A Clinical Study in the management of ViswachiWith Sinduvaradi Yoga along with Ksheerabala taila Nasyam Thesis Submitted in Partial Fulfillment for the Degree of Doctor of Medicine (AYURVEDA) in KAYA CHIKITSA BY Dr. G.LAVANYA GUIDE: Dr.Prakash chander (Ay) H.O.D Dept. of Kayachikitsa, P.G. UnitPOST GRADUATE DEPARTMENT OF KAYACHIKITSADr. B.R.K.R. GOVT. AYURVEDIC COLLEGE / HOSPITAL HYDERABAD Affiliated to Dr. N.T.R. University of Health Sciences Vijayawada, A.P. 2007 Dr. NTR UNIVERSITY OF HEALTH SCIENCES VIJAYAWADA, A.P. Dr. NTR UNIVERSITY OF HEALTH SCIENCES VIJAYAWADA, A.P.POST GRADUATE DEPARTMENT OF KAYA CHIKITSADr. B.R.K.R. GOVT. AYURVEDIC COLLEGE / HOSPITAL HYDERABAD, A.P., INDIA 2007
CERTIFICATE This is to certify that Dr.G.Lavanya final year PostGraduate Scholar, Dept. of Kaya Chikitsa has submitted her dissertation work entitled “A CLINICAL STUDY IN THE MANAGEMENT OF VISWACHI WITH SINDUVARADI YOGAM ALONG WITH KSHEERABALA TAILA NASYA” under our direct supervision.We are satisfied with the work carried out by her and recommend the same for the acceptance and approval of the adjudicators. H.O.D. Dr. Prakash Chander, M.D. (Ay) Professor Dept. of Kaya Chikitsa, P.G. Unit Dr. B.R.K.R. GOVT. Ayurvedic College / Hospital, Hyderabad.Date:Place:
Dr. NTR UNIVERSITY OF HEALTH SCIENCES VIJAYAWADA, A.P. POST GRADUATE DEPARTMENT OF KAYA CHIKITSA Dr. B.R.K.R. G0VT. AYURVEDIC COLLEGE / HOSPITAL HYDERABAD, A.P., INDIA 2007 CERTIFICATE This is to certify that the present thesis of Dr.G.Lavanya, entitled by “A clinical study in the management of Viswachi with Sinduvaradi yoga along with Ksheera bala taila nasya” has been completed by the candidateherself under our direct supervision. She has devoted the required time for the purpose and her work has been checked periodically. This originality of the work holds good of its kind to enlighten the branch of Kaya Chikitsa. Guide: Dr.Prakash chander M.D., H.O.D Dept. of Kaya Chikitsa, P.G. Unit Dr. B.R.K.R. GOVT. Ayurvedic College / Hospital, Hyderabad.Date:Place:
LIST OF TABLES1. Table showing features of typical cervical vertebrae2. Table showing origin, nervename, muscle name & action3. Table showing nidanas explained in various classics4. Table showing differentiating features of disorders of urdhwa saakha5. Table showing vitamin contents in cow’s milk6. Table showing minerals contents of cow’s milk7. Table showing the incidence of sex8. Table showing the incidence of age9. Table showing the incidence of religion10. Table showing the incidence of occupation11. Table showing the incidence of socio-economic status12. Table showing the incidence of nature of work13. Table showing the incidence of food habits14. Table showing the incidence ofaddictions15. Table showing the incidence of prakriti16. Table showing the incidence of duration of illness17. Table showing the incidence of duraion of pain18. Table showing the incidence of side involved19. Table showing the incidence of type of pain20. Table showing the incidence of times of occurence21. Table showing the incidence of intensity of pain22. Table showing the incidence of bahu karma kshaya23. Table showing the incidence of clinical features24. Table showing the incidence of paraesthesia25. Table showing the incidence of weakness
26. Table showing the results of intensity of pain after treatment27. Table showing the results of subjective symptoms28. Table showing the results of scores of NPR & NSFT29. Table showing the results of functional disability after treatment30. Table showing the statistical analysis of NPR & NSFT31. Table showing the total outcome of the treatment LIST OF ILLUSTRATIONS1. Schematic representation of Viswachi samprapti2. Schematic representation of Nasya karmukata3. Images of anatomical structures involved in Viswachi4. Images of pathology in cervical spondylosis5. Images of drugs6. Images of compound preparation7. Graph showing incidence of sex8. Graph showing incidence of age9. Graph showing incidence of occupation10. Graph showing incidence of nature of work11. Graph showing incidence of type of pain12. Graph showing incidence of clinical features13. Graph showing NPR curve during treatment14. Graph showing NSFT curve during treatment15. Graph showing the pain relief16. Graph showing the functional disability response to treatment17. Graph showing the total outcome of the treatment
ACKNOWLEDGEMENTSI humbly owe every successful endeavour of my life to my beloved parents. I utilize this prospect to express my unfathomable gratitude to thepersons who helped directly or indirectly; I would like to pick few names,which doesnot mean that others are not remembered; human heart is not justtwo pages of paper. I express candid gratefulness with a deep admiration to my GuideDr.Prakash chander M.D., professor, H.O.D, Post Graduate Department ofKayacikitsa, Dr.B.R.K.R Govt. Ayurvedic College/ Hospital, Erragadda,Hyderabad for his able guidance, valuable support & affection. Iamundoubtedly benefitted by his suggestions through out the period of myP.G.studies. I feel great pleasure to express my sincere gratitude to Dr.V.Vijayababu M.D., Reader, Post Graduate Department of Kayacikitsa, Dr.B.R.K.RGovt.Ayurvedic College/ Hospital, Erragadda, Hyderabad for his thoughtprovoking lectures; had it not been for his valuable suggestions & constructivecriticisms this work would not have achieved its present form & standard. I humbly express my heartfelt gratitude to Dr.M.Srinivasulu for hisdiligent support & encouragement in the attempt of understanding concepts ofAyurveda. I am particularly indebted to Dr.G.Purushottamacharyulu M.D., forhis valuable advices and kind support in clarifying my doubts. I thank Dr.M.L.Naidu, Dr.Bhaswanth Rao, Dr.S.RamalingeswaraRao Dr.K.Vijaya Lakshmi, for their co-operation during this work. I acknowledge Dr.B.R.K.R Govt.AyurvedicCollege/Hospital PrincipalDr.Sadashiva Rao & Dr.L.R.K.Murthy Hospital Superintendent forproviding the necessary facilities during my study.
Dr.V.V.S.Rama Sastry, Dr.Chalapathi Rao, & Dr.Suresh Babu fortheir valuable suggestions. I gratefully acknowledge the contributions of all my teachers sinceprimary education that inspired, guided and nurtured my interest in acquiringknowledge and scientific enquiry at various stages of my career. Especially I thank Dr.P.Murali Krishna & Dr.A.R.V.Murthy of myparent institution S.V.Ayurvedic College, Tirupati for their encouragementthrough out my career. I acknowledge the valuable support of my friends & colleaguesDr.Ratnapriyadarshini, Dr.Neelayathachi, Dr.J.Sivanarayana, DrP.Himabindu,Dr.Prasuna, Dr.K.Sireesha, Dr.Haritha, Dr.Binod, Vd.Pranita joshi & otherswho helped me a lot in one way or the other in successful completion of thistask. As a token of gratitude I acknowledge my beloved sisters G.S.Madhavi,G.v.lakshmi & my brother G.S.Sanath for their attentive support and care inevery endeavour of mine. I sincerely express my thanks to Swapna Bhupathi (M.P.T) & Amruthashah B.P.T for their timely co-operation and help extended in collecting thebooks required. I sincerely express my heart felt thanks to Mr.Sridhar for giving hispersonal laptop, with out which the task of typing had been a challenge. I acknowledge the staff of our college library, British library & I.M&Hlibrary for their co-operation. Lastly I thank all my patients, with out whom I could not havecompleted my dissertation.
SOURCE ACKNOWLEDGEMENT I sincerely express my gratitude to the authors of all the books andarticles which have been utilized by me, as the source of information, in thisdissertation work.
INTRODUCTION Pain is the most complicated area of human experience. Pain is derivedfrom the Greek poine (a tax) and the Latin poena (a punishment or reality). Thelatter had both physical & mental implications in classical Latin. The International Association for the study of pain defines pain as “anunpleasant sensory & emotional experience associated with actual or potentialdamage or described in terms of such damage.” Pain is whatever the experiencing person says it is, and it existswherever he says it does”. Pain, when it does occur, usually signals tissue disorder. Pain as asymptom is often used by the physician in establishing the diagnosis. Severaldiseases include pain as an important feature alerting the patient to take action. One of such disease is Viswachi, affecting the upperlimbs. Greatmobility characterizes the upper extremity; they possess great range ofmovement. They are also prey to many diseases & disorders. Present daylifestyle has led to many diseases which though does not kill a person, buthamper his day-to-day life It seems totally unnecessary to champion the argument for the economicimportance of the hand when one considers the magnitude of person’seconomic limitations if hand function is impaired or lacking. Aristotle contended that hand as “The organ of organs, the activeagent of the passive powers of the entire system.” It has been estimated by research group that the hand performsapproximately thousand different functions in an ordinary day’s activity. Quitner and Elvey postulated that mechanical tension upon neuralstructures either distally (for instance at the wrist) or proximally(for instancewithin the cervical spine), generates abnormal discharges within the nervous
system, and that such neural entrapment is the primary precipitating event inthe development of chronic upper limb pain. Historically the relationship between diffused pains around the shouldergirdle and cervical lesions has been recognized (Cyriax, 1969). It is universally accepted that radicular symptoms in the arm usuallyindicate nerve root entrapment secondary to a paracervical disc protusion or inthe older population to the foraminal bony hypertrophy. Nerve root pain maybe very distressing and is often compatible with manual or office work for avariable period of time, depending upon the pathology. The present study of viswachi is limited to the cervical spine lesions.The degenerative diseases of the cervical spine, cervical spondylosis isclinically correlated with Viswachi of vatavyadhi. Cervical spondylosis is a chronic progressive degenerative disease. Theincidence of cervical spondylosis is becoming much more now a days becauseof many reasons. It is occurring in more than 90% of adults over the age of 50years and almost 100% by 70 years. Cervical degenerative disorders lead to a wide spectrum ofpresentations. Often a subtle mix of axial neck pain, radicular upper extremitydysfunction and even myelopathic states exist. The most frequent reason forseeking medical assistance is arm pain. The treatment of cervical spondylosis is difficult and absolute cure ofthis condition is impossible owing to the fact that the underlying structuralchanges are irreversible and is part of the generalized ageing process. Theprinciple of treatment is therefore aimed at reducing the symptoms andpreventing the development of new ones and their complications. Scope of present study includes the understanding of Viswachi diseasecompletely, with respect to cervical spondylosis and evolving an AyurvedicCompound which can manage the pain effectively along with delaying thedegenerative process in the cervical spine.
Vedana (pain) being the pratyatmika lingam (prime feature) ofViswachirequires great attention. Ayurvedic texts have mentioned a lot of vedanasamaka dravyas from which Sinduvara (Vitex negundo), Suranjan (Colchicumluteum), Parijatha (Nyctanthes arbortristis) are selected due to their potentialpain relieving property. Apart from the oral administration of these drugs, Nasya karma isconsidered for tarpana of uttamanga. Since this is purely vata disorder, tailambeing best vatasamaka dravya, Ksheera bala tailam is selected for nasya karmawhich is mentioned in most of the authentic classics of Ayurveda. This study has been taken up to make observation of these drugs, theirclinical efficacy and to put on record with statistical data. This thesis contains two parts. First part includes Introduction, Reviewof literature- Historical review, Sareera (both Ayurvedic & modern aspects),Disease review (both Ayurvedic & modern aspects), and Drug review. Secondpart includes the clinical study i.e Materials & methods, observation & results,Discussion, Summary and Conclusion. Bibliography and Annexure containingthe case sheet & questionnaire mark the end of this sincere attempt done instudy of Viswachi.
HISTORICAL REVIEW Mahabharat, one of the greatest epics of India, describes Ithihas(history) as a destroyer of veil of Ignorance1. It would be profiting to study thepresent in the light of past. So, review of references of disease Viswachi, fromthe age old scriptures have been taken up. There is no direct reference of term Viswachi in the Vedic literature.Only indirect references are available, which indicate possible prevalence ofvata diseases during that period.Vedic Period: The term vata vyadhi was mentioned for the first time in Adharvaveda2.Whereas the term vata has been used for wind in both Rigveda3 andAdharvaveda4. Vata is also said as bhisak in Rigveda and A.V.S5. In AdharvaVeda many synonyms were used for vata like maruta, vatajeeetc6. There is a hymn offering prayer to God of Vata (Marut-Storm Gods) toprotect the body & bear the limbs till old age. Anatomical description of Bahu, hasta & amsa7 is seen in Vedicliterature. There are certain references from both Rigveda8& Adharvaveda9quoting that there are certain diseases affecting the bahu, pani & anguli10, byoffering some prayers that parts will become disease free. This denotes that, at that time though direct term viswachi was notcoined but the disease with same symptoms might have been present.Upanishad Period: The other literary works like Upanishads contain facts and conceptsrelated to medicine. Chandogya & Brihadaranyaka has mentioned five types of vata,whereas in the Agni Purana ten types of vata are described.
In Garuda Purana medicine is dealt in elaborate way and in nidanavata vyadhi is dealt. These are all the evidences which show occurance of viswachi, type ofvata vyadhi affecting upper limbs though unnamed at that times. In some puranas (vahnipran’s ganabhednadhyaya) the word viswachi isthere but it is not applied as disease instead it is stated that viswachi was one ofthe twelve apsaras in the court of Indra.Samhita Period: In the samhita period, Caraka Samhita has to be given credit ofdescribing vata in an explicit manner. Stating it to be shareera vayu, loka vayu& again classifying it into five types allotting separate chapter named vatakalakaleeyam, only for vata. The pathological aspects are dealt in a separate chapter (28) of cikitsastana. Though the term viswachi is not seen in samhita but khalli is described.There is mythological reference for the vyadhi affecting the upper limbs11. Thatis while mentioning about miracles of Aswinis, the divine physicians, and thestupefaction of arms of Indra has been quoted. Caraka has described ekangavata where shoola, toda, sankocha of either upper limb or lower limb is present. In Bhela Samhita vata rogas are classified into two sarvanga & ekangarogas. In Haritha Samhita “viswachi gridhrasi choktah khalli teevrarujanvita” has been mentioned. In the Susruta Samhita many important observations pertaining tobasics of vata are dealt. Vata vyadhi, first chapter of nidana sthana, explainsdiseases specifically afflicting upper limbs. In those, viswachi is described forthe first time along with apabahukam and amsasosha. In Astanga Hrdya & Sangraha, viswachi is explained in vata vyadhiadhyaya.
Sarangdhara Samhitha is the samhita explaining viswachi as one ofthe ashitivatajavikara i.e., as vatajananatmaja vyadhi for the first time. Both Madhava Nidana & Bhavaprakasha have detailed explanationof Viswachi, quoting “Bahvo Prasarana Akunchanadi Karma Ksyayakari”. The later on evolved literature of ayurveda like Vangasena, Gadanigrahaall contain detailed description of Viswachi. Dr. C. Dwarakanath in his book Introduction to KC quotes as follows“Functions ascribed to sharira vayu, in the ancient medical classics are exactlythose which modern physiology ascribes to the nervous system”. The historical aspect of the neurological aspects has been describedas follows: Rufus of Ephesus, who flourished under the reign of Emperor Trozan,was the first medical writer that adopted a global view of the function ofnervous system. Later on Galen, Vesalius made significant contributions. Herophilus, Greek Physician and Anatomist in Egypt (335-280 B.C.)was probably the first to differentiate between nerves, tendons and motor,sensory nerves.1621-1675 - Thomas Villis, English Physician and Anatomist, described the spinal nerves.1648-1730 - Joseph G. Duverney named the nerves which form the brachial plexus in 1697. Before this nerves were designated by numbers.1748-1791 - The developments in clinical neurophysiology are closely linked to the discovery of electricity.1783-1855 - Francois Magendie confirmed that the anterior roots of spinal nerves are motor in function, posterior root stimulation elicited pain.
1791 - Galvani, discovered nerves to be good conductors of electricity.1806-1875 - Duchene was first to systematically study neuromuscular diseases.1817 - James Parkinson described a case whose clinical features suggest cervical radiculopathy.1836-1921 - Henric wilhelmgottfried waldeyer hartz proposed neuron theory.1857-1952 - Charles Scott Sherington studied the distribution of ventral and dorsal spinal nerve roots.1873-1930 - Henry Verger devised classification of neuralgias in 1904.1892 - Gowers described cases 0f cervical spondylosis under the “vertebral exotoses.” Though lesions of cervical cord had been diagnosed earlier, it was not until 1892 that the first successful operation on the cervical spine was done by Horsley. (Taylor & Collier 1901)1926 - Elliot described after Gowers how spinal arthritis involving cervical region might give rise to radicular symptoms through narrowing of the intervetebral foramina.1934 - Nachlas first drew attention to the fact that pain in the chest could result from lesions involving the cervical spine1936 - Hanflig discussed cervical spondylitis as a cause of pain in the shoulder and arm referred to pain in the chest wall as an associated symptom.1943 - Semmes & Murphy discussed production of radicular symptoms by acute protrusion of a cervical intervertebral disc.
1944 - Scoville reported 12 verified cases of ruptured cervical intervertebral disc; they thought that the dorsal protrusion was usually the result of trauma where as lateral protrusions were result of degeneration and cause pain in the shoulders & upper limbs resulting from root compression.1944 - Seddon and his co-workers elucidated the nature of different types of nerve injury.1948 - Bull correlated the anatomy of joints of cervical spine with the mode of production of the symptoms caused by their disease and their abnormal radiological appearances.1948 - Brain discussed importance of vascular factors as a cause of disturbance in the function of the cervical cord below the site of compression.1950 - Acute traumatic disc herniation process was distinguished from the chronic spondylotic process.1951 - Frykholm published detailed study of patients with cervical root compression along with comprehensive review of various aspects of degeneration of intervertebral disc.1954 - Pallis, Jones & Spillane stressed the fact that cervical spondylosis was a common disease of elderly people.1954 - O’connel distinguished three types of lesions occurring in cervical spondylosis.1963 - Fullerton and others shown that local ischaemia due to pressure is one factor giving rise to signs and symptoms when peripheral nerves or roots are compressed.
1965 – James found that in general the outcome in cervical spondylosis was independent of age, sex, trauma, the extent of degenerative changes and the clinical picture but did depend on duration of symptoms & level of protein in C.S.F. He thought cervical spondylosis could produce two types of changes in the spinal cord: firstly an acute “exudative”, a revesible condition & a second process of gradual loss of neural tissue with subsequent demyelination & gliosis.1974-1975 - Repeated prolonged pressure upon a nerve leads to ischaemia but also to mechanical deformation of the myelinsheath with local edema (rudge, Ochoa and gilliatt, neary and Eames).1978 - Nakano comprehensively reviewed entrapment neuropathies.1986 - The brachial plexus tension test (BPTT), devised by Elvey. It is used particularly by physiotherapists with an interest in spinal disorders.1995 - Rowland described brachial plexus neuropathy disorder of unknown cause that is characterized by sudden onset of severe pain usually around the shoulder12.
REFERENCES: 1. Mahabharat, Adiparava, 1.27 2. Adharvaveda, 9-8-20 3. Adharvaveda, 8-4-13 4. Rigveda, 2-33-13 5. A.V.S, 4-13-3 6. Adharvaveda, 8-4-18 7. Adharvaveda, 2-13-2, 10-2-5 8. Rigveda, 10-163-2 9. Adharvaveda, 20-16-18 10. Adharvaveda, 20-16-22 11. History of Indian Medicine, P.V.Sharma 12. Medical Discoveries, Who & When By Schimdt.
SAREERA Human body is divided into shadangas according to Ayurveda.1Shadangas include Siras, madhyasareera, saakhas (4).2 Saakhas are urdhwasaakha & adhosaakha. These are concerned with all the locomotor activities ofthe body. Ekadasa indriyas are explained in Ayurveda.3 Pancha karmendriyas area part of those eleven indriyas. Bahu is one of the panchakarmendriya. Itsfunctions are prasarana, akunchana, grahana & daana.4 Functional or physiological part in the body is carried out by thetridoshas. Vata is the one which is responsible for every activity in the body.5The term Vata is derived from the root Gati & Gandana, describing twopotential functions of vata. Gati indicates to move or cause movement. Whereas Gandana is knowledge. Vata in its prakritha avastha engazes all the elevenindriyas in their normal function. It integrates all these indriyas and derivesspecific work by co-ordination. 6 Out of panchavidha vatas 7 described, the vata that invades through outthe body being responsible for all the movements is Vyana vata.8 Movement isspecially attributed to this, though pranavata and udanavata control importanrtvegetative functions of life.9Functions of vyanavata are: 1. Gati- voluntary movements of skeletal muscles 2. Apakshepa- abduction 3. Utkshepa- throwing up 4. Unmesha- opening of eyelids 5. Nimesha- closing of eyelids 6. Rasavikshepa- circulation 7. Asrk sravana- circulation of blood 8. Sweda sravana- perspiration This vata controls all the movements of the skeletal muscles.10
11 12 13 Qualities like Amurta , Anavastitha / chalatva , Swayambu ,Sukshma etc of vata indicate that the phenomenon of vata can be assumed asphenomenon of nerve impulse. The vata or nerve impulse is conducted invatavaha srotases / nerve fibres and its sustained propagation is maintained bythe constituents of nerve fibres only.According to function, there are two types of vatavaha srotases- i. Chesta vaha srotas: to conduct motor function ii. Sagna vaha srotas: to conduct sensory functionAccording to structure, these are again of two types- i. Samvrita: well covered or concealed –myelinated fibres ii. Asamvrita: not covered or open – non myelinated fibres.14Since vata is amoorta (invisible), its chalanaswabhava is expressed by themovements of the mamsapeshis, snayus, kandaras, asthi, and sandhi. Movements are effected by the activation of muscles, which activatethrough their nerve supply. The nerves which supply the skeletal musculaturetake origin from the anterior horn cells of the spinal cord execute the functionsof vyanavata.15Disease in most instances has a visible component and the study of morbidanatomy has been the classic approach to its understanding. The cervical spine is surely the most complicated articular system in thebody; there are 37 separate joints whose function is to carry out the myriadmovements of the head and neck in relation to the trunk, and subserve allspecial sense organs. The seven small cervical vertebrae with their ligamentous, capsular,tendinous and muscle attachments appear poorly designed to protect theircontents, compared to skull above and the thorax below. The contents of thisanatomical cylinder interposed between skull and thorax include carotid and
vertebral arteries, the spinal cord, and all anterior and posterior nerve roots and,in its uppermost portion, the brain stem. Normally the neck moves over 600 times an hour, awake or asleep; noother part of the musculoskeletal system in such constant motion. The cervicalspine is subject to stress and strain in ordinary everyday activities. The cervical spine is a superb example of the biological principle ofadaptation of structure to function. It supplies support for the head, a flexibleand buffered tube for the transmission and protection of the upper spinal cord,provision for the entry and exit of spinal nerves, and extremely serviceablemobility.15 The posterior landmarks of the cervical spine include the occiput, theinion, the superior nuchal line and the mastoid process. Cervical vertebrae form the bony skeleton of the neck. These aresmallest of the 24 movable vertebrae, and bear less weight than do thevertebrae inferior to them. The cervical vertebrae as a whole are characterized by the fact that theirtransverse processes contain a foramen, the transverse foramen. The bodies arerelatively delicate, their greatest diameter being the lateral one. The articularprocess is short; the facets on the superior articular process face upward andbackward, those on the inferior articular process are forward and downward. The first two cervical vertebrae are markedly different from theremainder. The first cervical vertebra, known as Atlas, is especiallydistinguished by the fact that it has no body but only an anterior arch. Thesecond cervical vertebrae or Axis is also peculiar in structure, as it bearsprojecting up from its body a tooth like process, the dens. This processarticulates with the anterior arch of the Atlas, to which it firmly held byligaments in such a fashion that it acts as a pivot around which the atlas rotates.
1. Table showing features of typical cervical vertebrae (C3 –C7)16: PART DISTINCTIVE CHARACTERSTICS Body Small and wider from side to side than anteroposteriorly; superior surface is concave and inferior surface is convex Vertebral Large and triangular foramen Transverse Transverse foramina (foramina transversaria); small or absent in process C7; vertebral arteries are accompanying venous and sympathetic plexus pass through foramina, except C7, which transmits only small accessory vertebral veins; anterior & posterior tubercles. Articular Superior facets directed superoposteriorly; inferior facets processes inferoanteriorly; obliquely placed facets are most nearly horizontal in this region. Spinous Short (C3-C5) and bifid (C3-C5); process of C6 is long but that of process C7 is longer (for this reason C7 is called Vertebra prominens.)Blood supply of cervical vertebra: Vertebra and longitudinal muscles aresupplied by segmental arteries that give multiple branches. Other arteries aredeep cervical, occipital and transverse cervical arteries.Nerve supply of cervical vertebra: Joints between vertebral bodies areinnervated by small meningeal branches of each spinal nerve as it exits theforamina. Joints between articular processes are innervated by branches ofposterior rami of spinal nerve.Joints of the cervical spine: i. Joints of the vertebral bodies ii. Joints of the vertebral arches iii. Atlantoaxial joints iv. Atlanto occipital joints
The joints of the vertebral bodies are secondary cartilaginous jointsdesigned for weight bearing and strength. The articulating surfaces of adjacentvertebrae are connected by intervertebral discs and ligaments. The discs are not solid lumps of inert gristle resembling rubberpads,but living structures which flatten slightly during day and re-expand atnight17. The disc is a symphysis between each pair of vertebrae and with twoposterior facet joints, allows movement between vertebrae, acts as shockabsorbers, and their varying shapes produce the secondary curvatures of thevertebral column.Each intervetebral disc consists of:i. The center is a semi-liquid, mucocartilagenous mass, the remnant of the embryonic notochord, called the nucleus pulposus. It is a gelatinous substance with high water content in which the collagen network is masked by a rich layer of chondroitin sulphate. The collagen fibers form a fine network resembling a porous system. It contains primarily type 2 collagen which functions in resisting compression forces.ii. The nucleus is maintained by a thick fibrous band called the annulus fibrosus. It has a considerably denser and more regular collagenous pattern. The fibrils are grouped in bundles of varying thickness that pass in a spiral course from one vertebra to the next. It consists of water, proteoglycans and type 1 collagen whose function is to resist tensile forces. The intervertebral disc is further stabilized by the superior and inferior cartilage end plates that fix the structure to the vertebral bodies above and below.Blood supply: It is derived from the segmental vessels derived from the subclavianartery. The nucleus pulposus is avascular throughout foetal and postnatal life,but annulus receives a peripheral blood supply which gradually diminishesduring the first two decades until it is virtually avascular.
Innervation and nutrition of the disc: Outer annulus is supplied by vertebral and sinu vertebral nerves. Nonerve supply in nucleus pulposus. • Nutrition is by diffusion through central portion. The joints of the vertebral arches are the zygapophysial joints. Thesearticulations are plane synovial joints between the superior & inferior articularprocesses. Each joint is surrounded by a thin, loose articular capsule. Those inthe cervical region are especially thin & loose. These permit glidingmovements between the vertebrae. These are innervated by articular branchesthat arise from the medial branches of the dorsal primary rami of spinal nerves. The Atlanto occipital joint is between the Atlas and the occipital boneof the skull. This is a synovial joint of condyloid type. The Atlanto axial joint is between the Atlas & Axis. There are threeatlanto axial articulations. These are synovial joints with no intervertebraldiscs. They are designed to give wider range of movement than in the rest ofthe vertebral column. Uncovertebral joints are between the uncinate processes of C3 throughC6 and the beveled surfaces of the vertebral bodies superior to them. The jointsare at the lateral and posterolateral margins of the intervertebral discs. Thesejoint like structures are covered with cartilage and contain a capsule filled withfluid. These are the frequent sites of spur formation that may cause neck pain.Ligaments: Ligamentous attachments of cervical spine are: 1. Anterior longitudinal ligament: The anterior longitudinal ligament runs along the anterior and lateral surface of the vertebral bodies from sacrum to C2 attached firmly to the vertebral bodies, but only loosely at the disc area the ligament is compressed in flexion and is stretched in extension. The ligament may become slack in neutral position of spine when the normal height is reduced. 2. Posterior longitudinal ligment: This ligament runs within the vertebral canal along the posterior surfaces of the vertebral bodies from C2 to sacrum. It is stretched in flexion, slack in extension. This ligament is
firmly attached to the disc but loosely to the vertebral body surface. In the cervical spine it is 3 to 5 fold thicker and more. 3. Ligamentum flavum: t is a thick, elastic ligament, which is located on the posterior surface of vertebral canal. The fibres connect lamina of adjacent vertebra which runs from C2 to sacrum. It gets stretched when spine is in flexion and is under constant tension even when spine is in neutral position. 4. Interspinous ligaments: This ligament varies from region to region. In cervical region it connects and covers the margins of adjacent spinous processes. The parallel fibres run diagonally and fill up the space between the spinous process. The ligament is slack in extension and stretched in forward flexion, when they resist the separation of spinous processes. 5. Supraspinous ligament: This ligament is cord like which connects the tips of spinous processes from C7 to L3-L4. In cervical region it becomes ligamentum nuchae. It is stretched in flexion and its fibres resist separation of spinous process during forward flexion. 6. Intertransverse ligament: This ligment is paired and passes between the transverse processes and attaches to deep muscles of back.This ligament is alternatively stretched and compressed during lateral bending.Nerve root exits: The spinal cord passing through the vertebral column gives 31 pairs ofspinal nerves. Each spinal nerve is attached to the spinal cord by a dorsal root,which is sensory and a ventral root which is motor. All the branches of a spinalnerve contain both sensory & motor fibres. At the C3-C4 level the anterior and posterior nerve root sites through thedural sleeves are below the level of the intervertebral discs by approximately4mm. This is as a consequence of the formation of nervous system, beingfollowed latter by rapid growth of the spine. With growth and extension of thecervical spine, physiological traction is exerted on the cord and nerve roots and
the dural sleeve exit sites are at the level of vertebral bodies rather than at thedisc level; the root exit zone is generally below the level of the disc. The anterior nerve root is normally situated low in the intervertebralforamen and hence is very unlikely to be compressed. The posterior nerve rootis well protected from the point of any disc herniation. There is normally a considerable individual disparity between the spinalcord volume and space available in the bony canal. This seems a constitutionalor genetic, characteristic. After mixed spinal nerve passes through the intervertebral foramen, itdivides into two branches, a dorsal branch that turns backward to supplymuscle and skin of the back. Ventral branch runs laterally and forward,supplies the limbs and the anterolateral aspects of the trunk. Except in the thoracic region, the ventral branches run close togetherand exchange branches with each other, such an exchange being known as anerve plexus. The area of distribution of spinal nerve to skin is known asdermatome. On the limbs the dermatomes bear no relation to the distribution ofvarious peripheral nerves. The ventral rami of the upper four cervical nerves, unite to form thecervical plexus; union of ventral rami of the lower four cervical nerves and thegreater part of the ventral ramus of the first thoracic nerve form brachialplexus. The muscles of head & neck receive innervation from C1 to C4 where asthe muscles of arm are supplied by C5, C6, C7, C8 & T1 nerve roots. The following table shows the origin of nerve, name, muscle supplied &action.18
2. Table showing, origin, nerve name, mucle name & action:S. Origin Nerve Name Muscle Name ActionNo1. C2 , C3 Accesory/muscular Sternocleidomastoid Lateral flexion& rotation of head2. C3,4 Accessory/muscular Trapezius Elevation of tip of shoulder3. C3,4 Nerve to levator Levator scapulae Elevation of scapula scapulae4. C5 Dorsal scapular Rhomboidei(both) Retraction of scapula5. C5,6 Nerve to subclavius Subclavius Depression of shoulder6 C5,6 Axillary Deltoid,Teres minor Abduction & Ext.rot. of arm7. C5,6 Upper subscapular Subscapularis Int.rot. of arm.8. C5,6 Lower subscapular Teres major Extension & int.rot.of arm9. C5,6 Suprascapular Supraspinatus,Infraspinat Abduction & us ext.rot.of arm10. C5,6,7 Long thoracic Serratus anterior Upward rot. Of scapula11. C5,6,7 Lateral pectoral Upper pectoralis major Adduction,flexion of arm12. C8,T1 Medial pectoral Lower pectoralis Adduction,extension major,Pectoralis minor of arm; depression of shoulder13. C6,7,8 Thoraco dorsal Latissimusdorsi Extension,adduction of arm14. C5-7 Musculocutaneous Biceps,Coracobrachialis, Flexion, adduction Brachialis supination of forearm15. C5-8 Radial Triceps, anconeus, Extension of extensors forearm, adduction at wrist16. C5-TI Median Flexors of forearm, 5 Pronation of hand muscles forearm,flexion of wrist17. C8-T1 Ulnar 11/2Flexors of forearm, Flexion of skin of hand phalanges,adduction at wrist
Bio-Mechanics Of Cervical Spine From C4 To C7 • Biomechanics is study of mechanics in human body. • It includes kinetics and kinematics.Kinetics: Area of biomechanics concerned with forces producing motion ormaintaining equilibrium.Kinematics: Area of biomechanics concerned with motion. • Cervical spine is designed for large amount of motion. • The motion of flexion, extension and lateral rotation are permitted in cervical spine from C4-C7. Predominent translation at C2-C7 occurs in sagital plane from C4 to C7.Range of Motion and Muscles Acting:Movement : ExtensionMuscles : Longissimus Cervicis, Semispinalis Cervicis, Splenius Cervicis.Range of motion : 0’ to 30’Movement : FlexionMuscles : Scalene Muscles, Posterior SternocleidomastoidRange of Motion : 0’ to 35-45’Movement : Lateral flexionMuscles : Sternocleidomastoid, Splenius Cervicis, Scalenii, Erector spine.Range of motion : 20’ to45’Movement : RotationMuscles : Splenius capitis, splenius cervicis on same side. Sternocleidomastoid on opposite side.Coupling characterstics: The coupling pattern in the lower spine isimportant. • The coupling is such that with lateral bending the spinous process goes to the convexity of the curve.
• In lateral bending to left, the spinous process goes to the right and in lateral bending to right the process goes to the left. • This coupling phenomenon plays an important role in that some ratios of axial rotation and lateral bending may result in a unilateral facet dislocation.Stability of cervical spine: • Cervical region bears less weight and is generally more mobile. • The loads imposed on cervical region vary with position of head and body and are minimal in a well supported reclining body posture. • In cervical region compressive forces are transmitted in three parallel columns: A single anterocentral column formed by veterbral bodies and discs Two rod like posterolateral column composed of left and right zygopophyseal joints. Compressive forces are mainly transmitted through bodies and discs andless than 1/3rd by posterolateral column. • Compressive loads are low during erect stance, sitting posture and during flexion and extension movements. • Cervical motion segments exhibit stiffness in bending, axial rotation and compression.C2 to C5 exhibit more stiffness in compression and extension than C5 to T1. • Head should be held in non rotated position during flexion, extension activities to reduce the risk of injury. Joint capsules of cervical region are lax and therefore provide fewer restrictions to motion.Mobility of cervical spine: • The motion of flexion, extension and rotation occur here. • Lateral flexion below C2 is coupled due to articular facets. • Flexion and extension occur between C4 and C 6.
• The height of disc plays role in determining the amount of motion of spine. • Large amount of motion occurs at each segment at younger age because of large amount of water in disc. • At older age disc appear ligamentous, dry and no evidence of nucleus pulposus. • Thus disc are more prone for protusion and degeneration. • Highest occurs between C5 and C6 followed by C6 and C7, C4 and C5. • A normal cervical spine shows anterior convexity that is a lordotic curve. • More degeneration occurs at C5 and C6 because of greater flexion and extension movements at this region.Factors affecting mobility and stability: • Excessive extension is limited by passive tension in anterior longitudinal ligament, spinous procces and anterior neck muscles. • Forward flexion is limited by posterior longitudinal ligament, ligamentum nuchae and flavum. • Lateral flexion and posterior translation is limited by uncinate process. • Rotation and anterioposterior and lateral tilting are limited by fibres of annulus fibrosis.19
References:1. Su.Sa.5/32. Su.Sa.5/33. Su.Sa.1/84. As.Sa.Sa.5/58,59 & Bh.Pr.5. Ca.Su.17/1186. Ca.Su.12/87. Ca.Ci.28/58. Neurological concepts in Ayurveda- 4th chap ; pg no:999. Essentials of Basic Ayurvedic concepts- Dr.V.V.S.Sastry- 1st chap ; pg no:1710. Tridosha theory- Dr.V.V.S.Sastry11. Ck on Ca.Su.12/20 & Su.Ni.1/712. Ck on Ca.Su.12/313. Su.Ni.1/514. Essentials of Basic Ayurvedic concepts- Dr.V.V.S.Sastry- 1st chap ; pg No:1015. Tridosha theory- Dr.V.V.S.Sastry16. The clinical anatomy & management of cervical pain17. Clinically oriented anatomy18. Orthopaedic medicine-a practical approach19. Gray’s anatomy20. Role of physiotherapy in lower cervical spondylosis- project work
NIDANA Rogotpadaka hetu is called nidana.1 A particular factor capable ofproducing a complete disease process in the body either immediately or aftercertain period is termed nidana.2 Acharya Caraka described Trisutra i.e Hetu-Linga-Aushadi.3The sumtotal of these three is Ayurveda. Where as Susruta stated nidana parivarjana asone of the methods of treatment.4 These two statements denote the importanceof nidana in production as well as curative line of approach. There are many and varied factors i.e both intrinsic (Nija) & extrinsic(Agantuja) factors causing disease. The actual intrinsic factors which becomeexcited and imbalanced, either conferring a predisposition or actually causingdisease are, the Tridoshas.5These are susceptible to imbalance and vitiation. There are no separate nidanas described for Viswachi. The generalnidanas of vatavyadhi and factors causing vataprakopa are applicable. Acharya caraka explained vatavyadhi nidana in 28th chapter of cikitsasthana. Susruta explained vataprakopa nidana along with other dosaprakopahetus in sutrasthana.Similarly Vagbata explained vatasanchaya hetus insutrasthana and vataprakopa hetus in nidanasthana. Basically nidanas are classified into sannikrista & viprakrista6 varieties.Sannikrista nidana includes aharaja, viharaja, manisika, agantuja, anya factors. In Vaidyacintamani viprakrista nidana for vatavyadhi is mentioned. Itstates that “the person who steals the wealth of God or Brahman and whodeceives his master or who apposes his teacher will suffer fromvatavyadhi.”7 There is another description of horoscope status which predictsoccurrence of vatavyadhi. It is as follows “If during birth Sun is in the Karkataka rasi & viewed by Saturn, thenthe person will suffer from vatavyadhi.”8 Though so many factors are explained a few act as primary aetiologicalfactors causing the pathology where as others act as sahayaka nidanas.
Aharajahetus:Gunas:• Excessive intake of ruksha, laghu, seeta ahara increases the vata. As samanyam is vriddhi karanam9, all these three factors are characters of vata which get increased by excessive intake ruksha guna causes dhatukshaya resulting in stamba, khatinyata of snayus and kandaras. Balanasa is noticed.• Laghuguna causes sroto riktata and rukshatwa, excites vata results in increased chalatwa.• Seetaguna causes stamba opposing movement of any kind results in stiffness10Rasa:• Kashaya, katu, tikta, rasas are vata kopaka rasas11.• Katu rasa by its laghu and ruksha gunas vitiates vata causing piercing and stabbing pain along with bala vighatam12.• Tikta rasa by its laghu seta ruksha gunas leads to dhatu kshaya and vata prakopa13.• Kashaya rasa by its ruksha, visada, seeta, and vistambi gunas causes soshana, stambana and srotorodha14.• Khara guna causes lekhana results in dhatukshaya and vata prakopa15• Excess sushka ahara sevana causes increased dryness in all the dhatus resulting in kshaya of all the dhatus.Sevana vidhi:• Food taken following the matra, kala, Agni is digested and absorbed properly, nourishes the body. Decreased quantity of food taken results in improper nourishment of the dhatus resulting in dhatu kshaya. Abstinence from food leads to lack of nourishment.• Food taken in irregular fashion not following matra, kala, Agni leads to improper paka of food, causing srotorodha and ultimately tridosha prakopa.• Eating incompatable foods (viruddasana) affects Agni and malnourishment of the dhatus. Vidahi bhojana vitiates rakta dhatu and is difficult to digest.
• The foods such as kalaya, chanaka etc comes under the vistambi, virudhaka category. These are heavy to digest and cause stambana resulting in sroto rodha, dosha prakopa and vyadhijanaka. The materials required for incorporation into the structure of seat of vata(mastishka and vatavahanadis) are produced in kosta by the in taken food. Allthe improper sevana vidhis results in nutritional deficiencies. Among all the nutrients B-complex, vitamins are very much essential forthe maintenance of normal health and activities of certain parts of the nervoussystem. Thus improper sevana vidhi may result in neurological diseas16.Viharajahetus:• Primary one is ativyayama i.e excessive exercise which also includes langhana (jumping), Plavana (swimming), dhavana (running), utkshepa, vikshepa, bharaharana (lifting heavy weights), vichesta and atichesta.• Due to excess of vyayama vata is vitiated along with pitta, rakta causing srama, klama, dhatukshaya17. All these causes excessive strees and strain on the spine. Ruksha, khara, laghu and visada gunas of vata increase.• Dukhasayya and asana are specially described by Caraka. Improper posture gives more and more pressure over the spine and disturbs the muscular integrity provoking vata.• The factors like gaja, turanga, ratha, pathadi charya and ati advagamana also vitiates vata due to increased chalatwa causing excessive stress and strain on the spine.• Diwaswapna causes srotorodha excites kapha vata, leads to vataprakopa.18• Ratrijagarana excites vata, pitta and kshaya of kapha. Rukshatwa is increased.19• Veganirodha and udirana both cause vata prakopa due to marga avarana. These are the almost always adisease causing factors in all diseases.• Ativyavaya can also be included under ativyayama but here along with vitiation of vata and pitta, dhatukshaya that to sukra kshaya occurs. This causes sandhi saitilya, rukshata and dourbalya20.
• Atichankramana leads to pain in both lower limbs, angamarda, amsabhitapa which are resultanat of vata prakopa21.Laghu guna, rukshaguna vriddhi occurs.• Excessive dosha srava or rakta srava from the body leads to dhatukshaya resulting in vata prakopa by increasing visada, laghu, and ruksha gunas in the body.• Occupational factors causing vata prakopa also comes under this category.Manasika hetus: Susruta defined swastha as one with healthy mind and body .22 Themanasika factors also influence the health of an individual. Chinta, soka, bhaya, krodha are due to rajasa guna, where as vata is alsorajo guna pradhana.23 Thus all these aggrevate vata. These factors also causenidra viparyaya leading to vata pitta prakopa along with kapha kshaya.Agantuka hetus: This includes abhighata i.e. patana, bhanga, where injury to the organsleads to diseased states. Marmas are 107 in number. They are vital points ofprana in the body. Marmaghata results in diseased conditions depending on thetype and the site of the marma.Kalaja hetus: In the classics swabhavika vata prakopa is described in certain periodsof time in a day and a year, they are ahoratri, bhuktante, vruddha vayah,greeshma and sisira and varsha ritus.24 During these times vata prakopa occursnaturally without any reason. All the factors which excite vata i.e. inducing the rukshatwa, laghutwa,seetatwa, dharunatwa, kharatwa, visadatwa and sushiratwa in the body, are vatavyadhi nidanas.25 In the Viswachi disease, the viharaja hetus are pradhanafactors and the aharaja and manasika factors are vyanjaka nidanas. Thus all the described nidanas increases rukshadi gunas resulting indecreased snehadi properties essential for proper vata function is the ultimateresult.
SAMPRAPTI The process of manifestation of disease by morbid doshas which arecirculating all over the body is known as samprapti.1 In otherwords it briefly the course of development of disease right fromthe vitiation of doshas to affliction of different parts of the body. Ultimatelyresulting in either structural or functional changes in the part.Acharya Susruta, vagbhata, Madhavakara described Viswachi as “ the diseasein which the enranged vata affecting the kandara which run to the tips of fingerfrom behind the roots of the upper arm, making them incapable and deprivingthem of their power of flexion & extension.2 Dalhana while commenting upon the above verses of Susruta stated thattalakandara means internal kandara and bahu prista denotes the externalkandara. And further he mentions that both the arms may also be affectedsometimes. Arundatta commenting upon Astanga Hrdya considers kandara as thesite of snayusanghata and extended upto the dorsal side of the arm. Thesekandaras when affected by vitiated vata, forsakes the activity of the arm.Samprapti of any Vata vyadhi occurs as follows: “ Due to the naidanik factors, vata prakopa occurs and it moves all overthe body and where, it comes in contact with snehadirahita rikta srotases itfills them up producing either sarvanga or ekanga vyadhi.”3 In Viswachi disease, the prakupita vata while moving all over the bodysettles in the greeva making it the adhistana. As the khavaigunya is in griva,vata fills those srotases doing soshana of the sleshaka sleshma of grivakaserukasandhis along with the grivakaseruka vikara.This inturn leads to dusti ofkandara of bahu manifesting the symptoms of Viswachi i.e radiating pain allalong the arm & weakened or loss of movements of the arm.Samprapti of Viswachi involves two major steps- i. Vitiation of vata ii. Kandara dusti
Caraka explained two ways for vataprakopa, causing disease. They are i. Dhatu kshaya ii. Margavarodha “Dhatukshayat iti sara kshayam “cakrapani on Ca.Ci.28/58Cakrapani states that in this context Sara has to be understood as the innerpartof kapala & kshaya as the decreased snehadi qualities or change incomposition, as a very minute change can upset the equilibrium.4 Nidanas explained in earlier chapter leads to increased ruksha, khara &visada gunas of vata resulting in dhatukshaya i.e reduction in snehadi gunas tolarge extent and further vitiating already prakupita vata. Margavarodha may be to kapha, ama etc. three doshas spread all overthe body, amongst them vatadosha is sukshma having property of prerakatwa.Thus it being sukshma, when in vitiated stage reaches everywhere in the bodystimulate pitta & kapha dosha.These pitta & kapha then obstruct the flow ofvata thus vitiating it more & more.5 Obsruction to the flow / movement of vata blocks the transmission, thusexcites vata, causing diseases.6 As explained in the nidana chapter few factorssuch as abhigata etc cause margavarodha resulting in disease. Thus the prakupita vata due to its rookshadi gunas does soshana of thesleshaka sleshma of griva kaseruka sandhis. Stanasamsraya of vata occurs atgriva. In samprapti of a disease, the sthana has a special importance becausethe dosha ultimately settles in the vaigunya sthana & treatment is directedagainst correction in such sthana dusti.7 Enraged vata not only dries up the sleshakasleshma but also causesvikriti in griva kaserukas. This depends on the strength and type of nidana. Kaseruka vikriti can be understood as follows: Vata & asthi shareasrayee and asraya relation respectively.8Even though the basic rule is that thematerials which cause increase of asraya should also effect the increase ofasrayee and the materials that cause decrease of asraya cause decrease ofasrayee, the reverse is true in case of vata & asthi. A material which causes
increase of asthi will produce decrease of vata & viceversa. Thus creatingimbalance in the relationship between the asraya & asrayee.9 Thus kaseruka vikriti along with soshana of sleshaka sleshma causesdusti of bahu kandara which precipitates Viswachi vyadhi.Schematic representation of Viswachi samprapti: Nidanas Dhatukshaya Margavarodha Vataprakopa Stanasamraya at griva Sleshakasleshma Soshana & Kaseruka vikriti Bahu Kandaradusti Viswachi
Samprapti ghatakas:i. Dosha : Vata; Vyana Vataii. Dushya : Kandaraiii. Srotas : Chestavaha (Srotases Conducting Both Drishya & Adhrihya Movements; Manas & Buddhi Considered As Moolas.)10iv. Srotodushti : Sangav. Adhistana : Greevavi. Vyaktasthana : Bahuvii. Rogamarga : Madhyamaviii. Vyadhisvabhava : ChirakariSamprapti through various types:i. Sankhya : Oneii. Vikalpa : Ruksha, Khara, Laghu, Visada Gunas of Prakupita Vataiii. Pradhanya : Vata (vyana vata )iv. Bala : Krichra Sadhyav. Kala : Vata Prakopaka Kala.As the Scope of this study includes understanding Viswachi withrespect to Cervical Spondylosis, an explicit explanation of themorbid condition follows:AETIO-PATHOGENESISPredisposing factors: • Poor posture associated with anxiety and habit. • Occupational stress eg: typist, coal miners, drivers…. Etc. • Body type: Thick necks [dowgers hump] and long backs are prone for spondylosis.11
The aetiology of cervical spine pathology is thought to includeprogressive degeneration, trauma and aberrant neurological reflex pattern(Mootz, 1995).In addition to degenerative changes that occur with the ageingprocess, it has been speculated that frank trauma such as injury from a whiplashmechanism or microtrauma produced by faulty sleeping posture and otherhabitual positions that produce repetitive strain can cause the pathology. The vulnerability of the neck is created by the 3.5-5.5 kg head sittingon top of the cervical spine with its multitude of joints, 50 pairs of muscle anda complex ligamentous/ capsular network. From this perspective we have a ball(the head), a flexible chain (the neck) and a rigid base (the upper back). It is notsurprising that this structure is subject to degenerative & subluxationsyndromes accompanied by soft tissue damage.A) The process and mechanics of spinal degeneration:• Single most important cause for the cervical spine disease is degeneration. Degenerative disease of the cervical spine is an extremely common clinical problem. The pathological changes in the conditions of cervical disc degeneration, degenerative arthritis of cervical spine and herniation of cervical disc are quite similar, differing only in degree. It is the generalized disease process affecting the entire cervical spine and related to chronic disc degeneration. It occurs in more than 90% of adults over the age of 50 yrs and almost 100% by 70 yrs.• The intrinsic factors that make the healthy spine a comparatively stable and mobile mechanical unit are vested in the elastic properties of some structures of the spine. Forces acting on the typical cervical motion segment include the axial pressure of the head on the nuclei pulposi and the tension exerted by ligaments holding each segment together, thus forming an intrinsic equilibrium. Relatively little muscular force is required from the contractile elements to maintain erect posture when this intrinsic equilibrium is preserved. Degeneration of the cervical disc represents premature ageing of this particular tissue.12
• It is characterized by dehydration, fissuring, annular disruption and osteophytosis.• Rapid depolymerization of the acid mucopolysaccharide and dehydration of the nucleus pulposus of the disc, converts this normally gel like substance into a thinned fibrous scar tissue that can no longer function as an adequate shock absorber.• The tension within the disc is maintained by fluid imbibition at the cellular level. If imbibition fails for any reason the pressure within the disc falls, the disc collapses, increased movement occurs between the adjacent vertebrae, the annulus fibrosus is exposed to increased stress and this is accompanied by vague pain.• Advancing degeneration of the nucleus pulposus and annulus fibrosis means lessening of the mechanical efficiency of the disc to act as shock absorber or insulator between two vertebral bodies.• Subsequently tears in the posterolateral region of the annulus occur.13• When the intervertebral disc degenerates, the intrinsic balance mechanism is disrupted with reduced turgidity, as nucleus pulposus looses its hydrophilic properties, segmental instability occurs because the inelastic ligaments cannot shorten to compensate for the loss of disc height. The resultant increase in muscle activity required to stqbilize the degenerating spine leads to the familiar-pain-spasm-cycle.• With the collapse of the disc space, the axis of motion shifts posteriorly to the apophyseal joints. These joints cannot withstand the stress and deteriorative changes soon follow to alter the smooth contour of the apophyseal joints.• The longitudinal ligaments degenerate and form bony spurs at their insertion into the vertebral body.• Hall (1965) reviewed the pattern of degeneration of the cervical spine. In early stages he noted cavities at the lateral margin of the annular fibres of the intervertebral disc that spread from oneside to other with accompanying loss of disc height and ligamentous laxity. In the final stage, the
intrevertebral distance is greatly reduced and the bone structure becomes distorted by osteophyte formation that results in stabilization of the excess mobility allowed by intersegmental ligaments.• Following the initial stage of dysfunction, loss of the intrinsic equilibrium creates an unstable phase of kinesiopathology during which subluxation occurs.In the final stage, stabilization occurs, when motion in the zygapophysial joints and disc becomes restricted by osteophytic proliferation: this stage is characterised by cartilage degeneration, loss of disc substance, soft tissue fibrosis, and the formation of osteophytes (anterior margin) of involved vertebrae.• The converging of the cervical disc space may result in buckling of the ligamentum flavum, with further narrowing of the spinal canal.• Segmental injury will result in hypertrophic formation of osteophytes by the uncovertebral joint of Lushchka and the facet joints. These prominent spurs will compress both the neural foramina and the spinal canal.• In the cervical spine the joints of Lushchka aiso exhibit degenerative changes, with the joint between the bodies of vertebrae altered from a fibrocartilagenous amphiarthrosis to a ball i.e. sockets shaped dysarthrosis (Hall, 1965).• When a disc protrusion becomes symptomatic, there has usually been a long period of silent degenerative change, first with fissure formation. If there are multiple fissures, a loose fragment will develop and this causes a major alteration in the disc mechanics. Under relatively small loads, the fragment will be displaced posteriorly, tearing the inner annulus and causing a protrusion. If the fragment displaces further the whole thickness of the annulus gives way and the fragment is extruded as a herniation.14B) The mechanics of cervical spine injury:• In general, spinal injuries are classified according to the mechanism of injury. Hyperflexion most commonly result from blows to the back of the head & forceful deceralations as in motor vehicle accidents (MVA) whereas
hyperextension injuries likely to occur from a blow to forehead or from whiplash injury.• Displaced fragments can produce cord injury in otherwise stable (structure) segments.• Cervical disc herniation occurs across a broad spread of age ranges from 20 to 60 yrs, being most common in individuals in their 30’s.• Herniation after the age of 30 is unlikely to occur since the gelatinous nucleus pulposus has been replaced by fibrocartilage.• The male to female ratio is approximately 1.4 to 1.Cervical disc herniations are less common than lumbar disc herniations and linked risk factors include smoking, diving and lifting heavy objects.• The most common levels of involvement are C6 to C7 (60%) & C5 to C6 (30%).• Cervical disc herniations are often referred to according to their consistency, being soft, when gelatinous nucleus pulposus extrudes and are unassociated with posterior osteophytes.• So called hard herniations are fibrocartilagenous annular bulges which occur in tandem with posterior osteophytes.• Lateral herniations are less common due to relative anatomical barrier of the uncovertebral joints and tend to select a single nerve root producing features consistent with lower motor neuron involvement.• Almost 50% of posterior herniations are intraligamentous lying between deep and superficial layers of the ligament.• Two main types of disc protrusions occur. They are- 1. Nuclear herniation 2. Annular protrusionNuclear Herniation: In this a circumscribed mass is formed by the extensionof the nuclear material through a tear of the annulus fibrosis as a result of thestrain put upon it by excessive movements of the neck. Thus it is traumatic andis the type of lesion commonly encountered in young people.
Annular Protrusion: This occurs usually in the middle aged and elderlypersons. During the ageing process the disc becomes dehydrated & looses itselasticity. As a result of this it collapses and the annulus bulges in all thedirections, which may be A. Central B. Lateral C. Dorsal D. Ventral E. Combination of any theseDepending on the direction of protrusion signs & symptoms occur.1. Dorsolateral: protrusion which does not invade the invertebral foramen but may compress the intrameningeal nerve roots against the vertebral lamina.2. Intraforaminal: Protrusion which comes from the uncinate part of the disc and compress the radicular nerve against the articular process. In this case the compressing agent may be the usual spur formation from the disc. Above said changes cause the nerve root compression along with the root sleeve fibrosis. The sleeves become thickened and adhesions form between the nerve filaments, with fibrosis of the arachnoid membrane.C) Athletic injuries: Injuries to cervical spine include those from athletic activities such as football, soccer, skiing etc. The mechanical vulnerability of the head neck coupling increases the risk of severe disruption of the motion segments. Bony elements, ligaments, discs and muscular supporting structures as well as neurovascular structures can be affected.D) Occupational and life style factors: A variety of occupational risk factors have been suggested for degenerative and mechanical disorders of the neck. The introduction of modern technology has resulted in monotonous tasks that impose static and
repetitive loads. These tasks affect the joints and muscles which, inturn can contribute to subluxation & degenerative syndromes. Consequently, a relationship has been found between times spent working with office machines, including visual display units and the occurrence of musculoskeletal symptoms. Other factors contributing to these disorders are mental strain, lack of situational control and low job satisfaction.15E) Congenital narrowed spinal canal since birth.F) Compression due to neuroma, lymphoma, extradural tumour or metastases: With any duration of compression the blood supply to the nerve is compromised, changes in the spinal cord and nerves due to insufficient blood supply result in tingling later numbness and weakness appear in the territory of the affected nerve. These degenerative changes occurring in the spine, the protruded disc or the osteophytes formed reduce the spinalcanal sagittal diameter lead to nerve root compression or and cord compression. It is thought that disc releases inflammatory mediators causing abnormality in the function of a compressed root. This is time dependent, and although the disc may continue to compromise the nerveroot, the inflammation can resolve and the symptoms settle. A large disc protrusion which compresses the nerve root will cause increased intra radicular venous pressure. This reduces the blood flow and impairs the arterial supply to the root. There will be nerve root edema as extra vascular fluid collects in the root, and nerve function is then impaired.16
REFERENCES:1 As.Hr.Ni.1st chap2 Su.Ni.1/353 Ca.Ci.28/184 Basic concepts of essentials of ayurveda 1st chap page 215 Ca.Ci.28/606 Ck on Ca.ci.28/587 Thesis “ A clinical trial of parijatha in Grdhrasi “ chap 20, page 308 As.Hr.Su.11/26,279 Basic concepts of essentials of ayurveda 1st chap, page 810 Basic concepts of essentials of ayurveda 8th chap, page 20011 Role of physiotherapy in lower cervical spondylosis- project work12 The clinical anatomy & management of cervical pain-vol 313 Fundamentals of orthopaedics- Gartland14 The spine and medical negligence- R.W.porter15 The clinical anatomy & management of cervical pain-vol 316 Orthopaedic medicine-a practical approach
POORVA ROOPA Poorva roopa marks the beginning of the disease. After doshas getsexcited and spread to other parts of the body i.e stana samsraya, occurs, thenpoorva roopa is manifested.1 Certain features that develop before the complete clinical featuresdevelop are called prodromal symptoms. In Vata vyadhi poorva roopa is stated as “avyaktam lakshanamtesham poorva rupamiti smritam”2 Avyaktam means incomplete in symptoms due to slightness. In thisdisease there is no poorva ropa different from roopa, but only in latent form.So, one may not appreciate them. Roopa slightly manifested before theappearance of disease is poorva roopa.3 In this context of Visvaci pain and other symptoms in milder form(alpatwa) can be taken as poorvaroopa.
References: 1 Ca.Ni 1/8 2 Ca.Ci.28/ 19 3 Ck on Ca. Ci.28/19
ROOPA Roopa is manifestation of signs &symptoms.1 It is the vyaktaavastha.2During this stage dosha dushya samoorchana gets completed.3Thisleads to manifestation of all lakshanas including pratyatmika lakshana, basedon which the disease is diagnosed.4 In description of Viswachi Susruta mentioned bahu karma kshaya as theonly symptom.5Vagbata quoted bahu chestapaharana as the lakshana 6 where asMadhavakara also described bahu karma kshaya as the only symptom.7 While commenting on the verses of Acharyas, various commentatorshave described in the following way: Dalhana opines that this diseaseresembles Grdhrasi affects one arm or sometimes both the arms.8The othercommentators like Gayadasa, Vijayarakshita and Arunadatta stressed the pointof occurrence of pain as the cardinal feature in this disease.9 They have also concluded that whenever there is severe pain in Visvaci& Grdhrasi they should be termed as “Khalli”. For all practical pueposes, innidana and cikitsa the diseases are to be considered as separate entities exceptin the above said references of “Haritha samhita”.10 The poorva acharyas alsohave dealt them separately.The word Viswachi is derived from two words: Visva + anc Visva means entire / whole / all pervading Anc means turned to / directed towards / to move / wander about Thus Viswachi literally means spread through out i.e.pain throughout or whole of the upperlimb.11 Viswachi is vedana pradhanaja vyadhi. Here stanika lakshanas areexhibited rather than sarva daihika lakshanas. Classics described Pain as ofradiating nature in viswachi. The description of pain given in this context in contemporary medicinesuits exactly to the description given in our classics. It is as follows-Pain is described as severe and sharp usually follows a radiating pattern fromthe shoulder to the arm and frequently into the forearm to the fingers.
Pain often has a neuritic quality – described as throbbing, burning,stabbing, electric shock like& aching. Sometimes it is cramping paraesthesiaoften felt in the fingers. These descriptions of pain are available in our classicsas vyadha, bhedana etc. Weakness& occasional tenderness occurs. The pratyatmika lakshana of Viswachi is radiating pain from the bahuprishta to the hasta talam & pratianguli.14In fact, this typical pain readilygives the diagnosis. Bahu karma kshaya is emphasized as pratyatmika lakshana by Susruta.Prasarana, akunchana, grahana, & daana are bahu karmas.Kshaya literallymeans loss/diminished/decreased/weaken. In this context diminished orweakened movements of the arm is appropriate. 15 As Viswachi is described similar to Grdhrasi of lower limbs, thelakshanas described in Gridhrasi can also be considered in Viswachi. Thusalong with vedana, bahu karma kshaya other signs & symptoms of Viswachican be considered as follows-1. Stambha : There is a feeling of tightness or rigidity throughout the upperlimb. This is also manifested by way of restricted movements.2. Ruk : Ruk is nothing but ruja /vedana /shoola i.e. pain. It is differentfrom the pain which has been described as the cardinal feature of Viswachi i.e.radiating pain. But ruk is dull aching pain of continous nature. It is feltthroughout the hand and is not localized to one portion. It is muscular in originresult of stambha. Ruksha & sheeta gunas are responsible for it.3. Toda : Toda is nothing but pricking type or lacerating type of pain feltin some region or felt at the intervals especially when Viswachi vedana isintense. This can be considered as pins& needles type of paraesthesia.4. Spandana : Along with pains of various types there is many times asensation of something pulsating or throbbing. This is due to musculartwitching. This may be in any region of the upper limb, can also alternate withthe stambha, ruk, toda.
After the classical description of lakshanas of Viswachi, the contemporaryexplanation of the Clinical features are as follows: The development during adult life of chronic disc protrusions, combinedwith osteophyte formation on the vertebral bodies and soft tissue changes in theparavertebral tissue frequently cause compression of the cervical cord and orroots.This slowly progressive degenerative process is known as cervicalspondylosis and become increasingly common with age. Spondylotic changes affect almost all individuals with advancing age,but in many remain only as an asymptomatic radiological finding.Spondyloticchanges are most common in the mid to lower cervical cord, with the maximalfrequency and severity of involvement at C5/6 level.14 Generally pain, paraesthesia, weakness, muscle spasm and limitationof movement are symptoms observed. Pain is dull, aching, superimposed by sharp stabbing pain and from timeto time as cramp type throbbing. It is initially intermittent but later constant.Pain is worse and can get altered with sleep. Paraesthesia is pins and needle type with altered sensation in the areasupplied by an impinged nerve root. Pressure applied on nerve root causes weakness.Postural muscles likeflexors of upper cervical spine and extensors of lower spine and side flexors areoften weak. Neck movements are bilaterally limited.During acute episode of painone side is more affected than other.Upper cervical spine flexion is moreaffected than extension of lower spine.15These above said symptoms can be broadly classified into followinggroups:1. Cervical radiculopathy2. Cervical myelopathy3. Occipital headache4. Pain in the neck
5. Vertebrobasilar syndrome Cervical radicuopathy can be grouped under three headings basing onthe cause of compression i.e.acute disc protrusion or the secondarydegenerative changes of the cervical spine. 1. Acute radiculopathy-I 2. Acute radiculopathy-II 3. Chronic radiculopathy The chronic variety is the continuation of acute variety withoutremission of symptoms but leaving some permanent sensory disturbances. The symptoms are extensive topographically i.e. pain & sensory loss inthe appropriate dermatome along with segmental weakness, wasting, and reflexloss affecting the relevant myotome. The manifestations depending on thenerve root involved are as follows16:C1 – C3: • It is rare condition. • Motor supply to number of neck muscles is interrupted but is not usually clinically apparent. • Sensory loss is found over the back (C2) and side (C3) of the neck.C4: • It is also a rare condition. • There is sensory loss in a cape distribution between the side of the neck and the top of shoulder. • Unilateral lesions cause weakness of Rhomboids.A C2, C3, & C4 root palsy weakens scapular elevation.The muscles of the arm are supplied by the C5, C6, C7, C8,& T1 nerve roots.C5: • Disc lesions are fairly common. • Pain in the neck, shoulder, lateral arm to elbow. • Pins & needles are usually absent; if present, extends from the outer surface of the shoulder down into the lateral arm and forearm.
• Weak Deltoid, Supraspinatus -- resisted abduction • Weak Biceps -- resisted elbow flexion • Weak Infraspinatus – resisted lateral rotation • Biceps jerk – absent/sluggish • Brachioradialis jerk – absent/sluggish/inverted.C6: • Disc lesions are fairly common. • Pain in the neck, lateral arm to thumb & index finger. • Pins & needles in the thumb &index finger. • Weak Extensor carpi radialis – resisted wrist flexion • Weak Brachialis & Biceps – resisted elbow flexion • Weak Subscapularis – resisted medial rotation. • Biceps jerk – sluggish/absent.C7 : • Disc lesions extremely common, probably 90% of cervical disc lesions causing a root palsy at the sixth level compresses the seventh root. • Pain in the lateral arm to middle, index & ring fingers. • Pins & needles in the index, middle, & ring fingers, and a strip in the middle of the hand both on the palmar & dorsal surface. • Weak Latissimus dorsi – resisted arm adduction. • Weak Triceps – resisted elbow extension. • Weak common flexor muscles – resisted wrist flexion. • Triceps jerk – rarely affectedC8: • Disc lesions are fairly common. • Pain in the medial forearm and hand; occasionally it can also be in lower scapular area and back or innerside of the arm & forearm. • Pins & needles in middle, ring & little fingers. • Weak thumb adduction • Weak thumb extension.
• Weak ulnar deviation. • Weak adduction of the index finger.T1 : • An electric shock like sensation elicited by neck flexion and radiating down the spine from the neck (Lhermitte’s symptom). • This usually indicates cervical or upper thoracic (T1 – T2) spinal cord involvement.17 True radicular pain is often severe and may be present nocturnally.Recumbency may not relieve the pain. Symptoms are activity dependant andposture dependant, their longevity determined by the nature of the causation ofspinal pathology.Cord compression: Main initial symptoms are dysaesthesia in the hands,weakness & clumsiness of the hands & spastic weakness of the lowerlimbs.The clinical course of the myelopathy is usually progressive, leading tocomplete disability over period of weeks to months.Deep aching pain of the extremity, broad based gait, loss of balance, loss ofhand dexterity and general muscle wasting are found in patients with advancedmyelopathy.Impotence is not uncommon in these patients.Occipital headache: Headache is due to upper cervical pathology. It may bepresenting symptom in few people. Usually, the headache is worse in themorning and improves throughout the day. It is commonly located in theoccipital region and radiates toward the frontal area.Pain in the neck: Neck ache is due to mid cervical pathology. Acute discprotrusion is likely to be associated with severe pain, muscular spasm andrigidity of neck muscles. In chronic cervical spondylosis pain is usuallycomparatively mild and tends to be more severe in the morning.Vertebro basilar ischaemia: Often rotation to one or other side or extension ofthe neck and, less frequently flexion may precipitate a brief attack of giddinessor a drop attack. Probably pressure on the vertebral arteries with consequentimpairment of the blood supply of the hind brain.18
References: 1) Ma.Ni.1/7 2) Su.Ni 21 3) Su.Su.24 4) Ca.Ni 1/9 5) Su.Ni.1/75 6) As.Hr.15/44 7) Ma.Ni.22/57 8) Dalhana on Su.Ni.1/75 9) Ma.Ni.22/57 10) Ha.sam. 11) Sanskrit to English dictionary 12) Su.Ni.1/75 13) Su.Ni.1/74 14) Lange’s current diagnosis & treatment in orthopaedics 15) Role of physiotherapy in lower cervical spondylosis-Project work 16) Brain’s neurology 17) Cyriax’s illustrated manual 18) Golwalla medicine .
EXAMINATION The need for a detailed history and a comprehensive musculoskeletalexamination that includes the cervico dorsal spine is paramount in theassessment of all upper limb disorders. Assessment of function is a particularly important aspect of theexamination. Topographically, function of one part of the limb, for instance thehand, can only be evaluated if the rest of the limb, the axial skeleton and thecontralateral limb are examined.1Examination of neck: The neck can move in all directions, but forexamination purpose they are reduced to six primary ranges. If these prove fulland painless, the lesion must be sought else where. • First active movements are assessed, starting with extension. • Next passive movements, starting with extension. • For the passive side flexions, care must be taken to limit the movement to the neck by counter pressure to the thorax; otherwise trunk movements will complicate the clinical picture. • When the passive rotations are tested, rotation of the patient’s trunk is precluded by the exaaminer’s elbows, one placed in front of the shoulder and the other behind, against the opposite scapula. • Passive flexion is normally omitted as any disc lesion may be exacerbated. • Next, the six resisted movements are tested. • In particular, the arm is examined for weakness to establish any neurological deficit. • The provocative test of combined passive extension & ipsilateral rotation is highly sensitive for the detection of nerve root irritation / compression at the intervertebral foramen; an increase in this manoevre indicates neural compression. • Root signs are looked for in logical order, working down the arm.
• Along with active shoulder movements all the resisted movement of the arm is to be examined primarily to check weakness caused by nerveroot pressure. • If weakness is found, the good side is compared. But pain on resisted movements suggests a lesion of the appropriate contractile structure. 2 Functional assessment is done by performing a series of functionaltests or movements to determine the functional capacity keeping in mind thepatient’s age and health.These tests include activities of daily living.3Special Tests: Special tests for neurological symptoms performed on cervicalspine, almost exclusively, by physiotherapists, they are 1. Foraminal compression (spurling’s) test 2. Distraction test 3. Upper limb tension test 4. Shoulder abduction test1. Foraminal compression test (spurling tests): In this test the patient bends or side flexes the head to the unaffectedside first and then to the affected side.The examiner carefully presses straightdown on head.Result: The test is positive if patient complains of pain radiating into arm whenhead is compressed towards the affected side, indicating pressure on the nerveroot.2. Distraction test: In this test, the examiner places one hand under patients chin and otherhand around the occiput, and then slowly lifts the patient’s head in effect ofapplying traction to the cervical spine.Result: The test is positive if the pain is decreased or relieved when the head islifted or distracted, indicating of nerve root pressure, that has relieved.3. Upperlimb tension tests (ULTT):
The tests of neural tension proposed for the upper limb have beendeveloped much more recently than those used for the lower limb and trunk.These are equivalent to the straight leg raise (SLR) test in the lumbar spine.Indications:• Routine for any upper quadrant symptoms ie, cervical spine, arms, thoracic spine.• For any patient indicating that a similar functional position produces their symptoms.Tests for assessing neurodynamics: ULTT 1 – Median Nerve ULTT2a – Modified Median Nerve ULTT2b – Radial Nerve ULTT 3 – Ulnar Nerve.The test is positive if • Reproduce local and referred symptoms • Restriction of movement which is assymetrical and can be altered by changing a remote component of the test that implicates neural structure. • The test is significant if • Reproduces symptoms • There is asymmetrical restriction of movement that relates to symptoms • There is diffirent symptoms response from either normal or the other side. 44. Shoulder abduction (relief test): This test is used for C5-C6 nerve root involvement.The patient is insitting or lying position, the examiner passively or the patient actively elevatesthe arm through abduction, so that hand or forearm rests on top of head.Result: The test is positive if pain decreases because of abduction of arm. Thisis because of lengthening of neurological pathway and decreases the pressureon lower nerve rootsIndications: Extra dural compression problem such as herniated disc, epiduralvein compression usually in C4-C5 area.
INVESTIGATIONS1.Blood tests : Complete blood picture ; E.S.R : Blood sugar levels : Serum proteins : C R P; C- reactive proteins2. X-rays : Spinal – cervical spine – A.P ; Lateral views3. Imaging : M.R.I – Excellent for cord, root lesions : CT- For bony lesions : CT with contrast, intra thecal – for root, cord lesions : Myelography – if MRI not possible4. Electrodiagnostic : Nerve conduction studies5. Isotopescans : Bone (metastases), infective lesions( gallium)6. C.S.F : Presence of infection / inflammation ; demyelinationThe specific diagnostic tools areI.Conventional Radiography :• Degenerative changes are graphically depicted, such as loss in disc height, osteophytes and displacement.• Loss in vertical height is assessed by comparision with adjacent discs. Normally disc height is less at C6-C7 and C7-T1 as the transition is made to the thoracic spine.• Bony outgrowhs from vertebral bodies occur initially at the insertion of the anterior longitudinal ligament.• Loss of lordosis occur commonly from the segment above degenerative disc changes have occurred, due to segmental extension as the uncovertebral joints approximate.• This has a limited role in detection of herniation.• Canal size can be estimated on the lateral view from the point of posterior mid vertebral body to the adjacent spinolaminar line and normally is around 17mm in AP diameter.