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Management of sukragatavata with vidarighrita a comparative study w.s.r to premature ejaculation, by naik praveen laxman, Department of Kayachikitsa, Post graduate studies and research center D.G. …

Management of sukragatavata with vidarighrita a comparative study w.s.r to premature ejaculation, by naik praveen laxman, Department of Kayachikitsa, Post graduate studies and research center D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, Gadag - 582 103

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  • 1. “MANAGEMENT OF SUKRAGATAVATA WITH VIDARIGHRITA A COMPARATIVE STUDY W.S.R TO PREMATURE EJACULATION” By NAIK PRAVEEN LAXMAN Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore J In partial fulfillment of the degree of Ayurveda Vachaspati M.D. In Kayachikitsa Under the Guidance of Dr. Shiva Rama Prasad Kethamakka M.D. (Ayu) (Osm), C.O.P. (German) M.A., [Ph.D] (Jyotish) Department of KayachikitsaPost Graduate Studies & Research CenterD.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG 2007-20010
  • 2. D.G.M.AYURVEDIC MEDICAL COLLEGE POST GRADUATE STUDIES AND RESEARCH CENTER GADAG, 582 103This is to certify that the dissertation “MANAGEMENT OF SUKRAGATAVATA WITHVIDARIGHRITA A COMPARATIVE STUDY W.S.R TO PREMATURE EJACULATION” isa bonafide research work done by NAIK PRAVEEN LAXMAN in partial fulfillment of therequirement for the post graduation degree of “Ayurveda Vachaspati M.D. (Kayachikitsa)” UnderRajeev Gandhi University of Health Sciences, Bangalore, Karnataka. Date: Guide Place: Prof. Dr. Shiva Rama Prasad Kethamakka M.D. (Ayu) (Osm), C.O.P (German), M.A., [Ph.D] (Jyotish) Professor in Kayachikitsa DGMAMC, PGS&RC, Gadag
  • 3. J.S.V.V. SAMSTHE’S D.G.M.AYURVEDIC MEDICAL COLLEGE POST GRADUATE STUDIES AND RESEARCH CENTER GADAG, 582 103 Endorsement by the H.O.D, principal/ head of the institution This is to certify that the dissertation entitled “MANAGEMENT OF SUKRAGATAVATAWITH VIDARIGHRITA A COMPARATIVE STUDY W.S.R TO PREMATUREEJACULATION” is a bonafide research work done by NAIK PRAVEEN LAXMAN under theguidance of Prof. Dr. Shiva Rama Prasad Kethamakka, M.D. (Ayu) (Osm), C.O.P (German),M.A., [Ph.D] (Jyotish), Professor in Kayachikitsa in partial fulfillment of the requirement for the postgraduation degree of “Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajeev GandhiUniversity of Health Sciences, Bangalore, Karnataka.. Professor & HOD (Dr. G. B. Patil) Dept. of Kayachikitsa Principal, PGS&RC DGM Ayurvedic Medical College, Date: Gadag Place: Gadag Date: Place:
  • 4. Declaration by the candidate I here by declare that this dissertation / thesis entitled “MANAGEMENT OFSUKRAGATAVATA WITH VIDARIGHRITA A COMPARATIVE STUDY W.S.R TOPREMATURE EJACULATION” is a bonafide and genuine research work carried out by me underthe guidance of Prof. Dr. Shiva Rama Prasad Kethamakka, M.D. (Ayu) (Osm) M.A. (Jyotish),[Ph.D (Jyotish)], Professor in Kayachikitsa, DGMAMC, PGS&RC, Gadag.DatePlace NAIK PRAVEEN LAXMAN
  • 5. Copy right Declaration by the candidate I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall havethe rights to preserve, use and disseminate this dissertation/ thesis in print or electronic format for theacademic / research purpose.DatePlace NAIK PRAVEEN LAXMAN© Rajiv Gandhi University of Health Sciences, Karnataka
  • 6. Acknowledgement Any research is not an individual effort. It is a contributory effort of manyhearts, hands and heads. I am very much thankful to the subjects of this study. “Many hands make a work lighter”. I take this opportunity to mention mydeep gratitude to several personalities who have helped me in the successfulcompletion of this work. I am extremely happy to express my deepest sense of gratitude to my belovedand respected guide Prof. and H.O.D. Dr. K. Shiva Rama Prasad, M.D. C.O.P.(German), M.A. [Ph.D.], for his guidance and timely help. I am sincerely grateful to Dr. G. B. Patil, Principal, for his encouragement andproviding all necessary facilities for this research work. I extend my gratitude to Dr. R. V. Shettar for their kind support and co-operation in completing this work. I am extremely thankful to Dr. Madhav diggavi, for their support during myclinical trial and for their co-operation in completing my research work. I am thankful to Dr. P.V. Joshi for their co-operation in completing this work.I should be thankful to all my Teachers, senior and junior friends and all my batchmates for their co-operation. I express my deepest thankfulness whose names are nottaken here but helped me a lot along with my kith and kilns to my family members. Lastly I pay my deepest respect for those patients who took part in the studyand share my success with them. This work carries some sweet memories to express and record about somedistinguished personalities by whom I had been inspired during the course of thisstudy.
  • 7. My gratitude, which is the mother of all virtues and most capital of all duties,has all the order and diligence to all those who graciously involved in this venture ofmine. There is much greatness of mind in acknowledging a good turn, as in doing it. I humbly seek this opportunity to bow my head to the feet of the AlmightyLord Ganesh and Swami samartha for showering their blessings and empowering meto this eventful outcome without any impediments. My main inspires are – “My father who gave me wings and taught me to fly and My mother who gave me an open sky to fly” My deep senses of gratification to my inspirations of this study are my parentsShri Laxman. J. Naik and my mother Smt. Kasturi. L. NaikDate: Signature of the scholarPlace:]
  • 8. ABBREVATIONSAH. : Asthanga Hridaya Ke. : KelikutuhalamAg.Pu : Agnipurana Ke. Up. : Kena UpanisadaAr. : Anangaranga K.S. : Kashyapa SamhitaArun. : Arundatta Ks. : KamasutraAS. :Asthanga Samgraha M.N. : Madhav NidanaA.V. : Atharva Veda Na. : NagarsarvaswamaBH. : Bhela Samhita Ni. : NidanasthanaB.P. : Bhavaprakasha Pa. : PanchasayakaB.Pu. : Bramhapurana Pu. Kh. : PurvakhandaB.Up. : Bramha Upaniŝada Rm. : RatimanjariCa. : Caraka RR. : RatirahasyaCakra. : Chakrapani Rrp. :Rati Ratna PradipikaChi. : Chikitsasthana R.V. : Rig-VedaCh. Up. :Chandogya Upanisada Sd. : SmaradipikaDal. : Dalhana Sh. : SharirasthanaGang. : Gangadhara Sha. : Sharangadhara SamhitaG. Pu. : Garudapurana Si. : SiddhisthanaHam. Ni. : Hams raja Nidana Srdi. :Sringara-rasa-prabandha-dipikaHem. : Hemadri Ss : Suprajotpatti ShastramH.S. : Harita Samhita S. : SushrutaJej. : Jejjata Su. : SutrasthanaKa. : Kalpasthana TA. : Taitirya AranyakaK.Cu. :Kandarpa Chudamani Ut. : UttarasthanaUtt. : Uttaratantra V.S. : Vangasena SamhitaVi. : Vimanasthana V.Pu. : VishnupuranaYd. : Yashodara Y.R. : Yogaratnakara
  • 9. “Management of Shukragatavata with Vidari Ghrita a Comparative study w.s.r.to Premature Ejaculation”Key words: Premature ejaculation, Ghrita- Vidaryadi Ghrita Achievement of Scientific integrity and credibility of the concepts can only bewith well designed and conducted research studies. In Ayurveda Vata is explained aslife and vitality, supporter of the all embodied beings and sustain long life free ofdisorder1. Sukra is the terminal tissue element and nourishes of the supreme vitalessence2. Both concepts attained superior considerations in Ayurvedic classics.Shukragatavata is a clinical condition described under the gatatva concept of vata. The tread of sexuality is woven densely into the febric of human existence.The rich heritage of Indian Culture Considered “Kama” as one among thePurusharthas, the objective of life the concept of ‘Kama’ reveals that the recreationalaspect like enjoyment of pleasure is equally important to its procreation aspects. Anapparent disparity between the subjective sense of pleasure and objective performancewas always present. The American psychiatric association (APA) defines Premature ejaculationw.s.r.to Shukragatavata as persistent or recurrent ejaculation with minimal sexualstimulation or before upon or shortly after penetration and before the person wishesit3. A global prevalence of PE is of approximately 30% across all age group4. Ayurveda believes that the management of Prakupita Vata which leads toSukragatavata vis-à-vis. premature ejaculation includes Snehana Chikitsa5 such asSnehapana6 and Uttara basti, etc with Vata shamaka dravya7. The literary material is an ideal one to study the activities of Vata onPsychological Parlance8 to formulate suitable scales for assessment and to evaluate theefficacy of Ayurvedic treatment modalities. The present study was aimed with
  • 10. connectional and applied exploration of Shukragatavata in term of prematureejaculation. The chinta, shoka and bhaya etc considered as the hetu for Vata prakopa. ThePrakupita Vata enters into Shukradhatu and causes early ejaculation i.e.Shukragatavata16. It indicates involvement of Psychological factors in this Vyadhi17for the convenience this study after analyzing the signs and symptoms carefully saidby different authors it is concluded as simulating to Shukragatavata vis-à-vispremature ejaculation where the person unable to exert voluntary control over theejaculatory reflex, reaches orgasm very quickly once aroused18. Vidaryadi Ghrita mentioned by Bhavaprakasha19 said to be time tested yogacontains mainly vata shamaka20 and shukra stambhak dravyas. Vata specificallyApana Vata is a chief component of Shukra Pravruthi either for it’s normally orvitiation21. So the Vidarighrita is proposed various routes of administration. To checkthe efficacy of Vidarighrita from various routs for comparisons, the Abhyantara 22(internal) and Intra Penile Uttara basti (IPUV) is undertaken as the present clinicaltrial. So here an effort is made to compare the efficacy of Vidaryadi Ghrita by oraladministration and Uttara basti.
  • 11. Contents of “Management of Shukragatavata with Vidarighrita a Comparative study w.s.r.to Premature Ejaculation” By Naik Praveen LaxmanChapter Content Pages1 Introduction 1-142 Objectives 15-163 Literary Review 17-1894 Methods 190-2235 Results 224-2646 Discussion 265-2867 Conclusion 287-2888 Summary 289-2909 Bibliographic References I-XII10 Annex 1 – Master charts data of trial 1-1711 Annex 2 - Case sheet 1-712 List of Shloka 1
  • 12. List of Tables “Management of Shukragatavata with Vidarighrita a Comparative study w.s.r.to Premature Ejaculation”SL TITLE OF TABLE PAGE1 Physical properties of vata 452 Pathway of gati of individual components of vata 463 Adhishthana (sites) of gatadosha 48-494 Gatatva of pitta and kapha 505 Comparative analysis of dhatugatavyathi and dhatugatavata 536 Comparative analysis of avritavata and gatavata 567 Showing the Samprapti ghataka of Vata vyadhi 578 Physical properties of Shukra 619 Differences between Shukragatavata and Shukravritavata 8310 Showing the physical causes of PE 9811 Male Sexual response cycle 13312 DSM-IV Phases of sexual response cycle & associated sexual dysfunctions 13413 Showing Drug Review 167-17014 Vidaryadi Ghrita 24 gms as single dose with hot water before food at night 21815 26 Group – B: Uttara basti 21916 27 Investigations 22217 28 Assessment of Results a) Subjective Criteria 22218 29 b) Objective Criteria 22219 Grading for Variables used in study Subjective Criteria 22220 Grading for Variables used in study Objective Criteria 22321 showing the distribution of patient’s age group 22422 showing the distribution of patients according to sex 22523 showing distribution of patients by Religion 22624 showing distribution of patients by Economical status 22725 Showing distribution of patients by Occupation 22826 Showing distribution of patients by Vihara (Nature of work) 22927 Showing distribution of patients by Matra of ahara 23028 Showing distribution of patients by Kala of ahara 23129 Showing distribution of patients by Rasa 232
  • 13. 30 Showing distribution of patients Type of diet 23331 Showing distribution of patients by Vyasana 23332 Showing distribution of patients by Kula vrittanta 23433 Showing distribution of patients by Agni 23534 Showing distribution of patients by Kosta 23635 Showing distribution of patients by Nidra 23736 Showing distribution of patients by Vyayama Shakti 23837 Showing distribution of patients by Chief Complaints 23938 Showing distribution of patients by previous illness 24038 showing the distribution of patients according to Snana 24139 Showing distribution of patients by Undergarments 24140 showing the distribution of patients according to Development of 242 Secondary Sexual Character41 showing the distribution of patients according to Masturbation 24342 showing the distribution of patients according to First coital experience 24443 showing the distribution of patients according to Family sexual life 24544 showing the distribution of patient’s Family sexual life 24645 showing the distribution of patients according to Sexual act 24746 showing the distribution of patients according to fore play 24847 showing the distribution of patients according to Mano pareeksha 24948 showing the distribution of patients according to Dehaprakriti pareeksha 25049 showing the distribution of patients according to Manasika prakriti 25150 showing the distribution of patients according to Sara pareeksha 25251 showing the distribution of patients according to Sahanana pareeksha 25352 showing the distribution of patients according to Satmya pareeksha 25453 showing the distribution of patients according to Satwa pareeksha 25554 showing the distribution of patients according to Pramana pareeksha 25655 showing the distribution of patients according to Vyayama Shakti 257 pareeksha56 showing the distribution of patients according to Aharshakti pareeksha 25857 showing the distribution of patients according to Vaya pareeksha 25958 showing distribution of patients by Shukravaha sroto dusthi laxanas 26059 Showing the distribution of patients according to response 26160 Comparative Study of Group A and Group B after treatment Table -1 26261 Comparative Study of Group A and Group B after Follow up Table-1 263
  • 14. 62 Individual study of the Group A Table - 2 A 26363 Individual study of the Group B Table - 2 B 26464 Group – A Showing Demographic Data in Patients I65 Group –B Showing Demographic Data in Patients I66 78 Showing Chief complaints II67 Showing Previous illness II68 Kula Vrittanta II69 Nature of work wise distribution of 20 patients III69 Diet wise distribution of 20 patients III70 Agni wise distribution of 20 patients III71 Matra of ahara wise distribution of 20 patients IV72 Regularity in Timing of food wise distribution of 20 patients IV73 Rasa wise distribution of 20 patients IV74 Kostha wise distribution of 20 patients IV75 Snana wise distribution of 20 patients V76 Undergarments wise distribution of 20 patients V77 Vyasana wise distribution of 20 patients V78 Nidra wise distribution of 20 patients VI79 Vyayama wise distribution of 20 patients VI80 Development of Secondary Sexual Characters wise distribution of 20 pts VI81 Masturbation wise distribution of 20 patients VII82 First coital experience wise distribution of 20 patients VII83 Family sexual life wise distribution of 20 patients VII84 Sexual act wise distribution of 20 patients VIII85 Fore play wise distribution of 20 patients VIII86 Dashavidha Preeksha VIII87 Manasika prakriti wise distribution of 20 patients IX88 Sara pareeksha wise distribution of 20 patients IX89 Sahanana pareeksha wise distribution of 20 patients IX90 Satmya pareeksha wise distribution of 20 patients X91 Satwa pareeksha wise distribution of 20 patients X92 Pramana pareeksha wise distribution of 20 patients X93 Vyayama shakti wise distribution of 20 patients XI94 Aharshakti wise distribution of 20 patients XI95 Vaya pareeksha wise distribution of 20 patients XI
  • 15. 96 Mano pareeksha wise distribution of 20 patients XII97 Shukravaha sroto dusthi laxanas XII98 Subjective criteria - Group –A XII99 Subjective criteria - Group –B XIII100 Objective criteria - Group –A XIII101 Objective criteria - Group –B XIII
  • 16. List of Graph “Management of Shukragatavata with Vidarighrita a Comparative study w.s.r.to Premature Ejaculation”SL TITLE OF GRAPH PAGE1 showing the distribution of patient’s age group 2252 showing the distribution of patients according to sex 2263 showing distribution of patients by Religion 2274 showing distribution of patients by Economical status 2285 Showing distribution of patients by Occupation 2296 Showing distribution of patients by Vihara (Nature of work) 2307 Showing distribution of patients by Matra of ahara 2318 Showing distribution of patients by Kala of ahara 2319 Showing distribution of patients by Rasa 23210 Showing distribution of patients Type of diet 23311 Showing distribution of patients by Vyasana 23412 Showing distribution of patients by Kula vrittanta 23513 Showing distribution of patients by Agni 23614 Showing distribution of patients by Koshta 23715 Showing distribution of patients by Nidra 23816 Showing distribution of patients by Vyayama Shakti 23917 Showing distribution of patients by Chief Complaints 24018 Showing distribution of patients by previous illness 24119 showing the distribution of patients according to Snana 24220 Showing distribution of patients by Undergarments 243
  • 17. 21 showing the distribution of patients according to Development of 244 Secondary Sexual Character22 showing the distribution of patients according to Masturbation 24523 showing the distribution of patients according to First coital experience 24624 showing the distribution of patients according to Family sexual life 24725 showing the distribution of patients according to Sexual act 24726 showing the distribution of patients according to fore play 24827 showing the distribution of patients according to Mano pareeksha 24928 showing the distribution of patients according to Dehaprakriti 250 pareeksha29 showing the distribution of patients according to Manasika prakriti 25130 showing the distribution of patients according to Sara pareeksha 25231 showing the distribution of patients according to Sahanana pareeksha 25332 showing the distribution of patients according to Satmya pareeksha 25433 showing the distribution of patients according to Satwa pareeksha 25534 showing the distribution of patients according to Pramana pareeksha 25635 showing the distribution of patients according to Vyayama Shakti 257 pareeksha36 showing the distribution of patients according to Aharshakti pareeksha 25837 showing the distribution of patients according to Vaya pareeksha 25938 showing distribution of patients by Shukravaha sroto dusthi laxanas 26039 Showing the distribution of patients according to overall response 261
  • 18. List of Flow Chart “Management of Shukragatavata with Vidarighrita a Comparative study w.s.r.to Premature Ejaculation”SL TITLE OF FLOW CHART PAGE1 Etiological Factors of PE 822 The spectator effect of performance anxiety 1043 Shukragatavata Samprapti 1404 Management of Premature Ejaculation 1555 Vasti Dravya Pramana 183 Figures and Photos of “Management of Shukragatavata with Vidarighrita a Comparative study w.s.r.to Premature Ejaculation”SL TITLE OF FIGURES AND PHOTOS PAGE1 Reproductive system of the male 222 Foreskin 343 The sexual response cycle 1004 Ejaculation 1205 Physiology of Ejaculation 1286 Hypersensitivity in the glans 1357 Squeeze Technique 151
  • 19. Chapter – 1 IntroductionIntroduction of PE Shukragatavata is a clinical condition explained in Ayurvedic classics. It comes under thegatatva concept of vata characterized by a group of clinical presentations, which includeejaculatory as well as seminal impairments. Premature ejaculation – a psychosexual orgasmic disorder is dealt in Ayurveda underShukragatavata. The concepts of gatatva or Shukragatavata are not critically analyzed by eitherauthors or commentators of Ayurvedic classics. Research works on gatatva are few and exclusiveclinical trials on Shukragatavata or premature ejaculation were not done till now. Taking all theseinto consideration an exclusive research work were planned on the topic. The three major forms of male sexual dysfunction are ejaculatory dysfunction, erectiledysfunction (ED), and decreased libido. PE is the most prevalent male sexual dysfunction.Erectile dysfunction and decreased libido are less common 1. The World Health Organization(WHO) includes the right to sexual health among its fundamental rights for the individual. Thereshould be “a freedom from organic disorders, disease and deficiencies that interfere with sexualand reproductive freedom”. PE has been associated [2]With erosion in sexual self- confidence and low sexual satisfaction in men and their female [3]partners . Before the last decade, the major approach to treating PE was behavioral andpsychotherapy, relying on such techniques as the `pause and `squeeze methods 4, 5 PE and the co-occurrence of other sexual problems, particularly ED. About 30% of men with PE have co-occurring ED, which typically results in early ejaculation without full erection. A wide degree ofseverity is seen, with patients ejaculating on or prior to penetration in the most severe cases. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 1
  • 20. Ejaculation is the squirting out of semen from the penis during an orgasm. Problems withejaculating occur quite commonly and these include premature (early), delayed or absentejaculation. Other problems include unusual discharge, pain upon climax, or a dry ejaculation. Most men experience some form of erection or ejaculation problem during their lifetime.For example, around 3 out of 10 men have had a problem with premature ejaculation. Suchproblems often cause anxiety and self-doubt which can make the problem worse. Fears andworries can also lead to abstinence or a decrease in frequency of intercourse or masturbation;again aggravating the problem. Many ejaculation problems can be resolved with simple self-help techniques, but youshould see your doctor if you feel it is severe or on going. It is important to remember that theseproblems happen to a lot of men occasionally. Studies such as that by Dr Alfred Kinsey have found that 75% of men reach orgasmwithin two minutes of penetration, and that the average duration of a mans orgasm is 3-5 seconds.However, it is important to note that there is no rule defining how soon is too soon. Many men wonder if they last in bed as long as their partners would like them to last.They are afraid that women are not completely satisfied with their sexual abilities and that theirerection is not strong enough. Nobody knows what the ideal number of minutes that a man shouldmaintain his erection is. Specialists say that it depends on the couple’s sexual rhythm and on thepartner’s desire. There are many differences between couples and that is why it is very difficult toset some strict rules as far as the erection and the ejaculation are concerned. People say that the man’s performance is ok as long as he can maintain his erection untilthe woman reaches her orgasm. In other words, the sexual act is perfect when both partners cumtogether in the same time. When the man ejaculates without being able to give his partner anorgasm, we can talk about premature ejaculation. These kinds of problems are very frequentnowadays and the causes are many. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 2
  • 21. There are many types of premature ejaculation. You can call premature ejaculation thesituation when the man ejaculates before penetration. This happens often when the man is toosensitive and when he can’t control his emotions and his body. The simple idea of penetrating hispartner makes him ejaculate. There is also another type of premature ejaculation: the ejaculationthat happens after some minutes of penetration. Sometimes, this can be the result of thestimulation of the penis’s head or the result of a strong emotion. Unfortunately, premature erection is associated to sexual problems. You must know thata man who ejaculates fast is not necessarily sick. There are cases when the man suffers of sexualdysfunctions, but many times the premature ejaculation can be produced only by somepsychological problems. Moreover, specialists have noticed that lately more and more mensuffering of stress and anxiety face this problem of premature ejaculation. The stress influencesdirectly the sexual life. A stressed man becomes sometimes incapable to maintain his erection fora long time. The mind can’t control the penis anymore and that is why the premature ejaculationoccurs. Premature ejaculation (initialized as PE; also known as rapid ejaculation, rapid climax,premature climax, or early ejaculation) affects 25%-40% of men in the U.S. Other sex researchershave defined premature ejaculation as occurring if the man ejaculates within two minutes ofpenetration; however, a survey by Alfred Kinsey in the 1950s demonstrated that three quarters ofmen ejaculate within two minutes of penetration in over half of their sexual encounters. Selfreported surveys report up to 75% of men ejaculate within 10 minutes of penetration. Today,most sex therapists understand premature ejaculation as occurring when a lack of ejaculatorycontrol interferes with sexual or emotional well-being in one or both partners. Most men experience premature ejaculation at least once in their lives. Because there isgreat variability in both how long it takes men to ejaculate and how long both partners want sexto last, researchers have begun to form a quantitative definition of premature ejaculation. Currentevidence supports an average intra vaginal ejaculation latency time of six and a half minutes in “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 3
  • 22. 18-30 year olds.6 If the disorder is defined as an IELT percentile below 2.5, then prematureejaculation could be suggested by an IELT of less than about one and a halfminutes.7Nevertheless, it is well accepted that men with IELTs below 1.5 minutes could be"happy" with their performance and do not report a lack of control and therefore do not sufferfrom PE. On the other hand, a man with 2 minutes IELT may have the perception of poor controlover his ejaculation, distressed about his condition, has interpersonal difficulties and therefore bediagnosed with PE. To clarify, a male may reach climax after 8 minutes of sexual intercourse, but this is notpremature ejaculation if his partner regularly climaxes in 5 minutes and both are satisfied with thetiming. Another male might delay his ejaculation for a maximum of 20 minutes, yet he mayconsider this premature if his partner, even with foreplay, requires 35 minutes of stimulationbefore reaching climax. If intercourse is the method of sexual stimulation for the second exampleand the male climaxes after 20 minutes of intercourse and then loses his erection, satisfying hispartner (at least with intercourse), who needs 35 minutes to climax, is impossible. Because many females are unable to reach climax at all with vaginal intercourse (nomatter how prolonged), this situation may actually represent delayed orgasm in the female partnerrather than premature ejaculation in the male; the problem can be either or both, depending on thepoint of view. This high lights the importance of obtaining a thorough sexual history from thepatient (and preferably from the couple). Ayurveda mentions diet, sleep and Brahmacharya as the Tripods of life. Sex is a basicinstinct, but sexual behavior is a learned ability. Dharma, Artha, Kama and Moksha are amongthe four Purusharthas, objectives of life mentioned in Ayurveda. The achievement of each ofthese is the basic need of every individual. The concept of Kama reveals that the recreationalaspects like pleasure are equally important to its procreation aspects. An apparent disparitybetween the subjective sense of pleasure and objective performance is always present. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 4
  • 23. The topic of sex is often kept under wraps and talking openly about it in society isconsidered prohibited. Therefore the knowledge of the public in this regard remains insufficientdue to which misconceptions abound leading to unwarranted problems. The act of seminalejaculation, likewise, is poorly understood by most. Erotic films and literature depicting`bucketfuls of cum squirted several feet tend to confuse even the well informed. Magnesium is one of the elements present in human semen, and it is required forenzymes that act on phosphate containing substrates. A decrease in magnesium level will result inan increase of thromboxane A2 (TxA2), and this will lead to a rise in endothelial intracellularcalcium, and subsequently, a decline in nitric oxide (NO).8,9 Since NO is a vascular smooth-muscle-relaxing factor,(10) cavernosal smooth muscle contraction, resulting from decreased NO,may be a contributing factor to premature ejaculation. The magnesium ion has an essential role in enzyme activation in the body. It is knownthat seminal plasma magnesium in each person (> 70 mg/L) is much higher than its serum levels(17 mg/L to 24 mg/L).11 There is tremendous evidence that a long duration of physical effort inmen leads to a decrease in extra cellular magnesium due to a transient shift between extra cellularand intracellular magnesium components and a simultaneous increase in urinary excretion.12,13This transient hypomagnesaemia may be manifested by uncontrolled contractility of the malegenital tract, causing emission and ejaculation. The increase in male factor infertility in recent times is believed to be caused by alteredlifestyle, stressful living conditions, diverse pollutants, certain prescription and several nonprescription drugs, dietary toxins, and certain nutritional deficiencies.14-15 The causative factorsproduce many types of derangements that directly or indirectly cause various kinds sexualdysfunction. The remedy for male sexual dysfunction in modern medicine is limited. The fact remainsthat, other than correction of obstruction, infections, varicose, and certain endocrine “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 5
  • 24. abnormalities, in most cases there is practically no successful therapeutic measure for maleinfertility or erectile dysfunction except for surgical implants. The allopathic drugs used for erectile dysfunction are believed to produce side effectsand affect other physiological processes and, ultimately, general health. Ayurveda realized theproblem of male sexual dysfunction thousands of years ago and developed a separate specialty,namely, reproductive medicine (Vajeekarana). It realized, among other things, the role of thenervous system, cardiovascular system, and psychological aspects of fertility and male sexualperformance; it has also recommended an appropriate use of plant-based remedies, a properlifestyle, and nutritious diet for improving overall health and treating male infertility and erectiledysfunction. Over 600 plants are described in the original Ayurvedic compendia like Caraka Samhitaand Sushruta Samhita. The potential of Ayurvedic and other traditional medicinal plants in thedevelopment of invaluable standardized phyto medicines and allopathic type of drugs is great,particularly in the context of male sexual dysfunction. An attempt to review the Ayurvedic concepts of male sexual dysfunction and thepotential of Ayurvedic treatments for the same, with plant-based remedies as seen in the classicalAyurvedic treatises as well as in the modern practice. An attempt has also been made to reviewthe pharmacological and biochemical studies on the plants and plant products that are in use inAyurvedic therapy for problems in male reproduction. The need for more elaborate scientificinvestigations on the Ayurvedic therapy for male sexual dysfunction is emphasized.History of PE During the last century, premature ejaculation has been considered from both a medicaland a psychological view, often resulting in contrasting psychotherapeutic and drug treatmentapproaches. For a better understanding of the current debate regarding its etiology and treatment,it is important to consider the history of how clinicians thought about and treated prematureejaculation. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 6
  • 25. 16 17 Waldinger distinguishes four periods in the approach to and treatment of prematureejaculation.The First Period (1887–1917): Early Ejaculation 18 In 1887, Gross described the first case of early ejaculation in medical literature. A 19second report of von Krafft-Ebing followed in 1901. Although publications were rare, it isworth noting that during the first 30 years of its existence in the medical literature, earlyejaculation was viewed as an abnormal phenomenon but not significantly as a psychologicaldisturbance.The Second Period (1917–1950): Neurosis and Psychosomatic Disorder 20 In 1917, Abraham described early ejaculation as ejaculatio praecox and stated that itwas a symptom of a neurosis caused by unconscious conflicts. Treatment should consist of classicpsychoanalysis. On the other hand, some physicians stated that premature ejaculation was due toanatomical urological abnormalities, such as a too short foreskin frenulum or changes in theposterior urethra, which had to be treated with incision of the foreskin or electrocautery of theverumontanum. 21 In 1943, Schapiro argued that premature ejaculation was neither a pure psychologicalnor a pure somatic disorder, but a psychosomatic disturbance caused by a combination of apsychologically overanxious Male Ejaculation and Orgasmic Disorders 223 constitution and aweak ejaculatory system. Schapiro described two types of premature ejaculation, type B in whichearly ejaculation existed from the first intercourses and type A, which led to erectile dysfunction.Many years later, both types became distinguished as the primary (lifelong) and secondary(acquired) forms of premature ejaculation 22The Third Period (1950–1990): Learned Behavior The biological component of PE and therefore also drug treatment, advocated bySchapiro, was ignored by the majority of sexologists who advocated psychoanalytic treatment. 23This neglect became even more pronounced after Masters and Johnson claimed the high “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 7
  • 26. success rates of behavioral therapy in the form of the squeeze technique, an adaptation of the 24stop–start technique published by Semans in 1956. Masters and Johnson stated that men withpremature ejaculation had learned this rapidity behavior as a result of their rushed initialexperiences of sexual intercourse.Fourth Period (1990 to present): Neurobiology and Genetics Since the 1990s, there have been an increasing number of publications on the efficacy ofSSRIs, clomipramine, and topical anesthetic creams in delaying ejaculation. At the same time, in 251998, Waldinger postulated a new neurobiological view arguing that premature ejaculation isrelated to disturbance of serotonin (5-HT) receptors in specific areas of the central nervoussystem with a possible genetic vulnerability. 26 Really, in some genitourinary clinics in the UK, itappears that a predominance of men from Islamic/Muslim countries present with prematureejaculation.17 Men from the Indian subcontinent may present with the ‘Dhat’ syndrome, a culturebound symptom complex of pre-occupation with excessive loss of semen, weakness, fatigue,sleeplessness, palpitations and hypochondiasis. A number of psychodynamic theories have been suggested along with psychosocial andrelationship factors .Prevalence of PE Male sexual dysfunction is considered the most commonly experienced, affecting 27globally. In India no much survey are noted. MSD in American men suggest that as many asone third of all sexually active men suffer from PE. PE is the most frequently encountered sexualcomplaint of men and couples. This condition could have profound effects on the psychosexualrelationship of a couple, and in its most severe form can lead to secondary impotence or even tomale infertility. The prevalence of PE is difficult to determine. Nevertheless, it is typically cited as beingthe most common sexual dysfunction (Kaplan, 1974). There is extremely large range of estimatesof the current prevalence of PE in sexual health clinic samples. Malatesta and Adams (1984) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 8
  • 27. indicate that 60% of the men entering sex therapy did so with the presenting problem of PE. Morerecently, Metz et al (1997) concluded that PE is the most common male sexual dysfunction andempirical estimates range from 0% (Bhue et al., 1994; Catalan et al., 1992b) to 77% (Verma et al.(1998) across five studies. The highest estimate (77% Verma et al. 1998) is from a northernIndian population. If the estimate of Verma et al, (1998) is considered an outlier, a more accuraterange is 0% to 22%. The problem of sexual dysfunction in patients with chronic prostatitis and chronic pelvicpain syndrome is gaining interest. Recently, Liang et al (2004) reported that the prevalence ofpremature ejaculation and erectile dysfunction (49%) is greater in Chinese men with chronicprostatitis than it is in persons in the general population. They also showed that the developmentof sexual dysfunction in patients with chronic prostatitis is positively linked with the duration ofprostatitis. Screponi et al (2002) reported a high prevalence of chronic prostatitis in patients withpremature ejaculation, and Keltikangas-Ja¨rvinen et al (1981) reported a high incidence ofdecreased libido in patients with chronic prostatitis, and they also concluded that this syndromeshould be viewed as a psychosomatic disorder. Berghuis et al (1996) reported that chronicprostatitis reduced the frequency of sexual intercourse, and they concluded that depression andpsychological disturbances were common in patients with chronic prostatitis. Mehik et al (2001)reported that psychological difficulties are common in men with chronic prostatitis, and theseauthors showed that men with chronic prostatitis tend to be more nervous and meticulous thanmen without this disorder. They also reported that sexual disturbances and erectile dysfunctionare common in these men (43%). But in all of these reported papers, the prevalence rates ofsexual dysfunction were lower than in the present study (77.3%). A survey in American men,aged between 18 and 59 years, found that 31% admitted to PE occurring for at least one monthover the past 12 months. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 9
  • 28. A more detailed study in the UK of 5000 16–44-year-old men found that 11.7% said thatthey had experienced PE for at least one month in the past year, but only 2.7% had experiencedthe problem for at least six months in the past year, suggesting that the problem affects many mensome of the time. Data from a large observational study show overlapping distributions ofejaculation times in men, who subjectively had premature ejaculation compared with those whowere subjectively normal. A substantial number of men who do not have premature ejaculation have shortejaculation times and conversely some men who complain of premature ejaculation appear tohave long ejaculation times. This suggests that other features of premature ejaculation have to beconsidered, as well as time, i.e. degree of control and distress. In a study carried out at 186 Italian medical centers it was reported that out of 2,658 mensuffering from PE 569 men suffered from lifelong PE, 1,855 had acquired PE and 234 had PE.Men with PE were younger than those without, but after adjusting for concomitant erectiledysfunction the risk of PE significantly decreased with aging. Men more educated, or who hadexperienced a divorce had a slightly increased risk also, lifestyle and occupational status affectedthe risk of PE. Concerning medical history, a decreased risk of PE emerged in men with treateddiabetes and no association was found with hypertension, cardiopathy, hypercholesterolemia andperipheral or central neuropathy. With regards to medical history, the findings showed a protective effect of diabetes onthe risk of PE. It is well known that diabetic patients may develop failure of emission, both due toneuropathic changes of the sympathetic fibers innervating the bladder neck and due to aperistalsis of the vas deference. These changes act in opposition to the mechanism of PE, so itappears that diabetes gives a protective effect against such a condition. The exact prevalence, however, is unknown as this appeared difficult to determine.Although it has been estimated that as many as 36% of all men in the general populationexperience premature ejaculation, other estimates have been lower. For example, Gebhard and “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 10
  • 29. Johnson, from a reanalysis of the Kinsey data, determined that 4% of the men interviewedreported ejaculating within 1 min of intromission. The large differences in prevalence numbersare mainly due to the use of various and often totally different definitions of prematureejaculation that have been used. Only by the general use of an empirically defined definition andidentical tools to measure the ejaculation time, methodologically correct epidemiological studiescan provide reliable prevalence data. Such studies have not been performed yet. It has been reported as the most common sexual problem in men with prevalence ratesranging from 9% to 31 %. It has been shown that the prevalence of PE in patients younger than40 and older than 70 years is higher than 40% and less than 10%, respectively. Moreover, theassociation between PE and sexual function and satisfaction emphasizes clinical importance ofthis symptom.Prevalence of PE in the Global Study of Sexual Attitudes and Behaviors In a recent article, Nolazco et al. reported a high prevalence of sexual dysfunction amongArgentinean men28. The study analyzed 2,715 sexual health questionnaires completed by menattending a prostate awareness campaign. The results indicated a 28.3% prevalence of PE basedupon the very much in line with the results of the Global Study of Sexual Attitudes and Behaviors(GSSAB), which has surveyed the attitudes, beliefs, and overall health of people in sexualrelationships from 29 countries 29. The GSSAB collected data from more than 27,000 participants aged 40–80 years (13,882women and 13,618 men) via face-to-face and telephone interviews and self-completed mailedquestionnaires. The data have provided information on the prevalence of a number of sexualdysfunctions, as well as the treatment-seeking behavior of people who suffer these conditions.Notably, and in agreement with Nolazco et al., the GSSAB reported that the prevalence of PE inLatin America was 28.3%. Overall, although the GSSAB showed that approximately one-third ofall men may have PE, there were significant geographical differences. The lowest prevalence wasreported in the Middle East (12.4%), while the highest recorded prevalence occurred in Southeast “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 11
  • 30. Asia (30.5%). Importantly, the GSSAB assessed the prevalence of self reported PE by includingonly those patients who reported experiencing PE “sometimes” or “frequently.” Therefore, thesemen, who presented as self-diagnosed as PE sufferers, do not represent a population with atransient condition, but rather a cohort who have a chronic complaint that is often associated withsignificant quality-of-life issues for the couple.Factors Influencing Regional Variation in the Prevalence of PE Several well-established factors may account for the regional variation in the prevalenceof PE. For example, the popularity of circumcision in certain regions could affect the prevalenceof PE, as this procedure is associated with glans penis keratinization and desensitization 30. Thevariations may also partly reflect religious and cultural influences. For example, the attitudes to,and recognition of PE may be different among “puritan” Protestant and “liberal” Catholicpopulations, and it is interesting that in many demographic studies, Northern and SouthernEurope are considered as distinct entities. Additionally, the rates of PE are likely to be greater inthose regions where sex has special importance, such as East Asia which is heavily influenced bythe Tantra philosophy and in Central and South America, where sex is regarded as very importantand female sexuality is fully accepted. However, compared with Europe, the Middle East isrepresented by predominantly Muslim, patriarchal societies, where females occupy a lower socialposition. In these communities, PE may be viewed less as a medical condition than as a sign ofvirility. Studies from the United States have shown equivocal data on the association of ethnicitywith the prevalence of PE. The National Health and Social Life Survey (NHSLS) conducted in1992, surveyed 1,410 men between the ages of 18 and 59 years and found that the prevalence ofPE among Caucasian, black, and Hispanic men was 19%, 34%, and 27%, respectively. However,this finding of an apparently higher incidence among black men was not supported by a morerecent study that reported a corresponding prevalence of 16%, 21%, and 29% in Caucasians, 31blacks, and Hispanics, respectively However, this study was conducted in an older population “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 12
  • 31. (40– 80 years)., unlike ED the incidence of which increases with age, the prevalence of PE is not 32associated with age . Indeed, the prevalence is essentially constant over the 18–59 years agerange. This highlights the fact that, in contrast with ED, PE often occurs in younger individuals.This places a particular importance on the discovery of effective management strategies as PEoften occurs at a time when the instigation, development, and maintenance of relationships are acritical part of the life experience. Overall, the GSSAB found few definitive correlates for theprevalence of PE. For instance, a preliminary association between vascular disease and PE wasnegated after controlling for the simultaneous presence of ED—a likely consequence of confusionabout the two conditions among respondents. However, the GSSAB suggested that education isnegatively associated with PE. For instance, in Central/South America and the Middle East, menwith no college education were twice as likely to report PE [odds ratio or 2.3–2.6, P < 0.05 andOR 2.2–2.3, P <0.05, respectively], compared with men who had received “at least some college”education. Other factors associated with PE included financial problems, although this wasstatistically significant only in the Middle East (OR 1.8, P < 0.05) and, perhaps unsurprisingly, atrend for association of PE with infrequent sex.Frequency of PE Estimates of premature ejaculation in European countries and India mirror the prevalencein the US.8 The prevalence in other parts of Asia, Africa, Australia, and elsewhere is unknown.Anestimated 30%-70% of American males experience premature ejaculation. However, varioussurveys have shown that many men do not report premature ejaculation to their physician,possibly because of embarrassment or a feeling that no treatment is available for the problem.Some men might not even perceive premature ejaculation as a medical problem. Such survey datasuggest that the percentage of men who experience premature ejaculation at some point in theirlives is almost certainly more than the 30% reported in the NHSLS. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 13
  • 32. Purpose of the study Ayurveda being the ancient unique system of medicine aims not only curing butpreventing the disease too. Ayurveda stressed the treatments in two broad classifications such asShodhana and Shamana. The American psychiatric association (APA) defines Prematureejaculation w.s.r.to Shukragatavata as persistent or recurrent ejaculation with minimal sexualstimulation or before upon or shortly after penetration and before the person wishes it33. A globalprevalence of PE is of approximately 30% across all age group34. Ayurveda believes that the management of Prakupita Vata which leads to Sukragatavatavis-à-vis. premature ejaculation includes Snehana Chikitsa35 such as Snehapana36 and Uttara basti,etc with Vata shamaka dravya37. The literary material is an ideal one to study the activities ofVata on Psychological Parlance38 to formulate suitable scales for assessment and to evaluate theefficacy of Ayurvedic treatment modalities. The present study was aimed with connectional andapplied exploration of Shukragatavata in term of premature ejaculation. The chinta, shoka and bhaya etc considered as the hetu for Vata prakopa. The PrakupitaVata enters into shukradhatu and causes early ejaculation i.e. Shukragatavata39. It indicatesinvolvement of Psychological factors in this Vyadhi40 for the convenience this study afteranalyzing the signs and symptoms carefully said by different authors it is concluded as simulatingto shukragatavata vis-à-vis premature ejaculation where the person unable to exert voluntarycontrol over the ejaculatory reflex, reaches orgasm very quickly once aroused41. Vidaryadi Ghrita mentioned by Bhavaprakasha42 said to be time tested yoga containsmainly vata shamaka43 and shukra stambhak dravyas. Vata specifically Apana Vata is a chiefcomponent of Shukra Pravruthi either for it’s normally or vitiation44. So the Vidari Ghrita isproposed various routes of administration. To check the efficacy of Vidari Ghrita from various 45routs for comparisons, the Abhyantara (internal) and Intra Penile Uttara basti (IPUV) isundertaken as the present clinical trial. So here an effort is made to compare the efficacy of VidariGhrita by oral administration and Uttara basti. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r.to Premature Ejaculation” 14
  • 33. Chapter – 2 Objectives of the study Why this problem has been selected for Research work? There are certain specific reasons behind the selection of problem. Everybody wants tomarry and get child and “Sexceed” in his life. But all married couples do not enjoy the sexual lifetoo, many times orgasm is dream and is having high expectation of sexual life not fulfilled andcontinued after marriage with the same zeal or strength. Sex has its own importance in the busylife and all the young and old used to it is evident by market advertisements and sex pills likeViagra sales. Present study of Shukragatavata patients’ vis-à-vis PE and ED is selected to offersame ages old skilled practices of Ayurveda. Ayurveda is gaining a global popularity for its effective treatments especially inShukragatavata vis-à-vis PE as much are with sexual dissatisfaction and no satisfactorytreatments available contemporary. Inclination towards Ayurvedic treatment after the repeatedconsultations of contemporary managements is getting more. Vidaryadi Ghrita is classical herbal combination which is mentioned in Bhava Prakasha.Here Vidaryadi Ghrita is given as oral administration for Group – A and Vidaryadi Ghrita isadministered intra urethral (Uttar Basti) for Management of Shukragatavata with Vidarighrita aComparative study w.s.r. to Premature Ejaculation Therefore, there is a need for properunderstanding of such problems of the society through Ayurvedic perspectives and to find someeffective steps of management. The present research work has been planned with following aimsand objectives.Aims and objective of the study Shukragatavata is explained under gata vata concept in different classical texts. In thiscondition by the intake of vataprakopaka hetus at first vata becomes prakupita and enters in toshukravaha srotas, and causes early ejaculation of shukra. So in this condition mainly “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 15
  • 34. vatashamaka chikitsa like snehana is needed. As Vidaryadi Ghrita is mainly indicated forshukradusti, it is used for snehapana in this clinical trial. The procedure Uttara basti is consideredas a one of the best chikista for shukradusti. So Uttara basti with vidaryadi Ghrita is taken forclinical trial. 1. To evaluate the effect of Vidaryadi Ghrita internal in improving IELT (Intra-vaginal ejaculatory latency time) 2. To evaluate the effect of Vidarighrita Uttar basti in improving IELT 3. An observation of Vidarighrita (internally) over Shukragatavata. 4. An observation of Vidarighrita (Uttara basti) over Shukragatavata. 5. To compare the efficacy of Vidari Ghrita w.s.r.to. Above 1 to 4.Reasons to Choose Following Therapies for Present Study: Ayurveda believes that the management of Vata vyadhi, which are giving agony tobody and Manas, disability of functioning, burden for family, dissatisfaction in sexual life,depression due to premature ejaculation and erectile dysfunction. Considering these factorspresent study is undertaken to minimize the Disability, which is the typical nature of this disease.Here an attempt is estimated to make the sufferer free from clinical symptom. Vidaryadi Ghritamentioned in Bhava Prakasha said to be time tested. This Vidaryadi Ghrita contains mainly Vatashamaka dravays. Vata doshas is the main culprit to cause Shukragatavata, so Vidaryadi Ghrita isadministered orally in Group – A and Vidaryadi Ghrita is administered intra urethral (UttaraBasti) efficacy on Oral use and Uttara Basti effect is compared.Research question:Whether Local (Uttara Basti) or Oral medicine good at Shukramucchanti with the selectedVidaryadi Ghrita? The Hypothetical answer is –(1) Oral administration of VG will act as Vatahara (Apana) and Vrishya (Aphrodisiac).(2) VG administered Intra urethral (Uttara Basti) will act as Vatahara (Apana) and Vrishya(Aphrodisiac). “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 16
  • 35. Chapter – 3 Review of literatureHISTORICAL REVIEWThe Vedas The ancient most written treatise of knowledge are having plenty of references regardingthe different aspects of the present context. Three words are mainly used shukra, veerya and retasto denote male reproductive factor in Vedas. Though the word shukra is occasionally used todenote male factor for reproduction it is generally used to denote qualities such as deepta(bright)); nirmala (pure) shubhra, sveta and shukla (white)). Retas is considered as Sara (extract)of all dhatus The word retas has been widely used in the Vedic literature and it generally meant forreproduction. The word veerya is used in multiple references to implicate meaning as manlinessstrength), energy) and power. In the first chapter of Rigveda and 6th and 9th chapter ofAtharvaveda, veerya has been used as a synonym of retas. Different terminologies were used todenote impotency like mritbhaja, krisata and glayta. The sexual act is described in brief. No directreferences are found regarding the duration of sexual act in Vedic literature. Also there is nodescription found about the gatatva of vata.Bramhana and Upanisada Qualities of shukra and functions are described in Taittariya aranyaka. Two functions ofpenis have been mentioned as retosarjana (ejaculation) and mootravisarjana (micturition).Purana Daivavyapasraya method of virilification different medicines for improving potency andtheir different modalities of application are explained. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 17
  • 36. Upanisada He who desires that pregnancy should not take place through the coitus performance shallwith hold his breath so that the semen may not be discharged. This is a clear indication of methodof mental distraction to prevent ejaculation. Locations, properties and functions of vata have beenmentioned in detail Cala guna of vata has been highlighted in Candogyopanishad. Laghu, sita andatirooksha have been described as properties of vata dosha in Vishnupuranas. Vayu has also beensaid as a factor which emaciates the body. In the Sanskrit literature, plenty of references are available regarding the sexual act.Panini has mentioned in Ashtadhyayi about drugs which vitiates and alleviates vata. First timePaniny has coined the term vataki for disorders of vata dosha.Erotic literature As an art as well as science the different ancient Indian erotic literature deal with thevarious aspects of ‘kama’ (love and sex) along with its social, cultural and medicinal importance.Class of women with who sexual relation should be avoided is described .Descriptions of organsof the body of women to be stimulated during foreplay for better gratification according to thelunar cycle of progression and regression has been available. Classification of unions betweenmen and women on the basis of time of sexual act is made. According to this three types of sexualunions are present- short timed, (seeghra sambhava) moderate timed (madhyama sambhava) andlong timed (cira sambhava). Degree of arousal which varied from person to person according tothe stimulation (kriya) is described in three types – laghu (easily aroused), madhyama(moderately aroused), and cirodaya (late aroused). Likewise the speed of reaching orgasm in man and woman may be quick, medium orslow .However passionate he may be a man can remain indefinitely potent during intercourse ifhe directs his thoughts to rivers, woods, caves, and mountains or other pleasant places andproceeds gently and slowly. If he imagines a particularly nimble monkey signing on the branch ofa tree, he will not ejaculate even though his semen is already at the tip of the penis. Prohibited “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 18
  • 37. places for sexual act are described .The need of clitoral manipulation for satisfaction of thefemale partner is also described .A number of recipes for hastening the orgasm of the femalepartner in an intercourse are enlisted in different erotic classics. It is advised to do purushayita(female on top) to satisfy the curiosity of her lover, or her own desire or novelty .Kalyanamallaprescribed a number of recipes for the delaying of orgasm (shukra stambana) in man and for theperfection for the dalliance of love. The shukrakasharańa (ejaculation) is described as two types –syndana (oozing) and visrishti (forceful ejaculation). Syandana leads to moistening only butvisrishti along with coital friction leads to orgasm.Classical Ayurvedic LiteratureCaraka Samhita The detailed description of shukra is available in this prime classic. Shukra kshayalakshanas, Shukra pradoshaja vikaras different types of napumsaka, general nidanas of klaibyaspecific nidanas management etc are explained in detail. Caraka has given much importance toVajeekarańa which is justified by inclusion of one separate chapter with four ‘padas’ inchikitsasthana. Caraka has devoted a special chapter for explaining merits and demerits of vata(vatakalakaleeya. The chapter is an ideal example of symposium held in ancient days and thesummary of the proceeding is given nicely. Apart from the properties, locations and functionsvitiated symptoms are detailed in different chapters. Gatatwa concept of vata is presented in thechikitsasthana – 28th chapter and in this Shukragatavata lakshanas and treatments are suggested.Susruta Samhita Susruta also explained the shukra and its disorders in detail. He attributed the propertiesof dhairya, cyavana and preeti to the shukradhatu. Different shukradushti lakshanas and theirtreatments are explained. The vitiation of vyana and apana are explained as responsible for theshukradosha. Shukragatavata laksanas and treatments are described. But no description regardingshukravrta vata is available in Susruta samhita. Susruta explained vajeekarana yogas in excellent “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 19
  • 38. descriptions regarding madhutailaka basti is present in the 38th chapter of chikitsasthana. Susrutaexplained vata vyadhi in the first chapter of nidana.Ashtanga Samgraha and Ashtanga Hridaya Vriddha Vagbhata compiled the detailed description of shukra from Caraka and Susrutaand regularly formatted. The gatatva of pitta and kapha is only described by Vriddha Vagbhata.The detailed explanations of the functions of the individual components of vata are present in thedosha bhedeeya chapter of sutrasthana. Ashtanga Hridaya contains more or less same descriptionsof Ashtanga Samgraha.Other classical texts Four types of klaibya have been described along with scattered references of vajeekaranain the available Bhelasamhita. Kasyapa samhita also contains different references like shukradoshas indication of lasuna in kshayavastha etc. The description of vata is explained in.Medieval and post medieval Ayurvedic literatureMadhavanidana 22nd chapter of Madhavanidana deals with the vata vyadhinidana. Shukragatavatalakshanas were explained in it. Madhavacharya has followed Caraka in the descriptions.Sarngadhara Samhita Acharya Sarangadhara has made certain distinct advances in the field by dividing thedrugs acting on shukra as shukrala, shukra pravartaka, shukra rechaka, and shukrastambhaka andshukra soshaka. Jateephala is exampled as shukra stambaka.Bhavaprakasa Seven types of klaibya are explained in the Bhavaprakasa along with their management.Bhavaprakasa discussed vata vyadhi in 24th chapter of Madhyasama khanda in which the gatatvaof vata is also explained. Apart from the above the different shukra stambhana yogas are explained in Cakradatta(vajeekaranadhikara). In Yogaratnakara detailed etiology, pathology and types of klaibya are “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 20
  • 39. explained with numerous vajeekarana yogas. Rasa dhatugata vata has been mentioned only byyogaratnakara. Shukragata vata lakshanas were mentioned under the vata vyadhi adhikara ofHamsaraja nidana .Previous Research Literature Around hundred thesis works were conducted all over India at P.G. and Ph.D. levels onshukra, vajeekarana and similar aspects. Very few works have been conducted to explore theconcept of gatatva of vata. Many of the works on gatatva were dealt with asthigata or sandhigatavata. No work has been carried out on Shukragatavata till now. One research work has beenconducted on premature ejaculation with special reference to shukravaha srotas in the disciplineof fundamental principles. Clinical research works on sexual dysfunctions were dealt in generalunder the heading of ‘klaibya’. But exclusive clinical works on Premature Ejaculation were notconducted. Analyzing the different source material it can be concluded that even though the conceptof gatatva has been explained in different classical and other textbooks, it has not been elaboratedmuch, particularly regarding the process and features of gatatva compared with other pathology.The clinical research works on gatatwa concept of vata are few. Shukragatavata has not beenstudied yet. Exclusive clinical research works in this regard has also not been conducted yet. A critical review of the Ayurvedic literature showed that the concept of shukra AvritaVata had not yet been clarified by either the Acharyas or the commentators. No research workhad been done on this topic. Premature ejaculation too remains an incompletely understooddisorder in modern medicine as well. In the context of Ayurveda Premature ejaculation remainsincompletely researched with only three research works performed on it by M. D. Patel et al.,1990, P Manglasseri et. al., 2002 and Dr. Basil Cardozo et al., 2006 at Jamnagar. The different drug trials on Premature Ejaculation were aimed to klaibya in general,without considering the disease in specific (vyadhi pratyaneeka); probably due to the same, theresults were inconsistent. Modern research findings established a better efficacy in the “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 21
  • 40. management of Premature Ejaculation with sex therapy (Masters and Johnson, 1970) which ispractically rarely possible in an Indian community. Ayurveda one of the medical system still achoice of all strata of society has a lot to contribute in this regard.As the problem is having an established psychological base in its causation, the efficacy ofAyurvedic drugs and treatment modalities have to be compared with keeping psychologicalcounseling as uniform control. The medication should possess vrishya, balya, Madhya andshukrastambhaka properties on considering different pathological aspects of Shukragatavata i.e.Premature Ejaculation.THE REPRODUCTIVE SYSTEM OF THE MALE Figure no 01 .the reproductive system of male The male genital organs include the testes, epididymes, deferent and ejaculatory ductsand penis, with the accessory glandular structures; seminal vesicles, prostate and bulbo-urethralgland. The spermatic externally in a cutaneous - muscular pouch the scrotum.1) Penis It conducts urine to the exterior and introduces semen into the female vagina duringintercourse. The penis, the male copulatory organ, comprises an attached radix or root in theperineum and a free, normally pendulous corpus or body completely enveloped in skin. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 22
  • 41. A) Root of penis The root of the penis is situated in superficial perineal pouch. It is composed of threemasses of erectile tissue, namely the two crura and one bulb.a) Crura penis Each crus is firmly attached to the margins of the pubic arch, and is covered by theischiocavenosus.b) Bulb Penis The bulb is attached to the perineal membrane in between the two crura. It is covered bythe bulbospongiosus. Its deep surface is pierced (above its centre) by the urethra, which traversesits substance to reach the corpus spongiosum (located in the body).This part of the urethra (withinin the bulb) show a dilation in its floor, called the intrabulbar fossa.B) Body of penis The free portion of the penis is completely enveloped by skin. It is continuous with theroot in front of the lower part of the bubic symphysis. It is composed of three elongated masses oferectile. During erection of the penis these masses become engorged with blood leading toconsiderable enlargement. These masses are the right and left corpora cavernosa, and a mediancorpus spongiosum. The penis has a ventral surface that faces backwards and downwards, and a dorsal surfacethat faces forwards and upwards. The two corpora cavernosa are the forward continuation of the crura. They are in closeapposition with each other throughout their length. The corpora cavernosa do not reach the end ofthe penis. Each of them terminates under cover of the glans penis in a blunt conical extremity.They are surrounded by a strong fibrous envelope called the tunica albuginea has superficiallongitudinal fibres enclosing both the corpora, and deep circular fibres that enclose each corpusseparately, and also form a median septum. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 23
  • 42. The corpus spongiosum is the forward continuation of the bulb of the penis. Its terminalpart is expanded to form a conical enlargement, called the glans penis. Throughout its wholelength it is traversed by the urethra. Like the corpora, it is also surrounded by a fibrous sheath. Its base has a projecting corona glandis, overhanging an obliquely grooved neck of thepenis. The navicular fossa of the urethra is in the glans and opens by a sagittal slit on or near itsapex. The skin covering the penis is very thin and dark in colour. It is loosely connected withthe fascial sheath of the organs. At the neck it is folded to form the prepuce or foreskin whichcovers the glans to a varying extent and can be retracted backwards to expose the glans. On theundersurface of the glans there is a median fold of skin called the frenulum. The potential spacebetween the glans and the prepuce is known as the preputial sac. On the corona glandis and on theneck of the penis there are numerous small preputial (sebaceous) glands which secrete asebaceous (waxy) material called the smegma, which collects in the preputial sac 46. Unfortunately, smegma can be an excellent source for bacteria. Mild inflammation andinfections in this region are common, especially if the area is not washed thoroughly andfrequently. One way of avoiding trouble is to perform a circumcision, surgical removal of theprepuce. In Western societies (especially the United States), this procedure is generally performedshortly after birth. Although the practice of circumcision remains controversial, strong religiousand cultural biases and epidemiological evidence (Uncircumcised male have a higher incidence ofurinary tract infections and are at a greater risk of developing penile cancer than are circumcisedmale) suggest that it will continue 47. The superficial fascia of the penis consists of very loosely arranged areolar tissue,completely devoid of fat. It may contain a few muscle fibres. It is continuous with themembranous layer of superficial fascia of the abdomen (above) and of the perineum (below). Itcontains the superficial dorsal vein of the penis. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 24
  • 43. The deepest layer of superficial fascia is membranous and is called the fascia of the penis(deep fascia of the penis, or Bucks fascia). It surrounds all three masses of erectile tissue, but doesnot extend into the glans. In resting state, the arterial branches are constricted, and the muscularpartitions are tense. This combination restricts blood flow into the erectile tissue. Theparasympathetic innervation’s of the penile arteries involves neurons that release nitric oxide(NO) at their synaptic knobs. The smooth muscles in the arterial walls relax when NO is released.Deep to it there are the deep dorsal veins, the dorsal arteries and dorsal nerves of the penis.Proximally it is continuous with the dartos and with the fascia of the urogenital triangle. The supports of body of penis are: 1) The fundiform ligament which extends downwards from the linea Alba and splits to enclose the penis. It lies superficial to the suspensory ligament. 2) The suspensory ligament lies deep to the fundiform ligament. It extends from the pubic symphysis and blends below with the fascia on each side of the penis.Arteries of the penisA) The internal pudendal artery gives off three branches which supply the penis. 1) The deep artery of the penis runs in the corpus cavernosum. It breaks up into arteries that follow a spiral course and are, therefore, called helicine arteries. 2) The dorsal artery of the penis runs on the dorsum deep to the deep fascia, and Supplies the glans penis and the distal part of the corpus spongiosum, the prepuce and the frenulum. 3) The artery of the bulb of the penis supplies the bulb and the proximal half of the corpus spongiosum.B) The femoral artery gives off the superficial external pudendal artery which supplies the skinand fasciae of the penis. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 25
  • 44. Veins of the penis 1) The superficial dorsal vein lies in the superficial fascia. It divides into right and left branches which drain into superficial external pudendal veins. 2) The deep dorsal vein lies subjacent to the deep fascia. At its proximal end it passes through the gap between the perineal membrane and the pubic symphysis, and drain into the prostatic plexus of veins. Other veins draining the penis correspond to the arteries. 3) Nerve supply of penisThese come from the second, third and fourth sacral spinal segments via the pudendal nerve andpelvic plexuses. On the glans and bulb of penis some cutaneous filaments connect with lamellatecorpuscles and many end in characteristic end bulbs 48.Lymphatic Drainage Lymphatic from the glans drain into the deep inguinal nodes (glands of cloquet)Lymphatics from the rest of the penis drain into the superficial inguinal lymph nodes.Mechanism of Erection of the Penis Erection of the penis is a purely vascular phenomenon. The turgidity of the penis duringits erection is contributed to by the following factors. 1) Dilatation of the helicine arteries pours an increased amount of arterial blood into the cavernous spaces of the corpora cavernosa. Blood is also poured into the corpus spongiosum and into the glans by their arteries. As the spaces within the erectile tissue fill up the penis enlarges. 2) This enlargement presses on the veins preventing outflow of blood through them. Contraction of the ischo - cavernosus muscles probably has the same effect. 3) Expansion of the corpora cavernosa, and to a lesser extent of the corpus spongiosum, stretches the deep fascia. This restricts enlargement of the penis. Further flow of blood increases the pressure within the erectile tissue and leads to rigidity of the penis. 4) Erection is controlled by parasympathetic nerves (Nervi erigentes, S2, 3, 4). “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 26
  • 45. Function of male reproductive system As in the female, the male reproductive organs are stimulated by the gonadotrophichormones from the anterior lobe of the pituitary gland. The follicle stimulating hormone stimulates the seminiferous tubules of the testes toproduce male germ cell, the spermatozoa. The spermatozoa pass through the epididymis, deferent duct, seminal vesicle, ejaculatoryduct and the urethra to be implanted in the female vagina during coitus. In the epididymis and deferent duct the spermatozoa become more mature and arecapable of independent consists of 2 to 5 ml of semen containing 40 to 100 million spermatozoaper ml. If they are not ejaculated, spermatozoa are reabsorbed by the seminiferous tubules. Thestored spermatozoa can retain their fertility for several months. During ejaculation the muscle inthe walls of the deferent duct contracts, propelling the spermatozoa towards the urethra. Successful spermatogenesis takes place at a temperature about 3oC lower than normalbody temperature. This lower temperature is possible because the testes in the scrotum arecovered by only a thin layer of tissue containing very little fat. Semen is the fluid ejaculated from the urethra during coitus. It consists of 1) Spermatozoa 2) A viscid fluid which is secreted by the seminal vesicles and facilitates motility and contains the sugar fructose that helps to nourish the spermatozoa. 3) A thin lubricating fluid produced by the prostate gland 4) Mucus secreted by glands in the lining membrane of the urethra. 49FUNCTIONAL ANATOMY OF PENIS Before approaching to the pathological aspects it is essential to know the physio-anatomical aspects for the better understanding of the disease. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 27
  • 46. 2) SCROTUM The scrotum is a cutaneous bag containing the right and left testis, the epididymis and thelower part of the spermatic cord. (The spermatic cord is composed of arteries, veins, lymphatics,nerves, and the excretory duct of the testis. These structures are connected together by areolartissue). The scrotum skin is very thin of brownish colour and often thrown into fold or rugae. The Testes (two egg-shaped structures) remain in the Scrotum, outside the body, wherethe temperature is about 3O C Cooler than the body internal temperature (270 C. Spermdevelopment in the Testes Requires the Lower Temperature). Externally, the scrotum is divided into right and left parts by a ridge or raphe which iscontinued forwards on to the undersurface of the penis and backwards along the midline of theperineum to the anus. 1) The left half of the scrotum hangs lower than the right (in correspondence with the greater length of the left spermatic cord) it is also contains numerous sweat glands, pigment cells and nerve endings. 2) Under the influence of cold, and in young and robust persons, the scrotum is short, corrugated and closely applied to the testis. This is due to contraction of the subcutaneous muscle of the scrotum, called the dartos. However, under the influence of warmth, and in cold and debilitated persons, the scrotumis elongated and flaccid due to relaxation of the dartos. From this it appears that the dartos musclehelps in regulation of the temperature within the scrotum.Layers of the scrotum 1) Skin 2) dartos muscle (which replaces the superficial fascia) 3) The external spermatic fascia 4) The cremasteric fascia 5) The internal spermatic fascia. The dartos muscle is prolonged into a median vertical septum between the two halves ofthe scrotum. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 28
  • 47. Blood supplyThe scrotum is supplied by the following arteries 1) Superficial external pudendal 2) Deep external pudendal 3) Scrotal branches of internal pudendal 4) Cremasteric branch of inferior epigastric.Nerve supply The anterior one third of the scrotum is supplied by segment L1 of the spinal cordthrough the ilioinguinal nerve and the genital branch of the genitofemoral nerve. The posterior two thirds of the scrotum are supplied by segment S3 of the spinal cordthrough the posterior scrotal branches of the pudendal nerve, and the perineal branch of theposterior cutaneous nerve of the thigh. The areas supplied by segments L1 and S3 are separatedby the ventral axial line. The dartos muscle is involuntary and is supplied by sympathetic fibres passing throughthe genital branch of the genitofemoral nerve.Applied anatomy 1) Due to laxity of the skin and its dependent position the scrotum is a common site for oedema. Abundance of hair and of sebaceous glands also makes it a site of sebaceous cysts. 2) The common cause of scrotal swelling is complete inguinal hernia and hydrocele. Hydrocele is a condition in which fluid accumulates in the cavity of the tunica vaginalis testis. 3) As the scrotum is supplied by widely separated dermatomes (L1, S3) spinal anesthesia of the whole scrotum is difficult to achieve. 4) Elephantiasis may involve the scrotum, when the skin and subcutaneous tissue may become hypertrophied to grotesque dimensions. It may also be affected by fungal infections and allergic reactions. 5) The scrotum is bifid in male pseudoherma phroditism. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 29
  • 48. 3) Testes The testis, the primary reproductive organs or gonads in the male and are the equivalentof the ovaries in the female. It is suspended in the scrotum by scrotal tissues including the non –striated dartos muscle and the spermatic cord, the left testis usually being about 1cm lower thanthe right. The testis is oval in shape, and is compressed from side to side. It is 4.5cm long, 2.5cmwide and 3cm thick. An adult testis weights about 10 to 15 g.External Features 1) Two pole (ends), upper and lower pole 2) Two border, anterior and posterior border 3) Two surface, medial and lateral surface. The upper and lower poles are convex and smooth. The upper pole provides attachment to thespermatic cord. The anterior border is convex and smooth, and is fully covered by the tunica vaginalis. Theposterior border is straight, and is only partially covered by the tunica vaginalis. The epididymislies along the lateral part of the posterior border. The lateral part of the epididymis is separatedfrom the testis by an extension of the cavity of the tunica vaginalis. This extension is called thesinus of the epididymis. The medial and lateral surfaces are convex and smooth.Attached to the upper pole of the testis, there is a small oval body called the appendix of thetestis. It is a remnant of the paramesonephric duct.Coverings of the Testis The testis is covered by three coats. From outside to inside, these are the tunica vaginalis,the tunica albuginea and the tunica vasculosa. The tunica vaginalis is the outer covering of the testes and is a down growth of theabdominal and pelvic peritoneum. During early fetal life the testes develop in the lumbar regionof the abdominal cavity just below the kidneys. They then descend into the scrotum taking with “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 30
  • 49. them coverings of peritoneum, blood and lymph vessels, nerves and the deferent duct. Theperitoneum eventually surrounds the testes in the scrotum, becoming detached from theabdominal peritoneum. Descent of the testes into the scrotum should be complete by the 8thmonth of fetal life. The tunica albuginea is a dense, white fibrous coat covering the testis all around. It iscovered by the visceral layer of the tunica vaginalis, except posterior where the testicular vesselsand nerves enter the gland. The posterior border of the tunica albuginea is thickened to form anincomplete vertical septum, called the mediastinum testis, which is wider above than below.Numerous septa extend from the mediastinum to the inner surface of the tunica albuginea. Theyincompletely divide the testis into 200 to 300 lobules. The tunica vasculosa is the innermost, vascular coat of the testis lining its lobules.Structure of the testis In each testis there are 200 to 300 lobules and within each lobule there are 1 to 4convoluted loops composed of germinal epithelial cells, called seminiferous tubules. Between thetubules there are groups of interstitial cells (of Leydig) that secrete of the hormone testosteroneafter puberty. At the upper pole of the testis the tubules combine to from a single tortuous tubule,the epididymis, which leaves the scrotum as the deferent duct (vas deferens) in the spermaticcord. Blood and lymph vessels pass to the testes in the spermatic cords.Arterial supply The testicular artery is a branch of the abdomen aorta given off at the level of vertebraL2. It descends on the posterior abdominal wall to reach the deep inguinal ring where it enters thespermatic cord. At the posterior border of the testis it divides into branches. Some small branchesenter the posterior border, while larger branch (medial and lateral) pierce the tunica albuginea andrun on the surface of the testis to ramify in the tunica vasculosa. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 31
  • 50. Nerve supply The testis is supplied by sympathetic nerves arising from segment T10 of the spinal cord.They pass through the renal and aortic plexuses. The nerves are both afferent (for testicularsensation) and efferent (vasomotor).Epididymis The epididymis lies along the posterior border of the testis. It is firm and can be feltthrough the skin of the scrotum. The epididymis consists of a tubule almost 7 meters (23 ft) long,coiled and twisted so as to take up very little space. The epididymis is a mass made up highly coiled tubes that act as reservoirs ofspermatozoa. Its upper end is called the head. The head is enlarged and is connected to the upperpole of the testis by efferent ductless. The middle part is called the body. The lower part is calledthe tail. The head is made up of highly coiled efferent ductless. The body and tail are made up ofa single duct, the duct of the epididymis which is highly coiled on it self. At the lower end of thetail this duct becomes continuous with the ductus deferens.Vessels and Nerves The epididymis is supplied by the testicular artery through a branch which anastomoseswith the tiny artery to the ductus deferens. The venous and lymphatic drainage are similar tothose of the testis. Like the testis the epididymis is supplied by sympathetic nerves through thetesticular plexus the fibres of which are derived from segments T11 to L1 of the spinal cord.5) Spermatic cordThere are two spermatic cords, one leading from each testis, consists of; 1 Testicular artery 1 Testicular venous plexus Lymph vessels 1 Deferent duct (vas deferens) Nerves “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 32
  • 51. The spermatic cord suspends the testis in the scrotum. It is composed of blood and lymphvessels, nerves and a deferent duct within a sheath of fibrous and connective tissue and smoothmuscle. It passes through the inguinal canal. At the deep inguinal ring the structure within thecord diverges. The testicular artery branches from the abdominal aorta, just below the renal arteries. The testicular vein passes into the abdominal cavity. The left vein opens into the left renal vein and the right into the inferior vena cava. The lymph drainage is through lymph nodes around the aorta. The deferent duct is some 45 cm long. It passes upwards from the testis through the inguinal canal and ascends medially towards the posterior wall of the bladder where it is joined by the duct from the seminal vesicle to form the ejaculatory duct. The nerve supply is provided by branches from the 10th and 11th thoracic nerves.Seminal vesicles The seminal vesicles are two small fibro muscular pouches lined with columnarepithelium, lying on the posterior aspect of the bladder. At its lower end each seminal vesicle opens into a short duct which joins with thecorresponding deferent duct to form an ejaculatory duct. They secrete and expel a viscous fluidthat helps to keep the spermatozoa alive.Ejaculatory ducts The ejaculatory ducts are two tubes about 2 cm long, each formed by the union of theduct from a seminal vesicle and a deferent duct. They pass through the prostate gland and join theprostatic urethra, carrying seminal fluid and spermatozoa to the urethra. The ejaculatory ducts arecomposed of the same layer of tissue as the seminal vesicles.Prostate gland The prostate gland lies in the pelvic cavity in front of the rectum and behind thesymphysis pubis, surrounding the first part of the urethra. It consists of an outer fibrous covering,a layer of smooth muscle and glandular substance composed of columnar epithelial cell. Itsecretes a thin lubricating fluid that passes into the urethra through numerous ducts. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 33
  • 52. AYURVEDIC VIEWUpastha In Ayurveda upastha is the term used for penis having the synonyms like Sepha, Sisna,Medhra, Dhvaja etc. Its normal length is 6 Angula and circumference is 5 Angula It is made up ofone Sevani and one Pesi thus having two muscles in total. In modern anatomy three muscles areconsidered, Susruta may have taken two corpora cavernosa as one Pesi. The consideration of upastha as Karmendriya shows its importance. Further the functionAnanda i.e pleasure attributed to it indicates its psychological importance also in parlance to otherKarmendriyas. According to the size of the penis Vatsayana has classified males into 3 types Sasha(Rabbit), Vrisha (Ox) and Ashva (Horse). Its main use is to impregnate women(Garbhadhanakarma), to void urine and ejaculate semenVrishana (Mushka) Vrshana, mushka, phala and anda are the synonyms used for representing testes in theAyurvedic classics. The derivation of the word vrshana as follows -vrshati anena iti -meansshowering of shukra. It has an oval shape as that of an egg, so known as a, and due tocontainment of numerous seeds named as phala. Vrishna are two in number embryologicallyoriginated from prasada of mamsa, rakta, and kaphaand meda. They are suspended outside thebody within a sac behind the penis and between the two thighs Vrshana is also considered moolaof shukra vaha srotas.Foreskin Figure no.2 Foreskin “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 34
  • 53. Sexual Effects of Circumcision There is considerable controversy over the sexual effects of circumcision. Anti-circumcision groups claim significant detrimental effects, though offer only anecdotal evidence.Sexual Function 50, 51, 52 Three prospective studies have investigated effects of circumcision Fink et alreported: "Adult circumcision appears to result in worsened erectile function (p = 0.01),decreased penile sensitivity (p = 0.08), no change in sexual activity (p = 0.22) and improvedsatisfaction (p = 0.04)."Erectile Function None of the other studies confirmed the finding of worsened erectile function, and it ispossible that this may reflect the consequences of aging rather than circumcision. Indeed,Laumann et al reported that circumcised men exhibit less erectile dysfunction than uncircumcisedmen, particularly amongst older males.Penile Sensitivity As Fink et al noted the finding of decreased sensitivity "bordered on statisticalsignificance" Confusingly, the scoring for sensitivity included time required to orgasm, includingcomplaints of premature ejaculation. Senkul et al reported an increase in time required to orgasmfollowing circumcision. Laumann et al found that uncircumcised men were more likely toexperience premature ejaculation. It is widely believed that the glans penis keratinises (cornifies) following circumcision,and this causes desensitization. However, Szabo and Short examined this issue in 2000, andfound no difference in level of keratinisation between circumcised and uncircumcised men.Masters and Johnson, in a 1966 investigation found no difference in glans sensitivity betweencircumcised and uncircumcised men. Bleustein et al confirmed this finding in a thorough 2003investigation. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 35
  • 54. Taylor et al reported indirect evidence suggesting a sensory role for the foreskin though ithas not been demonstrated that this is associated with increased sexual pleasure. 53, 54Sexual Activity While Fink et al noted no change in sexual activity; Laumann et al noted that circumcisedmen enjoy a greater variety of sexual practices. Williamson and Williamson investigated womens preferences in sexual partners. 71%preferred circumcised partners for sexual intercourse, 83% for giving fellatio and 75% for givingmanual stimulation. When asked for the reason for their preference, 92% responded that thecircumcised penis stays cleaner, 90% that it looks sexier and 85% that it feels nicer to touch. Kebaabetswe et al found that in the generally non-circumcising Botswana, 50% ofwomen preferred a circumcised penis (43% had no preference or were unsure). After aninformational session, this figure rose to 79%. Echoing this, Bailey et al found that 62% ofwomen in the non-circumcising Luo tribe would prefer a circumcised partner. 90% said it waseasier for circumcised men to keep clean. Both men and women believe that being circumcisedmade sex more pleasurable. Another survey, by OHara and OHara, that found opposing results55 has been criticizedfor surveying female members of an anti-circumcision organization, and is probably notrepresentative of the wider population. 56The penis and foreskin Preputial anatomy and sexual functionMusculature The prepuce has a sheath of smooth muscle tissue inside the skin which is called theperipenic muscle.57,58 The muscle fibers are arranged in a coil at the end of the foreskin to form asphincter. The muscle fibers keep the foreskin closely against the glans penis.59Skin and mucosa The outer surface of the prepuce is skin; however the inner surface is mucosal membranealthough it resembles skin in appearance. There is a muco-cutaneous boundary just inside the tip “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 36
  • 55. of the prepuce. The prepuce normally covers the glans penis and protects it from foreign matter,friction, drying, and injury.Sub-preputial moisture The sub-preputial area is normally slightly moist. Taylor et al. reported finding no sweator sebaceous glands however, Fleiss et al. reported apocrine glands that produce cathepsin B,lysosyme chymotrypsin, neutrophil elastase, cytokine, and pheromones such an androsterone.39Prostatic, vesicular, and urethral secretions also contribute moisture. Moisture may also beexuded through the mucosa of the foreskin. Indian scientists reported that the sub-preputialmoisture contains lytic material Lytic material has an anti-bacterial and anti-viral action. Thenatural oils lubricate, moisturize, and protect the mucosal covering of the glans penis and innerforeskinFrenulum The prepuce is usually tethered at the bottom by the frenulum. The frenulums function isto provide pleasure by stretching during sexual intercourse. In fact, the frenulum is coloquiallyknown as the "sex nerve" in France and perhaps throughout Europe. By destroying this stretchingaction, circumcision completely destroys this fundamental means of sexual pleasure in the humanmale. Taylor hypothesizes that stretching of the frenulum during coitus is provides a stimulus forejaculation60.Effects on sexual and marital relations associated with a missing prepuce Hughes reports a study in which intact (uncircumcised) males appear to enjoy bettersexual compatibility in marriage which apparently contributes to marital happiness. Zwang statesthat it is more difficult for the partner to manually stimulate the circumcised male duringforeplay. Depending on the individual, the permanently exposed glans may experience an excessof stimulation, or the wrong kind of stimulation, during intercourse which can lead to prematureejaculation (lack of "staying power") in the circumcised male61. The tight foreshortened “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 37
  • 56. immobilized skin of the circumcised penis is more vulnerable to laceration, bleeding and painduring intercourse62. Erectile dysfunction (impotence) is now known to be usually caused by circulatoryproblems. As noted above, circumcision inteferes with penile circulation by destroying severalimportant blood vessels that provides circulation to the penis. Circumcision may also contributeto erectile dysfunction by destroying some of the erogenous sensory tissue in the prepuce thatparticipates in the erectile response. OHara and OHara surveyed 138 women who had experiencewith both circumcised male partners and intact complete male partners. 20 of the 138 preferredcircumcised male partners while 118 (85.5%) preferred intact male partners with anatomicallycomplete penises over circumcised males. The respondents reported that circumcised partnerstended to ejaculate prematurely more frequently than intact male partners. Some respondentscommented that unaltered male partners appeared to enjoy coitus more than their circumcisedcounterparts63.All males are born with a foreskin A foreskin is a loose collection of skin that surrounds the glans. This skin attaches to theshaft of the penis just proximal to the head. When the penis is flaccid, this foreskin extends overthe glans. When the penis is erect the glans protrudes from the foreskin.You may or may not have a foreskin depending on whether or not you were circumcised A circumcision is a simple surgical procedure during which the foreskin is removed.Most male Americans are circumcised as infants shortly after birth. Most males in Asia, SouthAmerica, and many European countries are uncircumcised. Some religions such as Judaism andIslam practice circumcision for religious reasons. Other people decide whether or not to havetheir child circumcised simply based on the convention in their society. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 38
  • 57. Circumcision is rarely required for health reasons Phimosis is a condition in which the foreskin will not retract. Para phimosis is a conditionin which the foreskin will not extend over the glans once retracted. One of these two conditionsoccurs in 1 to 2 percent of males medically requiring them to be circumcised.Cancer Myth Are uncircumcised men more at risk for penile cancer? False! As long as a man practicesgood hygiene, an uncircumcised man is no more at risk for penile cancer than a circumcised man.Balanitis Is a fancy word for an infection of the genitals caused by yeast organisms. A YeastInfectionSymptoms Itching of the glans or foreskin A burning sensation in the glans or foreskin A red rash on the glands or foreskinTreatment Practicing good hygiene Antifungal medications If the problem is a recurrent one, circumcision may be considered. There may be little to no symptoms occurring during a yeast infection. So if you are diagnosed with one, you should consider having your sexual partner treated as well, especially if your yeast infections are recurrent.Risk groups Uncircumcised men and men with diabetes that dont wash underneath their foreskin on aregular basis with soap and water may be at greater risk for a yeast infection than circumcisedmen. However, good simple hygiene can prevent this problem.Hygiene for uncircumcised males First of all we recommend a shower with soap and water once a day to every teenager regardless of sex or circumcision status. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 39
  • 58. While showering, men should wash their penis and the areas around it with soap and water, especially the surfaces between the penis and scrotum, and the recesses where the penis and scrotum meet the rest of the body. Uncircumcised men should pull back their foreskin and wash their head with soap and water. You dont need to scrub vigorously until youre sore. Just apply soap and rinse well. Once your shower is complete, dry your body well including those recesses around your penis before putting on clothes. Uncircumcised men should dry the head of their penis well and then pull their forsekin back over the head before getting dressed.Size Circumcision does not affect the size of an erect penis. Since the glans extends beyondthe foreskin while the penis is erect, size is not dependent on the presence or absence of aforeskin. In fact an erect penis with a foreskin doesnt appear to be much different than an erectpenis without a foreskin.Sex There is no medical evidence that circumcision makes a man better or worse off when itcomes to sex.Sensitivity The glans of a circumcised penis is exposed when the penis is flaccid allowing the glansto rub against a mans clothes. This may cause the glans to become less sensitive. Its a matter ofopinion whether this is a good or bad thing. Some people assume that less sensitivity makes sexless pleasurable. However, those men who often experience premature ejaculation will tell youotherwise. There are actually lubricants on the market with the sole purpose of making a manspenis less sensitive so he can last longer during sexual intercourse before ejaculation occurs.Appearance Some people like the look of a circumcised penis. Others like the look of anuncircumcised penis. If you are an uncircumcised man considering a circumcision for cosmetic “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 40
  • 59. reasons, consider this: It can be very difficult to regain a foreskin once you have it removed.There is a way to grow a foreskin through constant stretching of the skin, but it could take yearsto accomplish. If you feel weird because most men you know have a different circumcision statusthan you, remember there are millions of other men in the world with a penis that looks just likeyours. We dont recommend altering your penis unless it is medically required. If you do decideto get a circumcision or to grow a foreskin, make sure you discuss it thoroughly with a medicalprofessional and get all the facts to avoid making a decision you could later regret.Male Urethra Embryology from internal urethral meatus to sinus pocularies (uterus masculinus) theurethra is developed from urogenital diaphragm sinus portion of male urethra correspond to theentire female urethra from sinus pocularies to fossa navicularies the male urethra is formed by thefusion of the edges of medial labial fold which also form carpous spongiosum the urethratransversing the glans is the last to be developed is formed by the down growth of a solid pencilof ectoderm, which become canalized shortly before birth. Male urethra is 18 to 20 cm longextended from an internal orifice in the urinary bladder to ext opening or meatus at the tip ofpenis.It may be considered into three regional parts - 1) Prostatic 2) Membranous 3) SpongiosePresent a double curve in the ordinary flaccid state of penis.1) The Prostatic Part It is widest and most dilatable part of urethra and about 3 cm long. It runs almostvertically through prostate. It is wide in middle and narrow below. On section it is cresentric,convex vertically due to presence of posterior wall of narrow median longitudinal ridge form byelevation of the mucus membrane and its adjacent turn, termed as urethral crest. On each side of “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 41
  • 60. crest there is shallow depression, prostatic sinus the floor which is perforated by orifice ofprostatic duct about middle elevation on which the slit like orifice of prostatic utricle is situated.On each side of this orifice or just with in this orifice there is small opening of ejaculatory duct.The prostatic utricle is a 6 mm long sac situated upward and backward into prostatic substancesand behind the median lobe.2) Membranous Part Shortest, least dilatable and narrowest portion of urethra (except the external orifice) itdescends with slight ventral concavity from prostatic to bulb of penis, passing through perinealmembrane about 2.5 cms poster inferior to Pubic symphysis. It is 1.25 cm to 2 cm in length. Themembranous urethra is surrounded by fibres of urethral sphincter on bulbo urethral gland is sitedon each side of this part of urethra.3) The Spongiose Part It is continued in carpous spongiosum of penis. It is about 15 cm long and extends fromthe end of membranous urethra to external urethral orifice i.e. on glans penis it continuesvertically concave curve of membranous urethra to a point anterior to lowest level of symphysispubis. From here when the penis is flaccid it curves downward in the free part of penis. It isnarrow with a uniform diameter of about 6 mm in penis. It is dilated at its commencement asinterbulbar fossa. The bulbo urethral glands open into the spongiose of urethra about 2.5 cmbelow the perineal membrane. External urethral orifice except in its most anterior part, presents the orifice of numeroussmall mucous glands and follicles situated into the sub mucous tissues and named urethral glands.Besides these there are a number of small pit like recesses or lacunae of varying sizes the openingof which directed anteriorly. On larger lacuna, the lacuna magna is situated on the roof of thenavicular fossa. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 42
  • 61. Urethral Sphincter Two sphincters surround the urethra. The internal vesical sphincter controls the neck ofthe bladder and prostatic urethra above the opening of the ejaculatory ducts. It is composed ofnon-striated muscle is not under the voluntary control and is supplied by sympathetic andparasympathetic fibres derived from vesical plexus. The external urethral sphincter surrounds themembranous urethra and consists of striated muscle it is supplied by perineal branch of pudendalnerve (S 2, 3, 4,) and under voluntary control.Male Urethral Structure The urethra is composed of mucus membrane supported by sub mucous coat (tissue)which connects it with various structures through which it passage. The mucus membrane of the urethra is continues internally with that of bladder andexternally with skin covering glans penis. It is prolonged into the duct of urethral, bulbourethral,prostatic gland and into the different ducts and seminal vesicles through the ejaculatory duct. Inmembranous and spingiose urethral region it is arranged into longitudinal folds when urethra isempty. The urethral epithelial lining is transitional variety as far as ejaculatory duct there after itis composed of patches of pseudo stratified columnar and stratified epithelium amongst which aresituated diverticula’s of various sizes, some extending into the lamina propria as mucous glands,near the external urethral orifice the epithelium is stratified squamous in type. The sub mucous tissue consist of a vascular erectile layer outside this there is a layer ofnon striated muscular fibres, arranged into an inner longitudinal and outer circular layer and bestmarked in the prostatic and membranous urethra. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 43
  • 62. DISEASE REVIEW Before startling any research on a disease, the researcher should have the knowledge ofAnatomy and physiology of related disease. The researcher should explain etiology,Parthenogenesis and available different treatment modalities of the disease. If necessary theinformation available in other system of science can be collected and correlated. Considering allthese points here, Shareera Rachana and Kriya of Shukragatavata, Nidanaa panchaka anddifferent types of Chikitsas for vyanga are explained in detail. In this study Shukragatavata iscompared with Premature ejaculation of contemporary science and its Physiopathology isexplained in detail.CONCEPTS ON VATA Ayurveda is a monumental contribution of India to the world. As the name implies, itis an organized body of knowledge of healthy living. It represents a well-codified humancare system and speaks of the art and science of health and healing. Ayurveda is the science oflife, which explains the knowledge of various strategies to follow in order to make a healthyliving. Health is defined as a state where in the dynamic balance of doshas, dhatus andmalas is maintained, the metabolism is at optimum level and soul, mind and sense organsassume sublime position. This definition fully agrees with the integral vision of health envisagedby W.H.O. the former has an additional dimension of sound spirituality. The living body canfunction normally only when its doshas, dhatus, malas and agni are in a state of equilibrium.The importance of Vata Due to the three important properties vata is entirely different from other doshas. 1. Asamghata (Incorporeal) 2. Anavasthita (Unstable) 3. Anasadhya (Inaccessible) Pitta and Kapha have appendages and relatively compact. On the contrary vata isincorporeal (avayavasamghatarahita). It can be termed as rarified in nature. The vata is “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 44
  • 63. anavasthita (unstable) too. These two properties are due to its bhoutic composition. Vata isformed by Akasa and Vayu predominantly. The biological vata (which is present in the livingbeing) is self originated (svayambhoo), subtle (sookshma) and all pervasive (sarvagata). It is notsensible (avyakta) but its activities are patent or manifest (vyaktakarma).Physical properties of vata There is difference of opinion regarding the number and nature of physical properties indifferent classics and different contexts of same classic. Table No. 1 Physical properties of vataNo. Physical Ca. Su. Ca. Su. Ca. Vi. Su. Ni. AH. Su.1 Properties 1/59 12/4 8/98 1/7 A. S. Su. 11 Rooksha + + + + +2 Sita + + + + +3 Laghu + + + + +4 Khara + + - + +5 Visada + + + - -6 Cala + - + - +7 Sookshma + - - - +8 Daruna - + - - -9 Parusha - - + - -10 Seeghra - - + - -11 Bahu - - + - - Total 11 7 6 8 4 6 Among the properties of vata, chalatva is the most important and it is the subjectpertaining to the present thesis context. Here the gati as well as gatatwa concept of vata.The concept of Gati Three functional status of vata are necessary for the maintenance of life without ailment. 1. Akupita (equilibrium stage) 2. Sthanstha (Normal habitat) 3. Avyahata gati (unimpeded course of activity) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 45
  • 64. The Pathway of gati Due to the continuous movement (sadagati) it is not possible to define particular positions(sthana) for Vayu Still according to functions their seats and pathways of activity are described. Table No. 2 Pathway of gati of individual components of vataNo. Component Adhisthana (seat) Pathway (Pravartana)1 Prana Moordhva (A.S. Ca.) Kanda, urah (A.S.); vaktra (Su.) Nabhi (Su. Sa.) Kandha, jihwa, asya, nasika (Ca.).2 Udana Uras (A.S.) Kandha, Nasika, Nabhi (A.S.) Nabhi, Urah, Kandha (Ca.)3 Vyana Hrit (A.S.) Krisnadeha (A.S.) Sarvadeha (Ca.)4 Samana Antaragni Samipa Sarvakoshtha (A.H.) (A.S.) Amapkwasayacara (Su.)5 Apana Apana pradesa (A.S.) Vasti, Sroni, medra, vrishaaa, Pakvadhana (Su) vamkshana, ooru (A.S.) Vrishna, vasti, medhra, nabhi, ooru, vamkshana, guda, antra (Ca.)Concept of Gatatva The sequentials happening from the contact of etiological factors till to the establishmentof disease and further advancement if any are termed as Samprapti. The mode of Samprapti is thekey factor which decides finally the manifestation of the disease when nidanas and amount ofdoshas vitiation etc. are identical. Occurrence of sthanasamsraya (lodgment to particular site)followed by doshas dooshya sammoorccana is the most important part of Samprapti. Thisdepends on the integrity and Excellency of dhatus and srotases. Khavaigunya (deformity ofsrotasas) and dhatu dourbalya (inferior qualities of dhatu) decides the sthanasamsraya of doshasand hence Samprapti itself. Different phenomenon has been put forward to explain the pathogenesis of variousdiseases. Gatatva is one such complex phenomenon mentioned in all classical texts. AcharyasVagbhata deals the gatatva of doshas just after explaining the Samprapti of rogas. The vitiateddoshas cause vitiation of rasa and other dhatus together vitiates malas which in turn vitiatechannels of their elimination which include two below (urethra and anus), seven in the head “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 46
  • 65. (eyes, nose, ears and mouth) and the channels of sweat; from the vitiated channels manifest theirconnected diseases. Only Vriddha Vagbhata explains the gatatva of pitta and kapha. But he does not mention thegatatva of vata in the same context instead of which advice to refer the context of vata vyadhiNidana. This may be due to relatively significant importance of gatatva of vata as far asmanifestation of diseases is concerned.Various terminologies or synonyms are used to denote gatatva in the classics. 1 Gate, Gatam 2 Prapte 3 Sthite/sthitam 4 Avasthite 5 Asrite/samasritam 6 Sthe 7 Gam/go 8 Saptami vibhakti of the word. Analyzing the above referred meanings and synonyms it can be concluded that the wordgata has two implications. One related with the movement and the other related with occuipment. Subjected to gati (movement) of Vayu Gata Subjected to adhishthana (Site) Hence ‘gatatva’ of vata implies an undesirable movement of vata and its unnecessaryoccupation of certain sites.Sthanas (Sites) of Gatadosha Different adhishthanas (sites / abode) are explained in the context of gatatva of vata indifferent classics. Texts like Gadanigraha, Bangasena, and Yogaratnakara etc. followed eitherCaraka or Susruta in this regard. Description given by Vagbhata regarding ‘gatatva’ of pitta andkapha has been also incorporated in the table.Dhatugata Vata The symptomatology and treatment of all dhatugatavata are explained in classics exceptthat of rasadhatu. Rasagata vata lakshanas are mentioned only by Yogaratnakara. Here the “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 47
  • 66. functional status of dhatu is analyses to understand the dhatugatava. The doshas are drawingnutrition from the kittamsa (waste) of ahara (food substance) after digestion. The prasadamsa(essence of food) provides nutrition to rasadidhatus (tissue elements), ojus, indriyas, sandhis etc. .When the food articles are producing more kittamsa in comparison to prasadamsa the chance ofdoshavriddhi and kopa (aggravation and vitiation) along with dhatudourbalya (diminution oftissue elements) is likely to take place. For example Vatahara will increase the formation ofkittamsa for production of more vata and decrease the production of tissue elements like rasa,rakta, mamsa, meda etc. When vata get vitiated it attains more cala property and starts its abnormal movements(gati). Dhatudourbalya causes Riktata (vaccum) in dhatus, makes more space enhances themovement of vata again. Thus, the vitiated vata abnormally move in situ tissues and get occupiedthere. Like wise viharas are also possible to create the vitiation of vayu and weakness of dhatus. Table No. 3 Adhishthana (sites) of gatadoshaN Site/ Gatatva of Vatadosa Pitta Kaphao Adhisthana Ca.Ci.3 Su.Ni.1/ As.Ni.1 Ah.Ni.1 Ma. Bh. As.Su.19 0 Ci.4 5/Ci.23 5/Ci.21 Ni. Pr.Dhatu1 Rasa # -- -- -- -- -- -- -- --2 (Tvak)3 Rakta4 Mamsa5 Meda6 Asthi7 Majja8 ShukraUpadhatu9 Snayu10 SiraAsaya11 Amasaya12 Pakvasaya13 Kukshi14 Koshtha “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 48
  • 67. Avayaya15 Guda16 Basti17 Adhonabhi18 Sirah19 Hridaya20 SandhiOthers @21 Garbha * * *22 Indriya23 Sarvangam{*Described treatment only # Rasagatatva described in Yogaratnakara only @ Gatatva of vata atBahu, skandha, vamkshnaa, trika, manya - explained by Susruta in Chikitsa-4. } Dhatus have two forms viz. asthayidhatus (nutrient to the concurrent dhatus) andsthayidhatus (Formed and stable tissue elements). In dhatugatatwa, the sthayidhatus are weakenedand aggravated vata gets lodged there in. Due to the same fact, line of treatment also should be toimprove the quality of dhatus and to pacify the vata. According to the complexity of the pathogenesis, dhatugatatva may producesymptomatology suggesting a single disease, a group of disease or even diseases which areopposite in nature. How ever it may be, the clinical presentation may be generally having thenature of dhatus dourbalya. It seems that ‘rasa’ is also mobile as vata, so rasadhatu gatavata is notexplained in classics; instead tvak gata vata lakshanas.Upadhatugata Vata The gatatva of vata has been mentioned in the sira and snayu as upadhatus. Thesereferences explain the dilatation and hollowness of siras and diseases related to posture andmovements. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 49
  • 68. Asayata vata Vitiation of vata in certain Asayas is causing disorders. These Asayas include Kostha,Amasaya, Pakwashaya and Kukshi. Even though Amasaya and pakwashaya are included in thekostha, their gata vata lakshanas are separately mentioned. This may be due to its higherincidence and importance. The symptomatology of certain avayavagata vata like that of Hridayacan also be understood from kosthagata vata lakshanas.Avayavagata Vata The symptomatologies as well as treatment of gudagata vata and sandhigata vata weredescribed. But regarding vasti, nabhi, sirah and Hridaya only treatments were prescribed.Gatavata phenomena were also explained for garbha, indriya and sarvanga. Susruta in thetreatment context describes gatatva of vayu in bahu, skandha, vaksha, trika and manya. Sarvangavata is the most serious condition as the vitiation of vata is not limited to any area of the body, butaffects the whole body.Gatatwa of Pitta and Kapha The Gatatva of Pitta and Kapha have been explained by Vridha Vagbhata Only(A.S.Su.21/19). The different disease entities caused by pitta and kapha due to gatatva are Table No.4 Gatatva of pitta and kaphaNo. Sthana Pitta Kapha1 Twak Visphotaka, Masoorika Stambha, svetavabhasata2 Rakta Visarpa, Daha Panduroga3 Mamsa Mamsapaka, Kothana Arbuda, Apachi, Ardracharma vanadhabhagatrata, atigourava4 Meda Sadaha granthi, atisveda, trishna Sthoolata, meha5 Asthi Bhrisa daham Asthisthabdhata6 Majja Haridra nakha, haridra netra Shuklanetrata7 Shukra Putisukram, pitavabhasa Sukram Shukrasanchayam, Shukra vbandham, governasam.8 Sira Krodha, pralapa Stabdhagatrata9 Koshta Mada, trishna, daha Udara, arocaka, avipaka “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 50
  • 69. Dhatugata Vyadhi and Dhatugata vataApart from the dhatugatatva of doshas, dhatugatatva is explained 1) Dhatugatatva of Jwara 2) Dhatugatatva of Kushtha 3) Dhatugatatva of Masoorika 4) Dhatugatatva of Sarpavisha vega Some scholars have tried to explain the dhatugatatva of roga and dhatugatatva of dosha. Sharma K.S. has discussed dhatugata vyadhi in detail and concluded that the examples of dhatugatatva given in kushtha can be taken as a model for understanding the symptomatology of dhatugatatva of kapha pradhanvyadhies. Like wise dhatugatatva of jwara for pittaja vyadhi and dhatugatatva described in vata vyadhi for vata in understanding other vata diseases also. But Shilpa D, Baghel M.S. et. al (1998) had critically approached the problem and made some relevant explanations in this regard. Here an attempt has been made to modify and add some more details to this observation. 1) In Dhatugatatva of vyadhi, the process of Samprapti eventually progresses to the dhatus. All the doshas, which are involved in the basic Samprapti, also affect the dhatus according to the progress. But in case of dhatugatatva of vata, the vata doshas alone affects the dhatus and then produce a disorder. Hence, as rasagata Kushtha is used in terminologies, dhatugata Vata vyadhi has not been used. In short, in dhatugata vyadhi the disease process it self is advancing, but in dhatugata vata the phenomenon is related only to vata doshas not with vata vyadhi. 2) In dhatugatatva of vyadhi only dhatus are getting involved. But in the context of dhatugatatva of vata dhatus, upadhatu, asaya, avayava etc. are getting involved. 3) Rasagata vyadhi are explained but rasagata vata lakshanas are not explained in classics. 4) In diseases showing processes of dhatugatatwa, dhatus show specific vitiation (vaiseshika dushti) on chronic of disease, which in turn leads to successive advancement of roga to “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 51
  • 70. dhatus but in the case of Dhatugatatva of vata such vaiseshika dushti is not seen. Only dhatu dourbalya is seen in Dhatu gata vata.5) The involvement of dhatus in dhatu gatavyadhi is in a specific krama starting from rasa and ending in Shukra. No karma is observed in dhatugata vata. Vitiated vata can affect and get lodged to any dhatus without any krama. Neither it follows any krama in affliction nor does it advance further to successive dhatus in sequence.6) Dhatugata vyadhi process manifests after the vyakti (establishment) stage of the Samprapti of the disease. So it may be considered as bheda stage of Samprapti. Due to the same fact it will severe in nature. But one thing to remember here is dhatugatatva of roga in dhatus which already exist in basic Samprapti should not be considered as bheda or gambhira stage. For example, the dhatugatatwa of kushtha in rasa, rakta and mamsa are not bheda or gambheera stage. Like wise, dhatugatatva of jwara in rasadhatu and dhatugatatva of masoorika in rasa rakta dhatus are part of the Samprapti till vyakti stage. This is evident from the symptomatology and prognosis of the above conditions explained. In case of dhatugatatva of vata the process of gatatava occurs before sthana samsraya stage. As sthana samsraya is accomplished it is called as ‘sthita’.7) Sadhyasadhyata of dhatugata vyadhi was described in the classics. Many a time the treatments were also not mentioned in advancements of roga to deeper dhatus (e.g. asthigatakushtha) Sadhyasadhyata of dhatugatavata has not been explained. But treatments were explained in each and every condition.8) Dhatugatatva may occur in many vyadhi, for e.g. Gambheera stage of vatarakta. The above descriptions may be summarized as follows. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 52
  • 71. Table No.5Comparative analysis of dhatugatavyathi and dhatugatavataNo. Dhatugatavyadhi Dhatugata vata1 The whole Samprapti advances to dhatus The phenomenon related to vata doshas only2 All the doshas of basic Samprapti affect Dhatus Only vata doshas affects the particular dhatus involved3 Only dhatus get involved Along with dhatus, upadhatus, asayas and avayava etc are involved4 Rasagatatva of vyadhi is explained Rasagatavata is not explained5 Vaiseshika dushti of dhatus present Dhatudurbalata is present. No vaiśeshika dushti.6 The involvement of dhatus are in a specific karma No specific krama is observed7 The involvement of dhatus is progressive according Not progressive to chronicity.8 Dhatugatatva of vyadhi is happening after vyakti Gatatva is the sthanasamsrayavastha of stage of samprapti. It may be termed as bheda or disease in dhatugatatva gambheera stage.9 Symptomatology of disease is already present No symptomatology before before dhatugatatva of vyadhi dhatugatutva of vata10 Sadhyasadhyata is clearly mentioned Sadhyasadhyata is not mentionedGata Vata and Avrita vata Avarana is special pathological condition of vata characterized by an obstruction in the‘gati’ of vata, paralysing it in performing its activities and lead to different disorders. The gatatwaand avritatva are entirely two different phenomenons. Here an attempt is being made todifferentiate the both path physiologies.1) In the process of avarana generally the vitiation of vata will be passive. When the vitiated doshas or any other things obstructed the pathway of vata, avarana happens. So initially vata will be in normal state, and when the process of avarana goes on vata also gets vitiated. The substance which obstructs the pathway of vata is called as ‘avaraka’ and the dosha (vata in general or its components) which affected by avarana is called as avareeya or avrita. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 53
  • 72. Normally the avarana is caused by the etiological factors for the vitiation of avaraka. Etiological factors for the vitiation of vata will be absent. In case of Gata vata the vitiation of vata will be active. Here its own etiological factors are operating in the vitiation of vata and the vitiated vata adopts specific pathway and abnormally localize at particular sites in the pathogenesis.2) In the process of avarana ‘cala’ property of vata is diminished due to obstruction. Other properties are not involved in the process till obstruction. But in case of gatatva the vitiation of vata takes place by involvement of other properties like rooksha, laghu, khara, vishada etc along with cala.3) In avarana the ‘gati’ of vata is obstructed partially or fully. Once get obstructed the vata may simply get lodged there (baddha marga, marga rodha), try to nullify the obstruction (udhooya), may get covered by the obstructing substance (avrita), adopt an opposite direction (pratiloma) or alter the direction (viloma). The different terminologies have been used to denote avarana in different contexts according to the nature of avarana and the state of vata and marga. In case of gatatwa the gati of vitiated vata get aggravated and starts moving abnormally leading to localizations at particular sites.4) Avarana is caused by poornata (filling) of other doshas in the srotas/marga of vata. In gatatwa the srotases or sites of occupation of vata are rikta and the aggravated vata fills the srotas/site5) In the avarana of vata, svakarmavriddhi (exaggerated activities) of avarakas is manifested. The avrita (i.e. vata) will show swakarmahani (diminished activity). This is the general feature of avarana. The excessively increased strong avaraka suppresses the normal action of avrita (i.e. vata). Therefore when the obstruction is complete it may lead to the prakopa of vata resulting in the presentation of vata vitiated symptoms as well as its disorders (Cakra. on. In case of gatatwa the symptomatology will be predominantly of vata vitiation and pain will be a common and chief complaint in all the conditions of gatatva. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 54
  • 73. 6) Avarana is possible by other doshas (pitta and kapha), dhatus, anna, malas, and individual components of vata each other. Avarana is not described by upadhatus and causation of avarana by asayas or avayavas are not possible. Gatatwa of vata is happening in dhatus, upadhatus, Asayas and avayavas. Gatatwa of vata in other doshas or non-bodily substances like anna and malas and in between the individual components of vata is not possible.7) Generally in dhatvavarana the dhatus will be in a state of vriddhi or samata so that they produce poornata in srotas and are capable of obstructing vata. In dhatugatavata the Excellency of dhatus will be diminished (dhatudourbalya) so that they produce riktata in srotases or sites and the vata get enough space for abnormal gati.8) Accordingly the symptomatology of dhatvavrita vata will be vriddha or samadhatu lakshanas associated with diminished activities of vata and of dhatugata vata will be dhatudourbalya lakshanas associated with vitiated vata lakshanas. Obviously exceptions are possible according to the complexities of processes of avarana or gatatva.9) In case of avarana of vata, the avaraka gets importance in treatment since the vitiation of vata is passive. When avaraa is removed vitiated vata gets pacified. But in cases of gatatva the vitiated vata has to be treated first along with correction of adhisthana.10) Diagnosis of avarana is made with the help of upasaya – anupasya (trial and error) method. Diagnosis of gatatva is made according to the symptomatology.11) Complications of avarana are explained in case of improper diagnosis and delayed treatment like hridroga, vidradhi, gulma etc. No complication is explained in gatatva.12) Avarana of vata may cause affliction of nutrition to dhatus (dhatugati Sama) leading successive diminution of rasadi dhatus (rasadeemschopasosayet). No such reference available in case of gatatva. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 55
  • 74. Table No. 6 Comparative analysis of avritavata and gatavata Avrta vata Gata vata1. Vitiation of vata is passive 1. Vitiation of vata is active2. Normally svanidanas of vata are not 2. Vitiation of vata by svanidanasOperating3. Only cala property of vata is involved and it is 3. Other properties of vata are also involveddiminished in the phenomenon and the cala property aggravated in the phenomenon4. Gati of vata is obstructed 4. Gati of vata is aggravated5. Poornata in srotas / marga 5. Riktata in srotas / sites6. Vata shows svakarma hani 6. Vata shows svakarma vriddhi7. Dhatus are in vriddha or sama 7. Dhatudourbalya present8. Avarana is possible with other Doshas 8. Not possible/anna/mala/individual components of vata9. Avarana by avayava or asaya not possible 9. Gatatwa in asayas and avayavas explained.10. Avaraka gets importance in treatment 10. Vata gets importance in treatment11. Diagnosis made with upasaya anupasa 11. Diagnosis with Roopa12. Complications of avarana possible 12. Not explainedSamanya Samprapti of Vatavyadhi1) Aharajanya Nidana 1) Ruksha ahara sevan 5) Sheeta ahara sevan 2) Adhyasan 6) Asatmya ahara 3) Vishamashan 7) Niyam viruddha ahara 4) Alpa ahara 8) Katu, tikta, kashaya rasa pradhan aharaVishama ahara2) Viharajanya Nidana 1) Ati maithuna 8) Ati jagaran 2) Ativicheshta 9) Upavasa 3) Ati adhyana 10) Ativyayama 4) Divaswapna 11) Abhighat 5) Kama 12) Plavana 6) Dukhasayanasan 13) Ratri jagarna 7) Vishama Shayya ShayanaManasika 1) Chinta 3) Soka 2) Bhaya 4) Krodha The way in which the dosha gets vitiated and the course it follows for the manifestationof disease is called Samprapti. For any disease to manifest, it requires two basic things namely “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 56
  • 75. dosha and dhatu. The earlier acquires later to generate certain sets of signs and symptoms. Fromthe onset of Dosha Dushya Dushti till the evolution of the Vyadhi there occurs various Vikriti.Samprapti explains such series of pathological stages involved. Acharya Caraka explained – due to the intake of Vatakara Ahara Vihara Vata vitiationtake place. This vitiated Vata lodges in Rikta Srotas i.e. Srotas in where Shunyata of SnehadiGuna is present. Vata after settling in Rikta Srotas produce disease related to that Srotas. Acharya Vagbhata frames the Samprapti of Vata Vyadhi like – Dhatukshaya aggravatesVata and the same is also responsible to produce Riktata of Srotas. Thus the vitiated Vata travelsthrough out the body and settles in the Rikta Srotas and further vitiates the Srotas leading to themanifestation of Vata Vyadhi. For the purpose of understanding the Samprapti of Vata can be studied under twoheading. They are,1. Dhatu Kshaya Janya and 2. Avarana Janya Vata.Samprapthi GhatakaTable:7 Showing the Samprapti ghataka of Vata vyadhiDosha VataDooshya Rasa raktadi dhatuSrotas Vatavaha srotusAgni VishamgniAdhisthana Anga pratyaga, sarvaga, Kostha, Kandara, Sira, snayuSroto drusti prakara Sanga, vimarga gamanVyadhi swabhav Navin- Mrudu Jeerna- DarunSadhyasadhyata Navin- Sadhya / Kruccha sadya Jeerna- Yapya / Asadya “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 57
  • 76. CONCEPTS ON SHUKRADHATUShukradhatu Shukra is the terminal tissue element of the body, which is considered as the Sara(essence) of all other tissue elements.Grammatical considerations The word ‘Shukra’ is derived grammatically as follows.“Shuc Souce” or “Shuc Klede”- applying the aphorism “Rujrendragravyaretian” to the dhatus‘suc’ which implies the meaning of purity. Both derivations are made by adding the suffix ‘ran’.The derived word Shukra is having multiple meanings. 1. Bright 2. Resplendent 3. WhiteTechnically in different contexts term ‘Shukra’ is used to denote different substances. 1. A name of fire 6. Semen 2. The planet Venus (Shukragraha) 7. Sperm 3. Prec eptor of daityas (Shukramuni) 8. Silver (Rajatam) 4. Morbid affection of the iris of the eye 9. The sclera of eye 5. Butter (Navaneetam) – (Shabdakalpadruma, Monnier Williams – 1993)In the present context a white and silvery substance ejaculated during sexual act is considered asshukra. It is clarified from the following references.1. “Shuklayati tyjayati Shuklam rejatam shuklam veeryam”2. “Shocati Anena, Shocayati va iti Shukram, shukre sarjane tyaja” (Amarakosa “Aharasyaparam dhaman shukram tadrakshya atmanam”DEFINITION OF SHUKRA The factor which is responsible for the formation of the embryo is known as Shukra.2SHUKRA DHATU STHANA Shukra dhatus is present all over the body like the juice is present in sugarcane, ghee ispresent in curd and oil is present in Tila, similarly Shukra present in an inconceivable manner inthe whole body3. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 58
  • 77. Chakrapani while commenting on the above statement categorizes individual into threegroups according to the duration of sexual act and the effort needed to express out the Shukra. Inone group Shukra is ejaculated without much effort (extracting juice from sugar cane). Anothergroup requires moderate effort and time (removing ghee from curd). The last group needs mucheffort and time (extraction of oil from sesame seed).Synonyms of Shukra The final tissue element ‘Shukra’ is having a number of synonyms.Paurusham (Virility) Retah (Semen)Beejam (Sperm) Veeiryam (Potency)Pumsthvam (Manliness) Tejah (Resplendid)Indriyah Annavikara (Food derivative)Majjasarah (Essence of marrow) RohanamBalam (Strength) Anandaprabhavam (Born out of pleasure)Kittavivarjitam (No waste materials) Majjasamudbhavam (Derived from marrow)Dhatus Sara Dhatus Sneha– tissue essence (S.K.D. / A.K.)Roopa dravya (That which imparts structure to all substancesShukradharakala Kalas are the functional basement situated at the ‘borders’ of the different tissue elementsand other fundamental functional entities. Shukradharakala is the last and seventh one amongkalas, which extends of throughout the entire body of all living creatures.. The simile used here isas ‘ghee in the milk’ or ‘sugar in the expressed juice of sugar cane’. At the time of ejaculation theShukra is coming out through the ducts situated about two-finger breadth on either side and justbelow the neck of the basti and finally flows out through the urinary meatus. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 59
  • 78. Shukravaha srotas (Channels of metamorphosis of Shukra) Regarding the origin different Acharyas are having varied opinions of shukravaha srotas1. According to Caraka i. Vrishanou (Both testicles) ii. Sepha (Penis)2. According to Susruta i. Stanou (both breasts) ii. Vrishnou (both testicles)3. According to Vagbhata iii. Stanou (Both breasts) IV. Mushkou (Both testicles) V. Majja (Bone marrow) Apart from these, Acharyas have given references of the two pairs of shukravahadhamani(Su.Sa.9/17), shukravahasira shukraharani, sepha sevani shukravahanadi and shukrasaya.Shukravahadhamani, Sira / Nadi, Shukrasaya, Shukraharani Acharyas Susruta mentions the term shukravaha sira in the context of physiology oferection and explains as the filling of shukravaha sira with blood, under the influence ofpsychological and physical stimulation (harshat) result in tumescence. In the context of dhamanis Susruta includes two dhamanis for shukrapradurbhava andtwo for shukra visarga. Bhaskara Govinda Ghranakkar, the famous commentator of Susrutasamhita, Sareerasthana opines that blood vessels supplying testes, testicular and spermatic arteriesform shukrapradurbhava dhamanis and arteries supplying epididymus, ductus deferens, andseminal vesicle and prostrate for shukravisarga dhamanis. But some others consider theepididymus itself shukrapradurbhava dhamani and ejaculatory ducts as shukravisarga dhamanis.Caraka in Sidhisthana has mentioned shukravaha nadi for the ejaculation of semen to the exteriorof the body which again can be taken as epididymus and seminal vesicles. Caraka mentionedshukrasaya and Susruta, shukra harani in contexts of shukrasmari. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 60
  • 79. TABLE NO. 8 PHYSICAL PROPERTIES OF SHUKRA Characteristics Caraka Susruta A. Samgraha A. Hridaya1 Colour 1.Sukla (white) 1.Taila Nibham 1. Suklam (white) 1.Suklam 2.Kshoudranib- 2.Ghritatailaksh- 2.Ghritamakshika Ham oudraanyatamavarńa tailabham2 Taste 2.Madhuram 3. Madhuram 3. Madhuram 3. Madhuram3 Smell 3. Avisram 4.Madhugandhi 4. Madhugandhi -4 Consistency 4. Bahalam 5. Dravam 5. Soumyam 5. Guru 5.Snighdham 6. Snigdham 6. Snigdham 6. Snigdham 6.Guru 7.Sphatikabham 7. Guru 7. Bahalam 7.Picchilam (Su.Sa.2/11) 8. Picchilam 8. Bahu 8.Bahu 9. Bahu 9. Khanam 10. Bahalam 10.Sphatika sannibham 11. Saratvam5 Other 12. Anubhavam 13.Pravanabhava 14. AvidahiQuantity of Shukra Shukra is considered as a liquid material and its quantity is mentioned as half Anjali (192ml). This is the measurement of the whole Shukra pervaded all over the body. Acharyas Bhelasuggested quantity of Shukra as one anjali.Bodily location of Shukra dhatus Ayurveda considers shukra as located all over the body by its pervading nature just as theentire sugarcane is pervaded with its juice, the whole curd is contained with ghee which isavailable on manthana (churning) and oil is contained in all parts of the sesame seed which can beextracted. The sugarcane juice, ghee and oil are not visible till the process of extraction. Susrutaalso expressed the same opinion.FORMATION OF SHUKRA DHATU 1. Origin according to Mahabhuta and Six Rasa’s. 2. Produce from Majja Dhatus. 3. Produce from Ahara Rasa. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 61
  • 80. 1) Origin according to Mahabhuta and Six Rasa’s It is composed of Vayu, Agni, Jala and Pruthvi in state of their excellence. All thesefactor individually shares ¼ of the attributes of each of Mahabhuta; this also shares Madhuradishad rasas. Chakrapani comments over that, Shukra is made of five Mahabhuta but this concept isconcerned with functional aspect of Shukra, which is movement of the Shukra. In AkashMahabhuta Gaman abhavata is there, so that property is not considered. And Shukra originatesfrom Shadrasa but Madhura rasa is Shukra janaka and Amladi pancha rasa are Shukra VighataKara.202) Production of Shukra from Majja About the production of Shukra Agnivesa raises is question that if shukra is formed fromMajja, then how it can be explained as it is pervading the whole body as wise men advised earlier.Physically there are no holes in the bones, which contain majja for the release of Shukra. Thepreceptor Punarvasu Atreya clarifies this query as follows. The unctuous substance of the majjagives rise to shukra. Porosity of asthi is caused by Vayu and akasa etc. and through these poresexudation of shukra takes place. This happens on the analogy of exudation of the water fromporous walls of the new earthen pot. Fine channels carrying shukra pervade the entire body.When a person gets sexually excited semen comes out from the entire body and gets filled in bastiand from there gets ejaculated. Based on the references of Dalhana’s commentary on Susruta that mastishka ormastulunga is also majja, the well-known scholar Prof. V. J. Thakar opines that brain andpituitary gland can be taken as functional representative of majja. The production of shukra aswell as smasru (secondary hair growth) at a particular age can be understood in this way.Moreover the psychological factors incorporated with functions of shukra (explained later) canalso be attributed to the relation to brain “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 62
  • 81. 3) Production of Shukra from Ahararasa Shukradhatu is the final tissue element produced from the progressive metabolictransformation of annarasa. Metabolic transformation in the different tissues happens in two waysas kittapāka and prasadabhaga (transformation of nourishing material). The bifold metabolictransformation of all the dhatus is justifiable, even though shukra the seventh dhatu does not havekittapaka at all. The tissue element nourished from the nutrient portion of shukra is garbha. Allthe three laws ksheeradadhi nyaya (law of transformation), kedarikulya nyaya (law oftransmission) and khale kapota (the law of selectivity) can be attributed to the formation ofshukra.SHUKRA DHATU UTPATTI KALA The formation of dhatus take place in the following orders – Rasa, Rakta, Mansa, Meda,Asthi, Majja and Shukra, the Uttarotra dhatus will formed by the previous dhatus. Regarding the origin of dhatu there are four views are explained23 – 1) Ksheera dhadhinyaya 2) Kedara kulyanyaya 3) Khalekapotanyaya 4) Ekkala dhatuposhana karma. Some authorities suggest that food gets converted into shukra with in one day. There areopinions that shukra is formed after 6 days or after one month by undergoing a series of paka.The transformation of nutrient tissue is continued like this. But vrishya drugs etc. by their specialeffect produce shukra immediately. Shukra is formed by ksheeradadhi method of transformationwithin one month, by kedarikulya method within six days and by khalekapota method suddenlymay be within one day.Physiological stages of formation of Shukra From the above descriptions the formation of shukra may be understood in differentstages. On the basis of following explanations of Cakrapani and Dalhana the formation of shukracan be divided into the following stages1. Shukrajanana (production of shukra) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 63
  • 82. a. Production of Shukradhatu (pervaded all over the body and invisible) b. Transformation of Shukradhatu into Roopa dravya (visible)2. Shukra pravartana (Ejaculation of shukra – roopa dravya)Production of Shukradhatu The production of Shukradhatu from ahararasa and the time taken for it has been alreadyexplained. Cakrapani clarified the different opinions regarding the time taken for production ofshukra as follows. The time for transformation of tissue elements depends on agni. As describedby Susruta in the context of movement of rasa three grades of speed can be imagined for thetransformation.1. Waves of water 2. Waves of sound 3. Waves of Fire/ light The transformation take place in slow speed as of water wave in the case of power ofagni is less, in moderate speed as of sound wave in a better status of agni and will be fastest asthat of light in the excellent status of agni. The Shukradhatu formed by the evolutionary metamorphosis of shukra pervades all overthe body in the shukradharakala. Shukradharakala performs the following functions. 1. Abode for the pervading Shukradhatu. : It holds and provides the abode for performing the whole body (sarvadaihika) functions of shukra. 2. Helps further transformation of Shukradhatu into Roopa dravya.Transformation of Shukradhatu into Roopa dravya The ejaculated part of Shukra is termed as Roopa dravya. It is the only visible part of theShukradhatu. The formation of the ‘Roopa dravya’ takes place in the vrishana, the moolasthana ofShukravaha srotas.Expulsion of Roopa dravya The formed Roopa dravya is expelled out from the tip of the penis by physical,physiological and psychological varieties of stimuli. The process of ejaculation has beendescribed later. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 64
  • 83. Functional characteristics of Shukra The specific function of shukra is garbhodpadana. Besides shukra a number of functionalcharacteristics are attributed to shukra. These all references are very necessary to formulate thestructural as well as functional identity of Shukradhatu. A. Specific function (visishťa karma) 1. Garbhodpadana B. Functions related to sexual act 2. Harsha 3. Preeti 4. Cyavana C. Psychological functions 5. Dhairya 6. Preeti 7. Soumyata D. General body functions 8. Bala 9. Upacaya 10. Utsaha 11. Ojoposaha E. Other functions 12. Ksheerapoornalocanatvam 13. Vitta 14. Snigdhavrittasarasamhata sighara dasanah 15. Mahasphik 16. Prasanna and snigdha svara 17. Bhrajishnuta 19. Shukha 20. Aisvarya 15. Prasanna and snigdha varna.Functions Related to Sexual Act Acharyas Susruta has beautifully narrated certain important functions of the Shukradhatuviz. Cyavana, Preeti and harsh which have particular importance regarding sexual act. ‘Dhairya’also have relation with sexual act as well as general psychological and behavioral features. Theapplied meanings of Dhairya, Cyavana, Preeti and harsh are being analyses here in detail.1. Dhairya The term ‘Dhairya’ have wider implications. It has been explained as the remedy formental morbidity. Commenting on this Arundatta explained as Dhairya is the control over mind,stability and adherence by which one follows the good and avoids the bad. by this property, onecan stand difficulties with strong will. Caraka suggested examining the ‘Dhairya’ of patient by “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 65
  • 84. virtue of ‘avishada’ nature. Bhaya (fear) is the exact opposite quality of Dhairya. Dhairya is thestrength of mind even in dangerous situations without much disruptive anxiety. According toDalhana Dhairya are valour and courageousness (souryam, sooratvam) and due to the same theimpotent is coward.2. Cyavana Cyavana means the ejaculation of semen. It should be timed optimum. The timing ofejaculation depends on Dhairya.3. Preeti Preeti has been explained as the love towards female sex. According to Caraka Preeti is avariety of pleasure. Preeti is the pleasure from satisfaction which is reflected by joyousappearance of the face or eyes etc4. Harsh Harsh is characterized by ‘amoda’ which is shown by indulgence in dancing, singing,playing musical instruments and remaining in festive mood Harsh in particular to the sexual actmay be termed as an anxiety optimal of course about female sex. Due to harsh the man amorouslydisposed towards female sex. From the above descriptions it is very clear that the functional characteristics of Shukraexplained by Susruta can be incorporated in the human sexual response cycle. Harsh is thepleasure, joy and the attraction making the arousal, Cyavana is the optimal timed ejaculation andPreeti, the resultant satisfaction of sexual act. Dhairya is the maintenance of anxiety only at theoptimal level, never disruptive and it is the conditional factor to harsh, Cyavana and Preeti. Theseall stages seem to be interrelated. The pathological manifestation of these functionalcharacteristics is explained later.Psychological functions Dhairya and Preeti have already been explained. These two characteristics can beattributed to general psychological functioning also. The Shukradhatu imparts a courageous “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 66
  • 85. nature and a stable will power to the individual in his every activity at its optimal excellence.Likewise person will be satisfied with all his performances and enjoyments. By virtue of theexcellence of Shukradhatu the individual will be gentle (soumya) in all his dealings.General body functions Shukradhatu imparts physical power to the individual. explained the provision ofdehabala by shukra in two ways. 1. Utsahalakshanam 2. Upacayalakshanam Utasaha, the enthusiasm to perform any activity is dependent on the Shukradhatu, can beexplained as a physical as well as mental attribute. Upacaya the physical fitness is characterizedby the maintenance of optimal level of all dhatus which impart bala to the individual. Shukra alsohave the function of production ojus.Other functions of Shukra While explaining the shukrasarata (excellency of shukra) Acharyas Caraka attributescertain characteristic. They include gentle look; having eyes as filled with milk (clarity in thesclera); cheerfulness; unctuousness, round, strong, even and beautiful teeth; clean and unctuouscomplexion and voice; dazzling appearance and prominent buttocks. Such individuals are lovedby women; they are strong, endowed with happiness, power, health, wealth, honour andoffspring.Structural and Functional Identity of Shukra From the different descriptions given regarding shukra, its structure and functionalidentity can be understood in a broader sense. The term shukra represents androgens, semen andsperm itself according to the suitability of the contexts. Moreover, the term shukra representscharacteristics in various known and unknown psycho neurological activities. Here the alreadyanalyses details are collectively listed to show the different structural and functional entity ofshukra.Shukra as Androgen “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 67
  • 86. Androgens are the substances having masculanising properties. They are producedmainly from the interstitial cells of testes and from the adrenal cortex in traces. They areresponsible for the growth of sex organs, development of male secondary sex characters, facilitatespermatogenesis muscular development etc. Its activity and production are controlled by thepituitary and hypothalamus. The following references identify shukra as androgen representative.A. Synonyms 1. Pauruhsam 2. Veerya 3. Bala 4. Teja 5. PumsatvamB. Physical characteristics 1. Anubhavam 2. PravańabhavamC. Location - pervaded all over the bodyD. Functional characteristics 1. Harsham 2. Upacayam 3. BalaE. Shukrasarapurusha lakshanasShukra as semen Semen is the suspension of spermatozoa in the secretion of the prostrate, seminal vesiclesand Cowper’s gland ejaculated at the end of sexual act. The following references identify shukraas semen.A. Synonym 1. Retas 2. Anandasamudbhava 3. RoopadravyaB. Anatomical features 1. Vrishana as moola of srotas 2. Sepha as moola of srotas 3. Shukrasaya 4. Shukraharani 5. Shukravahadhamani 6. Shukravaha siraC. Physical characteristics 1. Shukla varńa 2. Madhura rasa 3. Avisra 4. Madhugandhi 5. Bahala 6. Snigdha 7. Picchila 8. Guru 9. Taila kshoudraghritnibhamD. Functional characteristics 1. Process of ejaculation 2. CyavanaE. Description of shukravaha srotas by Caraka “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 68
  • 87. Shukra as spermatozoa Spermatozoa are the male gamete produced from the germinal epithelium of the testis bythe process of spermatogenesis. Its union with ovum leads to fertilization.A. Synonyms: BeejaB. Physical characteristics: Bahu – sperm count Guru – sperm density Ghanam – sperm density Phalavat – viabilityC. Functional characteristics: GarbhodpadanaROLE OF AUTONOMIC NERVOUS SYSTEM Pelvic region is the site where Apana vata is active. Its functions are to bring about theactivities like ejaculation, menstruation, defecation, micturition and parturition. There is enough proof to say that all these activities are influenced in one or the otherway by Autonomic Nervous system.64Grammatical Derivation of Apana “Apanastu apanayati” Grammatical explanation of the word Apana points to take away, to breathe out, to expireto direct downwards etc. That means Apana vata is a type of vata which possess the functionto expel out the excretory products of the body.Location of Apana vata Apana is the one among five subdivisions of the vata, and perhaps the most important 65among them. Acco to Caraka, Apana vata is located in the following areas 1. Two testes (vrushana) 2. Urinary bladder (Basthi) 3. Penis (medhra) 4. Umbilicus (nabhi) 5. Thighs (ooru) 6. Groin (vamkshana) 7. Rectum (gudam) 8. Lower part of intestine (anthra) Susruta in nidana sthana states that the exact seat of Apana vata is the capital place of 66vata itself i.e.in the pakwashaya the capital for all the subdivisions of vata. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 69
  • 88. 67 Pakawadhana is the receptacle of the fully digested food But there is no such separatereceptacle for the fully digested food, since pakwashaya being a place of digestion, contains onlypartly digested food which is received from amasaya and the digestion of such food iscompleted in this region. The nutrients which are the products of digestion are simultaneouslyabsorbed from the intestine. Therefore, pakwadhana can only be assumed as that part of theintestine where the kitta bhaga is left at the end of the digestion, to be transformed intopureesha by the pureesha dharakala of the koshtha. Therefore, pakwadhana may beinterpreted as the lower part of small intestine, colon and rectum. Apana vata is stated to move through the regions of urinary bladder, hips, 68penis, testes, groin and thighs . The word Apana indicates the lower most end. The pakwashayais declared as the most important site of vata, where in vata and its five subdivisions aregenerated. So the pakwashaya is the place where the materials necessary for growth andmaintenance of the body are generated and absorbed, and also the most important humorthe “tanthra yanthra dhara” vata is generated and located. Looking towards these importancesand Apana in prakritha and vaikrithavastha of vata, an effort has been made to study the Apanavata in its totality. According to Cakrapani, pureeshadhana is pakwashaya. But since Caraka mentionedboth pureeshadhana and pakwashaya in the same sloka as seats of vata, it is clear that bothare not one and the same and therefore the argument of Cakrapani is not correct.Pureeshadhana should be considered as that portion of the intestines where in is located thepureeshadhara kala. This pureeshadhana also includes the guda which is mentioned bySusruta as the seat of vata.Gunas of Apana vata Apana vata is having Rookshadi gunas and mala mootradi vikshepana karmas. Here theApana vata is the asraya sthana for its gunas and karmas with samavaya sambhandha in “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 70
  • 89. 69between them, that means can not have their own entity without each other . Guna is the factor having samavaya sambandha with dravya with no chesta (actions) init, but is the cause for the chesta. Here the relation between gunas and karmas are like the causeand effect relationship. Guna is the reason and karma is the effect of that cause. Like thesamavayi relation between Apana and rookshadi guna, no such relations are between guna(rookshadi) and karma (vikshepanadi), though they have cause and effect relationship. Gunaswhenever in samyak yoga with dravya then become able to produce normal karma. If these gunasare in ksheena or vruddhi avastha, then they are not able to produce their normal karmas, eitherless or excess in that order. Apana being a subtype of the vata, have the same guna as that of vata. Taking into consideration of the importance of doshas, always first preference given tovata dosha in every context Rooksha guna of vata both are sneha sadhya, so always rookshaguna has given first preference for vata guna in every context.Functions of Apana vata The action which has to be happened is called as karma. Here karma means not 70karmakaraka but it is the kriya. The word kriya is derived from kru + manina" pratyaya . Apadartha, residing in dravya and responsible for all samyoga and viyoga of the dravya is called askarma. Lots of lakshanas are available in the Classics for karma, but perfect one is "An actionwhich has to be happened as the duty without any other expectation”. In the living body, vata isdominantly responsible for all the normal and abnormal karmas (activity). There is no difference of opinion among the authors regarding the functions of Apana 71vata. They are the following 1. To facilitate the excretion of feces and urine, 2. Ejection of the semen, 3. To cause the menstrual flow, 4. To bear down the fetus at the time of delivery. The principal place of Apana vata is the pakwashaya - a capital of vata also. From this “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 71
  • 90. place, Apana vata keeps control over the karmas happening in its vasti medhradi area. Being inpakwashaya, Apana vata is also in connection with other sub types of vata. Therefore, anyqualitative or functional change in its area as well as in the other subdivision will mayleads to vitiation in pakwashaya as well as Apana vaigunya. So the Apana vata has moreimportance in its sub division group. In addition, the place of Apana vata has its own importance in the contest of vata. It hasbeen stated by vagbhata that Kostha, presently the pakwashaya is the place where vata and its 72five varieties are generated . Here "Generated" means the materials necessary for maintenanceof the structural integrity and also the materials essential for maintaining the functional 73integrity are produced. In short it gives strength to the Dhahran karma of the vata . Vata, the one among the three basic constituents of the living body has its entity mainlybecause of its chala guna and it remains as such until, there is nithya sambhandha in between ayuand sareera. For this nithya sambandha, pitta provides materials from food, kapha is the materialfor that structure and vata creates structure from that material and hold (dharana) it. The meaningof dharana karma is not just limited up to the word dharana. Here it has broad meaning. From thevata, dharana karma expected to maintain the nithya sambandha in between ayu and sareera by itsprakritha guna karmas. Here also ‘dharanat dhathvaha’ of the saptha dhatus and that of vata also differ. Thesaptha dhatus are the structural entity with the functions of nourishment and that of vata isin avyaktha swaroopa with the function of nourishment supply. It is the basic different betweenthe dharana karma of dhatus and vata dosha. Human body is the unique creation of the Almighty. It has the unique property in itsliving state to retain the substances inside the body until it has use and then immediately expulsethat substance when it is of no use. This function is happening through out the body from a celllevel up to the level of all system. In the same pattern, vata performs its dharana karma in the “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 72
  • 91. body by the two ways as follow. 1. Dharana of the shresta dhatus (sara) needful for the living body. 2. Vikshepana of malas (unnecessary substances) By vikshepana, it keeps the body or organ clean and indirectly helps for the dharanakarma. Always the vikshepana is not mean to drive out of the body, but vikshepana may bethe removal of matter from that particular place where it was hold. To detached, from the dravya (dharana of annarasa in the grahani and the dharana of the agni by the samana vata and after pachana kriya, sarakitta vibhajana with vikshepana intheir concerned srotases). This dharana and vikshepana karmas of all subdivision of the vata isgenerated from the Pakwashaya. This also supports the importance of Apana vata. Now in shortthe dharana karma of the five subdivisions of the Vata. It is clear that prana vata performs the dharana karma of its sthana i.e. murdha anddharana of indriya vishaya. This prana vata also performs the function of viyoga in betweenindriya and indriya vishaya with the Co- ordination of Manas. Apana vata also performs thedharana karma of its pakwashaya and dharana of mala mootra, garbha, shukradi vishaya fortime being and at the time of vikshepana of mala mootradi, Apana vata is responsiblefor viyoga of its sthana with its vishaya. In this way, Apana vata, being in pakwashaya, generateother subdivisions of vata, means give strength to other sub-division of vata for their dharana andvikshepana karma as it processes maximum dharana capacity because of its sthira guna andmaximum vikshepana karma. Niskramana karma of Apana vata is not just limited to theexpulsion kriya, but the proper withholding and ejection in the proper direction of sukladi isexpected with the proper functioning of the Apana vata. Apana vata keeps functioning throughout the life, but it shows variation in its retentionand expulsion with its subjects. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 73
  • 92. CONCEPTS ON SHUKRAGATAVATA 1. Quick ejaculation 2. Delayed, retarded and No ejaculation. 3. Missed abortion. 4. Breach presentation of fetus and delayed labour. 5. Various types of deformities and abnormalities in the semen and fetus74.Shukragatavata Shukragatavata is a distinct pathological entity characterized by a group of clinicalpresentations either related with the impairment of ejaculation or with the impairment of seminalproperties. The clinical presentations of Shukragatavata are as follows.1. Early ejaculation Kshipra munccathi Shukrasya seeghram utsargam 75 Pravritti / Atiseeghra pravritti 762. Delayed ejaculation Badhnati / ciram dharayate Sangam Apravriti / Atimanda3. Seminal abnormalities Vikriti Vaikrita / Grathitavivaranadi yuktam4. Affliction of fetus / premature birth / delayed birth Garbhasya vikriti / Vyangatvadinana vikarayuktam garbham / Garbhamapi kshipram munccati va ciram dharayati The different clinical presentations of a same pathological process occur according to theaffliction of the vitiated vata on the various structural and functional attributes of Shukra. Indelayed ejaculation although the intra vaginal ejaculation eventually occurs, it requires a longtime and strenuous efforts at coital stimulation, and sexual arousal may be slow-moving. It maybe caused when the vitiated vata loses its drutatva or calatva after the enlodgement which leads tolack of sufficient stimulation for ejaculation. It may also happen when the vitiated vata causes the “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 74
  • 93. diminution of Shukradhatu by soshanasvabhava, and quantitatively less amount of Shukra isejaculated after long effort. Seminal parameters are impaired when the vitiated vata afflict thefunctional characteristics of shukra as semen or spermatozoa.77 When vata affects these characteristics, Shukradushti explained as phenila, tanu, rooksha78 , grathita, vivarnadi yukta, vatika shukra, grandhi shukra (vatakaphaja), ksheena (vata paittika)79,80 , alparetas, ksheena retas and visushka retas occurs. These are seminal abnormalities lackingin the qualities like count (azoospermia or oligospermia), motility and morphology. The physicalproperties of semen like volume viscosity, appearance, transparency etc may also be impaired dueto vata vitiation. Shukragatavata may afflict the resulting garbha and fetus. Shukra affected by vitiatedvata may cause different disorders like vyangata, premature birth, and delayed birth. In thepresent context the pathological features of the early ejaculation as a result of Shukragatavata aredealt in detail. To analyze the pathology of early ejaculation on Ayurvedic line, the functionalapproximation of Shukra, manah and vata along with activities of vata on psychosexual parlancehas to be traced out.Functional approximation of Shukra, Vata and Manah 1. Shukra, Manah and vata are located all over the body. 2. Shukra is explained as tvakstha, tvak is in samavayi sambandha with Manah and thus to vata.81 3. Shukra is explained as sookshma or anubhava 82, Manah ha anutva property and vata is also sookshma. 4. Shukra is having the property of saratva; Manah and Vayu are explained as gatiman. 5. Vata is explained as stimulator (pranetah) and controller (niyantah) of Manah. 6. Different functions attributed to Shukra viz Dhairya, Cyavana, Preeti, harsh, etc. can be explained on neuropsychological axis. 7. Vata is explained as the yoni receptacle for harsh and utsaha which are functionally attributed to shukra. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 75
  • 94. 8. All indriyas (including upastha) are under the control of Manah and Manah itself at the control of vata 9. Harshasakti depends on dehashakti as well as satvasakti.83 10. Su-prasannah Manah is necessary for harshana.84Activities of vata on psychosexual parlance Vata is described as the agent who restrains and impels mental activities.85 It isresponsible for the functional format of mind. The control and stimulation are the bifold activityof same initiation which is antagonistic in nature. A balance between these two is necessary for an optimal arousal, activity andachievement of target action. A vitiated vata may cause the mental activities adversely indifferent dimensions. As far as the particular problem of premature ejaculation is concernedvitiated vata causes over stimulation leading to lack of control over physiological andpsychological activities. In premature ejaculation vitiated Vata causes over stimulation of Mana leading to lack ofcontrol over physiological and psychological activities. Dhairya, Cyavana, Preeti and Harsha arethe functions of Shukra. Optimum Cyavana occurs due to optimum Dhairya which is controlledby Mana which in turn is controlled by Vata. Harsh, Cyavana and Preeti are also under thecontrol of Vata and Mana. If there is proper Samkalpa and any of the 5 senses are stimulated thenharsh results, this should culminate into optimum Cyavana, for the individual to experienceoptimum Preeti. Over stimulation occurs as a result of vitiation in Vata and increase in Rajo Gunaand Calatva of Mana as a result of which the optimum time from the commencement of Harsh toachievement of Preeti due to timely Cyavana is cut short as a result of which prematureejaculation occurs. This can be understood on the basis of Suchi Patra Nyaya according to whichthough 100 lotus petals seem to be penetrated by the needle at once, though the needle ispenetrating one petal at a time ultimately penetrating all the petals. In the same fashion Preeti isachieved when every part of the sexual response cycle is enjoyed slowly and steadily and notthrough immediate climaxing. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 76
  • 95. All the subcomponents of vata have influence on physiology of shukradhatu. Out of thesubcomponents pranavayu, udanavayu, vyanavayu and apana vata are having direct relationshipin the psycho neurophysiology and haemodynamics of the sexual response cycle in male. Prana isexplained having the functions of manodharana and budhuidharana (holding proper intellect andmental faculties). Udana have the functions of manobodhana, dheebodhana dhriti bodhana andsmritibodhana. The word bodhana is used to denote samvahana (carrying out) and pariposhana(excitation) etc. So it is responsible for the recollection, imagination, fantasying etc. along with acontrol (dhriti) over the stimulation. So prana and udana unitedly make the cognitive aspects ofsexual response. They constitute the appetite phase of sexual response cycle. These componentsof vata also causes psychogenic and reflexogenic erection. An optimal activity of prana associated with udana stimulates vyana vayu which issituated in the hridaya. Vyana vata is explained to be having the functions deposition of semendeep in the vagina. Indu while commenting on the above opines that the vyana vata present in thefemale partner directs the semen ejaculated by male to the interior of vagina. But considering thelocation, activity and other features of Vyana vayu the above description is suitable for explainingthe haemodynamics in mechanism of erection. The activities of Prana, Udana and Apanaconstitute the excitement and plateau phase of male sexual response. It is generally assumed thatparasympathetic system facilitates the process of erection. At the peak level of continuous stimulation Vyana vata itself responsible for theemission; this is controlled by sympathetic activity. The further steps of ejaculation i.e. ante gradeejaculation with forceful spurts and bladder neck closure is controlled by Apana vata. Apana vatais responsible for the nishkramana of shukra, mootra etc. The release (nishkramańa) of shukraalong with dharana (retention by bladder neck closure) is Para sympathetically activated. It is alsoobserved that before ejaculation the level of oxytocin (the hormone responsible for the expulsionof fetus during delivery- an activity of Apana vata) is raised in man. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 77
  • 96. From the above description it is clear that a coordinated activity of Prana, Udana, Vyanaand Apana vata are very necessary for a good erection and rigidity, sufficient vaginal containmentand penile thrust and an optimal timed ejaculation. A derangement in this, probably caused by animpairment in the activities of sub components of vata ultimately leads to a poor erection andearly ejaculation as in the case of an over activity of sympathetic nervous system.Pathogenesis of Shukragatavata leading to early ejaculation Gatatva mode of pathogenesis of vata is the key phenomenon occurring in themanifestation of Shukragatavata. Pathological advances happen in three spheres – vata, Shukraand Mana, the psychoneuro sexual axis. Here an attempt has been made to formulate thepathogenesis of Shukragatavata leading to PE on the basis of shadkriyakalas; via Sancaya,Prakopa, Prasara, Sthanasamsraya, Vyakti and Bheda.Kriyakala in of Shukragatavata (Seeghram utsargam) i.e. PESancaya (Stage of accumulation) In the prime stage the etiological factors which are responsible for vata vriddhi(svanidana) causes an increase in the qualities like rooksha, laghu, khara, sookshma, cala, seeta,etc. The accumulation of vata is at its own seat. This accumulation of vata is of a condensed formand seta Guna is always favorable for such a condensation. Shukradhatu viguna aharaviharas (etiological factors antagonistic to shukra) causesreduction in the excellency of shukradhatu. Many a time certain Nidana are (like Katu Amlasevana, shukra Vega dharna etc). Vata provocative as well as antagonistic to Shukra. Thediminution of shukradhatu is characterized by diminution of properties like guru, snighdha,bahala etc. of shukradhatu. Diminution of shukra may take place by rasakshaya also (Klaibya isincluded in rasapradoshaja vikaras also). Nidana causing manoabhighata (Psychological stress) lead to derangement in the mentalfaculties. It may produce a comparative aggregation of raja and tama and reduction of satva onpsychic sphere. An increase of rajah causes development of dukha, akarunya, dama, Manah, “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 78
  • 97. harsha, Kama, krodha, matsara, etc. Likewise tamo vriddhi leads vishada, nastikya,adharmaseelata, budhirnorodham, anjanam, bhayam, akarmaseelata etc. In brief these factorscause gradual development of anjana adhairya, bhaya, vishada, adhriti, shoka, cinta and krodha.Again they cause further vatavriddhi and shukrakshaya. Moreover, Nidanas explained related tosexual act intersperse with manah as well as shukra. Over worrying also causes rasavahasrotodusti.Prakopa (Excitation) Prakopa is characterized by a liquefaction of samhatadosha in caya stage at its own site.In this stage dosha gets more free movements at its own site. The aggregation of rookhsa, laghu,khara gunas and Vishada contributes the attainment of more cala Guna in situ. On advancementof Samprapti gradual diminution of shukra quantitatively and qualitatively continues. Theimpairment of mental faculties also progresses in this stage.Prasara (spreading) In this stage doshas are in a state of spreading and extending to other parts of the body.When the etiological factors of Prakopa stage continues the doshas expand, increase and thenoverflow the limits of their respective sites. By taking advantage of aggravated cala guna vataattains increased gati and follows specific pathway. Continuous diminution of shukradhatu causes Riktata in Shukradhatu and shukravahasrotas. Riktata will also be present in rasavaha srotas. The direction of vata which adoptedabnormal gati will be towards shukra taking the benefits of Riktata in the dhatu. The impairmentof mental faculties may also be attributed to the abnormal functioning of components of vata viaPrana and Udana. The imbalance in the activities of Prana and Udana in psycho sexual parlance causesimpairment in manobudhi dharańa and mano budhi dhriti smriti bodhana respectively. This leadsto misconception and performance anxiety in the affected.Sthanasamsraya (Enlodgement) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 79
  • 98. The vata with aggravated gati advancing to the shukrasthana which is rikta gets localizedin the specific site. Here the dosha dooshya samoorchhana happens. The specificity of the Nidanaproduces affinity to vitiated vata for localization in the particular site or dooshya. Precisely thestage can be called Shukragatavata. After sthanasamsraya the manifestation of the disease starts.Vyakti (Clinical presentation) The Shukragatavata when occupies the localized site and advances the samprapti it maybe called Shukrasthavata precisely. The vitiation of vata in the shukra may produce functionaland morphological impairment of shukra; accordingly the clinical presentations will be found.The morphological impairment will cause shukravikriti and successive affliction of garbha. Thefunctional abnormalities may be of two types. 1. Apravritti 2. Atipravritti If the vitiated vata cause apravritti in the shukravaha srotas the clinical presentation willbe of delayed ejaculation (Badhnati / sangam / ciram dharayate).Seeghram utsargam (Premature ejaculation) If the vitiated vata causes atipravritti functionally in the Shukravaha srotas it leads toearly ejaculation during sexual act. Vata is causing the control (niyanta) and stimulation (praneta) of mental activities andthus by shukrapravritti. A balance between these two is necessary for an optimal arousal activityand achievement of target action. Vitiated vata responsible for atipravritti in shukravaha srotascauses over stimulation leads to abnormally steep arousal and activity with lack of control overejaculation. Vata in particular if considered as subcomponents, Prana and Udana causes impairedactivity on mana, budhi, dhriti and smriti faculties of mind. This phenomenon leads to mentaldisturbance during sexual act, cognitive impairment and lack of control over sexual act. Vyanavata that is responsible for the deposition of shukra in the vagina along with apana vayu, which isresponsible for dharana as well as nishkramańa of shukra cause early ejaculation. As the vitiated “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 80
  • 99. vata affects the shukra, the psychosexual functions attributed to it also get impaired. Thus thesefunctions are resultant of the co-ordinate activity of Prana, Udana, Vyana and Apana vata. Dhairya, Cyavana and Preeti are interdependent and their chronological order issignificant in the context of human sexual response. An impairment of these functions leads tolack of dhairya (performance anxiety), seeghracyavana and preetyabhava (lack of satisfaction).Many a time this impairment continues in a vicious circle.Bheda (Complications) On persistent failure in having Dhairya, controlling Cyavana and enjoying Preeti it maymake so many inter personal difficulties. The problem may make frustration in the individual andpartner (sadarabaaha). It may further cause extreme manovibhramsa and allied symptomatologylike generalized anxiety and even suicidal tendency etc. The etiopathogenesis of shukrasaya seeghram utsargam in Shukragatavata is shown in theflow chart following.Etiological Factors Etiopathogenesis of Shukragatavata with clinical presentation of shukrasya seeghramutsargam. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 81
  • 100. Etiological Factors Dhatuvigunahara Vataprakopaka Manoabhighata Viharas aharaviharaRasadhatu Shukradhatu Caya of vata (Svasthana) Vriddhi of (Vridhi of rooksha, laghu, Tama & Raja Sukshma, cala, sita, GunasRasakshaya Dhatudourbalya in Anjana, Adhairya, Prakopa of vata Shukradhatu Bhaya, Vishada, (Svasthana) Adhriti, soka, (Diminution of guru, (Vridhha rooksha, cinta, krodha Snigdha etc) laghu etc. favours cala Guna)Rasaprodosha Riktata in shukradhatu Prasara of vata (Gamana) and Shukravaha srotus (Attains Gati) Sthana samsraya in Shukrasthana (Shukrastha) Vyakti (Shukrastha) Prana Udana Apana Vyana Affliction Manaha, Bhuddi, Driti, Smriti, Sukrapradipatana and Shukravisrga Lack of Dhairya Lack of Preeti Early Cyavana“Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 82
  • 101. Shukragatavata and Shukravritavata The symptomatology of Shukragatavata and shukravritavata looks alike. Treatmentsuggested by Caraka and Vagbhata for shukravrita vata is to follow the line of treatment ofShukragatavata (Poorvavat retasavrite). Susruta has not explained Shukravritavata. On a closeanalysis of the symptomatology of both clinical conditions shows certain differences in betweenthem. Table No. 9 Differences between Shukragatavata and ShukravritavataNo Shukragatavata No Shukra Avrita Vata1. Kshipram Munchati (Ca.) 1. Ativega (Ca. and AH.) Sukrasya Seeghram utsargam AH. Atiseeghrapravritti (Dal. on. S.)2. Badhnati / Ciram dharayate 2. Avega (Ca. Ci. 28/34)3. Shukravikriti 3. Nishphalatvam (Ca.) Garbhajanana phala rahitatvam (Gang. on Ca)4. Garbhavikriti 4. - In Shukravritavata the clinical symptomatology are different. ‘Ativega’ may bemanifested by early, forceful or repeated ejaculation which is not clear. The commentators alsokept silent in this regard. The term Vega means pravrityunmukhatvam (about to act) orgatidayako gunaha (property giving movement). The term is also used to denote episodes ofattack of disease like akshepaka, jwara, etc. within intervals. But ‘avega’ clearly indicatesanejaculation. It is entirely different from delayed ejaculation as in the case of Shukragatavata.Anejacation may be due to retrograde ejaculation. The ‘shukra ’in case of shukravrita vata isexplained as ‘Nishphala’. It means that it will be never capable to impregnate. In the caseShukragatavata the shukra is capable of impregnation but may cause deformities or abnormalitiesin the fetus. As the impregnation is not at all possible chances of delayed or premature birth as inthe case of Shukragatavata is not relevant in Shukravritavata. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 83
  • 102. Still Shukragatavata and Shukravritavata are having similarly in symptomatology. So thatAcharyas suggested the same treatment for both.Physiology of ejaculation - Ayurvedic perspective The virility is dependent upon physical and mental strength and the sexual urge born ofvirility. So it is important to consider both physical and psychological factors to explain thephysiology of sexual act. Ejaculation of semen is a frequent accompaniment of erection andfollowed by sexual act, where erection is a necessary prerequisite to accomplish the sexual actculminating in ejaculation may be divided into 4 stages according to the description given inAyurvedic classics 1. Samkalpa 2. Ceshta 3. Nishpeedana 4. Shukrasravana1) Samkalpa (Passionate attachment) The mental preparation for sexual act may be termed as samkalpa. This includesenjoyment by all sensory organs except tvak. It also comprises the cognitive aspects of sex likerecollection, imagination, fantasy etc. This is the psychic element which causes erection. Theclarity of mental faculties is necessary for a good arousal. A person who is free from fear, complexes and diseases, habituated to daily sexualintercourse, who is having intimate companions, having accomplished their objectives, who aremutually helpful, who are endowed with noble lineage, magnanimity, skill, character and purity,who are free from grief and pain who have lovable and pleasant disposition pleasant in speech;such a man gets promotion in his virility. Erotic articles work as sex stimulants in variousseasons. A broad mind which is free from anxiety, a sense of achievement, new love, presence ofmuch-loved etc. are weapons which cupid wields. Various psychic stimuli obtained from theobjects of different sensorium initiate arousal. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 84
  • 103. Roopa (Sight) Beautiful, youthful and exhilarating female partner is considered as an aphrodisiac parexcellence. Similarly big ponds having lotus flowers, mountains with blue peaks, onset of blackclouds, rise of beautiful moon at night etc are extremely sensible to erotic stimulation.Rasa (Taste) Articles which are madhura, snigdha and jeevaniya etc. excite the mind thus act asstimulant to copulate with women. Alcohol has the capacity to lengthen the sexual act probablydue to the fact that in desirable quantity it is the excellent article for promoting exhilaration.Pleasing diet and drinks also promote sexual arousal.Gandha (Odour) In erotic classics woman are divided into different types according to the body odour viz.padmini (lotus odour), citrini (honey odour), shankini (alkali odour) and hastini (odour ofelephant tear). This may be compared with the concept of pheromones which cause arousal inanimal. Apart from this the fragrance of jati, utpala and other pleasing odours improves the sexualresponse.Sabda (sound) Melodious songs, pleasing sounds of birds, sounds of ornaments of women, sound ofriver waves, thundering of clouds, sound of music initiates the erotic feelings to cohabit withwoman.2) ChestaSparsa (Touch) The main object and mean of sexual arousal is tactile stimulation. Shukra is explained allover the body seated on the sparśanendriya (tactile sensorium). The mind is in inseparable union(samvayi vyapaka) with tvak. The sense of touch alone pervades all the senses the tactilestimulation results in erection and is necessary for the maintenance of rigidity and culmination inejaculation. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 85
  • 104. The Shukra present in the tvak (tvggatam Shukram) by continuous erotic stimulation getsejaculated. The classical erotic books explain certain erogenous zones classified as candrakala orkāmakala Cumbana (Kissing) mardana (caressing), dantakshata (biting with teeth), nakhakshata(nail scratching) etc. are advised to optimum level of arousal in sex classics.3) Nishpeedana (Specific stimulation /Rubbing) Specific stimulation of the local genital parts especially in the glans penis causes theejaculation and orgasm. The sensitivity of the tvagindriya producing apparent sensory stimulationis important in regard to the process of ejaculation.4) Shukra Nishkarana (Ejaculation) Shukra pervades the entire body which has the sensation of tvak. As water comes out of awet cloth when squeezed, similarly, the semen trickles out from its site during copulation betweenthe man and woman, because of sex act (ceshta), passionate attachment (samkalpa) and physicalpressure or rubbing (Nishpeedana). Compares the ejaculatory physiology with that of lactationsince both are deeply associated with psychological factors. Susruta explains the physiology ofejaculation as a combined activity of vata which is heightened by the heat generated in the act ofcopulation as a result of the rubbing of female and male genital organs which dispels the ShukraYasodhara explains the Shukraksharana (semen fall) as two types. 1. Syndana (Oozing) 2. Visrishti (Forceful ejaculation) Syandana leads to moistening only but visrishti along with coital friction gives rise toorgasm. Syndana may be termed as emission and visrishti as ejaculation. There are three kinds ofvisrishti according to duration of sexual act as cira sambhava (long timed), madhyama sambhava(moderately timed and seeghrasambhava) short timed. Three examples have been cited by Caraka to explain the pervasion of semen in theentire body of the individual they are (1) Juice present in the entire sugar cane, (2) Ghee available in the whole curd and “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 86
  • 105. (3) Oil available in the all parts of sesame seed. Cakrapani while citing these three examples, explains categorization of persons into threegroups according to the duration of sexual act viz. one group in which Shukra is ejaculatedwithout much effort, (as that of extraction of juice from sugar cane), the second group withmoderate effort and time (as in the case of removal of ghee from curd) and thirdly with mucheffort and time (as in the case of extraction of oil from sesame seed). 1 Harshat 5 Gouravat 2 Tarshat 6 Anubhavat 3 Saratvat 7 Pravanabhavat 4 Paicchilyat 8 Marutasya drutatvatHarshat (Due to excitement) Harsh is termed as stimulating pleasure to initiate the sexual act by psychologicalmeans.Otherwise ‘harsh’ can be explained as the desire produced from Samkalpa (fantasy)leading to erection and ejaculation. The word ‘harsh’ has been used to denote different meaningslike ananda, thinjhinika (numbness), Preeti, Kama, tushti etc. Terms like padaharsha, rom harshaetc. are also used. In the present context the term harsh means the psychological processingdeveloped from the enjoyment of different sensorium leading to the arousal and an alteration ofconsciousness which is gradually developing.Tarshat (Due to Desire) Tarsa is the desire on female partner (vanitanamabhilasha). The word tarsha is also usedto denote Trisha and trsinha, both means thirst. In the present context tarsha may be termed assatisfy for having sexual union with female partner. Both the above two (harsh and tarsha) arepsychological entities.Saratvat (Due to fluidity) Instability (asthairyam) is termed as saratvam because of fluidity the Shukra is unstable.The substance which is having the potency of prerana (stimulation) is called Sara. Sara propertycauses anulomana and it is said as pravartaka. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 87
  • 106. The opposite quality of Sara is sthira. The substance which possesses the quality ofretention is called sthira. So due to natural quality Shukra it tends to flow with out any retention.Paicchilyat (Due to sliminess) It is said that due to sliminess the Shukra flows out. Picchilata due to its lepan svabhavacause easy flow without any friction.Gauravat (Due to heaviness) Heaviness of Shukra also helps in ejaculation. Gourutva is the character which causespatanakarma (falling down).Anu Bhavat (Due to Atomicity) Shukra is possessing atomicity. Anubhava favour saraguna also by which ejaculationhappens.Pravanbhava (Tendency to flow out) Shukra possess bahirnirgamanasvabhava tendency to come outeven though it is anu.Pravana is used to denote the unmukhtata in the context of action of vamana drug. The factors Sara, paicchilya, guru, ańubhava and pravańabhāva are the physicalproperties of Shukra which helps in ejaculation. The edition of Caraka with Gangadharacommentary has a different version of sloka in this context. In this text ‘tarsha’ has been deletedand instead ‘soukshmya’ has been added. ‘Soukshmya’ is similar to the property of anubhava.Including Soukshmya, the six qualities starting from saratva and ending in anupravańabhava aredescribed as inherent action (naisargika karmas) of Shukra.Marustsya Drutatvat (Due to fastness of Vayu) The activity of ejaculation is carried out by vata, which have drutgati (Fast movingnature). The local vata which controls and stimulates the sex organs specially the sites of semen,exerts force during the sexual act, as a result of which the semen comes out of its place and getejaculated through the genital organ. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 88
  • 107. From the description of the eight factors responsible for ejaculation, it can be pointed outthat psychological, neurological as well as physical properties of shukra have their role in theprocess of ejaculation. Alteration in any of the above characteristics may lead ejaculatoryimpairment. The four stages of sexual act described in Ayurvedic classics Samkalpa, chesta,Nishpidana and Shukrasravana have similarity with the different stages of sexual responsedescribed as desire, excitement, plateau, orgasm and resolution.DEFINATION of Premature ejaculation Premature ejaculation is defined as “stressful recurrent ejaculation with minimal sexualstimulation and before the subject wish it” which is associated with “marked distress orinterpersonal difficulty.” 86 Premature ejaculation occurs when man orgasms during intercourse sooner than he or hispartner wishes. 87 A universally accepted definition has yet to be established. Masters and Johnsonproposed that premature ejaculation is the inability of a man to delay ejaculation long enough forthe woman to reach orgasm 50% of the time.88 Some authors have defined premature ejaculation as the number of vaginal thrusts theman makes before ejaculation. 89-90 Clinical studies have used intra vaginal ejaculation times asmeasured by a stopwatch to define premature ejaculation. Standardized inventories may beavailable in the future, which will generate individual data on the subjective perception of lack ofcontrol and associated distress. The Second International Consultation on Sexual and Erectile Dysfunction has definedPE as ‘ejaculation with minimal stimulation and earlier than desired, before or soon afterpenetration, which causes bother or distress, and over which the sufferer has little or no voluntarycontrol’. There are a number of definitions, none of which is wholly satisfactory. Most men withPE readily recognize their problem and there is no lack of self-assessment. Most men who report “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 89
  • 108. PE usually ejaculate prior to or within 1–2 min after vaginal intromission. A small proportion ofmen ejaculate prior to intromission. 91 Prematurity is a condition where in a man is unable to exert voluntary control over hisejaculatory reflex, with the result that once he is sexually aroused, he reaches orgasm veryquickly. Masters and Johnson diagnose a man as a premature ejaculator if he reaches orgasmbefore his wife does more than 50% of the time. It is very clear that a universally accepted definition of premature ejaculation has notbeen agreed upon. In a review of literature, Metz, Pryor, Nesvacil, Abuzz Ahab and Koznar(1997) point out that the time to ejaculation after penetration is not a useful criterion for definingpremature ejaculation because this time varies from 1 minute to 10 minute in published studies.DSM – IV-TR has avoided using objective criteria and has relied on clinical judgment to makethe determination. Basically these definitions conceptualize prematurity in terms of time; it takes a man toreach the plateau stage in the sexual response cycle. Prematurity cannot be defined in quantitativeterms because the essential pathology in this condition is not really related to tome. Rather thecrucial aspect of prematurity is the absence of voluntary control over the ejaculatory reflex,regardless of whether this occurs after two thrusts of five, whether the female orgasm or not.Prematurity can thus be said to exist when orgasm occurs reflex, i.e. when it is beyond the man’svoluntary control once an intense level of sexual arousal is attained. Conversely, an ejaculatorycontrol may be said to be established with the man can tolerate the high levels of excitement. Premature ejaculation (ejaculation praecox, rapid ejaculation, or early ejaculation) is themost frequent male ejaculatory disturbance.92 Excessive stimulation of the ejaculatory centre in the hypothalamus is usually of corticalorigin, caused by over-excitement or anxiety. The recommended definition of PE is an ejaculationthat occurs within 1 min after vaginal penetration or experiencing ejaculation that occurs too earlyfor partner satisfaction in at least half of attempts at intercourse.93-94 “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 90
  • 109. Defining “Normal” in Premature Ejaculation Rosen (2000) highlighted how the lack of clear diagnostic criteria has led to problems indefining the prevalence of PE and that prevalence values varying from 25% to 60% have beenreported, depending on the criteria used. However, despite the lack of diagnostic acuity, Rosenconfidently states that PE is the most frequent sexual complaint in men. 95 An accurate determination of the prevalence of any condition depends on an accuratedefinition of what is “normal.” Such a definition has been lacking for PE. In many respects thisreflects the multifactor influences on ejaculatory latency, and therefore defining normalejaculatory latency is difficult. First, there is a wide variation in men’s, and their partners’,perception of what is normal. In the Multi Country Concept Evaluation and Assessment of PEincidence study the perception of how long it takes for the “average” man to ejaculate variesbetween 7 and 14 minutes.96 These estimates show substantial geographical variation inperceptions. Among the countries included in this study, the perceived average latency time forGerman men was only 7 minutes, but was over 13 minutes for men from the United States. Theperceived average for men in the United Kingdom, France, and Italy was similar, at around 9.6minutes. Generally, women’s estimates of the “average” ejaculatory latency were similar to men’s,albeit a slight underestimation. The most striking disparity was observed between U.S. men andwomen, with female partners consistently estimating lower ejaculatory latencies than theirpartners (11.2 and 13.6 minutes, respectively). Conversely, German women were more generousin their estimation of “average” time to ejaculation than their partners (7.4 vs. 6.9 minutes,respectively). The difficulties in defining “normal” ejaculatory latency are mirrored in the absence of auniversally accepted clinical definition of PE. The most obvious limitation of such definitions liesin the subjectivity of the diagnostic criteria, which individually do not provide a basis for eitherthe definition of the condition or the study of the effects of treatment there upon. This problem “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 91
  • 110. was highlighted by Rowland et al. (2001) who emphasized the wide variations in the definitionsof PE used in some 45 studies conducted between 1963 and 2000.97 Quantifiable ejaculatorymeasures (e.g., latency, number of thrusts) or subjectively assessed PE criteria, such as perceivedlack of control, were reported in less than 50% of studies. Furthermore, while intra vaginalejaculatory latency time (IELT) was the most commonly used index of PE, the cut-off points forlatency varied from 1 to 5 minutes. While most men who present to practitioners with a premature ejaculation problem haveaccurately self-diagnosed their condition, it is less apparent that men, collectively, are aware thatPE is a medical and therefore a treatable condition. This accents the need for studies that willdefine attitudes toward PE. Such studies should generate a clear definition of PE and facilitatedevelopment of validated tools to measure ejaculatory control and the associated levels of sexualsatisfaction.Premature Ejaculation – Various authors to define premature ejaculation have suggested a number of definitions.But an exact definition of PE is rather difficult. It is due to the fact that in most instances therewill be a disturbance in both subjective sense of pleasure or desire and objective performance.The standards of normality regarding the time of sexual act or satisfaction depend upon numberof variables. For example the length of foreplay varies from couple to another, which is having adirect link with the amount of satisfaction. Due to the same fact of difference in the preferencesand approaches in sexual act, standards of normality to the western population may not be fit foreastern population. However, here an attempt has been made to collect the different definitionsput forward by various experts of the field. Many of the definitions were made on the basis ofsurvey studies. 1) Jon Meyer (1970) suggests that an ejaculation any time prior to, or during the first fifteen thrusts is premature. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 92
  • 111. 2) O’Connor (1976) reports that an ejaculatory delay of 1 – 1½ - 2 minutes may be considered as premature. 3) Alfred Kinsey considers premature ejaculation as a clinical condition when a man discharges within 30 seconds of penetration. 4) According to Helen Singer Kaplan in “The New Sex Therapy”, the essence of prematurely is the absence of voluntary control over the ejaculatory reflex once a high level of sexual excitement is reached. A premature ejaculator cannot control his orgasm and secondly, he does not feel the intense erotic pleasurable sensation when he is aroused. Dr. Kaplan calls this phenomenon as ‘genital anesthesia’. 5) International sex therapist Dr. Kothari (Bombay) says that prematurely ejaculating person is actually suffering from the premature or early orgasm. 6) He refers the condition as early orgasmic response. So it can be defined as it indicates a state of gap between person’s expectation and his performance vis -a-vis his orgasm. 7) Premature ejaculation is defined as an inability to delay ejaculation less than one minute. 8) Ejaculation prior to ten pelvic thrust is also termed as premature. 9) Absence of voluntary control over the ejaculation, regardless the duration of penetration, number of thrusts or frequency of the partner’s orgasm. 10) In ‘Human Sexual Inadequacy’ Masters and Johnson (1970) made an attempt to define premature ejaculation in terms of the interaction between sexual partners, not just the male alone. A man was considered to ejaculate prematurely if his partner was not orgasmic in at least 50% of the coital episodes.The all above mentioned definitions are based on the following four factors. a. Duration of sexual act b. Number of penile thrusts c. Satisfaction of the partner d. Voluntary control of ejaculation Older definitions that used a specific duration of intercourse as the dividing line or thatspecified a minimum number of penile thrusts before ejaculation have now been discarded.Masters and Johnson comments on this as it is fortunate because some men actually tried to timethemselves with a stop watch to determine if they were normal and others tried to hurry theirthrusting although this usually speeds up ejaculation instead of delaying it. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 93
  • 112. The definition suggested by Masters and Johnson on the basis of female satisfaction alsolacks precision. Specifically, it could not be applied situations in which woman was in frequentlyorgasmic or never had orgasms during intercourse, and it was an arbitrary way of estimatingnormality at best. Helen Kaplan’s definition regarding absence of voluntary control overejaculation is also not exactly applicable as most sex therapists agree that an absolute voluntarycontrol over timing of ejaculation is not possible. It is an exception rather than a rule. The American Psychiatric Association has recentlyside stepped these issues of defining premature ejaculation in terms of ‘reasonable voluntarycontrol’. According to American Psychiatric Association in Diagnostic and statistical manual ofmental disorders fourth edition (DSM IV) premature ejaculation is defined as- 1) Persistent or recurrent ejaculation with minimal sexual stimulation before on or shortly after penetration and before the person wishes it. The clinician must take into account factors that effect duration of the excitement phase, such as age, novelty of the sexual partner or situation and recent frequency of sexual activity. 2) The disturbance causes marked distress or interpersonal difficulty. 3) The premature ejaculation is not due exclusively to the direct effect of a substance (e.g. withdrawal from opioids). The above said diagnostic criteria clarify different aspects of the clinical condition. Stillthere are some problems with this definition also. What is minimal? Sexual stimulation. (Mostmen are not premature in ejaculation with stimulation other than intercourse) What does shortlyafter mean? (According to Kinsey data 75% of men ejaculate with two minutes intermission).And what if a person “Wishes” it to last 3 hrs but in actually able to last “only” 30 minutes? Despite the shortcomings of these definitions it is usually not too difficult to decide whenrapid ejaculation is problematic in a sexual relationship. For this all aspects of sexual act and its “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 94
  • 113. objectives should be considered with giving equal importance to subjective sense of pleasure ordesire and objective performance. Such an approach is made in the present study. The International Classification of Diseases, Tenth Edition (ICD-10) [WHO] defines PEas a condition characterized by, These definitions of PE concentrate on three central criteria of diagnoses, 1) A reduced intra vaginal ejaculatory latency time (IELT). 2) Diminished control over ejaculation. 3) Decreased satisfaction with sexual intercourse. Ejaculatory latency of 2 minutes or less may qualify a man for the diagnosis, whichshould include consistent inability to delay or control ejaculation and marked distress about thecondition. All three components should be present to qualify for the diagnosis. Subtypes of thedisorder are symptom-based, including lifelong versus acquired, global versus situational PE, andthe co-occurrence of other sexual problems, particularly ED. About 30% of men with PE have co- occurring ED, which typically results in early ejaculation without full erection. A wide degree of severity is seen, with patient’s ejaculation on or prior to penetration inthe most severe cases. Even this hasnt been standardized. Many additional parameters need to belooked at and the importance of physical factors (increasingly incriminated in PE) mentioned inetiology below need to be incorporated. Medical literature contains several one dimensional andmulti dimensional operational definitions of PE. The lack of agreement as to what constitutes PEhas hampered basic and clinical research into the etiology and management of this condition.Quantitative measures of intercourse such as the intra vaginal ejaculatory latency time (IELT), thenumber of thrusts between penetration and ejaculation, the extent of partner sexual satisfactionand the patients assessment of his voluntary control over ejaculation have been described. Eachof the three criteria above has been operational zed, although not always with consistency.Operationalization of PE using the quantifiable and objective number of intra vaginal thrustsbetween penetration and ejaculation has been reported by several authors; however these “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 95
  • 114. definitions were subjective, and not supported by normative data. Operationalization of PE usingthe length of time between penetration and ejaculation, the intra vaginal ejaculatory latency time(IELT), forms the basis of most current clinical studies on PE. There is considerable variance ofthe latencies used to identify men with PE with IELTs ranging from 1 to 7 minutes and none ofthe definitions offer any supportive rationale for their proposed cut-off time or normative data.The inability to control and defer ejaculation until the female partner was sexually satisfied on atleast 50% of intercourse attempts were proposed as a definition of PE by Masters and Johnson,however these definitions were subjective, and not supported by normative data.Operationalization of PE using the length of time between penetration and ejaculation, the intravaginal ejaculatory latency time (IELT), forms the basis of most current clinical studies on PE.There is considerable variance of the latencies used to identify men with PE with IELT rangingfrom 1 to 7 minutes and none of the definitions offer any supportive rationale for their proposedcut-off time or normative data. The inability to control and defer ejaculation until the femalepartner was sexually satisfied on at least 50% of intercourse attempts was proposed as a definitionof PE by Masters and Johnson. An inherent problem exists in defining a man as dysfunctionalbased on the sexual responsively of his partner, as only 30% of women achieve orgasm duringsexual intercourse regardless of the extent of their partners ejaculatory control and latency. The lack of a reliable operational definition for PE has severely limited clinical researchinto the understanding of PE as studies that fail to define PE offer meaningless or difficult tointerpret results. The lack of a universally accepted operational zed definition makes comparisonof different studies difficult or impossible as experimental group subjects in one study may verywell have been placed in the control group of a second study. The following multivariatedefinition of PE was proposed at, The WHO 2 nd International consultation on Sexual Dysfunction as "persistent orrecurrent ejaculation with minimal stimulation before, on, or shortly after penetration, and beforethe person wishes it, over which the Sufferer has little or no voluntary control which causes the “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 96
  • 115. sufferer and/or his partner bother or distress." However, the limitations of these criteria areemphasized by the fact that very few men or their partners know what constitutes a "normal"ejaculatory latency.Etiological considerations of premature ejaculation It is habitual to classify the causes of sexual dysfunction in general as organic (physicalor medical factors such as illness, injury or drug effects), physiological or psychosocial (includingpsychological, interpersonal, environmental and cultural factors). The precise cause of prematureejaculation in a given individual cannot always be identified, and in some instances, it may becombination of several different factors. The various etiological factors operating in themanifestation of premature ejaculation are collected and listed under the following threeheadings. 1. Organic 2. Physiological 3. Psychosocial1. Organic causes Although it is often stated that premature ejaculation can be caused by local pathologicalstatus such as prostitis or urethritis (Kaplan 1974) no evidence of such causation is available. Norit is any evidence of drugs causing premature ejaculation. But certain stimulants drugs likecocaine (a general CNS stimulant; augments sympathetic nervous system functions) andAmphetamines (a general brain stimulant) may enhance the orgasm. THC (Tetra hydro cannabin)included in the group of Hallucinogens is also suspected to be having enhanced orgasm response.Ephedrine, an anti asthmatic agent which is having alpha-adrenergic stimulator property was usedfor treatment of failure to ejaculate. Some times withdrawal from opioids may cause prematureejaculation. Neurological disorders should be considered when ejaculatory control was previouslygood such as diabetic neuropathy. But these all factors are now a day not taken as valid. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 97
  • 116. The etiology of PE is based on a genetic predisposition and, although cognitive andemotional influences interact with these primary defects, the psychological disturbancesassociated with PE may be secondary phenomena. Moreover, this genetic predisposition couldunderpin the other organic theories for the etiology of PE, which include penile hypersensitivity,a hyper excitable ejaculatory reflex, and central 5- HT receptor sensitivity. Another theory suggests that PE is the result of a defective or hyper excitable ejaculatoryreflex leading to a faster emission and/or expulsion phase of ejaculation. The bulbocavernosusmuscle surrounds the urethral bulb and is one of several key muscles involved in the expulsionphase of ejaculation. A study by Colpi et al. suggested that PE sufferers have a hyper excitablebulbocavernosus reflex (BCR). In over 500 cases of premature ejaculation seen at the Masters and Johnson institute, theyhave found only one instance where an organic condition proved to be of importance. Still JohnBancroft in his book “Human Sexuality and its problems” wrote as “whilst it is difficult toidentify local physical causes, we should be cautious in attributing the problem solely topsychological factors. Fasolo et al., 2001 examined a sample of 12,558 men attending the Andrology PreventionWeek 2001, out of which 2,658 men were with and 9,900 men were without PE. From this largedata set it was concluded that the frequency of PE did not change with age, smoking habits andphysical activity. A short frenulum and hypospadia were both positively related to PE. Loweroverall health is also cited as a cause. Rarely there could be other physical causes such as, Table No. 10 Showing the physical causes of PEPelvic fractures Local genitourinary diseaseProstatic hypertrophy and prostatitis Local sensory impairmentUrethritis PolycythemiaDiabetes PolyneuritisArteriosclerosis Cardiovascular diseaseEndocrine abnormality (hypogonadism, abnormal leptin level)Injury to sympathetic nervous system (e.g. following surgery for abdominal aortic aneurysm) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 98
  • 117. 2. Physiological Causes Stress, depression and other factors that affect mental and emotional health can aggravatethis condition. Certain physiological factors may interfere with the timings of ejaculation. a. Penile hypersensitivity b. missing of internal cues c. Shortness of nerve latency time d. Increased rapidity of all reflexes e. Increased cortical evoked potentials. f. Prolonged abstinence from sex Tactile stimulation of the penis especially glans during coitus results in the orgasm reflexin male penile hypersensitivity characterized by a decrease in the threshold for the receptors issupposed to cause an early ejaculation. But there is no correlative evidence of low incidence ofchances of PE in Muslims and Jews who perform religious circumcision which causes constantrubbing of the glans with cloths gradually increase threshold for receptors. Bernie Zilbergeld 1978, who wrote ‘The New Male Sexuality’, interviewed men whocould last a long time sexually to discover their secrets. Unlike premature ejaculators these menwere better able to identify their point of ejaculatory inevitability and take corrective actionbefore the point is reached. As stated earlier according to Helen Kaplan a premature ejaculator cannot control hisorgasm, and secondly, he does not feel the intense erotic or pleasurable sensation before theejaculatory inevitability, which is referred as genital anesthesia. Some researchers categorize a group of men who experiences premature ejaculation asthey are physiologically predisposed to climax quickly because of shorter nerve latency time. Theterm latency refers the state of being latent. In conditioning it means the period of apparentinactivity between the time the stimulus in presented and the moment of response occurs. Due toshortness of the nerve latency time the gap between the continuous stimulation when becomespeak level during sexual act and the effect or response as ejaculation and orgasm is reduced. It can be analyzed how the so explained penile hypersensitivity, genital anesthesia andshortness of nerve latency time effects the ejaculatory time. In most cases, premature ejaculation “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation” 99
  • 118. is associated with the man’s failure to perceive the erotic sensation of the late excitement stagewhich occurs prior to orgasm. Premature ejaculation will often report that they experience anatypically steep curve of excitement. Instead of the gradual rise of excitement, which manynormal men experience, they go from law level of excitement directly and steeply to the intensesensation of excitement which are premonitory to orgasm. Early mild excitement is well tolerated by these men, but a high level of excitementseems to evoke anxiety and its defense which in this case is repression, suppression anddistraction from the clear perception of the erotic sensation. This defense mechanism orimmediate antecedent produces the symptoms of inadequate ejaculatory control for the perceptualdefense against the sensation of erotic pleasure interferes with the normal process of learningejaculatory control. It may be speculated that in order to acquire control over this or for thatmatter any other reflects, one must be able to experience and register the sensation that occurpremonitory to the discharge of that reflex. Apart from anxiety a number of psycho-socio-behavioral elements operate along with the physiological causes. [The sexual response cycle in normal subjects (AA) and in premature ejaculators (BB) in the second case an abnormally steep arousal and plateu can be seen A1 represents a second arousal after an orgasm.] Figure no.3 The sexual response cycle A Sexual act after a long abstinence causes PE. Here the amount of ejaculate will be alsomore. If there is an increase muscular tone (increased beta afferent neurological response) causesthe person to ejaculate rapidly due to increased rapidity of all reflexes. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”100
  • 119. 3. Psychosocial causesThe different causative factors in this group can be classified as follows: I. Sexual Dysfunction in women II. Psychological Factors 1. Performance anxiety 2. Negative cultural conditioning 3. Phobias 4. Higher expectations 5. Situational 6. Inexperience 7. Excessive concern over partner’s satisfaction III. Social Factors (Interpersonal environmental and cultural) 1. Developmental factors 2. Ignorance/misconceptions 3. Partner’s contribution 4. Male prerogative ness IV. Behavioral 1. Adaptation 2. Early experiences of hurried sexual actI. Sexual Dysfunction in women There is evidence of an association between the prevalence of PE in men and sexualdysfunction in women [Abdo C., 2004], particularly anorgamia or a sexual pain disorder (e.g.,vaginismus). Negative conditioning and penile hypersensitivity are the most frequently citedetiological factors in PE, although neither mechanism has received adequate experimental supportto date.2. Psychological Factors Since the psychosocial factors are operating a great deal in the manifestation ofPremature Ejaculation it should be analyzed thoroughly.1. Performance Anxiety It is widely assumed that anxiety has a disruptive effect on sexual response. Themechanism involved in influencing sexual responses was considered to be based on a dualisticmodel of the autonomic nervous system; where the peripheral nervous system on beingstimulated by anxiety produces vaso constrictive effect on the vaso congestive sexual response ofthe cycle. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”101
  • 120. Different experimental studies conducted to assess the degree of erotic arousal to thenon-sexual but arousing situations- many of these being frightening (anxiety provoking) reportsfacilitation in the sexual arousal (Ramsey 1943, Bancroft 1980, Hoon et. al 1977, Wolchick et.al1980, Barlow et. al 1983, Lange et. al 1981). In the above experiments anxiety producing film, frightening measures, electric shock,adrenaline subcutaneous injection etc. were performed. This is in the case of an optimal level ofanxiety. Based on the available evidence Bancroft (1989) concluded that “anxiety per se doesn’tnecessarily impair sexual response and many in certain circumstances enhance it, and that anxietymay be a signal that the sexual situation is threatening in some way, though the individual mayrespond to that threat in a variety of ways including direct inhabitation of genial response andcognitive process. Therefore, it can be defined a number of different relationship between anxietyand sexual response. 1) Anxiety produces peripheral autonomic effects, which interfere with sexual response (As yet the evidence for this is most convincing in relation to speed of ejaculation). 2) Anxiety disrupts cognitive processes which would otherwise facilitate sexual response to erotic stimuli. 3) Anxiety and neurophysiologic inhibition of genital response co-exist both being reactions to some perceived threat. 4) Sexual responses are inhibited to avoid anxiety. 5) Anxiety occurs as a reaction to failure of sexual response. 6) Anxiety may facilitate sexual response. Helen Kaplan also suggested the term of ‘optimum range of therapeutic anxiety’ as apatient cannot be expected to modify his behaviors without experiencing some anxiety, so thetherapeutic progress may be constructed as taking place at an optimal level of anxiety. Sexually related anxiety when it reaches in disruptive magnitude may be considered asthe ‘final’ common pathway through which multiple psycho pathogens may producedysfunctions. The sexually disruptive anxiety is always evoked by and related to sex, but it is notspecific to content or intensity. It can have many origins and intensities and can play various roles “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”102
  • 121. in the psychodynamic structure of the person and relationship. It can result from deepunconscious conflict derived in early childhood or it can be a product of simple performancefears. It can be the result of fears of sexual success or fears of sexual failure. Deep fears ofejaculation and vulnerability that derive from the past events can cause sexual problems.However it may be, the physiological concomitants of anxiety are always the same; no matterwhat its source or depth or intensity, no matter the relationship to conscious experience, and nomatter what the level of insight. Sexual symptoms are produced by the interaction of anxiety with the physiologicexpression of sex and different symptoms are produced when anxiety arises at different times orpoints in the sequence of sexual response. Orgasm phase problem occur when anxiety anddefenses against this are evoked late, at the highest point of arousal just prior to orgasm and sothese patients sexual response is normal until the climax, which is impaired. The performance anxiety causes release of adrenaline to neuro receptors causingfight/flight/fear mechanism and increased activity of sympathetic nervous system. An oversympathetic activity causes an PE on a long term basis performance fears may lead to loweredinterest in sex, loss of self esteem, struggles to control by different means later cause sex to beeven more of a ‘performance’ instead of just being ‘fun’.2. The spectator effect of performance anxiety Fears of performance often cause one or both partners to become spectators during theirsexual interaction, observing and evaluating their own or their partner’s sexual response. Bybecoming a spectator, a person usually becomes less involved in the sexual activity because of thedistraction of watching and evaluating what is going on. Thus premature ejaculation leads toperformance fears which lead to the spectator role, which results in distraction and loss oferection as well as rigidity which heightens the fears of performance. This continues as a viciouscircle. Unless this cycle is broken, there is strong possibility that sexual dysfunctions will befirmly established. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”103
  • 122. Spectator Role Distraction Performance anxiety Loss of erection and or rigidity Premature ejaculation Performance anxiety Flow chart. 02 The spectator effect of performance anxiety3. Negative cultural conditioning Negative cultural conditioning is the after effect of bad experiences of the past. It is acardinal feature of depressive tendency. It is characterized by the following features. a. Negative interpretation of the experiences –First or previous sexual exposure became premature. b. Negative expectation of the future - Anticipation of the worst regarding sexual act. c. Negative views of self. - Low self esteem.4. Phobias Some men, fixated at the phallic stage of development, are fearful of the vagina believingthat they will be castrated if they approached it – a concept of Freud figuratively called Vaginadentate because according to him, they believe unconsciously that vagina has teeth. A traumaticfirst coital experience either physically or psychologically painful is a common problem found inthe background of many people with sexual dysfunctions. Likewise unresolved oedipal complexand castration anxiety also worth mentioning5. Higher expectations In art and media (particularly erotic books, male magazines and movies) there is atendency to describe the sexual act in an imaginary dimension so that the distortion reflects the “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”104
  • 123. triumph of anxious perception versus reality. Regarding orgasm, all orgasms are intense, earthshattering explosive events after a very lengthy sexual act. But the fact is that sex is very variablelike eating, drinking and sleeping, so as the case of ejaculation also. But when the person isunable to cop-up with the expectation leads to failure in a normally timed ejaculation.6. Excessive concern over partner satisfaction Premature ejaculation is more common today among college educated men than amongmen with less education and is thought to be related to their concern for partner satisfaction.Kinsey et. al. (1953) noted that ‘at lower educational levels, it is usual for the male to try toachieve an orgasm as soon as possible after effecting genital union. Upper levels more oftenattempt to delay orgasm. Men whose educational level is higher and sophistication is greater, aremore likely to lead that their masculinity is threatened by failure to satisfy their wives.7. Situational Many a time the complaints of an individual of premature ejaculation only are situational;not generalized. It may be due to novelty of sexual partner, situations, surroundings or even lackof enough privacy.8. Inexperience Premature ejaculation is a common problem in newly wedded couples. At first when thenewlyweds discover that the husband cannot delay ejaculation, they lovingly console each otherand assure themselves that the situation will improve after they become accustomed to marriedlife. Eventually many men do gain control; and of-course many not, which needs therapeuticassistance.III. Social factors1. Developmental factors Several developmental factors, for e.g. a rigid religious background during childhoodseem to be associated with many sexual dysfunctions. A child brought up believing that sex isdirty, sinful or shameful may be handicapped in later sexual enjoyments. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”105
  • 124. 2. Misconceptions/ Ignorance The important psychosocial causes of Premature Ejaculation are ignorance andmisconcepts. Most of the lay public is ignorant about the psychophysical aspects of sex. Forexample parents do not talk freely about sex, they feel rather uneasy, embraced and ashamedwhen forced by children to talk about it and use euphemism while referring to sexual organs andtheir functions. The after effect is that curious youngsters turn to other sources like cheapunscientific books unscrupulous quacks who exploit their ignorance finally creating undue alarmin their young minds. Misconceptions about sex are formed by socio-cultural beliefs playing upon an ignorantmind. The may be about masturbation, nocturnal emission, value of semen, size and shape ofgenital organ etc. Further there are misconceptions about sexual standards and normality; when aperson find he is not able to meet the so called “normal standards” whether in terms of size ortime, he starts feeling guilty and anxious and even consider himself a failure.3. Partner contribution The partner has a great influence on premature ejaculator. As already explainedPremature Ejaculation is a common problem among newly wedded couples. Initially they willconsole each other and hope for a gradual improvement. When the problem persist the wife’sattitude begin to change. She starts to feel that she is being inconsiderably used, that her husbandis concerned only with his own pleasure and he has no appreciation of her sexual needs. At everysexual counter, her husband ejaculates so quickly that she has no opportunity to reach climaxespecially after stimulating foreplay, the wife is left with no means of release and a lot ofresentment. They feel angry and get ‘used’ leading them to seek professional guidance, to seekanother lover, or to avoid sex. Avoidance is likely to worsen the problem as the quickness ofejaculation considerable increases according to the period of abstinence. Similarly if the man tries “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”106
  • 125. to reduce his arousal by shortening the time of non-coital play, his tactic not only ineffective butalso make backfire by further convincing the women of her partner’s selfishness. There is an opposite end of the spectrum, some females may actually grateful to ‘get itover with’ quickly. They may even fake orgasm. If the partner is repeatedly criticizing him on hispoor performance may develop erectile failure or lack of rigidity also. The partner should beappropriate, understanding and communication between the partners should be good. Some timespartners lack enough communication and expect their spouse to automatically understand thesexual needs and desires without their telling them. After effect is the partner cannot make theexpected responses and gestures and this taken by the spouse as rejection or lack of concern. Sexual dysfunction like premature ejaculation develops when the partner is negative, shyor having fear during sexual act or late aroused, unaroused. Age difference between the couples isalso an important factor. Relationship with the partner in the non-sexual areas also should begood. A stressful marriage always exacerbates the problem.4. Male prerogative ness As Kinsey et. Al. suggested that rapid ejaculation was a signs of biological competence;many men consider sexual pleasure as a male prerogative. This is a common misconceptprevalent in different strata of society.IV. Behavioral Factors Researchers have noted that many a time premature ejaculators are behaviorallyconditioned to their quickness. Rapid masturbatory behaviors in the adolescence may result inpremature ejaculation in married life. Premature Ejaculation may originate from early sexualexperiences in which ejaculating quickly was desirable. Such experiences might include situations with a risk of being discovered by some oneelse, as in sex in a parked car; sex with a prostitute who typically encourages speed so that shecan have more customers; or group masturbation where ejaculatory speed was a sign of virility. If “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”107
  • 126. the conditioning is powerful enough, it cannot be easily unlearned even when circumstanceschange.Psychological Factors PE is believed to be a psychological problem and does not represent any known organicdisease involving the male reproductive tract or any known lesions in the brain or nervoussystem. The organ systems directly affected by PE include the male reproductive tract (i.e. penis,prostate, seminal vesicles, testicles, and their appendages), the portions of the central andperipheral nervous system controlling the male reproductive tract, and the reproductive organsystems of the sexual partner (for the purpose of this discussion, the partner is assumed to befemale) that may not be stimulated sufficiently to achieve orgasm. Premature ejaculation may also be caused or aggravated by psychological factors such asguilt (believing the activity is sinful e.g., premarital or extramarital sex); fear (associated withconcerns regarding potential pregnancy, sexually transmitted diseases, or getting caught ordiscovered); performance anxiety (especially in the inexperienced partner or with partners new toeach other); and interpersonal issues affecting the couple.While men sometimes underestimate the relationship between sexual performance and emotionalwell- being, premature ejaculation can be caused by temporary depression, stress over financialmatters, unrealistic expectations about performance, a history of sexual repression, or an overalllack of confidence. Interpersonal dynamics strongly contribute to sexual function, and prematureejaculation can be caused by a lack of communication between partners, hurt feelings, orunresolved conflicts that interfere with the ability to achieve emotional intimacy. Some physical illnesses, such as a prostate infection, are also known to induce prematureejaculation. In other instances, PE is caused by a physical injury that affects the nervous system.Certain medications, such as cold medications containing pseudo ephedrine, also cause premature “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”108
  • 127. ejaculation. Sexual dysfunction is a common symptom of psychiatric afflictions ranging frombipolar disorder to post-traumatic stress disorder. In these cases, it is best to discuss the issuesopenly with a physician. It is most common in adolescents, young adults, and other sexually immature males.Increased risk is associated with lack of sexual experience, lack of knowledge regarding normalmale and female sexual responses, and with those individuals who highly associate psychologicalfactors (such as fear, guilt, and anxiety) with sexual activity. Most men experience prematureejaculation at least once in their lives. Often adolescents and young men experience prematureejaculation during their first sexual encounters, but eventually learn ejaculatory control. You don’t have a premature ejaculation problem unless you frequently ejaculate before orshortly after beginning intercourse. The following are not typically causes of PrematureEjaculation 1) Men are too excited to focus on bodily sensation. 2) Some men’s first experience with intercourse was in a tense situation where hurrying was beneficial, like in a car, and then learned a bad habit. 3) Being so concerned about performance they didn’t pay attention to their own sensations. 4) Guilt about enjoying sex or pleasure of any kind. 5) Worrying about maintaining erections. 6) Unresolved relationship issues. 7) General life stress.Psycho-behavioral origin Bad habit of excess of masturbation, during adolescence, in order to evacuate rapidly asexual tension, without making last the pleasure nor to appreciate the pleasure which come beforethe ejaculatory reflex. A very strong incontrollable emotional tension during sexual relations,stress, anxiety and tiredness can be responsible of PE Finally; a relational conflict with the partnercan also be responsible of a premature ejaculation. It is important to know that, a premature ejaculation, which occurs first occasionally,could happen more frequently and, then, to occur at every sexual relation. Indeed, as soon as a “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”109
  • 128. premature ejaculation occur several time, the fear of failure and the stress will be, responsible of arepeated and lasting premature ejaculation. Thus, the anxiety, the fear of failure, the fear of notbeing good, a very strong incontrollable emotional tension, are the causes the more often at theorigin of premature ejaculation.As to treating premature ejaculation, here are lists of things that don’t work 1) Getting drunk 2) Testosterone injections 3) Creams that numb the penis 4) Biting one’s cheek as a distraction 5) Concentrating on something other than sex while having sex 6) Tranquilizers 7) Frequent masturbation 8) Using one or more condomsThe Cause of Severe Premature Ejaculation Extreme levels of arousal caused by the over production of sex hormones. Simply stated -Hormones control “everything” that happens during a sexual performance - from the erection tothe ejaculation. A normal ejaculation occurs when sexual excitement triggers glands, located inside yourbody, to begin a slow release of chemicals (hormones) into your blood stream. The slow releaseof these hormones tells your brain to gently stimulate the nerves at the glans (head of your penis).As you become more and more sexually excited, your body produces more and more of thesehormones. The sensitivity becomes greater and greater until you reach the point at which timeyou ejaculate. Under normal circumstances the production of hormone is gradual and a man hasthe ability to control the sensations of sex. When nerve endings in the penis are stimulated signals are sent to the brain whichtriggers ejaculation. Topically help to prevent premature ejaculation by alternating neurologicalsensation to the penis. These altered sensations are new to the brain and will not register as asignal to ejaculate prematurely. Thus allowing the male total control over Premature ejaculation. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”110
  • 129. Premature Ejaculation occurs when your body produces too much hormone too fast. Yourbody becomes “over stimulated”. The head of the penis becomes so sensitive that you ejaculatealmost immediately. There is absolutely no control. This Extreme Sensitivity on the head of your penis causes the ejaculatory mechanism,inside your body, to go into “spasms”. It’s these spasms that cause the overpowering Urge toEjaculate. The head of your penis becomes so sensitive and the urge is so strong that youejaculate immediately. If you slow down the production of excess hormone - you slow down theejaculation.Severe premature ejaculation is an extremely complex condition the causes of prematureejaculation are both physical and psychological. Over the past few years that I have been evaluating and treating men with impotence andpremature ejaculation (in excess of 3,000 men), we have noticed that men with prematureejaculation have increased sensitivity to vibration in the penis when compared to men withoutpremature ejaculation. It is likely that premature ejaculation, at least in some men, may be due toa combination of hypersensitivity of the penis and hyperspasticity of the pelvic muscles. I shouldstress, though, that this is my idea and not one that’s been evaluated in controlled trials. There is also a biochemical explanation for premature ejaculation that is showing a greatdeal of promise. The first hints of this came with the release of several anti-depressivemedications called selective serotonin reuptake inhibitors (SSRIs), the best known of these beingProzac. One common side effect of SSRIs is delayed ejaculation or even inability to ejaculate.Since serotonin in his brain is one of the molecules involved in ejaculation, this led to the ideathat low serotonin levels might cause premature ejaculation. We’ll discuss this further in thetreatment section. Currently, my approach to premature ejaculation consists of a history and a physicalexamination specifically geared to determine the amount of sensitivity of the penis and detect anyneurological problem. In many of my cases, the patients problem relates to hypersensitivity of “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”111
  • 130. the penis. Causes of ejaculation problems vary, depending on the person involved and the type ofproblem can be complicated by having multiple causes include Physiology (natural body shapes). Some men simply take longer than others to climax.This can be related to their shape and size, lack of technique, or sexual positions used. Discomfortcan also be caused by the physiology of a female partner, who may not be sufficiently aroused orlubricated. Impotence some ejaculation problems are connected to inability to get or maintain anerection (erectile dysfunction). Other medical conditions may cause ejaculation problems, which can be temporary orpermanent. These include diabetes, prostate disease, cancer of the testicle, and benign proslastichyperlasia (BPH). Dry or delayed ejaculation is often caused by conditions such as diabetes, orafter surgery (for example on the prostate gland). Sexually transmitted infections (STIs) such as gonorrhea may cause smelly or discoloreddischarge. If blood appears in the semen it could be the result of an infection or inflammation inthe urethra or prostate gland, but you should also check whether it might have come from yourpartner (for example, a female partner may be having her menstrual period). Medication delayedejaculation is a side-effect of some medicines such as anti-depressants. Alcohol abuse often leadsto sexual problems including delayed ejaculation and erectile dysfunction. Psychological reasons among the most common for ejaculation problems. It is commonto ejaculate prematurely when having sex for the first time, or with a new partner due to intensearousal or worry about performance. Other psychological problems may stem from negativecomments about performance from previous partners, from worries about cultural or religioustaboos (such as sex outside marriage), distraction because of stress or a busy day at work, or fearof being overheard making love. Conditioning is a particular form of psychological cause. A manwho is used to masturbating with a very fast motion may not feel satisfied with the slower processof intercourse, and thus find it difficult to climax. In the case of young men, they may initially betrying to reach orgasm in a short space of time, because they do not have a comfortable or safe “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”112
  • 131. location in which to have sex, and this can condition them to climax quickly, even when theyreach a more stable environment. A combination of the above particularly psychological causes once a problem hasoccurred, even on a single occasion, worrying about it can cause it to re-occur. A man may facedelayed ejaculation because he is worried that he did not climax last time and is thus distractedfrom taking pleasure in the sensations. He may avoid or abstain from sex if he is worried abouthis performance.Possible psychological and environmental factors Psychological factors commonly contribute to premature ejaculation. While mensometimes underestimate the relationship between sexual performance and emotional well-being,premature ejaculation can be caused by temporary depression, stress over financial matters,unrealistic expectations about performance, a history of sexual repression, or an overall lack ofconfidence. Interpersonal dynamics strongly contribute to sexual function, and prematureejaculation can be caused by a lack of communication between partners, hurt feelings, orunresolved conflicts that interfere with the ability to achieve emotional intimacy. Neurologicalpremature ejaculation can also lead to other forms of sexual dysfunction, or intensify the existingproblem, by creating performance anxiety. In a less pathological context, premature ejaculationcould also be caused simply by extreme arousal. According to the theories developed by Wilhelm Reich, premature ejaculation may be aconsequence of a stasis of sexual energy in the pelvic musculature, which prevents the diffusionof such energy to other parts of the body. One study of young married couples reported that the husbands IELT seems to beaffected by the phases of the wifes menstrual cycle, the IELT tending to be shortest during thefertile phase. Other studies suggest that young men with older female partners reach theejaculatory threshold sooner, on average, than those whose partners are their own age or younger. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”113
  • 132. Symptoms Ejaculation happens before the individual or couple would like (prematurely). This mayrange from before penetration to a point just after penetration, and may leave the couple feelingunsatisfied. Since premature ejaculation is not a disease, it does not have the classic "symptoms".An individual realizes that he is suffering from it when sexual intercourse ends before eitherpartner is completely satisfied. It is diagnosed by a physical examination, in addition tointerviews with the couple regarding their relationship. There are different symptoms dependingon the type of ejaculation problem: 1. Premature ejaculation: There are no precise rules about how soon ejaculation should take place after intercourse or masturbation begins. Instead, the general principle is that ejaculation is premature if it happens more swiftly than the individual or the couple would prefer. It may occur a few seconds into intercourse, or even prior to penetration and it may not provide satisfaction for the man, or for his partner. 2. Delayed ejaculation: There are no clear rules, but if it seems to take a long time or if a man feels that he is ready but cannot climax, there may be a problem. 3. Absent ejaculation an inability to ejaculate 4. Dry orgasm this is when a man experiences the feeling of climax but no semen comes out. 5. Pain in the pelvic area upon ejaculation or intercourse 6. Discharge: The penis has an unusual smell or appearance; semen is unusually thick or discolored; or there is blood in the fluid. Anxiety or worries about performance will often accompany physical symptoms. Recently, the prevalence of chronic pelvic pain syndrome in patients with prematureejaculation and the prevalence of sexual dysfunction and premature ejaculation in patients withchronic pelvic pain syndrome were studied.Classification of Premature EjaculationSchapiro (1943) divided a large series of cases of premature ejaculation into two groups. 1) Those in whom the sexual arousal and excitement was high and in whom rapid ejaculation appeared to be a symptom of general sexual hyper excitability. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”114
  • 133. 2) Those in which there was a general sexual hypo excitability and frequently impaired erection, as well.Cooper (1969) defined three main types of premature ejaculation in a study of total 30 patients.They are as follows: 1) Habituated PE with strong erection present constantly since adolescence. 2) Acute onset of PE generally with erectional insufficiency occurring in younger men usually in response to a specific psychological or psycho physiological stress 3) Dangerous onset of PE generally with erectional insufficiency and other evidences of declining sexual responsiveness occurring generally in older man.According to DSM IV, premature ejaculation is having the following subtypes. A. 1. Lifelong 2. Acquired B. 1. Generalized 2. Situational C. 1. Due to psychological factors 2. Due to combined factorsI. Lifelong PEA syndrome characterized by the cluster of following core symptoms. Ejaculation occurs too early at nearly every intercourse. Nearly every woman From about the first sexual encounter onwards The majority of the cases (90%) within 30-60s or between 1-2 min (10%) Remains rapid during life (70%) and can even aggravate during aging (30%) The ability to delay ejaculation may be lacking however drug treatment may diminish the symptoms by the induced delayed ejaculation. In the life long type, individual was never able to make sexual act with a reasonable voluntary control.II. Acquired PE (Underlying somatic or psychological problem) Early ejaculation (before penetration or as soon as their penis touches the vagina) Manhad normal ejaculation experiences before the start of complaints. There is either a sudden or gradual onset. The ability to delay ejaculation. The dysfunction may be due to urological dysfunction like erectile dysfunction or prostatitis, thyroid dysfunction or psychological or relationship problems. It can be cured by treatment of the underlying cause. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”115
  • 134. In acquired variety the man had successfully achieved sexual act at some time in his sexual life but in later is unable to do so.III. Natural variable PE Men only coincidentally and situational experience early ejaculation this type of PEshould be regarded as a symptom or manifestation of true pathology but of normal variation insexual performance. Early ejaculations are inconsistent and occur irregularly The ability to delay ejaculation Experiences of diminished ability to delay ejaculation go along with either a short of normal ejaculatory time. Situational premature ejaculation is characterized by a failure to perform with enough time at certain circumstances but not in others, for example a man may be failure with his wife but effectively perform sexual act with an old girl friend or with a prostitute.IV Premature like ejaculatory dysfunction Complain of PE while the ejaculation time is in the normal range, i.e. around 3-6 min.Psychological factors have an abundant role in the sexual dysfunction. Probably it may be theonly cause. But in certain instances local irritating causes like prostitis or behavioral conditioningetc may operate along with psychological factors.Another classification can also be made according to the prognosis of the disease. A. Progressive B. Non-progressive Progressive type of ejaculatory dysfunction is characterized by improvement of thecontrol over ejaculation where as in non-progressive type the severity of the problem is stable.Some researches divide men who experiences premature ejaculation into two groups- 1. Those who are physiologically predisposed to climax quickly because of shorter nerve latency time. 2. Those with a psychogenic or behaviorally conditioned etiology. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”116
  • 135. A few words about different premature ejaculation types The primary reason premature ejaculation is so prevalent is that it can be induced byvarious, and offends irrelevant condition. Generally there are four types of PE. 1. “The teenager PE” occurs during adolescence or preadolescence mostly because of inappropriate masturbation habits. Teenagers that masturbate on a daily basis may have this type of premature ejaculation while being unaware of it. 2. A similar PE type is the “young adult PE”, which affects young men as a result of consistent stress, anxiety or emotional tension. These two types of premature ejaculation can be treated easily if diagnosed timely. 3. If not, after a couple of years they may develop into PE type 3, which is characterized by a persistent unbalance of serotonin and dopamine levels in the brain. This type of premature ejaculation is as treatable as the aforementioned, but requires more work and patience. At this stage medication is a preferable treatment since increasing serotonin level in the brain is crucial to treat premature ejaculation type 3. Untreated or inappropriate treated type 3 will become more complex and persistent over time, and eventually turn into type 4. 4. It is most severe PE that interrupts ejaculatory reflex and the central nervous system. Patient should start premature ejaculation treatment immediately before it triggers more sexual disorder or even nervous system damage.98 Ejaculation of semen occurs following erection of the penis and its insertion into thevagina. The disorders of ejaculation are premature ejaculation (PME), anejaculation, retrogradeejaculation.(1) Premature Ejaculation The term PME may be used when a man, unable to exert voluntary control over theejaculatory reflex, reaches orgasm very quickly once aroused. However the American “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”117
  • 136. Psychiatric Association (APA) defines this as persistent or recurrent ejaculation with minimalsexual stimulation, or before, upon or shortly after penetration and before the person wishes it.(2) Ejaculation (Synonyms - Ejaculatory incompetence, Dry run, Non - ejaculation) This disorder has been defined as inability to ejaculate within the vagina despite a firmerection and relatively high levels of sexual arousal. It must be differentiated from retrogradeejaculation (in which semen spurts backwards into the urinary bladder and sperms are found inurine) and retarded ejaculation (which is opposite of PME). Psychogenic cause include negative attitude towards sex in childhood, psychosocialtrauma, fear of pregnancy and ejaculating urine during intercourse.(3) Retrograde Ejaculation In this disorder, the semen enters the urinary bladder during intercourse. The diagnosis isconfirmed by detection of sperms in the urine immediately after intercourse. It is possible to have an orgasm without the expulsion of fluid and it is also possible forfluid to go backward into the bladder. This is called retrograde ejaculation and most commonlyoccurs in men who have had prostate surgery or in men who have had surgery that results indamage to the sympathetic nerves. Another very common cause of retrograde ejaculation ismedication, particularly newer medications used to treat prostate blockage symptoms. Because much can happen along this complex chain of events to disrupt the process,there are many causes of ejaculatory dysfunction. These include congenital problems that affectthe structures involved with both orgasm and ejaculation, and more commonly, acquired causesdue to trauma including urologic surgery to treat prostatic obstruction. In these men, retrogradeejaculation is common because the bladder neck, which normally acts as a dam, has been cut andthe ejaculate, rather than being propelled forward through the penis, follows the easier pathbackwards into the bladder. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”118
  • 137. There are two types of premature ejaculators, primary and secondary1. Primary ejaculators The person suffering from PE from adolescence and have never had satisfactory sexualrelationships before? The main cause of this type of premature ejaculation is bad masturbationhabits during adolescent where the subject over excites himself trying to reach orgasm as soon aspossible for enjoyment or because of lack of privacy.2. Secondary ejaculators The person who had control and lost it at some point of their lives? The main causes forthis type of PE are stress, an emotional shock or a long period of sexual inactivity. Where assecondary premature ejaculation describes individuals who develop the condition after years ofsatisfactory sexual activity.Defining normal ejaculatory latency (period between penetration and ejaculation) isdifficult - Men and womens ideas of what is normal is not consistent the perception of thenormal period before ejaculation varies widely between 7 and 14 minutes, with significantgeographical variation. For example, in Germany, the perceived average latency time is only 7minutes, but in the US it is over 13 minutes. The perceived average for men in the UnitedKingdom, France, and Italy is around 9 minutes. Generally, the time before ejaculation as estimated by women was similar to the timeestimated by men, though slightly lower in most cases. The difficulty of agreeing what is the"normal" ejaculatory latency is reflected in the lack of a universally accepted definition ofpremature ejaculation.EjaculationEjaculation is the ejecting of semen from a penis, and is usually accompanied by orgasm. It isusually the final stage and natural objective of sexual stimulation, and an essential component ofnatural conception. In rare cases ejaculation occurs because of prostatic disease. Ejaculation may “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”119
  • 138. also occur spontaneously during sleep (a nocturnal emission or "wet dream"). Anejaculation is the condition of being unable to ejaculate Phase. 1. Stimulation A usual precursor to ejaculation is the sexual arousalof the male leading to the erection of the penis, though not every arousal or erection leads toejaculation. Penile sexual stimulation during vaginal, oral or anal sexual intercourse, or manualstimulation (masturbation) may provide the necessary stimulus for a man to achieve orgasm andejaculation. There are wide variations in how long the sexual arousal needs to be beforeejaculation occurs. Premature ejaculation is the term used when ejaculation occurs before thedesired time. If a man is unable to ejaculate in a timely manner after prolonged sexualstimulation, in spite of his desire to do so, it is called delayed ejaculation or anorgasmia. Anorgasm that is not accompanied by ejaculation is known as a dry orgasm.2. Ejaculation [Figure no.4 Ejaculation] When a man has achieved a sufficient level of stimulation, ejaculation begins. At that point, under the control of the sympathetic nervous system, semen containing sperm is produced. The semen is ejected through the urethra with rhythmic contractions.99 These rhythmic contractions are part ofthe male orgasm. They are generated by the bulbospongiosus muscle under the control of a spinalreflex at the level of the spinal nerves S2-S4 via the pudendal nerve. The typical male orgasm canlast up to 17 seconds but may vary from a few seconds up to about a minute. Also males will onlyejaculate or (cumm) about a tablespoon each time. After the start of orgasm, pulses of semen begin to flow from the urethra, reach a peakdischarge and then diminish in flow. The typical orgasm consists of 10 to 15 contractions. Oncethe first contraction has taken place, ejaculation will continue to completion as an involuntary “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”120
  • 139. process. The rate of contractions gradually slows during the orgasm. Initial contractions occur atan average interval of 0.6 seconds with an increasing increment of 0.1 seconds per contraction.Contractions of most men proceed at regular rhythmic intervals for the duration of the orgasm.Many men also experience additional irregular contractions at the conclusion of the orgasm.100 Ejaculation begins during the first or second contraction of orgasm. For most men thefirst spurt occurs during the second contraction. The first or second spurt is typically the largestand can contain 40 percent or more of the total ejaculates volume. After this peak the flow ofeach pulse diminishes. When the flow ends, the muscle contractions of the orgasm continue withno additional semen discharge. A small sample study of seven men showed an average of 7 spurtsof semen (range between 5 and 10) followed by an average of 10 more contractions with nosemen expelled (range between 5 and 23). This study also found a high correlation betweennumber of spurts of semen and total ejaculate volume, i.e., larger semen volumes resulted fromadditional pulses of semen rather than larger individual spurts.1013. Refractory periodMost men experience a refractory period immediately following an orgasm, during which timethey are unable to achieve another erection and a longer period again before they are capable ofachieving another ejaculation. The duration of the refractory period varies considerably, even fora given individual. Age affects the recovery time, with younger men typically recovering fasterthan older men, though not necessarily universally so. However, many men are able to achieve sufficient sexual arousal immediately afterejaculation, and others may have refractory periods of less than 15 minutes. A short recoveryperiod may allow them to seamlessly continue sexual play from one ejaculation to sexualstimulation in preparation for the next. However, other men are averse to stimulation during theearly part of the refractory period. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”121
  • 140. 4. Volume The force and amount of semen that will be ejected during an ejaculation will varywidely between men and may contain between 0.1 and 11 milliliters.102 Adult semen volume isaffected by the time that has passed since the previous ejaculation; larger semen volumes are seenwith greater durations of abstinence. It is not clear whether frequent ejaculation increases103, 104 105reduces or has no effect on the risk of prostate cancer. The duration of the stimulationleading up to the ejaculation can affect the volume.106 Abnormally low volume is known ashypospermia, though it is normal for the amount of semen to diminish with age.5. Quality The number of sperm in an ejaculation also varies widely, depending on many factors,including the time since the last ejaculation,107 age, stress levels,108 and testosterone. An unusuallylow sperm count, not the same as low semen volume, is known as oligospermia, and the absenceof any sperm from the semen is termed azoospermia.Development of sperm1. During puberty The first ejaculation in males often occurs about 12 months after the onset of puberty,either through masturbation or nocturnal emission (wet dreams). This first semen volume issmall. The typical ejaculation over the following three months produces less than 1 ml of semen.The semen produced during early puberty is also typically clear. After ejaculation this earlysemen remains jellylike and, unlike semen from mature males, fails to liquefy. Most first ejaculations (90 percent) lack sperm of the few early ejaculations that docontain sperm, the majority of sperm (97%) lack motion. The remaining sperm (3%) haveabnormal motion.109 As the male proceeds through puberty, the semen develops mature characteristics withincreasing quantities of normal sperm. Semen produced 12 to 14 months after the first ejaculation “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”122
  • 141. liquefies after a short period of time. Within 24 months of the first ejaculation, the semen volumeand the quantity and characteristics of the sperm match that of adult male semen.[11]2. Control from the central nervous system To map the neuronal activation of the brain during the ejaculatory response, researchershave studied the expression of c-fos, a proto-oncogene expressed in neurons in response tostimulation by hormones and neurotransmitters. 110 Expression of c-fos in the following areas hasbeen observed: 111, 112 Medial preoptic area (MPOA) Lateral septum, bed nucleus of the stria terminalis Para ventricular nucleus of the hypothalamus (PVN) Ventromedial hypothalamus, medial amygdala Ventral premammillary nuclei Ventral tegmentum Central tegmental field Mesencephalic central gray Peripeduncular nuclei Parvocellular sub para fascicular nucleus (SPF) within the posterior thalamusHealth issues For most men, no detrimental health effects have been determined from ejaculation itselfor from frequent ejaculations, though sexual activity in general can have health or psychologicalconsequences. Some men experience a transient Post Orgasmic Illness Syndrome followingejaculation. In one study, more frequent ejaculation earlier in ones life predicted lower rates ofprostate cancer later on. Researchers have proposed that ejaculation may "flush out" carcinogensthat accumulate in the prostate. However, no definitive reason for the link has been found, nor hasit been proven that ejaculation is the direct cause of the reduced risk (but because the ejaculationoccurred many years before cancer developed, it is not just that cancer causes reducedejaculation). “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”123
  • 142. The researchers note that increased sexual activity can increase the risk of sexuallytransmitted infections. Gathering direct experimental evidence for the ability of increasedejaculation to reduce cancer risk many years later would be extremely challenging.EJACULATORY DISORDERS There exists a spectrum of disorders of ejaculation ranging from mild premature toseverely retard or absent ejaculation. Normally, by age 17 or 18 yr, 75% of men are able tocontrol their ejaculation113. Premature ejaculation is the most common male sexual dysfunction114.Several surveys among different populations estimate its prevalence at 29%, with a range between1% and 75% depending on the population and criteria used to define the condition115,116 Premature ejaculation and sexual desire disorders were the frequent reported problems inyoung adult males with adverse familial relationship to attachment figures117. Prematureejaculation was also found to be associated with anxiety in a recent survey of 789 men inEngland118. Painful ejaculation has been reported as a side effect of tricyclic antidepressants in at leasttwo patients119. Psychogenic post ejaculatory pain syndrome (PEPS) is a rare sexual disorder ofmale dyspareunia that was first described in 1979120as a persistent and recurrent pain in the genitalorgans during ejaculation or immediately afterward. Detailed descriptions of clinical features,pathogenesis, and treatment of this syndrome have recently been reviewed by Kaplan121. Ejaculatory pain in the testicular region may result from epididymal congestion aftervasectomy122or from duct obstruction and/or infection123, testicular torsion, mass lesion orprostatitis124. In some cases, specific etiological factors other than psychological stress cannot beidentified125.Other dysfunctions - Other dysfunctions are caused by parasitic infections or healed venereal diseases and stillothers may be the result of traumas such as back injuries that cause paraplegia, colon cancersurgery, or even testicular cancer. One of the most common causes is drug therapy. Many drugs “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”124
  • 143. are known to impair ejaculation, including alcohol, medications used to treat depression such asamitriptyline, and Valium type drugs. Even cold and flu pills can create the conditions forretrograde ejaculation. Many physicians are not aware that these medications may cause problemswith ejaculation. Some new studies indicate that premature ejaculation may be related tohypersensitivity of the nerves that go to the penis and there may even be an organic basis for thisproblemCurrent Concepts in Ejaculatory Dysfunction Although erectile dysfunction has recently become the most well-known aspect of malesexual dysfunction, the most prevalent male sexual disorders are ejaculatory dysfunctions.Ejaculatory disorders are divided into 4 categories: 1) Premature ejaculation 2) Delayed ejaculation 3) Retrograde ejaculation 4) An ejaculation / anorgasmia Pharmacologic treatment for certain ejaculatory disorders exists, for example the off -label use of selective serotonin reuptake inhibitors for PE. Unfortunately, the other ejaculatorydisorders are less studied and not as well understood. This review revisits the physiology of thenormal ejaculatory response, specifically explores the mechanisms of an ejaculation, and presentsemerging data. The neurophysiology of the ejaculatory reflex is complex, making classification ofthe role of individual neurotransmitters extremely difficult. However, recent research has elucidated more about the role of serotonin and dopamineat the central level in the physiology of both arousal and orgasm. Other recent studies that look atdiffering pharmacokinetic profiles and binding affinities of the 1-antagonists serve as anindication of the centrally mediated role of ejaculation and orgasm. As our understanding of theinteraction between central and peripheral modulations and regulation of the process ofejaculation increases, the probability of developing centrally acting pharmaceutical agents for thetreatment of sexual dysfunction approaches reality. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”125
  • 144. For centuries, the field of male sexual dysfunction lacked evidence-based, scientificfoundations, making both clinical diagnosis and management somewhat arbitrary. With theadvent of effective pharmaceutical treatments (i.e. phosphodiesterase type 5 [PDE-5] inhibitors)for the treatment of erectile dysfunction (ED), public awareness of the prevalence and therapiesof sexual dysfunction has expanded. The notion that diminishing sexual function is exclusively aproblem in the aging population is now being challenged. In a landmark 1999 study, Laumannand colleagues analyzed a group of young adult men aged 18 to 59 years and observed that 31%of this group suffered from some form of sexual dysfunction.126 Male sexual dysfunction can be divided into 3 main categories: hypogonadism, ED andejaculatory disorders. The latter can be further subdivided into premature ejaculation (PE),delayed ejaculation (DE), retrograde ejaculation (RE) and an ejaculation (AE) / anorgasmia. Male hypogonadism refers to a decrease in 1 of the 2 primary functions of the testes:production of sperm and testosterone. Hypogonadism can result from intrinsic disease of thetestes (primary) or a dysfunction of the pituitary or hypothalamus (secondary). Testosteronedeficiency can have multiple presentations depending on the age of onset. ED is defined as the inability to attain or maintain an erection of sufficient rigidity forsatisfactory sexual intercourse. With the success of the PDE-5 inhibitors (sildenafil, vardenafil,and tadalafil), ED has become the most publicly recognized male sexual dysfunction. DespiteED’s notoriety, the most prevalent male sexual dysfunction is the ejaculatory dysfunction PE.127 The ejaculatory disorders fall into 1 of 4 major categories. Most experts agree that PE isdefined as ejaculation occurring from a lack of ejaculatory control that interferes with sexual oremotional well-being in 1 or both partners. DE is characterized by a man’s inability to ejaculatein a reasonable period under normal sexual stimulation. RE occurs when the semen intended forpropulsion out the urethral meatus is directed backwards into the urinary bladder. This is mostcommonly due to intrinsic problems with the internal sphincter of the bladder. AE andanorgasmia are often mistakenly used interchangeably. AE specifically refers to the lack of “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”126
  • 145. ejaculation that may or may not be coupled with an orgasm. Anorgasmia is simply the lack oforgasm that is not necessarily a coupled response with ejaculation. Orgasm can be perceived asphysical (most commonly occurring at the time of ejaculation), psychological, or emotional, or acombination of these. Pharmacologic treatments for PE exist, and off-label therapy with selective serotoninreuptake inhibitors (SSRIs) is currently the most favored clinical approach. SSRIs exhibit thewell-established side effect of delaying ejaculation and, at higher doses, causing AE andanorgasmia. Further research on the development of US Food and Drug Administration–approved medications for the primary intent of controlling PE is ongoing. The other ejaculatory disorders— DE, RE, and AE/anorgasmia—are less studied and lesswell understood. The etiologies of these ejaculatory dysfunctions are numerous and multifactorpsychogenic, congenital, anatomic, neurogenic, infectious, endocrinological and iatrogenicfactors secondary to medications may all play a role. In a 2003 study, The Multinational Survey of the Aging Male (MSAM-7), Rosen andcolleagues investigated the relationship between lower urinary tract symptoms (LUTS)/benignprostatic hyperplasia (BPH) and sexual problems in aging men (between the ages of 50 and 80years).3 Specifically, 46% of the population able to achieve erections reported reducedejaculation, and another 5% of these men noted AE.4,5 The prevalence of ejaculatory dysfunctionshowed a direct correlation to both increasing age and severity of BPH/LUTS. Interestingly,when asked, most of these men were equally bothered by their symptoms of ED and ejaculatorydisorders, regardless of age.128 BPH/LUTS is a common condition in men aged 50 to 80 years and numerous reportshave suggested a link between BPH/LUTS and sexual dysfunction. The recommended first-linetherapy of BPH symptomatology is _1-blocker medications. The longstanding precept holds that_1- blockers exert their benefit by mediating smooth muscle relaxation in the prostate, urethra,and bladder neck.6 One agent in particular, tamsulosin, exhibits a much higher rate of RE and “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”127
  • 146. AE.7 The mechanism for this ejaculatory dysfunction has been proposed by many to be aselective receptor blockade and subsequent relaxation of the bladder neck region. Althoughclinical advances have been made in the diagnosis and treatment of hypogonadism and ED, basicconcepts on the physiology of ejaculation and treatment options for ejaculatory disorders havelagged. This article aims to review the physiology of the normal ejaculatory response; explore ourcurrent understanding of the mechanism of AE, especially in light of animal experimentation; andpresent emerging clinical trial data that bridge the gap in our knowledge about this importantclinical subject. A landmark 1999 study analyzed a cohort of young adult men aged 18 to 59years and observed that 31% of this group suffered from some form of sexual dysfunction. MODERN CONCEPTS Figure no.5 Physiology of EjaculationPhysiology of Ejaculation The orgasmic phase of sexual response is a genital reflex governed by spinal neuralcenters. Ejaculation is a complex process and relates to three discrete phenomena. They areseminal emission, antegrade ejaculation and bladder neck closure. Continuous sexual stimulation,especially the glans penis makes reflex afferent sensory stimuli initially relayed from the genitaliavia the pudental nerve to the cerebral cortex. The efferent neural fibers travel through the anterolateral column to the thoracolumbar sympathetic outflow emerging through T12 to L3 “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”128
  • 147. sympathetic ganglia. This sympathetic neural out put produces stimulation of adrenergic receptorsof the smooth muscles of the male reproductive organs cause the following events which aretermed as emission. 1) Reflex contraction of the smooth muscles of ductus deferens, stimulating peristalsis with propulsion of semen from the cauda epididymus to the ampulla. 2) Smooth muscle contraction of the ampulla and along with the contraction of prostrate and seminal vesicles which add their fluids. Partial closure of the bladder neck also happens along with this. These processes makedeposition of bolus seminal fluid in the posterior urethra, which is termed as emission. Thisemission response is not pleasurable. It is reported to be perceived as a slight physiologic signal,the first sense of ejaculation which has been called as the sensation of ejaculatory inevitability byMasters and Johnson’s. Further efferent neural control is mediated through the parasympathetic sacral outflow.This causes rhythmic 0.8 per second contractions of the striated muscles of the base of the pelvis,penis the ishiocavernous and bulb cavernous muscles, and the muscles of the lower extremitiesand trunk. These responses together with the complete closure of the bladder neck, the internalvesical sphincter result in rhythmic projectile ejaculation through the urethra in a series of squirts.These contractions are accompanied by the typical pleasurable orgasmic sensation. A largeejaculate is subjectively more pleasurable than small amount which may account for the fact thatthe first orgasm of several days of abstinence in the male is reported to be more pleasurable. From the above it is clear that ejaculation is a process controlled by both the sympatheticand parasympathetic nervous system. Thoracolumbar sympethectomy abolish seminal emissionwithout disturbing erectile potency or sensation of orgasm. Likewise a lesion of the parasympathetic pathway causes impotence due to failure oferection and ejaculation, where as an over activity causes priapism. Over activity of thesympathetic division causes weak erection and premature ejaculation. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”129
  • 148. Physiology of orgasm The neurophysiologic mechanisms underlying the orgasm remain obscure, but from theavailable evidence one can postulate that the central excitation in the spinal centers build up insuch a way and to such a level that spread of excitation occur involving emission and themuscular contraction accompanying it. The spread at which the critical level is reached and thedegree of which excitation spreads presumably depends on to a larger extent on excitatory orinhibitory influences from higher centers as well as individual differences in reactivity at thespinal level. Kinsey et.al (1953) regarded an orgasm as an explosive discharge of neuromusculartension and described it as the individual approaches a peak of sexual activity, suddenly becometense, momentarily maintain high level of tension, rise to a new peak of maximum tension andthen abruptly and instantaneously release all tensions and plunge into serious of muscular spasmsor convulsions through which he or she returns to normal or even subnormal physiologicalchanges. But orgasms vary from person to person and in different times in a single person itself.Different intensities of orgasm arise from physical factors such as fatigue and the time since lastorgasm as well as from a wide range of psychosocial factors including mood, relation to partner,activity, expectations and feelings about experiences. Some orgasm may be mild, fluttery orwarm while others are blockbusters. The following changes can be normally observed during orgasm.1. Genital responses a. Emission b. Feeling of ejaculatory inevitability c. Ejaculation2. General muscular responses As the excitement increases certain motor responses becomes more predictable and lessvoluntary, especially pelvic thrusting and contraction of the rectus abdominuas muscles, “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”130
  • 149. sternomastoid, facial musculature and some times carpopedal spasm. During orgasm spasm ofthese various muscle groups are maximal muscle tension decline rapidly once orgasm has passed.3. Cardiovascular and respiratory responses Changes in heart rate and blood pressure together with other peripheral vascularresponses occur during sexual excitement; however, there is a predictable though short lived risein heart rate, B.P. and respiratory rate during orgasm.4. Somatic sensations Apart from the sensation of ejaculation a wide variety somatic sensation occurs may beconfined to perineum or spread all over the body.5. Altered consciousness An orgasm may leave the subject completely in control, at its most extreme there may bevirtual loss of consciousness, certainly loss of control and alteration in the consciousness.Ejaculation and Orgasm Although the sensation resulting from emission and ejaculation form a characteristic partof the male orgasmic experience, it is clear that neither ejaculation nor emission is an essentialpart of orgasm. Pre adult boys not uncommonly experience orgasm without ejaculation and casesof ‘dry run orgasm” occurs as a result of adrenergic blocking agents in some cases.Post ejaculatory Refractory period Immediately after ejaculation the male enters a ‘refractory period’ a recovery time duringwhich further orgasm or ejaculation is physiologically impossible. A partial or full erection maybe maintained during this refractory period, but usually this erection subsides quickly. There is agreat variability in the length of the refractory period both within and between individual male,and it may last any from few minutes to many hours. For most males, this interval usually gets longer with each repeated ejaculation withintime span of several hours. In addition, as a man gets older the refractory period gets longer. Thepost ejaculatory refractory period is having a clinical implication also as far as Premature “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”131
  • 150. Ejaculation is concerned. Erection returns in a relatively short time after an ejaculation that hasoccurred quickly due to high arousal and a long interval since the last ejaculation. As against this,in patients with genuine Premature Ejaculation, the post ejaculatory refractory period is rathervery much prolonged.Sexual dysfunction Normal sexuality is difficult to define. Sexual behaviour is diverse and determined by acomplex interaction of factors. Sexual response is a true Psycho physiological experience.Normal men and women experience a sequence of physiological response to sexual stimulation.William Masters and Virgina Johnson observed the different physiological responses duringsexual response. It includes four stages via excitement plateau, orgasm and resolution. DSM IV consolidates the Master’s Johnson excitement and plateau phase into a singleexcitement phase. In the plateau phase high levels of sexual arousal are maintained andintensified potentially setting the stage for orgasm. For men who have difficulty in controllingejaculation, this phase may be exceptionally brief. Male sexual response cycle given in IV thedition of Diagnostic and statistical manual (DSM-IV) is reproduced here (Table No-12). According to DSM IV a sexual dysfunctions is defined as a disturbance in the sexualresponse cycle or as pain with sexual intercourse.Seven major categories of sexual dysfunctions are listed in DSM IV 1. Sexual desire disorders 2. Sexual arousal disorders 3. Orgasm disorders 4. Sexual pain 5. Sexual dysfunction caused by general medical condition 6. Substance induced sexual dysfunction 7. Sexual dysfunction not otherwise specifiedDSM –IV phase of sexual response cycle and the sexual dysfunctions usually associated with itare shown in the Table No. - 13. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”132
  • 151. Table No.11 Male Sexual response cycleOrgan Excitement phase Orgasmic phase Resolution phase Lasts several minutes to several 3 to 15 seconds 10 to 15 minutes; if hours; heightened excitement no orgasm, ½ to 1 before orgasm, 30 seconds to 3 day minutesSkin Just before orgasm: Sexual flush Well developed flush Flush disappears in reverse inconsistently appears; order of appearance, maculapapular rash originates on inconsistently appearing abdomen and spreads to ant. film of chest wall, face, neck and can perspiration on soles of include shoulders and forearms feet and palms of hand.Penis Erection in 10 to 30 seconds Ejaculation; emission phase Erection : partial caused by vasocongestion of marked by three to four involution in 5 to 10 erectile bodies of corpus contractions of 0.8 seconds of seconds with variable cavernosa of shaft; loss of vas, seminal vesicles, refractory period, full erection may occur with prostate; ejaculation proper detumescence in 5 to 30 introduction of asexual stimulus, marked by contractions of 0.8 minutes. loud noise; with heightened second of urethra and ejaculatory excitement, size of glans and spurt of 12 to 20 inches a age 18, diameter of panile shaft increase decreasing with age to ceepage at further 70.Scrotum Tightening and lifting of scrotal No change Decrease to baseline sizeand testes sac and elevation of testes; with because of loss of heightened excitement, 50% vasocongestion; increase in size of testes over un Testicular scrotal descent stimulated state and flattening within 5 to 30 minutes against perineum, signaling after orgasm; involution impending ejaculation may take several hours if no orgasmic release takes place.Cowper’s 2 to 3 drops of mucoid fluid that No change No changeglands contains viable sperm are secreted during heightened excitementOther Breasts: inconsistent nipple Loss of voluntary muscular Return to baseline erection with heightened control Rectum: rhythmical state in 5 to 10 excitement before orgasm contractions of sphincter minutes Myotonia: semispastic H.R.: up to 180 beats a contractions of facial, Minute BP: up to 40 to 100 mm abdominal, and intercostals systolic; 10 to 50 mm muscles Tachycardia: up to 175 Diastolic Respiration: up to 40 a minute, B.P. rise in systolic 20 respirations a minute to 80 mm; in diastolic 10 to 40 mm, Respiration : increased “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”133
  • 152. Table No.12 DSM – IV Phases of sexual response cycle and associated sexual dysfunctionsPhases Characteristics DysfunctionsDesire This phase is distinct from any Hypoactive sexual desire disorder; sexual aversion identified solely through physiology disorder; hypoactive sexual desire disorder due to a and reflects the patient’s general medical condition (male or female); motivations, drives, and personality. substance induced sexual dysfunction with impaired The phase is characterized by sexual desire. fantasies and the desire to have sex.Excitement This phase consists of a subjective Female sexual arousal disorder; male sense of sexual pleasure and erectile disorder; male erectile disorder due to a accompanying physiological general medical condition; dyspareunia due to a changes. All the physiological general medical condition (male or responses noted in Masters and female); substance – induced sexual dysfunction with Johnson’s excitement and plateau impaired arousal phases are combined and occur in this phase.Orgasm This phase consists of a peaking of Female orgasmic disorder; male orgasmic disorder; sexual pleasure, with release of premature ejaculation; other sexual dysfunction due sexual tension and rhythmic to a general medical condition (male or female); contraction of the perineal muscles substance induced sexual dysfunction with impaired and pelvic reproductive organs. orgasmResolution This phase entails a sense of general Postcoital dysphoria; postcoital relaxation, well-being and muscle Headache relaxation. During this phase men are refractory to orgasm for a period of time that increase with age, where as women are capable of having multiple orgasms without a refractory periodPremature ejaculation comes under dysfunctions of the male orgasmic phase.The problem is in the mind, not the penis Although many people blame their "penis" on this issue, the truth is different. Theproblem is in the mind (brain) because its responsible for collecting and managing the sexualimpulses related to physical and mental arousal during sex. How you mind reacts to the sexualstimulus is the difference between a good sexual encounter and premature ejaculation. You mind “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”134
  • 153. is your best tool or your worst enemy during sex. During masturbation (since there is no externalexcitation) the subject must create a sexual fantasy on his mind in order to get the desired arousallevel and erection to masturbate. This excitement or arousal level if mismanaged fromadolescence, in which the person voluntarily attempts to ejaculate as soon as possible, is the maincause of primary and some cases of secondary premature ejaculation.Hypersensitivity in the glans [figure no, 6 Hypersensitivity in the glans ]Many men who suffer from premature ejaculation complain from feelinghypersensitivity in the glans or head of the penis. Hypersensitivity in theglans is a physical effect to a psychological problem. Again, the problem isthe mind. During sexual arousal, the brain sends sexual energy to the penisfor it to become erected and ready. Once with the desired erection, the body channels the energyspreading it throughout the body. For the premature ejaculator this doesnt happen like this, theenergy is blocked in the penis causing the feeling of hypersensitivity which in turn causespremature ejaculation.What is that pre-ejaculatory secretion?The pre-seminal liquid is a secretion from the Cowpers gland produced for cleaning the urethraprior to ejaculation and it indicates a high level of arousal and an imminent ejaculation. Prematureejaculators experience this secretion much sooner than normal ejaculators.Patho physiology of PE Premature ejaculation is believed to be a psychological problem and does not representany known organic disease involving the male reproductive tract or any known lesions in thebrain or nervous system. The organ systems directly affected by premature ejaculation include themale reproductive tract (i.e. penis, prostate, seminal vesicles, testicles, and their appendages), theportions of the central and peripheral nervous system controlling the male reproductive tract, andthe reproductive organ systems of the sexual partner (for the purpose of this discussion, thepartner is assumed to be female) that may not be stimulated sufficiently to achieve orgasm. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”135
  • 154. If the premature ejaculation occurs so early that it happens before commencement ofsexual intercourse and the couple is attempting pregnancy, then pregnancy is impossible toachieve unless artificial insemination is used. Perhaps the most affected organ system is thepsyche of the partners. Both partners are likely to be dissatisfied emotionally and physically bythis problem. From an evolutionary perspective, logic may dictate that males who can ejaculate rapidlywould be more likely to succeed in fertilizing a female than males who require prolongedstimulation to reach climax. The genes of a male who ejaculates rapidly (but not so rapidly thatejaculation occurs before intromission) would be more likely to be passed on to succeedinggenerations. In a primitive sense, a male who could not complete the fertilization process quicklymight be pushed away or killed by a competing male because of his obvious vulnerability duringintercourse. Premature ejaculation has historically been considered a psychological disorder. Onetheory is that males are conditioned by societal pressures to reach climax quickly because of fearof discovery when masturbating as teenagers or during early sexual experiences "in the back seatof the car" or with a prostitute. This pattern of rapid attainment of sexual release is difficult tochange in marital or long-term relationships. The fact that female arousal and orgasm requiremore time than male arousal is being increasingly recognized, and this may result in increasedrecognition and definition of premature ejaculation as a problem. Some have questioned whether premature ejaculation is purely psychological. A numberof investigators have found differences in nerve conduction/latency times and hormonaldifferences in men who experience premature ejaculation compared with individuals who do not.The theory is that some men have hyper excitability or oversensitivity of their genitalia, thuspreventing down-regulation of their sympathetic pathways and delay of orgasm. Recently, acertain group of nerves in the lumbar spinal cord has been identified as the possible generator ofejaculation. This nerve site is thought to be linked to excitatory and inhibitory dopamine “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”136
  • 155. pathways in the brain, which play significant roles in sexual behavior. This knowledge, whilecontinuing to be researched, is providing the foundation for possible development of medicationsspecifically targeting delay of ejaculation. Other questions have been raised regarding possible biochemical factors in prematureejaculation. Testosterone is thought to play a role in the ejaculatory reflex. Higher testosterone(free and total) levels have been demonstrated in men with premature ejaculation than in menwithout premature ejaculation. Research published in a Chinese andrology journal showed that semen from men withpremature ejaculation contained significantly less acid phosphates and alpha-glucosidase than didthe semen of controls. These researchers concluded that these biochemical parameters may reflectdysfunction of the prostate and epididymis, possibly contributing to premature ejaculation;however, these have yet to be supported by subsequent studies. In other biochemical parameters, many men with premature ejaculation have been shownto have low serum levels of prolactin However, in this same study of prolactin in men with sexualdysfunction, men in the lowest quartile of serum prolactin levels who had premature ejaculationalso demonstrated associated metabolic syndrome, erectile dysfunction, and anxiety. In otherwords, while biochemical markers such as prolactin may contribute to premature ejaculation,organic and psychological associations (i.e. anxiety) suggest that biochemical parameters playonly a partial role in premature ejaculation. Further research is needed. While other factors may play roles of unknown significance, psychological factors havebeen found to contribute greatly to premature ejaculation beyond merely the time to ejaculation.While patients with premature ejaculation show significantly lower intravaginal ejaculatorylatency time (IELT), the IELT in those who fit the DSM-IV-TR criteria for premature ejaculationoverlaps with the IELT in patients who do not fit the criteria. However, while a shorter IELT hasbeen the measure of premature ejaculation in many studies, the perception of ejaculation controlhas been shown to mediate patient and/or partner satisfaction with sexual intercourse and “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”137
  • 156. ejaculation-related distress. While premature ejaculation is most likely not a purely psychologicaldisorder, such associations demonstrate a significant psychological role in the disorder.SHUKRAGATAVATA vis-à-vis (PREMATURE EJACULATION)NIDANA PANCHAKA Starting from the indulgence in the causative factors up to the complete manifestation ofthe disease including prognosis comes under Nidana panchakas. The perfect knowledge of whichis very much essential for a proper diagnosis and a line of treatment.Etiological considerations of Shukragatavata Etiological factors have not directly mentioned in the context of Shukragatavata. Butconsidering the pathological features of gatatva etiological factors mentioned elsewhere causingShukradhatu dourbalya, manoabhighata and vataprakopa relevant to the disease context arecollected and presented here.Shukradhatu dourbalyakara Nidana 1. Excessive intake lavana, katu, tikta and kashaya rasas 2. Excessive intake of Amla rasa and articles having amlavipaka and katu vipaka. 3. Intake of kshara 4. Intake of viruddhahara 5. Aharaviharas antagonistic to rasavaha srotas 6. Anasana (Fasting long) 7. Alpasana (Consumption of lesser quantity of food) 8. Shukravega nigraha 9. Sastraksharagnivibhramat (Iatrogenic)Nidana related code of conduct of Maithuna 1. Akalamaithuna 7. Ayonigamana 2. Anutthita nareeseva 8. Atimaithuna. 3. Dushta samkeerńa mehana nareegamana 9. Rajasvalagamana 4.. Atisthoolakrisanareegamana 10. Apriyagamana 5. Apriyacara nareegamana 11. Anyayoshitagamana 6. Maithuna in restricted places caitya, smasana, catvara. 12. Garbhini gamana Nidana causing Manobhighata “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”138
  • 157. Many of the Nidana explained in the earlier sub heading may cause manobhighatamainly. The following also cause manobhighata 1 Cintyanam cati cintanat 5 Shoka 2 Bhaya 6 Krodha 3 Utkanťha 7 Irshya etc 4 AtiharshaNidana causing vata prakopa 1 Ativyayama 2 Ativyavaya 3 Prapatana 4 Ratri jagarana 5 Katu, tikta, kashaya rasa 6 Rooksha, laghu aharas 7 Varaka, uddalaka etc 8 Shukravega vighata 9 Dhatoonam samkshaya 10 Cinta 11 Shoka 12 Bhaya 13 Duhkha sayya 14 Divasvapna 15 Marmabhighata 16 Aticamkramana 17 Heenabhojana 18 Sushkabhojana 19 Pramitasana 20 Vegodeerana 21 Veganigraha 22 Kriyati yoga 23 Yanasamkshobha 24 Vishamasana 25 Utkatakasana 26 Vishada 27 HarshShukravruta vata lakshanaOcclusion of vayu by semen gives rise to the following signs and symptoms 1. Non ejaculation or excessive ejaculation (premature ejaculation) of semen. 2. Sterility. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”139
  • 158. SHUKRAGATAVATA SAMPRATI Nidan Ahara Vihara Manasika Vyadi Kshataj Katu tikta Ativyavaya Chinta Vyadhi alpabhojan Ativyyama Shoka karshan abhojan Dhatukshaya Laghuta Calatva of vayu increase Vata prakopa Prakupita vayu enters into shukravaha srotus Cause Kshipramuncchati of shukraFLOW CHART NO. 03 SHUKRAGATAVATA SAMPRATI “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”140
  • 159. SAMAPRAPTI GATAKA –Dosha - Vata (Apana vata)Dushya - ShukraUddbhava sthan - KosthaAgni - VishmagniSanchara sthan - Shukravaha srotusSrotus - Shukravaha and vatavaha srotusSrotodrusti prakar - AtipravrutiRoga marga - BahyaSamprapti of Shukragatavata By the intake of heatus like katu, tikta aharas, alpa bhojana and abhojana, by the viharaslike atimaithuna and ativyayama etc, laghu guna of Vayu increases. Because of manasika viharaslike chinta, shoka etc, by vyadhikarshana and Kshata, dhatukshaya occurs. Due to dhatukshayaintern laghu Guna of vayu increases. This laghu guna of vayu is responsible for increase in thechalatva of Vayu. Then prakupita Vayu enters in to shukravaha srotas. Because of increased chalaguna kshipramunchanti of shukra i.e., early ejaculation of shukra occurs, which is the pratyatmalinga of shukragatavata. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”141
  • 160. MANAGEMENT OF SHUKRAGATAVATA If the (vitiated) vata is located in the semen, then the patient should be given therapies forsexual excitement. Food and drinks which promote strength as well as semen should also begiven to him. If there is obstruction in the seminal channel, then purgation therapy should beadministered. After purgation therapy, the patient should be given food, and thereafter, the earliermentioned therapies (for sexual excitement and promotion of strength as well as semen) shouldbe administered129. In the case of the aggravated vata having contaminated the semen, measures andremedies for seminal disorders (shukra dosha) should be employed. The intelligent (physician)would take recourse to measure, such as blood letting, immersion or bath in a vessel, fomentationwith heated stones, as well as in the manner karsu sweda, kuti sweda, anointment, Basti karmasetc. In the event of the aggravated vata having extended throughout the whole organism; where asbleeding by means of a born (cuffing) should be regarded as the remedy when the aggravatedDoshas would be found to have been confined in any particular part of the body130.Management of Shukragatavata The lines of management described by Acharyas for Shukragatavata in the classics aremore or less same. Praharsha anna, balya and Shukrakara drugs should be administered inShukragatavata. If Shukra is obstructed virechan should be performed. After virechan the aboveline of treatment should be done.. Shukradosha chikitsa can be adopted in Shukragatavata. Thetreatment explained in the ‘putrakasmeeya’ chapter can be employed in the management ofShukragatavata. While commenting on Carakasamhita, Cakrapani clarifies ‘praharsha’ as‘manoharshana’. Exhilarating food articles improves the quality of sexual arousal andfunctioning. The drugs should posses’ balya and Shukrakara properties. As the excellent sexual “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”142
  • 161. functioning depends on the physical and mental strength balya drugs will help in themanagement. In Shukragatavata, Shukradhatu dourbalya is present, and it causes gatatva of vata;so Shukrakara drugs should be administered to enhance the Excellency of dhatu. Above to theseall the drugs should be basically Vatahara, since vata vitiation is too countered to bring back it toits normal site. Acarya Susruta and Vriddha Vagbhata suggest Shukradushti chikitsa for Shukragatavata.Dalhana suggest vajeekarana and mootra dosha chikitsa. Indu specifies it as vatasukradushtichikitsa. Application of shukradushti chikitsa will be more relevant in cases of Shukravikriti inShukragatavata. The line of treatment in Shukragatavata varies according to the clinicalpresentation. For example classical virechan will be a must in case of vibadhamarga (e.g.Anejaculation, retrograde ejaculation, obstructive azoospermia etc), the whole treatment up toUttara basti in cases of Shukradosha (e.g. Azoospermia, maturation defect, oligospermia,astenospermia, terato spermia etc) should be performed. In medieval classics certain measures have been explained for long retention of semenduring sexual act. They include application of bhoomilatakalkasiddha kusumbha taila on soles,keeping mercury purified in brihatkaranja beeja and covered in leaf of dhattoora in the mouth,application of ajiaksheera and ushtra ksheera along with Goghrita in both legs during sexual actetc. (Cakradatta vajeekaranadhikara). These measures seem to be for distracting the mind duringsexual act. Such measures are also suggested in erotic classics. They included external applicationof different pharmaceutical modification of drugs like lajjalu, snuhi, kusumba, punarnava,kakajanghas, samyaka, kokilamoola, saptaparna, sarapunkha etc. However, it may be the line oftreatment of early ejaculation in Shukragatavata should be aimed vrishya, balya, vatahara,medhya and Shukrastambhaka properties. Among panchakarmas basti is an ideal choice as itcontrols vata at its own site. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”143
  • 162. CHIKITSA: Various Ayurvedic texts prescribed the various types of effective medicines for thedisease Shukragatavata. In addition certain special yogas are mentioned which not only cure theShukragatavata but also they are said to be Vrishya, Balya, Medhya, shukrastambhaka, Unmada,Vajeekaran and Vatahara properties. So all the action and effect of above said combination i.e.Vidaryadighrita is choosen for the present sudy. On the other hand there is a good amount of research done from contempotrary science isas follows –MANAGEMENT of PE Men with premature ejaculation should be evaluated with a detailed medical and sexualhistory, a physical examination and appropriate investigations to establish the true presentingcomplaint and identify obvious biological causes such as genital or lower urinary tract infectionshould be evaluated with a detailed medical and sexual history, a physical examination andappropriate investigations to establish the true presenting complaint and identify obviousbiological causes such as genital or lower urinary tract infection. In many relationships PE causes few if any problems. In others, the couple may reach anaccommodation of the problem through various strategies. Young men with a short refractoryperiod may often experience a second and more controlled ejaculation during an episode oflovemaking. Frequently, however, PE eventually leads to significant problems in the relationshipwith partners regarding men as selfish and developing a pattern of sexual avoidance. This onlyworsens the severity of the prematurity on the occasions when intercourse does occur. Since PE has been of human concern for centuries, every system of medicine and everyculture boasts its own unique `cures for the condition. Many of these have acquired a reputationfor efficaciousness because of their strong placebo effect. Since PE is often a psychologicaldisorder, even substances without any real pharmacological effect on the ejaculatory apparatuscan work by the power of suggestion (placebo). “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”144
  • 163. Several management options are available following initial assessment and diagnosis. Inparticular, men with PE secondary to ED, other sexual dysfunction or genitourinary infectionshould receive appropriate etiology specific treatment. Men with lifelong PE should be managedwith pharmacotherapy, while those with acquired or situational PE can be treated withpharmacotherapy and/or behavioral therapy according to patient/partner preference. Men withsignificant contributing psychogenic or relationship factors may benefit from concomitantbehavioral therapy. Recurrence of PE is highly likely to occur following withdrawal of treatment.Behavioral therapy may augment pharmacotherapy to enhance relapse prevention.Management according to severity(A) Very mild cases In a mild case of PE (for instance, if one can last a good five minutes but would like tolast 10), theres probably no point in going to a doctor. Why? As one should be able to improvematters by simple distraction techniques this means turning your mind to something else whenyou sense that a climax is near. For instance, you can: Mental distractions. Local anesthetic gel.(B) More severe cases If PE is causing much significant problems, it is best to consult an expert for treatment.Some people claim that its possible to self treat using the special grip mentioned later on. It isnot recommended instead it is advisable to go to a doctor, psychotherapist or counselor who istrained in the Masters-Johnson method of curing PE.(i) Treatment with drugs mentioned in detail below.(ii) A new technique At the end of the year 2000, a clinical trial of a new technique for treating PE waspublished in the medical press. It is emphasized that the new method has so far only been tried on “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”145
  • 164. a small number of patients. It involves wearing a constricting ring below the head of the penis for30 min. each day, to try and make the organ less sensitive(iii) Mental distractions Include thinking of a business problem, recalling a vacation trip, counting backwardsfrom hundred to one etc. These methods instead of helping may worsen the problem by causingerectile or rigidity failure. If these methods fail men may resort to concentrating on contractingthe anal sphincter, pinching them, biting the pillow etc. However the total result is dishearteningas distraction keeps the man from losing himself fully in the sexual experience as he cannot enjoyintercourse in an uninhibited passionate way. His partner becomes aware of his distance andrestraint and her pleasure is diminished.(iv) Sexual positions Sexual positions can affect a mans ability to control his ejaculation. The typicalmissionary position (Man on top) is not the best position while attempting to control ejaculation.Try lying on your back, allowing the partner to control copulation. In this position you are morerelaxed, and can guide your partner easily.(v) Masturbation before sex This technique is used by many young men to increase their level of control. It is thoughtthat masturbation before sexual activity will lessen the amount of desire a man feels therebyincreasing control. This technique is not very effective, however, as level of arousal is only partof what contributes to the condition.(vi) Topical anesthetics Local anesthetic gels are advertised to the public as a good way to damp down sexualsensation in the penis. The use of topical local anesthetics such as lignocaine and/or prilocaine asa cream, gel or spray is well established. They are moderately effective in retarding ejaculation,but do so at the price of possibly causing significant penile hypoanesthesia, possible trans vaginal “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”146
  • 165. absorption and distressing skin sensitivity reaction resulting in vaginal numbness and resultantfemale anorgasmia unless a condom is used.(vii) Desensitizing creams or lotions These are products which lessen the sensations felt by men during intercourse so that theycan last longer. The limitation of these creams is that they make intercourse less pleasurable bydecreasing stimulation. In 1999, a Korean product called S S Cream was claimed by Chinesedoctors to be helpful in treating PE, SS cream has been reported to improve ejaculatory control ina high percentage of patients. Local irritation can occur with herbal preparations and significantpenile hypoesthesia may occur. This latter effect can be severe enough to prevent the patient fromachieving an orgasm.(viii) Use of condom Condoms are an effective means of reducing the amount of stimulation experiencedduring sex. Some men find that a condom helps them prevent PE by lowering their arousal. If onecondom does not decrease the stimulation enough, then put on one more. Condoms provideexcellent protection against STDs and pregnancy, so theyre certainly worth a try.(ix) Avoidance of foreplay This method is ineffective because if a man tries to reduce his arousal by shortening thetime of foreplay as it may back fire by further convincing the women of her partners selfishness.(x) Second try mature ejaculationSome men find controlling ejaculation is no problem ‘the second try around’ i.e. after having oneorgasm and attempting intercourse within the next 2 – 3 hours. If this helps in any way it is at thecost of not feeling much or by the power of suggestion.(xi) Kegel exercises for pre mature ejaculationKegel Exercise These exercises, which have little risk and virtually no side effects, are a series ofconditioning of the pelvic floor muscles that have most commonly been used in patients suffering “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”147
  • 166. from urinary incontinence. However, it has recently been demonstrated that Kegel exercises arean effective treatment for premature ejaculation.131 These exercises consist of contracting thepelvic floor muscles or the pubococcygeus muscles for variable intervals of time (Patientinformation) and are usually first attempted during urination; by starting and stopping the urinarystream, the man learns to identify the pubococcygeus muscles. The goal of the technique is tostrengthen the pubococcygeus muscles in order to augment control during orgasmic response.Make sure your patient understands that it takes 3 to 6 months for this technique to make asignificant change in the latency period. Such alternatives may not offer a successful resolution to the ejaculatory problem asquickly as that off e red by any of the SSRIs, but these are less expensive and less riskyapproaches. When used in combination with drug therapy, they may assist the patient to graduallyregain control over the ejaculatory problem while allowing him to achieve sexual satisfactionduring that period of time, which in turn may enhance and expedite the recovery process.I) Psychological methodsAdopted in the treatment are as follows,1. Simple counseling Counseling can uncover and help resolve hidden conflicts or the emotions of anger andgrief long denied. Any issues about relationships may also be explored in this context, andcommunication between partners, often difficult in the presence of sexual problems, can befacilitated. An environment of emotional support and understanding can help patients work outtheir own solutions, with establishment of realistic goals and support for any changes in lifestyle. The basic elements of such simple counseling have been well described by Anon, 1974.The counselor should contribute in the following manner,i. Limited information The basic facts about normal sexual response, countering myths regarding sexualbehavior are provided to the patient. Such information need not be comprehensive but should be “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”148
  • 167. limited to specific problem area. (e. g. educating men that majority of women need some clitoralstimulation to achieve orgasm during intercourse.)ii. Specific suggestion Try female on top position to prevent PE so that the possibility of quickness may bereduced.iii. Permission and reassurance Permit the patient to try out new and previously unaccepted behaviors and reassureimprovement.iv. Facilitate communication This variety is based on commonsense and should occupy only one or two half-hoursessions.2. Couple therapy This method was developed by Masters and Johnson’s (1970) and the approach wasbased on the concept of treating the marital unit. Since both are involved in a relationshipinvolving sexual distress both should participate in the therapy. This is also called behavioralpsychotherapy. Improved communication in sexual and non-sexual areas is the specific goal oftherapy. Initial detailed history is taken individually, of the couple and again together with co-therapists. Psychiatric evaluation was suggested when needed. The treatment is short term andbehaviorally oriented, specific exercises are suggested and couples are made to learn to givebodily pleasure without the pressure of performance. The principle components of this therapyare behavioral, educational and psychotherapeutic.a. Behavioral Therapy Behavioral therapy offers one possible approach for treating PE. The cornerstones ofbehavioral treatment are the Semans "stop-start" maneuver which was later popularized by HelenSinger Kaplan and its modification proposed by Masters and Johnson, the squeeze technique. The"squeeze technique" is used more commonly. Both are based on the theory that PE occursbecause the man fails to pay sufficient attention to pre-orgasmic levels of sexual tension. As most “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”149
  • 168. men with PE are aware of their anxiety and the sources of that anxiety tend to be relativelysuperficial, treatment success with these behavioral approaches is relatively good in the shortterm but convincing long-term treatment outcome data are lacking.I. Stop and Start Technique The aim of these exercises is to learn to keep the patient below the point at whichejaculation seems inevitable for as long as possible. Men who do not have a partner can practicethe first three steps themselves. For the final four steps co-operation of a partner is needed.Step 1 Always masturbate with a dry hand. Avoid fantasizing and concentrate instead on thesensation in the penis. Allow the pleasure to build up but stop immediately as you feel you areabout to lose control. Relax for a while, still keeping your mind free of fantasies, until the dangerof ejaculation has passed, then begin again. Following the same pattern, aim starting for 15minutes without orgasm one may not be able to manage it at first, but keep trying. As one getsmore practice, he will probably find that he has to stop less often. When one has to completethree 15-minute sessions on three consecutive occasions (not necessarily one immediately afterthe other), proceed to the next step.Step 2 This involves masturbating with a lubricating jelly to heighten sensation and make delaymore difficult. Follow the technique in step 1 until one has completed three separate consecutivesessions as above.Step 3 One will now have gained a good measure of control. The next step involvesmasturbating with a dry hand for 15 min. before ejaculation. Keep focusing on the penis ratherthan fantasizing. When one feels dangerously excited, don’t stop, but instead, change rhythm oralter the strokes in such a way that the pressure to ejaculate fades. Experiment to see whichstrokes excite you most and which allow you most control. Work on this step until threeconsecutive sessions are completed as before.Steps involving a partnerStep 4 Lie on the back and get the partner to masturbate the penis with a dry hand, as in stepone. Concentrate on the sensations in the penis and ask the partner to stop every time one getstoo aroused before 15 min. are up. The aim is to last for three consecutive 15 min. sessions. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”150
  • 169. Step 5 Repeat step four, but ask the partner to use a lubricant while she masturbates your penis.It will be much more difficult to control ejaculation and one may have to ask the partner to stopmore often. Once the technique is mastered for three consecutive 15-minute sessions, one is readyto try the stop-start technique with intercourse.Step 6 The best position for delaying ejaculation is with the woman on top. Once inside, ask thepartner to move gently. Keep the hands on the hips so the woman so that one can let the womanknow with his hands when he wants her to stop, and when one is ready to start again. Again, aimto last for 15 minutes, but if one cannot, do not worry; one can start again on recoveringerection, and the second time he will probably have more control. During intercourse, one has toconcentrate entirely on himself. Give the partner full concentration and achieve orgasm eitherbefore or afterwards with oral or manual stimulation.Step 7 Move on to other positions. It is more difficult to delay ejaculation with the man on top,so save this until last.ii. Squeeze Technique [ Figure no.8 Squeeze Technique] A man with PE can learn to delay his ejaculation by means of aprogrammer of graded masturbatory exercises (the squeeze technique),with or without drug treatment. The aim of the exercises is to enablethe patient to recognize the feelings in his penis at different levels ofarousal and by modifying the stimulation, to learn to slow his desire to climax. When the coupleuse it after following careful instructions over a period of weeks, they can usually’re-train theman so that he can last longer. The squeeze action is designed to cause erection to subside and it can be applied everytime one gets too close to ejaculation. The partner placing her hand so that her thumb is on oneside of the mans erect penis (the nearer side to her - when she is facing him), while her index andmiddle fingers are on the other side. The index finger is just above the ridge of the glans (thehead or firemans helmet) while the middle finger is just below the ridge. When the man feelsthat hes near to a climax, he tells his partner. She then squeezes his shaft firmly between her “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”151
  • 170. thumb and the other two fingers. (It is painless) It is important to press fairly hard and not tomove the hand while doing so. Too light a touch could lead to ejaculation straight away.Step 1 Get your partner to masturbate you with a dry hand. Any time you get too close toejaculation, signal to her to stop and squeeze your penis. As with the stop- start technique, aim tolast for three consecutive 15 minute sessions before moving On to the next step.Step 2 Get your partner to masturbate you slowly and gently as before, but these times ask herto use a lubricant. Follow the procedure of step 1.Step 3 You are ready for intercourse, but not for thrusting. Lie on your back and ask yourpartner to sit on top of you, with your penis inside her. Neither of you should move. As soon asyou feel the urge to come, your partner should rise off you (dangerous movement as it appliesstimulation) and immediately hold your penis in the squeeze grip. Repeat the exercise a couple oftimes before ejaculating.Step 4 When you feel more confident about your self-control, ask your partner to move gentlywhile she sits on top of you in the same position. When you feel the urge to ejaculate, she shouldmove off you and squeeze as before, until you can last 15 minutes without ejaculating.Step 5 You are now ready to try other positions, but remember that with the man on top, you willhave least control. As with the stop-start technique, during intercourse you should focus allattention on yourself. Your partner will not feel neglected if you bring her to orgasm orally ormanually either before or after intercourse. If a man senses that he is about to experience premature orgasm, he interrupts sexualrelations. Then the man or his partner squeezes the shaft of his penis between a thumb and twofingers. The man or his partner applies light pressure just below the head of the penis for about 20seconds, lets go and then sexual relations can be resumed. The technique can be repeated as oftenas necessary. When this technique is successful, it enables the man to learn to delay ejaculationwith the squeeze. Behavioral therapy helps 60% – 90% of men with PE. However, it requires thecooperation of both partners. Also, PE often returns, and additional behavioral therapy may be “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”152
  • 171. needed. These techniques held sway for many decades, largely because of the unavailability ofother treatment methods. However, it soon became clear that the initial success rates claimed withthese were not sustainable and that over time the success rates had dwindled to 25%. Besides,these techniques are very tedious to employ and unsuitable for todays space age. Today, researchis centered on understanding the central and peripheral neurological control of the ejaculatoryprocess and regulating it with drugs. (andrology.com)a. Educational component To overcome ignorance and to counter false expectations in the minds of the couple theyshould be educated with regards to the normal human anatomy, physiology and how to enjoytheir sexual life.b. Psychotherapeutic component The assumption underlying this therapy is that the relationship between therapist andpatient provides a mirror of the relationship the patient has with his or her partner. It enablesunderstanding of any disturbed interaction with the partner and any hidden conflicts in thepatient. Initially, the doctor asks questions only when necessary, to minimize leading the patient.Medical investigations and questioning can sometimes be a way of avoiding painful andimportant emotional matters that the patient or the doctor may be afraid to face. It is most important to be aware of the feelings evoked in the doctor as well as the patientas the patients story unfolds and the physical examination takes place. These feelings need to bediscussed with the patient and can be used to inform him or her of the inner conflicts causing thedifficulties. Treatment is tailored to a patients individual needs to enable an understanding of theunique unconscious blocks hindering sexual fulfillment. This technique has been developed to be useful in a relatively short interview and so doesnot necessarily require any commitment to regular therapy sessions. Many general practitionersand some practice nurses have been trained in this approach, which lends itself well to the settingof a general practice or family planning clinic. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”153
  • 172. 3. Individual therapy An important development since 1970 when Master’s and Johnson first introduced theircouple therapy is the treatment of individuals who currently do not have a partner or whosepartner refuses to take part in the therapy. This is a common finding in clinical practice in India.In such cases the behavioral, educational and psychotherapeutic components are incorporated totreat the individual. Advise with regards to masturbation before sex and the stop and starttechnique can be employed.4. Group therapy This therapy provides a strong support system to patients who feel ashamed, anxious orguilty about their problem. It is a useful forum to counteract sexual myths, sexual misconceptionsand provide accurate information regarding sexual anatomy, physiology and varieties of sexualbehavior. In India however the main disadvantage is that couples often feel shy or are afraid ofexposure and loose confidence therefore are reluctant to join such group sessions.Current pharmaco therapeutically options for treating PE The most promising pharmaco-therapeutic agents have been serotonin reuptakeinhibitors. The potential of antidepressants to treat PE was first suggested by Ahlenius et al. in1979 who showed that the tricyclic antidepressant, clomipramine (a nonselective SRI), prolongedejaculatory latency in rats by blocking central serotonin reuptake. Clinical studies also provedefficacy of clomipramine in PE there is no evidence that the beneficial effects continue after thedrug is stopped. Tricyclic antidepressants have powerful side effects including anticholinergiceffects, reduced sexual desire, and genital anesthesia and as such, this treatment cannot becontinued for long. Other serotonergic antidepressants like paroxetine, clomipramine, sertralineand fluoxetine, are also used, a meta-analysis of drug treatment studies demonstrates thatparoxetine exerts the strongest ejaculation delay. Indoramin, an alpha blocker has less seriousside effects and is also effective. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”154
  • 173. Phosphodiesterase-5 inhibitors are widely used in treating erectile dysfunction and havealso been tested in clinical studies for the treatment of PE. However, to date, there is littleconvincing evidence to show that PDE-5 inhibition significantly increases IELT. Other drugswhich are of use include thioridazine and monoamine oxidase inhibitors. It is often preferred bymany therapists to use psycho-behavioral approach with special techniques like stop and start orsqueeze technique than mere drug therapy alone. Flow chart. No: 4 Management of Premature Ejaculation Premature ejaculation remains the most common sexual dysfunction in men132. Althoughprogress is being made in elucidating its causal mechanisms, the disparate variety of techniquesand drugs available for its treatment has met only limited success. For instance, behavioralinterventions were reported to be remarkably effective with initially satisfactory results in thevicinity of 90%; 133 unfortunately, the success rates decline markedly to less than 25% at 3 y. 134Systemic drugs have proven to have variable levels of efficacy, 135 but are plagued by side effectsthat are generally considered unacceptable, in the long term, in otherwise healthy men. Equallydiscouraging, the effect of these medications is temporary since the symptoms return upon their “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”155
  • 174. discontinuation. Therefore, it is evident that further avenues of treatment are an appropriate lineof inquiry for PE. The early Freudian-based causal hypothesis of PE has been revised and largelyabandoned in favor of physiological facts. A heightened sensitivity of the glans is currentlybelieved to be a fundamental initiating factor in PE. Therefore, it would be anticipated thatreducing the sensitivity of the glans would translate into a delaying effect on intra vaginalejaculation latency time (IVELT) without adversely affecting the sensation of ejaculation. Twostudies using topical local anesthetic creams have reported prolonged IVELTs, but exhibitsignificant drawbacks.136 The use of lidocaine–prilocaine (LP) cream reported by Berkovich et al137 required a 30-min application of the cream under a condom and resulted in numbness of thewhole shaft of the penis. A more drastic approach to desensitization involves ‘neurotomy’ of thedorsal nerves of the penis138. This invasive and irreversible measure is reported to be effective buthas failed to gain wide support in the medical community. We have developed a LP spray that is easy to administer, remains adherent to the skinafter application and only provides anesthesia of the glans139. The drug can be easily removedprior to vaginal penetration, circumventing the need for a condom that most patients findundesirable. Herein we report on a prospective open-label pilot study investigating the safety andefficacy of this novel delivery system for topical local anesthetic to the glans penis aimed atprolonging the IVELT in patients who self-reported having PE.Premature Ejaculation Exercises, Deal Premature Ejaculation with Exercises Premature ejaculation is mainly occurred during old age in males. But the investigationby doctors said that now a day’s premature ejaculation is also faced by every young male as theydo sexual intercourse in early age. Premature ejaculation is the commonest problem faced bymales once in their in life. Premature ejaculation makes life hell and frustrated because of unsatisfied sex. Prematureejaculation can destroy the marriage life because sometimes discharge quickly that man cannot “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”156
  • 175. have sex. Premature ejaculation can cause problem in fertility as man unable to do sexualintercourse. Premature ejaculation can be caused by two major factors physical and psychological likestress, depression, lack of sleep, restless, lack of confidence and lower level of testosterone. Thereare number of treatments to deal with the premature ejaculation. Many sex pills or antibiotics areoffered to deal with the premature ejaculation. But these pills can caused many problems likeexcess sweating, weight loss, insomnia, nasal problem and fatigue. So avoid consuming thesepills. Premature ejaculation also caused by excess consuming of hard drinks, smoking and drugs.There are some exercises to deal with the premature ejaculation Exercises are the best and easy way to deal with premature ejaculation or any othersexual problem. By doing exercises you will remain healthy throughout your life. Exercises giveus energy and increase the sex stamina. Performing exercises also increases the lower level oftestosterone. It also gives proper flow of blood to the penis as well as improves the bloodcirculation of the body. Secondly yoga is also the very effective and natural treatments to deal with thepremature ejaculation. By performing nude yoga increase the sexual power. Nude yoga posturesincrease your confidence. Yoga also helps to improve your stamina and delaying discharge. Breathing exercises also helps in delaying the premature ejaculation. By having sexualintercourse you have to take deep breathe and be calm this will help you in delaying thepremature ejaculation. Masturbation is also good to increase the sex ability and also help in delaying thepremature ejaculation. Masturbation can be done by yourself or by your girl partner.Masturbation can be done only by dry hands. Masturbation is the very effective technique tocontrol premature ejaculation and done by every men these days.Prognosis of premature ejaculation “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”157
  • 176. At the earlier stages of the problem the individual and the partner may try to comfort eachother and hope for a cure. When this is not achieved and recurrent ejaculatory failure occur theperformance anxiety increases according to the development of spectator role of both partners.Slowly the patient may adopt avoidance of sex, which may further worsen the ejaculatory controldue to long abstinence. In the usual course of events, the affected individual may develop erectile failure and lackof rigidity. The problems lead to deteriorate the marital harmony. The wife may try extramaritalaffairs and divorce. The affected individual may show associated clinical presentations likeheadache, backache, irritability, sleeplessness, lack of concentration, constipation, diarrhea, lossappetite, general debility and depression etc. In the later phase of the disease even suicidaltendency may develop.When does one need professional advice? Speak with your doctor if you consistently ejaculate before you want to. Remember, oneinstance of PE does not mean that you have a condition that requires treatment. Your doctor mayrefer you to a sex therapist if PE is causing major problems in your sex life or personalrelationships or if you would like to consider behavioral therapy.Expected duration of treatment Sometimes, PE goes away on its own over weeks or months. Working to relieve stress orother psychological issues may help the situation to improve. Other men have persistentdifficulties with PE, and require professional help. Some men respond to treatment promptly,while others struggle with this problem over a prolonged period. Effective treatment is available.PREVENTIONThere is no known way to prevent PE. However one should, “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”158
  • 177. 1. Maintain a healthy attitude toward sex. If you experience feelings of anxiety, guilt orfrustration about your sex life, consider seeking psychotherapy or sexual therapy. 2. Keep in mind that anyone can experience sexual problems. If you experience PE, trynot to blame yourself or feel inadequate. Try speaking openly with your partner to avoidmiscommunication.Pathya Apathya While commenting on Caraka, Cakrapani clarifies ‘Praharsha’ as ‘Manoharshana’.Exhilarating food articles improve the quality of sexual arousal and functioning. A man with vata disorder should change or maintain a vata-soothing diet. Follow a lowcholesterol diet if you have high cholesterol. Keep sugar intake low if you have diabetes as menwith this problem tend to experience premature ejaculation.Mental Exercises The importance of control over mind can be seen from the reference of Kokaka where hestates that if a person imagines a particularly nimble monkey swinging on the branch of a tree, hewill not ejaculate even though his semen is already at the tip of the penis. One should perform sex with Su-prasanna Mana. In the beginning of the act the personshould be fully focused on the act but as the act proceeds he should divert his mind to otheractivities. Yoga can be performed daily to attain stability of mind.Ten Dangerous Myths about Premature EjaculationMyth 1: You think you "learned to come too fast" and so you need to unlearn it. You’ve heard this one, right? You were masturbating as a teenager and didn’t want to getcaught so … Half truth. There may well be a learned behavior in PE but this is not the full story.In fact, there are differences in body chemistry between guys who come fast and guys who comeslowly, or even can’t come at all. How fast you ejaculate has a physical component, and it ismaybe even genetic (it runs in the family). So being nervous or excited may cause you to come quickly. But how quickly depends onyour underlying physical "set point". So guys have a longer set point than others.Good news You can do something to change this body chemistry. It will be a lot easier than"learning how to let go of your expectations".Myth 2: You think you are somehow "not normal". Deep down inside, you believe from all the "sex ed" on the web, in magazines etc. thatguys are all born studs. Half truth Normal is not average – normal is a range. It is obvious thatthere is a range of abilities in every area, and a range of differences in physical functioning. Justthe same as some guys have a bigger penis and others a smaller one, some guys will come fasterand others will come slower. And about 30% of guys come sooner than they or their partnerwant. So rapid ejaculation is pretty common. Most studies on how long is "normal" are inaccurate since most guys over-estimate their"staying power". But stopwatch measurements on 500 guys gave an average of about 5 minutes. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”159
  • 178. And about 2% came in less than one minute. However, among those men who sought treatmentfrom a medical practitioner, the majority ejaculated with 30 seconds…. Even though coming rapidly might be fairly common, it doesn’t mean that it is good foryour sex life. It can be devastating for both partners. In reality, everyone has to learn how to be agood lover. This includes learning your physical limitations and, more importantly what to do tocompensate for them, or even better to overcome them.Good news Changing your ‘set point’ for ejaculating is a lot easier than changing your penissize.Myth 3: No-one understands your condition. When you look at the information on the web, it’s easy to be forgiven for getting thisimpression based on the useless advice being offered. You have tried it and you know it won’twork for you. And if you have spoken to a non-specialist doctor they will probably quotequestionable research from decades ago…. The squeeze method or the stop starts method, oreven "don’t worry about it, it’s all in your head". So your assumption is based on personal evidence. But it is another half truth. In fact, PEis a hot area of research, after the success of Viagra followed from research in impotence. Andmedical researchers have a good general understanding of the mechanisms involved inejaculation. It is not a complete understanding by any means, but it is much better than theunderstanding decades ago.Good news Current medical understanding is not complete but it IS good enough to offer youeffective and rapid treatments. Getting curious? Keep reading because it is important tounderstand these issues and fix your condition soon.Myth 4: Therapy is the best ‘cure’. That’s the decades old understanding, but perhaps it is still touted by those who havevested interests in selling you expensive on-going therapy? Half-truth In fact, most guys either donot complete the therapy (you’d need a very understanding long-term partner and be preparedfor uncertain results) or they do make some improvement and then relapse to their old state. Thefirst two myths above give you some clues – the body easily returns to its natural rapidejaculation "set point". It is efficient to change your attitudes to change the body functioning. And it can be done.But it is much harder to shift attitudes and a belief, particularly about an area which is so centralto a man’s conception of himself and his sexuality. Let’s use an analogy. Do you change a guy’s confidence (for example to believe that theyare good in bed) and therefore change his sexual prowess, or is it better to give him sometechniques to change his prowess, and therefore let him automatically gain more confidence – aself-reinforcing process.Good news There are some things you can do which will get significant results right away. Soread on… Sign up below to find out about non-therapy treatments that work right away. And youwill get a free e-course!Myth 5: You can last longer by doing ‘Kegel’ squeezes doing sex. Kegels exercise a genital muscle called the Pubococcus Muscle (PC muscle). Some guyssay that by developing strong PC muscles and then clenching the PC muscle when you feel youare going to come will prevent ejaculation. This is another half truth. Here are the facts. The PCexercises do work for some guys. And these exercises will certainly increase the power andmaybe sense of pleasure you get from orgasm. But the squeezing during sex may worsen your problem. PC squeezing is more likely tohasten the onset of ejaculation for most guys. Or it may even cause retrograde ejaculation that iswhere the ejaculate is forced back into the bladder.Good news Doing Kegels might help you because premature ejaculation often occurs togetherwith erection problems. Straining to maintain an erection employs this very same squeezing “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”160
  • 179. technique and can hasten ejaculation. So improving PC muscle strength can help reduce theproblem but it is unlikely to remove it. Don’t go overboard but you can develop the health of these muscles easily over a fewweeks, and it is free! It is good to have strong PC muscles. But squeezing during sex is unlikely tohelp you. If you have problems getting or maintaining an erection after developing your PCstrength, you could also consider asking your doctor for a medication such as Viagra. Research shows that Viagra also tends to slow ejaculation slightly. So there is a doublebenefit for guys with erection issues for the reasons mentioned above.Myth 6: PE only affects your partner’s enjoyment of sex not yours. So you can compensate bybeing good at foreplay and stimulating her physically.... Many guys think this. After all, you can come anytime and it feels good, right? So yourmain problem is making her satisfied through lots of foreplay etc., and she will be OK. Half truthof course paying attention to her needs will be better than no foreplay! But here’s the real effectof PE on a sexual relationship. Her mental: most women are attracted to a dominant (but considerate) man, andalthough she will appreciate your thoughtfulness, not being able to stay hard and last a long timewill diminish her idea of your dominance and manliness. You are forced to be more passiveduring sex by your condition.You’re mental: You will never feel like you can really ‘deliver’ what you should be doing, andthis subtly reflects in your confidence about your sexuality. This is going to affect all aspects ofyour interactions with women: through the approach, seduction, sex to the relationship, andthereby limit your sexual options. She will pick up on this lack of deep inner confidence. Her physical: While pleasuring her with your fingers or tongue is good, it is not the sameto her as coming though intercourse alone with you on top of her and experiencing your ownexcitement, either mentally or physically. One of the biggest turn-on for a woman is when the guyis simultaneously turned-on. And most women need at least several minutes of vigorous vaginalstimulation to come from intercourse.You’re physical: Have you ever noticed that your orgasm is much more powerful when you havean extended build up of physical sensations, rather than ejaculating rapidly. So you pay for rapidejaculation with a reduction of your pleasure too.Good news: You can change your set point and last much longer on demand. Now you have thisunderstanding, the practical tips will make much more sense and if you apply them, it will make adifference!Myth 7: All Premature Ejaculation is the same. The half truth: PE is PE…. and it sucks. What you read and hear does not differentiatebetween types of rapid ejaculation: it is treated from the perspective of the symptom. It is a bitlike saying that allergy is one disease… in reality; there are many types of allergy with differentcauses although the allergy symptoms may be similar. The fuller truth: There are different causes of rapid ejaculation and there are differentcircumstances in which it occurs. From a time perspective, there is a difference whether youhave a lifelong condition (you have always come fast though whatever stimulation) or whether itdeveloped somewhat later in life or is just occasional. In the case where your condition hasalways existed, the cause is almost certainly that you have a biochemical set point that causesyou to come from little mental and physical stimulation. In other words, your body isprogrammed to do this.Good News and Bad news Men without PE slow down with age and tend to last longer. But research has shown thatit will not get better with age if you have lifelong premature ejaculation. In the case where the condition has developed recently, it could be due to a hidden orobvious health problem such as diabetes and you should get a thorough health check. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”161
  • 180. In case your condition is only occasional, it is more likely to have a mental "trigger". Forexample, you are with a new partner you feel under pressure. But there is a correspondingchange in your body. But it might just be that you are tired, sexually exhausted, stressed or otherwise not wellwhich leads to depleted chemicals in the nervous system. Or maybe you haven’t had sex for sometime: every guy knows that they will come faster in this situation.Good News In every case, there is an on-demand solution is available to solve your permanent ortemporary condition. This is because we now know enough how to manipulate the physiology tolengthen ejaculation time regardless of the cause or how long you normally last. Get ascientifically based on-demand solution and get a free e-course by registering below.Myth 8: Premature Ejaculation is defined by how long you can last. May be you have tried to find out how long the ‘average’ guy can last during sex tocompare yourself. Researchers tried to define PE in terms of a time measurement called IELT(intra-vaginal ejaculatory latency time) which basically means the time between when you insertyour penis into the vagina till you ejaculate. But these figures are not available or are very unreliable. They vary wildly depending onwhich source you get them from and how they are defined. One entry in Wikipedia defines thistime as 7.2 minutes for healthy guys while other research sources quote as little as 2 minutes.Anyhow, who cares? Comparing yourself is not as useful as making sure you last as long as youneed and you know how to satisfy a partner both physically and emotionally. Certainly, any guywho has a regular IELT of 2 minutes of less is likely to be unhappy or to have an unhappypartner. But IELT is not a good measure of PE because the time alone does not give an indicationof anything much to do with the experience during sex for both partners. Now researchers have decided on a composite definition: Premature ejaculation is amale sexual dysfunction characterized by ejaculation which always or nearly always occurs priorto or within about one minute of vaginal penetration; and, inability to delay ejaculation on all ornearly all vaginal penetrations; and, negative personal consequences, such as distress, bother,frustration and/or the avoidance of sexual intimacy. Just as some men come quickly, so do somewomen. Physical compatibility is an issue in sex, both in "responsiveness" and physical variablessuch as penis and vagina size. And the amount of foreplay, the relationship of the two partnersand the skill of the man as well as the attitudes and experiences of both man and woman create acomplex interaction that leads to the subjective experience of sexual satisfaction or not. The timetaken till the guy comes is only a part of that variable.Good news It doesn’t really matter how long other guys last, so you don’t need to suffer overwhether you are "normal" or not. Just focus on doing something about lasting as long as youwant, and see if it leads to an enhanced sexual experience for both of you. You may consider it more of a problem than she does, because of your desire for controlover the sexual interaction. But in any case, if you or she thinks you have a problem, regardlessof how long you last, you should take action to lengthen your time and it is possible.Myth 9: Lasting a long time will ensure she comes easily and you’ll be a stud. If you are like many guys who are not confident about their ability to perform well in bed,your three basic fears are probably: Am I big enough? Can I get it up? Can I last long enough?Probably in that order! Unless you have a big penis or unless you have one particular problem,in which case the order will change. This puts a tremendous pressure on you: this pressure mightnot reduce your penis size, but it is likely to impact on your ability to last longer or get hard.Penis size is somewhat important in spite of the politically correct information that states it is not.But it is not nearly as important for most women as you’re getting hard or lasting a reasonabletime before ejaculating. Delivering on these two things probably means you are an Ok lover. Butit is not enough to rock her world. Men and women are turned on by different things, and respondto different cues in sex. For a woman, a good sexual experience depends much more onemotional and mental stimuli, and for a guy it is initiated more by visual and physical stimuli. So “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”162
  • 181. the most important thing for a guy is to watch and see her reaction. Don’t go by what she says;go by what makes her aroused. When you find something that arouses her, keep on doing it. Justas attraction is not a choice, arousal is not a choice either. It is not an intellectual thing. It isvisceral.Good news: It is very possible achieve a good erection and to last longer. Then you have thephysical basis to experiment and observe or for a shortcut you can use the great materials thatare already available on dating, seduction and sexual technique to give you insights to get reallygood at being a desirable sex partner..... Something that it is normal for you to want, andsomething that is achievable. But you have to have the basics in place first. All the knowledge inthe world will not help you run if you can’t stand up and be there!Myth 10: You can’t change it, so learn to live with it. This is the biggest mistake of all. This is the mistake that will keep you from being a greatlover, ever! And that is a big loss to you and your current & future partners. Actually, let me tell you a secret. If you can control your PE, you might be a better loverthan other guys. Why? Because your experience will have made you more observant and morecaring in the bedroom. But you also need to be confident in your ability "to deliver" and thereforeable to take a dominant role too. Most women prefer a dominant but caring person. You don’twant to feel helpless or admit your problems. It’s not guy nature. So we sit on them. Experiencingthe sick feeling of being inadequate in some way? Trying to hide it? How about the pride andsatisfaction of the feeling that will come with lasting a lot longer? And having the choice! Ok, sowhat do you need to do to last longer? First let me give you a bit more information. A recentState of the Art Medical Conference on Premature Ejaculation found that mental factors docontribute to PE. But time to ejaculation is mostly a biological (physical) variable. And theynoted that the use of special medications lengthens the time from penetration to ejaculation.These medications act on the body’s serotonin system. Serotonin is a natural nerve chemical(neurotransmitter) which promotes relaxation. Guys who come quickly have lower levels of thisnatural body chemical. This is one of the primary reasons for rapid ejaculation. Bad news:These serotonin enhancers (medically called SSRI’s, for example Prozac) have side effectsleading to reduced libido (sex drive) or even impotence. Good news: There are medications thatwork to control premature ejaculation. Unlike older medicines, they have few side effects. Andeven better they can be used on demand, one hour before sex - just like the popular erectionenhancer Viagra.Myth: Premature ejaculation is a problem that is entirely in one’s mind.Fact: New studies have shown that a low level of serotonin, a natural substance that isproduced by nerves, may be a possible cause.Myth: Alcohol is a good method for controlling premature ejaculation.Fact: Although alcohol can delay orgasm, it is not an effective treatment for prematureejaculation.Myth: Premature ejaculation is a rare problem that affects few men.Fact: PE actually affects more men than people generally assume. Most experts on the subjectsestimate that somewhere between twenty and thirty percent of men suffer from prematureejaculation. This number could actually be far greater, since this figure solely is based on thosemen who seek medical attention for the disorder. You are not alone; there are plenty of men outthere who are unable to control when they climax.Myth: Premature ejaculation is a sickness or disease.Fact: Premature ejaculation is not a sickness or disease. It is a disorder generally related toemotional or psychological factors dependent upon the individual man, as well as low levels ofserotonin production in the brain. In very rare cases, climaxing early indicates a physical ailment, such as prostate cancer.Discussing the problem with your doctor is the only way to definitively rule out serious ailments. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”163
  • 182. Your doctor will ask you about your symptoms and may or may not wish to have you examinedphysically or refer you to another health professional.Myth: If you try and focus on something else, you’ll last longer in bed.Fact: Unfortunately, trying to shift your focus while in bed can exacerbate the problem ofpremature ejaculation. Subconsciously, your mind will revert to the subject matter you are tryingto avoid – climaxing. Although it sounds counterintuitive, you should pay attention to what yourbody is doing when you climax early. The root of the problem lies in the activity of sex itself.Since premature ejaculation is psychologically or emotionally driven, get in touch with theemotions you are experiencing during the sex act. Anxiety and tension only makes the problemworse in most cases.Myth: Some men are naturally better at controlling their ejaculation.Fact: Everyone is unique, and that is a definitive fact. Some men are better at controllingejaculations, but this has more to do with their emotional state. If you are well-adjusted, mostthings come more naturally, including the control over your ejaculations. You are not borngenetically predisposed to premature ejaculation. However, with natural supplements, such asCliminax, you can eliminate your premature ejaculation problems – giving you the confidenceand sex life you deserve.Myth: There is no treatment for premature ejaculation.Fact: This is patently untrue. There are many effective treatments for PE. You can speak with aqualified therapist, try PE creams and gels, utilize penis rings, conduct penis exercises, and alsotake supplements. The last option, taking pills such as Climinax, is the most effective and discreteoption – working quickly to eliminate your PE.Myth: Premature ejaculation means you can only last a few minutes.Fact: There is no set time limit that means you are a premature ejaculator or not, but medicalexperts generally agree that if you consistently ejaculate less than two minutes after insertion,you may have sexual dysfunction. The average man lasts slightly over seven minutes. That is an average; the only personwho can determine if you have premature ejaculation is yourself and your partner; if the two ofyou are unsatisfied with the length of time it takes for you to ejaculate, then you most likely areexperiencing erectile dysfunction.Myth: I have to wait until they develop a pill to treat premature ejaculation.Fact: Thankfully, you do not have to wait until a pill is developed. You can opt to take anantidepressant, such as Prozac, but that prescription is riddled with major side effects – such asthe inability to maintain an erection. Researching on the internet will yield plenty of results for treatments that others havetried. As with anything, there are varying degrees of success. One product that has been provento achieve results for a great deal of men is Climinax. Besides proven results, the product is100% guaranteed. It treats the core root of your premature ejaculation problem by providingyour brain with the needed ingredients to boost your serotonin production. Therapies followed at present study in Shukragatavata are - Virechana karma (Anulomana) - Anulomana: means sending or putting in right way. here the drug, which will digest the pakwa and apakwa (digested and undigested) malas and expels from the Adhomarga is called as Anulomana. e. g. Haritaki. Sushruta considers, Sara as the synonym for Anulomana. According to Dalhana, Anulomana causes expulsion of vata and kapha. Administration of Vidaryadi Ghrita “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”164
  • 183. DRUG REVIEW “Amantram aksharam naasti | Naasti moolam anaushadam||Ayogya purusho naasti | yojakastra durlabham” || There is no word which is not a chant. There is no Root of a plant which is not amedicine. There is no person who is not at all useful. But it is difficult to get a person who is ableto use all these things.ANALYTICAL CONCEPTS ON MANAGEMENT Shukragatavata with Premature Ejaculation as clinical presentation is characterized byVataprokopa, Shukradhatudourbalya and Manobhighata. The line of management should be toremove the cause. As already discussed in the conceptual contrive the medication should possessvrishya, balya, medhya, shukrastambhana and Vatahara properties. The selected combination ofdrugs for the clinical trial named as vidari Ghrita satisfies these properties.DRUG CONTRIVE “Yat Bheshajam Tat Amrutam, Yat Amrutam Tat Brahma”- (Gopath Brahman 1/3/4) Drugs are the tools of a Physician. According to Ayurveda, the success of treatmentdepends upon the Chikitsa Catushpada. Drug is a part of this quadruped of treatment, which isnext to the physician in importance. Thus the selection of proper drug in the management ofdiseases is very important. W.H.O. defines drug as ‘a substance or product that is used or intended to be used tomodified or explore physiology system or pathological status for the benefit of the recipient.’Ayurveda was the first to give an elaborate description of various therapeutic measures notmerely of radical removal of the causative factors but also to restore Doshika equilibrium. In Ayurvedic classics there are a lot of single and compound drugs which mentioned inseveral contexts. Most of them are not re-tested according to the current research methodology.Unless the efficacy of these drugs is not re-affirmed the drug may not receive proper recognitionin today’s scientific world. We also hope that by the use of phyto chemicals we would avoid “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”165
  • 184. many of the risks associated with synthetic chemicals. It is also high time that by keeping in mind the Samprapti of the disease and the basic principles of Ayurveda new herbal formulations are developed especially for those diseases that have not been aptly described in our texts. Shukragatavata as a clinical presentation is characterized by Vata Prakopa increased Rajo Guna and decreased Dhairya. The line of management should be to eliminate the cause. As discussed in the conceptual contrive the medication should possess Medhya, Balya, Rasayana, Vatashamaka and Vrisya properties. Table No. 13 Showing Drug ReviewSl. Drug Family Latin name Parts used Rasa Guna Veerya VipakaNo1 Vidari kanda Leguminosae Pueraria Kanda Madhura Guru, Sheeta Madhura tuberosa snigdha2 Vrishaka Acanthaceae Adhatoda Mula, patra, Tikta, kashaya Ruksha, Sheeta Katu (Vasa) Vasica puspa laghu3 Yuthi Oleaceae Jusminum Puspa, patra Kashaya, Laghu Sheeta Katu Auriculatum Panchaga Tikta, Madhura4 Matulunga Rutaceae Citrus Medica Phala Amla Tikshna Ushna Amla5 Bhustrana Gramineae Cymbopogon Patra, Katu, tikta Laghu, Ushna Katu Schoenanthus puspa, ruksha, Kanda tikshna6 Pashana Bedha Saxifragaceae Bergenia Mula Kashaya Laghu, Sheeta Madhura Ligulata Tikta ruksha,7 Kasturi - Moschus - Katu, tikta Laghu, Ushna Katu Moschieferous ruksha, tikshna8 Vasuka Asclepiadaceae Calotropis Mulatvaka, Katu, tikta Laghu, Ushna Katu (Araka) Procera Patra,puspa, ruksha, ksheera tikshna9 Gaja Pippali Piperaceae Scindapsus Phala, Katu Ruksha Ushna Katu officinalis Mula10 Chitraka Plumbaginaceae Plumbago Mulatvaka Katu Laghu, Ushna Katu Zeylanica ruksha, tikshna11 Punarnava Nyctaginaceae Boerhavia Mula, Madhura, Laghu, Ushna Madhura Diffusa Beeja, tikta, ruksha Panchaga kashaya12 Vacha Araceae Acorus Mula, Katu, Tikta Laghu, Ushna Katu Calamus Bhoumika tikshna kanda “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”166
  • 185. 13 Rasna Compositae Pluchea Patra, mula. Tikta Guru Ushna Katu Lanceolata14 Bala Malvaceae Sida Mula, Madhura Laghu, Sheeta Madhura Cordifolia Beeja snigdha pichhila15 Atibala Malvaceae Abutilon Mula, Madhura Laghu, Sheeta Madhura Indicum Beeja snigdha pichhila16 Kasheru Cyperaceae Scirpus Kanda Madhura Guru, Sheeta Madhura Grossus kashaya ruksha17 Kamala Nal Nymphaeaceae Nelumbo Mula, Kashaya Laghu, Sheeta Madhura Nucifera Beeja, Madhura snigdha Puspa Pichhila pichhila18 Shringataka Trapaceae Trapa Natans Beeja, Madhura Guru, Sheeta Madhura Stem kashaya ruksha19 Bhumyamlaki Euphorbiaceae Phyallanthus Panchaga Tikta, Laghu, Sheeta Madhura Urinaria Kashaya ruksha Madhura20 Shalaparni Leguminosae Desmodium Panchaga Madhura Guru, Ushna Madhura Gangeticum Tikta snigdha21 Prishniparni Leguminosae Uraria Picta Panchaga Madhura Laghu, Ushna Madhura Tikta snigdha22 Brihati Solanaceae Solanum Phala, Katu, Tikta Laghu, Ushna Katu Indicum Mula ruksha, tikshna23 Kantakari Solanaceae Solanum Phala, Katu, Tikta Laghu, Ushna Katu Surattense Mula ruksha tikshna24 Gokshura Zygophyllaceae Tribulus Phala, Madhura Guru, Sheeta Madhura Terrestris Mula snigdha25 Kusa Gramineae Desmostachya Mula Madhura Laghu, Sheeta Madhura Bipinnata Kashaya snigdha26 Kasha Gramineae Saccharum Mula Madhura Laghu, Sheeta Madhura Spontaneum Kashaya snigdha27 Shara Gramineae Saccharum Mula Madhura Laghu, Sheeta Madhura Munja Tikta snigdha28 Ikshu Gramineae Saccharum Mula, Madhura Guru, Sheeta Madhura Officinarum Swarasa, snigdha Sharakara29 Darba Gramineae Imperata Madhura Laghu, Sheeta Madhura Cylindrica Kashaya snigdha30 Yastimadhu Leguminosae Glycyrrhiza Mula Madhura Snigdha, Sheeta Madhura Glabra ruksha “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”167
  • 186. 31 Pippali Piperaceae Piper Longum Phala, Katu Laghu, Anu Madhura Mula snigdha Ushna tikshna Sheeta32 Draksha Vitaceae Vitis Vinifera Phala Madhura Snigdha, Sheeta Madhura Guru, Mrudu33 Gambhari Verbenaceae Gmelina Phala, Tikta, Guru Ushna Katu Arborea Mula Kashaya Madhura34 Parushaka Tiliaceae Grewia Phala, Kashaya, amla, Laghu Sheeta Madhura subinaequalis Mula madhura35 Ela Zingiberaceae Elettaria Beeja Katu, Laghu, Sheeta Madhura Cardamomum Madhura Ruksha36 Dhanvayas Zygophyllaceae Fagonia Panchaga Kashaya Laghu, Ushna Madhura Cretica Tikta, Snigdha Madhura Katu37 Kaunthi Verbenaceae Vitex agnus Beeja Katu, Laghu, Sheeta Katu Castus Tikta Ruksha38 Kesar Iridaceae Crocus Kesar Katu, Snigdha Ushna Katu (Kumkuma) Sativus (Stigma , Tikta Kukshibhaga)39 Nagakesar Guttiferae Mesura Ferrea Beeja, Puspa, Kashaya Laghu, Ushna Katu Patra Tikta Ruksha40 Jeevak & Leguminosae Pueraria Kanda Madhura Guru, Sheeta Madhura Vrashabhaka tuberosa snigdha (Vidarikanda)41 Kakoli & Solanaceae Withania Mula Katu, tikta, Laghu, Ushna Madhura Ksheerakakoli Somnifera Madhura Snigdha (Ashwagandha)42 Medha & Maha Liliaceae Asparagus Kanda Madhura tikta Guru, Sheeta Madhura medha racemosus snigdha (Shatavari)43 Vrudhi & Dioscoreaceae Dioscorea Kanda Katu, tikta, Laghu, Ushna Katu Vradhi bulbifera Madhura Snigdha (Varahikanda)44 Kankola Piperaceae Piper cubeba Phala Katu, tikta Laghu, Ushna Katu ruksha, tikshna45 Haridra Zingiberacae Curcuma Kanda Tikta, Katu Laghu, Ushna Katu longa ruksha46 Amalaki Euphorbiaceae Emblica Phala Pancha Ruksha, Sheeta Madhura officinalis (Lavanrahita), guru, Amalapradhana Sheeta47 Ghrita - Butyrum - Madhura Guru, Sheetha Madhura depuratu Snigdha, Mrudu “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”168
  • 187. 1) Vidari kanda140 Doshaghnata : Vatapittashamak Karma : Balya, Brihana,Varnya, Shonitasthapana, Vrishya, Shukrala, Prajasthapana, Stanyajanana, Rasayana. Prabhava : Balya Chemical composition : Resin, sugar and starch (In large quantity)2) Vrishaka (Vasa)141 Doshaghnata : Kaphapittashamaka Karma : Shotahara,Vedanastapana, Stambhana,Hridya, Kasahara, Swasahara, Mootrajanana, Jwaraghna142 Prabhava : Chedana Chemical composition : Aromatic volatile oil, fats, vasicin, adhatodic acid, Glycosides, resin, salt and dye.3) Yuthi143 Doshaghnata : Pittashamaka Karma : Prameha, Raktapitta shamaka, Shonitasthapana, Mukhapaka.144 Chemical composition : Sugandhi tail4) Matulunga145 Doshaghnata : Vatapittashamaka, Kaphavatashamaka Karma : Rochaka, Raktapitta, Swasa, Kasa, Hikka, Bhrama roga, Ashmari, Rajorodha, Arsha. Prabhava : Rochan Chemical composition : Citrene, Citrol, Cymene, Citronellal.5) Bhustrana146 Doshaghnata : Kaphavatashamaka Karma : Vedanasthapana, Rochana, Deepana, Pachana, Anulomana, Krimighna, Raktashodaka, Mutrajanana147 Prabhava : Stanyajanana “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”169
  • 188. Chemical composition : Palmarosa oil, Rusa oil, East Indian geranium oil, Ginger grass oil, and Geraniol.6) Pashana Bedha148 Doshaghnata : Tridoshashamaka Karma : Shothahara, Vranaropana, Stambhana, Mootral, Hridya, Raktapittashamaka, Ashmaribhedana, Jwaraghna. Prabhava : Asmaribhedana Chemical composition : Tannic acid, gallic acid, starch, calcium oxalate.7) Kasturi149 Doshaghnata : Vatakapha shamaka Karma : Sheetaprashamana, Balya, Vajikarana, Sheeghrapatana. Chemical composition : Cholestol, amonia, fat, albumin.8) Vasuka (Arka)150 Doshaghnata : Kaphavatashamaka Karma : Vedanasthapana, Shothahara, Krimighna, Dipana, Vranashodana, Jantughna, Vamanopaga, Pachana Prabhava : Teeksna virechaniya Chemical composition : Uscherin, Calotropin, Calotoxin, Amyrin, Giganteol.9) Gajapippali151 Doshaghnata : Vatakaphashamaka Karma : Deepana, Agnivardhaka, Malavishoshana, Kanthya, Stanya, Varnya, Krimighna, Balya. Prabhava : Kasahara Chemical composition : Piperine, Piplartine, Sesamin, Piplasterol.10) Chitraka152 Doshaghnata : Vatakaphashamaka Karma : Lekhana, Visphotajanana, Madaka, Deepana, Pachan, Grahi, Krimighna, Raktapittakopaka, Shothahara, Kaphaghna, Garbhasravakara, Vajikarana, Rasayana. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”170
  • 189. Prabhava : Dipana Chemical composition : Plumbagin,chloroplumbagin, chitranone, zeylinone, isozeylinone, droserone, plumbage acid.11) Punarnava153 Doshaghnata : Tridoshahara Karma : Kasahara, Vrishya, Mootrajanana, Rasayana, Hridya, Shothahara, Anulomana, Kushthaghna, Lekhana. Prabhava : Mutravirechaniya Chemical composition : Punarnavoside, rotenoids viz boeravinones A, B, C, D, E, lignans, liridodendrin, flavones, sterols, isofuroxanthone, boeravinr, hypoxanthine-9-L-arabinofuranoside.15412) Vacha155 Doshaghnata : Kaphavatashamaka Karma : Kanthya, Medhya, Shamaka, Vedanasthapana, Vamaka, Krimighna, Arshoghna, Anulomana, Mootrajanana Prabhava : Medhya Chemical composition : Asarone, Calamenol, Calamene, Methyl eugenol, Camphene, Various fatty acids, Calamol, Sugar, Glucosides- acorin, Asarylaldehyde.13) Rasna156 Doshaghnata : kaphavatashamaka Karma : Shothahara, Vatahara, Vedanasthapana, Amapachana, Kasahara, Vrishya, Rasayana, Raktashodhaka. Prabhava : Vedanasthapana Chemical composition : Sterol glycosides, flavone glycoside, choline chloride, taraxasterol, triterpene, neolupenol, pentacyclic. 14) Bala157 Doshaghnata : Vatapitta shamaka Karma : Balya, Prajasthapana, Vatasanshamana, Nadibalya, “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”171
  • 190. Vatahara, Shukrala, Mootrala, Ojhovardhaka Prabhava : Balya Chemical composition : Major components of seeds are alkaloids. Alkaloids Contain mainly ephedrine. It also contains fatty acid, mucin, potassium nitrate and resin.15) Atibala158 Doshaghnata : Vatapittashamaka Karma : Vatahara, Rasayana, Mutrajanana, Snehana, Vajikara, Kasahara, Krimi, Mridurechana. Prabhava : Balya Chemical composition : Flavones, gossypetin-8 and 7-glucoside, cyaniding-3 rutinoside, glucosyloxybenzoic acid,caffeic, fumaric acid, glucovanilloyl, fructose, galactose, glucose.15916) Kasheru160 Doshaghnata : pittashamaka Karma : Grahi, Kaphavatavardhaka, Vishtambhi, Prajasthapana, Raktastambhana, Vrishya, Stanyajanana, Mutral, Balya. Prabhava : Prajastapana Chemical composition : Steroids, sugar, tannins, carbohydrate, amino acid, fatty Acids - caprylic, capric, myristic, pentadecanoic.17) Kamala Nal161 Doshaghnata : Kaphapittashamaka Karma : Dahaprashamana, Varnya, Medhya, Chhardinigrahana, Trishnanigrahana, Stambhana, Balya, Prabhava : Prajastapana Chemical composition : Nuciferine, roemerine, dimethylcoclaurins, glucose, palmitic acid, chlorophylls, methyl corypalline.18) Shringataka162 Doshaghnata : Pittashamaka “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”172
  • 191. Karma : Vrishya, Balya, Sara, Shukrala, Stambhana, Mootral, Prajasthapana, Shonitasthapana, Vishtambhi. Prabhava : Prajastapana Chemical composition : Galactopyranose, gallic acid, vita. A & C, ellagicacid, Citric acid, tannin, amylopectin, amylose, carbohydrates, Protein, fat, nicotinic acid, riboflavin, thamine.19) Bhumyamlaki163 Doshaghnata : Pittakaphanashaka Karma : Mootrajanana, Kasa, Swasa, Daha, Shothahara. Prabhava : Mutra virechaniya Chemical composition : Phyllanthin, tikta and kshara ghataka20) Shalaparni164 Doshaghnata : Tridosha shamaka Karma : Tridosahara, Blya, Vrsya, Rasayana, Angamarda, Nadibalya, Anulomana, Stambhana, Krimighna. Prabhava : Angamarda prashamana Chemical composition : Hydroxygenistein, dalbergioiden, diphysolone, kievitone, flavone glucoside.16521) Prishniparni166 Doshaghnata : Tridoshashamaka Karma : Vatahara, Nadibalya, Vrishya, Mutral, Balya, Shonitasthapana, Dahaprashamana, Vishaghna. Prabhava : Angamarda prashamana Chemical composition : Amino acid, fatty acid22) Brihati167 Doshaghnata : Kaphavata shamaka Karma : Raktashodhaka, Shothahara, Kaphaghna, Mootral Prabhava : Kasahara Chemical composition : Methyl protodioscin, lauric acid, oleic, stearic acid, “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”173
  • 192. solamargine, gitogenin, trilinolin.23) Kantakari168 Doshaghnata : Kaphavatahara Karma : Mootral, Garbhashayasankochaka, Vajikarana, Vedanasthapana, Kasahara, Swasahara, Shothahara. Prabhava : Kasahara Chemical composition : Alkaloids `solenin`, potassium chloride, potassium Nitrate, iron and organic acid, amino acid, cholesterol.24) Gokshura169 Doshaghnata : Vatapitta shamaka Karma : Vedanasthapana, Vatashamaka, Agnideepaka, Balya, Ashmarinashana, Vajikara, Vastishodhaka, Mootrala. Prabhava : Mutravirechana Chemical composition : Chlorogenin, diosgenin, acetate, gitogenin, astragalin, dioscin, gracillin, hecogenin, ruscogenin, frostanol, glycoside, glucoseamino acid, alkaloids harmine.17025) Kusa171 Doshaghnata : Tridosha shamaka Karma : Mootravirechana, Stanyajanana, Ashmari, Mutraghata Prabhava : Mutravirechana26) Kasha172 Doshaghnata : Pittanashaka, Vatapittashamaka Karma : Shukrashodhaka, Stanyajanana, Vrishya, Vajeekarana, Prabhava : Mutravirechana Chemical composition : Protein, calcium, phosphorus, hydrocyanic acid glycosides.17327) Shara174 Doshaghnata : Tridosha shamaka Karma : Vrishya, Mootrajanana, Raktashodhaka, “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”174
  • 193. Sukradourabalya. Prabhava : Mutravirechana28) Ikshu175 Doshaghnata : Vatapittashamaka Karma : Veerya vardhaka, Balya, Mootrala, brinhana. Prabhava : Mutravirechana Chemical composition : Sucrose, glucose, fructose, fibre, nitrogenous substance, Fat, waxes, gums, pectin, free acid, proteins, vitamin D Albuminoses, acid amides, carboxylic acid, inorganic Salts, amino acid, histidine, riboflavin.17629) Darba177 Karma : Rasayana, Vamaka, TridaÀahara,30) Yastimadhu178 Doshaghnata : Vatapittashamaka Karma : Medhya, Vatanulomana, Mootral, Shukravardhaka, Varnya, Jeevaneeya, Rasayana, Balya, Nadibalya. Prabhava : Chedan Chemical composition : glycyrrhizine, prenylated biaurone, licoagrone, glabrolide, liquiritic acid, isoglabrolide, glycyrin.31) Pippali179 Doshaghnata : Kaphavatahara Karma : Medhya, Vatahara, Vrishya, Balya, Rasayana, Uttejaka Garbhashayasankochaka, Vatanulomana, Mootrala. Prabhava : Kasahara Chemical composition : Sungadhi tail, Piperine, Piplartine, Sesamin, Piplasterol.32) Draksha180 Doshaghnata : Vatapittashamaka Karma : Medhya, Vrishya, Garbhasthapana, Jivaniya, Balya, Sandhanakaraka, Mootrala, Chakshushya, Hridya. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”175
  • 194. Prabhava : Snehopaga Chemical composition : Palmitic, stearic, oleic, linoleic, linolenic acid, caffeic, caffeyltartaric acid, malic acid, tannic acid, glucose, fructose, amino acid, galactose.33) Gambhari181 Doshaghnata : Tridosha shamaka Karma : Sheetala, Snehana, Medhya, Keshya, Vedanasthapana, Mootrajanana, Garbhasthapana, Vrishya, Rasayana, Brinhana, Vishaghna, Balya, Shothahara.182 Prabhava : Shothahara Chemical composition : Gmelanone, palmitic, oleic, linoleic acid,stigmasterol, campesterol, luteolin, apigenin, quercetin, cerylalcohol.34) Parushaka183 Doshaghnata : Vatapittashamaka Karma : Vishtambhi, Hridya, Brinhan, Shophahara, Jwaraghna, Pittashamaka, Trishnashamaka. Chemical composition : Phenyl alanine, sugar-glucose, xylose, arabinose, glutaric acid, phenylalanine, glucose, linoleic acid, betulin, triterpenoid- erythrodiol, taraxasterol.35) Ela184 Doshaghnata : Tridoshahara Karma : Mooyrajanana, Swasa, kasa, Balya, Dahaprashamana. Prabhava : Daha prashamana Chemical composition : Cineol, terpineol, terpinene, limonene, sabinene.36) Dhanvayas185 Doshaghnata : Vatapittashamaka Karma : Dahaprashamana, Kothaprashamana,Vranaropana, Stambhana, Raktaprasadaka, Kaphanissaraka, Mootral. Prabhava : Trishna nigrahana “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”176
  • 195. Chemical composition : Ceryl alcohol, chinovic acid, harmine, alanine, lysine, arginine, glycine, isoleucine, leucine, phenylalanine, valine, chinovic acid, alkaloids, fagogenin, oleanolic acid, proline, tyrosine, campesterol, stigmasterol.18637) Kaunthi187 Doshaghnata : Vata, kapha Karma : Kasa, Netraroga, Chemical composition : Castine, Katu, dahajanaka drava, amala drava, tail.18838) Kesar189 Doshaghnata : Tridoshashamaka Karma : Varnya, Uttejaka, Mastishkabalya, Vedanasthapana, Garbhashayashodhana, Garbhashayasankochaka, Rasayana, Vajikarana, Shothahara. Prabhava : Varnya Chemical composition : Isophorone, fatty acid – palmitic, stearic, oleic, salicylic acid, campesterol, stigmasterol.39) Nagakesar190 Doshaghnata : Kaphapittashamaka Karma : Vedanasthapana,Durgandhanashana, Swedapanayana, Uttejaka,Krimighna,Kaphaghna, Vajikarana, Balya, Mootrajanana, Kushthaghna, Shonitasthapana. Prabhava : Rakta stambhana Chemical composition : Mesuol, mesuaferrol, leucoanthocyanidin, mesuone, mesuagin, mammeigin, xanthone, euxanthone.40) Jeevak & Vrashabhaka ( Vidarikanda) 191 Same as described above in serial number 141) Kakoli & Ksheera Kakoli (Ashwagandha) 192 Doshaghnata : Kaphavatashamaka Karma : Mastishkashamaka, Vajikarana, Garbhashayashothahara “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”177
  • 196. Yonishoolahara, Mootrala, Balya, Rasayana, Kaphaghna Prabhava : Rasayana Chemical composition : Cuseohygrine, anahygrine, tropine, anaferine, cystine.42) Medha & Maha Medha (Shatavari) 193 Doshaghnata : Vatapittashamaka Karma : Medhya, Rasayana, Balya, Gharbhaposhaka, Stanyajanana, Shukrala, Mootral, Nadibaladayaka Prabhava : Sukrajanana Chemical composition : Sarsapogenin, glycosides of quercetin, rutin, diosgenin, Polycyclic, alkaloid, asparagamine A, furostanolic.43) Vrudhi & Vradhi (Varahikanda) 194 Same as described above in serial number 1 19544) Kankola Doshaghnata : Kaphavatashamaka Karma : Mootral, Vajikarana, Artavajanana, Bastishodhaka, Uttejaka, Shothahara, Daurgandhyanashana. Prabhava : Mootravirechaniya Chemical composition : Cubebol, cubebic acid, oleic, stearic, piperidine, sesamin, palmitic, arachidic.45) Haridra 196 Doshaghnata : Tridoshashamaka Karma : Varnya, Kushthaghna, Kanndughna, Raktastambhana, Vedanasthapana, Mootrasangrahaniya, Shwasahara. Prabhava : kusthaghna Chemical composition : Desmethoxycurcumin, bidesmethoxycurcumin, fatty acid, dihydrocurcumin, phytosterols,polysaccharides197 19846) Amalaki Doshaghnata : Tridoshashamaka, Prabhava : Rasayana “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”178
  • 197. 47) GHRITHA Synonyms : Grutha, sarpi, ajya, Latin Name: Butyrum depuratu Rasa : Madhura Guna : Guru, Snigdha, Mrudu Veerya : Sheetha Vipaka : MadhuraAction of cow’s ghee on different body system Nadivaha samsthana : Medhya, Insanity Pachana samsthana : Snehana, agnideepaka, anaha Swasana samsthana : Rajaksma Raktawaha samsthana : Visarpa Mutravaha samsthana : Mutral Prajanana samsthana : Sukra janana Karma : Daha Shamana, Swara Varna Prasadana, Gathra Mardavakara, Deepana, Dhee-Dhrithi-Smrithi Vardhaka. Doshaghnat : Vata Pitta Shamaka. Rogaghnata : Kshaya, udavartha, jwara, Unmada, Shoola, Anaha, Vrana, Visarpa.48) Ksheera (Milk)199 Sanskrit – Dugdha, Ksheera Rasa – Madhura Guna - Snigdha, Guru, Sheeta, Shlakshna, Pichila, Manda Veerya – Sheeta Vipaka – Madhura Dosha – Vatapittaghna Uses – Shoolahara, Balya, Rasayana, Jeevaneeya and Brumhana Rogaghnata – Pandu, Rakta pitta, Yoni roga, Shukra dosha, Mootra roga, Pradara roga etc and it is pathya in vata pittaja vikara. Cows milk promotes long life it is rejuvenator good for those emaciated after injury,increases intelligence, strength and breast milk. It cures shrama, kasa, trishna, jeerna jwara,mootra krichra and rakta pitta. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”179
  • 198. UTTARA BASTI Basti is one of the important treatments and considered as ‘Ardhachikitsa’ inKayachikitsa200It is mainly divided into three types 1) Asthapana 2) Anuvasana 3) Uttara bastiNIRUKTHI That which is administered through the Uttaramarga and has shreshta guna is known asUttara basti. 201 Uttaramarga means the mootra and shukramarga i.e. penis in male and the mootra margaand yoni marga i.e. urethral meatus and the vaginal orifice in the female. Which is administered after niruha basti and through the uttara marga is said to be Uttarabasti. In the present context, both the definitions of Uttara basti have been taken intoconsideration. Uttara basti which is administered through the apathyamarga or the vaginal orificehas been considered.Uttara basti Uttara basti (UB) is a purificatory procedure, where in the medicaments are injected intourinary bladder and into uterus in case of females. UB in males Intra vesicle Urethral route Intra vaginal UB in females Genital route Intra vaginal “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”180
  • 199. Contra indications Urethral Stricture Bleeding disorders Carcinoma of the Bladder Carcinoma of Pennies Hypo/epispadiasisUttara basti Yantra A like the usual vasti yantra, this yantra also consists of two parts.1. Basti putaka Since the quantity of kwatha or sneha administered is comparatively less, small sizedanimal bladders are used for the purpose. For instance, bladders of goat, sheep, pig, etc. are usedor else, even the leather of birds or any other smooth leather can be used.2. Basti netra It is also named as ‘pushpa netra’. It must be 10 angulis in length for administeringuttaravasti in women. It must be made up of gold or silver. Its shape should resemble the petal ofa flower or ‘Gopuchha’ (tail of a cow) i.e., broad at the base and tapering towards the end. Theopening at the top of the netra should be of the diameter of a mudga. The netra should have twokarnikas or circular marking rings – the first one at the distance of 4 angulas from the tip and theother at the base of the basti netra.About Length Acc to Charaka, Vagbhata, Sharagdhara - 12angulas Acc to Susruta - 14angulasAbout Karnika Acc. to Charaka - Dwikarnika Acc. to Susruta - TrikarnikaBasti Netra/ Puspa NetraFor Male Materials- Hema / Rajat “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”181
  • 200. Smooth Tip- like jati or ashwahna vrata resembles Gopuccha Opening – should pass Sarshapa beeja Length- 12 angulas.202Acc to Susruta Through Mutra marga – 10 angulas Through Yoni marga – Thickness of MedraAcc to Sharagadhara Through Mutra marga - Sukshma Netra Through Yoni marga - Length -10 angula - Thickness -Kanistik AguliUttara basti Dravya PramanaAcc to Charaka Sneha pramana – ½ pala. 203Acc to SushrutaA. Sneha Dravya Pramana For male – 1 prakuncha for 25 yr old person For Female – 1 prasrutha - Uttama matraB. Kwatha Dravya Pramana: For Male – 1 prasrutha For Female – In stree - Garbhashaya shodhanartha - 2 prasrutha In kanya - Basti shodhanartha - 1 prasrutha “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”182
  • 201. Vasti Dravya Pramana Sneha dravya pramana Kashaya dravya pramana Male Female Male Female 1 prakuncha 1 prasrutha 1 prakuncha (48ml) (50-60ml) (48ml Kanya Stree 1 prasrutha 2 prasrutha (50-60ml) (100-120ml) Acc toVagbhata Vasti Dravya Pramana For Male For Female 1 shukti (24 ml) For Sthree For Bala 1 prakuncha (96ml) 1 shukti (24ml) Flow chart no.05 Vasti Dravya Pramana“Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”183
  • 202. Pushpa Netra Pravesha For Male – Shepha: pramana/ 6 Angula For Female- In Youvanprapta Nari –Apatya marga - 4 Angula In Youvanprapta Nari – Mutra marga - 2 Angula In Bala - Mutra marga - 1 AngulaAdministration of Uttara bastiPooravakarma As per the derivation of the word Uttara basti, i.e. Uttara basti should be given after theadministration of niruha basti, according to Vagbhata, about 2 or 3 niruha basti should be givenbefore the administration of Uttara basti. Sometimes in practice, a course of ‘Yoga basti’ can alsobe given to the patient before the administration of Uttara basti. On the day of actual Uttara basti, the patient should be prepared priorly, following whichsnehana and swedana karmas should be done preferably over the kati, vamkshana and adhodara.Poorvakarma Should take bath Should take food –Mansarasa, Ksheera, Yavagu etc Should undergo snehana and swedana –Sthanika in Kati Pradesh [ Person should undergo Asthapanabasti before the Uttara basti] Preparation of the Medicine Take the medicated oil in required quantity in a pre-cleaned container. Autoclave the oil along with all the required materials. Freshly prepared and cooled Ksheerapaka can be directly used if the contamination is avoided during the cooling. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”184
  • 203. Preparation of the Patient Part should be prepared with local shaving of pubic hair. Patient is asked to void the urine just before the procedure starts.Pradhana Karma in Male Patient should sit straight and comfortably in a chair, having the height of knee. Should hold the penis firmly and should passGhrita shalaka i.e. the probe smeared with Ghrita or any sneha, into Urethral Orifice. It should be observed that, probe will moves inside freely or not. If Shalaka moves freely, then it should be removed and pushpa netra should be inserted. The pushpa netra should be inserted in the direction of Perineal suture Care should be taken while inserting the pushpa netra same as while doing basti karma in Guda. After the proper entry of pushpa netra, basti putaka should be squeezed slowly- with out shaking There after the netra should be withdrawn slowly. After the injected material comes out, the process should be repeated for the second and third timeProcedure Patient must lie down on supine position on the clean table by exposing the part. The hands are flexed and clasped below head. Wash the genitalia and the surrounding area with the savlon by using sponge holding forceps and gauze. Retract the prepuce completely and wash thoroughly the glans penis and then apply Beta dine to glans penis. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”185
  • 204. The physician having gloves after washing hands spread the surgical towel over patient, exposing the penis. Towel clips may be applied. When once the assistant transfers the autoclaved medicine in to steel bowel, the medicine is filled in to the syringe. Fix the catheter to the nozzle of the syringe, push the oil to the tip of the catheter. Lubricate the catheter with the Xylocaine jelly. Gently introduce the catheter in to the urethra. Slowly introduce the catheter into the bladder. Ensure the catheter has entered the bladder and then slowly inject the medicine into the bladder. If more amount of medicine has to be injected clamp the catheter with artery forceps, remove the syringe and then inject the medicine with same syringe or by another. When once the injection of medicine is over remove the catheter and allow the patient to lie down in the same position for 5 to 10 min and then patient may be sent home. Check the tip of the catheter to ensure that there is no any bleeding.DOSE Usually 25–30ml of medicine per UB is enough to maintain the good retention.Maximum dose of 200ml per UB has been given without complications.Retention Usually 3 - 6hrs in some cases up to 8 hrs retention of UB is seen.Precautions Patient should not hold the urge of micturition and other natural urges after the administration of Uttara basti. Brahmacharya If patient is willfully abstaining from the sexual life, it’s good; otherwise it may be beneficial to allow the patient for moderate sexual life “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”186
  • 205. (decreasing the frequency of the intercourse), as the suppression of sexual urge is one of the causative factor for Shukradusti.Diet Avoid Katu, Tikta and Kashaya Rasa.Basti Dravya Prathyagamana Generally Uttara basti dravya comes out in short period. If it does not comes out, should wait for one night. Then also, if the dravya doesn’t comes out Pippalyadi varthi should be inserted into the urethra.Complication during Procedure If the pushpa netra is inserted beyond the prescribed limit, then it will cause injury to the vasti and may produce pain. If it is inserted lesser than the limit, then the sneha will not enter inside.Paschat KarmaThe paschat karma explained in the context of Anuvasana basti should be followed.204Food Uttara basti should be given in the morning. After its pratyagamana, in noon ksheera, yusha or mamsa rasa should be given.205 Kapha vyadhi– Yusha Pitta vyadhi - Ksheera Vata vyadhi - Mamsa rasaManagement in Retention of basti Dravya Shodhana gana sidda vasti should be administered. Guda varthi prepared using the shodhana dravya. Should introduce Eshani / Shalaka. Should press Adho nabi pradesha with hand. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”187
  • 206. Varthi prepared using Aragvada patra, Nirgundi swarasa, Gomutra and Saindava should introduce into the mutramarga. Varthi prepared by Agara dhuma, Bruhathi, Pippali, Madhana phala, Saindhava lavana, Nagara mixed with Suktha or Gomutra or Sura. Vyapat ChikitsaUttara Basti in Male Apply sterile gloves and clean the genital part with aseptic solution. Smear the distal portion (2-5cm) of the catheter with sneha (usage of xylocaine gel is optional). Apply sterile drape. Hold the penis with non-dominant hand. Maintain hand position until preparing to inflate balloon. Pick up catheter with gloved (and still sterile) dominant hand. Hold end of catheter loosely coiled in palm of dominant hand. Lift the penis to a position perpendicular to patient’s body and apply light upward traction (with non dominant hand). Identify the urinary meatus and gently insert the catheter up to the bladder until the urine starts to flow. Drain the urine completely. Inflate balloon, using correct amount of sterile liquid. Gently pull catheter until inflated balloon is snug against bladder neck. Inject the sneha dravya taken in syringe into the catheter. Deflate the balloon by draining the sterile water. Remove the catheter slowly. Clean the glans and meatus again.206 “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”188
  • 207. About Pradhanakarma Position: sitting position in male, but in general for catheterization, supine position is more convenient. Avastha: ‘Hrusta medra’. (Sthabda). Some opines Hrusta means ‘Erected’. But we can consider it as firmly held. Insertion: 6 angulas (approximately 12cm). The male urethra is 17-23cm giving medicine in mid urethral region can produce rupture and leakage. Course of treatment: On the day of administration of Uttara basti, after pratyagamana of basti dravya, again 2-3 vasti are administered. And same is repeated for 3-4 days. Then 3 days gap should be given. Again same is repeated. Such 3 cycles are practiced commonly.Medicinal effect Basti is the site for Apanavata. The veerya of the medicine may get absorbed and may pacify the vitiated doshas. The posterior wall of the bladder is a smooth triangular area- Trigone of the bladder is permeable. The route of administrations exerts a considerable influence upon the activity of hormone preparation. Certain hormones are ineffective when given by oral route while others are highly effective. Steroids are comparatively readily absorbed without much local destruction by the surface epithelium. The local administration of Hormonal preparations has the additional advantage that comparatively small doses are sufficient to produce definite effect.Ex: Arkapushpa Taila - having Estrogenic activity and act as Presubstance of Estrogen.Endometrium is second important thing for consideration. Endometrium having lining ofepithelium, it absorbs estrogen without much local destruction. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”189
  • 208. Chapter – 4 Materials & MethodsCLINICAL CONTRIVE More so if it is sexual, erotic and carnal. Unassailability, the headiest aphrodisiacof them all, always turns taboo in to temptation. In today’s world of two minute noodles(Maggi) a one minute noodle in bed is a very disturbing for most women resulting indeep fissures in marital bliss, family and society. The male himself is equally unsatisfiedand finds himself guilty for the same increasing the problem all the more. Here anattempt is being made to contemplate on the lifestyle of premature ejaculators, theirincidence in society, cause of the disorder, their predicament etc. and try to give the bestsolution. To study the disorder in detail first a research Performa was prepared. The drugwas prepared as mentioned in the drug review and a single blind control clinical studywas carried out in 20 patients out of 30 approached patients, the results of which will bediscussed ahead. The occurrence of Sexual dysfunctions is increasingly relevant now a day due tochange in life style, food habits, socio-cultural changes and influence of media andrevolutionary changes in information technology. Premature ejaculation is a sexual dysfunction causing a lot of dissatisfaction andinterpersonal difficulties in the married life. The prevalence of the same is also very high.Sex therapy has proved to be most effective treatment method for the problem by variousstudies. But as in the Western population the methodology is not easy to apply in apopulation like that of India. Moreover due to high incidence of the problem and moral as “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”190
  • 209. well as social restrictions regarding sex, unethical medical practices are prevalent. Themostly unqualified practitioners utilize the eagerness, innocence and lack of awareness ofthe immature anxious youth in exploiting them mentally and economically. Most of the time the approach of these persons makes the condition of the patientsworse leading to more serious psychological problems like generalized anxiety anddepression. The present status emphasizes the importance of imparting adequateknowledge about sex and management of sexual dysfunction like premature ejaculation. In Ayurveda this clinical condition can be closely related to the concept of GataVata and is termed as Shukragatavata. This clinical presentation of Shukragatavata is anideal one to study the activities of Vata on psychosexual parlance. It opens new vistas forsearching the role of Vata in contribution to psychological and sexual problemsfunctionally (where structural relations are quite absent); for formulating assessmentscales to psychosexual problems and for evaluating Ayurvedic medications and treatmentmodalities to manage the problem. In the field of Ayurvedic research only three studieshave been carried out on premature ejaculation which has been dealt with in the review ofprevious literature. Individuals suffering from Premature Ejaculation are either physiologicallypredisposed to climax quickly because of short nerve latency time or have a psychogenicor behavioral conditioning for early ejaculation. Many a time neuro-physiological,psychological and behavioral factors coexist and contributes each other. The functionalapproximation in between Vata, Mana and Shukra are as explained in the conceptualcontrive. Considering all these aspects in total a protocol for single blind clinical trial wasplanned to manage Premature ejaculation under psychological, psychobiological and “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”191
  • 210. Neuro biopsychological approaches. For this purpose patients were randomly divided intwo parallel groups and managed with oral medication and with Uttarbasti. The firstgroup was managed through oral medication. The second group by Uttara basti – a selfdesigned combination of herbs possessing rejuvenating, Vatahara, aphrodisiac andstrength promoting activities properties also re-establishes the functional integritybetween Doshas; Mana and Vata as a result of its mechanical effect. (Neuropsychobiological interface)Clinical Study: Ayurveda is an established medical system, which has been developed by variousancient Acharyas after rigorous experiments and examinations. But today it’s necessaryto prove the Ayurvedic facts on the modern parameters, without altering its basicstructure as Methodical approach is the backbone of research. Research is a scientific study through which one can establish new facts,discarding the old facts or modifying the present facts. Utmost care is taken in designingthe methodology for conducting this study. Clinical research involves theexperimentation of a drug therapy on a population and recording the feedback based onwhich postulations are made regarding the usefulness of the drug therapy in the disease.Research Approach: In the present study, the main objective is to “Management of Shukragatavatawith Vidarighrita a Comparative study w.s.r.to Premature Ejaculation”. Theefficacy was determined by finding out the difference between the baseline data of theparameters to the after pariharakala data. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”192
  • 211. Reasons for selection of the study design: The results and conclusions of a clinical trial depend on the study design. The aimof this study was to find out the “Management of Shukragatavata with Vidarighrita aComparative study w.s.r.to Premature Ejaculation”. Before starting any research work it is necessary to list out the materials requiredand the methods used for research. So in this chapter materials and methods which arerequired for this clinical study are explained in detail.Sources of dataa) Patient: Patients are selected from O.P.D of D.G.M.A M.C. & H. after fulfilling theinclusion and exclusion criteria.DIAGNOSTIC CRITERIA FOR PREMATURE EJACULATION The diagnostic criteria of PE suggested by International Statistical classification ofdiseases and health related problems- 10th is as follows,A. General criteria for sexual dysfunction must be met which are as follows, 1) The subject is unable to participate in sexual relationship as he or she would wish. 2) The dysfunction occurs frequently but may be absent in some occasions. 3) The dysfunction has been present for at least 6 months. 4) The dysfunction is not entirely attributable to any of the other mental and behavioral disorders in ICD-10, physical disorders (such as endocrine disorders) or drug treatment.B. There is inability to delay ejaculation sufficiently to enjoy love making and manifesting as, 1) Occurrence of ejaculation before or soon after the beginning of intercourse. (Before or within 15 sec. of beginning of intercourse) 2) Ejaculation occurring in the absence of sufficient erection to make intercourse possible.C. The problem is not the result of prolonged abstinence from sex. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”193
  • 212. The existing definitions of PE take into consideration different aspects of this condition,including distress interpersonal difficulty, sexual satisfaction, and lack of control over ejaculation,persistency and latency time. Some definitions emphasize the importance of these effects on thepartner as well as the patient, although effects on partners have been less studied. Ejaculatory latency, most commonly quantified using intra vaginal ejaculatory latencytime (IELT), is a dominant component of PE assessment in clinical studies. IELT is defined as thetime between vaginal intromission and intra vaginal ejaculation. Although it has been suggestedthat an IELT of 2 minutes or less may serve as an adequately sensitive criterion for defining PE, astandard cut-off for ejaculatory latency does not exist and studies have used latency valuesranging from 1 to 7 minutes for defining PE. Results of previous studies have indicated that additional patient reported outcome (PRO)measures are important and non interchangeable measures of premature ejaculation that assessdistinct aspects of the condition including perception of ejaculatory control, satisfaction withejaculatory control, and satisfaction with sexual intercourse. These studies further suggested thata multidimensional approach to the assessment of PE would allow for a more in depth analysis ofthe condition. Conclusions were limited by the small sample size in each study (N = 57, N = 260,and N = 152) and by the lack of a comprehensive set of assessment tools for evaluating PE. On the basis of the available data it can be concluded that the most important primaryobjective assessment of treatment efficacy is intra vaginal ejaculatory latency time (IELT).Secondary efficacy outcome parameters include patient-reported outcomes obtained viainterviews, self-completed questionnaires or diaries. Subjective measures include subject assessment of ejaculatory control, satisfaction withejaculatory control, sexual satisfaction, and partner sexual satisfaction. As the importance of improving IELT and other treatment outcomes depends on theperceptions of the patient, PRO measures are needed to evaluate both observable and subjectiveaspects of the condition. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”194
  • 213. Diagnostic assessment All men who meet diagnostic criteria for PE should receive a medical and sexual history,physical examination and investigations of causal or maintaining factors for the patients PE suchas anxiety or interpersonal factors. The developmental history of the disorder should be carefullyassessed, such as whether the rapid ejaculation is global or situational, life long or recent in itsdevelopment, and the presence or absence of other sexual dysfunctions, such as ED. If ED ispresent, this should be evaluated according to the guidelines above. Details of the patients ejaculatory response should be obtained; particularly thesubjective assessment of ejaculatory latency, sense of ejaculatory control and level of sexualdissatisfaction or distress should be fully evaluated. Sexual and emotional responses of thepartner also need to be assessed, particularly the presence or absence of sexual dysfunction orpain in the partner Questionnaire measures or brief symptom scales are available for assessing PEalthough these are not well standardized to date. Laboratory based evaluations (e.g.,biothesiometry) are not recommended for routine evaluation.Barriers to Patient Diagnosis Those who deal with PE patients on a regular basis know that the individuals who presentwith the condition are often desperate for help. Those seen in the clinic are, in many respects,only a small fraction of the PE population. These patients have usually already tried a range ofself-help techniques prior to seeking help. Self-help techniques include using multiple condoms to reduce sensitivity, masturbationbefore sexual interaction, mental distraction exercises and harder and faster thrusting to try andsatisfy their partner. However, while partially effective in the short term, many of thesetechniques may ultimately exacerbate rather than alleviate PE, as they deliberately ignore or bluntthe sexual sensations that need to be controlled in order to improve the condition. Therefore,cases that present in the clinic often comprise "hard to treat” patients for whom effective therapiesare badly needed. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”195
  • 214. There is a striking disparity between the many who acknowledge the existence of aproblem and the few who take active steps to address their PE. This applies not just to PE. Ananonymous postal survey of a sample of the general UK population found a high prevalence ofsexual dysfunction, including a 14% prevalence of PE among the 617 male respondents. Thestudy also found that 64% of men with a sexual dysfunction would like to receive professionalhelp, although only 6% who wished for help had actually received it. There are many reasons why patients with PE delay or defer seeking medical advice. It isabundantly clear that PE carries a stigma and patients are sensitive to being labeled as prematureejaculators. Moreover, many suffer embarrassment at the thought of having to discuss theirproblem with a relative stranger, such as a physician. It is worth noting that, especially in the caseof primary care practitioners, there is often embarrassment on the part of the physicians too andmany of whom would prefer to give their patients written material to read rather than engage indetailed discussion. Many patients persuade themselves that the problem will go away with time or that PE ispurely psychological and therefore there is no need to seek treatment. Indeed, there is a widebelief among this patient population that there is no treatment and therefore that presenting totheir physician is pointless. Indubitably, all of these factors are barriers to the patient presentingwith his condition. However, the healthcare profession collectively erects its own barriers by notimplementing strategies such as routine screening for sexual dysfunction. Moreover, the verylanguage of the consultation and the terminology used can themselves be impediments to thesuccessful assessment of the patient. Although men are typically driven to seek treatment by factors such as a distress,frustration, and a desire to please their partner, the many barriers to treatment seeking are, moreoften than not, overwhelming. Evaluation of male patients with sexual dysfunction requires not only the thoroughunderstanding of the anatomical and the physiological bases of human male sexual dysfunction “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”196
  • 215. but also the ability of the physician to collect and properly interpret the patient’s history andphysical findings. Along with others, we 206,207,208 have previously advocated such an approach indiagnostic assessment of male sexual dysfunction.A. History Medical, psychological, and sexual histories are extremely helpful in providing clues tothe underlying cause of the dysfunction and they reduce the need for an expensive investigation torule out all possible etiologies.1. Medical history Historical events related to the presence of chronic disease (e.g., diabetes, hepatic failure,renal failure, cardiac failure, advanced pulmonary disease, tabes dorsalis, multiple sclerosis,cerebro vascular accident), use of pharmacological agents (e.g. antihypertensive, antihistamines,antipsychotic, anticholinergics) endocrine disorders (gonadal failure, pituitary tumors, thyroiddisease, adrenal disease), prior surgeries (prostatectomy, proctectomy, vascular surgery), andtrauma (temporal lobe and spinal cord lesions, blunt pelvic trauma) should all be carefullyevaluated. Further, vascular risk factors such as family history of cardiovascular disease,hypercholesterolemia, hypertension, diabetes, cigarette smoking, and pelvic radiation therapyshould be inquired about, and, if present, vascular etiology should be highly suspected. Potentiallyirreversible pathology should be anticipated in patients with evidence for other micro vasculardisease (peripheral neuropathy, retinopathy, and nephropathy). Patients with neurological disease should be questioned about the temporal relationshipbetween the development of the sexual dysfunction and that of the neurological disorder. Patientssuspected for hypogonadism should specifically be assessed for family history of the disease,deviation of adolescence from normality, recent changes in secondary sexual characteristics,symptoms of pituitary dysfunction, history of orchitis, testicular trauma, infertility, or exposure toradiation or cytotoxic agents. Patients should also be assessed for symptoms of thyroid andadrenal diseases. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”197
  • 216. 2. Psychological history Psychological factors associated with male sexual dysfunction have recently beenclassified into three categories 209,210 predisposing factors, precipitating factors, and maintainingfactors. Restrictive upbringing, disturbed family relationships, traumatic early sexual experiences,inadequate sexual information, and insecurity in the psychosexual role are among the frequentlyencountered predisposing factors. Unreasonable expectations, random failure, discord in therelationship, dysfunction in the partner, infidelity, reaction to organic disease, or depression oranxiety are some of the factors that could precipitate the onset of sexual dysfunction. Performanceanxiety, guilt, poor communication, loss of attraction between partners, and impaired self-imageare among the factors that lead to maintenance of the sexual dysfunction. Affective disorders or character pathology can lead to both precipitation and maintenanceof sexual problems. Evidence for the presence of any of these psychological or situationalconditions should be carefully assessed. Moreover, it should not be forgotten that the existence ofan organic disease does not preclude the possibility of a coexisting psychogenic factor. Suchomission could lead to diagnostic difficulties as well as to therapeutic failures.3. Sexual history One of the first goals of the differential diagnosis during history taking is to ascertain thenature of the sexual dysfunction. The patient should be asked to describe his problem, the timeand manner of onset, its course, its current status, and any associated medical or psychologicalproblems. Decreased libido should alert the clinician to three probable causes: endocrinopathy,affective disorder, or relationship discord. A history of frequent strong erections under anycircumstances (during foreplay, fantasy, or masturbation, with another partner or uponawakening) indicates that the endocrine, vascular, and neurological systems are probably intactand that the erectile dysfunction is predominantly psychogenic. Conversely, historical dataindicating the presence of decreased erectile turgidity in non coital activities are highly suggestive “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”198
  • 217. of an organic etiology. Moreover, a report of firm sustained erections during foreplay that are lostafter intromission or upon initiation of pelvic movements might suggest either a psychogenicetiology or a vascular problem (pelvic steal syndrome). A history of delayed or retrograde ejaculation is suggestive of a neuropathy or an adversedrug effect. Premature ejaculation, on the other hand, is more compatible with a psychogenicdysfunction. Finally, it must be remembered that absence of orgasmic sensations in patients withnormal erectile and ejaculatory functions is almost always due to psychogenic etiology, whereasfailure of datum essences is usually organic in nature, which should direct the investigationstoward ruling out local penile, neurological, and hematological etiologies. Other historical eventsmost useful in differentiating predominantly psychogenic from predominantly organic erectiledysfunctions.B. Physical Examination When detailed history is coupled with a careful physical assessment, clues to theunderlying pathology are frequently obtained. Thus, every effort should be made to elicit physicalsigns of suspected pathology. General chronic diseases (hepatic, renal, cardiovascular,granulomatous, neoplastic) must be ruled out, and, if present, state of disease control must bedetermined. Similarly, presence of chronic illnesses such as diabetes, hypertension, thyroiddisease, adrenal disease, or hematological disorder, and any degree of complications, must besought. For example, if diabetes is found, evidence for peripheral neuropathy, autonomicneuropathy, and macro- and micro vascular complications should be assessed. In addition to thegeneral and systemic evaluations, detailed assessment of gonadal function, vascular competence,neurological integrity, and genital organ normalcy should be performed on every patient. Patients suspected of hypogonadism should be assessed for evidence of muscledevelopment, size and structure of the penis (normal adult penis is > 6 cm in length in the unstretched flaccid state, 3 cm or more in width, has normal urethral opening, and no evidence ofhypospadias) and size and consistency of the testes and the prostate. Patients with moderate “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”199
  • 218. hypogonadism including some with Klinefelter’s syndrome and many patients with gonadotropindeficiency usually exhibit a decrease in testicular volume from a normal size of 15–30 cm3 to asize of 6–12 cm3 (2.9–3.7 cm length, 1.8–2.3 cm width) 9 Patients with severe hypogonadism andmany with Klinefelter’s syndrome usually have infantile size testis of 2–4 cm3 (2.0–2.5 cm length,1.2–1.5 cm width) 211. A careful vascular assessment should include the palpation of ankle, femoral, and dorsalpenile arteries. Penile systolic blood pressure should be determined with a 3-cm blood pressurecuff placed around the base of the penis and a Doppler stethoscope positioned over eachcavernosal artery.212,213,214,215 The penile systolic occlusion pressure is then obtained and comparedwith that of a brachial artery, and a penile brachial index (PBI) is derived.216,217,218,219 Valuesgreater than 0.7 are considered normal Studies by Chiu and colleagues suggested that PBI ishighly diagnostic in patients with evidence for peripheral vascular disease but no other risk factorssuch as diabetes or current intake of medications with potential adverse effects on the erectilefunction. The PBI is less predictive in patients with peripheral vascular disease and diabetes, andleast predictive in those without peripheral vascular disease, diabetes, or current drug intake.Repeating the measurements after 3–5 min of gluteal muscle exercise may enhance sensitivity ofthe test. Reduction in PBI by more than 0.15 is suggestive of redistribution of the blood supplyand its shunting away from the arterial penile bed to the gluteal region. Such a phenomenon is 220characteristic of patients with steal syndrome. Further, the significance of a low PBI may gobeyond aiding the diagnosis of vasculogenic erectile dysfunction. This is suggested by aprospective study in 130 impotent patients that were followed for 24–36 months in which a lowPBI (0.65 or less) was shown to predict occurrence of a future major vascular event (myocardialinfarction or cerebro vascular accident). 221 Physical signs of muscular atrophy, pallor, and/or lossof hair growth of the lower extremities are also consistent with vascular pathology. Neurologically, the patient should be evaluated for the presence of motor deficits,changes in deep tendon reflexes, loss of sphincter tone, or decrease in light touch or pinprick “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”200
  • 219. sensations, particularly in the genital area. Penile temperature sensation testing could also be 222performed with the use of alcohol swabs. In addition, the bulbocavernosus reflex should beelicited by squeezing the glans penis and assessing the evoked contractions of external anal 223sphincter or bulbocavernosus muscles. This reflex response is clinically detectable in 70% of 224 225 226normal males. The more sensitive penile vibration perception threshold testing may beperformed to confirm results of the bulbocavernosus reflex. Testing of penile vibration perceptionthreshold is performed by sequentially placing a tuning fork on the glans and bilaterally on midshaft of the penis. Vibration amplitude is then increased until the patient perceives the stimulus.The vibration perception threshold testing is the most predictive sensation testing procedure, butothers can also help in evaluating a loss of somatic innervation. The penis should also beexamined for evidence of masses or plaque formation, angulation, unprovoked persistent erection,or tight un retractable foreskin.C. Selective investigations for male sexual dysfunction A detailed patient history is important in the evaluation of male sexual dysfunction as itcan help suggest the underlying etiology and narrow the scope of the required investigation forselecting an appropriate modality of treatment. A thorough physical examination and brief office-based investigation with assessment of PBI and real-time penile tumescence may also besufficient to corroborate the nature of the problem and to suggest an etiological basis in most malepatients with sexual dysfunction. Once detailed history and physical examination are completed,focus of the medical investigation can then be shifted toward confirming the underlying pathphysiological abnormalities and devising a treatment plan. Patients with desire disorder, premature ejaculation, and/or post ejaculatory pain require acareful assessment of drug use, possible underlying hypogonadism, or presence of psychologicalor psychiatric conditions. Patients with HSD and absent or retarded emission or anorgasmia mayneed to be evaluated for the presence of CNS disease. Patients with prolonged or painful erectionshould be evaluated for the possibility of primary penile disease, hematological disorder, or other “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”201
  • 220. systemic diseases associated with penile complication, or the intake of pharmacological agents ordrugs of addiction that could potentially cause failure of datum essence. There remain the majority of patients with sexual dysfunction who present with problemsrelated to erectile insufficiency. The availability of erectogenic agents such as oral sildenafil orintrapenile vasoactive drugs (e.g., PGE1) tempts many treating physicians to use them as aprimary therapeutic modality without conducting any specialized investigations. Although thismay be suitable for a significant fraction of patients with erectile insufficiency, potentialcomplications from these modalities could be life threatening (in the case of sildenafil when takentogether with nitrates), and the possibility of finding a potentially correctable disorder (e.g.,psychosexual problem, hypogonadism, treatable chronic illness and/or correctable vascularinsufficiency) indicate the need to perform the appropriate investigations. Such investigations areneeded for patients at high risk for complications and those who may have experiencedcomplications from the intake of these newly approved erectogenic agents (e.g., changes in visionon sildenafil, systemic symptoms from intra urethral prostaglandin, or penile priapism or fibrosisfrom intra penile vasoactive injections) to establish the underlying path physiology, and hence toselect the proper therapeutic interventions. However, before commencement of such detailed investigations, patients with a clearevidence of chronic organic disease should be evaluated and treated for their primary illness.Those on drug therapy that is likely to be responsible for their erectile problem should have theirmedications changed or discontinued for a trial period while assessing for the return of potency. Discontinuation of substance abuse before a full diagnostic workup is also required. Theremaining groups of patients in whom history and physical examination are not conclusive inidentifying any specific etiology require an organized multidisciplinary approach involvingpsychological, endocrine, vascular, and neurological investigations to search for treatableetiological factors. The investigation may also help in counseling patients with uncorrectableetiologies such as micro vascular disease or neurological deficits. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”202
  • 221. 1. Psychological evaluations. All male patients presenting with sexual dysfunction should be evaluated forpsychological factors, even in the presence of an obvious organic etiology. Conversely, thepresence of psychogenic conditions, such as anxiety, anger, guilt, or marital discord, should notbe construed as evidence for a sole primary causation. 227 Initial evaluation can be done by administering a detailed sexual history questionnaireexploring current sexual interactions, social and sexual discords, history of sexual abuse ortrauma, gender identity conflicts and preferences, state of mood and affect, and cultural andreligious influences. Such questionnaires are helpful in identifying psychological contributions toerectile dysfunction. The co-existence of more than one condition is a frequent occurrence. 228 A well structured psychosocial interview with the patient alone, and if possible conjointlywith his partner, should follow the administration of any sexual questionnaire to ensure the mostcomplete understanding of all possible predisposing, precipitating, and/or maintainingpsychological factors. Features differentiating predominantly psychogenic from predominantlyorganic dysfunctions. 229 Several well established and validated self-administered psychosocial questionnaires havebeen developed and used to assess the frequency and nature of sexual dysfunction in men, andsome have been used to assess the adequacy of response to therapeutic modalities. The questionnaires useful in clinical practice include the Derogatis Interview for Sexual 230Functioning-Self Report (DISF-SR), International Index of Erectile Function, 231 and Florida 232Sexual History Questionnaire. For research purposes, the Derogatis Sexual Functioning 233 234Inventory (DSFI) and Leiden Erectile Dysfunction Questionnaire are useful. A generalcriticism of these inventories is the small number of patient samples used to validate them. Otherlimitations include the lengthy time required for completion of the questionnaire and lack ofaccuracy in distinguishing psychogenic from organic causes of sexual dysfunction. They are,however, helpful in assessing the presence of problematic personality features, comorbid affective “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”203
  • 222. disorders, and situational factors that may be important in predisposing, precipitating, and/ormaintaining the disordered sexual function.2. Measurement of reproductive hormones. Patients with a history of decreased libido diminished secondary sexual characteristics,developmental disorder, anosmia, headache, visual disturbance, and drug ingestion, or patientswith physical signs consistent with hypogonadism or androgen resistance, such as abnormalsecondary sexual characteristics, decreased testicular size, or abnormal testicular consistency,should have bioavailability serum testosterone and LH measured. Circulating blood testosterone exists in three states: free, albumin-bound, and SHBG-bound.235 While it is generally considered that SHBG-bound testosterone is not available foruptake by tissues, opinion is mixed as to whether the biologically active testosterone is restrictedto the small quantity of the hormone that is free ( 2%) or includes the larger amount of albumin-bound hormone (20–80%). Recent investigations suggest that both free and albumin-boundtestosterone is biologically available.236 However, measurement of total testosterone levels shouldbe performed only if the patient is free of conditions influencing serum SHBG and/or albuminconcentration or binding activities. The free testosterone level calculated from the totaltestosterone level and the level of SHBG is an alternative approach, and the correlations amongthis calculated index of bioavailability testosterone and the measured free testosterone byequilibrium dialysis are high.237 Patients with primary hypogonadism may provide a history of orchitis or exposure toradiation or toxins or may exhibit phenotypic signs of inherited disorders. These patients willhave high LH and low bioavailability-testosterone concentrations.238 Patients with androgenresistance will present with varying degrees of hypoplastic genitalia, lack of secondary sexualcharacteristics, and/or gynecomastia and feminization. Such conditions are heralded by anelevation in both total (or bioavailability) testosterone and LH. In subtle cases of androgen “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”204
  • 223. resistance, genital skin biopsy for assessment of receptor number and enzyme activities (5 -reductase and 3 -ketoreductase) may be required to establish the diagnosis.239 Patients with secondary hypogonadism and some men with obesity, advanced age, orreduced testosterone binding to carrying proteins may have low total testosterone and LH serumconcentrations.240,241,242,243,244,245 Aging is associated with an increase in SHBG and consequently agreater reduction in bioavailability than in total testosterone,246,247 whereas obesity and certainconditions of abnormal binding proteins may be associated with more suppression in totaltestosterone than in bioavailability or free testosterone.248 Androgen replacement therapy isusually not required in conditions associated with normal bioavailability or free but depressedtotal testosterone. Serum PRL concentration differentiates between hyper prolactinemia and otherdisorders of the hypothalamic-pituitary axis. In the latter cases PRL is normal or low, but bothtestosterone (total or non-SHBG-bound) and LH are usually below their respective normal ranges.PRL concentrations in excess of 100 ng/ml are frequently associated with PRL-producingadenomas, whereas lower concentrations may be seen in drug-induced or in idiopathic hyperprolactinemia. Other conditions of secondary hypogonadism are characterized by normal or lowserum PRL concentration. Further workup of these patients should be directed towardidentification of the primary site of deficiency (pituitary vs. hypothalamus) since this mayinfluence the selection of treatment modality. A recent study reviewed the reproductive hormone parameters in 508 men with sexualdysfunction.249 A normal free fraction of testosterone saved an unnecessary endocrine evaluationin 50% of patients with low total testosterone.3. Investigation of structural abnormalities of the penis Several techniques are available for evaluation of structural and functional integrity of thepenile tissue. The following is a brief description of some of these experimental methods and theirapplication. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”205
  • 224. a. Penile imaging Structural abnormalities of the penis can be evaluated by a variety of methodologiesbased on the nature of the suspected lesions. Peyronie’s disease and its effect on penile vascularcompetence can be evaluated with color duplex sonography.250 Arteri ovenous malformations andlymphohemangiomas can be assessed for lesion extent and involvement of adjacent structureswith MRI.251 MRI can also be used to assess for penile ruptures and tears of the tunicaalbuginea.252b. Penile biopsy Percutaneous core biopsy, using 19- and 20-gauge coaxial automatic devices under localanesthesia, has been developed as a safe and technically easy procedure to perform.253 In addition,computerized image analysis techniques of smooth muscle and elastic fibers of the corpuscavernosum tissue samples from normal and impotent men have been developed. Corporeal fibrosis may develop secondary to abnormalities in the regulation of normalcollagen synthesis and degradation, most likely as a result of chronic ischemia.254 Changes inoxygen tension have been shown to affect human corpus cavernosum smooth muscle cellexpression of TGF-ß1 and synthesis of PGE-1.255 Oxygen tension consistent with blood PO2observed in flaccidity (30 mm Hg) induces TGF-ß1 expression and suppresses PGE-1synthesis.256 TGF-ß1 is a pleiotropic cytokine that induces connective tissue synthesis and inhibitsgrowth of vascular smooth muscle cells, the two principal changes observed in corporealfibrosis.257c. Cavernosal electrical activity Single potential analysis of cavernous electrical (SPACE) activity has been measured innormal subjects and in patients who had pelvic surgery (including prostatectomy), spinal cordinjury, and long-standing insulin-dependent diabetes with presumed autonomic neuropathy, aswell as smooth muscle dysfunction.258 This study is done by placing two coaxial electrodes intothe corpora cavernosa, with the tip of one electrode being placed centrally into each corporeal “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”206
  • 225. body. The neutral electrode is placed on the body surface. The patient is allowed to rest to reducestress-induced sympathetic overtone, and single potential signals are processed usingelectrophysiological instruments.4. Penile tumescence monitoring A variety of procedures are available to assess the involuntary, unconscious peniletumescence that occurs during the REM stage of sleep or the cognitively induced erection thatoccurs during the exposure to sensual (audio, audiovisual, or fantasy) and/or local tactile (penilevibration) sexual stimuli, which can be used to differentiate between organic and psychogenicerectile dysfunction. Monitoring of penile tumescence after intra corporeal injection of vasoactive drugs hasalso been used to assess the response to local pharmacological therapies. Changes in penilecircumference can be measured in one (mid shaft) or two (proximal to the glans and at the base ofthe penis) locations, using mercury strain gauges,259,260 electronically controlled constrictiveloops,261 Snap Gauges consisting of pressure-sensitive plastic strips,262 or simple strips of postagestamps.263 Penile rigidity is assessed either directly using specially designed manual tonometers tomeasure the pressure required to "buckle" the penis (axial rigidity),265 or indirectly usingelectronic dynamometers266 or constrictive loops (cross-sectional rigidity) during maximumtumescence. Penile rigidity can also be inferred from breakage of three plastic strips incorporatedinto the Snap Gauge device. The three elements break at degrees of tension corresponding tointracorporeal pressures of approximately 80, 100, and 120 mm Hg, respectively.267,268,269 Basicassumptions and limitations of each of these methods are described below.a. Nocturnal penile tumescence (NPT) monitoring This procedure evaluates the presence or absence of the involuntary unconsciouserections, which normally occur during the REM stages of sleep, during 1–3 nights Normal nocturnal tumescence has been defined as a total night erection time greater than90 min and an increase in penis circumference in excess of 2 cm. A change in circumference of “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”207
  • 226. 16 mm or 80% of a full erection is thought to reflect a sufficient degree of penile rigidity forvaginal intromission. Subsequently, a penile buckling pressure of 100 mm Hg using the manualkonometers, or 100 Pen rig (unit used for the electronic dynamometer), was found to provide amore accurate assessment of the degree of penile rigidity required for vaginal penetration than thepercentage change in circumference. A buckling pressure less than 60 mm Hg is thought to beinadequate for vaginal penetration. Formal NPT testing is performed in a sleep laboratory andincludes monitoring the penile circumference and axial rigidity at or near the time of maximumtumescence, and should be reserved to investigate difficult cases, e.g., males in whompsychological factors are strongly suspected but in whom organic factors are questionable or theintake of pharmacological agents are not identified. An electronic home device (Rigiscan monitoring device, Timm Medical Technologies)270 has been developed to provide continuous recording of NPT and rigidity.271 The system usestwo loops, placed around the base and tip of the penis proximal to the coronal sulcus, to measurepenile circumference in millimeters. Radial rigidity as measured by the Rigiscan device was foundto correlate with the axial rigidity as measured by the buckling pressure, and both were related tothe intra corporeal pressure. Recently, Rigiscan data analysis software, in which a 20% increase inbase circumference lasting for 3 min or more is counted as an erectile event, has been describedby Levine and Lenting. Very recently, a new electro bioimpedance device was used to determine the number andduration of erectile events and the percentage increase in penile blood venous changes duringthese events.272 The NEVA System (Urometrics, Inc., St. Paul, MN) consists of a small recordingunit that attaches to the upper thigh, and three small adhesive electrode pads that are placed overthe hip and on the penile base and glans. A constant non detectable alternating current is deliveredto the tissue, and a potential difference is then measured between the electrodes and converted toimpedance. Since impedance changes with variation in blood flow, penile volumetric changes canbe calculated from the changing measurement of impedance. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”208
  • 227. Several pitfalls associated with NPT monitoring, which limit the value of using thisinvestigation as an initial screening test, have been discussed extensively by Levine and Lentingand by Schiavi.273 These pitfalls include, 1) The paucity of NPT norms for men older than 65 yr; 2) The lack of validation by an independent method other than NPT monitoring itself for the basic assumption underlying this investigation; 3) The lack of clear objective measures to relate the quality of sleep-associated penile erections to those occurring during usual sexual activity; 4) The presence of psychological factors (e.g., anxiety, depression, or loss of sexual desire) or dreams with anxiety content may influence the occurrence of NPT; 5) The first-night effect that may occur on the first night of sleep laboratory monitoring; 6) Sleep abnormalities such as apnea, periodic leg movement, and nocturnal myoclonus can adversely influence the quality of NPT recording; 7) The identification of NPT events is dependent on the arbitrary criterion of the minimum erection time required for an erection episode; and 8) The formal sleep laboratory testing is very costly and involves waking the patient when he has 80% of a full erection to measure the buckling pressure of the penis.b. Daytime penile tumescence monitoring Several adaptations for NPT monitoring were described to reduce the cost of nocturnalsleep laboratory testing and/or to improve the diagnostic efficiency of tumescence monitoring.These include monitoring during the following: 1) Morning naps preceded by modest sleep deprivation 274,275 2) Audio-visual and/or fantasy stimulation 276,277 3) Erectile response to intra cavernous vasoactive drug administration with or without audio- visual enhancement. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”209
  • 228. 4) Pulse Doppler analysis of penile arteries with audio-visual enhancement of the erectile response278,279 5) Erotic audio-visual enhancement of the erectile response to vibrotactile stimulation280 6) Affective and cognitive response to erotic audio and fantasy stimulation.281 However, several pitfalls of real-time tumescence and rigidity testing in its present form exist and need to be addressed before a suitable adaptation for general screening can be recommended. These include the following: 1) Real-time response to erotic stimuli may be adversely influenced by the psychological factors underlying the dysfunction or those related to the testing environment itself; 2) Content of the audio-visual material used may not be consistent with the subject’s preference, leading to a reduced or absent erectile response; 3) Criteria for normal tumescence and rigidity response to real-time erotic stimulation have not been established or validated. A careful medical history and physical examination with basic laboratory tests iscurrently the recommended initial investigation. The availability of sildenafil may also provide aninexpensive and practical first line of therapy, regardless of etiology, and preclude the need toseek more elaborate testing for many males with erectile dysfunction. However, this testing procedure could have a significant role in evaluating some patientswith sexual dysfunction, particularly when psychological factors are suspected as the cause of theproblem. Such patients could initially be evaluated with either a Snap Gauge band over 1–3nights, daytime nap monitoring, or erotic audio-visual/tactile/fantasy stimulation monitoring.5. Vascular investigations Patients suspected of having vascular lesions, based on history, physical signs, orabnormal PBI, and those with abnormal tumescence monitoring, and may undergo more detailedvascular evaluation of the penile vasculature to determine whether a surgically correctable factorunderlies the dysfunction. Earlier studies have used indirect measures to infer arterial blood “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”210
  • 229. supply to the penis, such as intra urethral temperature recording during gluteal exercise andsimultaneous graphic tracing of finger and penis pulse volume changes (plethysmography) beforeand after temporary occlusion of blood flow in both organs (postocclusive reactive hyperemia).282More recently, several tests were developed to directly evaluate penile inflow and outflowvasculatures.a. Pharmaco-penile duplex ultrasound (PPDU) A duplex scanner with color-flow imaging capability coupled with spectral-displayingsystem and 7.5-mHz linear-array transducer is the optimal instrument for performing this study.Using B-mode ultra sonography and color- image guidance, the device can assess the penile softtissue for the presence of structural abnormalities of the tunica albuginea such as fibrous plaquesor calcifications. It can also define the arterial tree, measure the diameter of the cavernosalarteries, and display the Doppler spectrum waveform of blood flow in the cavernosal arteries. The diagnostic classification based on PPDU testing is difficult in up to 20% of patients.Other secondary data that could be obtained from the PPDU examination may help to improve thediagnostic yield of vascular abnormalities. For example, Fitzgerald and colleagues found that thecombination of persistent dorsal vein flow and elevated end diastolic velocity (EDV) resulted in93% accuracy in diagnosing venous leakage when correlated with cavernosographic findings,even though the determination of dorsal vein flow velocity by itself did not prove to be useful inmaking such a diagnosis. PPDU examination may also provide significant information about theexistence of significant congenital vascular anomalies and functional or structural abnormalitieswith the helicine arteriolar system. Knowledge of these types of findings may be of benefit indetermining whether surgical intervention is possible or needed. Several pitfalls exist in the interpretation of data provided by the PPDU investigation.Some of these pitfalls may be eliminated by meticulous attention to technique, use of colorDoppler scanning, and correlation of results with the degree of penile rigidity. Repeatedvasoactive drug injections or exposure to visual erotic stimuli may also help to induce complete “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”211
  • 230. relaxation of trabecular smooth muscle, and hence, reduce the overestimation of corporealstructural disease. Also, sufficient erectile response, as assessed by a self-reporting instrument (apost investigation questionnaire), may help to reduce the false-positive diagnosis ofvenoocclusive dysfunction by as much as 50%. Venoocclusive dysfunction due to smooth muscledysfunction or venous incompetence can be ruled out using this approach.b. Dynamic infusion cavernosometry and cavernosography (DICC). This is a four-phase investigation in which corporeal body pressure at equilibrium isdetermined after injection of vasoactive agents (commonly 45–60 mg papaverine and 1–2.5 mgphentolamine) into one corpus cavernosum to relax the corporeal smooth muscles (phase I).Cavernosometry is then performed by infusing the penis with heparinized saline to raise thecorporeal body pressure to 150 mm Hg and observing the fall in pressure over 30 seconds aftercessation of infusion (phase II). Cavernosal artery systolic occlusion pressure is measured fromthe reappearance of the Doppler signal in the cavernosal artery during the decline in intracorporeal pressure following the termination of saline infusion (phase III). Finally,cavernosography is performed by infusing a radiocontrast material into the corporeal tissue andobtaining radiographic images of the penis and perineum (phase IV). DICC is widely accepted as the reference diagnostic technique for evaluation ofvenoocclusive dysfunction. Intra cavernous and systemic brachial blood pressure and penilecircumference are monitored continuously throughout. Valid DICC testing is dependent upon acomplete relaxation of penile smooth muscles with vasoactive drug administration. Failure toachieve such a state due to the patient’s anxiety, an inadequate dose of vasoactive agents, orintrinsic smooth muscle dysfunction may yield false-positive results. False-positive results canalso occur with psychogenic erectile dysfunction and in normal controls. At least two other variations of cavernosometry have been described, including pump andgravity cavernosometry. In the latter method, an intravenous infusion set is used instead of thepump, and complete corporeal smooth muscle relaxation is induced with local vasoactive drugs “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”212
  • 231. injections with or without audio-visual sexual stimulation. Gravity cavernosometry has beenconsidered by several investigators to be more physiological, safer, and cheaper than DICC orpump cavernosometry.c. Penile angiography This study is usually performed in selected patients before reconstructive vascularsurgery. These patients are usually young men with a history of blunt perineal trauma leading to ablockage at the origin of the cavernosal artery. Penile arteriography is not indicated in older mendue to low success rates for penile revascularization among this population. Selective pudendalangiography is helpful in defining the site of arterial block and thus in planning the appropriatesurgery. The sensitivity of procedures for detecting arterial lesions is in the order of 95%. Thevalue of arteriography in micro vascular disease is limited, as microsurgical reconstruction is notalways feasible. Further, the many variations of arterial supply to the penis and lack of normativedata may make the interpretation of the study difficult. Lastly, anxiety related to this proceduremay lead to excessive adrenergic discharge with arterial vasoconstriction and increased potentialfor false-positive results.d. Radio nuclear scintigraphy Several radio nuclear scintigraphy techniques have been described in the last threedecades. Radionuclide techniques can objectively measure the whole organ blood flow andcontinuously monitor penile blood volume changes from flaccidity through various phases oferection. Radionuclide techniques that continue to evolve include dynamic penile scintigraphy anddual-radioisotope.e. Cavernous oxygen tension Measurement of oxygen tension of corporeal blood during flaccidity and during peniletumescence has been suggested as a method for characterization of cavernous perfusion, and thuscorporeal vascular dysfunction. Aoki et al. reported a sudden increase in cavernous oxygentension at the onset of penile tumescence during visual sexual stimulation. Others have reported “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”213
  • 232. an increase in the corpus cavernosum oxygen tension from 25–40 mm Hg in the flaccid state to90–100 mm Hg in the erect state of the penis. More recently, Knispel and Andresen correlatedchanges in cavernous oxygen tension during PGE-1-induced penile tumescence to peak systolicvelocity (PSV) during Doppler ultrasonography. They found some impotent men to have lowcavernous oxygen tension (measured by new, unbreakable, small-caliber oxygen-sensitive probes,and defined arbitrarily as <65 mm Hg) despite normal blood velocity (defined as >25 cm/sec).Thus, a decrease in oxygen tension may occur as a result of arterial insufficiency and lead to adecrease in trabecular smooth muscle dysfunction (decrease in vascular smooth muscle cells andan increase in connective tissue formation, leading to corporeal fibrosis) in some men witherectile dysfunction. Such changes are probably mediated by an increase in TGF-ß1 with asimultaneous decrease in PGE-1 concentrations in corporeal tissue6. Neurological investigations A significant amount of research has been performed over the last few decades to definethe role of neurological factors in the genesis of male sexual dysfunction. However, much of theearlier work was restricted to studies of the somatic innervations of the penis. Only recently hassignificant attention been directed to the role of autonomic disorders in the development of sexualdysfunction. Still, many of the newly developed investigative procedures provide only indirectevidence for the presence of autonomic disturbances, and therefore, these procedures may notaccurately reflect the abnormality in autonomic nervous system control of the penis. Presence ofautonomic dysfunction in organ systems such as the cardiovascular or urological may signal asimilar abnormality in the erectile mechanism of the penis. However, most of the tests have notbeen adequately validated.a. Somatic innervation of the penis The somatic sensory innervation is important in the development and maintenance ofnormal erection, and the somatic motor innervation plays an important role in the control of “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”214
  • 233. ejaculation. The following provides a brief summary of available methods for testing the integrityof these innervations:i. Vibration perception threshold (biothesiometry) The test provides a biothesiometric screening method for abnormality within the penilesensory afferent pathway. It is performed with a portable hand-held electromagnetic vibrationdevice that has a fixed frequency and variable amplitude of vibrations. The loss of, or anabnormal decrease in, vibratory sensation suggests the presence of a peripheral neuropathy.ii. Dorsal nerve conduction velocity A sensory deficit of the dorsal nerve may reduce the ability to sustain erections duringcoitus. The decrease in sensory transmission from the penis is also often associated withejaculation difficulties. Since the penis is a distensible structure and the dorsal nerve of the penisis serpiginous at rest, gentle stretching with a one-pound weight is usually performed to straightenthe coiled nerve and permit optimal and more accurate measurement of the conduction velocity.iii. Bulbocavernosus reflex (sacral reflex arc) latency Bulbocavernosus reflex latency testing determines the time interval required for a reflexarc that utilizes the dorsal penile/pudendal afferent pathway, the S2-S4 spinal cord segment, andthe pudendal/perineal efferent pathway. The test may be helpful in documenting suspected sacralnerve root, cauda equina, or conus medullaris lesions (S2–S4) caused by multiple sclerosis, spinalcord trauma, spinal cord tumors, and herniated inter vertebral discs. Since parasympathetic sacralneurons are anatomically close to the central portion of the pudendal pathways, insults to thesomatic innervation at these sites may also cause parasympathetic dysfunction. The diagnosticsensitivity of the bulbocavernosus reflex latency measurement has been compared with othertesting procedures in several studies.iv. Pudendal nerve somatosensory (genitocerebral)-evoked potential This test allows the evaluation of the peripheral and suprasacral afferent pathways bystimulating the pudendal nerve at the penis. The evoked waveforms are recorded at various sites “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”215
  • 234. within the CNS, but most typically over the conus medullaris and parietal cortex. Patients withsacral lesions (distal to the sacral recording electrodes) caused by multiple sclerosis, spinal cordtrauma, or tumor may demonstrate prolonged peripheral and total conduction times. However,patients with suprasacral lesions (cephalic to recording electrodes) caused by transverse myelitis,cervical disc disease, tumor, or trauma may have prolonged total conduction time and centralconduction time, but normal peripheral conduction time. Further, performing both thebulbocavernosus and the pudendal nerve somatosensory-evoked potential testing may allow theevaluation of the different components of the pudendal nerve.v. Perineal electromyography The test identifies disturbances in pudendal motor pathways, which may be associatedwith metabolic or toxic disorders such as diabetes and alcoholism. Structural abnormalities of theperineal striated muscles also give rise to abnormal electromyographic recordings. Theinformation obtained can help in assessing the presence of neuropathic defects, the ability tocontract the bulbocavernosus muscle voluntarily, and the degree of motor-unit action potentialrecruitment during a bulbocavernosus reflex or cough.b. Autonomic innervation As previously discussed, the parasympathetic efferent pathways involve the spinal S2–S4segments and pelvic nerve, and the sympathetic efferent pathways involve spinal cord segmentT12-L2 and the hypo gastric nerve. Many of the available autonomic testing procedures providean indirect measure of the functional state of the autonomic control of the erectile function.However, autonomic parasympathetic, and autonomic sympathetic innervations hold the promisefor diagnosing various types of autonomic neuropathy that contributes to erectile dysfunction.b) Literary: “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”216
  • 235. Required literary information for the intended study is procured from both theAyurvedic and Modern textbooks and they are updated with recent journals of both thefaculties.c) Trail drugGroup – A: Vidaryadighrita282 24 gms as single dose with hot water before food at nightGroup – B: Uttara bastiPreparation of Ghrita All the constituents of the Vidarighrita identified and collected from the local areaafter proper identification. The useful parts and the ratio of the individual drugs are takenaccording to the reference Preparation is undertaken with Good Manufacturing Practiceaccording to Snehapaka vidhi explained in classical texts the Vidarighrita282 is prepared,It is used for Snehapana (internally) and Uttara basti.Method of collection of Data a) Study Design – The patients with Shukragatavata within the age group of 20 yrs to 60 yrs Simplerandom sampling technique comparative clinical observation. b) Sample Size – The study is planed in two groups 1) In group ‘A’ the minimum of 15 patients will be taken for Shaman Sneha. 2) In group ‘B’ the minimum of 15 patients will be taken for Uttar-basti.Exclusive Criteria – (ICD – 9 F – 52.4)283 1) Patient with secondary Systemic involvement like diabetic mellitus. 2) Psychogenic impotence. 3) Satyriasis. (Excessive sexual drive) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”217
  • 236. Inclusive Criteria – (ICD- 9 F -52.4)283 1) Patient with classical signs and symptoms sukragatavata. 2) Hypoactive sexual desire disorder. 3) Anhedonia (Inability to experience pleasure in normally pleasurable acts). 4) Patients between age group 20-60 year’s.Data Collection: Patients were thoroughly examined both subjectively and objectively. Detailedhistory pertaining to the mode of onset, previous ailment, previous treatment history,family history, habits, ashtavidhapareeksha and dashavidhapareeksha and physicalexamination findings were noted. Routine investigations were done to exclude otherpathologies. Radiological features were also investigated.Diagnostic Criteria – (DSM-IV) 284 Premature Ejaculation (Psycho sexually) 1) Orgasm inhabited male psychosexuallyPosology -Table No. 14 Group – A: Vidaryadighrita282 24 gms as single dose with hot water beforefood at nightSchedule Date Observation / instructions1 to 3 day = 1st Initiation Haritakyadi churna / Kosta shuddhi4 to 10 day = Snehapan11 to 13 day = 2rd Initiation Haritakyadi churna / Kosta shuddhi14 to 20 day = Snehapan21 to 23 day = 3rd Initiation Haritakyadi churna / Kosta shuddhi24 to 30 day = Snehapan60th day = Final Follow Up “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”218
  • 237. Table No. 15 Group – B: Uttara bastiSchedule Date Observation / instructions1 to 3 days = 1st Initiation Haritakyadi churna / Kosta shuddhi4th day = Uttara basti5th day = Uttara basti6th day = Uttara basti7 to 10 days = Rest11th to 13th days = 2nd Initiation Haritakyadi churna / Kosta shuddhi14th day = Uttara basti15th day = Uttara basti16th day = Uttara basti17 to 20 days = Rest21st to 23rd days = 3rd Initiation Haritakyadi churna / Kosta shuddhi24th day = Uttara basti25th day = Uttara basti26th day = Uttara basti27 to30 days = Rest60th day = Final Follow UpProcedure of Uttara bastiPoorvakarma:Instruments 5 to 6 Number rubber Catheter Sterile Gloves Antiseptic solution Cotton Swab holder Kidney tray Artery Forceps Syringe VidaryadighritaProcedure: At first, procedure is explained to the patient in detail. The genital parts areexamined to rule out any abnormality. After bath and light food, mrudu Snehana andswedana are done over the pelvic and lumbo-sacral region.Pradhanakarma: The patient is made to lie down in supine position and both the knee joints areseparated to view the genital organs properly. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”219
  • 238. Procedure: After wearing sterile gloves genital parts are cleaned with antiseptic solution.Distal portion (4-5 cm) of the catheter in smeared with Sneha and hold in right hand andthe penis with left hand. Loosely coiled in palm and penis is lifted in position,perpendicular to patient body and light upward traction is applied. Urinary meatus is identified and gently catheter is inserted up to the bladder untilthe urine start to flow. Urine is drained completely; the Sneha dravya (48 ml) is takeninto the syringe and injected into the bladder. Catheter is removed after few minutes,glans and meatus of penis are cleaned again. Classical text says that Uttara Basti done in erect penis, which is not practically.We insert the Basti netra upto 6 angula (Approximately 12cms). The male urethra is 17-23 cms, giving medicine in mid urethral region can produce rupture and leakage, and sogiving intra penile Uttara Basti is suitable.Pashchatkarma: The patient is advised to lie on the bed with his poison changing from side to sidea waiting for the medicine to come out within 30-40 mins. The retention time of Uttarabasti not specified and same is considered to the Anuvasana Basti i.e. up to 3Yaama(9hrs). If Aushadha dravya not comes out within the period then according to classicsPippalyadi varti should be kept in the urethra, still if the Aushadha dravya not comes outthen same varti kept in Guda. So that the Aushadha dravya comes out easily.Study Duration – Thirty days for both groups. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”220
  • 239. Follow Up – Thirty DaysAssessment of Result – The subjective and objective Parameters of base line data to pre and postmedication will be compared assessment of the result. All the result will be analysesstatistically for value using unpaired‘t’ test.Subjective parameter – 1) Shukra Kshipra MuchhatwamObjective parameters2851) Desire Phase a) Sexual Desire Score (SDS) b) Stress Score (SS) c) Hospital A & D Score (HADS)2) Excitement Phase d) Penile Erection Score (PES) e) Penile Rigidity Score (PRS)3) Orgasm Phase f) Orgasm Score (OS) g) Frequency of NPT4) Resolution Phase h) Androgen Deficiency Score (ADS) i) My Sexual Persona (MSP) j) Golombok- Rust Inventory of Sexual Satisfaction (GRISS) k) Golombok- Rust Inventory of Marital State (GRIMES)Investigations No special investigations are routinely necessary unless prostatitis is suspected. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”221
  • 240. Table No. 16 InvestigationsTest Before After Follow UpHb% Pus cells Pus cells Pus cellsUrine Microscopic Cyst Cyst Cyst Sperms Sperms SpermsTable No. 17 Assessment of Resultsa) Subjective CriteriaSl. No Criteria Before After Follow Up1. Premature ejaculation2. Anxiety / depression3. Impotence4. Erection5. Orgasm6. Infertility/ConceptionTable No. 18 b) Objective CriteriaSl. No Criteria Before After Follow Up 1) Ejaculation 2) No. of Pelvic ThrustTable No. 19 Grading for Variables used in studySubjective CriteriaPremature Ejaculation 0 = No Premature Ejaculation 1 = With few pelvic thrust 2 = Shortly after penetration 3 = Before insertion, Lack of control over ejaculation 4 = Rapid, uncontrolled, against wish, No orgasm, Both partnersAnxiety / depression 0 = No 1 = Mid 2 = Moderate rarely 3 = Severe afterlyImpotence 0 = No 1 = Mild, erection with minimum effort 2 = Moderate, Erection with more effort 3 = Severe, No erection at all Erection 0 = Good erection always 1 = Erection with minimum effort 2 = Erection with more effort 3 = Erection attained with partners support only 4 = No Erection at all even with the use of vibrator “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”222
  • 241. Orgasm 0 = Good orgasm to both partners always 1 = Orgasm attained in > 75 % of attempts 2 = Orgasm attained in > 50 % of attempts 3 = Occasionally attains orgasm in 25 % attempts 4 = Rarely satisfied, with more counseling 5 = No orgasm at all, and never satisfied in all attempts every Infertility 0 = No 1 = No semen dysfunction 2 = Semen dysfunction but miscarriage etc 3 = No conception at all and very poor semen parameter HADS (Hospital A&D) Score / Hamilton Anxiety Rating (HAR) 1. Anxious 2. Depression 3. Tension 4. Fear 5. Insomnia 6. Cognitive Intellectual 7. Depressive mood 8. Somatic (muscular) strength 9. CV symptoms 10. Respiratory symptoms 11. GI symptoms 12. Genitourinary symptoms 13. Autonomic symptoms 14. Behavior at interview Table No. 20 Objective CriteriaSl. No Criteria Grade G0 G1 G2 G3 G4 1) Ejaculation 1 to 5 min < 4 min < 3 min <2 min < 1 min 2) No. of Pelvic Thrust 15 to 2o < 15 > 10 < 10 > 5 <5 >2 1 to 2 GRISS QUESTIONAIRE (MALE) Do you have sexual intercourse more than twice a week? Do you find it hard to tell your partner what you like/dislike about your sexual relationship? Do you become easily sexually aroused? Are you able to delay ejaculate during intercourse if you thinks you may be coming too early? Are you dissatisfied with the amount of variety in your sex life with your partner? Do you dislike stroking and caressing your partner’s genitals? Do you become tense and anxious when your partner wants to have sex? Do you enjoy having sexual intercourse with your partner? Do you ask your partner what she likes and dislikes about your sexual relationship? Do you fail to get an erection? “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”223
  • 242. Do you feel there is a lack of love and affection in your sexual relationship with your partner Do you enjoy having your penis stroked and caressed by your partner? Can you avoid ejaculating too quickly during intercourse? Do you try to avoid having sex with your partner? Do you find your sexual relationship with your partner satisfactory? Do you get an erection during foreplay with your partner? Are there weeks in which u don’t have sex at all? Do you enjoy mutual masturbation with your partner? If you want sex with your partner do you take the initiative? Do you dislike being cuddled and caressed by your partner? Do you have sexual intercourse as often as u would like? Do you refuse to have sex with your partner? Do you loose your erection during intercourse? Do you ejaculate without wanting to almost as soon as your penis enters your partner vagina Do you enjoy cuddling and caressing your partner’s body? Do you feel uninterested in sex? Do you ejaculate by accident just before your penis is at least to enter your partner’s vagina? Do you have feelings of disgust about what you and your partner do during love making?Sex PE Questionnaires 1. Date of Birth ------------------- Place of birth ----------------- 2. Date of marriage -------------- Age difference between husband and wife ---------- 3. How was the first night experience? ---------------- Fear /Good /Ok / Not good 4. Do you consume alcohol? Yes/No 5. Do you smoke cigarette / Beedi? Yes /No 6. How is your sleep? Good / Disturbed 7. Do you get more Stress /Tension/Angry /Worries? Yes /No 8. In a week how many times you try sex? 9. Do you feel you get quick ejaculation? Yes/ No 10. How many minutes you do sexual act? 11. Can you perform second time sex after one sex act? Yes/No 12. Do you ejaculation before vaginal insertion? Yes/No 13. Do you get ejaculation just after vaginal insertion? Yes /No 14. Do you ejaculation within 2 or 4 pelvic thrusts? Yes /No 15. Are you bored by taking medicine for sex? Yes /No 16. Because of your sexual weakness does your wife get upset? Yes /No 17. Do you avoid sex because of this premature ejaculation? Yes /No 18. Do you get sexual strength whenever you wish? Yes/No 19. Before marriage did you experienced masturbation? Yes /No 20. Do you get burning sensation while passing urine? Yes /No “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”224
  • 243. 21. Do you get burning sensation during semen ejaculation? Yes /No 22. Have you taken treatment for premature ejaculation? Yes /No 23. Do you discuss about your PE with your friends? Yes /No 24. What is your wife’s opinion about your PE? Curable /Not curable 25. Are you taking PE treatment without telling to your wife? Yes/No 26. Have you experienced sex before marriage? Yes /No 27. Have you got extra marital affairs? Yes /No 28. Do you get PE even after changing the sex partner? Yes /No 29. Have you visited Hotel sex doctors? Yes /No 30. Have you purchased advertisement sex products? Yes /No 31. Do you get semen in your urine while passing urine ?Yes /No 32. Do you get semen ejaculation in dreams? Yes /No This is a sexual survey opinion poll for academic purpose. It will be maintained as confidential report. The person can voluntarily participate in this survey. If you want to share anything more, please write in detail.ASESSNMENT ON CLINICAL IMPROVEMENT: Clinical improvement of the disease was based on improvement in the clinicalfinding and reduction on the severity of the symptoms of the disease grading for theclinical improvement for individual variables.Overall Assessment of Clinical ResponseGood Response: 60 % improvement in clinical parameters.Moderate Response: 30 % improvement in clinical parameters.Poor Response: up to 10 % improvement in clinical parameters.No Response: 00 % or No improvement in clinical parameters. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”225
  • 244. Chapter – 5 Observations and Result Present study register 20 patients, out of 30 approached patients, fulfilling thecriteria of diagnosis and inclusive criteria. None of patient discontinued the procedures,so dropped out patients are not registered in this study. The observation of the patients and the disease was done by providing thequestionnaire to those patients who can fill the case sheet and from those who can’t fill;the information was collected by translating the questions in the local language. The casesheet is attached in the appendix. All the patients were examined thoroughly before theirinclusion in the study. The observation was done by considering the subjective andobjective parameters strictly. The observations were done in the following heading and are depicted in formand graphs are used where ever necessary; 1. Observation of demographic data. 2. Observation of the patient. 3. Observation of the disease. 4. Observation of the data related to the response of the patient. 5. Observation of the statistical out comes of the study.Observation of demographic data:A 1] Table No. 21 showing the distribution of patient’s age group No of patients and percentageAge group Group A Group B Total No. of patients % No. of patients % No. of patients %20-30 02 20% 02 20% 04 20%30-40 05 50% 04 40% 09 45%40-50 02 20% 04 40% 06 30%50-60 01 10% 00 00% 01 05% “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”224
  • 245. Group A: out of ten patients 02 (20%) were belonging to 20-30 age group, 05 (50%) wasfrom 30-40 age group, 02 (20%) were 40-50 aged and 01 (10%) were 50-60 years aged.Group B: out of ten patients 02 (20%) were belonging to 20-30 age group, 04 (40%)were from 30-40 age group, 04 (40%) were again from 40-50 age group and none of 00(00%) were from 50-60 age group.Overall: out of twenty patients 04 (20%) were from 20-30 group, 09 (45%) from 30-40age group, 60 (30%) from 40-50 group and 01 (05%) were from 50-60 group.Figure 01 showing distribution of patients by age 9987 66 5 20-305 4 4 4 30-404 40-503 50-60 2 2 22 1 11 00 Group A Group B TotalA 2] Table No. 22 showing the distribution of patients according to sexSex Group A no. and % Group B no. and % Group A and B no. and%Male 10 (100%) 10 (100%) 20 (100%)Group A: Among 10 numbers of patients 10 (100%) were malesGroup B: Among 10 numbers of patients 10 (100%) were malesOverall: Distribution of sex was; male 20 (100%) “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”225
  • 246. Figure 02 showing distribution of patients by sex 202018161412 10 1010 M al e 8 6 4 2 0 Gr o up A Gr o up B T o t al A 3] Table 23 showing distribution of patients by Religion Religion Group A no. and Group B no. and Group A and B no. % % and % Hindu 07 (70%) 05 (50%) 12 (60%) Muslim 02 (20%) 03 (30%) 05 (25%) Christian 01 (10%) 02 (20%) 03 (15%) Others 00 (00%) 00 (00%) 00 (00%) Group A: Out of 10 patients 07 (70%) were Hindus, 02 (20%) were Muslims, 01(100%) were Christians and none were others. Group B: Out of 10 patients 05 (50%) were Hindus, 03 (30%) were Muslims, 02 (20%) were Christians and none were others. Overall: Among 20 number of patients, Hindus were 12 (60%), 05 (25%) were Muslims, 03 (15%), Christian and none 00 (00%) were from other category. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”226
  • 247. Figure 03 showing distribution of patients by religion 1212108 7 Hindu6 5 Muslim 5 Christian4 3 3 Others 2 22 1 0 0 00 Group A Group B Total A 4] Table 24 showing distribution of patients by Economical status Economical status Group A no. and Group B no. and Group A and B no. % % and % Poor 03 (30%) 03 (30%) 06 (30%) Middle class 05 (50%) 04 (40%) 09 (45%) Higher 02 (20%) 03 (30%) 05 (25%) Group A: out of 10 patients 03 (30%) were belonging to poor status, 05 (50%) were of middle class and 02 (20%) were Higher class. Group B: out of 10 patients 03 (30%) were belonging to poor status, 04 (40%) were of middle class and 03 (30%) were Higher class. Overall: out of 20 patients 06 (30%) were poor, 09 (45%) were of middle class and 05 (25%) were Higher class. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”227
  • 248. Figure 04 showing distribution of patients by Economical status 9987 66 5 5 Poor5 44 Middle class3 3 3 3 Higher 2210 Group A Group B Total A 5] Table 25 Showing distributions of patients by Occupation Occupation Group A no. and Group B no. and Group A and B % % no. and % Sedentary 03 (30%) 04 (40%) 07 (35%) Active 04 (40%) 04 (40%) 08 (40%) Labour 03 (30%) 02 (20%) 05 (25%) Group A: out of 10 patients 03 (30%) was Sedentary, 04 (40%) were Active, 03 (30%) was Labour by occupation Group B: out of 10 patients 04 (40%) was Sedentary, 04 (40%) were Active, 02 (20%) was Labour by occupation. Overall: out of 20 patients 07 (35%) were Sedentary, 08 (40%) were Active, 05 (25%) was Labour. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”228
  • 249. Figure 05 showing distribution of patients by occupation8 8 776 55 4 4 Sedentary 44 Active 3 33 Labour 2210 G ro up A G ro up B T o tal A 6] Table No. 26. Showing distribution of patients by Vihara (Nature of work) Nature of work Group A no. and Group B no. and Overall % % Physical work 05 (50%) 06 (60%) 11 (55%) Mental exertion 04 (40%) 02 (20%) 06 (30%) Chemical 01 (10%) 01 (10%) 02 (10%) Thermal 00 (00%) 01 (10%) 01 (05) Group A: Out of 10 patients 05 (50%) were working Physical, 04 (40%) were working Mental exertion, 01(10%) were working Chemical and 00 (00%) none were working Thermal. Group B: Out of 10 patients 06 (60%) were working Physical, 02 (20%) were working Mental exertion, 01(10%) were working Chemical and 01(10%) were working Thermal. Overall: Out of 20 patients 11 (55%) were working Physical, 06 (30%) were working Mental exertion, 02 (10%) were working Chemical and 01(5%) were working Thermal. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”229
  • 250. Figure 06 showing distribution of patients by Vihara (Nature of work)12 11108 Physical work 6 66 Mental exertion 5 4 Chemical4 Thermal2 2 2 1 1 1 10 0 Group A Group B Total Vaiyaktika vruttanta of the patients: A 7] Table No. 27 Showing distribution of patients by Matra of ahara Matra of ahara Bahu Madhyama Alpa Group A 01 (10%) 07 (70%) 02 (20%) Group B 01 (10%) 06 (60%) 03 (30%) Overall 02 (10%) 13 (65%) 05 (25%) Group A: 01 (10%) patients were taking bahu matra ahara, 07 (70%) were taking madhyama matra and 02 (20%) was taking alpa matra ahara. Group B: 01 (10%) patients were taking bahu matra ahara, 06 (60%) were taking madhyama matra ahara and 03 (30%) were taking alpa matra ahara. Overall: out of twenty patients 02 (10%) were taking bahu matra ahara, 13 (65%) were taking madhyama matra ahara and 05 (25%) were taking alpa ahara. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”230
  • 251. Figure 07 showing distribution of patients by Matra of ahara14 1312108 7 Bahu 66 5 Madhyama4 2 3 2 Alpa2 1 10 Group A Group B TotalA 8] Table No. 28 Showing distribution of patients by Kala of aharaKala of ahara Regular IrregularGroup A 03 (30%) 07 (70%)Group B 02 (20%) 08 (80%)Overall 05 (25%) 15 (75%)Group A: out of 10 patients 03 (30%) were taking food at regular time, 07 (70%) weretaking irregularly.Group B: out of 10 patients 05 (50%) were taking food at regular time, 08 (80%) wastaking irregularly.Overall: out of 20 patients 05 (25%) were taking it regularly, 15 (75%) were not takingregularly.Figure 08 showing distribution of patients by kala of ahara16 15141210 8 8 7 Regular 6 5 Irregular 4 3 2 2 0 Group A Group B Total “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”231
  • 252. A 9] Table No. 29. Showing distribution of patients by Rasa Madhura Amla Lavana Katu Tikta KashayaGroup A 04 (40%) 08 (80%) 06 (60%) 04 (40%) 00 (00%) 00 (00%)Group B 04 (40%) 07 (70%) 08 (80%) 03 (30%) 00 (00%) 00 (00%)Overall 08 (40%) 15 (75%) 14 (70%) 07 (35%) 00 (00%) 00 (00%)Group A: out of ten patients 04 (40%) were like madhura rasa, 08 (80%) were like amlarasa, 06 (60%) was like lavana and 04 (40%) were like katu rasa. None liked tikta.andkashaya rasa.Group B: out of ten patients patents 04 (40%) were like madhura rasa, 07 (70%) werelike amla rasa, 08 (80%) liked lavana and 03 (30%) were like katu rasa. None liked tiktaand Kashaya rasaOverall: out of twenty patients 08 (40%) were fond of madhura, 15 (75%) were fond ofamla, 14 (70%) liked lavana and 07 (35%) were fond of katu rasa and none liked katu andkashaya rasa. Figure 09 Showing distributions of patients by Rasa16 15+ 141412 Madhura10 Amla8 8 8 8 7 7 Lavana6 6 Katu4 4 4 4 3 Tikta20 0 0 0 0 0 0 kashya Group A Group B Total “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”232
  • 253. A 10] Table No. 30. Showing distribution of patients Type of DietDiet Vegetarian MixedGroup A 04 (40%) 06 (60%)Group B 03 (30%) 07 (70%)Overall 07 (35%) 13 (65%)Group A: out of ten 04 (40%) were vegetarians and 06 (60%) were mixed diet.Group B: out of ten 03 (30%) were vegetarians and 07 (70%) were mixed dietOverall: out of twenty patents 07 (35%) were vegetarians and 13 (65%) were of mixeddietFigure 10 showing distribution of patients by type of Diet14 1312108 7 7 Vegetarian6 6 Mixed4 4 320 G ro up A G ro up B T o talA 11] Table No. 31. Showing distribution of patients by Vyasana Alcohol Tobacco Smoking Tea/coffee chewingGroup A 03 (30%) 03 (30%) 01 (10%) 03 (30%)Group B 05 (50%) 03 (30%) 01 (10%) 02 (20%)Overall 08 (40%) 06 (30%) 02 (10%) 05 (25%)Group A: out of ten patients 03 (30%) were alcoholics, 03 (30%) was tobacco chewer,01 (10%) were smokers and 03 (30%) was taking excess tea/ coffee.Group B: out of ten patients 05 (50%) were alcoholics, 03 (30%) were tobacco chewers,01 (10%) were smokers and 02 (20%) were taking excess tea/ coffee. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”233
  • 254. Overall: Out of twenty patients 08 (40%) were alcoholics, 06 (30%) were tobaccochewers, 02 (10%) were smokers and 05 (25%) were taking excess tea/ coffee.Figure 11 showing distribution of patients by Vyasana8 876 65 5 5 Alcohol4 Tobacco chewing3 3 3 3 3 Smoking2 2 2 Tea/Coffee1 1 10 Group A Group B TotalA 12] Table No. 32. Showing distribution of patients by Kula vrittantaKula Diabetes Hypertension Tuberculosis Acid peptic disordervrittantaGroup A 07 (70%) 06 (60%) 00 (00%) 02 (20%)Group B 02 (20%) 02 (20%) 01 (10%) 01 (10%)Overall 09 (45%) 08 (40%) 01 (05%) 03 (15%)Group A: out of 10 patients 07 (70%) were Diabetes, 06 (60%) was Hypertension, 00(00%) were Tuberculosis and 02 (20%) was Acid peptic disorder.Group B: out of 10 patients 02 (20%) were Diabetes, 02 (20%) was Hypertension, 01(10%) were Tuberculosis and 01 (10%) was Acid peptic disorder.Overall: out of 20 patients 09 (45%) were Diabetes, 08 (40%) was Hypertension, 01(05%) were Tuberculosis and 03 (15%) was Acid peptic disorder. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”234
  • 255. Figure 12 showing distribution of patients by Kula Vrittanta3 7 6 9 8 32 2 2 2 Diabetes Hypertension 1 1 1 Tuberculosis1 Acid peptic disorder. 00 Group A Group B Total A 13] Table 33 Showing distributions of patients by Agni Agni Group A no. and Group B no. and Group A and B % % no. and % Samagni 03 (30%) 02 (20%) 05 (25%) Mandagni 04 (40%) 06 (60%) 10 (50%) Teekshnagni 00 (00%) 01 (10%) 01 (05%) Vishamagni 03 (30%) 01 (10%) 04 (20%) Group A: Out of 10 patients, 03 (30%) were had Samagni, 04 (40%) were had Mandagni, none had Teekshna and 03 (30%) were had Vishamagni. Group B: Out of 10 patients, 02 (20%) were had Samagni, 06 (60%) were had Mandagni, 01 (10%) were had Teekshna and 01 (10%) were had Vishamagni. Overall: Out of 20 patients, 05 (25%) were had Samagni, 10 (50%) were had Mandagni, 01 (05%) were had Teekshna and 04 (20%) were had Vishamagni “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”235
  • 256. Figure 13 showing distribution of patients by Agni 1010 9 8 7 6 6 Samagni 5 5 Mandagni 4 4 4 Teekshnagni 3 3 3 Vishamagni 2 2 1 1 1 1 0 0 Group A Group B Total A 14] Table 34 Showing distributions of patients by Kostha Kostha Group A no. and Group B no. and Group A and B % % no. and % Mrudu 03 (30%) 01 (10%) 04 (20%) Madyama 04 (40%) 05 (50%) 09 (45%) Krura 03 (30%) 05 (50%) 08 (40%) Group A: Out of 10 patients 03 (30%) were had Mrudu Kostha, 04 (40%) were had Madyama Kostha and 03 (30%) had Krura Kostha. Group B: Out of 10 patients 01 (10%) were had Mrudu Kostha, 05 (50%) were had Madyama Kostha and 05 (50%) had Krura Kostha. Overall: Out of 20 patients 04 (20%) were had Mrudu Kostha, 09 (45%) were had Madyama Kostha and 08 (40%) had Krura Kostha. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”236
  • 257. Figure 14 showing distribution of patients by Kostha 99 8876 5 55 Mrudu 4 44 Madyama 3 33 Krura2 110 Group A Group B Total A 15] Table 35 Showing distributions of patients by Nidra Nidra Group A no. and Group B no. and Group A and B no. % % and % Normal 03 (30%) 02 (20%) 05 (25%) Disturbed 07 (70%) 08 (80%) 15 (75%) Group A: Out of ten patients 03 (30%) were had Normal nidra, 07 (70%) were had Disturbed nidra. Group B: Out of ten patients 02 (20%) were had Normal nidra, 08 (80%) were had Disturbed nidra. Overall: Out of twenty patients 05 (25%) were had Normal nidra, 15 (75%) were had Disturbed nidra. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”237
  • 258. Figure 15 showing distribution of patients by Nidra16 15141210 88 7 Normal6 5 Disturbed4 3 220 G ro up A G ro up B T o tal A 16] Table 36 Showing distributions of patients by Vyayama Shakti Vyayama Shakti Group A no. and Group B no. and Group A and B % % no. and % Heena 03 (30%) 03 (30%) 06 (30%) Madyama 03 (30%) 05 (50%) 08 (40%) Regular 00 (00%) 00 (00%) 00 (00%) Irregular 04 (40%) 02 (20%) 06 (30%) Group A: Out of 10 patients, 03 (30%) were had Heena, 03 (30%) were had Madyama Vyayama Shakti, none 00 (00%) were had Regular and 04 (40%) were had Irregular. Group B: Out of 10 patients, 03 (30%) were had Heena, 05 (50%) were had Madyama Vyayama Shakti, none 00 (00%) were had Regular and 02 (20%) were had Irregular. Overall: Out of 20 patients, 06 (30%) were had Heena, 08 (40%) were had Madyama Vyayama Shakti, none 00 (00%) were had Regular and 06 (30%) were had Irregular. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”238
  • 259. Fig No 16 showing the distribution of patient’s by Vyayama Shakti:8 87 6 66 55 Heen 4 Madyam a4 3 3 3 Regular3 Irregular 221 0 0 00 Group A Group B TotalII. Data Related to Disease: (Chief Complaints)B 1] Table 37 Showing distribution of patients by Chief ComplaintsChief Complaints Group A no. and Group B no. and Group A and B % % no. and %PE 10 (10%) 10 (10%) 20 (10%)ED 08 (80%) 08 (80%) 16 (80%)Infertility 06 (60%) 07 (70%) 13 (65%)Group A: Out of ten patients 10 (10%) were had PE, 08 (80%) were had ED and 06(60%) were had Infertility.Group B: Out of ten patients 10 (10%) were had PE, 08 (80%) were had ED and 07(70%) were had Infertility.Overall: Out of twenty patients 20 (100%) were had PE, 16 (80%) were had ED and 13(65%) were had Infertility. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”239
  • 260. Figure 17 showing distribution of patients by Chief Complaints 202018 161614 1312 10 10 PE108 8 8 ED 76 6 Infertility420 Group A Group B Total B 2] Table 38 Showing distribution of patients by Previous illness Previous illness Group A no. and Group B no. and Group A and B % % no. and % Stholya 03 (30%) 02 (20%) 05 (25%) Mutrasmari 00 (00%) 01 (10%) 01 (05%) TB 01 (10%) 01 (10%) 02 (10%) Mutrakrchhra 00 (00%) 04 (40%) 04 (20%) Arsa 04 (40%) 02(20%) 06(30%) Varicose scrotal cyst 01 (10%) 01(10%) 02(10%) Group A: Out of 10 patients 03 (30%) were had Sthoulya, 00 (00%) none were had Mutrasmari, 01 (10%) were had TB, none 00 (00%) were had Mutrakrchhra, 04 (40%) were had Arsa and 01 (10%) were had Varicose scrotal cyst. Group B: Out of 10 patients 02 (20%) were had Sthoulya, 01 (10%) none were had Mutrasmari, 01 (10%) were had TB, 04 (40%) were had Mutrakrchhra, 02 (20%) were had Arsa and 01 (10%) were had Varicose scrotal cyst. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”240
  • 261. Overall: Out of 20 patients 05 (25%) were had Sthoulya, 01 (05%) were had Mutrasmari, 02 (10%) were had TB, 04 (20%) were had Mutrakrchhra, 06 (30%) were had Arsa and 02 (10%) were had Varicose scrotal cyst. Figure 18 showing distribution of patients by previous illness6 65 5 Stholya4 4 4 4 Mutrasmari 33 TB 2 2 2 2 Mutrakrchhra2 Arsa1 1 1 1 1 1 1 Varicose scrotal cyst0 0 0 Group A Group B Total B 3] Table 39 showing the distribution of patients according to Snana Snana Group A no. and Group B no. and Group A and B % % no. and % Usna jala 03 (30%) 05 (50%) 08 (40%) Sita jala 01 (10%) 03 (30%) 04 (20%) Samasitoshna jala 06 (60%) 02 (20%) 08 (40%) Group A: Among 10 numbers of patients 03(30%) were use Usna jala, 01 (10%) were use Sita jala and 06 (60%) were use Samasitoshna jala. Group B: Among 10 numbers of patients 05 (50%) were use Usna jala, 03 (30%) were use Sita jala and 02 (20%) were use Samasitoshna jala. Overall: Among 20 numbers of patients 08 (40%) were use Usna jala, 04 (20%) were use Sita jala and 08 (40%) were use Samasitoshna jala. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”241
  • 262. Fig No 19 showing the distribution of patient’s Snana: 8 887 66 55 4 Usna jala4 Sita jala 3 33 Sam asitoshna jala 22 110 Group A Group B Total B 4] Table 40 Showing distribution of patients by Undergarments Undergarments Group A no. and Group B no. and Group A and B % % no. and % Tight 06 (60%) 06 (60%) 12 (60%) Loose 04 (40%) 04 (40%) 08 (40%) Cotton 05 (50%) 03 (30%) 08 (40%) Synthetic 05 (50%) 07 (70%) 12 (60%) Group A: Out of ten patients, 06 (60%) were using tight, 04 (40%) were using Tight, 05 (50%) were using Cotton and 05 (50%) were using Synthetic. Group B: Out of ten patients, 06 (60%) were using tight, 04 (40%) were using Tight, 03 (30%) were using Cotton and 07 (70%) were using Synthetic. Overall: Out of ten patients, 12 (60%) were using tight, 08 (40%) were using Tight, 08 (40%) were using Cotton and 12 (60%) were using Synthetic. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”242
  • 263. Figure 20 showing distribution of patients by Undergarments 12 121210 8 8 8 Tight 7 6 6 6 Loose 5 5 4 4 Cotton 4 Synthetic 3 2 0 Group A Group B TotalVyavaya VrittantaB 5] Table 41 showing the distribution of patients according to Development ofSecondary Sexual CharacterSecondary Sexual Group A no. and Group B no. and Group A and BCharacter % % no. and %Normal 06 (60%) 08 (80%) 14 (70%)Early 03 (30%) 01 (10%) 04 (20%)Delayed 01 (10%) 01 (10%) 02 (10%)Group A: Among 10 numbers of patients 06 (60%) were Secondary Sexual CharacterNormal, 03 (30%) were Secondary Sexual Character Early and 01 (10%) were SecondarySexual Character Delayed.Group B: Among 10 numbers of patients 08 (80%) were Secondary Sexual CharacterNormal, 01 (10%) were Secondary Sexual Character Early and 01 (10%) were SecondarySexual Character Delayed. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”243
  • 264. Overall: Among 20 numbers of patients 14 (70%) were Secondary Sexual Character Normal, 04 (20%) were Secondary Sexual Character Early and 02 (10%) were Secondary Sexual Character Delayed. Fig No 21: showing the distribution of patient’s Secondary Sexual Character; 14141210 88 Norm al 6 Early6 Delayed 44 3 22 1 1 10 Group A Group B Total B 6] Table 42 showing the distribution of patients according to Masturbation Masturbation Group A no. and Group B no. and Group A and B % % no. and % Yes 07 (70%) 08 (80%) 15 (75%) No 01 (10%) 00 (00%) 01 (05%) Rare 02 (20%) 02 (20%) 04 (20%) Group A: Among 10 numbers of patients 07 (70%) were masturbation, 01 (10%) were No masturbation, and 02 (20%) were Rare. Group B: Among 10 numbers of patients 08 (80%) were Yes, none 00 (00%) were Masturbation, and 02 (20%) were Rare masturbation. Overall: Among 20 numbers of patients 15 (70%) were masturbation, 01 (05%) were No masturbation, and 04 (20%) were Rare masturbation. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”244
  • 265. Fig No 22: showing the distribution of patient’s Masturbation16 15141210 8 Yes8 7 No6 Rare 44 2 22 1 1 00 Group A Group B Total B 7] Table 43 showing the distribution of patients according to First coital experience First coital Group A no. and Group B no. and Group A and B experience % % no. and % Easy 01 (10%) 04 (40%) 05 (25%) Traumatic 09 (90%) 04 (40%) 13 (65%) Depressed 10 (100%) 06 (60%) 16 (80%) Exited 01 (10%) 04 (40%) 05 (25%) Group A: Among 10 numbers of patients 01 (10%) were Easy First coital experience, 09 (90%) were Traumatic First coital experience, 10 (100%) were Depressed First coital experience and 01 (10%) were Exited First coital experience. Group B: Among 10 numbers of patients 04 (40%) were Easy First coital experience, 04 (40%) were Traumatic First coital experience, 06 (60%) were Depressed First coital experience and 04 (40%) were Exited First coital experience. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”245
  • 266. Overall: Among 20 numbers of patients 05 (25%) were Easy First coital experience, 13 (65%) were Traumatic First coital experience, 16 (80%) were Depressed First coital experience and 05 (25%) were Exited First coital experience. Fig No 23: showing the distribution of patient’s First coital experience14 131210 10 98 Easy Traum atic6 6 6 Depressed 5 5 4 4 4 Exited42 1 10 Group A Group B Total B 8] Table 44 showing the distribution of patients according to Family sexual life Family sexual life Group A no. and Group B no. and Group A and B % % no. and % Best 01 (10%) 00 (00%) 01 (05%) Moderate 07 (70%) 09 (90%) 16 (80%) Worst 02 (20%) 01 (10%) 03 (15%) Group A: Among 10 numbers of patients 01 (10%) were Best Family sexual life, 07 (70%) were Moderate Family sexual life and 02 (20%) were Worst Family sexual life. Group B: Among 10 numbers of patients none 00 (00%) of were Best Family sexual life, 09 (90%) were Moderate Family sexual life and 01 (10%) were Worst Family sexual life. Overall: Among 20 numbers of patients 01 (05%) were Best Family sexual life, 16 (80%) were Moderate Family sexual life and 03 (15%) were Worst Family sexual life. “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”246
  • 267. Fig No 24: showing the distribution of patient’s Family sexual life 16 16 14 12 10 9 Best 8 7 Moderate 6 W orst 4 3 2 2 1 1 1 0 0 Group A Group B Total B 9] Table 45 showing the distribution of patients according to Sexual act Sexual act Group A no. and Group B no. and Group A and B % % no. and % Satisfactory 02 (20%) 01 (10%) 03 (15%) Not Satisfactory 08 (80%) 09 (90%) 17 (85%) Group A: Among 10 numbers of patients 02 (20%) were Satisfactory Sexual act, and 08 (80%) were Not Satisfactory Sexual act. Group B: Among 10 numbers of patients 01 (10%) were Satisfactory Sexual act, and 09 (90%) were Not Satisfactory Sexual act. Overall: Among 20 numbers of patients 03 (15%) were Satisfactory Sexual act, and 17 (85%) were Not Satisfactory Sexual act. Fig No 25: showing the distribution of patient’s Sexual act18 1716141210 9 8 Satisfactory8 Not satisfactory64 3 22 10 Group A Group B Total “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”247
  • 268. B 10] Table 46 showing the distribution of patients according to fore play Fore play Group A no. and Group B no. and Group A and B % % no. and % Yes 05 (50%) 06 (60%) 11 (55%) Minimal 05 (50%) 02 (20%) 07 (35%) No 00 (00%) 02 (20%) 02 (10%) Group A: Among 10 numbers of patients 05 (50%) were Fore play, 05 (50%) were Minimal Fore play and none 00 (00%) were Fore play. Group B: Among 10 numbers of patients 06 (60%) were Fore play, 02 (20%) were Minimal Fore play and 02 (02%) were No Fore play. Overall: Among 20 numbers of patients 11 (55%) were Fore play, 07 (35%) were Minimal Fore play and 02 (10%) were No Fore play. Fig No 26: showing the distribution of patient’s fore play12 11108 7 6 Yes6 5 5 Minim al No4 2 2 22 00 Group A Group B Total “Management of Shukragatavata with Vidarighritha a Comparative study w.s.r. to Premature Ejaculation”248
  • 269. B 11] Table 47 showing the distribution of patients according to Mano pareeksha Mano pareeksha Group A no. and Group B no. and Group A and B % % no. and % Intact 02 (20%) 01 (10%) 03 (15%) Elevated 01 (10%) 01 (10%) 02 (10%) Depressed 07 (70%) 10 (100%) 17 (85%) Anxious 05 (50%) 03 (30%) 08 (40%) Fear 05 (50%) 06 (60%) 11 (55%) Anger 06 (60%) 07 (70%) 13 (65%) Worries 10 (10%) 08 (80%) 18 (90%) Phobias 00 (00%) 00 (00%) 00 (00%) Stress 09 (90%) 10 (100%) 19 (95%) Group A: Among 10 numbers of patients 02 (20%) were Intact, 01 (10%) were Elevated, 07 (70%) were Depressed, 05 (50%) were Anxious, 05 (05%) were Fear, 06 (60%) were Anger, 10 (100%) were Worries, none 00 (00%) were Phobias, and 09 (90%) were Stress. Group B: Among 10 numbers of patients 01 (10%) were Intact, 01 (10%) were Elevated, 10 (100%) were Depressed, 03 (30%) were Anxious, 06 (60%) were Fear, 07 (70%) were Anger, 08 (08%) were Worries, none 00 (00%) were Phobias, and 10 (100%) were Stress. Overall: Among 20 numbers of patients 03 (15%) were Intact, 02 (10%) were Elevated, 17 (85%) were Depressed, 08 (40%) were Anxious, 11 (55%) were Fear, 13 (65%) were Anger, 18 (90%) were Worries, none 00 (00%) were Phobias, and 19 (95%) were Stress. Fig No 27: showing the distribution of patient’s Mano pareeksha20 1918 18 1716 Intact14 Elev ated 1312 Depressed 11 Anxious10 10