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Amavata kc004 udp
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A COMPARATIVE STUDY OF ERANDA PAKA AND AJAMODADI CHURNA IN THE MANAGEMENT OF AMAVATA , DEEPAK S.M. 2002 – 2003, DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA, S. D. M. COLLEGE OF AYURVEDA, …

A COMPARATIVE STUDY OF ERANDA PAKA AND AJAMODADI CHURNA IN THE MANAGEMENT OF AMAVATA , DEEPAK S.M. 2002 – 2003, DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA, S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118.

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  • 1. A COMPARATIVE STUDY OF ERANDA PAKA AND AJAMODADI CHURNA IN THE MANAGEMENT OF AMAVATA Dissertation submitted to the Rajiv Gandhi University of Health Sciences,Bangalore, Karnataka in partial fulfillment of the regulations for the award of the degree of DOCTOR OF MEDICINE (AYU) By DEEPAK S.M., B. A. M. S. GUIDE DR.U.N. PRASAD, M.D. (AYU) Professor and H.O.D. Department of Kayachikitsa S.D.M. College of Ayurveda, Udupi CO-GUIDE DR. V.K. SRIDHAR HOLLA, M.D.(AYU) Assistant Professor Department of Kayachikitsa S.D.M. College of Ayurveda, Udupi DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118. 2002 – 2003
  • 2. DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA S.D.M. COLLEGE OF AYURVEDA, UDUPI – 574 118 CERTIFICATE This is to certify that the dissertation entitled “A comparativestudy of Eranda Paka and Ajamodadi Churna in the management ofAmavata” is the record of the research work conducted by Deepak S.M.under my direct supervision and guidance in S. D. M. College ofAyurveda, Udupi. The candidate has put in sincere effort in both the conceptual andclinical studies. This title has not been awarded Degree, Diploma, Associateship,Fellowship or similar honors from this University. I recommend and forward the same for being submitted forevaluation to the adjudicators.Place : Udupi Dr. U. N. Prasad, M.D. (Ayu)Date : Professor and Head of the Department of Post graduate studies in Kayachikitsa S. D. M. College of Ayurveda, Udupi.
  • 3. DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118 CERTIFICATE This is to certify that the dissertation entitled “A comparativestudy of Eranda Paka and Ajamodadi Churna in the management ofAmavata” is the record of the research work conducted by Deepak S.Munder my direct supervision and guidance. The candidate has put in sincere effort in both the conceptual andclinical studies. I recommend the same for being submitted for evaluation to theadjudicators.Place : Udupi Dr. U. N. Prasad, M.D. (Ayu)Date : Professor and Head of the Department of Post graduate studies in Kayachikitsa S. D. M. College of Ayurveda, Udupi.
  • 4. ACKNOWLEDGEMENTSI am Ever Indebted To Lord Almighty, My Venerated Parents, Respected Teachers And Affectionate Friends
  • 5. Dedicated toMy Beloved Father
  • 6. CONTENTS LIST OF CHARTS LIST OF TABLES LIST OF GRAPHS LIST OF ABBREVIATIONS Page NoPART - I: INTRODUCTION 1PART - II: CONCEPTUAL STUDY Chapter I - Historical Review 5 Chapter II - Vyutpatti of Amavata 11 Ama and Vata 12 Nidana 30 Samprapti 35 Poorvaroopa 41 Bheda 43 Roopa 46 Upadrava 55 Investigations 58 Upashaya Anupashaya 62 Sadhyasadhyata 65 Sapeksha Nidana 67 Chikitsa 69 Pathya-Apathya 76 Chapter III - Drug Review 79PART - III: CLINICAL STUDY Materials and Methods 87 Observations 99 Results 104PART – IV: DISCUSSION 128PART –V: SUMMARY AND CONCLUSION 145 BIBLIOGRAPHY APPENDIX-CASE SHEET
  • 7. LIST OF GRAPHSGraph No. Contents 1. Age groupwise distribution of patients 2. Percentage of patients of different sex 3. Percentage of patients of different religion 4. Incidence of Literacy 5. Percentage of patients of different marital status 6. Incidence of socio-economical status of patients 7. Occupation wise distribution of patients 8. Distribution of patients according to their habits 9. Prakriti wise distribution of patients 10. Vikruti wise distribution of patients 11. Percentage of patients according to Satva 12. Percentage of patients according to Sara 13. Percentage of patients according to Samhanana 14. Percentage of patients according to Satmya 15. Percentage of patients according to Abhyavaharana Shakti 16. Percentage of patients according to Aahara-Jarana Shakti 17. Percentage of patients according to Vyayama Shakti 18. Percentage of patients according to Vaya 19. Effect of Eranda Paka on cardinal symptoms of Amavata 20. Improvement in general symptoms recorded in patients treated with Eranda Paka
  • 8. 21. Over all effect of Eranda Paka on general symptoms of Amavata22. Effect of Eranda Paka on symptoms of Ama23. Effect of Eranda Paka on total symptom score of Ama24. Effect of Eranda Paka on different clinical parameters25. Effect of Eranda Paka on TLC26. Effect of Eranda Paka on Hb%27. Effect of Eranda Paka on ESR28. Over all effect of treatment in 10 patients of Amavata29. Effect of Ajamodadi Churna on cardinal symptoms of Amavata30. Effect of Ajamodadi Churna on general symptoms of Amavata31. Total effect of Ajamodadi Churna on general symptoms of Amavata32. Effect of Ajamodadi Churna on symptoms of Ama33. Total effect of Ajamodadi Churna on symptoms of Ama34. Effect of Ajamodadi Churna on different clinical parameters35. Effect of Ajamodadi Churna on TLC36. Effect of Ajamodadi Churna on Hb%37. Effect of treatment on ESR38. Overall effect of Ajamodadi Churna in patients of Amavata39. Comparison of the effect of treatment on the cardinal symptom of Amavata40. Comparison of effect of treatment on general symptom in two groups41. Comparison of effects on symptoms of Ama in two groups
  • 9. 42. Comparison of effects on range of joint movement43. Comparison of effects on foot pressure between the groups44. Comparison of the effect on hand grip power45. Comparison of effect on body weight46. Comparison of effect on haemoglobin percentage47. Comparison of effect on erythrocyte sedimentation rate48. Comparison of overall effect of the treatments in both the groups
  • 10. LIST OF TABLESTable No. Contents 1. Lakshanas of Amavata according to different authors 2. Properties and therapeutic effect of the individual drugs in Eranda Churna 3. Properties and therapeutic effect of the individual drugs in Ajamodadi Churna 4. Properties and therapeutic effect of the individual drugs in Panchakola Phanta 5. Age Group of Patients 6. Sex Incidence of Patients 7. Religion of patients 20 patients of Amavata 8. Literacy incidence in patients of Amavata 9. Marital status of Amavata patients 10. Socio-economic status of patients 11. Incidence of occupation in Amavata patients 12. Study of Habit incidence 13. Study of patients Prakriti in the study 14. Incidence of Vikriti 15. Incidence of Satva in the Study 16. Study of Saratah Incidence in the Study 17. Study of patients Samhanana in the study 18. Satmya Incidence
  • 11. 19. Study of patients Ahara-Abhyavaharana Shakti20. Study of Patients Ahara-Jarana Shakti the Study21. Study of patients Vyayama Shakti in the study22. Vaya incidence23. Effect of Eranda Paka on cardinal symptoms of Amavata24. Effect of Eranda Paka on general symptoms of Amavata25. Overall effect of Eranda Paka on general symptoms of Amavata26. Effect of Eranda Paka on the symptoms of Ama27. Overall effect of Eranda Paka on symptoms of Ama28. Effect of Eranda Paka on circumference of limbs29. Effect of Eranda Paka on different clinical parameters30. Effect of treatment on body weight of patients of Amavata31. Effect of Eranda Paka on different hematological values32. Over all effect of treatment in 10 patients of Amavata33. Effect of Ajamodadi Churna on cardinal symptoms of Amavata34. Effect of Ajamodadi Churna on general symptoms of Amavata35. Total effect of Ajamodadi Churna on general symptoms36. Effect of Ajamodadi Churna on symptoms of Ama37. Total effect of Ajamodadi Churna on symptoms of Ama38. Effect of Ajamodadi Churna on circumference of the limbs39. Effect of Ajamodadi Churna on different clinical parameters40. Effect of Ajamodadi Churna on body weight of patients of Amavata41. Effect of Ajamodadi Churna on different hematological parameters
  • 12. 42. Over all effect of treatment in 10 patients of Amavata43. Comparison of effect of treatments on cardinal symptoms of Amavata44. Comparison of effect on general symptoms45. Comparison of effect on symptoms of Ama between the groups46. Comparison of effect on different clinical parameters47. Comparison of the effect on body weight in both the groups48. Comparison of effect on different haematological values49. Comparison of overall effect of treatment in two groups
  • 13. LIST OF CHARTSChart no. Contents 1. Schematic representation of Nidana of Amavata 2. Schematic representation of Samprapti in the light of Kriyakalas 3. Schematic representation of the evolution of Poorvaroopa 4. Schematic representation of the evolution of Roopa 5. Schematic representation of the evolution of Upadrava
  • 14. LIST OF ABBREVIATIONS1. A.H. : Ashtanga Hridaya2. A.P.I. : A.P.I.Text Book Of Medicine3. A.S. : Ashtanga Sangraha4. A.K. : Amarakosha5. A.V.S. : Atharvaveda Sayana Bhashya6. Basa : Basavarajeeyam7. B.P. : Bhava Prakasha8. B.R. : Bhaishajya Rathnavali9. C.S. : Charaka Samhita A10. C.D. : Chakra Datta11. Ckr. : Chakrapani.12. D.P.P.M. : Davidson’s Practice and Principles of Medicine13. Dl. : Dalhana14. D.N. : Dhanvantari Nighantu15. D.G. : Dravya Guna Vijnana16. E.M.P. : Essentials Of Medical Pharmacology17. G.N. : Gada Nigraha18. H.P.I.M. : Harrison’s Principle Of Internal Medicine19. H.S. : Harita Samhita.20. K.S. : Kashyapa Samhita21. K.K. : Kalyanakaraka22. K.N. : Kaiyadeva Nighantu
  • 15. 23. M.K.A. : Malavikagnimitra24. Madhu. : Madhukosha25. M.N. : Madhava Nidana26. M.P.N. : Madanapala Nighantu27. R.P.B.D. : Robbin’s Pathologic Basis Of Disease28. R.R.S. : Rasa Ratna Samucchaya29. R.N. : Raja Nighantu30. R.V. : Rugveda31. S.N. : Saligrama Nighantu Bhushana32. S.K.D. : Shabda Kalpa Druma33. Sh.S. : Sharangadhara Samhita34. S.S. : Sushruta Samhita35. T.B.P. : Text Book Of Pathology By Harsh Mohan36. Vag. : Vagbhata37. Vang. : Vangasena38. W.I. : The Wealth Of India39. Y.R. : Yogaratnakara ABBREVIATIONS OF STHANAS AND KHANDAS1. Chi. : Chikitsa Sthana2. Ind. : Indriya Sthana3. Ka. : Kalpa Sthana4. Ma.Kha. : Madhyama Khanda5. Ni. : Nidana Sthana
  • 16. 6. Po.Kha. : Poorva Khanda7. Sha. : Shareera Sthana8. Si. : Siddhi Sthana9. Su. : Sutra Sthana10. Ut. : Uttara Tantra11. Vi. : Vimana Sthana
  • 17. Introduction INTRODUCTION “Necessity is the mother of invention”, true to this sermon the invention:“Ayurvedo Ayam” and the necessity “Rogastasysa Apahartaraha” Kasya?“Shreyaso Jeevitasya cha”. Roga was hence the research problem, which led todawn of a philosophy, a religion, a science and the second important milestoneafter the birth of man away from the land of immortals. “Jignyasa Nama Pareksha” is a virtue that develops as a response to thestimulus of a problem, which haunts a human being to restrict him in hispursuits. Inventions like the microscope by Robert Koch, penicillin by AlexanderFleming are examples of such responses from the recent past. The history of medical science hence begins with the advent of Ayurvedaand takes many twists and turns gifting the modern world with awesomediscoveries and inventions enough to create a revolution. The revolution inmedical science has been progressing a lot since then as rightly put below. “We can put it down as one of the principles learned from the history ofscience that a theory is only overthrown by a better theory, never merely bycontradictory facts. Attempts are first made to reconcile contradictory facts tothe existing conceptual scheme by some modification of the concept. Only thecombination of a new concept with facts contradictory to old ideas finally bringsabout a scientific revolution and when this has taken place then in short years 1
  • 18. Introductiondiscovery follows upon discovery and the branch of science in questionprogresses by leaps and bounds”. -James B. Somnant The process of research hence continues with renewed momentumwhenever a medical problem is encountered especially that which becomesmore knotty and mysterious each time attempts are made to decipher it. AmaVata or Rheumatoid arthritis (Y.N. Upadyaya) as perceived in modern parlanceis one such medical problems that cripples a man to an extent to render himunfit for independent living. The patient experiences pain, which is so miserableas to promote a statistical study on the suicide rates in Rheumatoid Arthritis(RA) patients. Leave alone the articular manifestation the extra articular effects on theother systems are even more deleterious. In the musculoskeletal system itcauses skeletal muscle atrophy and osteoporosis, pleuropulmonarymanifestation of respiratory system, the vasculitis phenomenon of the vascularsystem peripheral neuropathies of nervous system, scleritis and othermanifestation of opthalmic system, haematological manifestation like anaemiaand splenomegaly are the common complications of the disease. R.A. effectsapproximately 0.8% of the population without race bias. Females are affectedthree times more than males. Interestingly, studies indicate that climate andurbanization have a major effect on the incident and severity of R.A. studies todiscover the mechanism of etiology, pathogenesis and treatment have been 2
  • 19. Introductioninconclusive at best and the disease continues to elude the modern researchesin all perspectives of objectivity. In this situation, the Ayurvedic viewpoint on the disease assumessignificant relevance, according to which Ama the toxic byproduct of atransformative error in body’s metabolic homeostasis conjugates with Vata thesupreme controller of homeostasis and the prime Dosha to manifest thesymptoms of Ama Vata. Ama is produced whenever the factors governing mechanisms thatrender the gross nutrients assimilable and compatible to the body elements areoverwhelmed both at the digestive and metabolic levels. Though the majorsources of Ama is from the Adishtana of Jatharagni initiated by PrakupitaDoshas, it is also produced at the Dhatwagni level when the inherentcompatibility of an equilibrium of contradictions in the Gunas of Doshas aredisrupted, a concept consistent with the description of autoimmunity in modernmedicine. The Ayurvedic approach to the treatment is the need of the hour as nosystem is successful in providing the complete cure to this disease. Acomprehensive Ayurvedic management with Langhana-a concept over sightedby the modern scientists as accidental and inconsequential, promises to make asignificant difference in the management of R.A. Among the Ayurvedic drugsEranda and Ajamoda are among the best Amapachakas and their effects in 3
  • 20. IntroductionAmavata has been hailed in Yogaratnakara. A well-organized clinical studycomparing the effect of Eranda Paka and Ajamodadi Churna is another attemptto search an effective remedy for Amavata. 4
  • 21. Conceptual Study HISTORICAL REVIEW An offshoot of Atharva and Rigveda, this science of medicine is withoutbeginning, but Ayurveda saw throughout many people, who organized it intobeautifully woven treatises, incorporating newer diseases and their treatmentwhich cropped up during their times. It is evident in the Samhitas that the mostprevalent and deadly diseases have been devoted separate chapters wereincluded as secondary diseases under the major category. Amavata might not have been widely prevalent and severely crippling asit was during the time of Madhava Nidana, as we see only passing referencesto the disease have been made in the Bruhatrayees. Madhava was the firstperson to devote separate chapter for Amavata. Thus the birth of this diseaseand its formative years can be glanced, starting from Vedic period.Vedic period (5000 BC to 1000 BC): Clear cut explanations of Amavata are not available in Vedic Samhitas,but disease caused by Kapha have been more or less described under themajor heading Balasa, but the diseases of joints are not included here. Few ofreferences indicating arthritic syndromes have been quoted by Sayana. Suchas Rapasi1: Disease arising due to sin (Rigveda) characterized by pain inmultiple joints also referred to as Papa. Yakshma and treatment with Jala, VayuYava, Kushta have been indicated. 5
  • 22. Conceptual Study Jayanya1: This disease is said to effect the bones cervical vertebraeand arise from women through Sanga. Whether the disease refers torheumatoid arthritis is still not clear. Grahi1 (Rigveda and Atharvaveda): This has been described as thedisease of joints but characteristic features have not been clearly mentioned.Treatment of this disease with Dashavruksha has been mentioned. Vatikrut1: This disease has been described as a serious ailment causedby Vata and treatment with Pippali and Vishanashaka has been mentioned. Sandhivikruti1 (Atharvaveda): This disorder is caused by Sleshma andcan be treated with prayers.Samhita period (1000 BC TO 600 AD): Charaka Samhita: Charaka has described in detail Ama and AmaPradoshaja Vikara and their treatment with Langhana and Ullekhana.2 Charaka had described treatment for Amavata while dealing withAvarana Chikitsa in Vatavyadhi3 which indicate Pramehahara and MedoharaVidhi. Amavata finds a mention in the list of therapeutic indication of KamsaHareetaki4 in Shwayathu Chikitsa and Vishaladi Phanda in Pandu Chikitsa.5 The treatment of Shariragata Ama in Grahani Chikitsa by Charaka6 issimilar to the description of Amavata Chikitsa by Bhava Mishra i.e. Langhana, 6
  • 23. Conceptual StudyPachana and oral administration of Panchakola Phanta7, same is the case withAmavata Chikitsa of Chakrapani in Chakradatta7. Sushruta Samhita: The description of Amavata in Sushruta Samhita isconspicuous by its absence. Bhela Samhita: The tenth chapter in Sutra Sthana deals with AmaPradosha. This description has some resemblance with that of Amavata. Harita Samhita: A complete chapter on Amavata finds a mention inHarita Samhita9. The classification of Amavata is quite unique and not followedby any of the later works in this field. Anjana Nidana: This work is claimed to be written by AcharyaAgnivesha, contains detailed description about etiology, premonitory symptoms,clinical manifestations, complications.Sangraha Kala (600AD-1600AD): Astanga Sangraha and Astanga Hridaya have ignored the diseasethough the word Amavata is included in the therapeutic index of compoundsVatsakadi Yoga10 and Vyoshadi yoga10. Madhava Nidana11: Madhavakara accorded this disease the status of aindependent disease and has dealt the topic threadbare. Chakradutta: Chakrapanidutta has described the treatment forAmavata8. 7
  • 24. Conceptual Study Vangasena12 and Vrinda Madhava followed Madhava with few additionsin the treatment aspect. Works like Bhava Prakasha13, Yogaratnakara14 andBhaishajya Ratnavali15 have only corroborated the descriptions with additionalprinciples of treatment.Adhunika Kala (1600AD onwards): Mahopadhyaya Acharya Gananath Sen has coined the term Rasavatafor Amavata. In Yoga Shastra the practice of Shushka Basti for improving Jatharagniand treating Amavata has been mentioned16. Y.N.Upadhyaya (1955) hascorelated the disease with rheumatoid arthritis. Later research workers haveagreed with Y.N.Upadhyaya.Modern History of Rheumatoid Arthritis:17 First Century AD: The rheumatoid/rheumatology is derived from the root‘Rheuma’, which refers to a substance that flows and probably was derivedfrom phlegm, an ancient primary humor, which was believed to originate frombrain and flow to various parts of the body causing ailments.1642 A.D.: The word rheumatism is introduced into the literature by the Frenchphysician Dr.G.Baillou who emphasized that arthritis could be a systemicdisorder. 8
  • 25. Conceptual Study1800 A.D.: Landre Baervier a physician from Salta Petruver in Paris, seemed tohave described the disease for the first time he called it Gartte AsthaniquePrimitivae.1857 A.D.: Sir Garrod proposed the name Rheumatoid Arthritis, Bannatynealso in 1959 published his pathological observations on the disease but hecould differentiate it from Osteoarthritis only in his later edition.1928 A.D.: The American committee for the control of rheumatism isestablished in U.S. by Dr.R.Pemberton, renamed American Association for thestudy and control of rheumatic disease (1934), then American RheumatismAssociation (1937) and finally American college of Rheumatology (ACR) (1988).1940 A.D.: The terms Rheumatology and Rheumatologist are first coined byDrs. Hollander and Comroe respectively.1948 A.D.: Roses identified some criteria for diagnosis of RA.1958 A.D.: American Rheumatic Association suggested uniform criteria fordiagnosis.1987 A.D.: The criteria were revised. In the beginning it was thought to be an infective condition especially inearly 20th century. French scientists thought it to be due to tuberculosis. 9
  • 26. Conceptual Study Hench and Kendell introduced steroids in the management ofrheumatoid arthritis described paediatric onset, juvenile RA in 1896. Later FeltyA.R. described Felty’s syndrome. Recent advancement in immunology have opened new vistas in themanagement of RA. Unfortunately till date the etiology of RA is unknown thepathogenesis is speculative, the treatment is only palliative and there is no cureto this disease. 10
  • 27. HistoryREFERENCES: 1. History of Indian Medicine. P.V.Sharma 2. C.S.Vi. 2/13 3. C.S.Chi. 28/195 4. C.S.Chi. 12/51, 52 5. C.S.Chi. 16/162 6. C.S.Chi. 15/75-80 7. B.P.Madya.Kha. Amavata, Chi./14-16 8. Chakradutta 25/1 9. H.S.Tri.Stha. 21 10. A.H.Chi. 21/47 11. M.N. 25 12. Vang. Amavata Rogadhikara 13. B.P. 26 14. Yr.Po. Amavata Chikitsa 15. B.R. 29 16. Gheranda Samhita 1/49 17. Rheumatology Secrets.
  • 28. Conceptual Study AMAVATA In our classics depending upon the permutation and combination ofDoshas, involved Dhatus, Vedana, Adishtana, Avayava, Gati, speceficsymptoms and so on, naming of the disease is done. The disease Amavata is named after the involvement of pathologicalfactors – Ama and Vata. These two are the central phenomenon of the disease.Vyutpatti of Amavata:1. Amam Cha Vatam Cha Amavatam:1 The word Amavata comprises of twomeaningful terms Ama and Vata which form the pathogenic basis of thedisease.2. Amena Sahito Vata Amavata:2 This derivation highlights the propulsion ofAma by Vata to produce Amavata.3. Amo Apaaka Hetuh Vataha Swanaama Khyaata Rogavisheshaha:3 Thatwhich is the result of improper digestion is Ama and with Vata the disease ispopularly known as Amavata.Definition: Yugapath Kupithavantaha Trikasandhi Praveshakau Stabdham Cha Kuruthe Gatramamavathaha Sa Uchyate4 Amavata is a condition where Stabdhata of the body occurs due tolodging of vitiated Ama and Vata in the Trika Sandhi. 11
  • 29. Conceptual Study From the above definition it is clear that for well understanding of thedisease Amavata, it is necessary to know the role of Ama and Vata in detail.AMA: The first twin of the pathological duo of Amavata, Ama is the root causeof all Vikaras more so in Amavata and it prompts a detailed study as discussedbelow.Etymology:1. “Am+Nich”: ‘Am’ Dhathu with ‘Nich’ Pratyaya constitutes the word Ama.72. Amyate Gamyate Pakadyartham Iti Amah:7 The substance which goes intothe process of digestion is Ama.3. Amyate Ishath Pachyathe:3 It means substance which is incompletelydigested or uncooked is Ama.4. Amyate Peedyate Srotas Samooho Anena Iti Ama:7 Substance which harmsa group of Srotas is Ama. This etymology of Ama is nearer to the diseaseAmavata.Definition of Ama: In Samhitas various definitions of Ama are available. Some of them are:1. Usmano Alpa Balatvena Dhatumadyamapachitam Dushtam Amashaya Gatam Rasamamam Prachakshyate8 Due to hypo-functioning of Ushma (Agni), the first Dhatu - the Rasa isnot properly formed; instead the Annarasa undergoes Fermentation or 12
  • 30. Conceptual Studyputrefaction (Dushta) and remains in Amashaya. It is this state of Rasa which isspoken of as Ama.2. Amasayasthaha Kayagnerdourbalyadavipachita Adya Ahara Dhathuryaha Sa Ama Iti Keerthithaha9 This quotation gives the same meaning as above.3. Avipakvam Asamyuktam Dourgandhyam Bahu Picchilam Sadanam Sarvagatranam Amam Ityabhideeyate9 The substance which has not undergone Vipaka giving rise to foulsmelling and slimy substance causing Gatra Stabdhata in the body is termed asAma.4. Aharasya Rasaha Shesho Yo Na Pakvo Agni Laghavat Samoolam Sarvaroganam Ama Ityabhideeyate9 Because of Mandagni, the residue of Ahara Rasa which is immature,forming the root cause of all diseases is labeled as Ama.5. Amam Anna Rasam Kechit Kechit Malasanchayam Prathamam Dosha Dushtim Cha Kechit Amam Prachakshate9 Here, the 3 different opinions about Ama are compiled by VijayaRakshita. First view is about the improperly digested food and the seconddescribes the accumulation of Malas in the different parts of the body.According to the third view, the first stage of Dosha Dushti is Ama.9 13
  • 31. Conceptual StudyETIOLOGY OF AMA: The causative factors of Ama are described detailed in CharakaSamhita10,11. These can be classified into Aharaja, Viharaja, Manasika andAnya Hetuja.Aharaja Hetu: Abhojana (not taking food), Atibhojana (excessive consumption of food)Ajeerna Bhojana (taking food before the previous food gets digested), AsatmyaBhojana (taking unwholesome food), Viruddha Bhojana (simultaneousconsumption of food having antagonistic properties). Consumption of Dwishta(unpalatable), Ashuchi Ahaara (unclean food), Rooksha, Sheeta, Shushka,Vishtambhi Vidahi Bhojana.Viharaja Hetu: Improper administration of Samshodhana and Snehana, VegaVidharana, Prajaagara and Dukhashayya (sleeping on uneven mattress) canalso initiate production of Ama.Manasika Hetu: Food consumed by a person in the state of Bhaya, Krodha, Shoka alsoleads to Ama Utpatti.Anya Hetu: Desha, Kaala, Rutuvaishamya, Vyaadhikarshana are mentioned as thecausative factors for Ama. 14
  • 32. Conceptual StudyLAKSHANAS OF AMA:12 The following explains the generalized symptoms with theiretiopathogenesis of manifestation which may be later modified by individualDoshas to show its specific presentations. Symptoms Etiopathogenesis Srotodushti Picchila and Snigdha Guna of Ama Balabramsha Mandagni causing lack of nutrients Gourava Snigdha, Picchila, Guru Gunas of Ama Alasya Snigdha, Picchila, Guru Gunas of Ama Malasanga Disturbance to Vata by Srotorodha Anila moodhata Disturbance to Vata by Srotorodha Apakti The qualities of Ama in turn leads to Agnimandya forming a vicious cycle Nishteeva Madagni causing Kaphotklesha Aruchi As a result of Ajeerna Klama Due to Dhatvagnimandya Above said symptoms are the general symptoms produced by Ama.Further, when this Ama comes in contact with Dosha, Dushya and Mala it istermed as Sama Dosha, Sama Dushya and Sama Mala. Assessment of Sama-Nirama is very much helpful for the treatment. 15
  • 33. Conceptual StudySAAMA DOSHA LAKSHANAS:5 If Ama combines with the Vayu then it gives rise to Vibandha(constipation), Mandagni (impaired digestion), Stambha (stiffness), AntraKujana (gurgling sound). Further, Vedana (pain), Shopha (edema), Nistoda (pinprick sensation) gradually affects the body parts one after the other. TheLakshanas will aggravate during morning hours, night hours, during cloudydays, and by Snehana. Sama Pitta is durgandhayukta, Amlarasa, Harita-shyavaVarna and is Guru Sama Kapha is Durgandhayukta, Avila, Tantula, there bysticks to Kanta Pradesha, prevents Udgara.NIRAMA DOSHA LAKSHANAS:5 Nirama Vayu shows Alpa Vedana, Nirvibandha and has Ruksha andVishada qualities, Vedana subsides on Snehana. Nirama Pitta is of Tamra orPeeta Varna, Ushna, Katu Rasa, Sara, Vigandha and improves the Agni andRuchi. Nirama Kapha is Phenavat, Pindita, Nirgandhi and has Pandu Varna,Vaktra Shuddhi will be there as it comes out easily. Separate symptomatologyof Sama Dushya has not been mentioned as the manifestations are similar tothe Dhatu Pradoshaja Vikaras itself.CONCEPT OF AMA: In other words, Ama reflects the products of deranged homeostaticmechanisms in the body. This clogs the controlling centers and pathways ofnormal physiologic functions marking the beginning of pathogenesis in the formof Sammurcchana of Nidana, Dosha and Dushya. 16
  • 34. Conceptual Study In Ashtanga Hridaya Doshopakramaniya Adhyaya, Acharya Vagbhatahas described in length about the treatment of vitiated Doshas in the form ofVatasyopakrama, Pittasyopakrama, and Kaphasyopakrama. Later, he highlightsthe formation of Ama and its treatment. He has given equal importance to Ama,as that to Dosha. The presence or absence of Ama i.e. Sama Avastha andNirama Avastha decides the line of treatment of disease.5MECHANISM OF PRODUCTION OF AMA - A PERSPECTIVE:13Physiology: A normal homeostatic function involves input from the food, processingby the action of Agni at the levels of Amasaya, Mahabhoota and Dhatus,transformation of the raw materials in to the vital elements (Sara) consistentwith tissue compatibility and waste products (Kitta or Malas) warrantingexpulsion. This process affects the nourishment of Dhatus, development andmaintenance of Vyadhikshamatva (the capacity of the body to resist the diseaseonslaught) initiated by Kshut (appetite), Trit (thirst) and Malavisarjana(excretion). Hence, the total body homeostasis is the augmented effect of non-defective functioning of the multiple organizations called Srotases. Each Srotashas a feeding point, a target point, a controlling center (Srotomula) and apathway (Srotas) and its function is appropriate transformation of the input rawmaterial in to a finished product with elimination of the waste product, effectedby the transformative principle Agni. 17
  • 35. Conceptual StudyPathology: The Vikara or Dhatu Vaishamya is hence a defective transformation,giving rise to a morbid finished product. The cause for which may exist in theraw material provided, the Srotomula, the Srotas or in the target tissue, in thebackdrop of impaired Vyadhikshamatva, effected by vitiated Agni and inflictedby Doshas. The resulting incompletely transformed product or Ama exhibits certaincharacteristic features, it is neither suitable for absorption nor is the bodycapable of excreting it. It is toxic and hence hinders the normal functions of theSrotases. The severity of morbidity is directly proportional to its accumulation.LEVELS OF EXISTENCE OF AMA: As mentioned above, the Ama exists at three levels in the body.A) Ama at Jatharagni level: Amashaya is the substratum of Jatharagni, whenthe vitiated Agni acts upon the Ahara, it fails to completely transform Ahara intonourishing moieties. The resulting Ahara Rasa is a mixture of formed andunformed elements called Ama, which is thrown out of the Amashaya throughthe Urdhwamarga by the Chardi (vomiting) and through the Adhomarga(diarrhoea), or it may get displaced into the Grahani to remain stagnant. Due toprolonged stagnation, it may assume the properties of Visha. Further, Ama mayassociate with the Doshas, Dhatus and Malas after getting absorbed fromAmashaya and manifest symptoms related with each of them. Dietetic indiscretions and emotional stresses may between them impairthe functioning of the neurohumoral mechanisms responsible for ensuring 18
  • 36. Conceptual Studyproper secretion of the digestive juices, the disturbances of the pH in thegastro-intestinal environment and more often sluggish and sometime hyper-motility of the stomach and intestine, thus leading to Shuktata or Shuktapakawhere food will be Avipakva, Asamyukta, Bahupicchila and Durgandha, due tofermentation and putrefaction of the carbohydrate, fat and protein components.Thus causes the toxic state - Visharupatvam. This pathogenesis may cause the following metabolic disturbances • Toxic states: 1. Intermediate toxic byproducts of metabolism 2. Superadded microbial action • Malnutritional statesIntermediate toxic by products of metabolism: It is clear from the texts thatSama Ahara Rasa induces the production of various deranged metabolites like, i. Sama Dosha: In Avasthapaka, there will be Udeerana of the Doshas i.e. Madhura Avasthapaka – Kapha (Amashaya), Amla Avasthapaka – Pitta (Pittashaya) Katu Avasthapaka – Vata (Pakvashaya) But, due to Apakva Ahara produced by Mandagni, there will beUdeerana of Dushita Dosha called as Samadosha. Further in Nishthapaka, dueto affliction of Rasa and Rakta Dhatu, there will be further increase of vitiatedKapha and Pitta in the form of Mala thus contributing to Sama Dosha. 19
  • 37. Conceptual Study ii. Bhutagni and Dhatvagni Mandya: Jatharagnimandya will lead to Bhutagni and Dhatvagni Mandya also. Jatharagni is the Poshaka to the different Agni of the body, but Bhutagni and Dhatvagni can even get vitiated independently i.e. irrespective of Jatharagnimandya. Apakva Ahara from Avasthapaka when gets treated by Manda Bhutagni and Dhatvagni further causes Vikrita or Dushita Nishthapaka. a) Sama Dhatu: With affliction of both Avastha and Nishthapaka, the Dhatu Poshaka Rasa produced is Vikruta. Thus, with production of Sama Rasa Dhatu, succeeding Dhatu will also get vitiated producing Dhatu Pradoshaja Vikara. Sama Dhatu Utpatti is due to Bhutagni and Dhatvagni Mandya but it can even be independent of Jatharagni status.14 b) Sama Mala: The word Mala includes 2 entities. • Mala of Ahara Rasa i.e. Pureesha, Mutra and Sweda and also the other Dhatugata Malas. • Dushita Dosha and Dhatu are also called MalaSuperadded microbial action: Toxins in the intestines in the present days aregreatly attributed to the action of different microbes, thus leading to differentmanifestations like: • Infective gastro-enteritis • Toxic gastro-enteritis • Botulism 20
  • 38. Conceptual Study Intestinal flora in the human body exists in the state of symbiosis; thesecan be very well compared with Sahaja Krimi. Chakrapanidatta15 explains themas the one which exists within the body without causing diseases. Intestinalflora breaks the complex molecule which are not broken by the body,metabolises them into simple molecules by 2 kinds of actions. They areFermentation and Putrefaction. Putrefaction is similar to fermentation but it specifically refers toconversion of protein substances to smaller molecules with the liberation ofvarious gases viz. Indol, Skatole, Phenol, Hydrogen sulphate and Ammonia thatare characteristically pungent in odour. Fermentation is related to theCarbohydrate and fat metabolism by the microbes. Microbe’s metabolismreleases few of the waste products vital for the body like Vit. B groups. Among these microbes, there are some in borderline populations whichunder circumstances become parasitic. There are other groups of virulentorganisms which invade body through food and drinks, producing abnormalitiesin the body. e.g.: Salmonella, Staphylococcus, B. botulinus, B. typhosus andcoma bacillus of Koch. Hence, the normal food metabolism also includes themetabolism by Intestinal flora (Sahaja Krimi). The following are circumstances which make the body susceptible to theinfection. • Irradiation, metabolic abnormalities, emotional stress, overstrain, intense treatment with anti-microbial agents 21
  • 39. Conceptual Study • Tissue produces an anti-microbial substance called Properdin. It has been shown that a low concentration of this substance in an area coincides with the highest susceptibility to the invasion of the tissue even by otherwise friendly intestinal flora causing bacteremia. • Experiments carried out at the Rockfeller institute and other research centers in U.S.A. have shown that susceptibility to microbial disease can be caused by manipulation of metabolism. e.g.: with such simple measures as temporary deprivation of food or feeding an unbalanced diet rich in Citrate. The resistance was again seen to have been restored back to normal within 2-3 days by the correction of nutritional errors. • But in case of epidemics and pandemics the microbes strike human irrespective of body strength, constitution and other predisposing factors. Interestingly, this phenomenon is observed when a microbe is newly introduced in a susceptible population which serves as a virgin soil. Ama is the immediate cause of most human affliction, exposure todisease causing microbes results in the disease only in those people whereinternal conditions are ripe for colonization. Louis Pasteur and Claude Bernardargued for years over the primacy of infective agents versus internal conditions,and it was only on his deathbed that Pasteur finally admitted that Bernard wasright and that the milieu interior is more important than exposure to a pathogen.This is especially true of diseases in which no pathogen can be detected.6 22
  • 40. Conceptual Study Hence, different microbial infection occur in the body when it is madesusceptible by predisposing factors like metabolic abnormalities, emotionalstress, overstrain and other Agnimandyakara and Amotpattikara Nidana.Malnutritional states: In chronic disorders, due to Agnimandya or Amotpatti, there will bepredominant manifestation of Dhatukshaya as it is told in Vatavyadhi contextthat the Avarana will cause Rasadi Dhatu Kshaya. Depending on the speed ofmanifestation, disease can be • Acute • Sub-acute and Chronic Acute conditions include Visuchika, Jwara, Atisara, Pravahika and so on.Sub-acute and chronic conditions include Grahani Dosha, Udara roga, Pandu,Amavata, Prameha and so on.B) Dhatvagni level: The Ama at Dhatvagni level occurs due to vitiated Dhatvagni first as aresult of a direct influence from Jatharagni as the Dhatvagnis are derivatives ofJatharagni and Jatharagni hyperfunction or hypofunction results in respectivederangements of Dhatvagnis too16. Secondly, as a result of Dhatvagnimalfunction independent of Jatharagni. The hypofunction of Dhatvagni leads tomorbid increase of the Dhatu involved and hyperfunction leads to its morbiddecrease. The Ama hence formed gets associated with these morbid Dhatus to 23
  • 41. Conceptual Studyform Sama Dhatus resulting in manifestation of symptoms explained underDhatupradoshaja Vikara17.C) Bhutagni level: The Ama at the Bhutagni level occurs as a result of Bhutagnimandya, themechanism of formation is similar to that mentioned under Dhatvagni level. Thesymptoms produced are Shosha, Vrana, Vidradhi and similar diseases18.Ama as a result of Malasanchaya:9 The Malas (waste products) produced at various levels in the body, whenaccumulates beyond tolerable limits also constitutes Ama. The Mutra andPureesha are the Malas of Ahara, Kapha that of Rasa, Pitta of Rakta, Vasa andKhamala of Mamsa, Sweda of Medas, Loma, Asthi and Tvacha Sneha andAkshi Vit of Majja19. The Shukra is the essence of all Dhatus and it does nothave any Malas. The excessive accumulation of these Malas (Mala Sanchaya)therefore gets to be called Ama as they are harmful to the normal physiology ofthe body.Production of Ama independent of influence of Agni – as a result of DoshaAnyonya Sammurcchana: Strangely, the Doshas exist in the body in an equilibrium of mutuallyparadoxical Gunas of Doshas; this equilibrium is inherent and compatible withthe normal bodily functions. This has been called as “Sahajasatmya”32 byCharaka. This unique coexistence has been compared to the existence of fatalpoison in a serpent without harming it, by Vagbhata. Nevertheless this 24
  • 42. Conceptual Studyequilibrium sometimes may get disturbed due to excessive aggravation ofDoshas, and the Doshas start affecting each others’ Gunas resulting in theproduction of Ama. This process is on the analogy of the production of toxicmaterial when the grains like Kodrava are kept in water for a long time, thisAma is highly virulent and can cause incurable diseases. The schematicrepresentation of the same is given in the chart no. 1. An interesting feature of this concept is its close resemblance to theconcept of auto immunity in the modern parlance. The Major HistocompatibilityComplex determined by Human Leukocyte Antigens marks the surface proteinsof all the cells of the body. This helps the T cells (responsible for Cell mediatedimmunity) to recognize the self antigens from the non-self. When thismechanism fails, the immune system starts secreting antibodies against body’sself proteins producing crippling and fatal diseases. They are called Autoimmune diseases and Rheumatoid arthritis is one among them. 25
  • 43. Conceptual StudyVATA: The second of the duo Vibhu as it is called Vata in its Prakruta Avasthasustains the human body. When it becomes Vimarga is responsible for fatalailments. The pathogenic sequence of Vatic vitiation requires a comprehensivebackground as discussed below.Nirukti:20 The Nirukti of Vata is as follows, the term Vata is derived from the root“Va” with “Tan” Pratyaya, it forms the word Vata. The root Vata summerises theessential Karma of Vata-Gati and Gandhana.Guna: Ruksha, Sheeta, Laghu, Sukshma, Chala, Vishada, Daruna and Khara.21Bheda: There are five classification of Vata Dosha based on the location andfunction. They are Prana, Udana, Samana, Vyana and Apana.22Karma:23 Vata Dosha has complex psycho somatic integrative function. They are:Tantra Yantra Dhara (upholds the structure and function of body), ChestaPravartaka (motivates the movements), Praneta Niyanta Cha Manasa(controller and conductor of Mana), Sarvendriyanam Udyojaka (stimulates allsensory function), Sarvendriya Artha Abhivoda (carrier of all sensory impulses),Dhatu Vyoohakara (integrator of body elements), Shareera Sandhanakara 26
  • 44. Conceptual Study(integrates of bodily structure and function), Vak Pravartaka (stimulator ofspeech), Shabda Sparsha Prabrith (cause of feeling and audition), SrotaSparshayoho mula (primary source of auditory and tactile sensation), HarshaUtsahayoho Yoni (originator of excitement and animation), Agni Sameerana(stimulator of Agni), Dosha-Samshoshana (desicator of morbid Dosha), MalaKshepta (cleanses the body channels), Garbha Akriti Karta (gives shape to thefetus), Ayushya Anuvritti (sustainer of life).Importance: Following opinions shows the importance and supremacy of Vata: Charaka opines that the Vayu in its abode with unimpaired functions inits normalcy, facilitates the Ayus of an individual to be hundred years.24 The Pitta, Kapha, Mala and Dhatus are inert (Pangu) until mobilized byVata, which takes them to get localized in specific location and cause disease,hence Vata controls all other Doshas Dhatus and Malas.25 Vata, Pitta and Kapha are circulating all over the body, Vata the subtleamong them provokes Kapha and Pitta and causes them to lodge in variousplaces from where the disease originates. The Pitta and Kapha hence occludesthe channels of Vata, thus vitiating Vata; it also gets vitiated by diminution oftissue elements which may be an independent cause or an effect of occlusion.26Etiological factors of vitiation of Vata: Etiological factors which vitiate Vata can be brought under Aharaja,Viharaja, Manasika and Anya Hetuja. 27
  • 45. Conceptual StudyAhara: Ruksha Ahara (dry food) Sheeta Ahara (cold foods) Alpa Ahara(subnormal quantity), Laghu Ahara (light food).27Vihara: Vyavaya (excessive indulgence in sex), Atiprajagara (night vigil),Vishama Upachara (improper nourishment), Rakta Atisravana (removing Doshaand Rakta in excess), Langhana (excessive fasting), Plavana (excessiveswimming), Atyadva (walking excessively),27 Atichesta (excessive improperbody movement), Dukhashayya Asana (uneven mattresses), Divaswapna (daysleep), Abhighata (trauma), Marmaghata (injury to vital organs), Patana (falls).28Manasika Karanas: Includes Chinta (depressive episode), Shoka (depression), Krodha(excessive anger) and Bhaya (fear).28Anyahetuja: Dhatu Sankshaya (depletion of tissue elements) and Rogatikarshya(emaciation due to disease).28Symptoms of Vata Prakopa: Parva Sankocha (contractures), Stambha (immobolity), Asthi ParvaBheda (painful bones), Lomaharsha (piloerrection), Pralapa (irrelevant speech),Pani Prishta Shirograha (stiffness of hands, hip, joints of head), Kanja Pangu(disability of lower limbs), Kubjata (loss of normal lumbar curvature), Anga 28
  • 46. Conceptual StudyShosha (wasting), Anidrata (insomnia), Garbha Shukra Rajonasha (disease ofreproductory system), Spandana (involuntary movements), Gatra Suptata(sensory system abnormality), Shiro Hundana (disorders of scalp), NasaHundana (disorders of olfaction), Jatru Hundana (cervical ankylosis), GrivaHundana (stiffness of neck), Moha (altered consciousness), Alasya (lethargy)and Akshepa (convulsive fits).29Symptoms of Vata Kshaya: Kshaya of Vata leads to Manda Cheshta (decreased activity), Alpavak(decreased speech), Apraharsha (erectile dysfunction) and Mudha Samjnyata(altered consciousness).30Chikitsa: Sneha (fatty substance), Swadu, Amla Lavana, Ushna Bhojana (food ofsweet, saline and hot properties), Paishtika or Goudika (types of Madhya),Abhyanga (external oleation), Mrudu Samshodana (light eliminative therapies),Mardana (massage), Veshtana (tying clothes), Trasana (supportivepsychotherapy), Seka (stream of oil over the body) and Snigda Ushna Basti(enemas having Snigda Ushna properties).31 In Amavata, Ama formed will be circulated through out the body byvitiated Vata, this Sama Vata is responsible for vitiating other two Doshas. Sounderstanding of Vata is essential in treating Amavata. 29
  • 47. Conceptual StudyREFERENCES: 1. M.N. 25/2-5 2. M.N. 25/2 3. S.K.D. 4. M.N. 25/5 5. A.H.Su. 13/27-28 6. Ayurveda Life Health and Longevity, RE Svoboda, Pg.162 7. A.K. 8. A.H.Su. 13/25 9. M.N. 25/1-5, Madhu 10. C.S.Chi. 15/42-43 11. C.S.Vi. 2/8 12. A.H.Su. 13/23-24 13. Introduction to Kaya Chikitsa, Dwarakanath 14. S.S.Su. 15/13 15. C.S.Vi. 7/9 16. C.S.Chi. 15/39 17. C.S.Su. 28/8-22 18. Atanadarpana, M.N. 6/22 19. C.S.Chi. 15/18-19 20. S.S.Su. 21/5 21. C.S.Su. 12/4 22. S.S.Ni. 1/11-12
  • 48. Conceptual Study23. C.S.Su. 12/824. C.S.Chi. 28/425. Sh.S.Po.Kha. 5/2526. C.S.Chi. 28/60, 6127. S.S.Su. 21/1928. C.S.Chi. 28/15-1829. C.S.Chi. 28/20-2330. S.S.Su. 15/731. A.Hr.Su. 13/1-332. C.S.Chi. 26/293
  • 49. Conceptual Study NIDANA The word creation is a neologue. It should be actually called asevolution. Similarly destruction is called involution, because something cancome from something not from nothing. Circumstances favoring the evolution of a existence is the cause. Theeffect can be useful or harmful. Man’s indulgence governs the good or badeffects he has to enjoy. If his indulgence is Hita, leads to peace. If it is Ahita,leads to commotion. Besides, the contents of ahita are highly disease specific.Though being common to quite a few diseases, they lead only to Amavata. Identifying the causative factors and understanding the role of thesecausative factors in the manifestation of the disease is utmost important tomake a proper diagnosis, to predict prognosis and to plan treatment. Invariably two factors are responsible for the manifestation of the diseaseAmavata. As the name indicates, Ama and Vata are those two factors. TheAnjana Nidana author opines Ama and Vata get vitiated due to their ownrespective causes to promote disease. Hence, individual etiological factorsresponsible for the vitiation of Vata and those etiological factors which produceAma may also be considered as etiological factors of Amavata.Madhavakara has explained following Nidanas for Amavata.1 1. Viruddha Ahara (incompatible diet) 2. Viruddha Cheshta (Erroneous habit) 30
  • 50. Conceptual Study 3. Mandagni (diminished digestive fire) 4. Nischalata (Sedentary habits) 5. Vyayama soon after Snigdha Ahara. Besides this, Harita opines that a person consuming Guru Ahara, KandaShaka (tubers) in excess and indulging in excessive Vyavaya is the Nidana ofAmavata.2 To sum up, the causative factors of Amavata can briefly be classified into two. 1) Viruddha Ahara- unwholesome diet. 2) Viruddha Cheshta- erroneous habit. Now it is very important to know what is Viruddha, as Viruddha itself isthe root cause of the disease Amavata. The factors which cause DoshaUtklesha (vitiation) but do not have the capacity to eliminate those Doshas outof the body are considered as Viruddha.3 Charaka has elaborately mentioned regarding Viruddha Ahara andcategorized these into 18 types.4 They are Desa (Habitat) Viruddha, Kala(season) Viruddha, Agni (digestive power) Viruddha, Matra (dose) Viruddha,Satmya (compatibility) Viruddha, Dosha Viruddha, Samskara (processing)Viruddha, Veerya (potency) Viruddha, Koshta (bowels) Viruddha, Parihara(proscription) Viruddha, Avastha (state of health) Viruddha, Krama (order)Viruddha, Upachara (prescription) Viruddha, Paka (cooking) Viruddha, 31
  • 51. Conceptual StudySamyoga (combination) Viruddha, Hrit (palatability) Viruddha, Sampath (quality)Viruddha, Vidhi (rules of intake) Viruddha. Besides Charaka also considers the Brashta Niyama of Ashta VidhaAhara Vidhi Vishesha Ayatana5 as unwholesome. These Ashta Vidha AharaVidhi Vishesha Ayatana are Prakriti (Natural food habits), Karana (Method ofprocessing), Samyoga (Combination), Rashi (Quantity), Desha (Habitat), Kala(Time), Upayoga Samstha (Rules governing intake of food), Upayoktru (Theperson who is taking the food). Viruddha Cheshta includes a wide variety of causative factors. They areconsumption of Snigdha Ahara and doing Vyayama immediately, SheetoshnaVyatyasa (alternative use of Sheeta and Ushna), use of Sheetodaka at onceduring Bhaya Shrama and so on, Vega Vidharana (suppression of naturalurges), Vega Udeerana (provoking of natural urges), Diva Swapna (day sleep),Ratri Jagarana (night vigil), Sahasa (act beyond capacity), Karma Kalatipata(avoidance of medication). The causative factors of a disease operate in varied patterns in the bodyto cause the disease. This depends upon the level of predisposition, in otherwords the extent to which the environment is made favorable for the interactionof Nidana, Dosha and Dushya.6 The capacity of the body to resist this interaction is called Vikara VighataBhava or Pratyaneeka Bala. This Bala differs from person to person. That is 32
  • 52. Conceptual Studywhy we see that inspite of exposure to Nidanas, some people do not developthe disease and some develop severe disease with negligible exposure. Furtherit is also seen that a single causative factor leads to development of manydiseases and many Nidanas are needed for the manifestation of a singledisease.7 Hence, not withstanding the list of Nidanas implicated to cause thedisease Amavata, it is ultimately the Vyadhikshamatva which renders a patientvulnerable. Thus Viruddha Ahara and Cheshta are accepted as the causative factorsof disease Amavata. But Viruddha Ahara and Viruddha Cheshta need notcause same disease in everyone i.e. all the unwholesome diet and erroneoushabits may not vitiate the same Dosha and also vitiation need not be of samegrade as every individual do not have the same Vyadhikshamatva (immunity).8Schematic representation of Nidana is given in the chart no. 2.Etiology of Rheumatoid Arthritis:10 The disease Amavata is best compared with Rheumatoid arthritis in themodern parlance.9 Rheumatoid arthritis (RA) is a chronic multisystem diseaseof unknown cause. It has been suggested that RA might be a manifestation ofthe response to an infectious agent in a genetically susceptible host. Becauseof the worldwide distribution of RA, it has been hypothesized that if an infectiousagent is involved, the organism must be ubiquitous. A number of possiblecausative agents have been suggested, including Mycoplasma, Epstein-Barr 33
  • 53. Conceptual Studyvirus (EBV), cytomegalovirus, parvovirus, and rubella virus, but convincingevidence that these or other infectious agents cause RA has not emerged. Theprocess by which an infectious agent might cause chronic inflammatory arthritiswith a characteristic distribution also remains a matter of controversy. Recentwork has focused on the possible role of "superantigens" produced by a numberof microorganisms, including staphylococci, streptococci and M. arthritidis.Superantigens are proteins with the capacity to bind to HLA-DR molecules andparticular Vb segments of the heterodimeric T cell receptor and stimulatespecific T cells expressing the Vb gene products. The role of superantigens inthe etiology of RA remains speculative. Of all the potential environmentaltriggers, the only one clearly associated with the development of RA is cigarettesmoking. Sero positive RA aggregates in families Genetic factors versus theirinteraction with environmental facilitators is unclear HLA DR4 is found in 70% ofcausascian sero positive patients compared to 25% of controls. Increasedrelative risk of 4-5 times for the DR4 positive persons, although a minority areaffected African Americans tend not to exhibit this predilection.11 34
  • 54. Conceptual StudyChart No. 1-Schematic representation of Nidana of Amavata: NIDANA Vataja nidana Amaja nidana Amavataja nidana Aharatah Aharatah Aharatah kashaya, tikta, Atimatra, Guru katu ruksha Ruksha, Sheeta Viruddha ahara laghu, sheeta, Shushka, Dvishta Shaka shushka shaaka Vishtambhi Katu ahara vallura, Vidahi, Aruchi Guru ahara uddalaka, kora Viruddha Mandagnikaraka dusha, shamaka, Akala annapana vishamashana, adhyashana Viharatah Viharatah ViharatahShareerika manasika Shareerika Manasika ViruddhaAtivyayama, ati shoka, Vegavarodha, Kama, Cheshta-prapatana, chinta, Viruddha Krodha, Nischalata,bhagna, bhaya, cheshta, Lobha, Moha, Vyayama,ratrijagarana, krodha, Ratri jagarana, Irshya, Hree, Mandagnivegadharana, Ayoga of Shoka, Mana, Karaka. kshobha,ativyavaya, Vamana, Udvegaraktati Virechana and Bhaya,sravana. Snehana Bhojana with these Upatapta manas.
  • 55. Conceptual StudyREFERENCES: 1. M.N. 25/1 2. H.S. 21/1, 2 3. A.Hr. 7/45 4. C.S.Su. 28/86-89 5. C.S.Vi. 1/21 6. C.S.Ni. 4/4 7. C.S.Ni. 8/24 8. C.S.Su. 28/7 9. Y.N. Upadhyaya 10. H.P.I.M., 14th edition, pg.1880 11. CIMS, 5Min, Clinical Assistance, pg.88
  • 56. Conceptual Study SAMPRAPTI The pathology of a disease is not always simple; rather it involvesvarious intricate and sequential mechanisms. This has to be unraveled for theproper understanding of the disease and then to plan successful treatment.Intricate mechanisms of the disease process are best understood by means ofSamprapti of the disease. As elaborated under the title Nidana it is clear that the illness Amavata isbasically caused by the Viruddha Ahara as well as Cheshta. More over thisphenomenon of Viruddha Ahara may not be similar in every patients rather it isindividual specific. This etiology of Viruddha Ahara in the form of Bahya Nidanais said to be incriminatory in three distinct ways ultimately resulting in theestablishment of the disease. On exposure to Viruddha Ahara it may causemorbidity of Dosha, impair the functioning of the Jataragni or else it may lead tothe formation of more virulent Amavisha.1Dosha Dushti: Consumption of Viruddha Ahara precipitates morbidity of Doshas.2 Dueto the deleterious effect of the Viruddha Ahara, any Dosha may get vitiated orelse any combination of the two Doshas or all the three together. These vitiatedDoshas in turn afflicting the specific Dushya manifests as illness, pertaining toAmavata. By the deleterious effect of the Viruddha Ahara, there occurs themorbidity of the Vata Dosha. The clinical manifestations like Anaha, Antrakuja,Vibandha, Sandhi Sula, Sandhi Jadyata etc are suggestive of vitiation of Vata 35
  • 57. Conceptual StudyDosha at different levels. By definition, this Viruddha Ahara only influences thegeneration of morbid Doshas, and is incapable of its removal from the body.Agni Mandya and Amotpatti: Intake of Viruddha Ahara has detrimental effect on the functioning of theJataragni. As mentioned by Acharya Charaka, intake of Viruddha Ahara leadsto Agnimandya which in turn generates the virulent Ama in the body.3 Invariableinvolvement of Ama is characteristic of the disease Amavata. Both Koshtagataas well as Shareeragata Ama are the hallmarks of the pathogenesis ofAmavata. Reduction in the Abhyavaharana Shakti and Jarana Shakti,symptoms like Praseka, Aruchi, Apakti, Malasanga and similar other symptomsare indicative of Koshtagata Ama5. Shareeragourava, Alasya, Klama, SandhiShotha, Staimitya are the other common clinical features of Amavatasuggestive of Shareeragata Ama5,6. Moreover, the symptom complex ofAmavata is more indicative of combined effect of Ama as well as morbid Vataand is popularly known as Samavata4 state. Progressive involvement of thejoints in the form of severe pain and swelling, worsening of the symptoms bythe application of the oil, more severity of the symptoms at the time of sunrise,as well as on appearance of the clouds in the sky4, all are the typical featuresindicative of Samavata state in the disease Amavata. The Ama and morbid Vata, stemming out from Amashaya circulates inthe whole body. The properties of the Samavata being similar to that of theKapha Dosha, Ama and morbid Vayu exhibits an affinity to get lodged in the 36
  • 58. Conceptual StudyKapha Sthana. More particularly the vitiated Vata Dosha along with Ama tend toget localized in the joint. With in the joint, these two pathological factorsundergo a pathological union with the naturally present Doshas in the joints. It issaid that by the interaction with the naturally present Doshas in the joint theAma and morbid Vata acquires further virulence and then manifests asAmavata. Here, the interaction with in the joint causes the generation ofAmavisha1. Perpetuation of the illness for a long duration destroying the jointsis analogous to the effect of Garavisha12 in the body. Progressive damage thatoccurs for long is very characteristic of Garavisha. Similarly the pathologicalinteraction between normal Doshas present in the joint and the morbid Vata aswell as Ama getting localized in the joint, is akin to the damaging effect of theGaravisha, and hence is named as Amavisha. Thus relating this to thecausation of the illness, indulgence of Viruddha Ahara ultimately culminates inthe generation of Amavisha. Similar to Garavisha, this Amavisha graduallycauses destruction of the body. Later, during the course of the disease,permanent destruction of the joints results in the Anga Sankocha8, Jadyata8,Anga Vaikalya10 etc, totally incapacitating the patients and restricting him to thebed.Dhatu Dushti: Deleterious effect of the Viruddha Ahara is not restricted to the Doshaand Agni, rather it badly influences the Dhatu even. This nature of the ViruddhaAhara is described as Dhatupratyanika13 effect. It is worth mentioning here thatthe Viruddha Ahara is considered as an etiology of Majjavaha Sroto Dushti14 37
  • 59. Conceptual Studyand the Mula of the Majjavaha Srotas17 being Asthi and Sandhi, this implies thedetrimental effect of the Viruddha Ahara on the Asthi and Sandhi wherein thedisease Amavata manifests. The symptoms like Sandhi Shotha, Sandhi Shoola,Bhedanavat Shoola in Asthi and Parva Pradesha, Mamsa Kshaya, SandhiSankocha etc. are suggestive of Asthimajja Gata Vata15 and Sandhi GataVata16 in the disease Amavata. So to say, the indulgence of Viruddha Ahara causes morbidity of VataDosha, generates the Ama, afflicts the Dhatu Asthi and Sandhi, and in all thepathology perpetuates and destructs the body in the form of Amavisha. Viruddha produces some alteration in the humoral activity of the bodyand results in the production of Ama. This Ama is antagonistic to the bodilytissues (Dhatu Virodhi). Effect of this may be rapid or gradual. Viruddha hasDhatu Virodhi Karma by way of producing Ama as a intermediate product incase of Amavata. Because of Dhatuvirodhi quality of Ama it can be correlatedwith autoimmunity in modern parlance. Madhavakara18 has explained the Samprapti of Amavata as follows inthe presence of Mandagni, if one is exposed to Nidana then Ama is formed inthe Amashaya along with vitiation of Vata Dosha. This Ama circulates in thebody propelled by the vitiated Vata exhibiting an affinity to get lodged in theShleshma Sthana i.e. Sandhi. Further, this circulating Ama in the Dhamanisinteract with the normally present Vata Pitta and Kapha Dosha giving rise tovariegated color to the virulent Ama. It becomes qualitatively heavy and 38
  • 60. Conceptual Studyviscous, facilitating Sroto Abhishyandana and Srotorodha. Alteration in theSrotas endures Sthana Samshraya leading to the manifestation of symptomslike Hrutgourava, Dourbalya, Sandhi Shotha and Shoola etc.11Samprapti Ghataka:Dosha: Vata predominant Tridosha.Dhatu: Rasa, Mamsa, Asthi, Majja.Upadhatu: Snayu, Sandhi.Srotas: Annavaha, Rasavaha, Asthivaha, Majjavaha, Udakavaha, Purishavaha, Mutravaha.Srotodushti: Sanga, Vimargagamana.Udbhavasthana: Amashaya, Pakvashaya.Adhishtana: SarvashareeraVyakta Sthana: Sarva Shareera more particularly SandhiAvayava: SandhiVyadhisvabhava: Chirakari.Roga Marga: MadhyamaPathogenesis of Rheumatoid Arthritis:19 In contemporary medical science, Amavata can be best correlated toRheumatoid Arthritis (Y.N.Upadhyaya). It is described as an autoimmunedisorder. The propagation of Rheumatoid Arthritis is an immunologicallymediated event, although the original initiating stimulus has not been clear. One 39
  • 61. Conceptual Studyview is that the inflammatory process in the tissue is driven by T4 helper cellsinfiltrating the synovium. Evidence for this includes, • The predominance of T4 cells in the synovium • The local production of lymphokines by these infiltrating T cells • Amelioration of the disease by removal of T cells by thoracic duct drainage or suppression of their function by total lymphoid irradiation Since T lymphocytes produce a variety of cytokines that promote B cellproliferation and differentiation into antibody forming cells. T cell activation mayalso produce local B cell stimulation. The resultant production ofimmunoglobulin is rheumatoid factor that can lead to immune complexformation. With consequent compliment activation there will be exacerbation ofinflammatory process by the production of anaphylatoxins and haemostaticfactors. This tissue inflammation is reminiscent of delayed type ofhypersensitivity reaction occurring in response to soluble antigens or microorganisms. It is how ever unclear that whether this represents a response topersistent exogenous antigens or to altered auto antigen such as collagen orimmunoglobulins.20 40
  • 62. Conceptual StudyChart No. 2-Schematic representation of Samprapti in the light ofKriyakalas: Nidana-Viruddha Sanchaya Vata Prakopa Agnimandya Dhatu Virodhi Prakopa Vata Dushti Ama (Koshta) Majjavaha Srotas Samavata Dosha Prasara Dhamani (Amavisha/Garavishatulya) Sthana Trika Sandhi Samshraya Saruja Shotha Vyakta (in multiple joints) Sankocha Adi Bheda Upadrava
  • 63. Conceptual StudyREFERENCES: 1. C.S.Chi. 15/44 2. A.H.Su. 7/45 3. C.S.Vi. 2/9 4. A.H.Su. 13/27 5. A.H.Su. 13/23,24 6. A.H.Su. 13/26 7. A.H.Su. 13/27 8. M.N. 25/7-10 9. H.S.Tri. 21/4 10. M.N. 25/7 11. A.H.Su. 7/29 12. A.S.Su. 9/7 13. C.S.Vi. 5/18 14. C.S.Chi. 28/33 15. S.S.Ni. 1/28 16. C.Vi. 5/8 17. M.N. 25/1 18. H.P.I.M. 14th edition, pg.1881 19. A.P.I. 5th edition, pg-1118
  • 64. Conceptual Study POORVA ROOPA Poorva Roopa are alarms signaling the onset of an ambush, like cloudsindicate the arrival of rain. They sometimes simulate the symptoms of actualdisease and sometimes not, but in any case they indicate occurrence of anailment. Though the Poorva Roopa of Amavata is not explained in the Samhitas,we can consider few of the Samanya Amavata Lakshanas as its Poorva Roopa.It is understood from Ayurvedic classics that some of the Poorva Roopa maycontinue as Samanya Lakshana of any disease.1 In Amavata before the onset of disease, Ama is formed. The symptomsproduced when Ama only gets involved with Vata before getting lodged in theShleshma Sthana, can be considered as Poorva Roopa. The SamanyaLakshanas2 of Amavata though not very disease specific to Amavata, likeAgnimandya, Aruchi, Angamarda and Gourava can be considered as PoorvaRoopa.Agnimandya: Nidana Sevana effects the normal functioning of Agni.Aruchi: Vitiation of Rasa Dhatu and Bodhaka Kapha impairs the functioning of Rasanendriya.Anga Marda: Inadequate nourishment of Dhatu and presence of Ama leads to feeling of aching pain in the body. 41
  • 65. Conceptual StudyGaurava: Ama and vitiated Kapha causes feeling of heaviness in the body. Also Sama Rasa and vitiated Kapha generates Hritgourava, i.e. subjective feeling of heaviness in chest. The production of Ama is the central phenomenon in Amavata, hence allthe Ama Lakshana can be considered as Poorva Roopa of this disease.Prodromals of Rheumatoid Arthritis: Onset of rheumatoid arthritis in approximately two thirds of patients isinsidiously with, fatigue anorexia, generalized weakness and vaguemusculoskeletal symptoms until the appearance of synovitis becomes apparent.This prodrome may persist for weeks or months and defy diagnosis.3REFERENCES: 1. A.H.Ni. 1/5 2. M.N. 25/6 3. H.P.I.M. 14th edition, pg.1883 42
  • 66. Conceptual StudyChart No. 3-Schematic representation of the evolution of Poorvaroopas: Agnimandya Nidana-Viruddha Vata Prakopa Agnimandya Dhatu Virodhi Aruchi Vata Dushti Ama (Koshta) Majjavaha Srotas Angamarda Samavata Dosha Dhamani (Amavisha/Garavishatulya) Trika Sandhi Gaurava Saruja Shotha (in multiple joints) Sankocha Adi Upadrava
  • 67. Conceptual Study BHEDA For a better understanding, the disease Amavata can be broadlyclassified into two categories, the first, on the basis of clinical manifestation andthe second, on the basis of prognosis, with sub classification existing in eachcategory. The details are as follows;1. Based on clinical manifestations it is divided into:A) Dosha Bhedena: In Amavata, the Pradhana Dosha is invariably Vata. Due to somesupportive factors other two Doshas also get involved; accordingly, we canobserve the symptoms. Madhavakara has explained seven type of Amavata onthe basis of Dosha Pradhanyata1. They are as follows: 1. Vataja: In Vataja type of Amavata, Shoola will be the predominant symptom. This can be well correlated to the Sheeta and Chala Guna of Vayu. In Amavata, the path of the Vata is obstructed due to Ama. Hence the characteristics feature of Vata-shoola will be more. 2. Pittaja: Symptoms Raga and Daha are indicative of Pittaja Amavata. These are due to the Teekshna, Ushna Guna of Pitta. 3. Kaphaja: Symptoms Sthaimitya, Guruta, Kandu indicate the dominance of Kapha. Sthaimitya is produced due to Picchila, Sthira and Sheeta Guna of vitiated Kapha. As Ama and Kapha have similar qualities, Guruta and Kandu are seen in the Sandhis. 43
  • 68. Conceptual Study 4. Vatapittaja: Symptoms of Vata and Pitta are seen together in Vatapittaja type of Amavata. 5. Vatakapha: Here the symptoms of Vata and Kapha are seen together. 6. Pittakapha: Here the symptoms of Pitta and Kapha predominate. 7. Sannipatika: In Sannipatika type of Amavata, symptoms of all the three Doshas are profoundly seen.B) Avastha Bhedena:2 Based on the different stages of the disease, Madhavakara has broadlyclassified Amavata into two varieties they are, 1. Samanya 2. Pravruddha. The symptomatology of this has been discussed in chapter Roopa.C) Lakshana Bhedena:3 Acharya Harita’s classification of Amavata has been unique. Accordingto him, Amavata is of four types. 1. Vishtambhi: This type of Amavata presents with Shareera Guruta, Adhmana, and Basti Shoola. 2. Gulmi Amavata: Amavata having Jatara garjana, Gulmavat peeda and Kati jadata is called as Gulmi. 3. Snehi: Here Gaatra snigdhata, Jadhya, Mandagni and excretion of Vijala and Snigdha ama are characteristic. 44
  • 69. Conceptual Study 4. Pakva ama: This variety of Amavata presents with excretion of Shyava vijala pitta and Pakva ama along with Shrama and Klama.D) Based on prognosis: Based on the general principle of Sadhyasadhyata, Amavata can be oftwo types. 1. Naveena: If the duration of disease is not more than one year, it is called Naveena Amavata which is Sadhya. 2. Purana: If the duration of Amavata is more than one year, it is called Purana Amavata which is difficult to treat.REFERENCES: 1. M.N. 25/11 2. M.N. 25/6-10 3. H.S.Tri.Sth. 21/5-6 45
  • 70. Conceptual Study ROOPA Specific signs and symptoms of a disease when manifested distinctly isconsidered as Roopa Avastha1 or Lakshana of a disease. Roopa is one of thekey tool in arriving at the diagnosis. Of course this is also helpful in assessingthe Sadhyasadhyata and to plan the treatment. The Lakshanas of Amavata have been explained in length in the classicsand are listed in the Table No. 1 On keen observation and assessment of Lakshanas, they can be broadlyclassified into 3 categories. 1. Lakshana specific to involvement of Sandhi. 2. Lakshana specific to involvement of Ama. 3. Lakshanas produced as a consequence of the disease process. They are elaborated below:Lakshana specific to involvement of Sandhi: The Lakshanas such as Shoola and Shotha in Hasta, Pada, Shira,Gulpha, Trika, Janu2 and so on are very specific to involved Sandhi. FurtherLakshanas like Shunata Anganam3 (swelling in Sandhi) Sashabdha Sandhi4(crepitation in joints) also indicates the same. Gatrasthabdhata (immobility of Sandhi), Jadyata (unable to do thephysical work due to Vedana in the Sandhi Pradesha) Sandhi Vikunchana,Sankocha, Kanja and so on deformities in the limbs further shows involvementof Sandhi4. 46
  • 71. Conceptual Study As seen in the Samprapti, the vitiated Dosha and Ama will move to theKaphasthana9 i.e. Sandhi Pradesha. The involvement of the Asthi and Sandhi isvery much pathognomonic of the disease. Hence, it can be said that Sandhi Shoola and Shotha2 is one of thecardinal features of this disease. But keeping in mind the narration of multiplejoints involvement in other diseases in the text, we should consider multiple jointinvolvement with Ama Lakshana only as the cardinal symptom of the diseaseAmavata.Lakshana specific to involvement of Ama: Most of the Lakshanas other than Lakshana related with the Sandhi willrefer to Ama Dosha in the body. If we scrutinize these Lakshanas some of themare specific to Ama in the Annavahasrotas6, where as some other refer to effectof Ama on the Rasavahasrotas6. Chardi, Arochaka and so on are the features suggestive ofAnnavahasrotodushti6 specifically by Ama. The symptoms produced due toRasavahasrotodushti6 can be considered at two dimensional levels, theSthanika and Sarvadaihika Lakshanas3. Aruchi3, Anaha3 and so on are theSthanika Lakshanas suggestive of Ama, where as Angamarda3, Alasya3 areSarvadaihika Lakshanas suggestive of Ama. 47
  • 72. Conceptual StudyLakshanas produced as a consequence of the disease process: Remaining few symptoms such as Nidraviparyaya4, Bhrama2 Murcha2,are neither the cardinal features nor the Ama Lakshanas. Basically they are theeffect of pathological process in the body. Shoola is the culprit behindNidraviparyaya, where as Bhrama and Murcha point towards the involvement ofMajjavahasrotas10. Though in this disease is Vata predominant, involvement of Ama isinvariable. Hence, we see Sama Vata Lakshanas7 in the patients of Amavata.This might be the reason for not mentioning the disease Amavata separately byCharaka.Doshanubandha Lakshanas: (1) Vatanubandha8 : Sasulam (2) Pittanubandha8 : Sadaha, Saraga (3) Kaphanubandha8 : Stimitatam, Guru, Kandu 48
  • 73. Conceptual StudyTable No. 1-Lakshanas of Amavata according to different authors: LAKSHANA M.N B.P Y.R R.R.S G.N BRJ HS VGA TRA1. Angamarda + + + - + - - + -2. Aruchi + + + - + - - + -3. Trushna + + + - + - - + -4. Hrillasa + + + - + - - + -5. Gourava + + + - + - - + -6. Jwara + + + - + - + + -7. Apaka + + + - + - - + -8. Angasoonata + + + - + - - + -9. Sa Ruk Shotha Hasta + + + - + - - + -10. Sa Ruk Shotha Pada + + + - + - - + -11. Sa Ruk Shotha Shira + + + - + - - + -12. Sa Ruk Shotha Gulpha + + + - + - - + -13. Sa Ruk Shotha Trika + + + - + - - + -14. Sa Ruk Shotha Janu + + + - + - - + -15. Sa Ruk Shotha Uru + + + - + - - + -16. Agnidourabalya + + + - + - - + -17. Praseka + + + - + - + + -18. Utsaha Hani + + + - + - - + -19. Vyrasya + + + - + - - + -20. Daha + + + - + - - + -21. Bahumutrata + + + - + - - + -22. Kushikadhinata + + + - + - - + -23. Kukshishoola + + + - + - - + -24. Nidraviparyaya + + + - + - - + -25. Trut + + + - + + - + -26. Chardi + + + - + + - + -27. Brama + + + - + - - + -28. Moorcha + + + - + - - + -29. Hrutgraha + + + - + - - + -30. Vitvibhandha + + + - + - - + -31. Jadyata + + + - + - - + -32. Antrakoojana + + + - + - - + -33. Anaha + + + - + - - + -34. Vikunchana of Manya - - + - + - - - -35. Vikunchana of Prushata - - + - + - - - -36. Vikunchana of Kati - - + - + - - - -37. Vikunchana of Janu - - + - + - - - -38. Vikunchana of Trika - - + - + - - - -39. Sashabda Gatra - - + - + - - - -40. Srasta Gatra - - + - + - - - -41. Kati Vyadha - - - + - - - - -
  • 74. Conceptual Study42. Sandhi Shotha - - - + - - + - -43. Uthana Asamartha - - - + - - - - -44. Deha Pandura - - - - - + - - -45. Mootra Pandura - - - - - + - - -46. Peta and Ushna Netra - - - - - + - - -47. Peeta and Ushna Chardi - - - - - - + - -48. Jangha Vyadha - - - - - - - - +49. Uru Vyadha - - - - - - - - +50. Trika Vyadha - - - - - - + - +51. Hrut Vyadha - - - - - - - - +52. Nabhi Vyadha - - - - - - - - +53. Pada Vyadha - - - - - - - - +54. Prushta Vedana - - - - - - + - -55. Manya Vedana - - - - - - + - -56. Ama Atisara - - - - - - + - -57. Anga Vaikalya - - - - - - + - -58. Shosha - - - - - - - - +59. Visuchika - - - - - - - - +
  • 75. Conceptual StudyClinical Manifestations of Rheumatoid ArthritisArticular manifestations: Rheumatoid arthritis is characterized by chronic polyarthritis. It beginsinsidiously – the earliest manifestations being fatigue, anorexia, generalizedweakness and vague musculoskeletal symptoms and the later symptom beingthe appearance of synovitis. Specific symptoms usually appear gradually andsymmetrically as several joints, especially those of the hands, wrists, knees,and feet, become affected. In approximately 10% of individuals, there is acuteonset, with a rapid development of polyarthritis, often accompanied byconstitutional symptoms, mainly fever, lymphadenopathy, and splenomegaly.Symptoms may initially be confined to one or a few joints in nearly a third of thepatients. Although a symmetric pattern is more typical, the pattern of jointinvolvement may remain asymmetric in a few patients. Initially, pain, swelling, and tenderness may be poorly localized to thejoints. The most common manifestation of established Rheumatoid Arthritis ispain in affected joints, aggravated by movement. The pain corresponds to thejoint involvement in pattern but does not always correlate with the degree ofapparent inflammation. Generalized stiffness is frequent and is usually greatestafter periods of inactivity. Morning stiffness of greater than 1 hour duration is analmost invariable feature of inflammatory arthritis and may serve to distinguishit from various non-inflammatory joint disorders. The majority of patients willexperience constitutional symptoms such as weakness, easy fatigability,anorexia, and weight loss. Temperature in excess of 38°C is unusual; on 49
  • 76. Conceptual Studyoccasion the temperature may rise to 40°C, but this may suggest anintercurrent problem such as infection. Clinically, synovial inflammation results in swelling, tenderness, andlimitation of motion. Warmth is usually found on examination, especially of largejoints such as knee, but erythema is infrequent. Joint swelling is caused byaccumulation of synovial fluid, hypertrophy of the synovium, and thickening ofthe joint capsule. Initially, motion is limited by pain. The inflamed joint is usuallyheld in flexion as this position provides maximum joint volume and minimumdistention of the capsule. Later, fibrosis or bony ankylosis or soft tissuecontractures form, ultimately leading to fixed deformities. Although inflammation can affect any diarthrodial joint, Rheumatoidarthritis most often causes symmetric arthritis, characteristically involvingcertain specific joints such as the proximal interphalangeal andmetacarpophalangeal joints. Involvement of the distal interphalangeal joints israre. Synovitis of the wrist joints is a nearly uniform feature of RA and may leadto limitation of motion, deformity, and carpal tunnel syndrome (median nerveentrapment). When synovitis effects the elbow joint, flexion contractures oftendevelop, early in the disease. The knee joint is commonly involved with synovialhypertrophy, chronic effusion, and frequently ligamentous laxity. Baker’s cyst,caused by the extension of the inflamed synovium into the popliteal space, maycause pain and swelling behind the knee. Arthritis in the forefoot, ankles, andsubtalar joints can produce severe pain with ambulation as well as a number of 50
  • 77. Conceptual Studydeformities. Axially, involvement is usually limited to the upper cervical spine.Lower back pain cannot be ascribed to rheumatoid inflammation, asinvolvement of Lumbar spines is not seen. Occasionally, inflammation from thesynovial joints and bursae of the upper cervical spine leads to atlantoaxialsubluxation. This usually presents as pain in the occiput and rarely, may lead tocompression of the spinal cord. Persistent inflammation can lead to a variety of characteristic jointchanges. These can be attributed to a number of pathologic events, includinglaxity of supporting soft tissue structures; damaged or weakened ligaments,tendons, and the joint capsule; cartilage degradation; muscle imbalance; andunopposed physical forces associated with the use of affected joints.Characteristic changes of the hand include (1) radial deviation at the wrist withulnar deviation of the digits, often with palmar subluxation of the proximalphalanges ("Z" deformity); (2) hyperextension of the proximal interphalangealjoints, with compensatory flexion of the distal interphalangeal joints (swan-neckdeformity); (3) flexion contracture of the proximal interphalangeal joints andextension of the distal interphalangeal joints (boutonniere deformity); and (4)hyperextension of the first interphalangeal joint and flexion of the firstmetacarpophalangeal joint with a consequent loss of thumb mobility and pinch.Typical joint changes may also develop in the feet, including eversion at thehindfoot (subtalar joint), plantar subluxation of the metatarsal heads, wideningof the forefoot, hallux valgus, and lateral deviation and dorsal subluxation of thetoes. 51
  • 78. Conceptual StudyExtra-articular Manifestations: Rheumatoid arthritis is a systemic disease with various extra-articularmanifestations. In 20 to 30% of persons with Rheumatoid arthritis, rheumatoid nodulesdevelop, usually found on periarticular structures, extensor surfaces, or otherareas subjected to mechanical pressure; but they can develop elsewhere,including the pleura and meninges. Other common locations include theolecranon bursa, the proximal ulna, the Achilles tendon, and the occiput. Thenodules are of differing size and consistency and are rarely symptomatic, buton occasion they break down as a result of trauma or become infected. Theyare found almost invariably in individuals with circulating rheumatoid factor. Clinical weakness and atrophy of skeletal muscle are common. Muscleatrophy may be evident within weeks of the onset of Rheumatoid arthritis and isusually most apparent in musculature approximating affected joints Another associated pathological event, rheumatoid vasculitis, can affectnearly any organ system, and is seen in patients with severe Rheumatoidarthritis and high titers of circulating rheumatoid factor. When in severe form,rheumatoid vasculitis can cause polyneuropathy and mononeuritis multiplex,cutaneous ulceration and dermal necrosis, digital gangrene, and visceralinfarction. Such widespread vasculitis is very rare, but more limited forms arenot uncommon, especially in white patients with high titers of rheumatoid factor.Limited forms of vasculitis may present as Neurovascular disease either with 52
  • 79. Conceptual Studymild distal sensory neuropathy or mononeuritis multiplex as the only sign.Cutaneous vasculitis usually presents as crops of small brown spots in the nailbeds, nail folds, and digital pulp. Large ischemic ulcers may develope,especially in the lower extremity. Myocardial infarction secondary to rheumatoidvasculitis has been reported, as has vasculitic involvement of lungs, bowel,liver, spleen, pancreas, lymph nodes, and testes. Renal vasculitis is rare. Pleuropulmonary manifestations, which are more commonly observed inmen, include pleural disease, interstitial fibrosis, pleuropulmonary nodules,pneumonitis, and arteritis. Presence of pulmonary fibrosis can impair thediffusing capacity of the lung. Single or clusters of pulmonary nodules mayappear. Associated with pneumoconiosis, the nodules can cause a diffusenodular fibrotic process (Caplans syndrome). In other cases, pulmonarynodules may cavitate and produce a pneumothorax or bronchopleural fistula. ,Pulmonary hypertension, secondary to obliteration of the pulmonaryvasculature, is a rare occurrence. In addition to pleuropulmonary disease,upper airway obstruction from cricoarytenoid arthritis or laryngeal nodules maydevelop. Clinically apparent heart disease attributed to the rheumatoid process israre, but autopsy studies have revealed evidence of asymptomatic pericarditisin 50% of cases. Pericarditis may be asymptomatic, or on rare occasions deathhas occurred from tamponade. Chronic constrictive pericarditis may also occur. 53
  • 80. Conceptual Study Rheumatoid arthritis tends to spare the central nervous system directly,although vasculitis can cause peripheral neuropathy. Neurologic manifestationsmay also result from atlantoaxial or midcervical spine subluxations. Nerveentrapment secondary to proliferative synovitis or joint deformities may produceneuropathies of median, ulnar, radial (interosseous branch), or anterior tibialnerves. Rheumatoid arthritis involving the eye is seen in fewer than 1% ofpatients. Affected individuals usually have long-standing disease and nodules.The two principal manifestations are mild and transient episcleritis and scleritis. Feltys syndrome is most common in individuals with long standingdisease. It consists of chronic Rheumatoid arthritis, splenomegaly, neutropenia,and, on occasion, anemia and thrombocytopenia. These patients frequentlyhave high titers of rheumatoid factor, subcutaneous nodules, and systemicmanifestations of rheumatoid disease. Secondary osteoporosis, following rheumatoid involvement, is commonand may be aggravated by glucocorticoid therapy. Osteopenia in Rheumatoidarthritis involves both juxta-articular bone and long bones distant from involvedjoints. 54
  • 81. Conceptual StudyChart No. 4-Schematic representation of the evolution of Roopa: Nidana-Viruddha Vata Prakopa Agnimandya Dhatu Virodhi Vata Dushti Ama (Koshta) Majjavaha Srotas Samavata Dosha Dhamani (Amavisha/Garavishatulya) Trika Sandhi Saruja Shotha (in multiple joints) Sankocha Adi Upadrava 1. Angamarda 2. Daha 3. Sashabda Gatra 4. Aruchi 5. Bahumutrata 6. Srasta Gatra 7. Trushna 8. Kushikadhinata 9. Kati Vyadha 10. Hrillasa 11. Kukshishoola 12. Sandhi Shotha 13. Gourava 14. Nidraviparyaya 15. Uthana Asamartha 16. Jwara 17. Trut 18. Deha Pandura 19. Apaka 20. Chardi 21. Mootra Pandura 22. Angasoonata 23. Brama 24. Peta and Ushna Netra 25. Sa Ruk Shotha Hasta 26. Moorcha 27. Peeta and Ushna Chardi 28. Sa Ruk Shotha Pada 29. Hrutgraha 30. Jangha Vyadha 31. Sa Ruk Shotha Shira 32. Vitvibhandha 33. Uru Vyadha 34. Sa Ruk Shotha Gulpha 35. Jadyata 36. Trika Vyadha 37. Sa Ruk Shotha Trika 38. Antrakoojana 39. Hrut Vyadha 40. Sa Ruk Shotha Janu 41. Anaha 42. Nabhi Vyadha 43. Sa Ruk Shotha Uru 44. Vikunjana of Manya 45. Pada Vyadha 46. Agnidourabalya 47. Vikunjana of Prushata 48. Prushta Vedana 49. Praseka 50. Vikunjana of Kati 51. Manya Vedana 52. Utsaha Hani 53. Vikunjana of Janu 54. Ama Atisara 55. Vyrasya 56. Vikunjana of Trika 57. Anga Vaikalya 58. Shosha 59. Visuchika
  • 82. Conceptual Study
  • 83. Conceptual StudyREFERENCES: 1. A.H.Ni. 1/5 2. M.N. 25/7-10 3. M.N. 25/6 4. Y.R.Po. Amavata Nidana/1, 2 5. A.H.Su. 13/23,24 6. C.S.Vi. 5/8 7. A.H.Su. 13/27 8. M.N. 25/11 9. M.N. 25/1-5 10. C.S.Su. 28/17 11. H.P.I.M. 14th edition, pg.1883, 1884.
  • 84. Conceptual Study UPADRAVA Among the different scholars of Ayurveda, there is a wide range ofdifference in relation to Amavata Upadrava. Yogaratnakara1 has included all the advanced stage manifestations asits complications whereas Vachaspati includes all Vatavyadhis as itsUpadravas. But, other Acharyas differentiate symptoms of Amavata from itscomplications. Vijayarakshita mentions Sankocha and Khanja2 specifically.Bhavaprakasha3 includes Kalaya Khanja. Anjana Nidana4 includes Jadya,Antrakujana, Anaha, Trushna, Chardi, Bahumootrata, Shoola, Shayananashaas Upadrava of Amavata.Following are the Upadravas which are elaborated; 1. Granthi 2. Angavaikalya 3. Vatavyadhi 4. Sankocha 5. KhanjaGranthi (Rheumatoid nodules): Granthi is one of the feature of Snayu Dushti5. Develops in 20-30% ofpersons with RA. They are usually found on the peri-articular structures,extensor surfaces and other areas subjected to mechanical pressure, but arealso seen in pleura and meninges. Common locations include Olecranon bursa,Proximal ulna and so on. Nodules vary in size and consistency.6 55
  • 85. Conceptual StudyAngavaikalya:7 Angavaikalya, one of the Lakshana mentioned by Harita can beconsidered as an Upadrava of Amavata as most of the different deformities ofthe body parts are produced in the later part of the disease RA.Deformity of joints:6 • Swan neck deformity • Boutonniere deformity • Ulnar deviation • Eversion at the hind foot, plantar subluxation of the metatarsal heads, widening of the forefoot, hallux vulgus, lateral deviation and dorsal subluxation of the toes. • Z-Deformity of wrist and fingers.Vatavyadhi: Vachaspati mentions Vatavyadhi to manifest in the Upadravavastha ofAmavata. But, Vijayarakshita mentions Khanja, Sankocha. Different neurological manifestations in RA are: • The subluxation of Atlantoaxial joint is a severe complication and may lead to compression of spinal cord by the Odontoid process producing symptoms like bladder dysfunction, sphincter laxity, circummonal hypesthesia, and long tract signs may occur. It may even lead to sudden death due to the laceration of the cord by the Odontoid process. 56
  • 86. Conceptual Study • Affliction of Crico-arytenoid joints leads to hoarseness of voice and even life threatening upper airway obstruction. • Tenosynovitis in wrist causes Carpal tunnel syndrome due to median nerve compression. • Vasculitis vasonervorum cause motor and sensory type of neuropathy. • Autonomic nervous system dysfunction cause cold and damp extremities.Sankocha: Inability to extend the limbs or normal fixed state of limb in flexion isSankocha.8 Sankocha is due to the affliction of Snayu, Sira and Khandara9.Yogaratnakara has used the term Vikunchana of different Sandhis. Inflamed joint is usually held in flexion to maximize joint volume andminimize distension of the capsule. Later, fibrous and bony ankylosis or softtissue contractures lead to fixed deformities.6Khanja:2 Patients gait gets altered because of Akshepana of Khandara. Gayadasaclarifies Akshepana as reduced Gati10. This is usually due to painful joints,contractures and stiffness.6 57
  • 87. Conceptual StudyChart No. 5-Schematic representation of the evolution of Upadrava: Nidana-Viruddha Vata Prakopa Agnimandya Dhatu Virodhi Vata Dushti Ama (Koshta) Majjavaha Srotas Samavata Dosha Dhamani (Amavisha/Garavishatulya) Trika Sandhi Saruja Shotha (in multiple joints) Granthi Angavaikalya Sankocha Adi Vatavyadhi Upadrava Sankocha Kanja
  • 88. Conceptual StudyREFERENCES: 1. Y.R.Amavata Chi. 3-6 2. M.N. 25/7-10 3. B.P.M. Madhu 26/11 4. Anjana Nidana 5. C.S.Su. 28/21 6. H.P.I.M. 14th edition, pg.1883 7. H.S.Tri. 21/4 8. A.H.Su. 12/49 (Hemadri) 9. C.S.Su. 28/29 10. Gay-M.N. 25/7-10
  • 89. Conceptual Study INVESTIGATIONSImmunological assay:1,2 No tests are specific for diagnosing RA. However gamaglobulins withdemonstrable antigamma globulin activity have long been called Rheumatoidfactor (RF) because of their occurrence in serum of over 80% of patients. Thepresence of Rheumatoid factor is not specific to RA. It is found in 15% healthypeople and frequency of RF in general population increases with age. It doesnot establish the diagnosis of RA but can be of high value in prognosis becausepatients with high titers tend to have more severe progressive disease. Inaddition a number of conditions like systemic lupus erythematosis, Sjogren’ssyndrome, chronic liver diseases, sarcoidosis, intestinal pulmonary fibrosis,infective mononeucleousus, hepatitis B, TB, Syiphilis, subacute bacterialendocarditis, schistosomiasis and malaria.Blood picture:2 Normochromic, normocytic anaemia is frequently present in RA. Largeiron stores in bonemarrow are usually noted. In general anaemia andthrombocytosis correlate with disease activity. The WBC count is ususllynormal. But a mild leucocytosis may be present.ESR:2 The erythrocyte sedimentation rate is increased in nearly all patients withactive RA. In few patients, the ESR may be continuously elevated even after 58
  • 90. Conceptual Studythe disease activity subsides which may be attributed to elevation of serumglobulin level.Biochemical investigationsAntinuclear antibodies (ANA):1 Higher titers of ANA are usually associated with highly expressed RA,but attempts to differentiate SLE from RA is a key in diagnosing RA precisely.Anti DNA Antibodies (anti n DNA):1 Though higher levels of anti n DNA are associated with SLE, in about20% of RA patients the levels anti n DNA are usually found increased.C-reactive proteins and ceruloplasmin levels:1 The C-reactive protein and ceruloplasmin levels are elevated andgradually such elevations correlate with disease activity and likely hood ofprogressive joint damage.Synovial fluid analysis:2 The fluid is usually turbid with reduced viscosity, increased proteincontent and slightly decreased or normal glucose concentration. The white cellcount varies between 5-50,000 cells per microlitre, polymorphoneuclearleukocytes dominate. A synovial fluid WBC count of more than 2,000 cells permicrolitre with more than 75% polymorphoneuclear leucocytes is highlycharacteristic of inflammatory arthritis. The total haemolytic complement C3 andC4 are markedly diminished in synovial fluid relative to total protein 59
  • 91. Conceptual Studyconcentrations as a result of activation of classic compliment pathway by locallyproduced immune complexes.2Cellular morphology:1 In about 95% of patients, both phase and ordinary light microscopyreveals small dark cytoplasmic granules or 0.5-2.0 µ diameter within 5-100% ofneutrophils. Such neutrophils are called RA cells. A given RA cell may contain1-20 granules in its cytoplasm. RA cells are not specific fro RA but also occur inother conditions such as gout and septic arthritis (Scott 1975).Radiographic evaluation:2 Roentgenograms of the affected joints early in the disease are usuallynot helpful in establishing a diagnosis they reveal only that which is apparentfrom physical examination namely evidence of soft tissue swelling and jointeffusion. As disease progresses abnormality becomes more pronounceddiagnosis is supported by a characteristic pattern of abnormality including thetendency towards the systemic involvement. Juxta articular osteopenia maybecome apparent within weeks of onset. Loss of articular cartilage and boneerosion develop after months of sustained activity. The primary value ofradiography is to determine the extent of cartilage destruction and bone erosionproduced by the disease. 99m Other means of imaging bones and joints including TC biphosphonatebone scanning2 and magnetic resonance imaging2 may be capable of detecting 60
  • 92. Conceptual Studyearly inflammatory changes that are not apparent from standard radiographybut are rarely necessary in routine evaluation of patients with RA.2REFERENCES: 1. Clinical Diagnosis of Laboratory Methods, Bernard Hennry, pg.477, 478, 932. 2. H.P.I.M. 14th edition, pg.1884. 61
  • 93. Conceptual Study UPASHAYA ANUPASHAYA Oushadha, Ahara and Vihara which are responsible for relief from thesymptoms of Vyadhi are known as Upashaya and that which aggravate areknown as Anupashaya1. As said in the Amavata treatment2, Langhana, Tikta,Katu Deepana and Ushna Ahara Viharas are the Upashaya measures of thisdisease, since they carry out Ama pachana thereby giving relief from symptomslike Jwara, Sandhi Vedana, Angamarda and Gourava and so on. Ruksha Guna of Ruksha Sweda employed in Amavata is opposite toAma Gunas. viz. Snigdha, Picchiladi. It is Srotovishodhakara and Pachakahence effectively reduces pain. Besides, Ushna Jala suppresses symptoms ofthe disease as it is Pathya3. In brief Ruksha Sweda, Langhana, Ushnakala andSayamkala are the Upashaya in Amavata.Anupashaya: On the contrary, Sheeta Guru Snigdha Ahara Meghodaya Kala, PratahKala and Snigdha Sweda are considered as Anupashaya4 in this disease.Snigdha Sweda supports the formation of Ama in early morning hours, cloudyand rainy days because Sheeta Guna enhances the Vata and Ama. Henceconsidered as Anupashaya. This characteristic feature helps to differentiate Amavata from otherclosely related diseases of Sandhi. When the symptoms of two diseases are sosimilar as to confuse the physician (“Bhishak Mohakara”), the classics suggest 62
  • 94. Conceptual Studythe use of the concept of Upashaya and Anupashaya to bring out the occultsymptoms (Guda Linga) to diagnose the disease5. When application of oilrelieves the pain, the disease is free from Ama.REFERENCES: 1. A.H.Ni. 1/67 2. Chakradutta 25/1 3. B.R. 21/232-234 4. A.Hr.Su. 13/27 footnote 5. C.S.Vi. 5/7 63
  • 95. Conceptual Study SADHYASADHYATA Physician who wants to be successful should have clear knowledge ofcurable and incurable disease, and start treatment in time with wellunderstanding of various aspects of the disease. This will help inaccomplishing his goal of curing diseases. Physician treating incurablediseases would loose wealth, fame and earn bad reputation. He will becomevictim of legal sanctions.1 Generally Amavata is a Krichrasadhya Vyadhi as it includes MadhyamaRogamarga2. It is also difficult to treat because of opposite nature of Ama andVata. Diseases accompanied by Upadrava becomes Asadhya the same isapplicable to Amavata. Ekadoshaja Amavata3 caused by minimum Nidana, with fewLakshanas, of recent origin2 is Sadhya and Harita adds Pakwama type ofAmavata is Sukhasadhya4. When the disease is Dwidoshaja3, having manyNidanas and Lakshanas, then it become Yapya. Disease becomesKrichrasadhya by the involvement of Tridosha and when associated withSarvangashotha.3 Snehi ama, Vistambi, Gulmi types of Amavata areKashtasadhya.4 Shopha anana, Jadya, Ghana udara, Aruchi and AmathisarayukthaSnehi Amavata is Asadhya according to Harita.5 65
  • 96. Conceptual StudyPROGNOSIS OF RHEUMATOID ARTHRITIS:6 In Rheumatoid arthritis prognosis is variable. Life expectancy is reducedby 25%. 10-15 yrs mortality is increased in patient with functional impairment.The overall prognosis is much better in patients whose symptoms are not ofsuch severity as to require admission to hospital. Poor prognosis may beassociated with high titer of Rheumatoid Factor, insidious onset of disease,more than a year of active disease without remission, early development ofnodules and erosion, extra articular manifestation, severe functionalimpairment.REFERENCES: 1. C.S.Su. 7/8 2. C.S.Su. 10/18 3. M.N. 25/12 4. H.S.Tritiya sthana 21/21 5. H.S.Tritiya sthana 21/14 6. Davidson’s PPM 18th edition. pg. 848 66
  • 97. Conceptual Study SAPEKSHA NIDANA For the diagnosis of any disease physician should have clear knowledgeof other conditions which mimic particular condition. This can avoid thephysician from embarrassment and prevents the patient from taking theunwanted pain and complications. Therefore for the accurate diagnosis ofAmavata the disease having similar feature has to be excluded. Following arefew conditions which have to be differentiated from Amavata.1. Vata Shonita: In the disease process of Vata Shonita, Rakta Dushti plays an importantrole. Vata and Shonita1 get vitiated due to each others own causative factors.Though this disease presents with Shotha in Parshva Sandhi and big jointsalso, it classically begins with affliction of big toe2 with skin manifestations unlikeAmavata.2. Kroshtuka Sheersha: This is a disease of the knee joint and the question of involvement ofother joints does not arise. Swollen Knee has the appearance of head of ajackal (Jambuka Shira)3. Here too Vata and Shonita are the two factorsinvolved.3. Sandhigata Vata: Sandhigata Vata typically presents with swelling of the joint that gives afeeling of a bag inflated with air.8 Notably, use of oil here results in improvementof symptoms rather than aggravation. 67
  • 98. Conceptual Study4. Sandhiga Sannipata Jwara:11 In this disease the joint manifestations are secondary to Jwara which isthe cardinal symptom. Besides, excessive mucoid secretion from mouth,Insomnia and Saruja Kasa differentiates this condition from Amavata Along with the above mentioned diseases, Shotha and Shoola in Sandhi,like in Amavata can be seen in Vataja Atisara4, Grahani5, Kshayaja Kasa6,Vatodara7, Arsha9, Antarvega Jwara10. But these can be differentiated fromAmavata by their own characteristic features.REFERENCES: 1. C.S.Chi. 29/4 2. C.S.Chi. 29/4 3. A.S.Ni. 15/35 (Indu) 4. C.S.Chi. 19/5 5. C.S.Chi. 15/54 6. B.P. 11/35 7. A.S.Ni. 12/14 8. C.S.Chi. 28/37 9. A.S.Ni. 7/16 10. C.S.Chi. 3/39, 40 11. B.P.Mady.Kha. Sandhiga Sannipata Jwaradhikar/500 68
  • 99. Conceptual Study CHIKITSA The treatment modalities for Amavata listed by Chakradatta1 can beorganized into three groups, to be administered in the following order. 1. The treatment aimed at Amapachana - Langhana, Swedana, Tikta, Katu, Deepana drugs. 2. Shodhana - Virechana and Basti 3. Shamana - Snehapana.Amapachana: The first step in the management of Amavata is Amapachana, as it is thefirst step in the general management of all the diseases and as Ama is theprime pathogenic factor in Amavata. The modalities for Amapachana in the Chakradatta’s Chikitsa Sootra are, 1. Langhana 2. Swedana 3. Tikta, Deepana, Katu Oushadhis to be administered in order.Langhana: In the management of Amavata, Upavasa is the ideal line of treatment.Bhavaprakasha in the context of Jwara, considers Langhana as Upavasa.2 Asboth Jwara and Amavata are Amashayotha diseases, Upavasa3 can beconsidered as the ideal method of Langhana in Amavata also. This is alsobecause of unsuitability of the other methods of Langhana, analysed below. 69
  • 100. Conceptual Study o Chatushprakara samshudhi, cannot be employed because Samshodhana is contraindicated in the Samavastha of a disease.4 o Pipasa cannot be employed because in morbid patients Jala is Pranadharaka5. o Maruta and Atapa Sevana are less efficient for Jatharagni impairment when compared to Upavasa. o Deepana, Pachana cannot be employed as Agni affected by Ama is incapable of Dosha, Ahara and Oushadha Pachana.6 o Vyayama is incompatible in the disease Amavata. For these reasons, Upavasa is the ideal method of achieving Langhanain Amavata, which can be achieved by Anashana or Alpabhojana. TheLanghana thus achieved will have Amapachaka effects at the Koshta level aswell as Sarvadaihika level.7Swedana: The definition of Sweda8 includes its benefits, viz. Stambha, Gouravaand Sheetagna. Since these are antagonistic to the qualities of Kapha andAma, Swedana has an important role to play in the treatment of Amavata. Snigdha Sweda, Ruksha Sweda and Ekangasweda, Sarvangasweda arethe two fold classifications of Sweda9 and in Amavata, the Ruksha type ofSweda should be administered for the following reasons; 1. The pathogenesis of Amavata involves spread of Ama and Vata to the Sleshmasthana, specifically Amashaya and Sandhi.10 70
  • 101. Conceptual Study 2. In all conditions of Amashayagata vata, Ruksha sweda should be administered.11 As disease is localized in Sandhipradesha, Ekangasweda is ideal. TheRukshasweda can be advised to the affected Sandhi using Valukapottali orRukshopanaha.12Tiktam Deepanani Katuni Cha: Administration of Tikta, Katu Deepana oushadhis in Ama achievesAmapachana both at the Koshta level and Sarvadaihika level. The methodsused for Ama Pachana are potentially Vataprakopaka. But as Langhana isindicated in Sama Vata condition the danger of Vata Prakopa is minimalbecause,13 the Amapachana methods of Langhana, Swedana and Tikta KatuDeepana drugs are administered only until Niramavastha is achieved. After this,Nirama Doshas have to be eliminated from the body by Shodhana. TheShodhana methods which can be employed are Virechana and Basti.Virechana: Virechana is the best preferred form of Shodhana in Amavata becauseVamana (Ullekhana),14 though indicated by Charaka in Amachikitsa isunsuitable here as it aggravates the symptoms of Amavata caused byPratilomagati of Vayu like Anaha, Vibandha and Antrakoojana. They can bestbe relieved by Virechana. Besides, the production of Ama involves the Avaranaof the Pachaka Pitta by Kledaka Kapha. Virechana administered here provides 71
  • 102. Conceptual Studydual benefits of removing the Avarana produced by Kledaka Kapha and actingon the Sthanika Pitta Dosha.Basti: Basti forms the second method of Shodhana. Both Niruha andAnuvasana Bastis should be employed here. The Niruha Basti does theShodhana of the Doshas brought to Pakvashaya and the Anuvasana Bastialleviates Prakupita vata as a consequence of Niruha Basti.Shamana Snehapana: This is a third component in the plan of management of Amavata. Theobjective of Snehapana here is Shamana. It is important to administer Snehaonly after the disease has become Nirama. Shamana Snehapana in Amavataprovides the following benefits; o Snehapana prevents the aggravation of Vata and Rukshata as a result of the previously employed therapeutic measures.15 o It helps in increasing the Bala of the patient who has been debilitated as a result of previously employed therapeutic measures.15 o Shamana Sneha stimulates the Agni16 which is an important component in the treatment of Amavata. o Since the Snehapana has been prescribed in Asthi Majja Gata Vata, it can be comfortably used in Amavata. o Vataharana is the inherent property of Sneha, an essential requirement in the treatment of Amavata. 72
  • 103. Conceptual StudyGeneral principles in treatment of Rheumatoid Arthritis:17 The goals of therapy of RA are; 1. Relief from pain 2. Reduction of inflammation 3. Protection of articular structures 4. Maintenance of function 5. Control of systemic involvement The therapy of RA remains empirical and palliative since the etiology,pathogenesis and mechanism of therapeutic action is speculative till date. Theinterdisciplinary approach in the management of RA includes both physical andmedical modalities.Physical therapy and education: This includes rest, splinting to reduce unwanted motion of inflamedjoints, exercise to maintain muscle strength and joint mobility, arthrotic andassistive devices for support and alignment of deformed joints to reduce painand improve joint function, patient and family education to give the insight of thedisease and make necessary life style changes to minimize stress on the joints.Medical management:This includes four approachesI. First line of treatment with non steroidal anti-inflammatory drugs (NSAIDs): Besides aspirin, the new generation NSAIDs have shown to act byinhibiting cycloxygenase II pathways which is responsible for the inflammatory 73
  • 104. Conceptual Studyactivity. They have analgesic anti inflammatory, and anti pyretic properties.Though non aspirin agents are lesser gastric irritants, the NSAIDs in generalare associated with following side effects 1. Gastric irritation, 2. Azotemia 3. Platelet dysfunction 4. Rash 5. Liver function abnormalities 6. Bone marrow depletion 7. Toxicity in elderly on diuretic therapy. The NSAIDs have minimal effect on disease progression.II. Second line of treatment with disease modifying anti rheumatic drugs(DMARD): The DMARDs include Gold, Depencillamine, Antimalarials andSulphasalazine. They have the capacity to decrease elevated levels of acutephase reactants, like RA factor, C-reactive protein and ESR. Thus, they modifythe destructive capacity of the disease. They have been shown to induceremission, but have minimal anti inflammatory activity. Hence, NSAIDs must becontinued during DMARD therapy. The Folic acid antagonist Methotrexate is currently a frequently utilizedDMARD as its onset of action is more rapid than others. The toxicity ofDMARDs include GIT upset, oral ulceration, hepatic fibrosis and pneumonitis. 74
  • 105. Conceptual StudyConcurrent administration of folic acid may diminish the frequency of the sideeffects.III. Third line of treatment with glucocorticoids: Low dose (less than 7.5 mg/day) Prednisolone has been advocated as auseful additive therapy to control symptoms and retard progression of boneerosions.IV. Fourth line of treatment with immuno suppressants: Drugs like Azathioprim and Cyclophosphamide have same effects likethe DMARDs and are used when the DMARD therapy has completely failed. Inhigher doses the toxic effects include predisposition to malignant neoplasms.Recent trials have found that high dose cyclosporine therapy may induce rapidimprovement but are associated with renal and gastrointestinal toxicity.Cyclosporine has still not been approved for use in RA.V. Surgery: Surgery helps patients with severely damaged joints. Surgeries likeArthroplasty, total joint replacement (especially of hip and knees.), Arthroscopicsynovectomy and Tensosynovectomy can be adopted to give the patient relieffrom pain and deformity. 75
  • 106. Conceptual StudyREFERENCES: 1. Chakradutta 25/1 2. C.S.Chi. 3/142 3. B.P.Madhy.kha.Prathambhaga.1/9 (AnashanamUchyate) 4. A.H.Su. 13/28 5. B.P. 1/14 6. A.H.Su. 8/18 7. C.S.Chi. 15/75 8. C.S.Su. 22/4 9. C.S.Su. 14/66 10. M.N. 25/2 – Madhu 11. C.S.Su. 14/9 12. B.P. Madhya 26/14-15 13. C.S.Chi. 3/283 - Chakrapani 14. C.S.Vi. 2/13 (Ullekhana) 15. C.S.Chi. 28/81 16. C.S.Chi. 15/201 17. H.P.I.M. 14th edition, pg. 1885-1888
  • 107. Conceptual Study PATHYAPATHYA Pathyapathya plays vital role in crushing the disease process as well asin the recurrence of the disease. Success of treatment depends upon thepractice of Pathyapathya. Vaidyakiya Subhashita quotes,” there is no need totake the medicine for the one who follows the Pathya properly, contrarily thereis no need to take the medicine for the one who does not follow the Pathya, asit will be of no use”. Purusha has been carved out of nature itself. That is whythere exists little difference between the constituents of his make and that of hisenvironment. The dimensions of man’s interaction with his environment includeAhara, Vihara and Oushadha. A beneficial interaction is termed Hita and aharmful one is called Ahita, this leads to homeostasis and homeostenosisrespectively. The factors governing this aspect of treatment constitutes theconcept of Pathya and Apathya. By definition, Pathya means “Patho Anapetam” and “Manasaha Priyam”1which can be interpreted as “Manoshareera Anupaghati”2. That which isharmless to both to Shareera and Manas is Pathya. On the contrary, Apathyameans otherwise. Among the Pathya Varga, the methods involved inadministration of Oushadha have been dealt in the chapter of Chikitsa. Thedetails of Ahara and Vihara are discussed here. Raja Nighantu has listed thefollowing Hitakara Dravya Samooha3. i.e. which are in general are Pathya for alldiseases. Ghrita, Saindhava, Dhanyaka, Jeeraka, Ardraka, Tanduleeyaka,Patola, Alabu, Godhuma, Jeerna shali, Gokshura, Hamsodaka and Mudga. 76
  • 108. Conceptual Study In Amavata, the Ahara and Vihara which are Vatahara, Kaphahara,Amapachaka, Agnideepaka and Rasaprasadaka are considered as Pathya. So,the diet and the Oushada having Katu, Tiktarasa, Ushna, Tikshna guna areconsidered as Pathya. They are as follows,Shuka Dhanya - Purana Shali, Purana Shastika Shali, Yava5Shami Varga - Chanayusha, Kalayayusha, Kulatta, Kodrava5Shakha Varga - Nimba Patra, Gokshura, Varuna, Sigru, Ardraka, Lashuna, Karavellaka, Patola5Mamsa Varga - Jangala mamsa, Lava mamsa processed with Takra4Paniya Varga - Ushna Jala, Panchakola siddha jala, Madhya4Ksheera Varga - Takra4Mutra Varga - Gomutra4 Harita opines that all the Pathya which are mentioned in JwaraRogadikara should be considered in Amavata also6.Apathya: The Ahara and Vihara which compliment or supplement the Prakruti ofthe Vyadhi are called as Apathya. In Amavata, to be a Apathya it should beAmakaraka and Vatakaraka. It should cause Mandagni and vitiate the RasaDhatu.Aharatah Apathya:Shami Dhanya - Masha Pistaka4,5,7,8 Dvidala dhanya6Mamsa Varga - Matsya, Anupa4,5,7,8 77
  • 109. Conceptual StudyKsheera Varga - Dhadhi, Ksheera, Guda9,5,7,8,10Mutra Varga - Gomutra9,11Jala Varga - Dushta jala9,11Anna - Viruddha, Asatmya, Vishamashana9,11 Guru7,9,11 Picchila Abhishyandi7,9,10,11, Ushna, Drava, Goulya6Viharatah Apathya: Poorva Vata, Vegavarodha, Jagarana, Vishamashana9,11 Harita opines that all the Nidana which are Atisarakaraka are Apathya inAmavata.6REFERENCES: 1. C.S.Su. 25/45 2. Chakrapani on C.S.Su. 25/45 3. Ra Ni 11/126 4. B.R.Amavata 21/232-234 5. Y.R. Amavata.1,2 6. H.S.Tritiya stana 21/47-49 7. B.P Ma.Amavata.26/129 8. G.N.Kaya chikitsakhanda.22/38. 9. B.R.Amavata 21/235-236 10. Vang.Amavata/123 11. Y.R. Amavata.3,4 78
  • 110. Drug Review DRUG REVIEW The therapeutic effect of any drug combination in the patients ofAmavata depends upon its ability to pacify the Ama and Vata Dosha, correctionof Rasa Dhatu abnormality, rectifying the Agni, correcting the structuralabnormality in Sandhis, ability to pacify and bring out reduction in pain,softening the stiff Sandhis, reducing morning stiffness and such measures. The drugs used in the clinical trial have been reviewed below: 1. Eranda Paka1 2. Ajamodadi Churna2 3. Panchakola Phanta3 4. Eranda Taila.4ERANDA PAKA: ContentsName of the drug Latin Name Quantity1. Eranda Ricinus communis 750 grams2. Ksheera Milk 6 liters3. Ghrita Ghee 375 grams4. Khandasharkara Sugar candy 1500 grams5. Pippali Piper longum Linn. 12 grams6. Maricha Piper nigrum Linn. 12 grams7. Shunti Zingiber officinale 12 grams8. Twak Cinnamomum zeylanicum 12 grams9. Ela Elettaria cardamomum 12 grams 79
  • 111. Drug Review10. Patra Cinnamomum tamala 12 grams11. Nagakesara Mesua ferrea 12 grams12. Pippalimoola Piper longum Linn. 12 grams13. Chitraka Plumbago zeylanica 12 grams14. Chavya Piper retrofractum 12 grams15. Shatapushpa Anethum sowa 12 grams16. Shati Hedychium spicatium 12 grams17. Bilwamoola twak Aegle marmelos 12 grams18. Yavani Trachyspermum ammi 12 grams19. Jeeraka Cuminum cyminum 12 grams20. Krishna jeeraka Carum bulbocastanum 12 grams21. Haridra Curcuma longa 12 grams22. Daruharidra Berberis aristata 12 grams23. Aswagandha Withania somnifera 12 grams24. Balamoola Sida cordifolia 12 grams25. Patha Cissampelus pereira 12 grams26. Hapusha Juniperus communis 12 grams27. Vidanga Embelia ribes 12 grams28. Pushkaramoola Inula racemosa 12 grams29. Goshura Tribulus terrestris 12 grams30. Kushta Saussurea lappa 12 grams31. Amalaki Embelica officinalis 12 grams32. Haritaki Terminalia chebula 12 grams 80
  • 112. Drug Review33. Vibheetaki Terminalia bellirica 12 grams34. Devadaru Cedrus deodara 12 grams35. Baboola twak Acacia arabica 12 grams36. Satavari Asperagus racemosus 12 gramsMethod of Preparation: Eranda Paka is herbal compound mainly contains Eranda Beeja, Milk,Ghee and 33 Prakshepaka Dravyas, tabled above. A special preparationmethod, mentioned in Yogaratnakara was followed in preparing Eranda Paka.Initially Eranda Beeja are collected and its outer covering is removed. Heatthese Eranda Beeja with milk on Mandagni till it turns to pasty consistency. Thispaste is grinded well and fried in ghee on an Iron pan. Then 33 PrakshepakaDravyas are added, mixed well till it gets granule form.Dose: Orally in a dose of 15 gms, thrice a day with hot water after food.Duration: For a duration of 30 days in patients of Group EP. Eranda is one of the main ingredient in Eranda paka. Eranda is Tikta,Kashaya and Madhura Rasatmaka, Ushna veerya and Madhura vipaka. Thuswith Madhura rasa and Madhura vipaka contradicts Vata and with Tikta rasaand Ushna veerya counters Ama. In Amavata, Vedanasthapana andShothahara properties plays an important role, which are also the main actionof the Eranda as Eranda is Vata Anulomana, Vedanasthapaka and Shothaharain nature. The rest 33 Prakshepaka drugs are added in very minute quantity.Most of them are Deepaka, Pachaka and Vata anulomaka in nature. The 81
  • 113. Drug Reviewdifferent properties and therapeutic effect of the individual drugs are shown inthe table below5 (Table No. 2) 82
  • 114. Table no. 2-Properties and therapeutic effect of the individual drugs in Eranda Paka: Sl. Name of the Latin Name Rasa Guna Veerya Vipaka Doshaghnata Karmukata No. Drug 1. Eranda Beeja Ricinus Madhura Guru Ushna Madhura Vatakapha Swedopaga Communis Katu Snigdha Prashama Shothahara Kashaya Teekshna Rasayana, Vedana Sookshma Shamaka 2. Milk Madhura Shigdha, Sheeta Madhura Vata Pittahara Jeevaniya Mrudu Rasayana Guru Vajikara Shlaksna Balya Picchila Bruhmana 3. Ghee Madhura Shigdha, Sheeta Madhura Vata Pittahara Dhatuvardhaka Guru 4. Kanda Sharkara Madhura Sara Sheeta Madhura Vata Pittahara Vrishya Snigda Bruhmana 5. Nagara Zingiber officinale Katu Laghu Ushna Madhura Kaphavata Deepaka, Pachaka Snigdha Shamaka Shoolaprashamana Vatanulomana 6. Pippali Piper nigrum Katu Laghu Ushna Katu Vatakapha Deepana, Teekshna Shamaka Triptighna, Vatanulomana, Mrudureehana,
  • 115. Balya, Rasayana7. Maricha Piper nigrum Katu Laghu, Ushna Katu Kaphavata Deepana, Teekshna Shamaka Pachana, Vatanulomana Pramathi8. Twak Cinnamomum Katu Tikta Laghu Ushna Katu Vatakapha hara Deepana Pachana Zeylanica Madhura Rooksha Vedanashamaka Teekshna9. Ela Elettaria Katu Laghu Sheeta Madhura Tridosha hara Deepana Pachana cardamomum Madhura Rooksha Vedanashamaka10. Patra Cinnamomum Katu Ushna Ushna Katu Kaphaghna Deepana Pachana tamala Laghu Vedanashamaka11. Nagakeshara Mesua ferrea Kashaya Laghu Ushna Katu Kaphapitta Deepana Pachana Tikta Rooksha Shamaka Vedanashamaka12. Pippali moola Piper longum Katu Laghu Anushna Madhura Kaphavata Deepana, Snigdha Shamaka Triptighna, Teekshna Vatanulomana, Balya, Rasayana13. Chitraka Plumbago Katu Teekshna Ushna Katu Kapha hara Deepaka, Pachaka Zeylanica Laghu Shoolaprashamana Rooksha Vatanulomana14. Chavya Piper Katu Laghu Ushna Katu Kaphavata Deepaka, Pachaka retrofractum Rookhsa Shamaka Shoolaprashamana Vatanulomana
  • 116. 15. Shatapushpa Anethum sowa Katu Laghu Ushna Katu Kaphavata Rochana, Tikta Rooksha Shamaka Deepana, Teekshna Pachana, Anulomana, Shothahara16. Shati Hedychium Katu Tikta Laghu Ushna Katu Kaphavata Deepana Rochana spicatium Kashaya Teekshna Shamaka Shoolaprashamana17. Bilwamoola Aegle marmelos Kashaya Laghu Ushna Katu Kapha Shamaka Vedana Shamaka Twak Tikta Rooksha18. Yavani Trachyspermum Katu Tikta Laghu Ushna Katu Kaphavata Rochana Deepana ammi Rooksha Shamaka Vatanulomana Teekshna Shoolaprashamana19. Jeeraka Cyminum Katu Laghu Ushna Katu Kaphavata Deepana, Pachana cuminum Rooksha Shamaka Vatanulomana Shoolaprashamana20. Krishna Jeeraka Carrium carvi Katu Laghu Ushna Katu Kaphavata Deepana Pachana Rooksha Shamaka Vedanashamaka21. Haridra Curcuma longa Tikta Katu Rooksha Ushna Katu Kaphavata Nashaka Vedanashamaka Laghu Varnya Deepana Anulomana22. Daruharidra Berberis aristata Tikta Rooksha Ushna Katu Kaphapitta hara Shothahara Kashaya Laghu Vedanashamaka Anulomana
  • 117. 23. Ashwaganda Withania Madhura Laghu Ushna Madhura Kaphavata Shothahara, somnifera Kashaya Snigdha Shamaka Vedanashamaka Tikta Rasayana24. Balamoola Sida codifolia Madhura Guru Sheeta Madhura Vata Shamaka Vedanahara Snigdha Shothahara Picchila25. Patha Cissampelos Tikta Laghu Ushna Katu Tridosha Nashaka Anulomana Pereira Teekshna Vedanashamaka Deepana pachana26. Hapusha Juniperus Katu Tikta Guru Ushna Katu Kaphavata Deepana Pachana communis Rooksha Shamaka Teekshna27. Vidanga Embelia ribes Katu Laghu Ushna Katu Kaphavata Deepana, Pachana Kashaya Rooksha Shamaka Anulomana Teekshna Krimighna28. Pushkaramoola Inula recemosa Tikta Katu Laghu Ushna Katu Kaphavata Shothahara Teekshna Shamaka Vedanasthapaka29. Gokshura Tribulus terestris Madhura Guru Sheeta Madhura Vatapitta Shamaka Balya anulomaka Snigdha Vedanasthapaka30. Kushta Saussurea lappa Tikta Laghu Ushna Katu Kaphavata Deepana, Pachana Katu Rooksha Shamaka Anulomana Madhura Teekshna31. Amalaki Emblica Amla Guru Sheeta Madhura Tridosha hara Rochana, Deepana officinalis Pradhana Rooksha Anulomana
  • 118. Pancharasa Sheeta Rasayana Lavana Rahita32. Haritaki Terminalia Kashaya Laghu Ushna Madhura Tridosha Shothahara, chebula Pradhana Rooksha Vedanasthapaka, Pancha Rasa Anulomana, Mruduvirechaka, Deepana, Pachana33. Vibhitaki Terminalia Kashaya Laghu Ushna Madhura Tridosha hara Shothahara bellerica Rooksha Vedanasthapaka34. Devadaru Cedrus deodara Tikta Laghu Ushna Katu Kaphavata Shothahara Snigdha Shamaka Vedanasthapaka Deepana pachana35. Babbula Twak Acacia arabica Kashaya Guru Sheeta Katu Kaphapitta Dahasamaka, Rooksha Shamaka Vrushya36. Shatavari Asperagus Madhura Guru Sheeta Madhura Kaphapitta Vedana sthapana recemosus Tikta Snigdha Shamaka Balya rasayana
  • 119. Drug ReviewAJAMODADI CHURNA: ContentsName of the drug Latin Name Quantity1. Ajamoda Carum roxburghianum 1 part2. Vidanga Emblia ribes 1 part3. Saidhava Sodium cloride 1 part4. Pippalimoola Piper longum Linn. 1 part5. Chitraka Plumbago zeylanica 1 part6. Devadaru Cedrus deodara 1 part7. Pippali Piper longum Linn. 1 part8. Maricha Piper nigrum Linn. 1 part9. Shatapushpa Anethum sowa 1 part10. Haritaki Terminalia chebula 5 part11. Vrudhadaru Argyreia speciosa 10 part12. Nagara Zingiber officinale 10 part Ajamodadi churna, a compound preparation contains above mentioned12 ingredients.Method of preparation: The first 9 drugs mentioned above are taken 1 part each, where asHareetaki is 5 parts, Nagara and Vruddhadaru are taken 10 parts each. Theseabove mentioned drugs are taken as per classics and made into Churna.Dose: 5 gms thrice a day with hot water before food.Duration: For 30 days in patient of group AC. 83
  • 120. Drug Review First 9 ingredients are used commonly in both Ajamodadi Churna andEranda Paka preparation. These drugs are Deepaka, Pachaka and VataAnulomana in nature.5 Details of which are explained in Table No. 3. 84
  • 121. Table no. 3-Properties and therapeutic effect of the individual drugs in Ajamodadi Churna:Sl. Name of the Latin Name Rasa Guna Veerya Vipaka Doshagnata KarmukataNo. Drug01 Ajamoda Carum Katu, Tikta Laghu Ushna Katu Kaphavata Vedanasthapaka, Deepana, roxburghianum Rookshna Nashaka Pachana, Vidahi, Teekshna Vatanulomana,02 Vidanga Embelia ribes Katu Laghu Ushna Katu Kaphavata Deepana, Pachana, Kashaya Rooksha Shamaka Anulomana Teekshna03 Saindhava Sodium Lavana Snigdha Sheeta Lavana Deepana Deepana, Pachana, chloride Teekshna Pachana Vatanulomana Laghu Vatanulomana Sookshma Tridoshahara04 Devadaru Cedrus Tikta Laghu Ushna Katu Kaphavata Deepana, Pachana deodara Snigda Shamaka Anulomana05 Chitraka Plumbago Katu, Tikta Teekshna Ushna Katu Kaphavata Vedanastapaka zylanicum Laghu Shamaka Deepana Rookshna Pachana06 Pippali moola Piper longum Katu Laghu, Anushna Madhura Kaphavata Deepana, Triptighna, Snigdha, Shamaka Vatanulomana, Balya, Teekshna Rasayana07 Pippali Piper longum Katu Laghu, Anushna Madhura Kaphavata Deepana, Triptighna, Snigdha, Shamaka Vatanulomana, Balya, Teekshna Rasayana08 Shatapushpa Anethum sowa Katu Laghu Ushna Katu Kaphavata Rochana, Deepana, Pachana, Tikta Rooksha Shamaka Anulomana, Shothahara Teekshna09 Maricha Piper nigrum Katu Laghu, Ushna Katu Kaphavata Deepana, Pachana Teekshna Shamaka Vatanulomana10 Nagara Zingiber Katu Laghu, Ushna Madhura Kaphavata Triptighna, Rochana, Deepana, officinale Snigdha Shamaka Pachana, Vatanulomana, Shothahara11 Vriddhadaru Argeria Tikta Laghu, Ushna Katu Kaphavata Vedanasthapana, speciosa Snigdha Shamaka Deepana, Pachana12 Haritaki Terminalia Kashaya Laghu Ushna Madhura Tridosha Shothahara, Vedanasthapana, chebula Pradhana Rooksha Anulomana, Mruduvirechana, Pancha Rasa Deepana, Pachana
  • 122. Drug ReviewPANCHAKOLA PHANTA:3 This yoga contains 5 ingredients which are taken in equal quantity andmade into coarse powder. Phanta is prepared according to the Phanta Vidhi. Inboth the group patients’, Panchakola Phanta 20 ml thrice daily administeredbefore food for a period of three days. The list of ingredients is given below: Ingredients Proportion Pippali 1part Pippali moola 1part Chavya 1part Chitraka 1part Nagara 1part As discussed earlier Agni Deepana and Ama Pachana holds itssupremacy in treating the disease Amavata Deepana-Pachana helps inSampraptivighatana by virtue of its qualities. In Panchakola phanta, most of thedrugs are having Tikshna guna and Ushna veerya. Because of these qualitiesit, does the Dosha Niramata and prevents further production of Ama6 (Table No.4). This in turn brings vitiated Dosha to Koshta so that later it can be removed.Hence the Panchakola Phanta is opted. 85
  • 123. Table no. 4-Properties and therapeutic effect of the individual drugs in Panchakola Phanta: Sl.No. Name Latin Rasa Guna Veerya Vipaka Doshagnata Karmukata Name 01 Pippali Piper Katu Lagu, Anushnasheeta Madhura Kaphavata Deepana, Triptigna, longum Snigdha, Vatanulomana, Mruduvirechana, Teekshna Balya, Rasayana 02 Pippali Piper Katu Lagu, Anushnasheeta Madhura Kaphavata Deepana, Triptighna, moola longum Snigdha, Vatanulomana, Mruduvirechana, Teekshna Balya, Rasayana 03 Chavya Piper chaba Katu Lagu, Ushna Katu Kaphavata Deepaka, Pachaka Rooksha Shoolaprashamana Vatanulomana 04 Chitraka Plumbago Katu Lagu, Ushna Katu Kaphavata Deepaka, Pachaka zeylanicum Rooksha Shoolaprashamana Teekshna Vatanulomana 05 Nagara Zingiber Katu Lagu, Ushna Katu Kaphavata Deepaka, Pachaka officinale Snigdha Shoolaprashamana Vatanulomana
  • 124. Drug ReviewEranda Taila: Action of Eranda Taila in the management of Amavata has beencompared to the supremacy of the lion in the rivalry between lion and elephant4.Eranda has Madhura rasa, Katu, Kashaya Anurasa; Snigdha, Tikshna,Sukshma are its Gunas. It undergoes Madhura vipaka and has Ushna veerya7. Due to the above said qualities, it does Vata and Kapha Shamana. It issaid that it does Srotovishodhana and thus can be employed in Samavatacondition. For the above said reasons, Taila has been selected for KoshtaShodhana7. After the Deepana, Pachana by administering Panchakola phanta for 3days, Eranda Taila administered 10 ml once in morning hours on emptystomach for 3 days.REFERENCES: 1. Y.R. Poorva Kha. Vatavyadhi Chi 1-5 2. Y.R. Poorva Kha. Amavata Chi. 1-3 3. B.R. 5/193 4. B.R. 28/23 5. D.G. vol. II by P.V.Sharma 6. B.P. Madhya Kha. 26/49 7. S.S.Su. 45/114 86
  • 125. Materials and Methods MATERIALS AND METHODSMATERIALS TAKEN FOR THE STUDY:Eranda Paka: Prepared according to the prescribed method in S.D.M.Ayurvedic Pharmacy.Ajamodadi Churna: Prepared according to the prescribed method in S.D.M.Ayurvedic Pharmacy.Panchakola Phanta: Prepared using Panchakola phanta churna procured fromS.D.M. Ayurvedic Pharmacy.Eranda Taila: Procured from S.D.M. Ayurvedic Pharmacy.METHODS:Objective of the study:1) To evaluate effect of Eranda Paka in the management of Amavata2) To study the efficacy of Ajamodadi Churna in Amavata3) To compare the efficacy of Eranda Paka and Ajamodadi Churna in Amavata.Source of data: 20 patients diagnosed as Amavata (Rheumatoid arthritis) from IPD andOPD of S.D.M. Ayurveda Hospital, Udupi. The patients were randomly groupedinto two groups of 10 each which were called Group EP (Eranda Paka group)and Group AC (Ajamodadi Churna group)Study design: Single blind comparative clinical study with pre-test and post-test design. 87
  • 126. Materials and MethodsInclusion criteria: • Patients aged between 16 – 70 years age • Signs and symptoms of Amavata • Criteria for diagnosis of Rheumatoid Arthritis as approved by American Rheumatism Association (ARA),1987 revisionExclusion criteria: • All connective tissue disorders other than Rheumatoid arthritis. • Systemic Lupus Erythematosus • With any other systemic disorderDiagnostic criteria: Patients were diagnosed on the basis of signs and symptoms ofAmavata and the criteria as approved by ARA, 1987 revision • Morning stiffness* (Stabdata) (>1hour) • Arthritis of three or more joints* (Shoola and Shotha in three or more joints) • Arthritis of hand joints.* • Symmetrical arthritis.* • Rheumatoid nodules. • Rheumatoid factor. • Radiological changes. * - Duration of 6 weeks or more. N.B. Diagnosis of R.A. made with four or more criteria. 88
  • 127. Materials and MethodsAssessment criteria: The patients were observed on the weekly basis and the change insubjective signs and symptoms assessed by suitable scoring method andobjective signs using appropriate clinical tools. Details of which are given below.A. Subjective criteria:1. Pain in the joints: Symptom Grading No pain 0 Mild (on motion only) 1 Moderate (at rest) 2 Severe (wakes patient from sleep) 32. Morning stiffness (duration in hours): Symptom Grading 0-5 min. 0 5 min. - 2 hrs. 1 2 - 8 hrs. 2 8 hrs. or more 33. Swelling in the joints: Symptom Grading Absent 0 Mild 1 Moderate 2 Severe 3 89
  • 128. Materials and Methods4. Redness: Symptom Grading Absent 0 Mild 1 Moderate 2 Severe 35. Warmth: Symptom Grading Absent 0 Mild 1 Moderate 2 Severe 36. Tenderness in the joints: Symptom Grading No tenderness 0 Says tender 1 Patient winces 2 Winces and withdraws 3 Not allowed to be touched 4 90
  • 129. Materials and Methods7. Alasya: Symptom Grading Fully active 0 Mild laziness, slow initiative in work 1 Initiative in some works, absent in others 2 Absolute lack of initiative even though capacity for work exists 38. Dourbalya: Symptom Grading No feeling of weakness 0 Slight weakness 1 Feeling of weakness but ability unimpaired 2 Ability to do duties affected 39. Knuckle swelling: Jewellers rings were used to measure the knuckle swelling. The ringwhich passes through knuckle with least resistance was noted. Any change inthe number of the ring after the treatment was recorded.10. Muscle wasting: The circumference of arm, fore arm, thigh and calf were measured incms using a measuring tape both before and after treatment to have anobjective view of muscle wasting. 91
  • 130. Materials and Methods11. Malabaddhata/Vibandha (Constipation): Symptom Grading Absent 0 Slight with one motion per day 1 Marked constipation with one motion after two days or more 212. Jwara (in degree Fahrenheit): Symptom Grading No fever 0 Mild (990 F-1010 F) 1 Moderate (1010 F-1030 F) 2 Severe (>1030 F) 313. Sadana - fatigue: Symptom Grading No fatigue 0 Works full-time despite some fatigue 1 Patient must interrupt to rest 2 Fatigued at rest 3 92
  • 131. Materials and Methods14. Bahumootrata (frequency of micturition per 24 hours): Symptom Grading Absent (less than 4 times/24 hrs) 0 Mild (upto 6 times/24 hrs) 1 Moderate (6-10 times/ 24 hrs) 2 Severe (> 10 times/ 24 hrs) 315. Chardi (frequency of bouts per 24 hours): Symptom Grading Absent 0 Mild (upto 2 vegas/24 hrs) 1 Moderate (2-4 vegas/24 hrs) 2 Severe (4 vegas/24 hrs) 316. The other symptoms like Angamarda, Aruchi, Gourava, Brama,Kukshishoola, Hrithgraha, Anaha, Praseka, Trishna, Hasta pada daha, Kanduare scored as mentioned below. Grading No symptoms 0 Mild symptoms 1 Moderate symptoms 2 Severe symptoms 3 93
  • 132. Materials and MethodsB. Functional assessment: To assess the objective improvements following functional assessmentswere carried out in patients of Amavata.1. Grip strength: The patient’s ability to compress the inflated ordinarysphygmomanometer cuff under standard conditions to assess the functionalcapacity of effected upper limb, both before and after treatment.2. Foot pressure: Foot pressure was recorded both before and after treatmentby the ability of the patient to press a weighing machine, to an objective view offunctional capacity of lower limb.3. Range of joint movement: By using the Goniometer the range of movementof all effected joints was noted both before and after treatment.4. General functional capacity: • Complete ability to carry on all usual duties without handicap 1 • Adequate normal activity despite handicap of discomfort or limited joint movement 2 • Limited only to little or none of the usual occupation or self care 3 • Bedridden or confined to wheel chair, little or no self care 4C. Investigations: To assess the general condition and to confirm the diagnosis followinginvestigation were conducted before after the treatment 1. Hemoglobin percentage (Hb% using Sahli’s method) 2. Total Leukocyte count (TC using Neubauer’haemocytometer) 3. Differential Leukocyte count (DC using Neubauer’haemocytometer) 94
  • 133. Materials and Methods 4. Erythrocyte sedimentation rate (ESR using Westergren’s method) 5. Rheumatoid arthritis factor (using immunoglobulin agglutination method) 6. If required other investigations to rule out other pathologies.D. Disease activity degrees: On basis of criteria laid down by American rheumatism association(1967) the degree of disease activity was estimated for the diagnosis andtherapeutic purpose. Details are as follows: Grade 0 1 2 3 Morning 5 minutes or 5 minutes to 2 2 to 8 hours 8 hours or stiffness less hours Fatigue None Works full time must interrupt Fatigue at rest despite some work to rest fatigue Pain None only on At rest Wakes patient movement from sleep. Patients Fine Almost well Pretty good Pretty bad estimation General Full activity Most activities Few activities Little self care function without difficulty but with difficulty cares for self mainly chair and bed Grip strength 200mm/Hg or 195 to 120 115 to 70 under 70mm/Hg more mm/Hg mm/Hg Spread of joint None 0to50 51to100 Over 100 Involvement Westergren 0to20mm 20to35 35to50 above 50 ESR Haemoglobin 12.5gms% 12.4to11gms% 10.9to9.5gms% Less than 9.5gms% Physicians Inactive Minimal active moderately severely active estimate active 95
  • 134. Materials and MethodsE. Overall assessment of the treatment: The overall effect of the therapies assessed on the basis of criteria laiddown by ARA (1967) was adopted. The results are classified as four groups aslisted below.Grade I: Complete remission • No systemic signs of rheumatoid activity. • No sign of inflammation. • No evidence of activity in any extra articular process, including nodules, tino-vaginitis and iritis. • No lasting impairment of joint mobility other than that associated with irreversible changes. • No elevation of erythrocyte sedimentation rate. • Articular deformity or extra articular involvement due to irreversible changes may be present.Grade II: Major improvement • No systemic sign of rheumatoid activity, with the exception of an elevated sedimentation rate and vasomotor imbalance. • Major signs of inflammation resolved, such as heat, redness of joint structures. • No new rheumatoid process of intraarticular or extraarticular structures. • Minimum joint swelling may be present. 96
  • 135. Materials and Methods • Impairment of joint mobility associated with minimum residual activity may be present. • Articular deformity or extra articular involvement due to irreversible changes may be present.Grade III: minor improvement Any decrease in the signs of rheumatoid activity inadequate to fulfill thecriteria of grade II. • Diminution of systemic signs of rheumatoid activity. • Signs of joint inflammation only partially resolved. • No evidence of extension of rheumatoid activity into additional articular or extra articular structures. • Decreased but not minimum joint swelling present. • Impairment of joint mobility may be present. • Articular deformity or extraarticular involvement due to irreversible changes may be present.Grade IV: Unimprovement or progression • Undiminished signs of rheumatoid activity, regardless of functional capacity. • Exacerbation of any previously involved joint or joints, or development of sites of rheumatoid activity. • Roentgenologic changes indicative of progression of the rheumatoid process, excepting hypertrophy changes. 97
  • 136. Materials and Methods • In the presence of one or more of the aforesaid criteria, involvement in other features, including a normal or lowered ESR, not significant. • Items which must be present.INTERVENTION:Deepana Pachana and Koshta Shodhana: • Patients were randomly divided into two groups of minimum 10 patients each. • Before administration of medication, all patients of both groups were given Panchakola phanta 20 ml thrice daily before food for first three days for Deepana - Pachana. • All patients of both groups were then given Eranda Taila 10ml on empty stomach in the morning for next three days for Koshta Shodhana.Eranda Paka and Ajamodadi Churna: • Patients of Group EP were given Eranda Paka 15 gms three times daily after food with warm water for 30 days. • Patients in group AC were given Ajamodadi Churna 5 gms three times daily after food with hot water for 30 days. 98
  • 137. Observations OBSERVATIONS In both the Eranda Paka and Ajamodadi Churna group, a total of 20patients suffering from Amavata fulfilling the inclusion criteria were studied. Theobservation and the results as well as statistical analysis of these areelaborated as mentioned below. • Descriptive statistical analysis. • Assessment of the effect of Eranda Paka and Ajamodadi Churna in patients of Amavata, and the assessment of the significance of the treatment by adapting the paired ‘t’ test. • Comparison of the effects of treatment between the Eranda Paka group and Ajamodadi Churna group, and statistical analysis of the comparison by performing unpaired ‘t’ test.Descriptive statistical analysis:Age group of patients: Out of 20 patients of Amavata studied in this work,maximum number of 6 (30%) patients belonged to the age group of 50 to 60years, against a minimum of 1 (5%) patient was in the age group of 10 to 20years. The details are given in the Table No. 5 and Graph No. 1.Sex incidence of patients: 15 (75%) of patients of Amavata were females asagainst only 5 (25 %) of males in the present study. The details are elaboratedin the Table No. 6 and Graph No. 2. 99
  • 138. ObservationsIncidence of Religion: As shown in the Table No. 7 and Graph No. 3 (65%) ofpatients were Hindus, 5 (25%) were Muslims and only 2 (10%) of patients wereChristians.Incidence of Literacy: Prevalence of literates was recorded in the presentstudy involving 20 patients of Amavata. 45% of the patients were illiterates andthe remaining 55% of patients had education, as detailed in the Table No. 8 andGraph No. 4.Incidence of Marital status: Among the 20 patients of Amavata taken for thisstudy, a maximum of 16 (80%) patients were married as against mere 4 (20 %)of unmarried people. The details are shown in the Table No. 9 and Graph No. 5.Socio-economical status of patients: The study revealed that most of thepatients belonged to either poor (35%) or lower middle socio-economical status(35%) category. None of the patients were either from rich socioeconomicstatus or from very rich socioeconomic status. Very poor percentage of patientswere from the middle class socioeconomic status (5%) and the upper middleclass socioeconomic status (5%) category. The details are given in the TableNo. 10 and Graph No. 6.Incidence of Occupation: It is observed that 12 (60%) of the females in thisstudy were house wives by their occupation. Also, this formed the largestcategory of patients leaving behind the patients engaged in other occupations. 100
  • 139. ObservationsNo patients from the business or student category were recorded in any of thegroups. Details are given in the Table No. 11 and Graph No. 7.Incidence of Habits: Large percentage of patients in this study did not haveany addiction. Only 6 (30%) patients reported addiction to tobacco chewing asagainst 14 (70%) of the non addicts. Table No. 12 and Graph No. 8 show thedetails of the habits of patients.Prakriti of patients: All the patients in the present study belonged to theDvandaja Prakriti. 6 (30%) patients were of Vatapitta and Vatakapha each. Themaximum 8 (40%) patients were of Pittakapha Prakriti Table No. 13 and GraphNo. 9.Severity of the Vikriti: The degree of Vikriti was assessed to be Madhyama, ina maximum of 16 (80%) patients in the present study followed by Avara in 3(15%) patients and Pravara Vikriti in 1 (5%) patient. Details of the distribution ofthe patients according to their degree of Vikriti is given in the Table No. 14 andGraph No. 10.Satva of patients: Majority of 14 (70%) patients belong to Madhyama Satva, 3(15%) were of Pravara Satva and Avara Satva each in this study. The detailsare shown in Table No. 15 and Graph No. 11.Sara of patients: The assessment of Sara in 20 patients of Amavata showedmaximum number of patients having Madhyama Sara 19 (95%) and remaining 101
  • 140. Observations1 (5%) patient belong to Avara Sara. Incidence of patients according to theirSara is detailed in the Table No. 16 and Graph No. 12.Samhanana of patients: Samhanana of every patient was assessed beforethe treatment, and it was observed that among the 20 patients 17 (85%) of thepatients had Madhyma Samhanana. Pravara Samhanana was recorded in just1 (5%) of the patients. Remaining 2 (10%) of the patients showed characters ofthe Avara Samhanana. The detail of the same are given in the Table No. 17and Graph No. 13.Satmya of patients: Observation of 20 patients of Amavata revealed that only1 (5%) of the patients had Pravara Satmya, and the remaining 19 (95%) ofpatients showed Madhyama Satmya. Table No. 18 and Graph No. 14 show thedetails.Ahara Abhyavaharana Shakti in patients of Amavata: Interrogation of the 20patients of Amavata revealed that 12 (60%) of the patients had MadhyamaAbhyavaharana Shakti and 4 (20%) each patients had either Pravara or AvaraAbhyavaharan Shakti. Details are given in the Table No. 19 and Graph No. 15.Ahara Jarana Shakti of patients: Jarana Shakti of 20 patients suffering fromamavata revealed that majority 12 (60%) had Madhyama Jarana Shakti. 4(20%) each patients had the Avara and Pravara Jarana Shakti. The same isshown in the Table No. 20 and Graph No. 16. 102
  • 141. ObservationsVyayama Shakti of patients: Madhyama Vyayama Shakti is recorded in 13(65%) of patients. 5 (25%) of the patients had Avara Vyayama Shakti and theremaining 2 (10%) patients had Pravara Vyayama Shakti. The same is given inthe Table No. 21 and Graph No. 17.Vaya of the patients: All the 20 patients in this study belonged to MadhyamaVaya. This has been shown in Table No. 22 and Graph No. 18. 103
  • 142. ObservationsTable No. 5-Age Group of Patients: Total Age in years No % 10-20 1 5 20-30 4 20 30-40 5 25 40-50 4 20 50-60 6 30Graph No. 1-Age groupwise distribution of patients: 30% 30% 25% 25% 20% 20% 20% 15% 10% 5% 5% 0% 10‫02ـ‬ 20-30 30-40 40-50 50-60
  • 143. ObservationsTable No. 6-Sex Incidence of Patients: Total Sex No % Male 5 25 Female 15 75Graph No. 2-Percentage of patients of different sex: 80% 75% 70% 60% 50% 40% 30% 25% 20% 10% 0% Male Female
  • 144. ObservationsTable No. 7-Religion of patients 20 patients of Amavata: Total Religion No % Hindu 13 65 Muslim 5 25 Christian 2 10 Others 0 0Graph No. 3-Percentage of patients of different religion: 65% 70% 60% 50% 40% 25% 30% 20% 10% 10% 0% Hindus Muslims Christian
  • 145. ObservationsTable No. 8-Literacy incidence in patients of Amavata: Total Education No % Illiterate 9 45 Literate 11 55Graph No. 4-Incidence of Literacy: 55% 60% 45% 50% 40% 30% 20% 10% 0% Literate Illiterate
  • 146. ObservationsTable No. 9-Marital status of Amavata patients: Total Marital Status No % Single 4 20 Married 16 80 Widowed 0 0Graph No. 5-Percentage of patients of different marital status: 80% 80% 70% 60% 50% 40% 20% 30% 20% 10% 0% Married Unmarried
  • 147. ObservationsTable No. 10-Socio-economic status of patients: Total S.E.Status No % Poor 7 35 Lower Middle 7 35 Middle 5 25 Upper Middle 1 5 Rich 0 0 Very Rich 0 0Graph No.6-Incidence of Socio-economical status of patients: 35% 35% 35% 30% 25% 25% 20% 15% 10% 5% 5% 0% 0% 0% Poor L.Middle Middle U.Middle Rich Very Rich
  • 148. ObservationsTable No. 11-Incidence of occupation in Amavata patients: Total Occupation No % Manual Laborer 6 30 House Wife 12 60 Student 0 0 Business 0 0 Others 2 10Graph No.7-Occupation wise distribution of patients: 60% 60% 50% 40% 30% 30% 20% 10% 10% 0% 0% 0% Laborer House-Wife Student Buisness Others
  • 149. ObservationsTable No. 12-Study of Habit incidence: Total Habit No % Alcohol 0 0 Tobacco 6 30 Smoking 0 0 None 14 70Graph No. 8- Distribution of patients according to their habits: 70% 70% 60% 50% 40% 30% 30% 20% 10% 0% 0% 0% Alcohol Tobacco Smoking None
  • 150. ObservationsTable No. 13-Study of patients Prakriti in the study: Total Prakriti No % Vata 0 00 Pitta 0 00 Kapha 0 00 Vata-Pitta 6 30 Pitta-Kapha 6 30 Vata-Kapha 8 40 Sama 0 00Graph No.9- Prakriti wise distribution of patients: 40% 40% 35% 30% 30% 30% 25% 20% 15% 10% 5% 0% 0% 0% 0% 0% Vata Pitta Kapha V-P V-K P-K Sama
  • 151. ObservationsTable No.14-Incidence of Vikriti: Total Vikriti No % Pravara 1 5 Madhyama 16 80 Avara 3 15Graph No. 10-Vikruti wise distribution of patients: 80% 80% 70% 60% 50% 40% 30% 15% 20% 5% 10% 0% Pravara Madhyama Avara
  • 152. ObservationsTable No.15-Incidence of Satva in the Study: Total Satva No % Pravara 3 15 Madhyama 14 70 Avara 3 15Graph No. 11-Percentage of patients according to Satva: 70% 70% 60% 50% 40% 30% 15% 15% 20% 10% 0% Pravara Madhyama Avara
  • 153. ObservationsTable No.16-Study of Saratah Incidence in the Study: Total Saratah No % Pravara 0 0 Madhyama 19 95 Avara 1 5Graph No. 12- Percentage of patients according to Sara: 95% 100% 90% 80% 70% 60% 50% 40% 30% 20% 0% 5% 10% 0% Pravara Madhyama Avara
  • 154. ObservationsTable No. 17-Study of patients Samhanana in the study: Total Samhanana No % Pravara 1 5 Madhyama 17 85 Avara 2 10Graph No.13. Percentage of patients according to Samhanana: 85% 90% 80% 70% 60% 50% 40% 30% 10% 20% 5% 10% 0% Pravara Madhyama Avara
  • 155. ObservationsTable No. 18-Satmya Incidence: Total Satmya No % Pravara 1 5 Madhyama 19 95 Avara 0 0Graph No. 14- Percentage of patients according to Satmya: 95% 100% 90% 80% 70% 60% 50% 40% 30% 5% 0% 20% 10% 0% Pravara Madhyama Avara
  • 156. ObservationsTable No. 19- Percentage of patients according to Abhyavaharana Shakti: Total Ahara-Abhyavaharana Shakti No % Pravara 4 20 Madhyama 12 60 Avara 4 20Graph No. 15-Percentage of patients of different Abhyavaharana Shakti: 60% 60% 50% 40% 30% 20% 20% 20% 10% 0% Pravara Madhyama Avara
  • 157. ObservationsTable No. 20-Study of Patients Ahara-Jarana Shakti the Study: Total Ahara-Jarana Shakti No % Pravara 4 20 Madhyama 12 60 Avara 4 20Graph No. 16- Percentage of patients according to Aahara-Jarana Shakti: 60% 60% 50% 40% 30% 20% 20% 20% 10% 0% Pravara Madhyama Avara
  • 158. ObservationsTable No. 21-Study of patients Vyayama Shakti in the study: Total Vyayama Shakti No % Pravara 2 10 Madhyama 13 65 Avara 5 25Graph No. 17- Percentage of patients according to Vyayama Shakti: 65% 70% 60% 50% 40% 25% 30% 10% 20% 10% 0% Pravara Madhyama Avara
  • 159. ObservationsTable No.22-Vaya incidence: Total Vaya No % Bala 0 0 Madhyama 20 100 Vruddha 0 0Graph No. 18- Percentage of patients according to Vaya: 100% 100% 90% 80% 70% 60% 50% 40% 30% 20% 0% 0% 10% 0% Baala Madhyama Vruddha
  • 160. Results RESULTSEranda Paka groupEffect on cardinal signs and symptoms: The oral administration of Eranda Paka had resulted in remission of allthe cardinal symptoms of Amavata as elaborated in the following paragraph.Effect on Stabdhata: Patients treated with Eranda Paka marked remission of the symptomStabdhata was recorded. 2.3 was the mean initial score of Stabdhata in 10patients of Amavata came down to 1.1 after the treatment. The improvement tothe tune of 52% is found to be statistically highly significant (P≤0.001) as shownin the Table No. 23 and Graph No. 19.Effect on Sandhi Shoola: Sandhi Shoola, one of the cardinal symptoms of Amavata relieved by65% as the initial score of Sandhi Shoola which was 2.3 reduced to 0.8 after thetreatment with Eranda Paka. This improvement when analyzed by the paired ‘t’test found to the highly significant (P≤0.001). Table No. 23 and Graph No. 19provides the details.Effect on Sandhi Shotha: 69% of improvement was observed in the symptom Sandhi Shotha.1.353 was the initial mean score of Sandhi Shotha recorded in the 10 patientsof Amavata in this group. This was brought down to 0.418 after the 104
  • 161. Resultsadministration of Eranda Paka. This improvement after the treatment is found tobe highly significant (P≤0.002) as per the paired ‘t’ test. The detail of thedifferent statistical values are shown in the Table No. 23 and Graph No. 19.Effect on tenderness: 1.649 was the mean initial score of tenderness before the treatment inpatients of Eranda Paka group. This initial mean score came down to 0.439after the treatment. The improvement to the tune of 73% was highly significant(P≤0.001) as revealed by the paired ‘t’ test. Details of the same are given in theTable No. 23 and Graph No. 19.Effect on Crepitation: Crepitation is another cardinal symptom of Amavata. None of thepatients in this Eranda Paka group presented this symptom. Therefore, theeffect of the Eranda Paka in relieving this symptom could not be assessed.Details of the same are represented in the Table No. 23 and Graph No. 19.Effect on general symptoms: Complete cure of the symptom Jwara was observed in all the patientstreated with Eranda Paka. The initial mean score of Jwara was 0.6, and itbecame 0 after the treatment. 91% remission of the symptom Aruchi wasrecorded in patients of Amavata. The initial mean score of Aruchi which was 2.2was reduced to 0.2 after the treatment with Eranda Paka. A minimal mean initialscore of 0.5 was observed in the symptom trit. Complete remission of trit wasrecorded after the treatment with Eranda Paka. 76% of the improvement was 105
  • 162. Resultsnoted in the symptom Alasya. The initial mean score of 2.10 was reduced to 0.5after the treatment. Before the institution of the treatment the initial mean scoreof the symptom Apaka was 2.3. This came down to 0.2 after the treatment. Theimprovement by the treatment recorded was 91%. Marked improvement wasobserved in the symptom Angamarda also. The initial mean score ofAngamarda was 2.3 and was reduced by 57% after the treatment. Thesymptoms like Angasunata, Raga, Staimitya, Angagourava, Kandu andAntrakujana was not found in any of the 10 patients studied in this group. Theinitial mean score of 1.3 of the symptom Daha was reduced by 92% after thetreatment. The mean score of Daha was 0.1 after the treatment. Completeremission of the Hrillasa was observed in all the patients treated with ErandaPaka. The initial mean score of 0.1 came down to 0 after the treatment. Theinitial mean score of Chardi was 0.10. Cent percent remission of this symptomwas observed after the treatment. Complete remission of the symptom Anahawas noted in all the patients. The initial mean score of Anaha, which was 1.0became zero after the employment of the treatment. 0.5 was the initial meanscore of the symptom Praseka in patients treated with Eranda Paka. Thesymptom got completely cured after the treatment. The initial mean score of thesymptom Kukshi Shoola was found to be 0.3. This initial score reached to zeroafter the treatment releaving 100% cure. 50% of improvement was observed inpatients complaining of disturbed sleep. The initial mean score of the symptomNidralpata was 1.0 and that dropped to 0.5 after the treatment. The details of 106
  • 163. Resultsthe effect of the Eranda Paka on different general symptoms of Amavata aregiven in the Table No. 24 and Graph No. 20.Effect on total score of general symptoms: The mean of the total score of general symptoms showed markedimprovement in these symptoms. Initially before the treatment the total score ofgeneral symptom was 18.6 and was reduced to 3.3 after the administration ofthe Eranda Paka. An over all improvement of 82% in general symptoms wasrecorded in this group. The improvement after the treatment is also statisticallyhighly significant (P≤0.001) as revealed by the paired ‘t’ test. The details aregiven the Table No. 25 and Graph No. 21.Effect of Eranda Paka on symptoms of Ama: Significant improvement was noticed in all the symptoms indicative ofAma by the administration of Eranda Paka. Bala of the patients was improvedby 64% as suggested by the change in the symptom score to 0.80 after thetreatment from the initial score of 2.20. The symptom Gaurava was notobserved in any patients studied in this group. The initial mean score of Alasya,which was 2.1 before the treatment dropped down to 0.50 after the treatment.Thus the treatment showed a reduction of Alasya by 76 %. Complete remissionof the symptom Apaka was recorded in patients of Amavata treated with ErandaPaka. The initial score before the treatment was 1.10, and which came down tozero after the treatment. The initial mean score of Nistiva was 0.5, which camedown to zero after the treatment recording complete remission of the symptom. 107
  • 164. Results91% of the improvement was recorded in the symptom Aruchi. The initial scoreof 2.20 reduced to 0.2 after the treatment with Eranda Paka. Proper bowel habitwas restored after the medication with Eranda Paka in patients of Amavata.Before the treatment the severity score of Vibanda was 1.1, and it became zeroafter the treatment suggesting the complete remission. Impaired taste in themouth was reduced by the treatment with Eranda Paka to the tune of 64%. Themean score of Aruchi was reduced by 2.0 from the initial score of 2.2 before thetreatment. Patients felt more comfortable after the treatment as the severity ofthe Klama was reduced by the treatment. 2.2 was the initial score of Klamabefore the treatment. This score dropped down to 0.8 following the treatment.Analysis of the symptoms of the Ama before and after the treatment iselaborated in the Table No. 26 and Graph No. 22.Statistical analysis of effect on symptoms of Ama: Before the treatment the total score of symptoms of Ama was 12.7. Afterthe treatment with Eranda Paka this reduced to 2.4. The total improvement wasto the tune of 81%. This improvement after the treatment was found to bestatistically highly significant (P≤0.001) as assessed by the paired ‘t’ test. Thedetails of the same is given in the Table No. 27 and Graph No. 23.Effect on clinical parametersEffect on circumference of the limbs: The circumference of the limbs that was assessed before and after thetreatment showed that there was neither increase nor decrease in the 108
  • 165. Resultscircumference after the medication with Eranda Paka. The details of the sameis given in the Table No. 28.Effect on the range of joint movement: Range of joint movement was increased after the treatment with ErandaPaka in patients of Amavata. Initially an average range of 61.98 degree of jointmovement was recorded. This range of joint movement was increased to78.864 after the treatment. The paired ‘t’ test revealed that this change after thetreatment was not because of the chance factor. The improvement of jointmovement was highly significant. The details are given in the Table No. 29 andGraph No. 24.Effect on foot pressure: Improvement in the foot pressure was recorded in patients of ErandaPaka group. Before the treatment the average foot pressure of the patients was30.4 kgs. And this was increased to 38.95 kgs after the treatment. This markedchange after the treatment was also statistically highly significant according tothe paired ‘t’ test. Table No. 29 and Graph No. 24 shows the detail of thestatistical values.Effect on hand grip power: After the treatment with Eranda Paka the hand grip power of the patientswas significantly increased. The average hand grip power before the treatmentwas 62.000 mm of hg. After the administration of the Eranda Paka it increased 109
  • 166. Resultsto 85.950 mm of hg. This increase in hand grip power after the treatment wasfound to be statistically highly significant (P≤0.001). Table No. 29 and GraphNo. 24 shows the detail.Effect on general functional capacity: Treatment with Eranda Paka has shown favorable effect on functionalability of patients of Amavata. The functional disability score before thetreatment was estimated as1.700. And this score came down to 0.800 recordingan improvement by 52%. Statistical analysis by adapting paired ‘t’ test revealedthat this change after the treatment is highly significant (P≤0.001). Details aregiven in the Table No. 29 and Graph No. 24.Effect on body weight: The body weight of the patients recorded before and after the treatmentshowed marginal change. There was very little increase of body weight by0.100 kg after the treatment. This change following the treatment is statisticallyinsignificant (P=0.343) as determined by the paired ‘t’ test. The details are givenin the Table No. 30.Effect on hematological valuesEffect on total leukocyte count: There was marginal decrease in total leukocyte count after the treatment.The initial TC was 10345.000 cu.mm and this came down to 8759.000 cu.mm.after the treatment. The details are shown in the Table No. 31 and GraphNo.25. 110
  • 167. ResultsEffect on differential count of WBC’s: Minimal change was also observed in the differential count of white bloodcorpuscles. The statistical analysis by adapting the paired ‘t’ test revealed thatthese changes after the treatment are insignificant. The details are given in theTable No. 31.Effect on haemoglobin percentage: Before the treatment the initial haemoglobin percentage was 10.175gm%. This was then increased to 10.970 gm% after the treatment. Thisincrease of hemoglobin by 0.795 gm% is statistically insignificant as shown bythe paired ‘t’ test. The details of the same are shown in the Table No. 31 andGraph No. 26.Effect on erythrocyte sedimentation rate: The erythrocyte sedimentation showed a marginal decrease. Before thetreatment the average ESR in patients of Amavata studied in this group was82.0 mm at 1st hour. A reduction by 38.400 mm at 1st hour was recorded afterthe treatment with Eranda Paka. This decrease in the ESR was also statisticallyhighly significant (P=0.006). Table No. 31 and Graph No. 27 shows the detail.Over all effect of treatment in 10 patients of Amavata: The assessment of the overall effect of the treatment revealed that 40%of the patients recorded complete remission. 30% of the patients showed majorimprovement. And an equal percentage of the patients also responded withminor improvement. All the patients studied in this Eranda Paka group showed 111
  • 168. Resultsdifferent degrees of remission. The details are given in the Table No. 32 andGraph No. 28. From the foregoing observations, it is clear that the patients who aretreated with Eranda Paka have shown favorable response in regards to cardinalsymptoms of Amavata, general symptoms of Amavata, clinical parameters,hematological investigations and overall effect of the medication. Most of theseimprovements are found to be statistically highly significant as per the paired ‘t’test except the few parameters like circumference of the limbs, body weight. 112
  • 169. Results Table No. 23-Effect of Eranda Paka on cardinal symptoms of Amavata:Signs and Mean score % of Paired ‘t’ testsymptoms B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ P Stabdata 2.3(0.483) 1.1 (0.316) 52 0.632 0.20 6.0 ≤0.001 Sandhi 2.3 (0.675) 0.8 (0.422) 65 0.527 0.167 9.00 ≤0.001 Shoola Sandhi 1.353 0.418 69 0.702 0.222 4.214 ≤0.002 Shotha (0.574) (0.498) 1.649 0.439Tenderness 73 0.269 0.0849 14.249 ≤0.001 (0.317) (0.277)Crepitation 0 0 - - - - - Graph No. 19-Effect of Eranda Paka on cardinal symptoms of Amavata: 2.3 2.3 2.5 2 1.65 1.5 1.1 1.35 BT 0.8 1 AT 0.5 0.42 0.44 0 0 0 Stabdata S Shoola S Shotha Tenderness Crepetation
  • 170. ResultsTable No. 24-Effect of Eranda Paka on general symptoms of Amavata: Mean score Percentage of Symptoms Initial After treatment relief. Jwara 0.600 0.000 100 Aruchi 2.200 0.200 91 Trit 0.500 0.000 100 Alasya 2.100 0.500 76 Apaka 2.300 0.200 91 Angamarda 2.300 1.000 57 Anga Sunata 0 0 0 Daha 1.300 0.1000 92 Raga 0 0 0 Staimitya 0 0 0 Gaurava 0 0 0 Kandu 0 0 0 Hrillasa 0.1000 0.000 100 Chardi 0.1000 0.000 100 Anaha 1.000 0.000 100 Praseka 0.500 0.000 100 Antrakujana 0 0 0 Kukshi Shoola 0.300 0.000 100 Vibanda 1.100 0.000 100 Shrama 2.200 0.800 63 Bahumutra 0.500 0.000 100 Bhrama 0.1000 0.000 100 Hridgraha 0.500 0.000 100 Nidralpata 1.000 0.500 50
  • 171. ResultsGraph No. 20-Improvement in general symptoms recorded in patientstreated with Eranda Paka: 0.5 Nidralpata 1 0 Hridgraha 0.5 0 Bhrama 0.1 0Bahumutra 0.5 0.8 Shrama 2.2 0 Vibandha 1.1 0Kuk si sula 0.3 0 Prasek a 0.5 0 Anaha 1 0 Chardi 0.1 0 Hrillasa 0.1 0.1 Daha 1.3 0.1Angamarda 2.3 0.2 Apak a 2.3 0.5 Alasya 0.2 2.1 2.2 0 0 Trit 0.5 0.6 Aruci Jwara 0 0.5 1 1.5 2 2.5 BT AT
  • 172. ResultsTable No. 25-Overall effect of Eranda Paka on general symptoms ofAmavata: Mean score % of Paired ‘t’ test Criteria B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ PGeneral 18.600 3.300 82 2.946 0.932 16.424 ≤0.001symptoms (3.406) (2.312)Graph No. 21-Overall effect of Eranda Paka on general symptoms ofAmavata: 18.6 20 15 10 3.3 5 0 B.T. A.T.
  • 173. ResultsTable No. 26-Effect of Eranda Paka on the symptoms of Ama: Mean score Symptoms Percentage of relief Initial After treatmentBalabhramsa 2.200 0.800 64Gaurava 0 0 -Alasya 2.100 0.500 76Apakthi 1.100 0.000 100Nistiva 0.500 0.000 100Malasanga 1.100 0.000 100Aruchi 2.200 0.200 91Klama 2.200 0.800 64Graph No. 22-Effect of Eranda Paka on symptoms of Ama: 2.5 2.2 2.2 2.2 2.1 2 1.5 Score 0.8 1.1 1.1 1 0.8 0.5 0.5 0.5 0 0 0.2 0 0 0 0 Apakti Aruchi Balabramsha Gourava Alasya Nishtiva Malasanga Klama BT AT
  • 174. ResultsTable No. 27-Overall effect of Eranda Paka on symptoms of Ama: Mean score % of Paired ‘t’ test Criteria B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ PSymptoms 12.700 2.400 81 2.111 0.667 15.431 ≤0.001of Ama (2.406) (2.221)Graph No. 23-Effect of Eranda Paka on total symptom score of Ama: 12.7 14 12 10 Total score 8 6 2.4 4 2 0 B.T. A.T.Table No. 28-Effect of Eranda Paka on circumference of limbs: Mean score % of Paired ‘t’ test Circumference B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ P 24.625 24.625 Arm - - - - - (2.698) (2.698) 23.425 23.425 Fore arm - - - - - (2.249) (2.249) 44.700 44.700 Thigh - - - - - (4.894) (4.894) 32.350 32.350 Leg - - - - - (3.859) (3.859)
  • 175. Results Table No. 29-Effect of Eranda Paka on different clinical parameters: Mean score Difference Paired ‘t’ testParameters B.T.(S.D.±) A.T.(S.D.±) in mean S.D.± S.E.± ‘t’ PRange ofjoint 61.980 78.864 27.24 14.267 4.512 3.742 =0.005movement (26.315) (37.491)in degreesFoot 30.400 38.950pressure in 28 2.640 0.835 10.242 ≤0.001 (9.216) (9.290)kgsHand grip 62.000 85.950 39 13.475 4.261 5.620 ≤0.001in mm of hg (16.700) (22.47)General 1.700 0.800functional 52 0.568 0.180 5.014 ≤0.001 (0.483) (0.632)disability Graph No. 24-Effect of Eranda Paka on different clinical parameters: 90 78.86 85.95 80 61.98 70 62 60 50 38.95 BT 40 30.4 AT 30 20 10 1.7 0.8 0 J motion F pressure H grip F disability
  • 176. Results Table No. 30-Effect of treatment on body weight of patients of Amavata: Criteria Mean score % of Paired ‘t’ test B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ P Body 51.000 51.100 0.100 0.316 0.1000 1.000 =0.343 weight (11.235) (11.140) Table No. 31-Effect of Eranda Paka on different hematological values: Mean score Paired ‘t’ testInvestigation BT-AT B.T.(S.D.±) A.T.(S.D.±) S.D.± S.E.± ‘t’ P 10345.000 8759.000TC /cu.mm. 1586.000 1850.064 585.042 2.711 =0.024 (1977.857) (1828.882)DC- 68.800 56.100 12.700 18.343 5.800 2.189 =0.056neutrophils-% (7.843) (14.594) 26.100 36.500Lymphocytes -0.400 16.748 5.296 -1.964 =0.081 (8.020) (13.534) 4.600 6.100Eosinophils -1.500 2.838 0.898 -1.671 =0.129 (0.966) (2.601) 0.400 0.700Monocytes -0.300 0.483 0.153 -1.964 =0.081 (0.516) (0.483) 0.1000 0.000Basophils 0.1000 0.316 0.1000 1.000 =0.343 (0.316) (0.000) 82.000 43.600ESR – I hour 38.400 34.069 10.774 3.564 =0.006 (35.640) (28.702) 10.175 10.970Haemoglobin 0.795 1.362 0.431 1.846 =0.098 (1.728) (1.259)
  • 177. ResultsGraph No. 25-Effect of Eranda Paka on TLC: 10345 10500 10000 9500 8759 9000 BT AT 8500 8000 7500 TLCGraph No. 26-Effect of Eranda Paka on Hb%: 10.97 11 10.8 10.6 10.175 10.4 BT 10.2 AT 10 9.8 9.6 Hb%Graph No. 27-Effect of Eranda Paka on ESR: 100 82 80 43.6 60 BT 40 AT 20 0 ESR
  • 178. ResultsTable No. 32-Over all effect of treatment in 10 patients of Amavata: Treatment effect No of patients Percentage Complete remission 4 40 Major improvement 3 30 Minor improvement 3 30 No change 0 00Graph No. 28-Over all effect of treatment in 10 patients of Amavata: 40 40 35 30 30 30 25 20 15 10 5 0 0 complete Major Minor No change
  • 179. ResultsAjamodadi Churna groupEffect on cardinal signs and symptoms: The oral administration of Ajamodadi Churna has resulted in remission ofall the cardinal symptoms of Amavata as elaborated in the followingparagraphs.Effect on Stabdhata: 69% of improvement was observed in the symptom Stabdhata. 2.200was the initial mean score of Stabdata recorded in the 10 patients of Amavatain this group. This was brought down to 1.000 after the oral administration ofAjamodadi Churna. This improvement after the treatment is found to bestatistically highly significant (P≤0.002) as per the paired ‘t’ test. The detail ofthe different statistical values are shown in the Table No. 33 and in Graph No.29.Effect on Sandhi Shoola: Reduction in the severity of the Sandhi Shoola was noted after themedication. 2.200was the initial mean score of Sandhi shoola recorded in the10 patients of Amavata in this group. This symptom score then reduced to1.200 after the administration of Ajamodadi Churna. This improvement after thetreatment is found to be statistically highly significant (P≤0.001) and is assessedby the paired ‘t’ test. The related statistical values are depicted in the Table No.33 and in Graph No. 29. 113
  • 180. ResultsEffect on Sandhi Shotha: Sandhi Shotha, one of the cardinal symptom of Amavata was relieved by58% as the initial score of Sandhi Shotha which was 1.377 then reduced to0.565 after the treatment with Ajamodadi Churna. This improvement whenanalyzed by the paired ‘t’ test found to the highly significant (P≤0.001). TableNo. 33 and the Graph No. 29 provides the detail.Effect on tenderness: 1.884 was the mean initial mean score of tenderness before thetreatment in patients of Ajamodadi Churna group. This initial mean score camedown to 0.897 after the treatment. The improvement to the tune of 52% washighly significant (P≤0.001) as revealed by the paired ‘t’ test. The relatedstatistical values are shown in the Table No. 33 and in the Graph No. 29.Effect on crepitation: None of the patients in this Ajamodadi Churna group presented with thissymptom. There fore the effect of the Ajamodadi Churna on this symptom couldnot be assessed. Table No. 33 and in Graph No. 29 shows the details.Effect on general symptoms: Best improvement was observed in all the general symptoms of Amavatain patients treated with Ajamodadi Churna. Following lines elaborate the exactpercentage of improvement. Marked improvement was observed in thesymptom Angamarda. The initial mean score of Angamarda was 2.3 and thenwas reduced by 48% after the treatment. The mean symptom score after the 114
  • 181. Resultstreatment was 1.2. By the administration of Ajamodadi Churna the fever camedown significantly in patients of Amavata. The initial score of Jwara was 0.500and that came down to 0.1000 after the treatment recording 80% ofimprovement. 91% remission of the symptom Aruchi was recorded in patients ofAmavata. The initial mean score of Aruchi which was 1.200 then reduced to0.1000 after the medication. A minimal mean initial score of 0.5 was observedin the symptom trit. This score came down to 0.200 after the treatment withAjamodadi Churna. This means 60% of improvement in the symptom Aruchi bythe medication. 58% of the improvement was noted in the symptom Alasya. Theinitial mean score of 1.900 was reduced to 0.800 after the treatment. Before theinstitution of the treatment the initial mean score of the symptom Apaka was1.400. This came down to 0.2 after the treatment. The improvement by thetreatment recorded was 86%. The symptoms like Angashunata, Raga,Staimitya, Angagourva, Kandu Hrillasa Chardi and Antrakujana was not foundin any of the 10 patients studied in this group. The initial mean score of 1.100 ofthe symptom Daha was reduced by 73% after the treatment. The mean score ofDaha was 0.300 after the treatment. Marked remission of the symptom Anahawas noted in all the patients. The initial mean score of Anaha, which was 1.100,became 0.200 after the employment of the treatment indicating 90% ofimprovement. 0.400 was the initial mean score of the symptom Praseka inpatients treated with Ajamodadi Churna. This reduced to 0.1000 after thetreatment. Thus an improvement by 75% was recorded by the treatment. Theinitial mean score of the symptom Kukshi Shoola was found to be 0.500. This 115
  • 182. Resultsinitial score reached to zero after the treatment releaving 100% cure. The initialmean score of Vibandha was 0.600, and this came down to 0.1000 after theadministration of Ajamodadi Churna. Thus 83% of improvement was recordedin this symptom. The symptom Shrama was reduced by 55% by the treatmentwith Ajamodadi Churna. The initial mean score of Shrama was 2.000 and whichreduced to 0.900 after the treatment. 25% of the improvement was recorded inthe symptom Bahumutra after the treatment. The initial mean score ofBahumutrata was 0.4 and that came down to 0.3 after the treatment. Completeremission of the symptom was noted in patients treated with Ajamodadi Churnain relation to the symptoms, Bhrama and Hridgraha. 57% of improvement wasobserved in patients complaining of disturbed sleep. The initial mean score ofthe symptom Nidralpata was 0.700 and that dropped to 0.300 after thetreatment. The details of the effect of the Ajamodadi Churna on differentgeneral symptoms of Amavata is given in the Table No. 34 and Graph No. 30.Total effect on general symptoms: The study showed that after the administration of the Ajamodadi Churnamarked remission of the symptoms was observed. Initially before the treatmentthe total score of general symptom was 15.2 and was reduced to 4.9 after theadministration of the Ajamodadi Churna. An over all improvement of 68% ingeneral symptoms was recorded in this group. The improvement after thetreatment is also statistically highly significant (P≤0.001) as revealed by thepaired ‘t’ test. The details are given in the Table No. 35 and in Graph No. 31. 116
  • 183. ResultsEffect of Ajamodadi Churna on symptoms of Ama: Symptoms indicative of Ama showed marked remission by theadministration of Ajamodadi Churna. Bala of the patients was improved by 55%as suggested by the change in the symptom score to 0.900 after the treatmentfrom the initial score of 2.000. Significant remission of the symptom Gouravawas seen in patients treated with Ajamodadi Churna. Before the treatment thesymptom score of Gourava was 2.300. This reduced to 1.100 after thetreatment. The initial mean score of Alasya, which was 1.900 before thetreatment dropped down to 0.800after the treatment. Thus the treatmentshowed a reduction of Alasya by 57%. Marked remission of the symptom Apakawas recorded in patients of Amavata treated with Ajamodadi Churna. The initialscore before the treatment was 1.400, and which came down to 0.200 after thetreatment. The initial mean score of Nistiva was 0.400, which came down to0.1000 after the treatment recording 75% remission of the symptom. 92% of theimprovement was recorded in the symptom Aruchi. The initial score of 1.200reduced to 0.1000 after the treatment with Ajamodadi Churna. Good restorationof the bowel habit was recorded after the medication with Ajamodadi Churna inpatients of Amavata. Before the treatment the severity score of Vibandha was0.600, and it became 0.1000 after the treatment suggesting 83% of remission.Patients felt more comfortable after the treatment as the severity of the Klamawas reduced by the treatment. 2.100 was the initial score of Klama before thetreatment. This score dropped down to 1.000 following the treatment. Analysis 117
  • 184. Resultsof the symptoms of the Ama before and after the treatment is elaborated in theTable No. 36 and Graph No. 32.Statistical analysis of effect on symptoms of Ama: Before the treatment the total score of symptoms of Ama was 11.9. Afterthe treatment with Ajamodadi Churna this reduced to 4.3. The totalimprovement was to the tune of 64%. This improvement after the treatment wasfound to be statistically highly significant (P≤0.001) as assessed by the paired ‘t’test. The details of the same is given in the Table No. 37 and in Graph No. 33.Effect on clinical parametersEffect on circumference of the limbs: The circumference of the limbs that was assessed before and after thetreatment showed that there was neither increase nor decrease in thecircumference after the medication with Ajamodadi Churna. The details of thesame is given in the Table No. 38.Effect on the range of joint movement: Range of joint movement was increased after the treatment withAjamodadi Churna in patients of Amavata. Initially an average range of 79.690degree of joint movement was recorded. This range of joint movement wasincreased to 94.200 after the treatment. The paired ‘t’ test revealed that thischange after the treatment was not because of the chance factor. Theimprovement of joint movement was highly significant. The details are given inthe Table No. 39 and in Graph No. 34. 118
  • 185. ResultsEffect on foot pressure: Improvement in the foot pressure was recorded in patients of AjamodadiChurna group. Before the treatment the average foot pressure of the patientswas 32.800 kgs. And this was increased to 40.050 kgs after the treatment. Thismarked change after the treatment was also statistically highly significantaccording to the paired ‘t’ test. Table No. 39 and Graph No. 34 shows thedetails of the statistical values.Effect on hand grip power: After the treatment with Ajamodadi Churna the hand grip power of thepatients was significantly increased. The average hand grip power before thetreatment was 71.750 mm of hg. After the administration of the AjamodadiChurna it increased to 98.500 mm of Hg. This increase in hand grip power afterthe treatment was found to be statistically highly significant (P=0.005). TheTable No. 39 and Graph No. 34 shows the details.Effect on general functional capacity: Treatment with Ajamodadi Churna has shown favorable effect onfunctional ability of patients of Amavata. The functional disability score beforethe treatment was estimated as 1.900. And this score came down to 1.000recording an improvement by 0.90 score. Statistical analysis by adapting paired‘t’ test revealed that this change after the treatment is highly significant(P≤0.001). Details are given in the Table No. 39 and in Graph No. 34. 119
  • 186. ResultsEffect on body weight: The body weight of the patients recorded before and after the treatmentshowed minimal change. There was mere an increase of 100 gms in the meanbody weight after the treatment. Also this change is statistically insignificant (P=0.343) as revealed by paired ‘t’ test. The details are given in the Table No. 40.Effect on hematological valuesEffect on total leukocyte count: There was marginal decrease in total leukocyte count after the treatment.The initial TC was 9245.000 cu.mm and this came down to 8425.000 cu.mmafter the treatment. This change is found to be statistically insignificant. TableNo. 41 and the Graph No. 35 show the details.Effect on differential count of WBC’s: Minimal change was also observed in the differential count of white bloodcorpuscles. The statistical analysis by adapting the paired ‘t’ test revealed thatthese changes after the treatment are insignificant.Effect on haemoglobin percentage: Before the treatment the initial haemoglobin percentage was 11.00 gm%.This was then increased to 11.63 gm% after the treatment. This increase ofhemoglobin by 0.625 gm% is statistically insignificant as shown by the paired ‘t’test. The details of the same is shown in the Table No. 41 and the Graph No.36. 120
  • 187. ResultsEffect on erythrocyte sedimentation rate: The erythrocyte sedimentation showed a marginal decrease. Before thetreatment the average ESR in patients of Amavata studied in this group was40.6 mm 1st hour. A reduction by 18.00 mm was recorded after the treatmentwith Ajamodadi Churna. This decrease in the ESR was also statistically highlysignificant (P=0.001). Table No. 41 and Graph No. 37 shows the details.Overall effect of treatment in 10 patients of Amavata: The assessment of the overall effect of the treatment revealed that 10%of the patients recorded complete remission. 30% of the patients showed majorimprovement. And 60% of the patients responded with minor improvement. Allthe patients studied in this Ajamodadi Churna group showed different degreesof remission. 121
  • 188. Results Table No. 33-Effect of Ajamodadi Churna on cardinal symptoms of Amavata:Signs and Mean score % of Paired ‘t’ testsymptoms B.T.(S.D.±) A.T.(S.D.±) relief S.D± S.E± ‘t’ P 2.200 1.000Stabdata 54 0.422 0.133 9.000 ≤0.001 0.422 0.667Sandhi 2.200 1.200 45 0.000 0.000 >1e20 ≤0.001Shoola 0.422 0.422Sandhi 1.377 0.565 58 0.173 0.0549 14.795 ≤0.001Shotha 0.501 0.399 1.884 0.897Tenderness 52 0.226 0.0715 13.805 ≤0.001 0.299 0.354Crepetation 0 0 - - - - - Graph No. 29-Effect of Ajamodadi Churna on cardinal symptoms of Amavata: 2.5 2.2 2.2 2 1.884 1.5 1.2 1.377 Score 1 BT 1 0.897 AT 0.569 0.5 0 0 0 Stabdata S Sula S Sotha Tenderness Crepetation
  • 189. ResultsTable No. 34-Effect of Ajamodadi Churna on general symptoms ofAmavata: Mean score Symptoms Percentage of relief. Initial After treatment Angamarda 2.300 1.200 48 Jwara 0.500 0.1000 80 Aruchi 1.200 0.1000 91 Trit 0.500 0.200 60 Alasya 1.900 0.800 58 Apaka 1.400 0.200 86 Angasunata 0 0 - Daha 1.100 0.300 73 Raga 0 0 - Staimitya 0 0 - Gaurava 0 0 - Kandu 0 0 - Hrillasa 0 0 - Chardi 0 0 Anaha 1.100 0.200 90 Praseka 0.400 0.1000 75 Antrakujana 0 0 - Kukshi Shoola 0.500 0.000 100 Vibanda 0.600 0.1000 83 Shrama 2.000 0.900 55 Bahumutra 0.400 0.300 25 Bhrama 0.300 0.000 100 Hridgraha 0.300 0.1000 66 Nidralpata 0.700 0.300 57
  • 190. ResultsGraph No. 30-Effect of Ajamodadi Churna on general symptoms ofAmavata: 0.3 Nidralpata 0.7 0.1 Hridgraha 0.3 0 Bhrama 0.3 0.3 Bahumutra 0.4 0.9 Shrama 2 0.1 Vibandha 0.6 0 Kuk si sula 0.5 0.1 Prasek a 0.4 0.2 Anaha 1.1 0 Chardi 0 0 Hrillasa 0 0.3 Daha 1.1 1.2 Angamarda 2.3 0.2 Apak a 1.4 0.8 Alasya 0.1 1.9 1.2 0.2 0.1 Trit 0.5 0.5 Aruci Jvara 0 0.5 1 1.5 2 2.5 BT AT
  • 191. ResultsTable No. 35-Total effect of Ajamodadi Churna on general symptoms: Mean score % of Paired ‘t’ test Criteria B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ PGeneral 15.200 4.900 68 4.620 1.461 7.050 ≤0.001symptoms (4.022) (2.132)Graph No. 31-Total effect of Ajamodadi Churna on general symptoms ofAmavata. 15.2 16 14 12 10 Score 8 4.9 6 4 2 0 B.T. A.T.
  • 192. ResultsTable No. 36-Effect of Ajamodadi Churna on symptoms of Ama: Symptoms Mean score Percentage of relief. Initial After treatment Balabhramsa 2.000 0.900 55 Gaurava 2.300 1.100 52 Alasya 1.900 0.800 57 Apakthi 1.400 0.200 86 Nistiva 0.400 0.1000 75 Malasanga 0.600 0.1000 83 Aruchi 1.200 0.1000 92 Klama 2.100 1.000 52Graph No. 32-Effect of Ajamodadi Churna on symptoms of Ama: 2.5 2.3 2 2.1 2 1.9 1.5 1.1 1.4 Score 0.9 1.2 1 1 0.8 0.6 0.5 0.4 0.2 0.1 0.1 0.1 0 Balabramsha Gourava Alasya Nishtiva Malasanga Klama Apakti Aruchi BT AT
  • 193. Results Table no. 37-Total effect of Ajamodadi Churna on symptoms of Ama: Mean score % of Paired ‘t’ test Criteria B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ PSymptoms 11.900 4.300 64 2.221 0.702 10.820 P=<0.001of Ama (1.524) (2.312) Graph No. 33-Total effect of Ajamodadi Churna on symptoms of Ama: 11.9 12 10 8 Score 6 4.3 4 2 0 B.T. A.T.
  • 194. Results Table No. 38-Effect of Ajamodadi Churna on circumference of the limbs: Mean score % of Paired ‘t’ test Circumference B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ P 26.775 26.775 Arm 0 - - - - (3.566) (3.566) 24.350 24.350 Fore arm 0 - - - - (2.404) (2.404) 45.050 45.050 Thigh 0 - - - - (4.036) (4.036) 31.375 31.375 Leg 0 - - - - (7.400) (7.400) Table No. 39-Effect of Ajamodadi Churna on different clinical parameters: Mean score improve Paired ‘t’ test Parameters B.T.(S.D.±) A.T.(S.D.±) ment S.D.± S.E.± ‘t’ PRange of joint 79.690 94.200movement in -14.510 8.256 2.611 5.558 ≤0.001 (25.072) (29.662)degreesFoot pressure 32.800 40.050 7.250 3.729 1.179 6.149 ≤0.001in kgs (7.220) (7.228)Hand grip in 71.750 98.500 26.750 23.035 7.284 3.672 =0.005mm of Hg (30.278) (40.624)Functional 1.900 1.000 0.900 0.568 0.180 5.014 ≤0.001disability (0.316) (0.667)
  • 195. ResultsGraph No. 34-Effect of Ajamodadi Churna on different clinical parameters: 94.2 100 98.5 90 79.69 80 71.75 70 60Score 50 40.05 BT 32.8 40 AT 30 20 10 1.9 1 0 J motion F pressure H grip F disabilityTable No. 40-Effect of Ajamodadi Churna on body weight of patients ofAmavata: Mean score Paired ‘t’ test Criteria BT-AT B.T.(S.D.±) A.T.(S.D.±) S.D.± S.E.± ‘t’ P Body 55.500 55.400 0.1000 0.316 0.1000 1.000 =0.343 weight (10.721) (10.741)
  • 196. Results Table No. 41-Effect of Ajamodadi Churna on different hematological parameters: Mean score % of Paired ‘t’ testInvestigation B.T.(S.D.±) A.T.(S.D.±) relief S.D.± S.E.± ‘t’ P 9245.000 8425.000TC /cu.mm 820.000 1413.074 446.853 1.835 =0.100 (2472.791) (2085.965)DC- 63.700 64.900 1.200 5.051 1.597 -0.751 =0.472neutrophils-% (7.394) (5.238) 31.600 30.600Lymphocytes 1.000 4.876 1.542 0.649 P=0.533 (7.106) (5.232) 4.100 4.800Eosinophils 0.700 2.359 0.746 0.938 P=0.373 (2.132) (2.348) 0.500 0.600Monocytes 0.1000 0.876 0.277 -0.361 P=0.726 (0.527) (0.966)Basophils 0 0 - - - - - 40.600 22.600ESR – I hour 18.000 10.995 3.477 5.177 P=<0.001 (15.116) (13.794) 11.000 11.625Haemoglobin 0.625 0.835 0.264 2.366 =0.042 (0.825) (0.981)
  • 197. ResultsGraph No. 35-Effect of Ajamodadi Churna on TLC: 9245 9400 9200 Cells per cubic mm 9000 8800 8425 BT 8600 AT 8400 8200 8000 TLCGraph No. 36-Effect of Ajamodadi Churna on Hb%: 11.63 11.7 11.6 11.5 11.4 11.3 gm % 11.2 11 BT 11.1 11 AT 10.9 10.8 10.7 10.6 Hb%Graph No. 37-Effect of treatment on ESR: 40.6 45 40 35 mm after 1st hour 30 22.6 25 BT 20 AT 15 10 5 0 ESR
  • 198. ResultsTable No. 42-Overall effect of treatment in 10 patients of Amavata: Treatment effect No of patients Percentage Complete remission 1 10 Major improvement 3 30 Minor improvement 6 60 No change 0 00Graph No. 38-Overall effect of Ajamodadi Churna in patients of Amavata: 60 60 50 40 % of patients 30 30 20 10 10 0 0 complete Major Minor No change
  • 199. Results COMPARISONComparison of effect on cardinal signs and symptoms: By observing the response to the treatments in both the group it is clearthat both the medicines are effective in relieving the cardinal symptoms of theAmavata. Comparison of the efficacy of the treatments is detailed in thefollowing paragraphs.Effect on the symptom Stabdhata: The effect of the treatment in both the group on the symptom Stabdhataappears to be equal. In both the groups the difference in the mean symptomscore before and after the treatment is 1.2. This explains equal efficacy of thetreatment in both the groups. Table No. 43 and Graph No. 39 represents thesame.Effect on Sandhi Shoola: The difference in means of Sandhi Shoola score before and after thetreatment in the Eranda Paka group was 1.5 as against1.0 in the Ajamodadigroup. This difference proves the better efficacy of the Eranda Paka in relievingthe symptom Sandhi Shoola in comparison to the relief obtained by theAjamodadi Churna. Table No. 43 and Graph No. 39 gives the detail.Effect on Sandhi Shotha: Favourable response was obtained in both the groups in regards toeffect of the treatment on the symptom Sandhi Shotha. Also, comparatively a 122
  • 200. Resultsbetter response was observed in the Eranda Paka group. The difference inmean symptom scores before and after the treatment was 0.935 in the ErandaPaka group, and is just higher than the one noted in the Ajamodadi Churnagroup. In patients treated with Ajamodadi Churna, the difference in meanscores before and after the treatment was 0.812. Though the statistical analysisof the same by adapting the unpaired ‘t’ test does not rule out the chance factorfor such a difference between the groups, the efficacy is marginally better inEranda Paka group. Details are given in Table No. 43 and Graph No. 39.Effect on joint tenderness: Severity of tenderness was reduced in both the groups after thetreatment. The difference in mean scores before and after the treatment in twogroups when compared reveals that the Eranda Paka is better in relieving thesign joint tenderness. In the Ajamodadi group the difference in mean scoresbefore and after the treatment was 0.987, and is lesser than the one noted inEranda Paka group. Here in patients treated with Eranda Paka the difference inmean symptom score before and after the treatment was 1.21. Here also thedifference observed between these groups could be due to chance. Statisticallythis difference was insignificant (P=0.060). Table No. 43 and Graph No. 39show the details. Joint crepetation another cardinal symptom of the illness was not presentin both the groups. 123
  • 201. ResultsEffect on general symptoms: In patients treated with Eranda Paka a difference of 15.3 was recorded inthe sum total of different scores of general symptoms before and after thetreatment. The value of the same in the Ajamodadi Churna group was 10.3.This difference in values states that the oral administration of Eranda Paka ismore efficacious in relieving the general symptoms of Amavata. But theunpaired ‘t’ test could not prove the statistical significance of the variations seenbetween the groups. Table No. 44 and Graph No. 40 represents the same.Effect on Ama: Comparison of effects on symptoms of Ama in two groups reveals that,better improvement was found in patients treated with Eranda Paka. Thevariance of symptom score before and after the treatment in Eranda Pakagroup was 10.3 and the same in Ajamodadi group was 7.6, confirming thebetter efficacy of the Eranda Paka in relieving the symptoms of Ama. Thechange observed between the groups was also statistically significant accordingto unpaired ‘t’ test. Same is represented in Table No. 45 and in Graph No. 41.Effect on clinical parametersEffect on circumference of the limbs: The circumferences of the arm, fore arm, thigh and legs were notedbefore and after the treatment in both the Eranda Paka group as well asAjamodadi group. Both the group showed no variation in the circumferencesafter the treatment. 124
  • 202. ResultsEffect on the range of joint movement: In an average the range of joint movement was increased by 16.884degrees in Eranda Paka group as against the increase by 14.51 degrees inAjamodadi group. This implies a better improvement in the range of jointmovements in patients treated with Eranda Paka though the statistical analysisby adapting the unpaired ‘t’ test does not justify the significance of variationbetween the groups. Table No. 46 and Graph No. 42 shows the details.Effect on foot pressure: Comparison of effects of treatments on foot pressure indicates thatEranda Paka has an edge over the Ajamodadi Churna in improving the footpressure after the treatment. The difference in the mean foot pressure in theEranda Paka group was 8.55 kgs as against 7.25 kgs in Ajamodadi group.Statistical analysis by unpaired ‘t’ test could not rule out the possibility ofchance factor in causing such a variance between the groups. Table No. 46 andGraph No. 43 gives the detail.Effect on hand grip power: Ajamodadi Churna was found to be more efficacious in improving thehand grip power in comparison to the Eranda Paka. After the treatment inEranda Paka group the increase in the mean hand grip power was 23.95 mm ofHg as against 26.75 mm of Hg in Ajamodadi Churna group. Of course thisvariation between the groups was statistically insignificant (P=0.744). Detailsare given in the Table No. 46 and Graph No. 44. 125
  • 203. ResultsEffect on general functional capacity: The analysis of the functional disability in both the groups showed thatfunctional capacity of the patients has increased following the treatment. Thefunctional disability score reduced to the tune of 0.9 in both the groups,recording no difference in the efficacy of two treatments when compared. TableNo. 46 represents the same.Effect on body weight: Marginal improvement in body weight was observed in Eranda Pakagroup and marginal decrease in body weight was recorded in Ajamodadi groupafter the treatment. However the difference is statistically insignificant(P=0.174). Table No. 47 and Graph No. 45 provides the details.Effect on haematological values: Haematological examinations carried out before and after the treatmentin both the groups showed that there was marginal change in TLC and DC. Thechanges also found to be statistically insignificant. Details are in Table No. 48. Better improvement of Hb% was noted in the Eranda Paka group incomparison to the Ajamodadi group. The average increase of Hb% followingthe medication with Eranda Paka was 0.795 gm%. And the same in Ajamodadigroup was just 0.625 gm%. This explains the Eranda Paka has an edge overthe Ajamodadi Churna in improving the Hb%. The variation noted in the twogroups when compared showed statistically insignificant change (P=0.740).Table No. 48 and Graph No. 46 shows details. 126
  • 204. Results Reduction in the ESR following treatment was recorded in both thegroups. However the Eranda Paka group patients showed a better fall in ESRlevel. The average fall in ESR after the treatment with Eranda Paka was 38.4mm after1st hour, as against 18.0 mm after1st hour in Ajamodadi group. Alsostatistical significance of this variation noted could not be confirmed by theunpaired ‘t’ test. Table No. 48 and Graph No. 47 shows the details.Over all effect of treatment in 20 patients of Amavata: Comparison of the overall effects of the treatment in both the groupsreveals that Eranda Paka is more efficacious. Complete remission of the illnesswas observed in 40% of the patients in Eranda Paka group as against mere10% of the patients in Ajamodadi group. 30% of the patients in each grouprecorded major improvement. In patients treated with Eranda Paka, 30% of thepatients showed minor improvement as against 60% of patients showing thisresponse in Ajamodadi Churna group. In both the groups no patients wereobserved in the “no change” category. Details of comparison are given in theTable No. 49 and Graph No. 48. In a nutshell, almost all the parameters of assessment have shownimprovement in both the groups following treatment. In most of theseassessment criteria the Eranda Paka group has shown a better response incomparison to the Ajamodadi group. The better improvement in the cardinalsymptoms and general symptoms was also statistically significant where as theclinical parameters as well as laboratory investigations have shown insignificantchange between the groups. 127
  • 205. Results Table No. 43-Comparison of effect of treatments on cardinal symptoms of Amavata: No. of BT - Difference Unpaired ‘t’ test Symptoms Group patients AT in mean S.D. S.E.M. ‘t’ P EP 10 1.2 0.632 0.200Stabdata 0.000 - - AC 10 1.2 0.422 0.133 EP 10 1.5 0.527 0.167Sandhishoola 0.500 3.000 P=0.008 AC 10 1 0.000 0.000 EP 10 0.935 0.702 0.222Sandhishotha 0.123 0.538 P=0.597* AC 10 0.812 0.173 0.0547 EP 10 1.21 0.269 0.0851Tenderness 0.223 2.007 P=0.060* AC 10 0.987 0.226 0.0715 EP 10 0 - -Crepetation - - - AC 10 0 - - Graph No. 39-Comparison of the effect of treatment on the cardinal symptom of Amavata: 1.5 1.6 1.4 1.2 1.2 Difference in m ean sc ores 1.21 1.2 1 1 0.987 0.935 0.812 0.8 EP 0.6 AC 0.4 0.2 0 0 0 Stabdata S Sula S Sotha Tenderness Crepetation
  • 206. ResultsTable No. 44-Comparison of effect on general symptoms: Group No. of BT-AT Difference Unpaired ‘t’ testSymptoms patients in mean S.D. S.E.M. ‘t’ PGeneral EP 10 15.300 2.946 0.932 5.000 2.886 P=0.010symptoms AC 10 10.300 4.620 1.461Graph No. 40-Comparison of effect of treatment on general symptom intwo groups: 15.3 16 14 Difference in mean scores 10.3 12 10 8 6 4 2 0 EP AC
  • 207. ResultsTable No. 45-Comparison of effect on symptoms of Ama between thegroups: No. of Difference Unpaired ‘t’ testSymptoms Group BT-AT patients in mean S.D. S.E.M. ‘t’ P EP 10 10.300 2.111 0.668Ama 2.700 2.786 P = 0.012 AC 10 7.600 2.221 0.702Graph No. 41-Comparison of effects on symptoms of Ama in two groups: 15.3 16 14 Difference in mean scores 10.3 12 10 8 6 4 2 0 EP AC
  • 208. Results Table No. 46-Comparison of effect on different clinical parameters: No. of Difference Unpaired ‘t’ testParameters Group BT-AT patients in mean S.D. S.E.M. ‘t’ PRange of EP 10 16.884 14.267 4.512joint 2.374 0.455 P=0.654*movement AC 10 14.51 8.256 2.611Foot EP 10 8.55 2.640 0.835 1.300 0.900 P=0.380pressure AC 10 7.25 3.729 1.179 EP 10 23.95 13.475 4.261 P=0.744Hand grip -2.800 0.332 AC 10 26.75 23.035 7.284Functional EP 10 0.9 0.568 0.180 0.000 - -capacity AC 10 0.9 0.568 0.180 Graph No. 42-Comparison of effects on range of joint movement: 16.884 17 16.5 Difference in range of jt 16 movement 15.5 15 14.51 14.5 14 13.5 13 EP AC
  • 209. ResultsGraph No. 43-Comparison of effects on foot pressure between the groups: 8.55 8.6 Difference in foot pressure in Kg 8.4 8.2 8 7.8 7.6 7.25 7.4 7.2 7 6.8 6.6 EP ACGraph No. 44-Comparison of the effect on hand grip power: 26.75 27 Difference in hand grip power in 26.5 26 25.5 mm of Hg 25 23.95 24.5 24 23.5 23 22.5 EP AC
  • 210. ResultsTable No. 47-Comparison of the effect on body weight in both the groups: No. of Difference Unpaired ‘t’ testCriteria Group BT-AT patients in mean S.D. S.E.M. ‘t’ PBody EP 10 0.100 0.316 0.1000 0.200 1.415 P=0.174weight AC 10 -0.1000 0.316 0.1000Graph No. 45-Comparison of effect on body weight: 0.1 0.1 Difference in body weight in Kgs 0.08 0.06 0.04 0.02 0 -0.02 -0.04 -0.06 -0.08 -0.1 -0.1 EP AC
  • 211. Results Table No. 48-Comparison of effect on different haematological values: No. of Difference Unpaired ‘t’ testInvestigations Group BT-AT patients in mean S.D. S.E.M. ‘t’ P EP 10 1586.000 1850.064 585.042TLC 766.000 1.309 P=0.207 AC 10 820.000 5.051 1.597 EP 10 12.700 18.343 5.800Neutrophil 11.500 1.911 P=0.072 AC 10 1.200 5.051 1.597 EP 10 10.400 16.748 5.296Lympthocyte 9.400 1.704 P=0.106 AC 10 1.000 4.876 1.542 EP 10 -1.500 2.838 0.898Eosinophil -2.200 1.885 P=0.076 AC 10 0.700 2.359 0.746 EP 10 -0.300 0.483 0.153Monocyte -0.400 1.264 P=0.222 AC 10 0.1000 0.876 0.277 EP 10 0.1000 0.316 0.1000Basophil 0 - - AC 10 0 EP 10 0.795 1.362 0.431Hb % 0.170 0.337 P=0.740 AC 10 0.625 0.835 0.264 EP 10 38.400 34.069 10.774ESR 20.400 1.802 P=0.088 AC 10 18.000 10.995 3.477 Graph No. 46-Comparison of effect on haemoglobin percentage: 0.795 0.8 0.625 0.7 Difference in hemoglobin 0.6 percentage 0.5 0.4 0.3 0.2 0.1 0 EP AC
  • 212. ResultsGraph No. 47-Comparison of effect on erythrocyte sedimentation rate: 38.4 40 Difference in ESR in mm/1st 35 30 25 18 hour 20 15 10 5 0 EP ACTable No. 49-Comparison of overall effect of treatment in two groups: Percentage of patients Treatment effect Group EP Group AC Complete remission 40 10 Major improvement 30 30 Minor improvement 30 60 No change 00 00Graph No. 48-Comparison of overall effect of the treatments in both thegroups: 60 60 40 Overall improvement in % 50 30 30 40 30 Group EP 30 10 Group 20 10 0 0 0 Complete Major Minor No change remission improvement improvement
  • 213. Discussion DISCUSSION The name of the disease Amavata represents Ama and Vata as the twopredominant pathological factors involved in the Samprapti of the disease.Vitiated Vata Dosha in association with Ama circulating ubiquitously in the body,gets lodged in the Sandhi, one among the Kaphasthana producing thesymptoms like Sandhi Stabdata, Sandhi Shoola, Sandhi Shopha and other localand generalized symptoms. Though the literature related to the disease isrestricted to the mentioning of the word Amavata in Brihatrayi, an elaboratedescription is found in Chakradatta and Madhava Nidana. All the diseasesaffecting the locomotor system are elaborated under the single name Vataraktain Charaka, Sushruta and Vagbhata Samhita. Another distinct clinical entity ofthe locomotor system, named as Amavata, and its clear clinical presentation isgiven in Madhava Nidana. Acharya Chakradatta has given the full account ofthe effective treatment of the same in his best work Chakradatta. Severely disabling as well as perpetuating nature of the illness isattributed to the unique pathogenesis of the illness. The specific etiologicalfactors in the form of unwholesome diet and regimen, causes generation ofAma, as well as morbidity of the Vata Dosha in the Abhyantara Roga Marga.Trivial involvement of Pitta and Kapha Dosha is also contended as pathologicalfactors. Ama along with morbid Vata Dosha circulated in the whole body moreparticularly in the Madhyama Roga Marga, and tend to get localized in the jointproducing the typical clinical signs and symptoms. During the course of the 128
  • 214. Discussionpathogenesis the morbid Dosha afflicts the Sandhi, and in turn its Dhatustructure viz. Mamsa, Snayu, Asthi, and Majja. Symptoms related to the jointslike Sandhi Shotha, Stabdhata and Shoola are the initial manifestations. And inthe later stages of the disease deformities like Sandhi Sankocha, SandhiJadhyata and Angavaikalya are the hall marks of the disease. In addition to thesymptoms related to the joints, patients are likely to suffer from certain othersymptoms like Sthaimitya, Dourbalya, Agnimandya, Apaka, Vibanda,Antrakujana, etc. Needless to say the disease cripples the patients in the longrun.Amavata in modern parlance: Rheumatoid arthritis a systemic disease, though it involves thecardiovascular, nervous respiratory and similar other systems, mainly affectsthe locomotor system is analogous to Amavata in terms of Ayurveda. Theeffective curative medical management of the illness is doubted by the chroniclingering nature of the illness as well as the risk of disabling deformities inpatients suffering from rheumatoid arthritis. In spite of continuous extensiveresearch works for years in this regard, ambiguity about the aetio-pathogenesisof the illness still persists. Autoimmune mechanism related to the connectivetissue more particularly the sinovium is mostly accepted as the pathology of theillness. The ambiguity in most aspects of the disease has impeded theexploration of effective and curative treatment for this dreaded illness. 129
  • 215. Discussion The abnormal activity of the immune system is said to be initiated by theexogenous or endogenous antigens. Probably these antigens are either viral orbacterial in origin. The presence of these antigens in the body causes theformation of RA factors and other antibodies. The combined activity of theantigen and antibody with in the connective tissues including the joint resultingin the inflammatory changes is the prime pathological event of the rheumatoidarthritis. This inflammatory response is always destructive. This uniquepathological process of Rheumatoid arthritis is analogous to the Samprapti ofAmavata in many respects as expounded in Ayurvedic literature. Unwholesomediet and regimen, mostly in the Vairodhika form causes the initiation of theillness by the production of Ama as well as morbidity of Vata Dosha. Propelledby the vitiated Vata Dosha the virulent Ama circulates in the body, and tends tolocalize in Sandhi. With in the Sandhi, in combination with the Doshas naturallypresent in the joint, the Amadosha and vitiated Vata Dosha acquires still morevirulence and thus produces the perpetuating and disabling illness. This typicalsequence of Samprapti may be compared to the aetiopathogenesis ofRheumatoid arthritis, beginning from the exogenous or endogenous antigens. Samprapti Vighatana and there by remission or cure of the illness isachieved by advocating the different therapeutic procedures. Deepana,Pachana, Shodhana and Shamana are the procedures said to be efficacious inpatients suffering from Amavata. Ama is the one among the predominantpathological factor in the Samprapti of Amavata, and is initially treated byDeepana and Pachana. Thus at the outset of the Samprapti Vighatana an 130
  • 216. Discussionattempt is made to eliminate the effect of Ama. As the morbid Dosha acquirethe Pakwa stage by these procedures, this renders ideal stage for thepurificatory procedures. Virechana or the Ksharabasti when employed inpatients of Amavata eliminates the excessive accumulation of vitiated Doshafurther causing the remission of the illness. To complete, Shodhana treatment isfollowed by Shamana procedure. Based on these principles of treatment thepresent study is planned to evaluate the efficacy of Eranda Paka in patients ofAmavata that constitutes both Shodhana and Shamana treatment. A controlgroup treated with Ajamodadi Churna is also maintained to prove the efficacy ofthe Eranda Paka.Selection of the regimen: In the present study, the Eranda Paka and Ajamodadi Churna is taken totreat the patients of Amavata and to explore the efficacy of these in bringingabout cure of the illness. Pancha Kola Phanta is administered initially for the purpose of achievingAmapachana. This herbal combination is said to possess Katu rasa, Katuvipaka and Ushna veerya and therefore likely to render Amapachana in patientssuffering Amavata. More over, Amapachana is considered to be an essentialprocedure before administering the Shodhana treatment. With this rationalityPancha Kola Phanta was opted to bring about Ama Pachana in the presentstudy. 131
  • 217. Discussion In the classics, Eranda Taila is considered as best among themedications for the Snigdha Virechana. Following the Deepana and Pachanathe elimination of the excessive accumulation of the Dosha is the treatment ofchoice. This is made possible by the oral administration of the Eranda Taila inprescribed dose. For the same purpose this oil is taken for the study in thepresent work. Eranda is a unique herb having both Shodhana as well as Shamanaeffect in patients of Amavata. Also, it is claimed that this is the best drug inAmavata and efficacious in bringing about the cure of the illness. It is arguedthat by virtue of the Snigdha property it alleviates the Vata Dosha. Vyadhiharaproperty of this drug is also contended. Drugs like Pippali, Chitraka, Sati, etcare efficacious in rectifying the Amadosha. With this idea Eranda Paka is optedfor this study. Ajamodadi Churna is an herbal combination containing drugs that renderAmapachana as well as alleviate the morbid Vata Dosha. Pippali, Pippali MoolaChitraka and similar other drugs in Ajamodadi Churna are efficacious inachieving the Amapachana. In addition to this the drugs like Devadaru, Bilvamoola, etc., are effective in alleviating the Vata Dosha. This is the rationality ofselecting the Ajamodadi Churna for treating the patients of Amavata in thisstudy. 132
  • 218. DiscussionPlan of the study: 20 patients suffering from Amavata are taken for the study and allcompleted the course of the treatment. The disease is mainly diagnosed on thebasis of signs and symptoms Amavata as mentioned in the Ayurvedic texts,aided by the A.R.A. criteria (Hollander et al, 1967). RA test was also carried outto confirm the diagnosis. To assess the general health status of the patients aswell as to rule out other possible pathologies routine haematological and urineexamination was carried out in all the patients. Routine blood examination wasrepeated after the course of the treatment. These 20 patients of Amavata selected for the study are randomlysegregated in to two groups irrespective of age, sex or creed as well as severityof the illness. In the first Eranda Paka group Deepana Pachana Shodhana andShamana treatment is carried out. Deepana and Pachana are achieved byadministering the Pancha Kola Phanta in a dose of 20 ml thrice a day for threedays. This was followed by Kostasodhana for another three days by oraladministration of Eranda taila in a dose of 10 ml in the morning in emptystomach. For the next one month course of treatment, Eranda Paka was givenorally in a dose of 15 gms thrice a day with warm water after food. In the second Ajamodadi Churna group also Deepana Pachanatreatment is initially carried out by the oral administration of Pancha KolaPhanta for first three days in a dose of 20 ml thrice a day. 133
  • 219. Discussion This was followed by the Koshta Shodhana by Eranda Taila given orallyin a dose of 10 ml in the morning in empty stomach for the next three days. Forthe next 30 days regimen, patients were orally treated with Ajamodadi Churnain a dose of 5 gms thrice a day with warm water after food.Descriptive statistical analysis of patients: In this study involving 20 patients of Amavata showed majority of thepatients belonged to the age group of 50 to 60 years. Though the illnessrheumatoid arthritis is said to be more common during the 3rd and 4th decade ofthe life, this study of 20 patients of Amavata being small could not represent thisgeneral observation. 75% of the patients were females among the 20 recordedin this study. This observation represents the general observation of prevalenceof the illness in females. Majority of the patients were Hindus in the presentseries. The religion has nothing to do with the causation of the illness, and thepredominance of Hindus accounting 65% in this study only represent thepopulation in around Udupi, which is dominated by Hindus. Most of the patients,females in particular revealed house hold as their occupation, once againreflecting the usual occupation of females in this area. As per the socio-culturalstatus of this geographical area females usually will not have any addiction. Inthe present study involving majority of females showed only 30% of the patientswere addicted and is true to the socio-cultural status of the general populationhere. Majority of patients accounting 80% were married as against remaining 20% of the patients who were unmarried. This only represents the adult age groupof the patients that is taken for the study, and further the illness is more 134
  • 220. Discussioncommon in the later decades of adult age group which is also the marriageableage of general population. More number of poor and lower middle class peoplewere recorded in this study, and the poor socio-economic status of the patienthas nothing to do with the causation of the illness, more over this incidence onlyrepresents the socio-economic status of the patients in and around Udupi. 45%of the patients were illiterates, and 35% of the patients had primary education.Once again education has no role in the predisposition of the illness, and thisonly correspond to the educational status of population at large from which thepresent sample is selected. Ekadoshaja Prakriti as well as Sama Prakriti was not observed in anypatients of Amavata. All the patients belonged to the Dvandvaja Prakriti, and inthat 40% of the patients had Pitta Kaphaja Prakriti. It is said that, diseases dueto morbidity of Vata is common in Vata Prakriti people and also such an illnessis severe in them. This nature of the incidence of the illness is not reflected inthis small sample of 20 patients of Amavata. To substantiate the preponderanceof Amavata in patients having Vata Prakriti a study of larger sample is needed.The study of the degree of the severity of the illness revealed that 80% of thepatients had Madhyama Vikriti. Interrogation of the patients revealed that 70%of the patients had Madhyama Satva as against 15 % of patients having AvaraSatva. It is understood that, mental tension and anxiety has some role to dowith the severity of the illness, and the present observation in this sampleshowing majority of the patients with either Madhyama or Avara Satva bear thesame understanding. Analysis of the Sara in 20 patients of Amavata revealed 135
  • 221. Discussionthat 95% of the patients had Madhyama Sara and the remaining 5% had AvaraSara. None of the patients showed the features of the Pravara Sara. In thepathogenesis of the Amavata it is clear that morbid Vata Dosha ispredominantly involved. And this morbid Vata has a tendency to causedepletion of the body elements and that may be reason the patients of Amavatashowing Madhyama or Avara Sara in their physique. In addition to this, most ofthe patients belonging to the poor or lower middle socioeconomic status in thisstudy may have poor nutrition. This further affects the Sara of the patients.Analogous to Sara of the patients, assessment of the Samhanana of thepatients showed the higher incidence of Madhyama Samhanana. 85% of thepatients had Madhyama Samhanana out of 20 patients of Amavata. MorbidVata Dosha has a role in reducing the excellency of the Samhanana of thepatients and poor physical activity due to sever joint pain may further contributein the same line. Madhyama Satmya was observed in 95% of the patients ofAmavata. Satmya of the patients has direct bearing with the Sara andSamhanana, predominance of Madhyama Satmya also explains preponderanceof Madhyama Sara as well as Madhyama Samhanana. Assessment of the Agniwas also carried out in all the patients suffering from Amavata. It was observedthat majority of 60% of the patients had Madhyama Abhyavaharana as well asMadhyama Jarana Shakti. 20% of the patients had Avara Abhyavaharana andJarana Shakti. Impairment of the Agni is a common phenomenon of Amavata.Impaired functioning leads to impaired ability to consume food as well asreduced digestive ability. The same is reflected in the present sample with a 136
  • 222. Discussionminimum 20% of patients showing good functioning of the Agni. Functionalability of the patients will be affected either due to the Sandhi Shoola orStabdata. Physical strength is likely to be reduced as the depletion of the bodyelement is a regular phenomenon in patients suffering from Amavata.Corroboratory to this phenomenon, in the present study also majority of thepatients had reduced ability to do the physical exercise. The therapeutic effect of the treatments in both the groups was assessedmethodically in regards to the salient features of Amavata, general symptoms ofAmavata, symptoms of Ama, functional disability of the patients, degrees ofdisease activity and haematological investigations. Overall effect of thetreatments was also analyzed. The results of the treatments in both the groupsare discussed in the following pages.Therapeutic effect of the treatments: The signs and symptoms of Amavata, both cardinal and generalsymptoms were scored depending upon the degree of severity of thesesymptoms, and the same is elaborated in the chapter on clinical study. Thechange in these initial scores of the symptoms after the treatment was noted toknow the therapeutic benefit of these treatments.Effect on the symptom Stabdhata: The effect of the treatment in both the group on the symptom Stabdhataappears to be equal. In both the groups the difference in the mean symptomscore before and after the treatment is 1.2. This explains equal efficacy of the 137
  • 223. Discussiontreatment in both the groups. And the improvement recorded after the treatmentwas statistically highly significant.Effect on Sandhi Shoola: The difference in means of Sandhi Shoola score before and after thetreatment in the Eranda Paka group was 1.5 as against 1.0 in the Ajamodadigroup. This difference proves the better efficacy of the Eranda Paka in relievingthe symptom Sandhi Shoola in comparison to the relief obtained by theAjamodadi Churna.Effect on Sandhi Shotha: Favorable response was obtained in both the groups in regards to effectof the treatment on the symptom Sandhi Shotha. Also, comparatively a betterresponse was observed in the Eranda Paka group. Though the statisticalanalysis of the same by adapting the unpaired ‘t’ test does not rule out thechance factor for such a difference between the groups, the efficacy ismarginally better in Eranda Paka group.Effect on joint tenderness: Severity of tenderness was reduced in both the groups after thetreatment. The difference in mean scores before and after the treatment in twogroups when compared reveals that the Eranda Paka is better in relieving thejoint tenderness. In the Ajamodadi group the difference in mean scores beforeand after the treatment was 0.987 and is lesser than the one noted in ErandaPaka group. Here in patients treated with Eranda Paka the difference in mean 138
  • 224. Discussionsymptom score before and after the treatment was 1.21. Here also thedifference observed between these groups could be due to chance. Statisticallythis difference was insignificant (P = 0.060). Joint crepitation another cardinal symptom of the illness was not presentin both the groups. In patients treated with Eranda Paka a difference of 15.3 was recorded inthe sum total of different scores of general symptoms before and after thetreatment. The value of the same in the Ajamodadi Churna group was 10.3.This difference in values states that the oral administration of Eranda Paka ismore efficacious in relieving the general symptoms of Amavata. But theunpaired ‘t’ test could not prove the statistical significance of the variations seenbetween the groups.Effect on Ama: Comparison of effects on symptoms of Ama in two groups reveals that,better improvement was found in patients treated with Eranda Paka. Thevariance of symptom score before and after the treatment in Eranda Pakagroup was 10.3. And the same in Ajamodadi group was 7.6, confirming thebetter efficacy of the Eranda Paka in relieving the symptoms of Ama. Thechange observed between the groups was also statistically significant accordingto unpaired ‘t’ test. 139
  • 225. DiscussionEffect on clinical parametersEffect on circumference of the limbs: The circumferences of the arm, fore arm, thigh and legs were notedbefore and after the treatment in both the Eranda Paka group as well as inAjamodadi churna group. Both the groups showed no variation in thecircumferences after the treatment.Effect on the range of joint movement: In an average the range of joint movement was increased by 16.884degrees in Eranda Paka group as against the increase by 14.51 degrees inAjamodadi churna group. This implies a better improvement in the range of jointmovements in patients treated with Eranda Paka though the statistical analysisby adapting the unpaired ‘t’ test does not justify the significance of variationbetween the groups.Effect on foot pressure: Comparison of effects of treatments on foot pressure indicates thatEranda Paka has an edge over the Ajamodadi Churna in improving the footpressure after the treatment. The difference in the mean foot pressure in theEranda Paka group was 8.55 kgs as against 7.25 kgs in Ajamodadi Churnagroup. Statistical analysis by unpaired ‘t’ test could not rule out the possibility ofchance factor in causing such a variance between the groups. 140
  • 226. DiscussionEffect on hand grip power: Ajamodadi Churna was found to be more efficacious in improving thehand grip power in comparison to the Eranda Paka. After the treatment inEranda Paka group the increase in the mean hand grip power was 23.95 mm ofHg as against 26.75 mm of Hg in Ajamodadi Churna group. Of course thisvariation between the groups was statistically insignificant (P=0.744).Effect on general functional capacity: The analysis of the functional disability in both the groups showed thatfunctional capacity of the patients has increased following the treatment. Thefunctional disability score reduced to the tune of 0.9 in both the groups,recording no difference in the efficacy of two treatments when compared.Effect on body weight: Marginal improvement of body weight was observed in the Eranda Pakagroup after the medication. Contrary to this marginal decrease in body weightwas recorded in the Ajamodadi group after the treatment. However thedifference noted in these groups when compared, is statistically insignificant(P=0.174).Effect on haematological values: Haematological examinations carried out before and after the treatmentin both the groups showed that there was marginal change in TLC and DC. Thechanges were also found to be statistically insignificant. 141
  • 227. Discussion Better improvement of haemoglobin % was noted in the Eranda Pakagroup in comparison to the Ajamodadi group. The average increase of Hb%following the medication with Eranda Paka was 0.795 gm%. And the same inAjamodadi Churna group was just 0.625 gm%. This explains the Eranda Pakahas an edge over the Ajamodadi Churna in improving the haemoglobin %. Thevariation noted in the two groups when compared showed statisticallyinsignificant change (P=0.740) Reduction in the ESR following treatment was recorded in both thegroups. However the Eranda Paka group patients showed a better fall in ESRlevel. The average fall in ESR after the treatment with Eranda Paka was 38.4mm after 1st hour, as against 18.0 mm after 1st hour in Ajamodadi Churnagroup. Statistical significance of this variation noted could not be confirmed bythe unpaired ‘t’ test.Over all effect of treatment in 10 patients of Amavata: Comparison of the overall effects of the treatment in both the groupsreveals that Eranda Paka is more efficacious. Complete remission of the illnesswas observed in 40% of the patients in Eranda Paka group as against mere10% of the patients in Ajamodadi Churna group. 30% of the patients in eachgroup recorded major improvement. In patients treated with Eranda Paka, 30%of the patients showed minor improvement as against 60% of patients showingthis response in Ajamodadi Churna group. In both the groups no patients wereobserved in the “no change” category. 142
  • 228. Discussion From the foregoing it is clear that both Eranda Paka as well asAjamodadi Churna are very effective in the patients suffering from Amavata.The sequential administration of Pancha Kola Phanta, Koshtashodhana byEranda Taila and Shamana Chikitsa by Eranda Paka is found to be veryeffective in alleviating signs and symptoms of the disease. Eranda is said to bevery effective as Vata Kaphahara and is helpful in the disease Amavata. Erandais described as drug of choice in patients of Amavata. The present clinical datajustifies the Vata Kaphahara as well as Vyadhihara effect of the drug Eranda.The complete or partial remission of the cardinal symptoms of Amavata provesthe Vyadhihara effect of the herb. The alleviation of the symptoms like Shoola,Antrakujana, Vibandha, etc., explains the Vatahara effect of the Eranda Paka.Further the alleviation of the symptoms like Agnimandya, Praseka and similarother symptoms of Kapha Dosha corroborates the Kaphahara effect of the drug.Ama is one of the predominant pathological factor in Amavata, the alleviation ofthe symptoms of Amavata like Balabramsha, Alasya, Apakti, Malasanga etc.,prove the therapeutic effect of the Eranda Paka as Amapachaka. Ajamodadi Churna consists of herbs that render Amapachana and thatpacify Vata Kapha Dosha. The herbs like Pippali, Chavya, Chitraka etc., aresaid to improve the digestive ability rendering Amapachana. In patients treatedwith Ajamodadi Churna, the remission of the symptoms like Apakti, Praseka,Hrillasa, Chardi, Malasanga etc., prove the efficacy of the drug in alleviating theAma. The herbal combination Ajamodadi Churna also contains herbs likeDevadaru that has proven efficacy to pacify Vata Dosha. Reduction in the 143
  • 229. Discussionsymptom score of Shoola, Stabdata, Sandhi Sankocha, Balakshaya in patientstreated with Ajamodadai Churna as observed in the clinical data justifies theefficacy of the drug in this regard. Kaphahara effect of the herbal combination isproved by the remission of the symptoms like Aruchi, Praseka, Hrillasa, Chardi,etc., in patients treated with Ajamodadi Churna. The comparison of the two treatments clearly showed that the ErandaPaka has an edge over the Ajamodadi Churna in the remission of cardinalsymptoms of Amavata, general symptoms of Amavata, symptoms of Ama,activity of the disease, functional disability, improvement in the laboratoryinvestigation findings, hand grip and foot pressure, etc. This corroborates thetextual reference in Bhavaprakasa : Amavata gajendrasya shareeravana charinaha | Eka eva nihantyaashu eranda taila keshari || (B.P. Madh. Kha. 26/50) 144
  • 230. Summary and Conclusion SUMMARY AND CONCLUSION This dissertation work entitled “A Comparative Study of Erandapaka andAjamodadi Churna in the Management of Amavata” comprises of five parts, viz.Conceptual study, Clinical study, Discussion and Conclusion.Introduction: In the first part, brief introduction to the disease Amavata and toRheumatoid arthritis in the modern parlance is given.Conceptual part: Conceptual the second part includes 3 chapters. The first chapter dealswith a brief historical review of the disease Amavata starting from Vedic periodto this age. Second chapter includes etymology of Amavata, the concepts ofAma and Vata in Amavata, Nidana, Poorvaroopa, Roopa, Chikitsa, Upadravaand Sadhyasadhyata. Along with that description of Rheumatoid arthritis is alsogiven. In the third chapter under the heading drug review, drug compound andingredients there in are described.Clinical study: The third part titled ‘Clinical study’ where in a detailed description ofmaterials and methods are given. Subsequently the results obtained weresubjected to statistical analysis and are given in the form of tables and graphs. 145
  • 231. Summary and ConclusionDiscussion: The fourth part entitled as ‘discussion’ includes logical interpretation ofresults obtained. The conclusion drawn from those are given below: 1. Among the patients studied in this work maximum of 6 patients (30%) belonged to age group of 50-60 years. Predominance of females (75%), Hindus (65%) and domestic workers (60%) was observed in this study. Addiction to tobacco is seen in 30% of patients and a majority of 45% of illiterates. Most of the patients were married (80%) and dominant part of the patients were economically poor (35%), lower middle class (35%). Predominance of patients using mixed diet (80%) was seen. 2. 40% of patients registered in the study belonged to Pittakapha Prakriti. Dominance of Madhyama Satwa (70%) along with Madhyama Saara (95%) and Madhyama Samhanana (95%). 3. Majority of patients showed Madhyama Satmya (95%) 4. Regarding Agni Abhyavarana Shakti and Jarana Shakti was Madhyama in most of the patients (60%) 5. Statistically insignificant improvement was seen on the symptom Stabdata in both the groups. 6. Highly significant relief in Sandhi Shoola is observed in Eranda Paka group against Ajamodadi Churna group. 7. Marginally better results were observed in Eranda Paka group in reducing the Sandhi Shotha and joint tenderness. 8. Joint crepitations were not observed in both group patients 146
  • 232. Summary and Conclusion9. Eranda Paka has shown edge over Ajamodadi Churna in reducing the general symptoms of Amavata.10. Statistically significant change is obtained in Eranda Paka group in reducing the symptoms of ama against Ajamodadi Churna group.11. No change observed in circumference of arm, forearm, thigh and calf in both groups before and after treatment.12. The range of movement increased by 16.884 degrees in Eranda Paka group against Ajamodadi Churna group (16.51 degrees). The difference was statistically insignificant.13. Comparatively better improvements in foot pressure test (8.55 kgs) observed in Eranda Paka group where as in Ajamodadi Churna group improvement of 7.25 kgs was seen. Chance factor could not be ruled out. Improvement in hand grip power was observed in Ajamodadi group but statistical analysis could not rule out chance factor. Efficacy in improving the general functioning capacity observed is equal in both the groups. Marginal improvement in body weight in Eranda Paka group contrary to marginal decrease in body weight in Ajamodadi Churna group was observed. But the difference is statistically insignificant.14. Average reduction of E.S.R. was more in Eranda Paka group against Ajamodadi Churna group (38.4mm in first hour, 18.0mm in first hour respectively). Marginal change observed in TLC and DC values in both groups. Better improvement in Hb% noted in Eranda Paka group. 147
  • 233. Summary and Conclusion 15. Complete remission is observed in 40% patients belonging to Eranda Paka group and 10% of patients in Ajamodadi Churna group.30% of patients in each group, recorded major improvement. Where as 30% of patients in Eranda Paka group showed minor improvement against 60% of patients in Ajamodadai Churna group. To brief, the Eranda Paka group patient showed comparatively betterimprovement. Eranda Paka found more efficacious in relieving the cardinalsigns and symptoms and general symptoms of Amavata, symptoms of Amaimprovement in functional ability. Deduction in above said signs and symptomscomparatively less in Ajamodadi Churna group. Hence it can be said as ErandaPaka has an edge over Ajamodadi Churna in the management of Amavata. 148
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  • 240. Bibliography48) Warrier P.K, Nambiar VPK, Ramanakutty C; Indian Medicinal Plants: 1st edition, 1994; Orient Longman.49) Williams Sir Monier; A Sanskrit English Dictionary (1999): 1st edition; Motilal Banarasidas publishers Pvt. Ltd, Delhi.
  • 241. Case Proforma DEPARTMENT OF KAYACHIKITSA S.D.M. COLLEGE OF AYURVEDA KUTHPADY, UDUPI RESEARCH PROFORMA FOR STUDIES ON AMAVATAGuide: Prof. U. N. Prasad Co-Guide: Dr. Sridhar Holla Researcher: Dr. Deepak S. M.Name : Serial No :Age : Group :Sex :M/F OPD No :Religion :H/M/C/O IPD No :Education : UE / P / M / MS / GR / PG DOA :Marital Status : UM / M / D / W DOD :Social Status : VP / P / LM / M / UM / RVR Diagnosis :Occupation : Result :Postal Address :MAIN COMPLANTS: OTHER Duration BT AT AT AT AT SYMPTOMS 1 2 3 4 Jwara Stabdatha Aruchi Mala Bhaddatha Angamarda Sadana Alasya Hrutgraha Anaha Preseka Trushna Hasta-Pada Daha Bahumootrata Kukshi Shoola Chardi Bhrama Shareera Bhara Antrakoojana Kandu
  • 242. Case ProformaHISTORY OF PRESENT ILLNESS:Onset: insidious / gradual / suddenSequence of joint involvement: 1……Since……2……Since……3……Since……4……Since…… 5……Since……6……Since……7……Since……8……Since……Course: Progressive / receding / relapsing / stationeryAggravating factors:Relieving factors:Symmetry of joint involvement: 1 2 3 4 5HISTORY OF PAST ILLNESS:FAMILY HISTORY:TREATMENT HISTORY: Drugs Dosage Duration Details NSAID’S STEROIDS OTHERSPERSONAL HISTORY:Vyasana: Coffee/Tea…… Alcohol…… Cigarette…… Tobacco Chewing…… Others…… Duration: Since………Occational / Regular / Stopped / Reduced / ContinuedAhara: Veg / Mixed Samasana / Visamasana / Adyasana / Anasana Dominant Rasa - M / A / L / K / T / Ka Dominant Guna – R / S / U / Sh / G / LNature of work: Manual /Sedentary / Labour / Traveling / Walking / Studying / Sitting/ Day/Night.Vishrama: ……Hours Proper / Less / ExcessiveVyayama: No / Proper / Excessive / IrregularNidra: Sound / Disturbed Night …… Day …… Difficulty in falling Asleep / Staying AsleepBowel: Frequency ……… Consistency ………… ColourMicturation: ………Frequency………quantity………
  • 243. Case ProformaOBSTETRIC HISTORY:No. of delivery ……. Normal…… Surgical Intervention……Abortions …… Miscarriages …… Last Delivery ……Years Back……GYNAECOLOGICAL HISTORY:Menstrual cycle: …… Regular / Irregular / Menarche …… yearsBleeding ….. days Menorrhagia / Metrorrhagia / Dysmenorrhoea / LeucorrhoeaMenopause since……yearsGENERAL EXAMINATION: DASHAVIDHA PARIKSHAPulse …… / min Prakrutitah:V/P/K/VP/VK/PK/KP/KV/PV/VPKB.P …… mm / Hg Vikrutitah: P / M / ATemperature……F Satwatah: P / M / ARespiratory rate…… / min Saratah: P / M / ANourishment: G / F / P Satmyatah: P / M / ABuilt: Samhanatah: P / M / ANails: Ahara Shaktitah: Abyavaharana: P / M / AConjunctiva: JaranaShaktitah: P / M / ASinuses: Vyayama Shaktitah: P / M / ALymph nodes: Pramanatah: P / M / ADeformities: Height …… cmsContractures: Weight …… KgsNodules: Y / N Vayataha; Bala / Madya / VradhaOthers:SYSTEMIC EXAMINATION:CNS :CVS :RS :GUS :P/A : ASSESSMENT CRITERIA FUNCTIONAL TEST Joint Motion BT 1 2 3 4 Rt Lt Rt Lt Rt Lt Rt Lt Rt Lt Flexion Extension Shoulder Abduction Adduction Lat. Rot. Medi. Rot. Flexion Elbow Extension Supination Forearm Pronation
  • 244. Case Proforma Uln. Devi.Wrist Radi. Devi. Flexion Extension Flexion ExtensionHip Abduction Adduction Lat. Rot. Medi. Rot ExtensionKnee Flexion Plant. Flex.Ankle Dorsi. Flex. InversionFoot EversionMCP1 Flexion Extension Abduction AdductionMCP2 Flexion Extension Abduction AdductionMCP3 Flexion ExtensionMCP4 Flexion Extension Abduction AdductionMCP5 Flexion Extension Abduction AdductionPIP1PIP2PIP3PIP4DIP1DIP2DIP3DIP4 FlexionTOE ExtensionSpine Flexion ExtensionNeck Lat. Bend. Rotation
  • 245. Case Proforma RING TEST No. BT 1 2 3 4 Rt Lt Rt Lt Rt Lt Rt Lt Rt Lt 1 2 3 4 5 BT 1 2 3 4 TEST Rt Lt Rt Lt Rt Lt Rt Lt Rt LtGrip TestFoot PressureGen.Functions Circumference BT 1 2 3 4 Rt Lt Rt Lt Rt Lt Rt Lt Rt LtArmForearmThighCalfINVESTIGATION: Test BT 1 2 3 4 HB% T.L.C D.C / N D.C / L D.C / E D.C / B D.C / M E.S.R RA Factor OthersRADIOLOGICAL EXAMINATIONS:TREATMENT:OBSERVATION:
  • 246. Pain Swelling Stiffness Tenderness Warmth Redness Joints Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 RtDIP Lt RtPIP Lt RtMCP Lt RtWRI Lt RtELB Lt RtSH Lt RtDIP Lt RtPIP Lt RtMTP Lt RtANK Lt RtKN Lt RtHIP Lt RtJAW Lt RtSTC Lt RtARC Lt SpineC/T/L/S

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