Pakshaghata kc024 gdg

EVALUATION OF THE COMPARATIVE EFFICACY OF SHODHANA AND SHAMANA IN THE MANAGEMENT OF PAKSHAGHATA

WITH SPECIAL REFERENCE TO ISCHAEMIC STROKES

Thesis submitted to the Rajiv Gandhi University of Health

Sciences, Bangalore, Karnataka in partial fulfillment of

regulations for award of degree of

DOCTOR OF MEDICINE (AYURVED VACHASPATI)

IN KAYACHIKITSA

BY

Dr. Umesh Veerbhadrappa Purad

GUIDE- DR.VANGEEPURAM VARADACHARYULU M.D. (AYU) (OSM)

Professor and Head of the department of

Kayachikitsa P. G. A. R. Center KAYACHIKITSA

DANAPPA GURSIDDAPPA MELMALGI AYURVEDIC MEDICAL

COLLEGE CUM RESEARCH CENTER, GADAG 582103.

Ayurmitra

TAyComprehended

Post graduate and Research CenterPost graduate and Research CenterPost graduate and Research CenterPost graduate and Research CenterPost graduate and Research Center(Kayachikitsa)(Kayachikitsa)(Kayachikitsa)(Kayachikitsa)(Kayachikitsa)

D.G.M. Ayurvedic Medical College, Gadag.D.G.M. Ayurvedic Medical College, Gadag.D.G.M. Ayurvedic Medical College, Gadag.D.G.M. Ayurvedic Medical College, Gadag.D.G.M. Ayurvedic Medical College, Gadag.

CertificateCertificateCertificateCertificateCertificateThis is to certify that the thesis entitled the

“Evaluation of comparative efficacy of shodhana andshamana with special reference to ischemic strokes” is arecord of research work conducted by Dr. UmeshVeerabhadrappa Purad under my direct supervisionand guidance.

The candidate has put in sincere effort aftermaking an intense study coupled with theoreticaland clinical observations.

This title has not formed title of degree as-sociation ship, fellowship and similar other stud-ies in this university.

I recommend the same for being submittedfor evaluation to the adjudication.

Guide :Dr. VangeepuramVaradacharyulu

M.D. (Ayu) (Osm)Date : Gold Medallist

Professor & Head of the department,Place : Gadag Kayachikitsa.

Post graduate studies and research center D.G.M. Ayurvedic Medical College,

Gadag.

J.S.V.V.S. Samsthe’s

SHRI D. G. M. AYURVEDIC MEDICAL COLLEGESHRI D. G. M. AYURVEDIC MEDICAL COLLEGESHRI D. G. M. AYURVEDIC MEDICAL COLLEGESHRI D. G. M. AYURVEDIC MEDICAL COLLEGESHRI D. G. M. AYURVEDIC MEDICAL COLLEGE

POST GRADUATE AND RESEARCH CENTERPOST GRADUATE AND RESEARCH CENTERPOST GRADUATE AND RESEARCH CENTERPOST GRADUATE AND RESEARCH CENTERPOST GRADUATE AND RESEARCH CENTER

GADAG – 582103.GADAG – 582103.GADAG – 582103.GADAG – 582103.GADAG – 582103.

CERTIFICATE

This is to certify that Dr. Umesh Veerabhadrappa Purad has worked

for his thesis on the topic entitled “Evaluation of the comparitive

efficacy of shodhana and shamana in the management of

Pakshaghata with special reference to Ischemic strokes”.

He has successfully done the work under the guidance of

Prof. Dr. V. Varadacharyulu M. D. (Ayu).

This particular study helps in treating dreaded disease Pakshaghata

(Stroke) with present scientific approaches.

I here with forward this thesis for the evaluation to the adjudicators.

Dr. G. B. PatilDr. G. B. PatilDr. G. B. PatilDr. G. B. PatilDr. G. B. PatilPrincipal / C.M.O.Principal / C.M.O.Principal / C.M.O.Principal / C.M.O.Principal / C.M.O.Place :Gadag.Place :Gadag.Place :Gadag.Place :Gadag.Place :Gadag.

Date :Date :Date :Date :Date :

ABBREVIATIONS

Ch. S. – Charaka Samhita

Su. S. – Sushruta Samhita

A. S. – Astanga Sangaraha

A. Hr. – Ashtanga Hridaya

M. Ni. – Madhava Nidana

C. D. – Chakradatta

V. S. – Vangasena

Y. R. – Yoga Ratnakara

B. P. – Bhava Prakasha

H. S. – Harita Samhita

K. K. – Kalyanakaraka

B. R. – Basavarajeeyam

Bai. R. – Bhaishajya Ratnawali

B. S. – Bhela Samhita

R. Y. S. – Rasayoga Sagara

S. Y. – Sahastra Yoga

A. V. – Atharvana Veda

Vach. - Vachaspathyam

S. T. M. – Shabdhasthoma Nidhi

S. K. D. – Shabdhakalapa druma

Sha. Sam. – Sharanghadhara

Samhita

R. T. – Rasa Tarangini

C. P. – Chakrapani datta

Dal. - Dalhana

Hem. - Hemadri

I. M. M. – Indian Materia

Mediaca

Vr. Vai. – Vrinda Vaidya

Chi. – Chikitsa sthana

Si. – Siddhi sthana

Ni. – Nidana

Vim. – Vimana sthana

Sha. – Shareer sthana

Su. – Sutra sthana

Kal. – Kalpa sthana

U. T. – Uttara tantra

Infn. - Infarction

M. C. A. – Middle cerebral artery

A. C. A. – Anterior cerebral

artery

P. C. A. – Posterior cerebral

artery

C. N. S. – Central nervous

system

C. T. – Computerized

tomography

HTN - Hypertension

DM – Diabetes mellitus

MI – Myocardial infarction

CHD – Congestive heart disease

ECG - Electrocardiography

C.V.A. – Cerebro vascular

accident

B.T. – Bleeding time

KBT – Ksheera bala taila

AT – After treatment

BT – Before treatment

N.I.N.D.S. – National Institute of

Neurological Disorders & Stroke

HDL – High density lipids

LDL – Low density lipids

VLDL – Very low density lipids

RBS – Random blood sugar

ATP – Adenosine triphospahte

K. S. – Kashyapa Samhita

LIST OF GRAPHS

Graph No. 01 : Showing the availability of the patients.

Graph No. 02 : Showing the age group incidence of the patients.

Graph No. 03 : Showing the sex incidence of the patients.

Graph No. 04 : Showing the religion incidence of the patients.

Graph No. 05 : Showing the occupation distribution of the patients.

Graph No. 06 : Showing the habits of the patients.

Graph No. 07 : Showing the risk factors of the patients.

Graph No. 08 : Showing the side affected of the patients.

LIST OF PHOTOGRAPHS

Slide No. 01 :

A. Showing the Functional areas of the brain.

B. Showing the motor activity areas of the brain.

C. Showing the Sensory activities of the brain.

D. Showing the arteries of the brain (Circle of Willi’s).

Slide No. 02 : Showing the ingredients of Pakshaghatari yoga.

Slide No. 03 : Showing the condition of the patients before and after the treatment.

LIST OF TABLES

Table No. 01 : Showing the divisions of the brain.

Table No. 02 : Showing the nidanas of Pakshaghata.

Table No. 03 : Showing the correlation of Pakshaghata with hemiplegia.

Table No. 04 : Showing the properties of the Trikatu Churna.

Table No. 05 : Showing the properties of the Moorcchita Tila Taila.

Table No. 06 : Showing the properties of the Gandharvahasta taila.

Table No. 07 : Showing the properties of the Bala taila.

Table No. 08 : Showing the properties of the Ksheera bala taila 101.

Table No. 09 : Showing the properties of the Brihat vata chintamani rasa.

Table No. 10 : Showing the properties of the Chatushatprahari pippali yoga.

Table No. 11 : Showing the properties of the Pakshaghatari yoga.

Table No. 12 : Showing the Barthel Indedx score.

Table No. 13 : Showing the availability of the patients.

Table No. 14 : Showing the age group incidence of the patients.

Table No. 15 : Showing the sex incidence of the patients.

Table No. 16 : Showing the religion incidence of the patients.

Table No. 17 : Showing the economical status of the patients.

Table No. 18 : Showing the occupational distribution of the patients.

Table No. 19 : Showing the educational status of the patients.

Table No. 20 : Showing the marital status of the patients.

Table No. 21 : Showing the habits of the patients.

Table No. 22 : Showing the food habits of the patients.

Table No. 23 : Showing the rasa satmya of the patients.

Table No. 24 : Showing the roga prarambha kala of the patients.

Table No. 25 : Showing the time of onset of the disease.

Table No. 26 : Showing the chronicity of the patients.

Table No. 27 : Showing the previous history of the patients.

Table No. 28 : Showing the habits of the patients.

Table No. 29 : Showing the risk factors of the patients.

Table No. 30 : Showing the treatment history of the patients.

Table No. 31 : Showing the general condition of the patients.

Table No. 32 : Showing the side affected of the patients.

Table No. 33 : Showing the sara of the patients.

Table No. 34 : Showing the prakriti of the patients.

Table No. 35 : Showing the samhana of the patients.

Table No. 36 : Showing the satwa of the patients.

Table No. 37 : Showing the distribution of bala of the patients.

Table No. 38 : Showing the condition agni of the patients.

Table No. 39 : Showing the vyayama shakti of the patients.

Table No. 40 : Showing the habit of nidra of the patients.

Table No. 41 : Showing the vaya of the patients.

Table No. 42 : Showing the distribution according to the desha of the patients.

Table No. 43 : Showing the bhara of the patients.

Table No. 44 : Showing the blood pressure of the patients.

Table No. 45 : Showing the nidana sevana of the patients.

Table No. 46 : Showing the poorva roopa of the patients.

Table No. 47 : Showing the motor function of the patients.

Table No. 48 : Showing the samsristaja dosha of the patients.

Table No. 49 : Showing the lakshanas of the patients.

Table No. 50 : Showing the ANOVA for NINDS.

Table No. 51 : Showing the least significance difference of groups for NINDS.

Table No. 52 : Showing the ANOVA for Barthel’s Index.

Table No. 53 : Showing the least significance difference of groups for Barthel’s Index.

Table No. 54 : Showing the ANOVA for Rankin’s Disability Scale.

Table No. 55 : Showing the least significance difference of groups for Rankin’s disability

Scale.

Table No. 56 : Showing the ANOVA for HDL.

Table No. 57 : Showing the least significance difference of groups for HDL.

Table No. 58 : Showing the ANOVA for Serum cholesterol.

Table No. 59 : Showing the least significance difference of groups for Serum cholestrol.

Table No. 60 : Showing the ANOVA for Hb %.

Table No. 61 : Showing the ANOVA for R. B. S.

Table No. 62 : Showing the ANOVA for Serum cholesterol.

Table No. 63 : Showing the least significance of different groups for Serum cholesterol.

Table No. 64 : Showing the ANOVA for Serum triglycerides.

Table No. 65 : Showing the ANOVA for LDL.

Table No. 66 : Showing the ANOVA for VLDL.

Table No. 67 : Showing the ANOVA for Serum creatinine.

Table No. 68 : Showing the coefficient of variations.

Table No. 69 : Showing the Master chart for group A (10 patients)

Table No. 70 : Showing the Master chart for group B (10 patients)

Table No. 71 : Showing the Master chart for group C (10 patients)

Table No. 72 : Showing the varieties of Pathya and Apathya.

ACKNOWLEDGEMENT

I express my deep sense of gratitude to his great holiness Jagadguru Shri

Abhinava Shivananda mahaswamiji for their divine blessings.

I express my gratitude to my respected guide Prof. Dr. V. Varadacharyulu M.D.(Ayu)

Head of the department of Kaya chikitsa in Post graduate studies D.G.M.Ayurvedic

medical college, Gadag. He has been very kind to guide me in the preparation of thesis

and for whose extraordinary efforts, tremendous encouragement and valuable thoughts

provoking advice me to complete this thesis.

I express my heart felt thanks to our respected principal Dr. G.B. Patil

D.G.M.Ayurvedic medical college cum Postgraduate studies and research center, Gadag

for their maximum encouragement, providing all necessary facilities for this research work.

I am ever thankful to Dr. K.S.R. Prasad Asst. Prof., Dr. R.V. Shetter Lecturer.

Department of Kaya Chikitsa D.G.M.A.M.C. P.G.A.R.C.,Gadag for their deep sensed

cooperation and guidance.

It gives me a pleasure to express my gratitude to Dr. A. K. Panda Lecturer,

Jayendra Sarswati Ayurvedic College, CHENNAI. for being kind affectionate through his

valuable suggestions and advice as and when approach.

I am very much grateful to Dr. M.C. Patil H.O.D. P.G. Rasashatra and

Dr. S. H. Doddamani Asst. Prof. P.G. Panchakarma, D.G.M.A.M.C. P.G.A.R.C., Gadag for

their valuable suggestions and moral support throughout the study.

I am very much thankful to Prof. Dr. G. S. Hiremath H.O.D., Dr. Kuber Sankh

Lecturer Depart. of Dravyaguna D.G.M.A.M.C., Gadag for their constant help in this study.

I wish to convey thanks to my teachers Dr.R.K. Gachinmath, Dr.C.S.Kudarikannur,

Dr. B.G. Swami, Dr. V.M. Sajjanar, Dr. G.S. Juktihiremath, Dr. S.H. Redder, Dr. S.A. Patil,

Dr. G.M. Kanti, Dr. Suresh G. Hiremath, Dr.C.S. Hiremth Dr.S.S. Avvanni, Dr.K.S.Paraddi,

Dr. B. S. Patil, Dr. P. C. Chappanmath, Dr. V. M. Malgoudar, Dr. M. V. Aiholi, Dr. R. R.

Joshi and Shri. C. S. Bhat for their enlightening the deep sensed study of Ayurveda since

U. G. level itself.

I am very much thankful to non-teaching staff for their valuable cooperation.

I am very grateful to Dr. R.I. Dugani, Dr. G.S. Mudgal, and Dr. V. S. Hosmath for

Dr. Katwe, their encouragement and help in my studies.

I thanks to Shri. P.M.Nandkumar for his help in the statistic evaluations.

I wish to convey my thanks to P.G. colleagues Dr. Shyju, Dr. Shankargouda,

Dr. Hanamantgouda, Dr. Vanita, Dr. Shakuntala Garwad, Dr. Subin, Dr. Febin, Dr.Ranjit,

Dr. Shajil, Dr. Satish, Dr. Ratnakumar, Dr.Udaykumar and Dr Chandramouli. for their

constant cooperation and help in P.G. studies.

I very much thankful to Dr.S.D. Yarageri R.M.O. and all the physicians, house

surgeons, non-teaching staff and hospital staff for their timely assistance to complete this

work.

I wish to convey my thanks to Shri.V.M.Mundinmani Librarian, Shri. S. B. Surreban

for providing me essential reference books.

I am very much thankful to Mr. Arunkumar Biradar for his constant help in making

dissertation.

I am thankful to Shri. B.S. Tippangouda Laboratory technician who extended his

co-operation in investigations.

I am highly indebted to my beloved mother Smt. Savantramma, elder brother

Shri. V.V. Purad, B.V. Purad, sisters, sister-in-law, brother-in-law and my whole family

members for their love and affections rendered throughout my career.

It is impossible to make this great success without the incredible moral support

and encouragement of my wife Smt. Jayashree and my childrens Shambu, Veeresh,

Vijayalakshmi and Muttu in all respect.

Let me express my thanks to all who were on the trial for their constant enrolling in

this clinical study and obedience to advice.

Lastly I pay my deep homage and tribute to my father -in-law, retired principal

D.G.M. Ayurvedic Medical College Gadag, Late Dr. S.V. Savadi for his advice and

encouragement for this valuable project. I remain ever grateful to him.

Dr. U. V. Purad.

Management of Pakshaghata

Introduction 1

INTRODUCTION

Movement is an important characteristic of all living organisms. Vata is responsible

for all types of movements and prime dosha among the three humors (three doshas).1

Normal functions of vata are motor functions (gati), sensory function (jnana),

congestive and connective functions (dharana, budhhi, indriya). Vata which is also known

as Maruta, Vayu, Anila,2 etc. and is capable of producing not only 80 vikaras but also

innumerable diseases. Madhavakara says that vata vyadhis are Ati balayukta,

Duschikitsa, and Ashukari.3

Pakshaghata is one among the 80 vata vikaras and being one among Mahagadas,

is capable of making cheshtahani, karmendriyakriyahani of the person.4

The word Pakshaghata reveals the definition that Paksha means half of the body

Aghata means loss or injury.5 Pakshaghata is vata vikara of rapidly or gradually

developing clinical signs of focal or global disturbances of limbs movements and

sensations and symmetrical loss of body functions. It manifests due to disturbances in the

vatavaha samsthana i.e. Mashtishka, leading to impairments of functions of Vata i.e.

cheshtahani (akarmanyata) either in left or right of the body.

Pakshaghata can be correlated with hemiplegia where stroke may be the main

etiological factor. The term stroke is used to describe an abrupt loss of function of some

parts of the central nervous system due to vascular lesions. The symptoms varying from

loss of cerebral functions to deep coma, motor and sensory functioning loss. There is a

wide range of sensitivity from recovery in a few days through a persistent disability to

death.6

Ischaemic infarction is a series of functional, neurological and neurophysiological

changes due to fall of cerebral blood flow which leads to lack of oxidative mechanisms of

glucose to provide energy in the form of ATP. Because in the brain stroke is due to


Introduction 2

negligible amount of glucose and obligatory arobe ; it drives all most all its energy from the

oxidative mechanism of glucose.7

Infarction is a local area of ischemic necrosis, usually caused by thrombosis and

embolism. It may be due to degeneration, head injury, encephalitis and other global

encephalitic conditions.8

Pakshaghata is as one of the major health hazard of the modern society. Studies

have demonstrated that 10% men and 15% women aged about around 45 years may

suffer by Pakshaghata. In the subsequent 30 years8 the incidence of Pakshaghata varies

through out the world more in black race than white race.

Pakshaghata occurs in about 5 to 8 per 1000 peoples after 25 years age and is

cause of 10 – 20 % of the deaths 9. Among the survivors approximately half will recover

completely. The remaining half will be left with persistent major disability.

One month case mortality rate vary between 17 – 34 % (average about 24 % )

depending upon the age structure and the health status of the population one year

mortality rate is about 40 %.9

Pakshaghata (stroke) is found to be the third most frequent cause of the death

next to ischemic heart disease and cancer. 9

The mode of onset of organ involved, degree of impairments, functional disability

and mental function varies from patients to patients according to the underlying etiology

and dosha-dushya sammurchhana.

The diagnosis of Pakshaghata is mostly depending on the signs and symptoms

according to the dominancy of doshas. Some clinicians believed that the signs and

symptoms differentiate the diagnostic factor of stroke like ischemic and hemorrhagic.

Since last one decade there is a lot of invention in neurodiagnosis where C.T. scan

of brain is an important tool to diagnose ischemic or hemorrhagic acute conditions. MRI is


Introduction 3

certainly more sensitive than CT scan. MRI is not available widely and more expensive

than CT scan.

The treatment of Pakshaghata takes much time and is costly too. The expense of

Pakshaghata ranks only second to mental illness in consuming national health services

and resources in foreign countries.

Pakshaghata treatment schedule adopted according to the stage (avastha) i.e. in

acute stage the immediate aim is to maintain the life style and to prevent the further

complications. The patient’s condition must be stabilized in the emergency room and

strategies to reestablish the circulation in the acute condition of stroke.10

Acharya Charaka prescribed snehana, swedana, virechana with unctuous drugs.

In the management of Pakshaghata Sushruta, Vagbhta added vasti and nasya karma in

their treatment.11 Patients should be adopted all physical and mental comforts.

Rehabilitation is a team effort involving disciplines of nursing, medicine

,physiotherapy, dietetics and speech therapy being as early as possible after the stroke.12

There is now increasing evidence that Ayurvedic therapeutics is very useful in

patients with Pakshaghata. It would be very efficient if the treatment starts immediately

after the stroke in medium to moderate conditions.

The assessment of stroke depends upon the neuro-physiology and neuro-

pschycology. Parameters include the motor function, sensory function, language

compansion, bladder control, bowel control, feeding, etc.

This clinical trial was undertaken to clarify the role of shodhana and shamana in

the management of Pakshaghata with special reference to the ishemic strokes.

NEED AND SIGNIFICANCE OF THE STUDY

Despite of its prevalence and its high cost management as well as disability

Pakshaghata has been paid proper attention and functioning for stroke researches in

scandalously.


Introduction 4

In spite of advance of modern medicine and neuro imaging it is surprised to note

that there is no standard medical treatment of strokes so far. It is reported that with a

present status of treatment the effect of infarction or hemorrhage cannot be reserved. The

dead neurons cannot be reviewed and the degree of improvement is commonly observed

is to be attributed up to some extent to the recovery of damage but viable cells of the

periphery to infarction. 13

Despite the wide spread of use of Mannitol , Glycerol in cerebral ischemia there is

no convincing evidence that these drugs can be liable for life. The use of steroids has

been demonstrated that there is no value in the controlled randomized trial of ischemic

strokes rather steroids should be avoided because of its measure adverse effect.14

Platelet inhibition is recently introduced in the management of prevention of

ischemic stroke. But there is no evidence had emerged either to prevent stroke in

transient ischemic attacks or previous stroke patients.

The use of thrombolytics, anticoagulants and vasodilators are found to be

ineffective and does not increase blood flow through the damaged area. There is no drug,

which improves series of mental functions particularly higher cortical functions such as

learning ability (especially language), memory, ability to think, consciousness, etc.

Recently Piracetam standard neurotrophic drugs are under the investigations.

Vascular surgery can alter the progress of stroke. But a very few patients are fit for

surgery and the effort put the high financial burden.

Ayurveda is gaining a global popularity for the effective majority of treatment in

Pakshaghata because almost all patients become victims of physical disability after the

latest treatment of modern medicine. Therefore, patients are also preferring to go to

Ayurvedic treatment after the acute phase of stroke.


Introduction 5

A very few controlled clinical reports have been published, in spite of majority of

general beds in Ayurveda hospitals appeared to be filled with patients of residual

Pakshaghata.

Ancient Ayurvedic physicians spent more time to achieve a considerable benefit to

patients. They treated empathetically without supporting data and multi centric trials.

There is no doubt that snehana, swedana, virechana and other oral medications are

effective in ischemic stroke.

Among all sneha, Bala taila 15 is said to be best oil for vata, Gandharvahasta taila

16 is choice for sneha virechana and Ksheerabala taila 101 is best for Nasya.17 They are

thought to be penetrate the minute channels and expel the waste materials.

Pakshaghatariyoga18 19,20 is herbomineral combination which is rationally

formulated on the basis of the individual action. Even some traditional practitioner claiming

this compound is a safe and effective in the management of Pakshaghata. The above

treatment putatively assumed that it can reduce the brain damage and increases the

process of repair.

STATEMENT OF PROBLEM

A clinical study is conducted to assess the efficacy of Ayurvedic management

(shodhana and shamana) in Pakshaghata with special reference to ischemic strokes.

Objectives of the study

To assess the efficacy of selected shodhana and shamana treatment modalities in

the management of Pakshaghata.

To achieve optimum out come in the treatment of Pakshaghata with special

reference to ischemic strokes.

To determine the side effect of given treatment clinically if any.

To assess the role of Ayurvedic treatment as an adjuvant to maintain the well

being of the patients.


Introduction 6

STUDY IN A NUT SHELL :

Patients in and around Gadag who have attended OPD / IPD of Postgraduate

department research center of D.G.Melmalgi Ayurvedic Medical College, Gadag.

Patients age group between 40 to 70 years.

The durations of the study is 90 days.

The assessment of results will be made on the basis of functional status scale

(Barthel’s index) NIH NINDS (National Institute of Health and National Institute of

Neurological disease and strokes), Rankin’s disability scales.

Before and after treatment the effect of the shodhana and shamana will be

statistically analyzed.


7 Historical Review

HISTORICAL PROSPECTIVE OF PAKSHAGHATA

Historical view is an essential part of the literature in which review is done about

the past events of the diseases, the drugs used for treatment and life style of people to

prevent it.

It gives the past medical ethnology of the subject before the scientific study of the

disease. Pakshaghata commonly found in olden age. Aging is inevitable process of the

living being. Therefore it is expected that the disease might exist since the human

civilization.

The Vedas are the first written documents of human civilization. Therefore the

available information can be formulated as follows –

A. Vedic Kala – 2500 B.C. – 1000 B.C.

B. Samhita Kala – 1000 B.C. – 100 A.D.

C. Sangrahakala – 100 A.D. – 800 A.D.

D. Nighantu Kala – 800 A.D. – 1700 A.D.

E. Aadhunika Kala – 17 A.D. – on wards.

In this study the evolution and progression in the study of Pakshaghata were

recorded.

Vedic Kala

Among the four Vedas, Atharvana Veda is considered as the chief source of

Ayurveda. Atharvana Veda describes a variety of Vata disorders and the location of Prana

vata in shiras.

One hymn of Atharvana Veda (Atha. 3/22/06) that offers prayer to God for active

limb movements till old age and maintain the harmony between the prana and apana vata.

This will indicate the existence of Pakshaghata that afflicts the limbs.

A clear description was found in Koushika Sutra [31-18-19] that explains the

treatment of Pakshaghata as follows –


8 Historical Review

The paralyzed part of the body is rubbed with mud collected from the foot prints of

dog and keep the part in passive movements then the affected part may be fumigated by

burning the insect taken from the dog. While doing the whole chikitsa the hymn has been

recited. In Vedic period they know better about the close relation between the Hridaya and

Shiras1

Samhita Kala

In this period more contribution was made by eminent acharyas with their scientific

view to Ayurveda. Most of the available treatises have dealt separate chapter pertaining to

vata, the physiological, pathological and clinical aspects of vata among with detailed

regimen of management Vata vyadhi.

Charaka Samhita2

Charakacharya has included the Pakshaghata in madhyama roga marga. In

chikitsa sthana3 he explained about Samanya vata karmas, lakshanas, chikitsa sutra along

with samanya chikitsa. Specifically for Pakshaghata he prescribed snehana along with

swedana and virechana.

Sushruta Samhita 4

In nidana sthana, Sushruta explained about samprapti and lakshanas of

Pakshaghata. He indicated the involvement of cerebral vessels and impairment of

opposite side of body. His explanation resembles the modern physiology and pathology of

stroke.

Sushruta knew the site of lesion of Pakshaghata i.e. Mashtishka and preferably

advocated that Mashtishkya chikitsa for Pakshaghata. He gave more importance to

shodhana and also shamana i.e. kayavirechana and nasya.5

Sangraha Kala 6

Both the Ashtanga Sangrahakara and hridayakara have explained the nidana of

Pakshaghata. For lakshana and chikitsa, Ashtanga sangrahakara has correlated with


9 Historical Review

Charaka and Sushruta views. They indicated the vikriti sthana in Shiras and Snayus and

suggested to adopt the hridroga chikitsa similar to Sushruta.

Bhela Samhita 7

Bhela samhita explained in detail about the functioning of manas. But he has not

mentioned about the Pakshaghata. In the context of vata roga he described sarvanga and

ekanga roga. According to Bhela, Pakshaghata is a type of sarvanga roga. Instead of

Pakshaghata he used the word Pakshagraha.

Nighantu kala

01. Madhava Nidana 8 : Madhavakara while explaining nidana, lakshana, bheda,

sadhyasadhyata of Pakshaghata classified into two types according to the

involvement of dosha i.e. Vata-pittaja and Vata-kaphaja.

02. Chakradatta 9 : Chakradatta noticed the efficacy of Masha in the management of

Pakshaghata by using the Yogas like Mashataila, Mahamashataila, Mashabaladi

nasapana, abhyanga and basti.

03. Vangasena 10: In his chikitsa sangraha he described the various yogas in the

treatment of Pakshaghata.

04. Basavarajeeyam 11: Pakshaghata is explained in different patterns ,which are not

described in Brihattrayi. Several rasoushadha yogas are found in his text. He

mentioned the details dietetic regimens in the systematic ways, which are followed

by subsequent authors.

05. Yoga ratnakara 12 : Mahalakshminarayana taila, Dwatrinshatika guggulu, etc. are

mentioned in the treatment including the nidana and lakshanas of Pakshaghata.

06. Sahasra yoga13 : Many effective yogas for the treatment of the Paskhaghata like

Prabhanjana vimardana taialm, Dhanwantaram tailam, Ksheerabala tailam,

Karpasatyadi tailam, Dhanwantaram gulika, etc. are narrated in Sahasra yoga

which are popular even today.


10 Historical Review

07. Adhunika Kala : During this period the treatment of Pakshaghata is more

delighted. Bhaishajya ratnawali mentioned teekshna virechana for Pakshaghata.

Other authors like Brihatyoga Tarangini, chikitsa Chandrodaya mentioned the

lakshana and chikitsa of Pakshaghata.

Historical Prospective Of Hemiplegia

Hemiplegia the counter part of Pakshaghata is prevalent through out the globe

since long. Ancient Greek, Chinese, Romans were also known about its existence.

01. Hippocratis (462-370B.C.) : Used the term apoplexy and described the features

like sudden loss of consciousness

02. Galen (130-200 A.D.) : He explained the involvement of the brain matter apoplexy.

He also proved that arteries are carrying blood. Further he described regarding

cranial nerves and sympathetic nervous systems. He made the first experiment of

dissecting of spinal cord and proved that it causes the paraplegia.

03. Gabriel Fallopius (1523 to 1562) : He was the first to describe the trigeminal,

auditory and glassopharyngeal nerves.

04. Thomas Willis (1621 to 1675) : He gave the most complete and accurate account

of the nervous system. He described the network of arteries in the base of the

brain, now known as “Circle of Willis”. He classified the cranial nerves and firstly

described the 11th cranial nerve and gave excellent account of general paralysis.

05. Wepfer : Published his account of four cases of apoplexy with autopsies in 1658.

In each he found a cerebral hemorrhage.

06. Morgagni (1682 to 1771) : He seems to have suspected that cerebrovascular

lesions can cause stroke.

07. Baillie : He suspected the deposition of bony or earthy matter in the arteries

especially the carotid arteries which is the causative factor for the stroke.



08. Fother gill (1712 to 1780) He had thought that generally apoplexy arises when

there is an increased blood flow to the brain

09. John cooke (1756 to 1838) : He first considers the term apoplexy commenting on

the disagreements.Ancient and modern in definition and interpretation written a

book entitled on apoplexy.

NIRUKTI

Pakshaghata has been derived from “Pakshyasya Aghata iti Pakshaghata”. The

word Pakshaghata is composed of two Sanskrit words i.e. Paksha + Aghata. The

individual meaning of these words is as follows –

01. According to Vachaspathyama – Paksha + Arch i.e. Parshva matre – means side

02. According to Shabdakalpadruma – Parshvamatram – means side Parshva

means dehanga.

03. According to Shabdasthambha mahanidhi – Parshwa means side. Dehardha

means half of the body.

04. Ghata – It derived as follows according to Vachyaspatya and Shabdasthmabha

mahanidhi

Han + Ghanj

Hanana – to kill

Vadha – to kill

Prahara – to kill with a blow.

Aghata : It derives as follows –

According to Vachyaspatya –

Aa + Han + Ghnaja.

Ahane – to kill

Vadhe – to kill

Hanana – to kill



Vadha – means death, destruction. Strikes, paralysis.

Pakshaghata : According to Shabdhakalpadruma Pakshaghata has been defined

as – “Pakshaghata Dehangasya Ghatam Vinashanam Yasmat Yatra Va.”

It means loss of function of one side of the body. Sir Williams confined the meaning of

Pakshaghata to one stroke or hemiplegia only.

Definition of hemiplegia –

The term hemiplegia is derived from a compound Greek word. Here hemi means

half and plegia means paralysis or stroke.

Paralysis (Part lysis) Para means besides and lysis means loosening or breaking

or death.

Paralysis means an abolishment of either motor or sensory functions. Paresis may

be used for slight loss of motor or sensory functions.

Therefore, hemiplegia can be defined as a clinical feature of one side weakness or

paralysis in upper and lower extremities and a part of face.

Hemiplegia is the commonest manifestation of a stroke with a paralysis effect on

the face, limbs and trunk or one side of the body.

Synonyms

In Ayurveda different paryayas or synonyms has been used to denote the disease

process, avayava, etiology, pathology, etc.

Pakshaghata, Pakshavadha, Pakshavata, Ardhangavata, Ardhanga shosha,

Pakshagraha, Ekanga vata, Pakshahata, etc.


Shareera 13

SHAREERA

Chakrapani says that without understanding the prakruti (Anatomy and physiology)

particular knowledge of vikriti is not possible. Siras is a part of shadanga and also called

as uttamanga. It is one among the pranayatana and it is counted under sadyo pranahara

marma.1 It is a seat of manas & controls gnanendriya & karmendria.

Siras is the seat of the prana (life), which controls the vital functions of the body

i.e. motor and sensory functions ( prana vata, pranvaha srotas, indriya, indriya vaha

srotas)2. Vagbhata has stated that the root of the human being is located in the seat of

sensory and motor functions.

Among tridoshas vata is prime dosha. Prana vata appears to be the prime dosha

among five types of vata. Pakwashaya is the main seat of the vata even though kati,

Sakthi, srotru, asthi, are the other sthanas of vata. Head appears to be functional seat of

vata. Kashyapa samhitakara considered asthi and majja dhatu are the seats of vata.

Vriddha Vagbhata has mainly mentioned about majja i.e. mastishka and sushumna

situated in the asthi (cranium & vertebral column) that resembles the modern anatomy

and physiology of central nervous system.

Shiras and Dhamanis

The word sira and dhamani has quoted in the vedas (Nadi tu dhamani sira)

according to Yaksha the word dhamani has been taken as a synonym of speech.

Dhamani mentioned in Rigveda was interpreted as reed or pipe. Atharvana Veda quoted

the term dhamani and shiras in the same passage. Hundred siras and thousand

dhamanis.2 According to SAYAM, dhamanis are the channels connected with the heart.

The blood comes out from them when they loses their continuity. The thicker blood

vessels are called as dhamanis and thinner blood vessels are called as siras.2 referring an

old theory that the siras and dhamanis and srotas are all the same. Susruta established

that they couldn’t be distinguished from one another because -


Shareera 14

01. Distinct characteristics

02. Different sources of origin

03. Different functions

Their uses in Ayurvedic literature in different contexts.

Classification of dhamani by Sushruta -

(A) Urdhwaga dhamani : They are 30 in number and carry out the functions like

shabda, sparsha, rupa, rasa, gandha, prasava ,uchhvasa jrimbha, bhashana and

nourishes the bahu, prishta, greeva and parshwa.

10 dhamani carries Vata, Pitta, Kapha and Rakta.

8 dhamani bhashana

2 dhamani ghoshana

2 dhamani Prathibodhana(awakening)

2 dhamani nidra

2 dhamani ashruvahini

2 dhamani stanya vahana

(B) Adhogami dhamanis : They carry out the vata, mutra, pureesha, shukra and

arthava in the downward direction of the body and nourishes, Pakwashaya, guda,

vasti, medra, etc.

10 dhamani carries Vata, Pitta, Kapha and Rakta.

8 dhamani annavahana

2 dhamani mutravahana

2 dhamani shukra visarjana

2 dhamani jala vahana

2 dhamani purisha visarjana

2 dhamani shukrotpatti.


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(C) Tiryag dhamani : They are four in number. Further divides into hundred and

thousands of branches and carry the functions like swedavahana , oushadha shoshana

(applied to skin in the from of abhyanga), lepa and sparsha gnana. The above description

has lead to controversy in interpretation of dhamani as per modern anatomy. Pandit

Gangadhara Shastry in his work ‘Dhamani Vivechana’ asserted that connotation of the

term Dhamani is nerve and nerve alone. Bhela states that nutrients fluids flows in

circulation from the heart spreads all over the body and return to the heart through the

Shiras. Therefore, heart is regarded as center of all the siras or blood vessels.

These vessels are stated to give of branches that transverse upwards and

transversely for nutrition, support, promote and migrate the entire body especially to the

brain.

The role of siras in pakshaghat is given more importance. Since hypertension is

one of the important contributing factor of Pakshaghata. It is essential to know the

physiology of circulation and blood pressure from Ayurvedic point of view.3

Lack of blood supply leads to less amount of oxygen to the tissues that leads to

tissue anoxia. It can occur in any where in the body. It takes places in the Shiras, ie,Brain

vessels leads to Pakshaghata and heart leads to coronary ischemic and infarctions.

Snayu

Muscles are said to be fixed or pastened to the bones by snayus. Dalhana

interpreted kandara as Mahasnayus. Many ligaments are able to sustain human weight.

Sushruta notes the injury to bones, muscles, vessels does not cause much disability as

compared to the snayu (Ligamets). The involvement of such structures in Pakshaghata

leads to akarmanyata (Loss of function).


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THE BRAIN

Neuroanatomy is structural aspect of nervous system. Nervous system is the chief

controlling and co-ordinating system of the body. It adjusts the body to surrounds and

regulates all the body activities i.e. both voluntary and involuntary. The sensory part of the

nervous system collects the information from the surroundings and helps in gaining the

knowledge and experiences where as motor part is responsible for responses of the body.

Brain is enclosed in the bony framework and covered by three protective layers viz. Pia

mater, Arachnoid mater, Dura mater.4

Divisions Of Nervous System 5

I. CNS (Central nervous system) –

1) Brain – Occupies the almost whole the cranial cavity.

2) Spinal cord – Occupies the upper 2/3 of the vertebral canal.

II. Peripheral nervous system –

1) Somatic nervous system (Cerebro spinal) – It is made of 12 pairs of cranial

nerves and 31 pairs of spinal nerves. It’s afferent fibers reaches the

receptors without interruption.

III. Autonomic (Splanchnic) Nervous system – It consists of sympathetic and

parasympathetic systems. Its afferent fibers relay in ganglions and then

postganglionic fibers pass to the effectors.

Nervous system consists of the peripheral components i.e. neurons and

neuroglia , neurons make up the nervous tissue that forms the structural and

functional portion of the system. Neurons highly specified for impulse condition

and neuroglia serves as a special supporting protective component of nervous

system.


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Table No. 01 : Divisions Of The Brain

Sl. No. Parts Subdivision Cavity

01. Fore brain

(Prosencephelon)

A. Telencephelon (Cerebrum) –

Made up of two cerebral

hemispheres & the median part in

front of the intraventricular

foramen

B. Diencephelon – Hidden by

cerebrum consists of a.

Thalamus b. Hypothalamus c.

Metathalamus including medial

and lateral geniculate bodies &

epithalamus including the penial

body.

Lateral ventricle

Third ventricle

02. Mid Brain

(Mesencephelon)

Crus, Cerebri, Substantia nigra,

Tagmentum & Tactum from

before backwards.

Cerebral

aqueduct.

03. Hind Brain

(Rhombencephelon)

a. Mylencephelon (Medulla

Oblongata)

b. Metencephelon – Made up of

Pons and cerebellum.

Fourth ventricle.

Fore brain

The cerebrum occupies the front and upper portion of the cranial cavity, termed

respectively as anterior and middle cranial fossa. It consists of two large hemispheres of

nerve cells (gray mater) & nerve fibers (white mater). The outer layer of the gray mater is

termed as cortex. Two cerebral hemispheres unite at their bases of corpus callosum.

Cerebral cortex is composed of many layers of nerve cells. It is the grey mater

cerebrum. It is arranged in irregular folds, which increases the surface area of the cerebral

cortex. Cerebral cortex contains the higher centers controlling mental behavior, thought,

consciousness, speech, intellect, and special senses. It is the origin of all voluntary &

motor impulses and controls the skeletal muscles & senses of touch, pain, pressure,


Shareera 18

temperature, vibrations, etc. In Pakshaghata more area of motor cortex involved to

produce the clinical features.

Basal ganglia

Mass of white mater of each cerebral hemisphere or certain small areas of gray

mater is known as basal ganglia or nuclei. Caudate nuclei and lentiform nuclei together

form the corpus stratum. It is likely that the system of nuclei and fibers which are the part

of the extra pyramidal system. In some way influences tone, posture, integrations and

coordination. The main voluntary muscles movements which are the concern of the great

descending motor path way or pyramidal system.

Diencephalons Or Mid brain

Thalamus, epithalamus, metathalamus, hypothalamus, and subthalamus are the

ventral parts of the diencephalons.

Thalamus

Thalamus is the large mass of gray mater situated in the lateral part of third

ventricle.

Cerebellum

It is the largest part of the hindbrain. Cerebellum separates the pons and the

medulla by the cavity of fourth ventricle. It is divided into two hemispheres viz. Right &

Left.

The cerebellum has connections of the many parts of the nervous system. It

regulates the posture & postural activities. It plays an important role in muscular

coordination & maintenance of balance. Where as the cortical spinal fibers running

between the cerebral cortex and spinal cord & cross the each other, thus the cerebral

cortex controls the movement of the opposite side of the body. A unilateral lesion causes

the disturbances in posture and muscle tone.


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Medulla oblongata

It is the lowest part of the brain stem. It is the point of vital centers i.e. respiratory

and vasomotor is situated in the lowest part of the fourth ventricle formed medulla. An

injury to medulla usually fatal lesions of posterio- inferior cererbellar artery and vertebral

artery causes lateral and medial medullary syndrome due to the thrombus in vessels.

Pons

Pons is the middle part of the brain stem connecting mid brain with medulla.In

vascular lesion the commonest pathogenesis is pontine hemorrhage. Crossed hemiplegia

or alternate hemiplegia is characterized by the paralysis of face on one side of the limbs

on the other side. The unilateral lesion in the lower part of the pons produces it.

Pyramidal tract

It is also called corticospinal and cortinuclear tract. It is a motor tract extending

from the cerebral cortex to the various motor nuclei of the cranial and the spinal nerves. It

constitutes the upper motor neuron in the motor pathway from the cortex to the voluntary

muscles. The tract passes through the following parts of the CNS i.e. Corona radiata,

Centrum semiovales & the part between the corona radiata and the internal capsule,

occupying jenu and anterior 2/3 of the posterior limb, Middle two third of the crus cerebri

of mid brain & basilar part of the pons. Pyramid of the medulla with decussation in its

lower part - about 75 % fibers crosses opposite side and descends lateral (Cross) &

Corticospinal tract – 20 % fibers remain uncrossed and run at anterior corticospinal tract.

Effect of lesion of pyramidal tract:

Lesions above the level of decussation cause the contra lateral paralysis, while

lesions below the decussation cause the ipsilateral paralysis. It is an upper motor type of

paralysis, which is characterized by loss of power of voluntary movements, hypertonia,

and tendon reflex exaggerated, superficial reflex lost, Bibniski’s sign is positive.


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Spinal cord

The spinal cord starts from the foramen magnum & ends into the lower border of

L1 or upper border of the L2. Transverse section of the spinal cord shows the arrangement

of the grey mater in the form of ‘H’ with its afferent and efferent tracts. In its center shows

one central canal, which contains the CSF. 31 pairs of spinal nerves run through the

different parts of the body to constitute the reflex arch.

BLOOD SUPLY TO CEREBRAL HEMISPHERE 1, 2

The cerebral hemispheres are supplied by the both internal carotid and vertebral

systems anastomosis with each other around optic chiasm and infundibulm of pituitary

stalk forming arterial “circle of Willi’s.” The communicating vessels allow equallisation of

blood flow between the two sides of brain and can allow anastomotic circulation ,if parts

are occluded the circle is formed in the following ways. The basilar artery from the

vertebral system divides at upper border of pons into right and left posterior cerebral

arteries and from each of these communicating artery runs forward to join the internal

carotid artery. Each internal carotid artery gives off an anterior cerebral artery, the circle of

Willis is completed by the anterior communicating artery, a small vessel that units

anteriorly to the cerebral arteries.

The arterial supply of the cerebrum is by the three cerebral arteries. The anterior

middle and posterior with contribution from anterior choriodal. Internal carotid emerges

from roof from cavernous sinus, gives off ophthalmic artery. It runs vertically upwards and

divides into middle and anterior cerebral branches; middle cerebral artery is the largest

branch of the internal carotid artery. It passes into lateral sulcus to supply cortex of insula

and over lying opercula. Many branches emerge in the deep sulci in its area of cortical

distribution lie the motor and sensory areas for opposite side excluding leg, foot and

perineum (which are in anterior cerebral territory) the auditory and speech areas.


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Anterior cerebral artery leaves internal carotid artery at anterior perforated

substance and posses forward above optic nerve. It is connected to follow of anterior

communicated artery. It is distributed to surface of frontal lobe adjutant to whole medial

surface of the hemisphere above corpus callasum as parito-occipital sulcus. The motor

and sensory areas of the opposite leg, foot and perineum including maturating and

defecating centers lie in its territory.

Posterior cerebral artery curls back around the cerebral peduncle, supplying it and

optic tract and surface of the temporal and occipital lobes. It branches supply inferior

temporal gyrus and a corresponding strip of cortex on lateral surface of occipital lobe.

Visual area for opposite side lies wholly in this territory.

The arterial supply of subcortical nuclei is by branches from the three cerebral

vessels and by anterior choridal vessels. Branches from cerebral vessels enter the post-

perforated substance to thalamus and basal ganglia post part of internal capsule.

The anterior choridal artery supplies choridal pluxes. The arterial branches to the

optic tract and gradiation and lateral geniculate body. Post part of the internal capsule,

basal ganglia and limbic system.

Cerebral veins:

The venous return doesn’t follow arterial pattern. Cortical veins travel superficially

them cross-subdural space to drain into nearest venous sinus or dura mater.

Superio-lateral surface of the hemisphere drains into superior sagital sinus by

superior cerebral vein. Drains orbital surface of frontal lobe at anterior posterior substance

striate veins draining corpus striatum. Emerge through the perforation they join deep

middle and anterior cerebral veins to form choridal vein. Thalamo strita vein. Two basal

veins join this and with inferior sagital sinus it enters the straight sinus.


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CEREBRAL CIRCULATION 1, 2

Blood flows to the brain mainly through the branches of the cerebral arterial circle

(circle of Willis) at the base of the brain. Brain receives 750 to 800 ml. of blood per minute.

It is about 15 to 16 % of total cardiac out put and about 50 to 55 ml/100 grams of brain

tissues per minute.

In adult, the brain represents only 2 % of total body weight, but it consumes about

20 % of oxygen and glucose used at rest. Neurons synthesize ATP almost exclusively

from glucose via reactions that use oxygen (through oxidative phosphorylation in

mitochondria). When activity of neurons and neuroglia increases in a region of the brain,

blood flow to that area also increases. Even a brief change of blood flow in brain may

cause unconsciousness. Typically, an interruption in blood flow for 1 to 2 minutes impairs

neuronal function, and total deprivation of oxygen for about 4 minute causes permanent

injury. Because virtually no glucose is stored in the brain, the supply of glucose also must

be continuous. If blood entering the brain has a low level of glucose, mental confusion,

dizziness, convulsions may occur. The existence of a blood – brain barrier (BBR)

protects brain cells from harmful substances from blood into brain tissues. Tight junction

seals together the endothelial cells of brain capillaries, which are also surrounded by a

continuous basement membrane. The pressure against the capillary processes the large

number of astrocytes (one type of neuroglia), which may create a selective passage for

some substances from the blood, but inhibit the passage of others. A few water-soluble

substances (for example glucose) cross the BBR by active transport; & other substances,

such as creatinine, urea, and most ions, cross BBR very slowly. Still other substances –

proteins and most antibiotic drugs – do not pass at all from the blood brain tissue.

However, the BBR dose not allow the passage of lipid-substances, such as oxygen,

carbon dioxide, alcohol, and most anesthetic agents, into brain tissue.


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Measurement of cerebral blood flow:

There are two methods to measure the blood flow to the brain viz.

01. Kety method

02. By using radio active substances

Regulation of cerebral blood flow

There are three methods of cerebral blood flow regulation.

01. Effective perfusion pressure and cerebral vascular resistance: l

Cerebral blood flow is directly proportional to the balance between effective perfusion

pressure and a vascular resistance in brain.

Effective perfusion pressure is the difference between the arterial blood pressure,&

venous blood pressure. Since venous pressure is zero in brain, the most important factor

regulating cerebral blood flow is the arterial blood pressure.

Autoregulation : Cerebral blood flow is regulated by the brain tissues itself between the

limit of 60 mm of Hg and 140 mm of Hg and this is known as auto regulation. If the mean

arterial blood pressure rises above 140 mm of Hg or falls below 60 mm of Hg, the

autoregualtion fails and the cerebral blood flow is altered.

Cerebral vascular resistance : This is offered by intracranial pressure, cerebrospinal

fluid pressure and viscosity of the blood, when the vascular resistance is more, the blood

flow to the brain is less.

Intracranial pressure and cerebrospinal fluid pressure: The increase in the

intracranial pressure is the pressure exerted by the cerebrospinal fluid which may cause

compression of the cerebral blood vessels leading to the reduction in the blood flow. The

elevation of these pressure occurs in conditions like increased venous pressure.

Cushing reflex : The increase in the intracranial pressure or cerebrospinal pressure can

reduce the cerebral blood flow only for a short period. The blood flow is stored

immediately by means of reflex called Cushing reflex or reaction. When cerebral blood


Shareera 24

flow is affected by the compression by the cerebral arteries, the cerebral ischemia

develops. This leads to activation of vasomotor center, peripheral vasoconstriction and

rise in the arterial pressure. The increased arterial pressure helps to restore the cerebral

blood flow. Thus, Cushing reflex plays the most important role in maintaining cerebral

blood flow.

However, when the intracranial pressure exceeds the arterial blood pressure, the

cerebral ischemia becomes severe leading to the irreversible damage of the brain tissues.

Monor-Kellie doctrine : Though the cerebral arteries are compressed by the increased

intracranial pressure and the cerebrospinal fluid pressure but the volume of the brain

tissue is not affected. This is because, the brain tissue is not compressible. This

phenomenon is called Monro Kellie doctrine.

Viscosity : Cerebral vascular resistance is increased if viscosity of blood is more, as in

polycythemia. The resistance is decreased if viscosity is less as in anemia. Cerebral blood

flow is inversely proportional to the viscosity of blood.

02. Chemical factors: Decreased oxygen tension, increased carbon dioxide and

increased hydrogen ion concentration are the important factors which increases

the cerebral blood flow.

Carbon dioxide is the most important factor as it causes dilatation of cerebral blood

vessel. A moderate increase in the carbon dioxide tension does not alter the blood flow,

due to autoregulation. When arterial partial pressure of carbon dioxide above 45 mm of

Hg, the cerebral blood flow is increased.

Carbon dioxide combines with water to form carbonic acid, which dissociates into

bicarbonbate ions and hydrogen ions. This hydrogen ion causes dilatation of blood

vessels in the brain.

Hypoxia causes an increase in cerebral blood flow by vasodilatation.


Shareera 25

03. Nervous factor : The blood vessels of the brain are supplied by sympathetic

vasoconstrictor fibers. But these fibers don’t take part in regulating blood flow under

normal conditions. In the conditions like hypertension, the sympathetic nerve causes the

constriction of cerebral blood vessels leading to reduction in blood flow. This prevents

cerebral vascular hemorrhage and cerebral stroke.

CEREBRAL MICRO CIRCULATION :

The overall metabolic rate of the gray matter of the brain, where the neuronal cell

bodies lie, is about 4 times greater than the white matter correspondingly the number of

capillaries and rate of blood flow is also about 4 times greater than the gray matter.

Another important structural characteristic of the brain capillaries are that they are

not so “leaky” as that of capillaries present in any other tissue of the body. The capillaries

are supported on all sides by “glial feet”, provide physical support to prevent out stretching

of the capillaries. In case of high pressure in addition the walls of small arterioles leading

to the brain capillaries become greatly thickened in the people who develop high blood

pressure and these arterioles remain significantly constricted, all the time to prevent

transmission of the high pressure to the capillaries. Whenever the system is protecting

against the transudation of fluid in the brain breakdowns, then serious brain oedema takes

place, which can lead rapidly to coma and death.

CORRELATION BETWEEN VATA AND THE CENTRAL NERVOUS SYSTEM

All the tridoshas are important for maintaining equilibrium of the body but various kinds

of disturbing influences operate on them. Still vata would appear to be the primary motive

force1. Without the vata dosha other two doshas may cease to operate. For the relation of

vata and C. N. S. Charaka quoted that “Vayus tantra yantra dhara:”. It clears that for the

maintenance of the body the psychosomatic activities should be normal. Here tantra may

correlates with psychic controller and yantra correlates with somatic i.e. physical


Shareera 26

controller. So, the vata dosha controls psychosomatic activities,2 as well as C.N.S. By

this, vata and C.N.S. are correlated.

The shareeragata vata, or biological vata is a force, which is self-generating and self-

propagating energy that is responsible for the conduction, regulation and integration of all

vital functions and structures of the body. It is a biophysical force, which cannot be seen,

but can be recognized from the functions and its performance. It is said that “Avyakta

Vyakta Karma Cha”.4

In respect to sthana of vata, we can state that mashtishka is the sthana of vata as well

as manas , so vata and manas are interrelated. The functions of vata can be observed in

sarva shareera. Main controller is mashtishka,3 where manas is also situated. Prana

vata appears to be the prime dosha among 5 types of vata due to its functions and

location in head. Prana vata facilitates the accomplishment of all the vital functions.4

Sushruta defines that vata as “Va gati gandhanayoho”.5 the meaning of gati is moving

or going and gandhana means intimation, or information. It clears that vata is having two

important functions i.e. movement and information. Here movement correlates with motor

functions and information is with sensory functions. CNS is also having motor and sensory

functions. It proves that CNS is vatavaha Samsthana .

“sarvahi chestha vaten sa: prana: praninam smruta: I”6 Charaka clearly mentioned that

vata is responsible for all the activities as well as vital functions of the body, which are

also impossible without CNS.

Bhela added, as long as vata remains in the body so long the life exists.7 Sushruta

says that vata is a cause for growth, origin, and destruction of all animated organisms. It is

invisible in nature but can be perceived by its functions.8

Charaka and Vagbhata described vata prakopavastha as –

1. The vata kopaka nidana sevana causes vata dusti which leads to dhatukshaya.


Shareera 27

2. Vata may also enter in such a srotas and can be obstructed there.9 The former

condition is of successive changes which takes place in the structure of the nerves

leading to their degeneration. It may be due to malnutrition or impaired nutrition

and the consequent change, which occurs, in its chemical structure and the

depletion of lipid nucleoprotein content. The second condition is showing the

obstruction of the passage of nerve impulses, which may be due to infections,

vascular accidents and tumors. So, the different variety of disease included under

the heading of vata vyadhis described in ayurvedic classics. They are more

correlated with the disease of nervous system.

3. If the sensory tract is affected, the symptoms like Shoola, sthamba [numbness]can

be arised, If motor tract is affected then stiffness and convulsions (sankuchan &

kampa) may be produced . Dharana or control of dhamanis is the function of prana

vata which is also located in the mastishka . The impairment of this function in intra

cerebral vessels occurs in Pakshaghata. In all the cases of the Pakshaghata, the

vikriti (lesion) is situated in the head itself.

All this matter shows that there is a great similarity in the vata and CNS.


Nidana 28

NIDANA

Common nidana have been told by different acharyas in the context of vata roga

adhyaya.1 There is no specific nidana which have been explained for Pakshaghata. Even

though Pakshaghata is one among the 80 types of vata roga. Hence, vata prakopa

karanas i.e. etiological factor relevant to doshas will also play some role in the

pathogenesis of Pakshaghata. Variety of etiological factors for the manifestation of the

Pakshaghata have been explained broadly and classified as follows –

Vata prakopaka - 1) Aharaja 2) Viharaja 3) Kalaja 4) Manasika 5) Panchakarma

6) Other

Vata prakopaka ahara, vihara, kala, manasika, etc other nidanas, also pitta and kapha

prakopa factors are having sanniikrishta nidana and viprakrishta nidana like guru, stealing

of ornaments of God, etc manifests vata rogas and Pakshaghata. Congenital

abnormalities like arteriovenous malformation aneurisms and birth injuries may lead to

Pakshaghata subsequently.

Table No. 02. Showing the Vata prakopaka nidanas by different authors.

Sl. No.

Vata prakopaka nidana

Cha Su Va Mn Yr Bp Hs

Aharaja gunapradhana

01. Rooksha + + + + + + +

02. Sheeta + + - + + + +

03. Alpa + - + + + + -

04. Laghu + - - + + + -

Rasa pradhana

05. Kashaya - + + - - + +

06. Katu - + - - - + +

07. Tikta - + + - - + -

Dhanya varga

08. Masoora - + - - - - +


Nidana 29

09. Kalaya - + - - - - +

10. Nishpava - + - - - - +

11. Raja masha - - - - - - +

12. Krishna kanya - + - - - - +

13. Kangu - + - - - - +

14. Nevera - + - - - - +

15. Rakta shali - + - - - - +

16. Kura dusha - + - - - - +

17. Shyama - + - - - - +

18 Yavagu - - - - - - +

19. Mudga - + - - - - +

20. Adhaki - + - - - - +

21. Harenu - + - - - - +

Harita varga

22. Kalinga - - - - - - +

23. Vastuka - - - - - - +

24. Palandu - - - - - - +

25. Gunjana - - - - - - +

26. Kandashaka - - - - - - +

27. Shushka shalaka - - - - - - +

Mamsa varga

28. Vallura - + - - - - -

29. Varaka - + - - - - -

Viharaja

30. Vishamanshana + + - + + - -

31. Atibhukta - - - - - - +

32. Kshara - - - - - - +

33. Abhojana - - + - - - -

34. Langhana + - - - + - -

35. Adhovatavarodha - + - - - - +

36. Mutra avoradha - + - - - - +

37. Pureesha

avarodha

- + - - - - +


Nidana 30

38. Nisha jagaran + - + + + + +

39. Ati vyavaya + + + + + - +

40. Ati vyayama + + + + + - +

41. Ati adwa + + - + + - +

42. Ati bhashana - - + - - - +

43. Ashwa yana + - - + + - +

44. Ushtra yana + - - + + - +

45. Ratha yana * - - - - - +

46. Gaja yana + - - + + - -

47. Plavana + - - + + + -

48. Ati cheshta + - - + + - -

49. Vega dharana + + + + + - -

50. Sheeghra yana + - - + + - -

51. Apatarpana + + - + + - -

52. Abhighata + + - + + + -

53. Bala vad vigraha - + + - - - -

54. Shayyasana + - - - + - -

Manseeka Karana

55. Shoka + - + + + + -

56. Chinta + - + + + + -

57. Dukha + - - - - - -

58. Krodha + - - - + - -

59. Bhaya + - - - - - +

Pancha karma apachara

60. Vishama

upachara

+ - - + - + -

61. Asamyak vamana - - - - + - -

62. Asamyak

virechana

- - - - + - -

63. Kriya atiyoga - - + - - - -

Kalaja

64. Sheeta dina - - - - - - +

65. Dur dina - - - - - - +


Nidana 31

66. Snana peete - - - - - - +

67. Apranhe - - - - - - +

68. Varsha rutu - - - - + - -

69. Payodhashamaye + - - - + - -

70. Jara - + - - - - -

71. Greeshma - + - - - - -

72. Ahoratri - + - - - - -

73. Nishayanye + - - - - - -

74. Diavasante + - - - - - -

75. Varshante + - - - - - -

Any karmas-

76. Dosha sravana + - - + - + -

77. Askrika sravana + - - + + + -

78. Dhatu kshataya + - - + + + -

79. Marma adhighte + - - + - + -

80. Ama dosha + - - + + + -

Vaya : Incidence of Pakshaghata is more in vriddhavasta. It is observed that due to

ageing the arterial wall becomes thickened and stiff. Progressively thickening of intima

layer of the vessels owing to the gradual accumulation of smooth muscles cells and

connective tissue, which may lead to the Pakshaghata. It can be correlated with vata

prakopa, which occur due to ageing. Incidence of Pakshaghata is 5 % in below 65 years

and 23 % in above 65 years.2

Sex : Males are prone to get Pakshaghata than females. Tendency of atheroscerosis is

less in females between the cases of 35 years. 2

Kala : Seasonal and climatic factors also takes part in provoking Pakshaghata. Rainy

season, cold, cloudy, hot atmosphere early morning, every end of the night, cold effect on

the vessels making in their constriction.2


Nidana 32

Ahara : Vata prakopaka ahara having the gunas like ruksha, laghu, sheeta, etc produces

the degenerative processes in the vessels.1 The nature of vessels like smooth, elastic

walls may undergo in precipitation by means of indulging into above-mentioned nidana,

the atherosclerosis may occur and the cerebral vessels are the most liable sites of these

changes. The circumstances any mild physical or mental strains may lead to rupture of

vessels resulting into hemorrhage leading to Pakshaghata.

Other causes lead to constriction of dhamanis which may resulting into ischemia or

infarction lead to Pakshaghata.

There is no doubt about vata prakopa karanas which manifests the vata vikaras

but indirectly association of pitta and kapha also plays an important role production of the

vata vikara of anubandhi dosha by making vata marga avarodha. Provocation factors like

pitta kapha by their respective karanas are able to manifests Pakshaghata as anubandhi

dosha.

The vata dosha provocation follows the different influencing factors like desha,

deha, kala, vaya, prakriti, etc. For instance the kapha prakriti person develops

Pakshaghata by means of indulging into kaphakara ahara vihara with upalepatwa of

kapha in srotases inflicted by vata dosha itself. Thses types of nidana increases the

viscosity of the blood particularly dislipidemic condition leads to upalepatwa i.e. dhamani

pratichayatwa may lead to coronary or cerebrovascular stenosis causing MI or stroke.

Genetic or acquired derangement influences the exogenous and endogenous

pathways of cholesterol metabolism results hyperlipoproteinaemia and predisposes to the

provoking to either sclerosis in kapha prakriti person.

The symptoms will appear as per the involvement of anubandhitwa of vitiated

doshas.


Nidana 33

The pitta prakoapaka nidana causes enhancement of drava and sara guna of pitta

along with vitiation of the rakta which may affects on the vessels that leads to cerebral

vasodilatation and rupture of blood vessels and results into hemorrhagic strokes.

Psychological factors : 3 Several psychological factors like chinta, shoka, bhaya,

krodha, or mentioned as the vata and pitta provoking factors. Because of their harmful

influences on the neurohormonal system can be considered as a risk factor for

Pakshaghata. Recently this has been studied. (Stroke Vol.1 Apr-Mar.2003) A positive

association between the psychological distresses to make fatal ischemic strokes.

Margavarodha : 4 Margavarana means avarodha of srotas i.e. cerebral vessels (Middle

cerebral arteries). Avarodha in the form of thrombus or embolia in cerebral arteies leads to

cerebral anoxia. More than three minutes of cerebral anoxia leads to death of brain

parenchyma i.e. cerebral infarction occur.

Asrik sravajanya : Excessive loss of blood or excessive letting of blood are mentioned

as provocative factors of vata by making dhatu kshaya leads to Pakshaghata, ekanga

vata, akshepaka, hikka, swasa, pandu, and even death. 5

It may lead to lack of blood supply to the brain causing infraction. Rupture of the

walls of the cerebral arteries leads to bleeding in brain due to the long-standing high blood

pressure. Asrik srava is one among the nidana of vata vyadhi that to Pakshaghata is

mentioned by Sushruta.

Abhighata : 6 Pressed, traumatic injuries leads to vata prakopa. Abhighata means the

traumatic injuries that of head injuries leads to disorder of the blood vessels in the brain

may lead to Pakshaghata. Due to abhighata there is formation of hematoma leading to

cerebral ischemia.

Marmabhighata : 7 injury to the marma is mentioned as vata prakopaka karana. Hridaya,

Basti, and Shiras are the trimarmas. The abhighata to these marmas leads to vata


Nidana 34

prakopa and may lead to Pakshaghata. Especially Snayu marma, Vaikalyakara,

Lohitaksha abhighata leads to Pakshaghata.

RISK FACTORS : 8

Most of the reliable evolution of stroke risk factor comes from Chohort studies such

as in Framingham. Where there has been no or little division of strokes into cerebral

infractions or hemorrhage and even less subdivision into lacunar infarcts. Most studies are

to do the risk factor for infarction. 39 The vast majority of stroke patients have well-

recognized risk factors fro vascular disease. The effect of risk factors on subsequent

stroke incidence is usually additive or multiplicative so that the presence of several risk

factors puts on individuals at particularly at high risk.

Age, sex, blood pressure, smoking, blood lipids, diabetes mellitus, plasma

fibrinogen factors VII coagulant activity, oral contraceptives, alcohol, obesity, race,

snoring, psychological factors, evidence of existing vascular disease, MI, Angina, cardiac

failure, transient ischemic attack, etc.

Hypertension : Hypertension is the major risk factor for stroke in both sexes. It is often

called as “silent killer”. Both elevated systolic and diastolic blood pressure are strongly

associated with stroke incidences. The relative risk factor of stroke in individuals with

definite hypertension is 3.1 in men and 2.9 in women.

The impact of hypertension stroke incidences seems to be lower in older

individuals. However, despite the fact that the absolute risk of stroke increases with age

hypertension remains a major determinant of stroke in older individuals. It is the single

most important controllable stroke risk factor.

Blood lipids : There is no doubt that increasing levels of total plasma cholesterol and to a

lesser extent decreasing level of high density lipoprotein cholesterol are strong risk factors

for CHD. A recent study revealed no significant association between blood cholesterol and

strokeThe author postulated the positive association with ischemic stroke might be


Nidana 35

counter balanced by a negative association with intracerebral hematoma. High levels of

cholesterols in blood stream can lead to the build up of place on the inside of the arteries

which can clog arteries and cause heart or brain attach.

Diabetes : The people with diabetes have a high risk. The Framingham study showed

that glucose tolerance an independent risk factor for stroke.This may be due to circulation

problems that diabetic can cause in addition barin damage may become more severe and

extensive. If blood sugar is high when a stoke happens treating diabetes may delayed

onset of complications that increases the stroke risk.

Smoking : Smoking doubles stroke risk. Smoking damages the blood vessels walls

speeds up the clogging up the arteries by deposits rises the blood pressure and makes

the heart work harder a meta analysis of these studies revealed that cigarette smoking is

associated with 50 % of increased risk of stroke compared with non smokers.

Alcohol consumption : The risk of stroke becomes on the amount of alcohol consumed.

Heavy alcohol consumption (> 3 drinks daily) is related to increased incidence of stroke.

The stroke mortality where as mild or moderate consumption (1 –3 drinks) daily seems to

be related to decreased risk.

Obesity : All though obese persons have a higher risk incidence of hypertension,

diabetes, heart disease and high serum lipid levels. Obesity seems to be a significant and

independent risk factor for stroke.

Heart disease : Heart disease such as atrial fibrillation increases stroke risk up to 6 times.

In the Framingham study 80.80 % of stroke patients had hypertension, 32.70 % patients

had coronary heart disease, 14.50 % of patients had previous cardiac failure, 14.50 % had

the atrial fibrillation and only 13.60% had the non of this. It is known that myocardial

infarctions increases the risk of stroke. Particularly in the first day after the event. Chronic

atrial fibrillation had been associated with five to six folds increase the risk of the stroke.

Risk because, it allows the blood to pool in the heart when blood pools, it tends to form a


Nidana 36

clots. Which can then be carried to the brain causing a stroke. In patients with left

ventricular hypertrophy risk of stroke increases four fold in men and six folds in women.

Hormone therapy : The use of oral contraceptives with high estrogen levels is

significantly related to stroke.

ATHEROSCLEROSIS : 9

Atherosclerosis is a specific form of arterio-sclerosis which affects primarily intima

(inner layer of muscular arteries) and is characterized by atheroma i.e. a fibro fatty

plaques. The term atherosclerosis is derived from athero + sclerosis. Here athero means

soft lipid rich material in the center of atheroma, sclerosis referring to a connective tissue

in the plaques. Atherosclerosis is the commonest and most important in the arterial

diseases. Large and medium size arteries may be involved in this. The most commonly

affected the aorta and the coronary cerebral artery systems are prime targets cirrhosis.

Myocardial infarcts (Heart attack), cerebral infarcts (strokes) are the two major

consequences of this disease, other less common sequel are peripheral vascular

diseases. CVD and CAD mostly related to atherosclerosis. Epidemiological investigations

revealed a number of risk factors, which are associated with increased risk of developing

clinical atherosclerosis. Often these risk factors are acting in combined rather than single.

Major constitutional risk factors.

Major acquired risk factors.

Minor risk factors.

Major constitutional risk factors :

Age, sex, familial and racial factor are explained in nidana.

Major acquired risk factors :

Hypertension, diabetes mellitus, hyperlipidaemia, cigarette smoking are acquired

risk factors.

MINOR RISK FACTORS :


Nidana 37

Environmental influences, obesity, lack of exercise type of behavioral patterns, use

of contraceptives, alcohol consumption, role of viruses, are the Minor risk factors.

Atherosclerosis is not caused by a single etiological factor but it is multi factorial

conditions. The clinical manifestations of atherosclerosis are as varied as vessels affected

and the extend of atheromatous change. The lesions themselves do not cause symptoms

or signs.

Narrowing the vascular lumen to cause ischemic atrophy.

Sudden occlusion of the lumen by the super imposed thrombosis or hemorrhage

into an atheroma producing a frank infarction.

Providing the site for thrombosis and then embolism.

Ischemic Stroke

Atherosclerotic occlusion generally thought to be the main cause of ischemic and

embolic strokes were considered to be less frequent. Angiographic studies in the very

early phase of hemispheric stroke demonstrated number of intracranial occlusions

exceeds the previously reported and that the embolism is most frequent cause of the

ischemic stroke.

The main source of embolism is the heart. Cardiac explorations such as ECG and

transthoracic and trans esophagus echolardiogrphy have allowed the identification of the

principal cardiac and aortic conditions leading to the formations and cerebral migration of

thrombi. Major emboli occlude the middle cerebral artery or the posterior cerebral artery in

a large number of ischemic strokes. Less frequently embolic may also called small

infarcts. In specific territory i.e. posterior division of the middle cerebral artery anterior

cerebral artery, cerebellum and multiple territorial.

Hemodynamical lesions : Cerebral haemodynamic lesions may results from a cardiac

arrest a shock or sudden drop in blood pressure or patient with the cardiac

dysarrhythmias or severe internal carotid artery stenosis.


Nidana 38

Infarction (Cause of stroke) :

An infarct is a localized area of ischemic necrosis in an organ or tissue resulting

from sudden on reduction on either of its arterial supply of venous drainage.

Interruption of the arterial blood supply to the tissue produces the ischemia and

necrosis.

Cerebral ischemia and infarction :

Cerebral ischemia and infarction are caused by sudden occlusion of artery supply

to the brain or less often by the reduced blood flow to the already occluded highly

stenosed artery. Occlusions or stenosis can be the result of disease of arterial wall.

Embolism from the heart, hematological disorders and various rare but sometimes

treatable conditions, which are more proportionally more common in young stroke

patients. But, which can be still be a cause of stroke in the elderly venous infarction is

considered later. Ischemia due to head injury encephalopathy and other global

encephalopathic conditions.

Typically the lesions involved brain areas located at the boundaries between the

arterial territories, where even the normal conditions perfusion is reduced. This type of

infarct is then usually border zone or water shed infarctions.

Lacunar lesions :

Lacunar infarcts are a lesion of less than 1.5 cm in diameter. The vessels involved

are pertaining to arteries or arterioles. Lacunas are commonly seated in the basal ganglia

thalami. Capsule interns Centrum semiovale and base of the pons. Recently, different

studies have demonstrated that the small lacunar lesions may be due to embolism from

the internal carotid artery or heart or to occlusion of the deep perforates or at their origin

from an athrosclerotic intracranial artery.

THROMBOSIS :10


Nidana 39

Thrombosis is the process of formation of a solid mass from the constituents of

blood with in living blood vessels or the heart. The resulting mass is termed as thrombus.

The thrombus formed by the complex process involving in the interaction in the

blood vessel walls. The formed element of blood notably the platelet and plasma

coagulants that constitute blood-clotting system.

The development of thrombus is life saving when a large vessel ruptures or is

served under these circumstances the thrombus called haemostatic plug. When thrombus

develops in the un-ruptured cardiovascular system. It may be life threatening.

Thrombi may diminish or obstruct vascular flow causing ischemic injury to tissue

and organs become dislodged or fragment to create emboli. The thrombosis and

embolism are closely interrelated as give rise to term thromboembolism.

Thromboembolism of occlusion of the vessel areas leads to ischemic necrosis of

tissues. Ischemic injury of heart lung and brain are secondary to thromboembolism.

Pathogenesis :

Human being posses inbuilt system by which the blood remains in fluid state

normally and guards against the hazards of thrombosis and hemorrhage. However, injury

to the blood vessel indicate haemostatic repair mechanism or thrombogenesis.

Virchow described three important factors, which predisposes thrombosis and is

typically known as “virchow’s traid”. They are –

1. Endothelial injury.

2. Alteration in the normal blood flow.

3. Alteration in the blood / hypercoagulibility.

Endothelial injuries :

It is clearly the major and most frequent influence in the induction of thrombosis.

Diabetes with their predisposition to severe atheroscerosis hyperlipidaemia is

extremely vulnerable to arterial thrombi.


Nidana 40

Thrombi also develop within the cardiac chambers when there is injury to the

endocardium as may occur with MI, infections of myocardium.

Inflammatory valve diseases.

In additions to these the hemodynamic stress in hypertension or turbulent flow in

arterial disorders is thought to be injuries to endothelial cells.

Other causes are –

Chemical agents of exogenous origin. Eg. cigarette smoking.

Chemical agents of endogenous origin. Eg. hypercholesterolaemia.

Bacterial toxins.

Alteration in blood flow :

Formation of arterial and cardiac thrombi is facilitated by turbulence in the blood

flow, while stasis initiates the venous thrombosis.

Role of turbulence / stasis :

These provide four important dimensions.

They disrupt laminar flow and bring platelets into contact with endothelium.

They prevent hepatic dilution and clearance of the activated coagulation factors by

the fresh flow of blood.

Turbulence could contribute to the endothelial injury and damage to the formed

elements of the blood.

Loss of normal blood velocity permits the build up of thrombi.

Hypercoagubility / alteration in blood :

Hypercoagubility is defined as unaltered state of circulating blood that requires smaller

quantity of clot promoting substance to induce intravascular coagulation then is required

to produce comparable thrombosis in a normal subject.


Nidana 41

It may occur by the following changes in the blood composition –

Increase in coagulation factors. Eg. fibrinogen, prothrombin, VII A, VIII A, & X A

factors.

Increase in platelet count and their adhesiveness.

Decrease level of coagulation inhibitors. Eg. antihtrombin III, fibrin split products,

etc.

Clinical condition predisposing to the thrombosis :

1) Heart disease. Eg. MI, CHF, Rheumatic fever, cardiomyopathy, etc.

2) Atherosclerosis.

3) Deanerysm of the aorta and other vessels.

4) Varicosities of leg veins.

5) Nephritic syndrome.

6) Late pregnancies and puerperum.

EMBOLISM :11

Embolism is a process of partial or complete obstruction of some part of CVS by

any mass carried in the circulation.

An embolus is detached intravascular solid, liquid or gaseous mass i.e. derived by

blood to a site distant from its point of origin. Virtually 99% of all emboli arise in thrombi.

Rare form of emboli includes fragment of bone or bone marrow, atheromatous debris from

ruptured atherosclerotic plaques, droplets of fat, bits of tumour, foreign bodies, etc.

Inevitably emboli lodge in vessels too small to permit their factors passage

resulting in partial or complete occlusion in the vessel.

Types of emboli

01. Depending on the matter

a. Solid – eg. thromboembolism, athromatomateria, tumour cell clumps,

tissue fragments, parasites, etc.


Nidana 42

b. Liquid – eg. fat globules, aminotic fliud, bone marrow.

c. Gaseous – eg. air or other gases.

02. Depending upon whether infected or mole

a. Bland – when sterile

b. Septic – when infected.

03. Depending upon the source of emboli

a. Cardiac emboli – from left side of heart.

b. Arterial emboli – eg. in systemic arteries in the brain, spleen, intestine, etc.

c. Venous emboli – eg. in pulmonary arteries.

d. Lymphatic emboli can also occur.

Arterial thromboembolism

01. Causes within the heart (80-85%) these are mural thrombo within the left

atrium or left ventricle.

02. Causes within the arteries – in case of athrosclerotic plaques, aortic

aneurysms. Pulmonary veins.

Effects of arterial thromboembolism :

01. Infarction of the organ on its affected part.

02. Gangrene following infarction.

03. Arteries and mycotic aneurysm formation from bacterial endocarditis.

04. MI may occur following coronary embolism.

05. Sudden death may occur from coronary embolism or middle cerebral artery.

Venous thromboembolism :

01. Thrombi in the veins of lower limbs are most common cause of venous emboli.

02. Thrombi in the pelvic veins.

03. Thrombi in the veins of the upper limbs.

04. Thrombi in cavernous sinus in the brain.


Nidana 43

05. Thrombi in the right side of the heart – pulmonary embolism.

Effect of venous thromboembolism :

Most significant effect of venous embolism is obstruction of pulmonary arteries

leading to pulmonary embolism.


Poorvaroopa and roopa 44

POORVA ROOPA

No specific poorva roopa have been explained for Pakshaghata, because

Pakshaghata usually occurs suddenly. It is very important to know the prodromal

symptoms of Pakshaghata [stroke]. Prodromal symptoms were seen in different

pathological conditions of the stroke. It is very difficult to identify the prodromal symptoms

of ischemic strokes. Even though slight numbness, heaviness of half the body, mild

headache, dysarthria may be present. Gradual increase in onset of clinical features may

be considered as prodromal symptoms.1

Sudden onset of severe headache, vomiting, giddiness may be seen. Transient

ischemic attacks are at risk of having another attack of 30 % of these cases develop

Pakshaghata within 5 years and the risk is greater in the first few weeks. High risk persists

up to 6 months. 2

Lakshanas Of Pakshaghata :

Akarmanyatwam (loss of function)

Vichetanatwam (loss of consciousness)

Sandhi bandha shaithilya (loosening of joints) are the roopas of Pakshaghata.

Akarmanyatwam 1, 2 : It is a main feature of Pakshaghata. It means loss of function of

affected part of the body. It denotes the motor deficit.

Charaka told that loss of movement occur either in right or left side of the body.

Sushruta and Vagbhata have used the word “Ardhakaya Akaramanyata” which is one side

of the body.

Acharya Dalhana has mentioned Akarmanyata as a state, when patient is not able

to perform normal activity and tend to fall.

According to ‘Arunadatta’ loss of strength to perform the required activities like

akunchana, prasarana, unnamana and vinamana and fine distal movements are not

possible.3



According to Madhavakara and Dalhana 4– Hasta and pada karma like dharana,

grahana and gamana karma are not possible to perform.

Vagindriyam : Speech may be affected according to the involvement of prana and

udana.

Pani : Inability to lift the hand and produce movements. It shows the involvement

of vyana.

Padam : Inability to walk and change in gait. It is due to vyana vata involvement.

Payu and Upastha : Involuntary micturition and unable to perform coitus.

Vichetanatwam: 5 The word Vichetanatwam means impaired consciousness and

impairment of all modalities. Achetana (Su), vichetanatwam (Va), alpacheshtana (Dal),

are different names of the impaired chetana by different acharyas to evaluate the

consciousness of the patients.

Impaired tactile sensation can be seen in lacunar infarcts, occlusion of vertebral

artery, anterior cerebral artery and in thalamic hemorrhage. Dalhana while commenting on

Achetana says if there is complete loss of consciousness the person may die as in cases

of hemorrhage.6

Sandhi bandha Shaithilya Sushruta, Vagbhata, Madhavakara, Bhavaprakasha, have

explained this symptom which means looseness of joints.

Doshanubandha lakshanas : Pittanubandha – daha, santhapa, murchha, etc.

Kaphanubandha : 8 Shaithilya, Shotha, gurutwa, etc.

Vak Sanga : It is due to Pranavayu and Udana vayu dushti. In this prana vayu is for

indriya dharana and udana vayu performs vak pravrutti. In hemiplegia also dysarthria or

aphasia is usually associated but not always present.

Other lakshanas are:

Ruja : 10 Present in affected side, coated by Charaka. In case of thalamic hemorrhage

severe pain can be observed.



Vak sanga: 10 vak sanga with Pakshaghata are mentioned in separate disease in

asheeta vata vikaras by Charaka and Vagbhata while describing vak sanga he mentioned

as a feature only. Speech disturbance is mentioned as a feature along with Ardita.

Ardita can be interpreted as facial paralysis, the facial paralysis may be associated

with hemiplegia and there may be slurring of speech as facial muscles become weak.

Language will be affected in hemiplegia if dominant hemisphere is affected. The Ardita

mentioned by charaka, vagbhata characterized by hemiplegia with U.M.N., Facial palsy

speech defect is almost resembles hemiplegia with aphasia. Following are the few more

laksahnas found in Pakshaghata –

Hasta pada sankocha 10

Supti

Parshwa shoola

shoola from shiras to pada 9

Clinical features of stroke : 11

Neurological defects fluctuate in stage wise fashion with a series of sudden events

so called as stroke in evaluation.

Middle cerebral artery syndrome

Middle cerebral artery occlusion is usually embolic and middle cerebral artery

stenosis with or without thrombotic occlusion is less common. When the entire territory of

the middle cerebral artery is affected, and resulting into clinical picture includes contra

lateral hemiplegia and hemi anesthesia, contra lateral homonymous hemiplegia and

hemianopia with impairment of conjugate gaze in the direction opposite the lesion,

aphasia with language dominant [usually left] hemisphere involvement and aprectognosia,

asomatognosia, and anosognosia, when with non dominant hemispheric involvement

middle cerebral branch occlusions occur which is often the case, incomplete syndromes



results; non fluent or Broca’s aphasia with contra lateral lower face and arm weakness

from upper division middle cerebral artery occlusion.

Anterior cerebral artery syndrome

Anterior cerebral artery occlusion also usually embolic may lead to paralysis of the

opposite foot and leg, Contralateral grasp reflex, gegenhalten rigidity, abulia, gait disorder,

and preservation and urinary incontinence.

Carotid artery syndrome

Carotid artery is severally narrowed and collateral flow is comprised, the most

regions supplied by the middle cerebral, anterior cerebral and at times, the posterior

cerebral artery may affect. These zones represent the areas of collateral realization

among the 3 arteries. The damage in this situation typically produces weakness or

paresthesia in the contra lateral arm.

Carotid artery disease is responsible for approximately 50 % of the cases of

transient unilateral loss of vision.

Posterior cerebral artery syndrome

It produces following neurological signs controlateral homonymous hemianopia,

memory loss, dyslexia without dysgraphia, coloranomia, mild contra lateral hemiparasis,

contralateral hemisensory loss and ipsilateral third nerve palsy with contra lateral

involuntary movements hemiplegia or ataxia.

Vertebro-basilar artery syndrome

Occlusion of branches of the basilar artery usually results in unilateral pontine or

cerebellar disfunction or both depending on the level of involvement .It shows clinical

features like ipsilateral ataxia, contralateral hemiplegia with sensory loss, internuclear

optholmoplegia, nystagmus, vertigo, nausea, vomiting, deafness, and tinnitis, and palatal

myoclonus.



Cerebellar infarction

Cerebellar infarction usually produces dizziness, nausea, vomiting, direction

changing, nystagmus and ataxia. There is often healing to skin or finger to nose ataxia.

Over one to three days there may be a resultant edema of the cerebellum and may

progress rapidly to coma and death.

Lacunar infarcts

A special type of vascular disease is characterized by hyaline thickening of the

small penetrating arteries of the brain and is most commonly seen in patients with

diabetes mellitus and hypertension. Often cystic infarcts referred to as lacunars infarcts

produces symptoms like pure motor stroke, pure sensory stroke, clumsy hand, disarthria

syndromes. Homolateral ataxia pure motor hemiparasis with contra lateral paralysis of

lateral gaze.

Hemorrhagic stroke

The most common variety of hemorrhagic strokes are intracerebral hemorrhage

secondary to hypertension or amyloid angiopathy and subarachnoid hemorrhage

secondary to ruptured saccular aneurysms or arterio-venous malformation.

Intracerebral hemorrhage

It is the small penetrating artery if damaged by hypertension and gives rise to

hypertensive intracerebral hemorrhage. It almost arises in following locations with

decreasing order of frequency – i.e. putemin, thalamus, pons and cerebellum.


Samprapti 49

SAMPRAPTI

Samprapti of a disease explains the process of derangement of doshas and the

pathological changes, which occur in a person leading to the formation of the disease and

manifestation of clinical features1.

The breaking of samprapti is called as chikitsa2.

The Samprapti of Pakshaghata follows the same pathway as that of other

diseases. But, Pakshaghata being as a vata vyadhi, it does not exhibit any sign and

symptom of the disease in its poorvaroopavastha (i.e. Avyakta poorvaroopa) and it

completes its pathway within no time3. Very few patients of Pakshaghata represent

poorvaroopa and manifestations before the onset of the disease (i.e. completion of all the

stages of the Samprapti.) 4

Stagewise samprapti of Pakshaghata

Though, the Pakshaghata is mentioned as a one of the vata vyadhi, its detail

description of Samprapti is not available in classics. Here is an attempt made for clear

understanding of the pathological consequences in terms of concepts of Shat kriyakala5.

As it is categorized in vatavyadhi, the disease manifests suddenly due to

ashuakaritwa of vayu6. However, there will be some underlying gradual dosha-dushya

samurchhana, which facilitates the sudden bursting of the clinical features of Pakshaghata

in most of the cases.

The Samprapti of Pakshaghata may pass through consecutive stages of the dosha

vikriti like Chaya, Prakopa, etc. During these stages if any interference occur by diets,

atmospheric changes or by other measures, it will reflect over the stages of the

Samprapti. (By the measure, which provokes the relevant doshas, will enhance the

parampara of the onset of the disease formation). By the measures, which alleviate the

relevant dosha, can subside the disease in either Chaya or in Prakopavastha itself7.


Samprapti 50

If the dosha involving in the formation of the disease are not treated in Chaya or

Prakopavastha, then the vikrita dosha will pass on to further stages like Prasaravastha,

etc8.

I. Sanchayavastha

Sanchayavastha means after nidana sevana, the dosha are begins to accumulate

at their own sites9.

The pradhana shareerika dosha vata gets vitiated by its specific nidana mentioned

in classics, exhibits following signs and symptoms –

Vata : The Pakwashaya is the main seat of vata where it undergoes moderate

accumulation in its own site and results in expression of symptoms like – Sthabdhapoorna

koshtata,viruddha kamitwa (i.e. liking towards the factors possessing opponent

properties.) 10

Pitta & Kapha: Even though the Pakshaghatajanya nidana trigger the vata mainly but

they shows their effect over pitta and kapha and result in their sanchayavastha, at their

own site.

II. Prakopavastha

Prakopavastha means maximum accumulation of dosha and which are ready to

expel form their location. (”Prakopastu unmarga gamita”)

Vata : After Sanchayavastha, the aswabhavika vriddhi of the vikrirta vata represents in the

from of – Koshta toda, Koshtagata vayu sancharana, etc11.

Pitta & Kapha : Simultaneously, the pitta and kapha advances in their Prakopavastha.

III. Prasaravastha

In prasaravastha, the prakupita vata spreads to all parts of the body through its

main seat12.

Vata: The sthanachyuta vata in prakopavastha manifests symptoms like – Atopa, etc13.


Samprapti 51

Pitta & Kapha: The sthanachyuta pitta and kapha are being consecutively proceeding in

this stage along with vata.

This stage enhances the vikrita bala of vata by getting anubandhitwa of pitta and

kapha. So, this stage lasts within short time and progresses into Sthanasamshrayavastha

quickly by Ashukaritwa of vata dosha.

IV. Sthanasamshrayavastha

If there is no pre-existing srotovaigunya in any part of the body, the doshas remain

in srotas itself and alleviates spontaneously. The provoked vata gets located at the site of

Mastishkagata srotovahinis (Cerebral arteries) and manifests the signs as per nidana and

circumstantial conditions and dominancy of anubandhitwa of dosha.

V. Vyakta & Bheda

Since it is vata vyadhi there may not be time to get exhibit poorvaroopavastha14.

So, the vyakta avastha of Shat kriya kala may be manifested abruptly.

The lakshanas expressed by means of pradhana and anubandhi dosha of

Sthanasamshrayavastha dominantly resemble lakshanas of Pakshaghata.

Patho-physiology of Pakshaghata

The vishesha samprapti of Pakshaghata is not explained in our classics we have

to go with the general samprapti of vatavyadhi even, which is not clear. So, it is very

difficult to understand the samprapti of Pakshaghata.

To elaborate the pathophysiology / pathological consequences we have to take

help of passive scriptural references.

So, here is an attempt made to understand the many aspects of impairment of

related dosha with analyzing the manifestations found in Pakshaghata patient.


Samprapti 52

A. Pranavayu :

01. The Ashtanga Hridayakara mentioned about the pranavata as it is situated in

Moordhaga (i.e. Mashtika) and does the dharana of buddhi and manas (i.e. higher mental

functions.) 15

The impaired consciousness, impaired memory, inability to calculation and

constructive inability to make skilled movements are found in pran vayu dushti.

02. Dharana of gnanendriya and their functioning is under the control of pranavayu.

Where as the findings in the patients are such as –

a. Difficulty in the identifying shape, size, texture, etc.

b. Disability of the limbs on the affected site.

c. Reduced sensation for pain, touch, temperature, etc.

d. Loss of sense of position, etc.

e. Loss of taste and appetite, etc.

03. Dharana karma of karmendriya and their functioning capacity is also under the

control of pranavata.

The most of the patients approaches with the main complaint of loss of functioning

of the limbs (i.e. may be either of one of the side or both) and loss of speech in terms of

aphasia, dysarthria.

04. Annapravesha and shteevana (i.e. deglutition and spitting) mechanisms are

regulated by the co-ordination of the various parts of the mukha. All these processes are

under the control of prana and udana vata.

Whereas most of the cases of Pakshaghata and Pakshaghata associated with

ardita show the symptoms like –

a. Expressive dysphasia

b. Receptive dyspepsia

c. Excessive salivation and trickling of saliva, etc.


Samprapti 53

B. Udana vata :

01. The main physiological function of udana vata is said to be vak pravritti16.

Most of the patients of Pakshaghata are associated with the involvement of

speech center. Among these the patients with left hemispheric stroke cases are more

prone to be involved with loss of speech.

In patients of Pakshaghata without involvement of speech center and if afflicted

with Ardita, will represents with inability to speak few words (i.e. lack of proper

articulation.)

02. Bala and varna both refers to strength and skin complexion respectively. The

patients of Pakshaghata mostly are of vruddhavastha. So, the symptoms like pallor, loss

of strength in a single or in a group of muscle (i.e. muscular wasting), can be considered

as the vikriti of udana vata.

03. Smriti is the higher mentallactual functioning carrying by the udana vata. Smriti

plays an important role in vak pravritti. The diminished score (i.e. less than 23) indicates

the deformed higher intellectual functions.

C. Apana vata :

01. As per the normal physiological functioning of apana vata i.e. dharana,

udeerana and nishkramana of the mala, mootra, garbha, etc17.

Impairment of the functioning of apanavata because of the influence of nidanas

like dharana, udeerana, vaya, etc. initiates the vikriti of vata dosha in terms of pathological

consequences of Pakshaghata.

02. Apana vata passively withholds the activities of agni which in terms represents

in likings, disliking and digestive processes of the person. So, the most of the patients

shows the signs and symptoms like digestive disturbances and lack of the appetite, etc.

Long term digestive disturbances and lack of Shad rasatmaka ahara reflects in

terms of nidana for dhatukshayajanya Pakshaghata.


Samprapti 54

IV. Vyana vata

01. The Ashtanaga sangrahakara stated in Sutrasthana that the main physiological

functions of vyana are supply of rasa, raktadi (i.e. requirements of body) to all parts of

body, continuously and constantly18.

In Pakshaghata, the main complaints are as per the involvement of the lesions

occupied area. The Pakshaghata originated by thrombo-embolic episodes / thrombotic

changes / atherosclerotic changes, etc. produces the obstruction affecting the needed

nourishment to the brain and results into partial inactivity of the respected center and the

part of the body.

02. The loss of partial function and inactivity of respected center in the brain is due

to malfunctioning of Vyana vata. The vyana vata has the control over all types of voluntary

and involuntary functions. The Pakshaghata patients usually approach with the main

complaint of loss of motor functioning19.

03. Vyana vata does the blinking of eyelids and their co-ordination.

`The patients of Pakshaghata associated with Ardita possess the cardinal

symptoms of ptosis, loss of co-ordination, etc20.

04. The vyana vata is responsible for annaswada, sara-kitta vibhajana and

dhatuposhana krama21. So, the impairment of vyana vata may be hetu for imbalance in

doshika avastha. Long term existence of this stage may results into Dhatukshayajanya

Pakshaghata.

The patient of Pakshaghata shows the major sign as debility of the afflicted part of

the body and muscle wasting selectively or in group from.

V. Ranjaka Pitta

The main physiological function of ranjaka pitta is said to be the formation of rakta

from rasa (i.e. the haemopiosis mechanism) 22.


Samprapti 55

Both the rasa and rakta dhatu does the preenana and jeevana function

respectively. These are the vital functions of rasa and rakta dhatu..

The incidence of occurrence of Pakshahghata is found to be more in old age

because of less preenana, jeevana functions of rasa and rakta dhatu.

VI. Alochaka pitta

The main physiological function of Alochaka pitta is related with visual perception

of roopa by chakshurendriya24.In case of Pakshaghata, this function is not found to be

more significant. But, very few cases like Hemianopia where the VII cranial nerve is

affected leading to loss of vision,

Samprapti Ghatakas

01. Dosha : Pakshaghata is one among the nanatmaja vyadhi, where kapha and

pitta may also play a role. But, vata is dominantly seen.

Shareeraka dosha – Pradhana dosha – Vata – Prana vata

Vyana vata

Apana vata

Udana vata

Manasika dosha – Raja

02. Dushya : Dhatu – Rasa, rakta, mamsa, meda and majja,

03. Upadhatu : Sira, Snayu, Dhamani.

04. Srotas : Rasavaha srotasa

Raktavaha srotasa

Mamsavaha srotasa

Medavaha srotas

Majjavaha srotasa

Manovaha srotasa

05. Adhisthana : Mastishka.


Samprapti 56

06. Udbhava sthana : Pakwashaya.

07. Sanchara sthana : Sarva shareera, especially afflicted side.

08. Vyakta sthana : Ardhakaya, mukha.

09. Agni : Vikruta.

10. Vyadhi swabhava : Onset is ashukari in most of the cases and chirakari in some

cases.

11. Avayava : Hasta, pada, mukha, netra, nasa, swarayantra, etc.

12. Srotodushti prakara : Sanga and Vimarga gamana.

13. Ama : Pachakagani and Dhatwagnimandyajanya ama.

14. Roga Marga : Madhyama roga marga.


Upadrava & Arishta 57

UPADRAVA

There is no direct explanation of Upadrava of Pakshaghata. But, indirectly

mentioned the upadrava of Pakshaghata along with some other vata vyadhis should be

treated earlier (recent origin). 1 Sushruta has clearly mentioned the upadrava of vata

vyadhis are prana kshaya, Mamsa kshaya, Jwara, Atisara, Murchha, Trushna, Hikka,

Chhardi, and Swasa 2 He again describes the upadravas for vata vyadhis which are

shotha, kampa, supta twacha, adhmana, bhanga, antaha ruja.3

Madhavakara has described the upadravas of the vata vyadhis along with

Pakshaghata are visarpa, daha, ruja, sanga, murchha, aruchi, agnimandya, ksheena

mamsa, and ksheena bala. 4

Systemic complications of stroke : 5

Good nursing care is essential to reduce the stroke patient’s complications. Ensure

that patient is comfortable. The air way should be cleared. Safe swallowing must be there.

The patient should be well hydrated and kept clean in suitable postures and turned

regularly. The frequency of complications after acute stroke depends on the severity of the

stroke. The quality of nursing care, age and site of the lesion relevant but not in exact

nature.

Pneumonia, venous thromboembolism, urinary tract infection, pressure source,

cardiac arrhythmia, failure, myocardial infarction, fluid imbalance, hyponitremia,

mechanical problems like spasticity, contractures, frozen shoulder, falls, fractures,

osteoporosis, ankle swelling, mood disorders, seizuers, etc.

ARISHTA LAKSHANA

Harita explained Shoola, Supta twacha, Bhagna, Adhmana, Ruja, as the arishta

and finally the patient dies. 6


Sadhyasadhyata 58

SADHYASADHYATA (PROGNOSIS)

The prognosis of Pakshaghata may be explained under two category i.e.

prognosis about survival of patient and recovery of function of vata as Pakshaghata is

deep-seated disease of mastishka.

Prognosis depends upon the earliest starting of emergency treatment

implementations. Because, vata according to its nature powerful, quick acting and causes

the Atyayeekata1. Vata disorders are difficult to cure with its nature of duschikitsitatwa.

1Yoga ratnakara says that vata vyadhis are asadhya but some times due to daiva yoga it

may be get cured. Physician should not make any assurance to patients. 2 As per

Madhavakara without having any complications, well-nourished patient’s vata vikaras are

sadhya. 3 As per Charaka mamsa kshayaja vata vyadhis does not yield to any treatment.

Cha. Ind. 9/8-9.

Madhavakara emphasized balavan rogi without complications of Pakshghata are

kashtasadhya or asadhya. 4

Sushruta says that vata vyadhis are maharoga having incurable nature. Suggest

the physician not to treat when the patient is suffering from plenty of upadravas.

Sushruta and madhavakara says that, shuddha vataja Pakshaghata is krichhra

sadhya. Dhatu kshayajanya is asadhya. Pitta and kaphanubandhi are sadhya.

Garbhini, Sutika, Balaka, Vriddha, Krisha patients are to be considered as

asadhya. Asrik sravajanya is also said to be the major cause for mortality by

madhavakara. 5 In Kalyanakaraka it is said that shuddha vataja is krichhra sadhya ,if it is

due to abhighata surely asadhya. Kaphanubandha leads to guruta and shopha and if it is

said to be with pitta probably daha, moorchha is observed which are said to be sadhya.6


Sadhyasadhyata 59

PROGNOSIS

Death within first week is usually directly caused by stroke. Eg. Extensive lesion

computable with survival massive cerebral oedema leading to cerebral herniation. The

occurance of post-ischemic oedema peaks at 48 to 72 hours after stroke onset. It is

particularly common cause of early death among the patients with infarcts in the territory

of internal carotid artery, middle cerebral artery and large cerebellar arteries. After the first

week death is more often due to general complications of stroke including cardiac

complications, pulmonary embolism and severe infections, etc.

Six months after stroke 50 % of the patients who survive after an acute phase are

living at home and regarded themselves as partially or totally independent and about 20 %

of survivors are living in institutional care centers. The remainder accounting for about 30

% of acute events has residual difficulty with caring for them. 7


Roga nirnaya 60

ROGA NIRNAYA 1,2,3

Detail history of vyadhi poorvarupavasta or vyaktavasta of the Pakshaghata must

be elicited properly. Cause and effect of the disease along with the ashtasthana and

sadvidha, trividha, dashavidha rogi pareeksha facilitates the clinical diagnosis.

Patient’s disability, identification of proper site of the lesion, proper evaluation of

cardiovascular diseases, diabetes, hypertension, etc. and doshic conditions are to be

thoroughly assessed.

Thorough observation of clinical signs and symptoms of dominance of doshas and

causes of pakshaghata should be differentiated from the following conditions of vata.

Ardita vata, Sarvanga vata, Ardhanga vata, Ekanga vata.

01. Sarvanga vata (quadriplegia) : The impairment of functions of vata occur in all

the organs i.e. four limbs are involved.

02. Ekanga vata (monoplegia) : One limb either urdhwa or adhaha shakha is

involved like gridhrasi, vishwachi, avabahuka etc may be regarded as specific

variety of ekanga vata.

03. Adharanga vata (paraplegia) : Both the legs are involved in ardhanga vata. In

Pakshaghata either left or right half of the body is involved.

04. Ardita vata : Different opinions between Charaka and Sushruta regarding ardita

vata.

According to Sushruta the clinical features of Arditavata are limited to face and neck

itself which correlate with Bell’s palsy and lesion of cerebellum and pontine angle.

According to Charaka the clinical features of Ardhita vata may be limited to face it self

or extended to half of the other part of the body. Hence, according to Charaka,

Pakshaghata may be of two kinds i.e. Kevala Pakshaghata and Pakshaghata with Ardita.

Similarly Ardita may be of two types i.e. Kevala ardita and ardita along with Pakshaghata.


Roga nirnaya 61

Clinical diagnosis :

Traditionally some clinical signs were believed to differentiate thrombotic from

embolic strokes, ischaemic from hemorrhagic stroke, such as sudden onset of embolic

stroke v/s gradual onset of thrombotic strokes. An abrupt onset of intracerebral

hemorrhage with loss of consciousness, headache, seizures. Neuroimaging is required for

correct diagnosis. Subarachnoid hemorrhage, sudden sever headache, vomiting, stiffness

of neck and loss of consciousness, minor bleeding may be undetected.

Instrumental diagnosis :

The CT scan is still most important diagnostic tool in acute stroke. It is the first

examination that should be performed immediately a stroke is suspected. CT scan

confirms the diagnosis of stroke, determine its type, location, and extension can exclude

non-vascular lesion. Causing a focal neurological deficit mimicking stroke, non invasive

safe and can be performed quickly.

MRI :

Magnetic resonance imaging (MRI) is more sensitive than the CT scan in acute

stroke. MRI is less widely available requires more collaboration than CT scan. Therefore it

is indicated in specific cases and is not usually used for diagnosis of acute stroke.

X-ray chest :

X- ray chest reveals the presence of lung and heart disease.

Ultra sound examinations :

An ultra sound examination is useful for significant, through etiological and

prognostic evaluation. The combination of B-mode pulsed and colour droppler can quite

accurately assess the degree of luminal narrowing,identify ulcerations and intraplaque

hemorrhage, and delineate the surface wall characteristic of the internal carotid artery.

Colour droppler is particularly good for demonstrating changes in blood flow near small


Roga nirnaya 62

plaques, and has a sensitivity and specificity of >80% in the detection of significant

occlusive lesions.

Transcranial doppler can be used to examine the internal carotid artery bifurcation

and posterior cerebral artery via the temporal window, and the internal carotid siphon and

ophthalmic artery via the transorbital window, and the proximal anterior cerebral artery,

middle cerebral artery and its major branches. The intracranial vertebral artery and the

proximal portion of the basilar artery via the sub occipital window. It is therefore useful in

the early detection of the arterial occlusion responsible for ischemic stroke.

Cerebral angiography :

Angiography remains the standard tested procedure for defining vascular

lesions, but it should never be performed before neuro imaging and ultrasound studies.

Angiography should be performed in patients believed to be treatable and in whom

ultrasonography has not yield sufficient data, and in some experienced centers in patients

in whom arterial fibrinolysis is possible. Moreover angiography is particularly indicated in

patients with subarchnoid hemorrhage or lobar intracerebral hemorrhage, to detect a

vascular malformation or an aneurysm that is not detected by MRI.

Lumbar puncture :

It is useful to differentiate the infarction and intracerebral hemorrhage however it is

contraindicated in brain tumor.

ECG :

It is useful to identify the status of heart condition and detect previous or recent

cardiac disorders.


Roga nirnaya 63

CORRELATION OF PAKSHAGHATA WITH HEMIPLEGIA

Recent researchers like Dr. Sahu, Dr. Arora, Dr. Parawara K. S. of Jamanagar, Dr.

Khare N. V. of Pune were correlated Pakshaghata with hemiplegia by below mentioned

features –

Table No. 03. Showing the correlation of Pakshaghata with Hemiplegia

Sl. No. Factors Pakshaghata Hemiplegia

01. Etiology Vaya, Margavarana, dhatu

kshaya, Marmabhighata,

Asruk srava, rooksha, alpa

ahara.

Age, Atherosclerosis,

Hemorrhage,injury to head,

nutritional imbalance.

02. Signs and

symptoms

Chesta nivritti, Ishat karma

kshaya in Ardha kaya,

Ardhanarishwaravat acheshta,

Vak sthambha, Sira-snayu

shosha.

Loss of power and movements

in half side of the body,minor

sensory deficit, dysarthria,

atrophy due to disease

stiffness.

03. Pathology Sanga in vata vaha siras,

Improper / no circulation of

blood to mashtishka.

Obstruction of cerebral

vessels,ischaemia depletion in

glucose metabolism, death of

nerve cells,


Chikitsa of Pakshaghata 64

CHIKITSA OF PAKSHAGHATA

Among the various vata vyadhis Pakshaghata is very complicated disease. The

cause for this complicated nature is due to the involvement of pranayatana and marma in

shiras.

Vata involvement is a major factor for its complications. Due to the negligence of

complications patient’s condition may worsen. Hence, the multi disciplinary syndromic

approach in the management of Pakshaghata is essential.

Treatment of Pakshaghata should be started as early as possible, which prevents

the progression of the complications. 1

Thorough history taking and proper examination with appropriate laboratory and

instrumental tools helps to assess the nidana, avastha of the disease and to modulate

proper line of treatment for Pakshaghata according to the avastha of the disease.

Nidana parivarjana

Variety of nidana sevana i.e. risk factors that are provoking the disease

Pakshaghata should be avoided.

General chikitsa of vata roga and Pakshaghata

Samanya vatopakramas that are explained in Astanga Sangraha as vata shamaka

ahara, snehana, swedana, mrudu samshodhana, bahir parimarjana and variety of basti

upakramas plays an important role to specify the vata. Hence, Pakshaghata being vata

pradhana vikara in which special treatment different Acharya in the texts has explained

modalities.

CHIKITSA OF PAKSHAGHATA

Acharya Charaka has explained Snehana, Swedana and Virechana. 2

Acharya Sushruta added abhyanga, mrudu shodhana, anuvasana, asthapana and

shiro basti. 3 Ashtanga Hridayakara opines the snehana, swedana, virechana.4 Dalhana

commented on above view, and added vamana karma if necessary and should followed



with Virechana and with a gap of 7 days patient should follow Anuvasana and Asthapana

Basti karmas as per the condition.

Bhaishajya ratnavali opines that only teekshna virechana is sufficient to treat the

Pakshaghata.5

Chakradatta added nasapana as a vishesha upakrama. In unconscious patients

the Nasya karma is helpful to regain consciousness. 6

Astangna sangraha kara advised kukkuta rasayan as a special remedy for

Pakshaghata.7

SNEHANA

It is one of the shad vidhopkrama according to Charaka.It is considered as first

line of treatment in vata vyadhis. Snehana therapy is best vata shamaka by making

mrudutwa, snigdhatwa and kledatwa in the body. It can be used for both external and

internal use. Bahya snehana karma like abhyanga, lepa, dhara, mardana, moorgni taila,8

etc. Internally it is used in several ways like bhojana, pana, nasya, Anuvasana, etc. Sneha

nourishes the shuskha dhatus and improves the bala and status of agni.9 charaka states

that taila is one of important treatment modality which can specify the vata. Avartita tailas

are more effective in sukshma srotogata vata vikaras.

Sneha kalpas

Ghrita, vasa, majja and taila are four mahasneha dravyas nourishes the mastishka

because of their gunas and potent or restore the functioning capacity of sira snayus.

Ghrita and taila are very useful in keval vata and samsrishatja vata conditions.

Dashamooladi ghrita, Dashamooladi majja Sneha, Chitrkadi ghrita, Pancha tiktadi ghrita,

pancha tikta ghrita guggulu, etc. are very useful in abhyanga, pana, basti karmas, etc.

Nirgundi taila, moolaka taila, laghu panchamooladi taila, are useful in

kaphanubandhi Pakshaghata. Yavadi taila is preferable to use in the sheetakalajanya

Pakshaghata.Sahacharadi taila, Bala taila, Prasarini taila, Karpasatyadi taila,



Mahanarayana taila, Masha taila, Mahamasha taila, Rasna taila, lashunadi taila, etc. are

useful in pana, abhyanga, nasya, anuvasana basti, etc.

SWEDANA

Swedana is one of the important poorva karma in panchakarma.

It not only opens the sweat pores also helps in release the avarodha of the srotases.

Swedana is useful where there is sankocha, ayama shoola, and stamba are present.10

Spasticity and contractures of the muscles are the main component of the various

desciplinaries of Pakshaghata.11.

In vata, vata-kapha avastha the Swedana is very useful. Nadi sweda, prastara

sweda, sankara sweda, kuti sweda, bhoo sweda, etc are pescribed in vata vyadhis. In

Pakshaghata particularly, salavana upanaha sweda,12 avagaha sweda, parisheka sweda,

with kwatha taila of vatahara actions are very useful. Upanaha sweda,13 niragni koopa

swedana is also useful.

In Pakshaghata cases those are associated with rakta pitta, visha, stoulya,

atisara, etc swedana is contra indicated.

SHODHANA

To expel out the excessive doshas in Pakshaghata the mrudu shodhana therapy

should be adopted to eligible patients.

VAMANA

Dalhana has advised the mridu vamana karma in Pakshaghata.14

VIRECHANA

Pakshaghata is vata-dominating disease even though the basti karma is given

prime shodhana karma instead of this charaka and vagbhata have advocated Virechana

is specific shodhana for Pakshaghata. Specifically, sneha virechana administered in case

of Pakshaghata but no specific virechana dravya has mentioned in shodhana. There is a

quite opposite opinion about virechana. Sushruta explained mrudu rechana15 where as



Bhaishajya ratnawali indicated the teekshana virechana. Eranda taila Tilwaka ghrita and

satala ghrita given with milk as sneha virechaka. It is necessary according to the

anubandhata of dosha.

Charaka advocated snehana, sneha yukta swedana, sneha virechana in

Pakshaghata, which are necessary to eliminate the deeply situated dhatugata malas.

Sarva shareeragata malas as well as mastiskhastitha waste materials. Rakta shodhaka

property of virechana helps to restore the rakta prasarana.

BASTI KARMA 16,17

Basti karma is the main treatment for vata disorder. Multi faceted action of basti

karmukata has taken a prime place among all the pancha karmas. Basti karma has

considered as the “ardha chikitsa.” Proper advocation of basti karma facilitates the

evacuation of pureesha ,shleshma ,pitta, adhovata and mootra which accomplishes the

strength.

Niruha basti eliminates the mala doshas from all the srotases. In kapha associated

vata conditions niruha basti is to be given. Where as anuvasana basti reduces the

rooksha, laghu, sheeta guna of vata. Ksheerabala taila sahacharadi taila dashamooladi

taila, etc. are very effective in anuvasana basti.

NASYA

Verities of nasyas indicated in Pakshaghata according to avastha of the disease

by different types of nasya yogas. In unconscious patients the avapeedana and

pradhamana nasya are indicated repeatedly to restore the consciousness. Sneha

dhoomapana and nasya beneficial in Pakshaghata to give the nourishment to the brain.

Ksheerabala taila, Mahamasha taila and also Mashabaladi nasya (B.R.) is very effective.



MASTISHKYA CHIKITSA 18

Sushruta and Vagbhata indicated the mashtishka chikitsa in Pakshaghata.

Application of sneha kalpas on the siras. It is a type of moordhni taila as that of pichu. It is

having less action than the shiro basti.

Sneha dhara 19

Vatahara tailas are used for dhara, abhyanga and luke warm taila used in the form

of dhara or stream blow.

Shiro Basti 19

Moordhni taila is most important and potent described by vagbhata. Pichu, shira

seka and shiro abhyanga are the other three forms of moordhni taila [A.H.Su 22/27-29]

Ksheerabala taila, Mahanrayana taila, Dhanwantara taila, etc are used in Pakshaghata.

Sushruta has specifically mentioned shiro basti in Pakshaghata because he postulated

that vatahara taila directly strikes to the site of the lesion of mashtishka.

BAHI : PARIMARJANA

Bahi: parimarjana chikitsa has an important role in Pakshaghata. Snehana

abhyanga, swedana, shirodhara, shiro basti, pichu, kaya seka, parisheka, avagaha, all

these upakramas are the variety of bahi : parimarjana.

Upaveshtana, mardana, peedana, vyayama are the physical manipulations.

Treatment of Pakshaghata in anubandhi dosha 20

Elimination of kapha and pitta in anubandhi Pakshaghata by appropriate

shodhana, which releases avarodha in pittanubandha Pakshaghata. Pitta shamana

followed with vata shamaka swedana to be advocated. In kaphanubandhi Pakshaghata,

kaphaghna churna with hot water is given. Eg. Hingwadi churna.



Avasthanuasara Chikitsa of Pakshaghata

Speech defects :

Mukatwa, min minatwa, gad gadatwa, in which ksheera dhooma, Sneha

gandusha, application of vacha on the tongue, Kalyanaka avaleha is beneficial in such

conditions.(B.R.)

Loss of memory :

Saraswata ghrita,29 Kalyanaka ghrita, Jyotishamti gulika, Shankapushpi, Vacha,

Saraswatarishta, Pancha gavya ghrita,29 Brahmi ghrita, 29etc are beneficial.

Drugs used in Pakshaghata :

Vatanashaka gana,21 vata shamaka gana,22 Vajeegandadi gana23 dravyas are

used for chikitsa of Pakshaghata.

Different yogas used in Pakshaghata :

Nirgundi taila, moolaka taila, laghu panchamooladi taila, Yavadi taila, Sahacharadi

taila,30 Bala taila30 etc. are used as pana, abhyanga, nasya, Anuvasana basti, etc Tailas

like Prasarini taila,30 Karpasatyadi taila,30 Mahanarayana taila,30 Masha taila, etc are being

used in treatment of Pakshaghata

Kwatha :

Maharasnadi kashaya,28 dashamoola kwatha, 28 manjisthadi kwatha,28

Kapikacchwadi kwatha, Mashabaladi kwatha, Rasonashtaka, rasona saptaka, Rasona

panchaka, etc. are useful in Pakshaghata.

Churna :

Shunthi churna, Vaishwanara churna, Brihata rasnadi churna, Dashamoola

churna, Rasona kalka 24and Rasonapinda,24 etc. are mentioned in the treatment of

Pakshaghata



Rasaoushadhis :

Ekangaveera rasa, 31 Vatagajankusha rasa, 31Vatavidwamsa rasa, 32 Kanjanakari

rasa, 33 Rasaraj rasa,34 Brihat vata chintamani rasa,32 Mallasindura,32 Vata kulantaka

rasa32 etc are mentioned as beneficial.

General management of all strokes 42,43

The general approach to management is identical whether the stroke is due to

recent cerebral infarction, intra cerebral hemorrhage, subarachnoid hemorrhage. The

main aims are –

To make the correct diagnosis of the stroke v/s not stroke.

To establish the reason for stroke in terms of pathological type (infarct or

hemorrhage) the underlying cause particularly if treatable (thromboembolism,

cardiogenic embolism, vascular malformation, etc).

Unless the patient is very seriously handicapped or expected to die rapidly the

attempt to reduce early mortality and lesser disability is made by –

a) Maintenance of pulmonary cardiovascular, fluid, electrolyte, nutritional

homeostasis.

b) Avoidance reorganization and treatment of systemic complications.

c) Avoidance of reorganization of any cause of neurological deterioration.

d) Minimize the extent of irreversible cerebral infarction or hemorrhage.

To rehabilitate the patients surviving the first few days.

To initiate secondary prevention in patients who might be benefited.

To treat any coincidental disorders such as cardiac failure, angina, etc. Current

approaches to the disease management Ischaemic infarction account for 85 % of

stroke and hemorrhagic lesions account for remainder. Preventive measures are

aimed at the vascular risk factors have been shown to have dramatic impact on

the prevalence of the major categories. Any elevations beyond normal blood



pressure level, age, Cigarette smoking, imperfect control of diabetes mellitus or an

increase of blood cholesterol is not to be tolerated. Individuals have no control

over the genetic inheritance.

When stroke occurs the goal of attending physician is to make every effort to ensure

the recovery of useful or perhaps even totally normal function. A large hemorrhage and a

large ischemic infarction will frustrate the best therapeutic intension. Even though many

patients are capable of encouraging degrees of recovery. Good care given quickly is now

known to make a decided and at times dramatic difference to the improvement of

prognosis.

General management guidelines

The ideal plan for every patient considered to have the symptoms and signs of sudden

loss of brain function is immediate admittance to the hospital on an emergency basis. The

patients condition must be stabilized in the emergency room and the essential laboratory

test, imaging to be done, must be decided en route to the in patient facility. Blood

chemistry, complete blood count, ECG, CT is the minimum requirements for planning

modern care and sooner they are done. The better it is for the physician who will execute

the urgent treatment program.

The air way :

The maintenance of good air way must never be compromised. Special vigilance is

demanded in the presence of impaired consciousness. Whenever there is imperfect

handling of secretions and whenever seizers are occurring.

Fluids and nutrition :

Careful chart notes will ensure adequate attention to the fluids and to the nutrition.

These are the fundamental to good care. Dehydration is to be avoided to further

complications. These conditions are detrimental to the accurately ischemic brain.



Avoidance of pressures source :

Avoidance of pressure source is must. Essential nursing staff that is familiar with the

management of unconsciousness, drowsy, immobile patients. When this distress does not

develops infections threatens, pelvic venous thrombus and pulmonary venous emboli are

more prevalent and active rehabilitation is delayed.

Convulsions :

Rigid control of seizers’ activity is mandatory. The ischemic brain is predisposed to

more damage from seizers than normal brain.

Cardiac function :

Optimum cardiac out put is required in all the cases, which have suffered from a

stroke. Abnormal cardiac function may call for antiarrhythemic drugs an appropriate

therapy for any evidence of cardiac failure.

The hazards of hyperglycemia :

The relationship of blood sugar can concentrate to the extent of ultimate brain tissue

damage, which has been affirmed in experimental ischemia. The unwanted effects of

hyperglycemia have been reported in clinical observational studies. Blood sugar

concentrations should be returned to normal and monitored to ensure that they are

maintained at this level. Intravenous administration to stroke patients must not contain

glucose.

Use of agency that affects brain edema

Agents affecting tissue osmolarity :

Urea, Mannitol and subsequent glycerol are known to reduce the detrimental affects of

brain edema in a number of disorders. They continued to be useful agents and are

recommended when the swelling of the brain is caused by trauma, tumor, pseudo tumor,

and encephalitis and by certain circumstances related to subarachnoid hemorrhage.



Despite the wide spread use of these agents in stroke related intracerebral haematoma.

There is no convincing evidence that they ever return such patient useful life.

Steroids :

Steroids are useful in variety of disorders in which the brain becomes edematous.

However, their use in the stroke has been demonstrated to be no value in controlled

randomized trials. Steroids may be detrimental because of their major adverse effects

despite the fact that they are still used quite frequently in patients with ischemic strokes.

Blood pressure manipulation :

Anti hypertensive therapy and its supervision by the patients, physicians must be

accepted as a life time commitment.

Anti thrombotics :

Platelet inhibitors : Many drugs interfere with platelet function and might serve anti

platelet agents. But, the experience is greatest with aspirin, depyridamole, Ticlopidin, has

been demonstrated to be the least as effective as aspirin in preventing the stroke.

Clopidogrel another platelet II b and III a receptors similar to ticlopidin was shown in one

study to have a marginal benefit over aspirin in the prevention of a stroke.

Piracetam :

Piracetam is associated with a significant improvement in motor weakness level of

consciousness and aphasia.

Anti coagulants :

A number of studies have been identified served clinical conditions which is an acute

ischemic infarction, an indication for the administration of anticoagulants. This is usually

requires heparin followed by warfarin. When the stroke has resulted from thrombo

embolism producing from heart to the cerebral arteries, heparin and 3 months of

subsequent warfarin are known to be beneficial and are recommended. Subjected to the

confirmation of stroke by CT scan of brain as ischemic infarction.



Thrombolytics and fibrinolytics :

Thrombolytic agents are not commonly used in the acute management of stroke.

These may be advised intravenously. Although these agents have ability to lyse the clot

with the potential for significant clinical importance they are also potentially hazards in

terms of hemorrhagic risk.

Rehabilitation :

Rehabilitation is a team effort involving the discipline of nursing, physical medicine,

physiotherapy, dietetics and speech therapy begins as early as possible after the stroke.

Skin care and expert assistance in the handling of secretions are easy to provide while

their neglect invites distressing pressure lesions and pulmonary complications. Urinary

catheter should be removed as early as possible. Passive movements of joints are

mandatory until active movement returns.

Patients and families will need to learn that maximum recovery of functions will be

reached at three months.

Speech therapy will assist the person with a moderate speech disorder to adopt to

the loss of communication skills. Rehabilitation will be brief duration for those with no

persisting disability. However, it will not be beneficial for the unfortunate person deprived

of significant cognitive function.


Pathyapathya 75

PATHYA-APATHYA 1,2

The role of Pathya and apathya also takes the importance in the management of

Pakshaghata. Pathya inhibits the future extension of the disease. Apathyakara bhava

sevana worsens the condition of the disease. The pathya ahara-vihara acharana plays an

important role in the recovery of Pakshaghata.

Some important and special ahara kalpas have been told by different acharyas

according to the conditions of vata roga and Pakshaghata. Charaka has mentioned the

sarpi, taila, vasa, majja are good. Bala, Dashamoola, and Panchamoola kwatha sidhha

ajamamsa is good for the vata vikaras.3

Yavagu processed with yava, kola, kulattha, moolaka, dadhi, ghrita and shunti should be

given with diet.

Table No. 72 : Showing the varieties of Pathya and Apathya.

Factors Pathyas Apathyas

Rasa pradhana

Madhura, Amla, Lavana. Katu, Tikta, Kashaya.

Peyas Ushna jala, Dugdha, Goudika,

Sura, Asava.

Udaka, manda

Ahara varga Kulattha, Masha, Godhuma,

Rakta shali, Patola, Varataka,

Dadima, Badara, Lashuna,

Ardraka, etc.

Chanaka, Kalaya, Shyamaka,

Karavindu, Nivara, Mudga, Raja

masha, Guda, Kramuka, etc.

Vihara Snehana, swedana, snana,

abhyanga, etc.

Vyayama, vega dharana, ashwayana,

chankramana, shrama,vyavaya, etc.

Mamsa varga

Chataka, Tittira, Kukkuta. All jangala mamsas.

Manasika Sukha Shoka, chinta, prajagara.


Drug Review 76

DRUG REVIEW

The main motto of this study is to assess the comparative efficacy of shodhana i.e.

virechana and nasya karma along with shamana chikitsa i.e. pakshaghatari yoga.

Trikatu churna1. Moorchhita tila taila, 2Gandhravahasta taila3, Balataila,4

Ksheerabala taila 1015 are used for shodhana treatment. In shamana a herbomineral

compound i.e. pakshaghatari yoga is used. It constitutes Ashwagandha 6, Bala, 6 Brahmi 7,

Vacha 6, Katuki6, Apamarga tandula 6, Choushat prahari pippali 7 Lashuna6 and Brihat vata

chintamani rasa 8 with Madhu9 as anupana.

Trikatu churna – the ingredients of Trikatu churna are Pippali, Maricha, Shunti.

Which does the deepana and pachana. Properties of the drugs are tabulated in the

Table no. 04.

Moorchhita tila taila – Tila taila moorchhana was carried in the manjishtadi

dravyas. It has madhura rasa, madhura vipaka. Madhura makes the vata shamana by

making srotoshuddhi, widening of the srotases. The properties are tabulated in

Table no. 5.

Gandharvahasta eranda taila – It is best vatahara, mrudu, nirapada rechaka,

madhura rasa, madhura vipaka, and ushna guna, properties are tabulated in

Table no. 6.

Bala taila – It is one of the best taila having the combination of bala and ksheera.

Ksheera, Bala are the best vata shamakas. It is best in vatavyadhis and preferably in

Pakshaghata Table No.7

Ksheera bala taila 101 – Avartita ksheera bala taila is very effective in vata

vikaras. 101 times avartita ksheera bala taila pacifies the aggravated vata. Preferably for

nasya karma the above medicine is best and does the brumhana. Table No.8

Pakshaghatari yoga – It is a herbomineral compound which is constituted by the

combination of Ashwagandha, bala, brahmi, vacha, pippali, lahashuna, apamarga, katuki,


Drug Review 77

Brihata vata chintamani rasa (Table No. 09.) Chaturshashtaprahari pippali (Table No. 10)

in different proportions. Drugs are having vata shamaka, kaphaghna, balya, medhya, and

rasayana in nature. They are said to be best in Pakshaghata. The properties of each drug

are tabulated in (Table No. 11).

Madhu – Madhu is used as anupana in this study. Madhu is having laghu, ushna,

ruksha, sukshma guna , grahi ,madhura rasa, kashaya anurasa. It is one of the yogavahi

dravya. As Sukshma srotogami it travels all over the body very quickly. It also acts as

lekhana and srotovishodhana.

78

Table No. 04 : Showing the properties of ingredients of Trikatu churna :

No. Drug Latin name

Rasa Guna Veerya Vipaka Prayukta anga

Dosha-ghnata

Karma-ghanata

01. Pippali Piper

longum

Katu Laghu,

snigdha,

teekshna

Anushna

sheeta

Madhura Phala,

moola

Kapha-

vata

shamaka

Swasa,

kasa,

agnimandya.

02. Maricha Zingiber

officinale

Katu Laghu,

snigdha.

Ushna Madhura Kanda Kapha-

vata

shamaka

Rochaka,

agnimandya.

03. Shunthi Pipper

nigrum

Katu Teekshna,

ushna

Ushna Madhura Twak Kapha-

vata

shamaka

Swasa,

79

Table No. 05. : Showing the properties of Moorchhita tila taila.

No. Drug Latin name Rasa Guna Veerya Vipaka Prayukta anga

Dosha-ghnata

Karma-ghanata

01. Tila Sesamum indicum

Katu, tikta, kashaya

Guru Ushna Katu Beeja. Vata nashaka

Vruna, shotha, kushta.

02. Manjishtha Rubia cordifolia

Madhura, katu

Guru Ushna Katu Moola. Kapha- pitta nashaka

Kushta, raktatisara,

03. Amalaki Emblica officinale

Amla pradhana, lavana varjita pancharasa

Guru ruksha

Sheeta Madhura Phala. Tridosha shamaka

Raktapitta, prameha.

04. Vibhitaki Terminalia bellerica

Kashaya Laghu ruksha

Ushna Madhura Phala. Tridosha shamaka

Bhedana, kasahara.

05. Mustha Cyperus rotendus

Tikta kashaya

Laghu ruksha

Sheeta Katu Kanda Kapha- pitta nashaka

Trishna jwara atisara

06. Haridra Curcuma longa

Tikta, katu Laghu ruksha

Ushna Katu Kanda Kapha- pitta nashaka

Twak vikara meha shosha pandu

07. Lodhra Symplocus racemosa

Kashaya. Laghu, ruksha.

Sheeta Katu Twak. Kapha- pitta nashaka

Raktatisara, jwaratisara.

08. Haritaki Termminalia chebula

Kashaya pradhana lavana varjita pancharasa.

Laghu, ruksha.

Ushna Madhura Phala. Tridosha shamaka

Brimhana, swasa kasa.

09. Kamala nala

Nelumbo nucifera

Madhura. Guru. Sheeta Madhura Stem. Kapha- pitta nashaka

Trishna, daha, visarpa.

10. Vata ankura

Fiucs bengalensis

Kashaya. Guru. Sheeta Katu Ankura. Kapha- pitta nashaka

Visarpa, daha, vrana.

80

Table No. 06. : Showing the properties of Gandharvahasta taila. (A.San.Chi.15/17)

Ingredients Qua. Rasa Guna Veerya Vipaka Doshaghnata Action

Gandharvahasta

Moola

1 tola Kashaya Laghu,

snigdha

Sheeta Madhura Vata-pitta

shamaka

Vatavyadhi

shamaka

Yava 1

Adaka

Madhura Guru,

snigdha


shamaka

Balya,

dhatuvardhaka.

Nagara ½

Kadava

Katu Laghu,

ushna

Ushna Mahdura Vata-kapaha

shamaka

Deepana,

pachana

Eranda taila 1

prasta

Kashaya Laghu,

snigdha


shamaka

Vidhradi,

gulma, shopa

81

Table No. 07. : Showing the properties of Bala taila.

Ingredients Qua. Rasa Guna Veerya Vipaka Doshaghnata Action Moorcchita tila taila

1.2 lit.

Madhura Guru, snigdha

Ushna Mahdura Vata-kapaha shamaka

Balya, varnya, mootrala

Bala moola 4.2 kg.

Madhura Laghu, snigdha

Sheeta Madhura Vata-pitta shamaka

Balya, varnya

Kalka dravyas Yahsti madhu


Sheeta Madhura Pitta-kapha shamaka

Kasahara, swasa

Manjishta Madhura Laghu, ruksha

Ushna Katu Pitta-kapha shamaka

Shoshahara

Ela Tikta Laghu, ruksha

Ushna Katu Pitta-kapha shamaka

Kasahara, swasa

Chandana Tikta Laghu, snigdha

Sheeta Katu Pitta shamaka

Twacha, kanthya, kasahara

Utpala Tikta Laghu, snigdha

Sheeta Madhura Pitta Mootravirechaneeya, shothahara

Padmaka Kashaya Laghu, snigdha

Sheeta Madhura Pitta shamaka

Mootravirechaneeya, shothahara

Pippali Kashaya Laghu, ruksha

Sheeta Madhura Pitta shamaka

Kasahara, swasa

Twak Katu Laghu, ruksha

Ushna Katu Kapha shamaka

Kasahara, swasa

Bruhat ela Katu Laghu, ruksha


Kasahara, swasa

Aguru Katu Laghu, ruksha


Sheeta prashamaka

Kushtha

250 gm

Tikta Laghu, ruksha


Kushatghna, kandughna

Dugdha 3.7 Lit.


Sheeta Madhura Vata-pitta shamaka

Ojovardhaka, Balya, dhatuvardhaka.

82

Table No. 08. Showing the properties of Ksheera bala taila 101.


Bala moola 240gm. Madhura Laghu,

snigdha


shamaka

Balya, varnya

Dugdha 1 Lit. Madhura Guru,

snigdha


shamaka

Ojovardhaka,

Balya,

dhatuvardhaka.

Tila taila 768 ml Madhura Guru,

snigdha

Ushna Mahdura Vata-kapaha

shamaka

Balya, varnya,

mootrala

Table No, 09. : Showing the properties of Brihat vata chanitamani rasa.

Ingredients Qua. Rasa Guna Veerya Vipaka Doshaghnata Action Suvarna Bhasma

3 parts

Kashaya, tikta, Madhura

Guru, snigdha, Picchila

Sheeta Madhura Vata-pitta-kapha shamaka

Balya, varnya, ojovardhaka, vishahara

Rajata bhasma

2 parts

Kashaya, amla

Guru, snigdha, sara

Sheeta Madhura Vata-kapha shamaka

Ojovardhaka, Balya, dhatuvardhaka.

Abraka bhasma

2 parts


Sheeta Mahdura Vata-pitta-kapaha shamaka

Swasa kasahara.

Louha bhasma

5 parts

Tikta, kashaya

Sara, guru, rooksha

Sheeta Mahdura Vata-pitta shamaka

Lekhana, balya, vrishya

Pravala Bhasma

3 parts

Kashaya, madhura

Guru, snigdha

Sheeta Madhura Tridoshaghna Deepana, pachana, rechana

Mukta bhasma

3 parts


Sheeta Madhura Kapha-pitta shamaka

Kshayaroga nashaka

Parada bhasma

7 parts

Kashaya, madhura

Guru, snigdha

Ushna Madhura Tridoshaghna Balya, medhya, dhatu vardhaka

83

Table No. 10 : Showing the properties of Chaturshashtaprahari pippali


Pippali As

needed

Katu Laghu,

snigdha

Anushana

sheeta

Madhura Kapha-pitta

shamaka

Medhya, mutrala,

vishamajwaraghna,

pleehavriddhihara

Gaja pippali

As

needed

Katu Laghu,

snigdha

Anushna

sheeta

Madhura Kapha-pitta

shamaka

Medhya, mutrala,

vishamajwaraghna,

pleehavriddhihara

84

Table No. 11. : Table showing the properties of the ingredients of Pakshaghatari yoga.

Sl. No.

Drug Latin name Rasa Guna Veerya Vipaka Prayukta anga

Dosha-ghnata

Karma-ghanata

01. Ashwagandha Withania somnifera

Tikta, kashaya

Laghu, snigdha.

Ushna. Madhura. Moola Kapha-vata shamaka

Balya, rasayana

02. Bala Sida cardifolia

Madhura Snigdha. Sheeta. Madhura. Moola Vata-pitta shamaka

Balya, rasayana, vrishya.

03. Brahmi Centella asciatica

Tikta, kashaya, amla

Laghu. Sheeta. Madhura. Panchanga Kapha-pitta shamaka

Medhya

04. Vacha Acorus calamus

Katu, tikta.

Teekshna. Ushna. Katu. Moola. Kapha-vata shamaka

Vamaka, kanthya, medhya.

05. Katuki Picrorhiza kurroa

Tikta. Sheeta, laghu.

Sheeta. Katu. Rhizomes. Pitta-kapha shamaka

Pitta rechaka, pachaka.

06. Lashuna Allium sativum

Amla varjita pancha rasa.

Snighda, ushna.

Ushna. Katu. Kanda. Kapha-vata shamaka

Swasa, jwara, vataja vikara.

07. Choushasta pippali

Piper longum

Katu. Laghu, snigdha.

Madhura. Mahdura. Phala. Vata-kapha shamaka

Deepana, pachana, rasayana, swasaghna.

08. Apamarga Achyranthes aspera

Tikta, katu.

Ushna, teekshna.

Ushna. Madhura. Beeja, panchanga.

Kapha-pitta shamaka

Pitta rechaka, vishaghna, krimighna.


Materials & Methods 85

MATERIALS AND METHODS

This clinical study is based on the classical explanations of Pakshaghata with

scientific well-designed research protocol.

Material taken to study

01. Trikatu churna1

02. Murchhita tila taila 2

03. Gandharva hastadi taila 3

04. Bala tail 4

05. Pakshaghatahari yoga

06. Madhu 9

07. Ksheera bala taila 1015

Ingredients of Pakshaghatahari yoga

The detail description of this drug is mentioned in drug review. The ingredients are

as below –

01. Ashwagandha churna 6 - 3 parts.

02. Bala moola churna 6 - 3 parts.

03. Brahmi 7 - 3 parts.

04. Vacha churna 6 - 3 parts.

05. Katuki churna 6 - 2 parts.

06. Lashuna 6 - 1 part.

07. Brihat vata chintamani rasa 8 - ½ part.

08. Apamarga churna 6 - ½ part.

09. Choshasta prahara pippali 6 - ½ part.

Criteria for selection of drugs :

All drugs in this compound are vata-kaphghna, pramathi, medhya, balya, rasayana. The

pharmacological action of individual drugs are vata shamaka and pitta rechaka.



Trikatu churna :

Maricha, pippali, shunthi are mixed in equal quantity and prepared a fine power in

our college pharmacy to use for ama pachana.

Murchhita tila taila :

For the purpose of sneha pana murchhita tila taila was prepared. The ingredients

taken for the preparation of tila taila were – Taila, Manjishta, Triphala, Musta, Haridra,

Hribera, Nalika, Lodhra, Khandasava, Vatankura. The taila was prepared in standard

process unit under the departmental guidelines of Rasashastra.

Brihat vata chintamani rasa :

This drug was purchased from Dabur, India limited Banglore. Brihat

vatachintamani rasa is a herbomineral compound and indicated in the disease

Pakshaghata. It is easily available in the local market. It is very easily processed drug.and

can be easily swallowed by the patient.

Preparation of Pakshaghatahari yoga :

All the ingredients of the yoga are identified with the help of Dravyaguna and

Rasashastra specialists. The drugs are made chaya shushka and processed into a fine

churna and mixed well. Lahasuna bhava has been extracted from ksheerapaka

procedure.

Ksheera bala taila 101 :

This oil is purchased from Swadeshi Oushadha Bhandara, Udupi.

Madhu :

The madhu was purchased from Coorg Company, Banglore for radical use.

Methods and research design :

Selection of the sample: Patients of Pakshaghata were selected from the OPD of

PGARC DGMAMC Gadag. They were included for this study, after confirming the CT

brain and on the basis of inclusive criteria.



Inclusive criteria :

Patients with motor loss or weakness with or without aphasia after an acute phase

or after the 10 days of infarction. Such cases are included in this study. Only the chronic

strokes were included after diagnosing by C.T. scan. M.C.A., A.C.A., and P.C.A. territory

and other mild to moderate infarctions with conscious stage. Patients are selected

irrespective of sex and race other than exclusion criteria.

Exclusion criteria :

Patients below the age of 40 and above the age of 70 years, pregnant women and

lactating mother, patients with severe hypertension, diabetes, M.I., hemorrhagic stroke,

infectious brain diseases and other systemic disease are excluded. Patients of stroke for

more than 1 year with concomitant therapy and with complications are also excluded.

Sample size :

Total 30 patients were randomly selected and divided into the three groups.

Each group was of 10 patients.

Group A : 10 patients were subjected to deepana – pachana, then snehapana

sarvanga abhyanga and swedana, kaya virechana with Gandharvahasta Tail. and

shirovirechana with Ksheerabala taila 101.

Group B : 10 patients were subjected to shamana therapy in the dose of 3 g. in 24

hours in three divided doses with madhu as anupana.

Group C : 10 patients were subjected to shodhana and shamana therapy.

Laboratory investigations :

Selected patients were subjected to the following investigations for the diagnosis

and over all prognoses of the patients.

Hb %, TLC, DC, VDRL, HIV, RBS, Lipid profile (i.e. serum cholesterol, serum

triglycerides, HDL, LDL, VLDL Serum urea and serum creatinin, ECG, CT brain.



Diagnostic criteria:

Patients were diagnosed clinically with doshic predominance.

Every patient was advised for CT of brain as main diagnostic criteria for ischemic

strokes. It is non-invasive safe procedure.

To exclude the pathological condition hematological, biochemical and serological

investigations were also carried out in this study.

On the basis of three-shad-ashta-dasha vidha rogi pareeksha described by various

acharyas.

Supplement of loss of function, muscle bulk, tone, power, gait and reflexes, etc.

Treatment schedule :

Group A :

10 patients were administered three grams of trikatu churna as deepana pachana

daily twice with luke warm water before food for three days.

After deepana pachana patients were administered Moorchhita tila taila in arohana

and sadya snehavidhi with hot water.

Sarvanga abhyanga with Bala taila and followed with sarvanga bashpa swedana

with Nirgundi patra for three days, each day 30 minutes.

After observing the samyaka sneha and sweda lakshana virechana is

administered with Gandharvahastadi taila depending on the koshta of the patient

i.e. 30 to 40 ml. was given at 8 am in empty stomach. Observing the samyaka

shudhhi lakshana, sansargajanya krama was advised in the form of Peya, etc.

After one month of virechana, patient was prepared for Nasya karma and it is

carried out with Ksheera bala taila 101 – 8 drops in each nostrils according to the

condition of the patient for 7 days.

Patient was strictly advised to follow the paschat karma after nasya karma.



Group B:

10 patients were administered deepana pachana with Trikatu churna and

Pakshaghatahari yoga in the dose of 1 gm thrice daily with madhu in the form of prashan.

Application made on and beneath the tongue for consecutive 90 days along with Bala taila

abhyanga and nadi swedana.

Group C:

10 patients were subjected to follow the schedule of both group A and group B.

Diet : All the group of patients were suggested high fibrous vegetarian diet i.e. laghu and

supachya ahara and not to take high calorie diet and salt restrictrion.

Follow-up: The follow up was made in the interval of 30,60 and 90 days consequently in

each group.

Assessment criteria: Assessment of results were made according to the clinical and

functional improvement. The clinical assessment was done on the basis of day to day

activities of the patients. A specially designed stroke scales were taken which were

Internationally accepted as assessment tools for the strokes.

NIH NINDS scale :

From National institute of health, National institute of Neurological disorders [NIH

NINDS] stroke scale was taken for primary evaluation. The stroke severity scales Barthel

index was also assessed before and after the treatment. Ran kin ‘s disability scales were

assessed and the residual disability of the patients if any.

Follow up study was made in 30, 60 ,90 days to assess complications and

mortality.

Reference: NIH & NINDS 10

Barhel s index 11

Rankin’s disability scale 12



The general assessment was done by the Hb%, lipid profile, RBS, before and after

the treatment and safety profile of the drug by renal profile before and after the treatment.

STROKE SCALE OF NATIONAL HEALTH-NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE (NIH-NINDS)

01. Date performed 02. a. Level of consciousness: Alert ( )0

Drowsy ( )1 Stuporous ( )2 Coma ( )3

b. Level of consciousness: Answers both correctly ( )0 Answers one correctly ( )1 Incorrect ( )2 Normal ( )0 c. Level of consciousness: Obeys both correctly ( )0 Obeys one correctly ( )1 Incorrect ( )2 Normal ( )0

03. Best gaze: Partial gaze palsy ( )1 Facial deviation ( )2

04. Best visual: No visual loss ( )0 Partial hemianopia ( )1 Complete hemianopia ( )2 Bilateral hemianopia ( )3

05. Facial palsy: Normal ( )0 Minor ( )1 Partial ( )2 Complete ( )3

06. Best motor arm right: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

07. Best motor arm left: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

08. Best motor leg right: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

09. Best motor leg left: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

10. Limb ataxia: Absent ( )0 Present in either upper or lower ( )1



Present in both upper and lower ( )2 11. Sensory: Normal ( )0

Partial loss ( )1 Dense loss ( )2

12. Neglect: No neglect ( )0 Partial neglect ( )1 Complete neglect ( )2

13. Dysarthria : Normal articulation ( )0 Mild to moderate dysarthria ( )1 Near unintelligible or worse ( )2

14. Best language: No aphasia ( )0 Mild to moderate aphasia ( )1 Severe aphasia ( )2 Mute ( )3

NIH-NINDS STROKE GLOSSARY:

Level of consciousness

0 Fully alert, immediate responsive to verbal stimuli, able to co-operate

completely.

1 Drowsy, consciousness slight impaired, arouses when stimulated verbally or

after shaking, responds appropriately.

2 Stuporous aroused with difficulty (often painful stimuli must be applied),

arousal usually incomplete, responds inadequately reverts to original state

when not stimulated.

3 Comatose, unresponsive to all stimuli or responds with reflex motor or

autonomic effects.

Level of consciousness questions

0 Patient knows age and month (only initial answer graded).

1 Patient answers one question correctly.

2 Patient unable to speak or understand or answers incorrectly to both

questions.

Level of consciousness commands

0 Patient grips hand and closes or opens eyes to commands.

1 Patients dose one correctly.



2 Patient dose neither correctly.

Best gaze

0 Normal

1 Partial gaze palsy, gaze abnormal in one or both eyes, but forced deviation or

total gaze paresis is not present.

2 Forced deviation or total gaze paresis not over come by oculocephalic

maneuver.

Best visual

0 Normal

Partial hemianopia, clear field cut.

Complete hemianopia.

3 Bilateral hemianopia

Facial palsy

0 Normal

1 Minor (asymmetry with smiling and spontaneous speech, good volitional

movement).

2 Partial (definite weakness but some movement remains).

3 Complete (no movement of entire half of face).

Right and left motor arm

Patient is examined with arms outstretched at 900 (if sitting) or at 450 (if supine).

Request full effort for 10 second. If patient’s consciousness or comprehension is

abnormal, cue patient by actively lifting arms in two positions while giving request for

effort.

0 No drift, (limb holds 900 for full 10 seconds).

1 Drift (limb holds 900 but drifts before end of 10 seconds).



2 Cannot resist gravity (limb cannot hold 900 for second, but some effort against

gravity).

3 No effort against gravity (limb falls no resistance against gravity).

4 No movement.

Right and left motor leg

While supine, patient is asked to maintain leg at 300 for 5 seconds. If patient’s

consciousness or comprehension is abnormal, cue patient by actively lifting leg into

position while giving request for effort.

0 No drift. (Leg holds 30 for 5 seconds.)

1 Drift. (leg falls to intermediate position by end of 5 seconds.)

2 Cannot resist gravity (leg falls to bed by five seconds but some efforts against

gravity).

3 No effort against gravity (leg falls to bed immediately, no resistance against

gravity).

4 No movement.

Limb ataxia

Finger – nose- finger and heal – to – skin tests are performed. Ataxia is scored

only if clearly out of proportion to weakness. (limb ataxia not testable in hemiplegia).

0 Absent

1 Present in upper or lower limb.

2 Present in both limbs.

Sensory

Test with pin if patients consciousness or comprehension is abnormal; score

sensation normal unless deficit clearly recognized (eg. clear – cut grimace asymmetry);

without asymmetry only hemi sensory losses are counted as abnormal.



0 Normal, no loss of sensation.

1 Mild or moderate (pin prick less sharp or dull on the affected side, or a loss of

superficial pain with pin prick but patient aware of being tested).

2 Severe or total (patient unaware of being touched).

Neglect

0 None

1 Visual, tactile, or auditory hemi-inattention.

2 Profound hemi-inattention to more than one modalility.

Dysarthria

0 Normal speech.

1 Mild to moderate (slurs some words, understands with difficulty).

2 Unintelligible slurred speech (in the absence of, or out of proportion to any

dysphasia.

Best language

0 Normal, no aphasia

1 Mild to moderate aphasia (word finding errors, naming errors, paraphrases or

impairment of communication by comprehension or expression or disability).

2 Severe aphasia (fully developed Broaca’s or Wernicke’s aphasia or variant.)

3 Mute or global aphasia.

Rankin disability score

Grade I: No significant disability; able to carry out all usual activities of daily living

(without assistance). Note: This does not preclude the presence of

weakness, sensory loss, language disturbance, etc, but implies that these

are mild and do not or have not caused patient to limit activities (eg. if

employed before, is still employed at same job).



Grade II: Slight disability; unable to carry out some previous activities, but able to

look after own affairs without much assistance. (example- unable to return

to previous job; unable to do some house holds chores, but able to get

along without daily supervision or help).

Grade III : Moderated disability ; requires some help but able to walk without

assistance (eg. needs daily supervision, needs assistance with small

aspects of dressing or hygiene, unable to read or communicate clearly).

Note : Ankle – foot orthosis or cane dose not imply leading assistance.

Grade IV: Moderately severe disability ; unable to walk without assistance and

unable to attain to own bodily needs without assistance. (eg. needs 24

hours supervision and moderate to maximal assistance on several

activities of daily living but still able to do some activities by self or with

minimal assistance.

Grade V: Severe disability; bed ridden, incontinent, and requires constant nursing

care and attention.

Reference:

Modified from Rankin J Cerebro-vascular accidents in patients over the age of 60: II

Prognosis. Scott Med J 2: 200-215, 1957.

FUNCTIONAL STATUS SCALES (STROKE SEVERITY SCALE)

Table No. 12. : Showing the Barthel index score.

Function Score Description BT AT

10 Independent, able to apply to any

necessary device, eats in reasonable

time

Feeding

5 Needs help

15 Movements of wheel chair Wheel chair or bed 10 Minimal assistance or supervision



transfers 5 Able to sit but needs maximal assistance

to transfer

5 Washes face, combs hair, brushes teeth,

shaves

10 Independent with toilet or bedpan,

handles cloths, whips, flushes, or cleans

pan.

Personal toilet (grooming) toilet transfers

5 Needs help for balance, handling clothes

or toilet

Bathing self 5 Able to use shower or complete sponge

bath without assistance

15 Independent for 50 feet, may use

assistive devices, except for rolling walker

10 Walk with for50 yards

Walking

5 Independent with wheel chair for 50 feet

only if unable to walk

Stairs, ascending & descending & dressing & undressing

10

5

10

5

Independent, may use assistive devices

Needs help or supervision

Independent, ties shoes,

Needs help but, dose not at least of task

within reasonable time

10 No accident, able to care for collecting

devices if use

Bowel control

5 Occasional accidents or needs help with

enema or suppository

10 No accidents, able to care for collecting

device if used

Bladder control

5 Occasional accidents or needs help with

device.

Total score



The Barthel scale scores 10 functions on a scale from fully dependant to

independent. If performance of the patients is inferior to that described, the score is 0; full

credit is not given for an activity if the patient needs minimal help or supervision. Adapted

from Mahoney FI Barthel evaluation: The Barthel index Md State Med J 14: 61-65, 1965.

A score of 0 is given in all of the above activities when the patient cannot meet the criteria

as defined above.

DEFINITION AND DISCUSSION OF BARTHEL INDEX SCOREING

Feeding

10 Independent. The patient can feed self a meal from a tray or table when

some one puts food within each. Patient must put on an assistive device. (If

needed),cut up food, use salt and pepper, spread butter etc.Patient must

accomplish this in a reasonable time

5 Some help in necessary (eg. Cutting food),as listed above

Moving from wheel chair to bed and return

15 Independent in all phases of this activity. Patient can safely approach bed in

wheel chair, move safely to bed, lie down, come to sitting position on the side

of the bed, change position of wheel chair (if necessary to transfer back into it

safely), and return to wheel chair.

10 Some minimal help is needed in some steps of this activity or patient need to

be reminded or supervised for safety of one or more parts of this activity.

5 Patients can come to sitting position without help of second person but needs

a great deal of help of help to transfer.

Doing personal toilet

5 Patient can wash hands and face, comb hair, clean teeth, and shave.



Patients may use any kind of rozor but must put in blade or plug in razor without

help and take razor from drawer or cabinet. Female patients must put on own

makeup, if used, but need not braid or style hair.

Getting on and off toilet

10 Patients is able to get on and off toilet, fasten and unfasten clothes, prevents

soiling of clothes, and use toilet paper without help. Patients may use wall bar

or other object for support if needed. If necessary to use bedpan instead of

toilet, patient must be able to place bedpan on a chair, empty bedpan and

clean it.

5 Patient need help because of imbalance or needs help handling clothes or in

using toilet paper.

Bathing self

5 Patients may use bathtub or shower or take complete sponge bath. Patient must

be able to do all step involved in whichever methods is used another person

present.

Walking on a level surface

15 Patients can walk at least 50 yards without help or supervision. Patients may wear

braces or prostheses and use crutches, canes, or walkerette but not rolling walker.

Patients must be able to lock and unlock braces if used, assume standing position

and sit down, place necessary mechanical aids into position for use, and dispose of

them when sitting. (Putting on and taking off braces is scored under “dressing”.)

10 Patient needs help for supervision in any of the above but can walk at least 50

yards with little help.

Propelling a wheelchair

5 Patient cannot ambulate but propel a wheelchair independently. Patient must be



able to go around corners, turn around, maneuver the chair to a table, bed, and

toilet, etc. Patient must be able to push a chair at least 50 yards. (Do not score this

item if patient receives score for walking.)

Ascending and descending stairs

10 Patient is able to go up and down a flight of stairs safely without help or

supervision. Patient may (and should) use handrails, canes, or crutches when

needed. Patients must be able to carry canes or crutches to ascend or

descend stairs.

5 Patients need help with or supervision of any of above items.

Dressing and understanding

10 Patient is able to put on, remove, and fasten all clothing and shoe laces

(unless necessary to use adoptions)or supervision. Activity includes putting on,

removing, and fastening corset or braces when these are prescribed. Special

clothing such as suspenders, loafer shoes or dresses that open in front may be

used when necessary.

5 Patients need help in putting on, removing, or fastening any clothing. Patient

must do at least half the work. Patients must accomplish this in a reasonable

time. (Women need not be scored on use of brassiere or girdle unless these

are prescribed garments).

Continence of bowels

10 Patient is able to control bowels and has no accidents. Patient can use

suppository or take enema when necessary (as for spinal cord injury who have

had bowel training )

5 Patients needs help in using suppository or taking enema or has

occasional accidents.

Controlling bladder

10 Patient is able to control bladder day and night. Patient with spinal cord injury

who wear external device and leg bag must them on independently, clean and

empty the bag, and stay dry day and night

5 Patient has occasional accidents or cannot wait for bedpan or get to the toilet

in time or needs help with external device.


Observation & Results 99

OBSERVATIONS AND RESULTS

Detailed examinations of the different groups of patients revealed the following

clinical features and were recorded here.

Table No. 13 : Showing the availability of the patients –

Availability No. of patients Percentages

Fresh 03 10 %

Treated 27 90 %

Out of 30 patients, 27 (90%) fresh cases were found, where as 3 (10%) cases

were treated with Ayurvedic treatment. Fresh cases were treated with modern medicines

as emergency treatment for the disease and risk factors.

Graph No. 01 : Graph showing the availability of the patients –

Availability of the patients

27

3

0

5

10

15

20

25

30

Fresh Treated

No.

of p

atie

nts

FreshTreated

Table No. 14 : Showing the age group incidence -

Age group No. of patients Percentages

40-50 12 40 %

51-60 05 16.7 %

61-70 13 43.33 %



Among 30 cases maximum number of cases 13 (43.33%) was from the age group

of 61 – 70 years and 5 (16.70%) were from 51 – 60 years. 12 patients (40.00%) were from

the age group of 40 – 50 years.

Graph No. 02 : Graph showing the age group incidences -

Age group incidence

12

5

13

40-50 51-60 61-70

Table No. 15 : Showing the sex incidences –

Sex No. of patients Percentages

Male 21 70.00 %

Female 09 30.00 %

Out of 30 patients, 21 (70.00%) patients were male and 09 (30.00%) were female

cases in this study.



Graph No. 03 : Graph Showing the sex incidences –

Sex incidence

21

9

0

5

10

15

20

25

Male Female

No.

of p

atie

nts

Male Female

Table No. 16 : Showing the religion incidences –

Religion No. of patients Percentages

Hindu 24 80 %

Muslim 05 16.7 %

Christian 01 03.33 %

Others 0 0 %

Maximum number of patients i.e. 24 (80.00%) belongs to Hindu community, 5

(16.70%) were of Muslims and only 1 (3.33%) patient was of Christian community. No

patient was reported from others community.



Graph No. 04 : Graph showing the religion incidences –

Religion incidence

24

5

1 00

5

10

15

20

25

30

Hindu Muslim Christian Others

No.

of p

atie

nts

Hindu Muslim Christian Others

Table No. 17 : Showing the economical status of the patients –

Economical status No. of patients Percentages

Poor 06 20 %

Middle 19 63.33 %

High 05 16.7 %

Observation of the socioeconomic status of the patients revealed that majority of

the patients belong to middle class i.e. 19 (63.33%), 6 (20.00%) patients belong to poor

class and 5 (16.70%) were of high class socioeconomic status.



Table No. 18 : Showing the occupation distribution of the patients –

Occupation No. of Patients Percentage

Agriculture 08 26.7 %

House hold 08 26.7 %

Business 03 10 %

Job 03 10 %

Others 05 16.7 %

Driver 03 10 %

Out of 30 patients, 8 (26.70%) each were agriculture and household, 5 (16.7%)

patients were with other works and 3 (10.00%) patients were businessmen, jobholders,

drivers.

Graph No. 05 : Graph showing the occupation distribution of the patients –

Occupational Incidences

8 8

3 3

5

3

0123456789

Ag Hh Bu Jo Ot DrOccupations

Ag Hh Bu Jo Ot Dr



Table No. 19 : Showing the educational status of the patients –

Educational status No. of patients Percentages

Illiterates 11 36.7 %

Primary 09 30 %

High school 06 20 %

College 04 13.33 %

Maximum numbers of the patients were illiterate i.e. 11 (36.70), 9 (30.00%)

patients with primary education, 6 (20.00%) patients were with high school level educated

where as only 4 (13.33%) cases were completed graduation.

Table No. 20 : Showing the marital status of the patients –

Marital status No. of patients Percentages

Married 30 100 %

Unmarried 0 0 %

Among 30 patients unmarried patient were not reported.

Table No. 21 : Showing the habitat of the patients –

Habitat No. of patients Percentages

Rural 16 53.33 %

Urban 14 46.7 %

Majority of the patients 16 (53.33%) were with native of rural area and 14 (46.70%)

patients were urban citizens.

Table No. 22 : Showing the food habitat of the patients –

Food habitat No. of patients Percentages

Pure vegetarian 16 53.33 %

Mixed 14 46.7 %

Most of the patients i.e. 16 (53.33%) were with food habits of pure vegetarian

and 14 (46.7%) were of mixed food habits.



Table No. 23 : Showing the rasa satmyata of the patients –

Rasa satmyata No. of patients Percentages

Pravara 15 50 %

Madhyama 09 30 %

Avara 06 20 %

Out of 30 patients most of the patients were of pravara rasa satmya i.e. 15 (50%),

9 (30%) were of madhyma and 6 (20%) were of avara rasa satmya.

Table No. 24 : Showing the roga prarambha kala of the patients –

Roga prarambha kala No. of patients Percentages

Sheeghra 10 33.33 %

Manda 20 66.7 %

Onset of the disease in 20 (66.70%) was manda in nature and 10 (33.33%)

was reported with all of a sudden nature.

Table No. 25 : Showing time of onset of the disease of the patients –

Time of onset of disease No. of patients Percentages

Prataha kala 15 50.00 %

Dina kala 03 10.00 %

Ratri kala 09 30.00 %

Nidrakala 03 10.00 %

Gamana kala - -

Krodha kala - -

Maximum number of the patients i.e. 15 (50.00%) were had the

symptoms at early morning, 9 (30.00%) patients generated the disease in ratri kala.

and 3 (10.00%) each developed the Pakshaghata in dina and nidrakala.



Table No. 26 : Showing the chronicity of the disease of the patients –

Chronicity No. of patients Percentages

Within 20 days 18 60 %

Within 40 days 09 30 %

Within 2 months 01 3.33 %

More than 6 months 02 6.7 %

Maximum number of the patients i.e. 18 (60.00%) were reported to

Ayurvedic treatment within 20 days after manifestation of the symptoms, 9 (30.00%)

Patients were reported within 40 days after the symptoms, 1 (3.33%) was reported within

60 days of onset of the disease and only 2 patients were reported more than 6 months

after the occurrence of the disease.

Table No. 27 : Showing the previous history of patients –

Family history No. of patients Percentages

Present 02 6.7 %

Absent 28 93.33 %

28 (93.33%) patients were not having a family history of Pakshaghata where as

only 2 (6.70%) cases were with the family history of Pakshaghata.

Table No. 28 : Showing the habits of the patients –

Habits No. of patients Percentages

Smoking 11 33.33 %

Alcohol 11 33.33 %

Tobacco chewing 11 33.33 %

Chinta 14 46.66 %

Krodha - -

Risk factors like chinta was affected to 14 (46.66%) patients. 11 (36.70%)

Patients each were suffering with the alcoholism and tobacco chewing and smoking.



Graph No. 06 : Graph showing the habits of the patients –

Habits incidence

11 11 11

14

002468

10121416

Smk Alc Tob.c Chn Krd

Habit

Smk Alc Tob.c Chn Krd

Table No. 29 : Showing the risk factors of the patients –

Risk factors No. of patients Percentages

HTN 24 80 %

DM 06 20 %

Hyperlipidaemia 04 13.33 %

Epilepsy 01 3.33 %

Alcohol 11 33.33 %

Smoking 11 33.33 %

Hormone therapy 0 0

Maximum number of the patient i.e. 24 (80.00%) had HTN as the main risk factor,

11 (33.33%) patients each were had the alcoholism and smoking, 6 (20.00%) patients

were with DM, 4 (13.33%) patients were with hyperlipidaemia and only one patient (i.e.

3.33%) was with epilepsy as a risk factor.



Graph No. 07 : Graph showing the risk factors of the patients –

24

64

1

11 11

00

5

10

15

20

25

HT DM HL Ep Al Sm HrT

Risk factors

No. of patients

Table No. 30 : Showing treatment history of the patients –

Treatment history No. of patients Percentages

Fresh 27 90.00 %

Treated 03 10.00 %

Among the 30 cases 27 (90.00%) cases were received the preliminary and major

modern line of treatment from local and specialists where as 03 (10.00%) patients were

directly approached to the Ayurvedic treatment.

Table No. 31 : Showing general condition of the patient –

General condition No. of patients Percentages

Good 07 23.33 %

Moderate 16 53.33 %

Bad 07 23.33 %

Maximum number of patients i.e. 16 (53.33%) were presented with moderate

health status, 7 (23.33%) patients each were with the good and worst physical status.



Table No. 32 : Showing the side affected of the patients –

Side affected No. of patients Percentages

Right 15 50 %

Left 15 50 %

30 patients presented with equal incidence of the affected right and left side i.e. 15

(50.00%).

Graph No. 08 : Graph Showing the risk factors –

Side affecetd

15 15

Right Left

Table No. 33 : Showing sara of the patients –

Sara No. of patients Percentages

Pravara 0 0 %

Madhyama 17 56.7 %

Avara 13 43.33 %

17 (56.70%) patients were with madhyama sara prakriti and 13 patients were with

avara sara prakriti. No patient with pravara sarata was reported in this clinical study.



Table No. 34 : Showing the prakriti of the patient –

Prakrirti No. of patients Percentage

V - -

P - -

K - -

VP 13 56.7 %

PK 05 16.7 %

VK 05 16.7 %

VPK 07 23.33 %

13 (56.70%) patients were of vatapitta prakriti, 7 (23.33%) patients were with

tridoshaja prakriti where as 5 (16.70%) cases each were presented with the pittakapha

and vatakapha prakriti.

Table No. 35 : Showing the samhanana of the patient –

Samhanana No. of patients Percentages

Pravara 0 0 %

Madhyama 23 76.7 %

Avara 07 23.33 %

Maximum numbers of patients i.e. 23 (76.70%) were of madhyama samhanana

and 7 (23.33%) of avara samahanana. No patient with pravara samhanana was reported.

Table No. 36 : Showing the satwa of the patient –

Satwa No. of patients Percentages

Pravara 02 6.7 %

Madhyama 21 70 %

Avara 07 23.33 %

Madhyama satwa 21 (70.00%) patients were presented, 7 (23.33%) patients were

of avara satwa and only 2 (6.70%) cases were of pravara stawa.



Table No. 37 : Showing the distribution of bala of the patient –

Bala No. of patients Percentages

Pravara 07 23.33 %

Madhyama 19 63.33 %

Avara 04 13.33 %

19 (63.33%) cases were with madhyama bala, 7 (23.33%) cases were with

pravara bala and only 4 (13.33%) cases were of avara bala.

Table No. 38 : Showing the condition of the agni bala of the patient –

Agni bala No. of patients Percentages

Manda 22 73.33 %

Teekshna 04 13.33 %

Vishamagni 04 13.33 %

Maximum numbers of patients 22 (73.33%) were suffering with mandagni and 4

(13.33%) patients each were afflicted with teekshanagni and vishamagni.

Table No. 39 : Showing the distribution of vyayama shakti of the patients –

18 (60.00%) patients were having avara vyayama shakti, 11 (36.66%) cases were

with madhyama vyayama shakti and only 1 (3.33%) patient was with pravara vyayama

shakti.

Table No. 40 : Showing the habit of nidra of patients –

Nidra No. of patients Percentages

Ati 01 3.33 %

Alpa 25 83.33 %

Vishama 03 10 %

Anidra 01 3.33 %

Vyayama shakti No. of patients Percentages

Pravara 01 03.33 %

Madhyama 11 36.66 %

Avara 18 60.00 %



Maximum number of the patients i.e. 25 (83.33%) were having disturbed sleep

(alpa nidra), 3 (10.00%) cases were vishama nidra habit and 1(3.33%) patients each were

reported with ati and anidra.

Table No. 41 : Showing the vaya of the patient -

Vaya No. of patients Percentages

Balya - -

Madhyama 12 40 %

Vardhakya 18 60 %

Dominancy of the old age incidence in the sample was found i.e. 18 (60.00%)

where as 12 (40.00%) cases were found in the middle age group.

Table No. 42 : Showing the distribution according to the desha of patient –

Desha No. of patients Percentages

Jangala 30 100 %

Anupa - -

Sadharana - -

All of the patients were residing the jangala desha. No patient was reported from

anupa and sadharana desha.

Table No. 43 : Showing the bhara of the patient –

Bhara No. of patients Percentages

50-60 10 33.33 %

60-70 8 26.66 %

70-80 12 40.00%

12 (40.00%) patients were in the weight of 70 – 80 kg, 10 (33.33%) patients were

of 50 –60 weight group and 8 (26.66%) patients were reported in the weight group of 60 –

70 kg.



Table No. 44 : Showing the blood pressure of the patient –

Blood pressure No. of patients Percentages

140/80 mm of Hg 02 6.7 %

160/90 mm of Hg 10 33.33 %

180/100 mm of Hg 16 53.33 %

200/100 mm of Hg 02 6.7 %

More number of cases observed in the category of 180/100 mm of Hg {i.e. 16

(53.33%) cases}, 10 (33.33%) cases were from the blood pressure group of 160/90 mm of

Hg and 2 (6.70%) patients each were with the blood pressure category of 140/80 and

200/100 mm of Hg.

Table No. 45 : Showing the nidana sevana of the patients –

Nidana Sevana No. of patients Percentages

Vatakaphakara 16 53.33 %

Vatapittakara 13 43.33 %

Pittakaphaja 0 0

Vataja 01 3.33 %

Maximum number of patients 16 (53.33%) were found to be in indulging into the

vatakaphakara nidanas, 13 (43.33%) cases were had habit of the vatapittaja nidana and

only 1 (3.33%) patient was with more number of vata vikritijanya nidanas.

Table No. 46 : Showing the poorva roopa lakshanas –

Poorva roopa No. of patients Percentages

No 25 83.33 %

Yes 05 16.7 %

Maximum number of patients 25 (83.33%), were reported with no history of poorva

roopa, where as only 5 (16.70%) patients were having the history of insignificant

poorvaroopa of stroke.



Table No. 47 : Showing the motor function loss -

Motor function test No. of patients Percentages

Grade 0 25 83.33 %

Grade I 05 16.7 %

Grade II - -

Grade III - -

Grade IV - -

Grade V - -

25 (83.33%) patients were reported with the grade 0 motor functional loss and 5

(16.7%) patients were reported with grade I loss.

Table No. 48 : Showing the samsrashtaja dosha of the patients-

Samsrashtaja dosha No. of patients Percentages

Shuddha vataja 01 3.33 %

Vata pittaja 13 43.7 %

Vata kaphaja 16 53.33 %

Dhatu kshayajanya - -

In the sample 16 (53.33%) cases were with involvement of vatakapha dosha as

the major causative, 13 (43.70%) patients were having the signs and symptoms with the

predominance of vatapitta dosha. Only 1 (3.33%) case was exhibited the signs and

symptoms of shuddha vatajanya Pakshaghata lakshanas.

Table No. 49 : Showing the lakshanas of Pakshaghata –

Lakshanas of Pakshaghata No. of patients Percentages

Akarmanyatva of half of the body 30 100 %

Shakti hrasata 1 3.33 %

Chesta kshaya 10 33.33 %

Vak sanga 12 40 %

Vak aspashtata 10 33.33 %

Shiraha shoola 07 23.33 %

Bhrama 02 6.7 %



All the cases were reported with the pradhana lakshana of Pakshaghata i.e.

Akarmanyatva of half of the body and 1 (3.33%) patient was reported of shakti hrasata of

half of the body. 10 patients (33.33%) each were reported with chesta kshaya and vak

aspashtata, 12 (40.00%), 7 (23.33%), 2 (6.70%)patients were reported with vak sanga,

shiraha shoola, bhrama respectively.

RESULTS : 30 patients were studied in three groups with 10 patients in each. Group A patiets

were treated with Abhyanga, Swedana, Snehana and Naysa. Group B patients were

treated with shamana, Abhyanga and Swedana. Group C patients were treated with only

shamana chikitsa.

The results obtained in all the three groups were assessed on the basis of

Rankin’s disability scale, Barthel index, NINDS, Hb%, RBS, Serum cholesterol, serum

triglycerides, HDL, LDL, VLDL, Serum urea and Serum creatinine.

Table No. 50 : Statistical analysis of assessment parameters in group A. Parameter Mean S.D. S.E. t-value P-value Remarks

NINDS 4.0 1.414 0.447 8.948 < 0.001 H.S.

Barthels 23.5 4.743 1.5 15.66 < 0.001 H.S.

Rankins 1.2 0.4216 0.1333 9.00 < 0.001 H.S.

Hb % 1.6 0.699 0.222 7.207 < 0.001 H.S.

R.B.S. 15.3 9.649 3.051 5.014 < 0.001 H.S.

Serum cholesterol

39.7 38.51 12.182 3.258 < 0.001 H.S.

Serum Triglycerides

28.8 24.48 7.743 3.719 < 0.001 H.S.

H.D.L. 3.8 1.619 0.512 7.421 < 0.001 H.S.

L.D.L. 11.3 9.499 3.00 3.766 < 0.001 H.S.

V.L.D.L. 3.1 2.131 0.674 4.599 < 0.001 H.S.

Serum Urea 3.9 2.183 0.69 5.652 < 0.001 H.S.

Serum Creatinine

1.4 0.699 0.221 6.334 < 0.001 H.S.



All the assessment parameters in group A showed a significant improvement and

the statistical analysis showed that the improvement is statistically highly significant

(p<0.001).

Table No. 51 : Statistical analysis of assessment parameters in group B

Parameter Mean S.D. S.E. t-value P-value Remarks

NINDS 4.8 0.788 0.249 19.277 < 0.001 H.S.

Barthes 40.00 17.32 5.477 7.303 < 0.001 H.S.

Rankins 1.7 0.483 0.152 11.184 < 0.001 H.S.

H.b.% 2.7 0.6749 0.213 12.676 < 0.001 H.S.

R.B.S. 10.4 7.705 2.436 4.267 < 0.001 H.S.

Serum cholesterol

14.4 10.469 3.31 4.34 < 0.001 H.S.

Serum Triglyseriods

11.6 5.66 1.79 6.48 < 0.001 H.S.

H.D.L. 4.5 1.5811 0.5 9.00 < 0.001 H.S.

L.D.L. 14.9 9.848 3.114 4.78 < 0.001 H.S.

V.L.D.L. 2.9 1.728 0.546 5.311 < 0.001 H.S.

Serum Urea 3.4 2.011 0.635 5.354 < 0.001 H.S.

Serum Creatine

2.0 0.816 0.258 7.75 < 0.001 H.S.



(p<0.001).



Table No. 52 : Statistical analysis of assessment parameters in group C.

Parameter Mean S. D. S. E. t-value p-value Remarks

NINDS 8.3 1.828 0.578 14.35 < 0.001 H.S.

Barthels 69.0 13.49 4.268 16.16 < 0.001 H.S.

Rankins 1.8 0.421 0.133 13.533 < 0.001 H.S.

H.b.% 2.9 1.911 0.604 4.801 < 0.001 H.S.

R.B.S. 18.6 21.27 6.728 2.764 < 0.001 H.S.

Serum cholesterol

7.0 7.149 2.26 3.097 < 0.001 H.S.

Serum Triglyseriods

14.3 9.546 3.018 4.738 < 0.001 H.S.

H.D.L. 6.2 4.131 1.306 4.747 < 0.001 H.S.

L.D.L. 9.6 11.616 3.673 2.613 < 0.001 H.S.

V.L.D.L. 3.9 2.923 0.924 4.22 < 0.001 H.S.

Serum Urea 3.2 2.043 0.646 4.953 < 0.001 H.S.

Serum Creatine

2.3 1.337 0.422 5.45 < 0.001 H.S.



(p<0.001).


Discussion on Observations 118

DISCUSSION ON OBSERVATIONS

For the clinical trial 33 patients were taken, out of these 3 patients were

discontinued the treatment during various stages of the study. Among the 3 patients, one

patient discontinued the treatment during the snehapana i.e. on the 5th day of the

treatment because of intolerance to the smell of the sneha. The cause of discontinuation

of the treatment of other two patients was obscure. So, the clinical study was carried on

30 patients only

Availability : All the cases were reported in D.G.M.A.M.C. P.G.A.R.C. hospital, Gadag. All of

them had an established clinical diagnosis. Before entering into the study, 27 patients had

the emergency treatment and different doctors treated 3 patients with Ayurvedic medicine.

Education : Majority of the patients were illiterate. Some of them had only primary and

secondary education. Four of them were graduates. This study only is made to observe

the relationship of the Pakshaghata with the educational level. The literate have

awareness and better position to understand the disease and follow the prescribed rules

and regulations.

Age : As it is known that majority of the patients had cerebrovascular accidents in the old

age, it was confirmed in this study that the maximum number of the patients were above

the age of 50 years.

Sex : It is evident that males are more prone to get hypertension, which may end up in

cerebrovascular accidents. This present study reports indicate that male (21) sufferers

are more than female (09) sufferers. The probable cause may be the expose to more

stress and strain. 1

Marital status : All the patients were married. None of the case was reported as unmarried. It is

because of age group of patient approached for the treatment was in between 40 to 70

years. No relation can be attributed to this disease.

Religion : The maximum numbers of patient reported were of Hindus (24), 5 of them belong

to Muslim and 1 case of Christian community was reported. It does not mean that Hindus

are prone to get this disease. It may be due to the method of sampling



Occupation: 8 patients reported were farmers, 8 patients were housewives, 3 patients were

businessmen, drivers and the jobholders, and other workers were 5 in numbers. More

number of patients were farmers and they had more physical stress and strain and it

might have led them to hypertension leading to Pakshaghata.

Economical status: Maximum numbers of patients (19) were of medium economical status , 6 were of

poor status and 5 patients reported higher economical status. It reveals that the

socioeconomic status of patients has significant role in this disease.

Habitat: More number of the patients i.e. 16 was from rural area and 14 were from urban

area. Urban people may have the more incidences due to the lack of exercise. But, in this

study it is very difficult to draw any conclusion on this basis.

Food habit: In this clinical study, it was observed that most of them belong to the non-

vegetarian group i.e. 16, where as 14 were reported as mixed. High calorie diet is more

prone to cause atherosclerotic changes and hypertension, which is said to be important

risk factors causing the hemiplegia. 2

Rasa satmya : Maximum number of patients (15) reported were taking pravara rasa satmya ahara

9 patients reported were of madhyama rasa satmya and 6 patients were of avara rasa

satmya. Rich calorie diet patients are more prone to get stroke. Roga prarambhakala : (Onset of the disease)

10 patients were having the sudden onset of the disease and 20 patients were

having the gradual onset; this can be attributed to the pathology of the thrombus formation

along with the risk factors. Onset varies from person to person with the site of lesion.

Time of onset of the disease: 15 patients were having the symptoms at prataha kala, 9 patients were having the

stroke at nighttime, 3 patients had at nidra kala and dina kala. None of the patients had

the disease at gamana kala and krodha kala. This information holds good as per as this

clinical trial is concerned. Pakshaghata is one of the vata prakopajanya disorders. Hence,

the time of onset of the disease noted at prataha kala. 3



Chronicity of the disease: Most of the patients reported with the less chronicity (60%), the reason could be

the people knowing the severity of the disease and trend towards to the Ayurvedic

treatment modalities.

Family history : Only two patients were reported with the family history, reason could not be

evaluated, as the sampling method is incidental.

Habits : 11 patients having the habit of smoking, alcohol, tobacco chewing and 14 patients

with chinta were observed. The habits are major risk factors for the stroke. Hence,

alcohol, smoking and tobacco are the main provoking factors for the stroke by making the

atherosclerotic changes.4

Risk factors: Maximum number of patients was reported with the risk factors like hypertension

(24), diabetes (6) and hyperlipidaemia (4). It is observed that hypertension, diabetes, and

hyperlipidaemia are the main risk factors for the stroke. Elevated systolic and diastolic

blood pressures have strong association with ischaemic stroke, which may be due to

increased blood lipids.

Only one case had presented with stroke after the attack of epilepsy. The

ischaemic brain is predisposed to more damage from seizers. It is evident that epilepsy is

also a risk factor for stroke.

General condition of the patient : More numbers of the patients were reported with moderate health conditions

Where as 7 patients were reported with good health conditions. Rest of the patients were

reported with worst health status, old age and severity of the disease. This has strong

relation with prognosis of the disease.

Side affected : 15 patients of each side were reported during the study. Here no conclusion can

be made because, the patients were selected incidentally.

Prakriti : Deha prakriti of the patients were assessed based on the major physical,

pathological and behavioral features. No patients having eka doshaja praktiti were

observed. 23 patients had dwandwaja prakriti. 7 were of sannipatika. Maximum numbers



of patients were of vata-pitta pradhana prakriti. Reason could be the Pakshaghata itself as

a vata pradhana and pittanubandhi, which supports the classics.

Satwa : More number of the patients 21 was reported with madhyama satwa, 7 were of

avarasatwa and only 2 were of pravara satwa.

Bala : More number of patients (19) was reported of madhyama bala. Avara bala of 4

patients, pravara bala of 7 patients. Pravara bala patients were prone to cure fastly than

the avara bala.

Agni bala : Majority of the patients belongs to the mandagni (22).

Vyayama shakti : There are 18 patients were reported of avara vyayama shakti, where as 11

patients were reported of madhyama vyayama shakti and 1 patient with pravara vyayama

shakti. It is assessed on the basis of nature of work.

Nidra : More number of patients having alpa nidra (25) and rest of them were having

vishama and anidra. This may be due to the stress and strain because of their life style.

Vaya : More number of the patients were of Vardhakya group (18). 12 patients were

reported of madhyama vaya group. This clinical study shows the incidence of disease in

vardhakyavastha.

Desha : All the patients were belonging to jangala desha where the aggravation of vata is

more and this could be the reason for getting the patients from jangala desha.

Bhara : 12 patients were reported with obesity i.e. 70-80 kg. 8 patients were with the 60-70

kg. 10 patients were with the weight 50-60 kg. This indicates the significant role of obesity

as a risk factor in Pakshaghata.

Blood pressure: In the present clinical study maximum number of patients (26) were with the

elevated blood pressure i.e. 160/90-180/100 mm of Hg.Hence there is linear correlation

between the hypertension and stroke.



Nidana : All the nidanas, which help in the manifestations of the disease of Vata vyadhis,

were observed in this study. In our classics there is no direct reference regarding the

cause of Pakshaghata. But, the high calorie diet which precipitates as a predisposing

factor of Pakshaghata.Atherosclerotic changes of the vessels, HTN, DM, etc are to be

considered as nidana for disease. So the maximum, 16 patients were observed with the

indulgence of Vata kaphakara ahara vihara. 13 patients with vatapittaja nidana and one

patient with vataja nidana sevana were observed.

Poorva roopa : Pakshaghata being the vata vyadhi it may occur all of a sudden by the ashukaritwa

of the vikrita vata. Hence, majority of the patients (i.e. 25) were of sudden onset of the

symptoms where as rest of 5 patients were represented with few nonsignificant prodromal

symptoms like bhrama, suptata, shira shoola, etc.

Roopa (Lakshanas of Pakshaghata) : Grahana, dharana shaktihani and cheshta nivritti are the cardinal symptoms of

Pakshaghata. This was observed in all cases. Along with this some patients were

associated with symptoms like cheshta kshaya (10 patients), vak stamba (12 patients),

vak aspatata(10 patients), shira shoola (7 patients) and bhrama (2 patients).

Type of Pakshaghata: Vata-kapahakarajanya Pakshaghata (15) were more dominantly seen and 13

patients with vatapittaja type and 1 patient of shuddha vatajanya Pakshaghata was

observed during the study.

Observation on Lab reports : Among 30 cases 4 patients showed high level of lipids in the blood i.e. elevated

triglycerids, low-density lipids and no variation in the serum creatinine was observed.

Where as, 17 cases were reported with decreased heamoglobin level i.e. less than

10 grams percentage, less percentage of the haemoglobin might be the cause for the

stroke.

CT brain : All 30 patients were showed the different lesions of the brain vessel occlusion led

to infarctions. More number of cases left and right MCA territory infarctions, sylvian, frontal

region, parietal, periventricualr infarcitons, pons, internal capsule infarction, PCA, ACA

territory infarction, coadate nucleus, gangliocapsular lesion, fronto-parietal, cerebellar

infarctions, were observed in this clinical study. CT scan reveals the exact lesion of the



infarction like large infarctions, lacunar infarctions and different areas of the brain lesions

and also prognosis of the disease. Hence, CT scan of brain is needed for diagnosis,

prognosis and treatment.

GENERAL OBSERVATIONS During the clinical trail the observations were made in the every step intervention.

Deepana – Pachana : All 30 patients were received the deepana and pachana with Trikatu churna had

showen agni deepti, shareera laghuta and vatanulomana. Some patients showed the

udardaha in such case advised take the more water.

Snehapana : 16 patients were received the madhyama matra snehapana (4-5 days) and 4

patients were received the 3 days avara matra snehapana. None of them received the

uttama matra of snehapana.

During the snehapana observation made on jeeryamana, jeerna and samyak

snigdha lakshana. Out of 20 cases 4 patients were of females received the avara matra of

snehapana. During snehapana vatanulomana, agni deepti and snigdha varchas were

noticed. Patients had the good sleep and blood pressure reduced.

Abhyanga and swedana : All the 30 patients were received the Abhyanga and swedana karma of 20-30

minutes for 90 days with Bala taila on sarva shareera more importance given to the

affected part. During this period in 3 patients Angamarda, Jwara were noticed and

Abhyanga and swedana was discontinued. Then same therapy was continued during this

course most of the patients attained the Shareera laghuta, Tanumardavata. Marked

improvement was observed in 3 patients mild elevation of blood pressure was noticed

immediate after snehana and swedana. Gate of the patient was improved during the

processes of treatment.

Virechana : On the basis of matra of snehapana dose of the virechana was fixed based on the

koshta i.e. 30-50 ml. 16 patients were received the 50 ml of virechana yoga and 30 ml in 4

patients. Virechana was given with luke warm water between 7-8 am. in the same

patients. Nausea, uneasiness were noticed after administration of virechana yoga. were

observed during this process.



After these procedure 18 cases attained the samyak virechana lakshanas in 2

cases Agnimandya, Aruchi and Shareera guruta were noticed except 2 cases in all the

patients madhyama shuddhi lakshana observed.

Nasya karma : 20 patients were received the nasya karma with Ksheerabala taila 101 for 7 days. After

the consequent one month of virechana therapy.

During this procedure 18 cases were attained the shareera laghuta good sleep in

most of the patients after the nasya karma. It is observed that pertaining to the motor

function improved. 2 cases developed with Sirogourava, Tandra, Kasa, etc laskhana. No

other complications were noticed during this therapy.

Shamana : 20 cases received the shamana i.e. Pakshaghatari yoga with Madhu as anupana

the application of shamana dravya on and beneath the tongue. During this procedure two

patients immediately got vomited twice. It may be due to the taste and smell of the yoga.

In these the case the yoga was administered with milk. 4 patients were showed the

Vibhanda these patients were advised to take more water.

During the shamana administration increased appetite was noticed. Improvement

in the motor function, Vak aspashtata, Vak sanga, Bhrama also responded. No

complications were observed during the shamana therapy. It is noticed that reduction in

the elevated blood pressure, blood sugar and blood lipids.


Discussion on Results 125

DISCUSSION ON RESULTS

Results are interpreted statistically analyzing grading given for the signs and

symptoms mentioned in the assessment criteria i.e. NIH- NINDS, Functional status scale

i.e.Barthel Index. Finally over all assessment was made by Rankin’s disability scale,

before and after the treatment. The results of the study showed that multi faceted therapy

is very effective in the management of Pakshaghata.

Best motor arm and leg:

Strength of the muscles was slightly improved after virechana, which was

statistically significant with p value < 0.01. Grade 4 to grade 3.

After Nasya procedure the muscles showed further improvement significantly with

p value < 0.001. Patients showed improvement from the grade 4 to grade 2.

After shamana the muscles power improved which was highly significant i.e. p value

< 0.001.

After 3 months of the complete treatment schedule muscle power increased as follows –

7 patients of grade 4 improved to grade 3




Group C showed the highly significant changes after the shodhana and shamana

therapy than the group A and group B. It may be due to shodhana of vikrita dosha. Vata

may be pacified after shamana by the use of vata shamaka dravyas.

Best language :

Mild improvement was seen after the virechana and nasya karma showed

statistically significance. After compete shodhana and shamana treatment slight

improvement was observed in the speech i.e. significant with p value < 0.01.



After complete treatment best language showed mute (03), severe aphasia (02),

mild / moderate aphasia (01).

Out of 12 patients of aphasia (Vak snaga) showed following changes after

complete treatment schedule of 3 months –

06 patients with mute (03) improved to severe aphasia (02).

06 patient with mute (03) improved to mild / moderate aphasia (01).

Out of 10 patients of dysarthria (Vak aspatata) showed following changes after

complete treatment schedule of 3 months –

06 patients with near unintelligible or worse condition (02) improved to mild /

moderate dysarthria (01).

04 patients with near unintelligible or worse condition (02) showed no

improvement.

Functional status scale (Stroke severity scale) :

Barthel index score results are interpreted with statistical grading given for signs

and symptoms mentioned in the assessment criteria. The result of the study showed that

the multi faceted action of the treatment is very effective in the management of

Pakshaghata.

Functions like feeding, wheel chair or bed transfer, personal toilet, grooming,

bathing, walking, staring (ascending and descending), dressing – undressing,

bowel control and bladder control showed improvement from D0 to D90 was

significant in all the three groups.

Mean of the Barthel index in group A is 23.5, group B is 40.0 and in group C is

69.0. Hence, the treatment protocol of functional status scale showed the

significant changes.



Rankin’s disability scale :

Rankin’s disability scales are interpreted the grading analyzing statistically for the

signs and symptoms mentioned in the assessment criteria before and after the treatment

was evaluated.

Grades of the disability scales were improved after 30, 60 and 90 days showed

statistically significant with p value < 0.001 with grade V to grade IV, grade IV to grade III,

grade III to grade II.

The mean of the Rankin’s score in-group A was 1.2, group B was 1.7 and in group

C was 1.8.

The Rankin’s disability scale showed highly significance in-group C.

At the time of treatment no patients had reported with reattach of stroke. No

complications were observed during the course of treatment. The clinical study showed

statistically highly significance with p value <0.001.

Assessment of blood pressure that is systolic blood pressure showed statistically

significant after virechana with p value < 0.01. After abhyanga and shamanoushadhi it

was highly significant with the p value < 0.001. Assessment of diastolic blood pressure

was highly significant with p value <0.001 after virechana.

The possible cause for such significance can be traced in the following reasons.

This can be attributed to the srotovishodhana (by dilating the constricted vessels) property

of tila taila, which also controls the vata. Virechana reduces dravata of pitta and rakta,

there by volume of the blood will be decreased. Lower the blood volume; lower the cardiac

out put and also the risk of rupture of blood vessels. Virechana does the mana, indriya

prasadana and so may be acted on the increased sympathetic activity. After abhyanga

and shamanoushadhi it was just significant.



Over all assessment :

In this clinical study special observation made on the three groups based on the

blood investigations and CT brain and also positive effect of treatment in all the cases –

Group A –

05 patients showed mild improvement as per the Barthel index, NINDS and

Rankin’s scorings. It may be due to old age, many risk factors such as – HTN, DM,

approach to treatment after 40-60 days etc. The above cases CT reveals large

infarcts due to occlusion of the MCA territories with old infarcts could be the cause

for mild improvement.

3 patients were responded moderately. It may be due to less risk factors and

having a shareera bala and manaseeka baladhikyata. Their CT shows other than

middle cerebral territory infarctions like fronto-parietal, parieto-occipital; cerebellar

infarctions, etc. could be the cause for the moderate improvement.

2 cases were also responded markedly. It may be due to less risk factors and

having a lacunar infarcts that could be the reason for the moderate improvement.

Group B –

5 patients were responded with mild improvement in NINDS, Barhtel’s index,

Rankins functional status scale. Above patients were having moderate risk factors;

large infarcts in gangliocapsular, fronto-temporal, parital region, lentiform nucleus,

cerebellar artery, and PCA territory lesions infarctions could be the cause for the

mild improvement.

3 patients were responded moderately in the assessing scale having less risk

factors. Their CT showed left fronto-parietal region infarction involving internal

capsule, which could be the cause for moderate improvement.

2 patients were markedly responded in scoring having least risk factors, shareerika

and manaseeka baladikyata, proper follows up and their CT involving



periventricular infarctions could be the cause for the marked improvement in the

scoring.

Group C –

3 cases were responded with mild improvement in the scoring due to more risk

factors having old age and CT shows MCA territory infarctions with occipito-parital

periventricular infarctions, basal ganglionic infarctions that could be the cause for

the mild improvement.

4 cases were responded significantly. It may be due to less risk factors included in

the trials early i.e. within 30 days of the stroke and having fronto-parital, ventricular

infarctions could be the cause for the significant improvement.

3 patients were markedly improved in the assessment grading. It may be due to

the less risk factors like adhika shareeraka and manaseeka bala and the CT

shows Anterior cerebellar artery infarction, external capsular and basal ganglionic

infarctions, fronto-temporal lanteforum nucleus infarction, could be the cause for

the best motor arm functions, language improvement and also independently to

carry their day-to-day activities.

More number of patients was recovered from severe bed ridden to best motor

functions. It could be because of the infarction other than MCA i.e. PCA, ACA temporal

regions were responded in both arms and leg motor functions. In this clinical study more

patients were able to walk with support and independently, whereas less number of the

patients got the arm motor functions. Mild to moderate motor function seen in the upper

limbs. The cause could be the size, area of the lesions.



Rankin’s disability scale :

Results were as follows –

06 patients were severe disability, bed ridden, incontinent and require constant

nursing care and attention.

04 patients were unable to do several day-to-day activities without assistance. But,

still they use to do some activities by self-disability and unable to carry out.

10 patients were had slight disability and unable to carry out some previous

activities, but able to look after own affairs without much assistance.

07 patients were responded by the disability, able to walk without assistance

03 patients were no significant disability and able to carry out all usual activities of

the day-to-day life.

131

INTER GROUP COMPARISION

Results obtained in-group A, B and C was compared using least significance

difference as per ANOVA test.

The least significance (L.S.D.) can be calculated by using formula

L.S.D.= t 5% √ 2 S2 \ K

Where t 5% is t-table value for error degrees of freedom at 5%

K is number of observation in each group

S2 is mean squares within groups.

Here L.S.D value is 1.523

Table No. 50 : Showing the ANOVA for NINDS

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares

F-Value P-Value Remarks

Between groups

2 145.67 72.63

Within groups

27 74.6 2.762

26.29

<0.01

H.S.

Total 29 219.867 ---

Table No. 51 : Showing least significance difference of groups for NINDS.

Group Mean gain

Difference from Group A

Difference from group B

A 8.1 -- --

B 6.3 1.8 --

C 2.8 5.3 3.5

132

Comparing the mean differences with the critical difference (Table 50 and 51) the

group C differs significantly from the group B and A. The conclusion for the parameter

NINDS Can be made as

1. Group A, B and C are not alike.

2. The least group mean effect is 2.8 in the group C (The patient is said to be

improved due to decreased grading after the treatment).

3. Hence if a choice is to make among the three groups, in parameter NINDS group

C is most effective than the group A & B. Moreover if a choice is made between

group B and group A that are differ significantly the group B is preferred (as

compared the mean in table 51).

Table No. 52 : Showing the ANOVA for Barthel’s Index.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 9215.00 4607.5

Within groups

27 3605.00 133.518

34.508

<0.01

H.S.

Total 29 12820.00 ---

Table No. 53 : Showing the least significance difference of groups for Barthel’s

Index.

Group Mean gain

Difference from Group C


C 87.0 -- --

B 60.5 26.5 --

A 44.5 42.5 16.00

The least significance( L.S.D.) can be calculated by using formula L.S.D. is 10.593

133



Barthels Can be made as


2. The highest group mean effect is 87.00 in the group C (The patient is said to be

improved due to increased gradings after the treatment). .

3. Hence if a choice is to make among the three groups, in parameter Barthels group

C is most effective than the group A & B. Moreover if a choice is made between

group B and group A that are differ significantly the group B is preferred (as

compared the mean in table 53).

Table No. 54 : Showing the ANOVA for Rankin’s disability scale.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 4.2 2.1

Within groups

27 6.1 0.225

9.33

<0.01

H.S.

Total 29 10.3 ---

Table No. 55 : Showing the least significance difference of groups for Rankin’s

Disability scale.

Group Mean gain



A 3.7 -- --

B 3.4 0.3 --

C 2.8 0.9 0.6

The least significance (L.S.D.) can be calculated by using formula L.S.D. is 0.434

134



Rankins Can be made as

1. Group A,B and C are not alike.


improved due to decreased gradings after the treatment).

3. Hence if a choice is to make among the three groups, in parameter Rankins

group C is most effective than the group A & B. Moreover if a choice is made between

group B and group A that are differ significantly the group B is preferred (as compared the

mean in table 55).

Table No. 56 : Showing the ANOVA for H.D.L.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 290.86 145.43

Within groups

27 911.806 33.77

4.306

<0.05

H.S.

Total 29 1202.66 ---

Table No. 57 : Showing the least significance difference of groups for H.D.L.

Group Mean gain



C 41.5 -- --

B 39.4 2.1 --

A 34.1 7.4 5.3


135



H.D.L. Can be made as

1.Group A,B and C are not alike.

2.The highest group mean effect is 41.5 in the group C (The patient is said to be

improved due to increased readings after the treatment).

3.Hence if a choice is to make among the three groups, in parameter H.D.L. group C

is most effective than the group A & B. Moreover if a choice is made between group B

and group A that are differ significantly the group B is preferred (as compared the

mean in table 57).

Table No. 58 : Showing the ANOVA for Serum Urea.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares

F-Value

P-Value Remarks

Between groups

2 104.06 52.03

Within groups

27 374.9 13.88

3.748

<0.05

H.S.

Total 29 478.96 ---

Table No. 59 : Showing the least significance difference of groups for Serum Urea.

Group Mean gain



C 21.5 -- --

B 25.6 8.8 --

A 21.6 12.8 4.00

The least significance( L.S.D.) can be calculated by using formula L.S.D. is 3.41.

136



Serum Urea Can be made as

1.Group A,B and C are not alike.

2.The least group mean effect is 34.4 in the group C. (The patient is said to be

improved due to decreased readings after the treatment).

3.Hence if a choice is to make among the three groups, in parameter Serum Urea

group C is most effective than the group A & B. Moreover if a choice is made between

group B and group A that are differ significantly the group B is preferred (as compared

the mean in table 59).

Table No. 60 : Showing the ANOVA for Hb %.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares

F-Value

P-Value Remarks

Between groups

2 1.866 0.933

Within groups

27 39.1 1.448

0.64

>0.05

N.S.

Total 29 40.966 ---

The inter group comparison of Hb % showed not much significance. (p>0.05).

137

Table No. 61 : Showing the ANOVA for R.B.S.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares

F-Value

P-Value Remarks

Between groups

2 147.8 73.9

Within groups

27 20789.4 769.97

0.095

>0.05

N.S.

Total 29 20937.2 ---

The inter group comparison of R.B.S. showed not much significance. (p>0.05).

Table No. 62 : Showing the ANOVA for Serum Cholesterol.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares

F-Value

P-Value Remarks

Between groups

2 5904.6 2952.3

Within groups

27 10020.9 371.144

7.954

<0.05

H.S.

Total 29 16003.5 ---

Table No. 63 : Showing the least significance difference of groups for Serum

Cholesterol.

Group Mean gain



C 144.2 -- --

B 151.4 7.2 --

A 176.9 32.7 25.5


138

Comparing the mean differences with the critical difference ( Table 8a and 8b) the


Serum Cholesterol Can be made as



improved due to decreased readings after the treatment).

3. Hence if a choice is to make among the three groups, in parameter Serum

Cholesterol group C is most effective than the group A & B. Moreover if a choice is

made between group B and group A that are differ significantly the group B is

preferred (as compared the mean in table 8b).

Table No. 64 : Showing the ANOVA for Serum triglycerides.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 3759.2 1879.6

Within groups

27 23547.6 872.13

2.155

>0.05

N.S.

Total 29 27306.8 ---


Table No. 65 : Showing the ANOVA for L.D.L.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 4791.8 2395.9

Within groups

27 32746.9 1212.84

1.975

>0.05

N.S.

Total 29 37538.7 ---


139

Table No. 66 : Showing the ANOVA for V.L.D.L.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 19.466 9.733

Within groups

27 806.4 29.86

0.327

>0.05

N.S.

Total 29 825.86 ---


Table No. 67 : Showing the ANOVA for Serum creatinine.

Source of variation

Degrees of freedom

Sum of Squares

Mean Sum of Squares


Between groups

2 13.866 6.933

Within groups

27 59.1 2.188

3.168

>0.05

N.S.

Total 29 72.966 ---


Table No. 68 : Showing the coefficient of variations.

Parameter Group A Group B Group C Conclusion

L.D.L 28.2 32.42 16.16 Group C is consistent

Hb% 8.75 6.8 6.8 Group C and group B are

consistent

Barthels 9.33 28.01 8.6 Group C is consistent

The Barthels and L.D.L. are more consistent in-group C and H.B.% is having equal

consistency in group B and group C. (by comparing the coefficient of variation values from

table 68).

Individually, all the three groups are shows highly significant in all the parameters.

However over all there is high significant in group C in parameters Barthels and Rankins.


Mode of Action of Therapies 140

MODE OF ACTION OF THERAPIES

MODE OF ACTION OF SNEHA

Literally “sneha” means to oleate or to make smooth. The process which produces

the sneha (i.e. unctousness), vishyandana (fluidity), mrudutwa (softness) and kledana

(smoothness) in the body is known as sneha karma . 1

Acahrya Charaka has clearly mentioned in the 13th chapter of sutrasthana before

going to procedure like vamana, virechana the snehana and swedana procedures should

be performed.2

Before starting the therapy physician should procedure the drug required for the

oleation and antidotes which will be helpful to manage complications. 3 On administering

snehana vata gets alleviated, while explaining the karmukta of shodhana Process.

Twak indriya is the main seat of vata dosha. Application of taila pacifies the vata-

kapha and promotes the muscles of affected site and initiates bulk and decreased

muscles tone by venture with the physical effects.4 Snehana karma is the poorvakarma of

the panchakarma, which will mitigate doshas and oleate the koshta which is more

utklishta also. Recent studies show that some of the pathological biochemical elements,

such as atheroma, amyloid, are only fat-soluble. Hence, snehapana dissolves the

metabolic wastes.

Sneha karma is the poorvakarma of the panchakarma.

MODE OF ACTION OF ABHYNAGA

Abhynaga or oil massage softens the skin makes the movements free and

increases the circulation of the blood to the muscles and helps in speedy removal of the

metabolic waste products through the skin.

Abhynaga or massage relieves the distress of illness by modifying sympathetic

nerve activity and



Encouraging the activity by parasympathetic nerve, which has the relaxing effects.

Shastrokta abhyanaga does the manipulation of the muscles, assists in the blood

circulation, lymphatic circulation etc. In Pakshaghata ,abhyanaga helps to reduce and to

prevent the spasticity and rigidity in joints as well as muscles. Also further muscles

wasting can be prevented.

Hypothetically blood amino acids like, triptophan increases after the massage.A

increase in plasma tryptophan subsequently causes a parallel increase in the

neurotransmitters (chemical between nerve ending and muscle) at motor end plates, and

serotonin which is made from the triptophan has been implicated in several psychiatric

diseases with low values of metabolite found in reaserches in depression and

schizophrenia. So by abhynaga blood circulation is increased. 5

MODE OF ACTION OF SWEDA

Swedana is one among the Shadvidhopkramas1. Swedana it self is a remedy for

wide range for diseases like vata-kapha dominance2. It is preoperative procedure in

panchakarma. In case of snigdha sweda additive effects due to the brimhanatwa of

snigdha dravya, snigdha guna gives smoothness to the body parts, strengthens the body

parts and guru guna the taila does the brimhana.

Swedana clears the srotodushti or sanga. The area in contact get more circulation,

relieves stiffness3 and variety of obstructions by widening of the pores which allows the

easy movement of the liquefied solid or semisolid materials.

Pharmacologically, it is evident that the drugs in oil or other lipid caring substances

can penetrate the epidermis. Heat temporarily changes the position of the cells in the

stratum corneum, creating channels that allow the drugs to penetrate.

MODE OF ACTION OF VIRECHANA

Virechana is a specific procedure among the panchakarma. Which eliminates

pitta dosha. It is indicated in pitta and kapha dosha vikaras and also in case of entry of



kapha dosha in pitta sthana 1 According to Kashyapa, virechana does the indriya shuddhi.

2 In Yoga Tarangini it is said that virechana gives indriya bala, dhatu sthirata, bala and

agni deepana.3

As virechana dravyas are having the gunas like ushna, teekshana, vyavayi, vikasi,

and adhobhagahara.4 Pakshaghata is vata pradhana vyadhi and in condition pitta and

kapha also seen. The action of virechana is helpful to make the adhogamita of doshas

and rakta shuddhi.

Even though Pakwashaya is the main seat of vata ,in Pakshaghata, mashtishka or

majja or mastulunga is involved. Vata sthana i.e. pakwashaya is much important because

in Sushruta, Dalhana commented that majja dhara kala is nothing but pittadharaa kala.

Seat of pittadhara kala is in grahini and pakwashaya. Hence, pakwashaya shodhana is

relevant. Charaka and Vagbhata indicated virechana as specific shodhana for

pakshaghata. 5 Jejjata commented on this says that snehayukta swedana, snehayukta

virechana, should be given. Snehana and swedana facilitates the transportation of malas

accumulated in various parts of the body including the target organ of pakshaghata i.e.

mashtishka. As mentioned in chikitsa aspect ,sneha virechana is indicated and also

mrudu virechana is preferable. Eranda taila is considered to be the best virechana dravya

in vata vyadhis.

Vagbhata has followed the Charakas line of treatment, but has adviced snehana

and snigdha virechana. Eranda taila6 and Tilwaka grita are best for virechana. Charaka

seems to have concentrated on the involvement of pranavata and vyana vata and has

recommended the same treatment of snigdha virechana in vyanavrita prana.

Snigdha, mrudu shodhana is adviced to expel out the malas which release the

srotosanga and does the anulomana of Vata.

Sira ,snayus are the uapadhatus of rakta. In pakshghata the main involvement of

siras and snayus dushti is seen. Rakta shodhana by virechana is preferable than the other



shodhanas. Rakta shodhaka property of virechana restores the rakta prasarana to the

mashtishka, which may relieves the blockage of brain arteries and may take part in

reducing the cerebral oedema by restricting body fluid.

Virechana is the line of treatment in mamsa pradoshaja vikara. In pakshaghata

there is evident involvement of mamsa kshaya. (Ch. Su. 24)

Besides the snigdha ahara dravyas are digested in pakwashaya, during

pakwavastha and processes such as digestion and absorption. Here, for the maintenance

of the structural status of the vatavaha samsthana and vatavahanadis the end products of

both protein and fats are being absorbed in gut. The main site of maximum absorption of

digested materials is pakwashaya which are needed for Vatavaha samsthana.

The two theories put forward Yu J in 1980 in management of neuronal damage are

reorganization and reestablishment. These two supports the pakwashaya shodhana by

virtue of virechana and basti.

It can be presumed that excitatory amino acids which cause the neurons damage

,are inhibited by the process of virechana.

The same study on pashaghata by Dr. M. M. Tilaka of Nagpur (Rheumatism Vol.

15 March 98). A study of 50 cases of pakshavadha was observed that vatakaphaja type

cases were well responded where as vatapittaja cases were moderately relieved and

shuddha vataja cases did not show any response. Dr. Bheem Bhat, Dr. C.P.Shukla, Dr.

Gurudeep Singh, & Dr. A.K.Patel – Pakshaghata a clinical study by them showed better

effect on the symptoms of pakshaghta, muscle power was increased markedly. Subjective

and objective parameters were also noticed marked improvement.

Oil is non-irritant one. When it reaches to duodenum, it’s surface tension reduces

(saponification) and converts into ricinoleic acid by pancreatic juice, which irritates the

bowel and stimulates the intestinal glands and muscular coat and causes purgation.

Hence, castor oil is the cheapest simplest and most important useful purgative of the



pharmacopia in all delicate conditions for children and old peoples.7 Snehana does the

vata shamana and virechana does the vatanulomana and vata pittaharana. Multi effect of

virechana can act on pakshaghata without any side effect. Exact mode of action needs

further studies.

MODE OF ACTION OF NASYA

Teekshna pradhamana and avapeedana nasyas are indicated in the impaired

consciousness conditions of Pakshaghata. Sneha nasya is helpful in Pakshaghata.

Sushruta explained the nasya karma in his commentary. But which type of nasya

is preferable in different Pakshaghatas, is not explained

In Pakshaghata (Ischaemic stroke) most of the patients will have the facial

paralysis. Hence it is better to consider the Charaka’s Ardita chikitsa 1 to explain the

mode of action of the nasya, in which the tarpana nasya,2 which is a part of the brumhan

A nasya,is preferred because acharya has explained, increased vayu is seen in

vata vikaras. In this particular condition also Astanga hridayakara has advocated the

bhrumhana as the treatment modality, which explains the treatment of the Ardita. Acharya

Charaka used the word tarpana in the shloka, Chakrapani commented over it as Tarpano

navana bheda and we get the reference from the part where in the management of

atiyoga of virechana nasya tarpana nasya is done. Chakrapani has commented that in

atiyoga of viechana nasya there is increase of vata seen. In this particular condition

acharya has advised to give tarpana nasya which suits the condition in Ardita or facial

paralysis due to infarctions.

Ksheera bala taila is mrudu , bhrumhan in nature which equals to tarpana. In

Astnaga sangraha Vagbhata cleared the mode of action of nasya is through the

Sringataka marma. Interestingly Sringataka marma is a meeting point of nutrient vessels

to nasa, akshi, karna and mukha. 3 Hence, it clears that the dosha nirharana takes place

through this way. And the santarpana must occur through the same way. The Sringataka



marma as discussed earlier is the opening of nutrient vessels to the four senses i.e. nasa,

akshi, karna, mukha where spreading of the oushadha dravya starts. So, the nasya plays

a major role in the treatment of pakshaghata.

Nose is the only place in CNS which is directly open to the external environment.

[NASA HI SIRASO DWARUM]. 4 Each olfactory receptor is a neuron. Therefore either to

stimulate or tickle the mucous membrane to cause beneficial effect in the CNS, nasya

karma is the best method of treatment in Pakshaghata.

Tila taila is the best pacifier of vata. Bala mentioned as the best single drug

remedy of vata rogas. When it is fortified with the Cow’s milk one time then the brumhana

character is going to get added into this preparation.

In ischemic strokes there is occlusion of the arteries due to blockage of the

cerebral arteries by thromboembolic factor. Adminstration of sneha nasya nourishes the

Mashtishka and its arteries by the sneha bhava of the K.B.T.101 nasya. 5 In collectively,

ksheerabala taila pacify the vata, manages the further dosha vitiation and works as

rasayana due to its brimhana character.

MODE OF ACTION OF PAKSHAGHATARI YOGA

Pharmacodynamics of drugs is mainly based on the panchamahabhoota and

tridosha siddhanta which govern the physio-chemical and bio-chemical phenomena

respectively. Pakshgatari yoga is a heromineral compound, which is rationally formulated

on the basis of individual actions. Traditional practitioners claming this compound as safe

and effective in the management of Pakshaghata. On assessing the ingredients of

Pakshaghatari yoga, the drugs like Ashwagandha, Bala are having actions like kapha-vata

shamaka, Balya, Rasayana with respect of madhura rasa and sheeta veerya and

madhura vipaka.

Drugs like Brahmi, Vacha, are having actions like Medhya, Swarya and having the

nerve stimulating action. Drugs like Chatushat prahari Pippali, Lahashuna, Katuki,



Apamarga are having ushna, teekshna, sukshma srotogami, amapachaka, deepaka and

having the action like srotoshodhaka. Lashuna is yogavahi and antihypertensive action

due to its ushna guna.

Brihat Vata Chintamani Rasa : It is prepared with the ingredients having mainly

madhura rasa, guru guna and madhura vipaka. All the drugs having Balya, Medhya, and

Dhatupushtikara. Roupya bhasma having Nadibalya action. It pacifies vata and promotes

the body strength, and increases the function of nerve impulses. This is one of the

efficacious drugs in treating the Pakshaghata.

Bala taila : It is formed by the base oil as tila taila with Balakwatha and by the

kalka of Vatashamaka and Jeevaneeya gana dravyas. Tila taila showing the activity like

Vatashamaka and Balya action due to its sara and madhura rasa. Bala is also showing

the vata shamaka activity because of its special alkaloids tannin and resins.

Ksheera Bala Taila 101 : It is a very excellent Paneeya taila, which mitigates

vata. The main ingredient is Bala, which has a Balya action, various glucocides, resins

and tannins which promotes the strength. Ksheera is Dhatuvardhaka and Balya. By

processing Bala with Ksheera gives more efficacious results. Sara and snighda guna of

Tila taila performs vata shamaka action.

Over all the drugs are showing the vata shamaka action and may be more

effective in cerebro-vascular diseases by reducing the blocked oxygen supply in three

ways –

Brain protection.

Enhancement of transmission functions.

Improvement of microcirculation.


Conclusion 150

CONCLUSION

Pakshaghata is a devastating disorder of vata. It is one of the third leading cause

for death. It is an important cause of long-term disability. It is most common life

threatening vata vikara. Pakshaghata can be correlated with hemiplegia. The stroke may

be the main etiological factor.

Ischemic infarctions accounts for 85% of the strokes. Infarct is a local area of

ischemic necrosis, it is usually caused by thrombosis, embolism. Alcoholism, smoking,

stress, hypertension, diabetes, etc are the important risk factors for the infarction. Vata

prakopaka nidanas provokes vata leads to Pakshaghata.

Cheshta nivritti of half of the body, with or without vak sanga is the main clinical

feature observed. However, modern diagnostic tools are very useful to know the cause of

Pakshaghata. CT-brain confirms infarction and hemorrhagic strokes.

Gandharva hastadi taila, kaya virechana, ksheera bala taila 101 shirovirechana

along with shamana chikitsa i.e. pakshaghatari yoga with anupana of madhu in the

prashana vidhi encouraging results in the management of Pakshaghata (ischemic

strokes).

It is very effective in fresh cases than old one. Only virechana does not help in the

management along with it appropriate shamana is effective. Virechana therapy helps in

reducing the elevated blood pressure. No complications observed in this study. Virechana

therapy was less effective in rigidity and spasticity conditions. In vak sanga (aphasia)

condition long-term treatment therapy and speech therapy helps to the patients of

pakshaghata. It is also necessary to conduct the clinical study for longer durations, as it is

time-consuming procedure to maintain the normal position of different vata involvement.

Treatment should be continued for 1 year.


Summery 151

SUMMARY

Since long period vata vyadhis (neurological problems) are considered as a major

subject with a very vast therapeutic intervention. Pakshaghata is mentioned in all the

classical texts. Our ancient physicians spent more time to achieve considerable benefit to

the patients.

Pakshaghata (hemiplegia) is the third major cause of death. Moreover, it is an

important cause of long-term disability and most common life threatening neurological

disease. It occurs in about 5 to 8 of 1000 persons. In spite of present available modern

approaches 50 % of the patients live with complete dependant or residual difficulty in their

routine life.

Pakshaghata is a cerebro-vascular disease leading to degeneration and

destruction of the nerve cells. Cerebral blood flow is essential aspect in the disease

process; brain functions are dependent on constant supply of oxygen and other nutrients.

The two internal carotid arteries and a vertebral artery branches supplies the brain. Lack

of blood supply due to the vascular accidents leads to the stroke.

Ischaemic infarctions account for 85% of stroke. Vascular risk factors, life style

have been shown to have dramatic impact on the prevalence even today. During the past

years there has been declining trend in stroke incidence patients with sufficient area of

ischemic strokes will frustrate with best therapeutic intervention like antithrombotic,

hyperosmatic and other neurotrophic agents.

The improved knowledge and consequently improvement in the management of

stroke factors, new trend in acute stroke treatment helps to achieve the optimum outcome

of the patients.

In these conditions capable of encouraging degree of recovery by Ayurvedic

approaches is evident.


Summery 152

The present study was carried out to evaluate the efficacy of Virechana, Nasya,

Abhyanga, Swedana and shamanoushadhis in the management of Pakshaghata.

This study is presented in two parts based on the descriptions available. First part

of work deals with introduction, literary review, shareera, concept of vata, nirukti, nidana

panchaka, sadhyasadhyata, arishta lakshana, chikitsa, pathyapathya and drug review.

The disease epidemiology, etiology, pathogenesis, clinical features, investigations,

diagnosis, complications and treatment of Pakshaghata (hemiplegia) were also reviewed.

Rest of the work on clinical trail i.e. evaluating the efficacy of Virechana, Nasya,

Abhyanga, swedana and shamana are delt. Ischaemic strokes, properly diagnosised with

the help of CT brain, also essential lab investigations strictly followed. The inclusive and

exclusive criteria and treatment schedule followed properly. The International stroke scale

of National Institute of Health and National Institute of Neurological Disorders and Stroke

(NIH, NINDS) to assess the general condition of patients are being used in present study.

Functional status scale (stroke severity scale), i.e. Barthel index, Rankin’s disability scales

were also followed.

The research design was single blind observational study. Assessment was made

before and after the treatment. 30 cases were selected of both the sexes between the age

group of 40 to 70 years. All the patients were received deepana, pachana with Trikatu

churna, Abhyanga with Bala taila followed with Sarvanga bhaspa swedana. These

patients made into three groups of each 10 patients. Group A patients received only

shodhana i.e. Gandharvahastadi taila for Virechana, Ksheerabala Tail 101 for Nasya.

Group B patients received Pakshaghatari yoga with madhu for 90 days as a shamana

oushadhi. Where as group C patients received both shodhana and shamana.

Group A and C patients were received sadhyo / arohana sneha pana with

Moorchhita tila taila followed with Gandharvahastadi taila for virechana and after a gap of


Summery 153

1 month patients received Nasya karma with Ksheerabala taila 101 for 7 days. The

duration of treatment was of 90 days. Follow up was done after 1 month of treatment.

In this clinical study keen observation was made on epidemiological features of the

disease and also nidana, lakshana, prakriti, agni, koshta, satwa, sara, samhana, kala,

bala, grade of loss of muscles strength, movement, gait etc.

In this study it is observed that more number of cases were reported in the age

group of 60 to 70 years. Patients belonging to the different religions, economical status,

mixed dietic regimens were reported. Patients with risk factors like smoking, alcoholic,

diabetic, and hypertension were reported. Among the sample selected, fresh cases i.e.

stroke with 30 to 40 days were dominantly seen. 12 patients with Vak sanga and Vak

aspashtata were also reported.

Assessment of result was made on monthly observations following the ANOVA

test. It is observed that group C patients were well responded to the treatment i.e.

combine therapy of shodhana and shamana. It is also observed that no patients have

reported the progression or relapse of the disease. It is equally effective in the follow up

treatment. This therapy is much beneficial in fresh cases rather than the old cases. Mild

improvement was found in old (i.e. more than 6 months) patient. Overall assessment

reveals marked improvement observed in 3 patients

Mild improvement observed in 10 and

Moderate improvement observed in 17 patients.

Snehapana, Sarvanga abhynga-swedana, Virechana, Nasya and shamana are

found to be more effective in the present study. The treatment of Pakshaghata associated

with Vak sanga / Vak aspastata was also significant up to some extent. Detailed

observations and literary works are submitted.


Recommendations and Limitations 154

RECOMMENDATIONS FOR FUTURE STUDY

The following recommendations are made on the basis of observations and

conclusions for the future studies as well as to over come the limitations.

Study can be conducted according to exact cause of Pakshaghata with good

sample size.

The same study can be conducted with large number of sample size.

Duration of the study should be prolonged.

Repeated virechana therapy can be conducted in the ischaemic strokes.

Modern investigation tools like MRI, helps better to under stand events of

pathological changes of the pre and post treatment of stroke.

Mashtishkya chikitsa can be done with other classica treatment like Shirodhara

Shirobhasti etc.

Different basti yoga should be adopted.

Physiotherapy ,speech therapy of modern technical procedures should be

followed appropriately.

LIMITATIONS OF THE STUDY

It is difficult to draw the conclusion because the sample size was small and

sampling method was incidental.

Though the study was single blind observational clinical trail. It is very difficult to

make complete recovery due to many risk factors.

Drug being a compound formation it is difficult to draw its mode of action.

Though the disease is in syndromic character it is difficult to approach with the trial

treatment.

REFERENCES INTRODUCTION

1. Cha. Su. 17/118 2. Su. Su. 21/5 3. M. N. 4. S. Ni. 1/62 Dal. 5. S. K. D. P. No. 2 6. Waltons Brain’s Diseases of the Nervous System 7. ibid 8. Devidson’s Principal of Internal Medicine 9. C. N. S. Drugs Page No 1.2.3. 10. ibid 11. Ch. Chi. 28/ 12. C. N. S. P.No 4,5

HISTORICAL REVIEW 1. A. V. Kosika Sutra 31-18-19 2. Ch. Su. 11/49 3. Ch. Chi. 28/51-53 4. Su. Ni. 1/60-61 5. Su. Chi. 5/10 6. A. H. Ni. 15/28-29

Ch. Chi. 21/44 7. B. S. Page No. 37 8. M. N. 23/29 9. C. D. Page No. 182 10. V. S. Page No. 182 11. B. R. Page No. 104 12. Y. R. Page No. 182 13. S. Y. Page No. Taila Prakarana

SHAREERA 1. Su. Ni. 1/5-17-18 2. Su. Sha. 9/7-9-10 3. Chourasia III Page No. 249-258 3. Ayurvedic management of stokes Dr.K.Nishteswar. p. no 19 4. Neuro-anatomy

CEREBRAL CIRCUALATION 1. Neuro-anatomy Medical physiology Page No. 497 2. Text book of Medical Physiology A. C. Guyton Page No. 1996

COOREALTION OF VATA AND CNS 1. Shar. Sam. Poo. 5/25 2. Ch. Sha. 1/23 3. Ch. Sha. 17/12 4. Su. Ni. 1/7 5. Su. Su. 21/5 6. Ch. Su. 17/118 7. B. S. 47 8. Su. Ni. 1/7 9. Ch. Chi. 28/18

NIDANA 1. Cha. Chi. 28/15-18

Su. Su. 14/31

M. N. 22/1 2. Waltons Brain’s Diseases of the Nervous System VIII Edi 2-160,217,218 3. Stroke Magazine Vol. April 2003 4. Ch. Chi. 28 5. Su. Su. 14/30-31 6. Ch. Si. 1/6 7. Su. Sha. 6/25 8. C. N. S. Drugs Supplements Page No. 213 9. Harshamohan Textbook of Pathology Page No. 254, 262 10. Robbin’s Textbook of Pathology Page No. 113-137 11. Devidson’s Principals of Internal Medicine Page No. 902-903

POORVAROOPA 1. Golwal Medicine Page No. 454 2. Waltons Brain’s Diseases of the Nervous System Page No. 235-236.

ROOPA 1. Su. Ni. 1/62 Dal. 2. Ch. Chi. 28/53 3. A. Hr. Ni. 15/36 4. Ch. Sha. 1/25-26 5. M. N. 22/39 6. Su. Ni. 1/60-62 7. Su. Ni. 1/62 8. A. Hr. Ni. 9 9. B. R. 104 10. Ch. Chi. 28/5 11. Manual of Neurological Therapeutics 232,233

SAMPRAPTI 1. Gangadhara commentary on Ch. Su. 10. 2. B. P. of Bhavamishra Poorva khanda 11. 3. Ch. Chi. 28/3 4. Walton’s Brains Neurology Page No. 235-236 5. Su. Su. 21/35. 6. Ch. Chi. 28/3. 7. Pakshaghata by – Dr. G.Purushothamacharyalu Page No. 38-39. 8. ibid. 9. Su. Su. 21/36. 10. Su. Su. 21/38. 11. Su. Su. 21/26. 12. Su. Su. 21/29. 13. Su. Su. 21/31. 14. Su. Su. 21/33. 15. A. Hr. Su. 12/4. 16. Ch. Chi. 28/6. 17. Ch. Chi. 28/9-10

A. Hr. 12/9. A. S. Su. 20.

18. A. Hr. 12/6-7. CH. Chi. 28/9-10. A. S. Su. 20.

19. A. Hr. Su. 12/6-7. 20. A. Hr. Su. 12/6-7.

21. A. S. Su. 20/4. 22. A. Hr. Su. 11/13.

S. Su. 21/9. Su. Su. 14/5-6. Ch. Chi. 25/27.

23. A. Hr. Su. 1. A. S. Su. 1/33.

24. A. Hr. 12/6-7 Ch. Su. 18/22.

UPADRAVA AND ARISHTA LAKSHANA 1. Ch. Chi. 28/22-74 2. Su. Su. 33/5-6 3. Su. Su. 33/7 4. M. N. 22/78-79 5. Waltons Brain’s Diseases of the Nervous System VIII Edi. 253,254 6. H. S. Dwi. 4/5

SADHYASADHYATA 1. Su. Su. 33/4 2. Y. R. 546 3. M. N. 22/74 4. M. N. 22/76 5. M. N. 22/44

Yoga Ratnakara Page No. 509 6. K. K. Page No. 127 7. C. N. S. Drugs Page No.

ROGA NIRNAYA 1. Davidson’s Principals of Internal Medicine Page No. 881, 834, 859 2. C. N. S. Drugs Supplements 3. Waltons Brain’s diseases of the Nervous System 8th Ed.

CHIKITSA 1. C. N. S. Drugs Supplements 12,13,14 2. Ch. Chi. 28/100 3. Su. Chi. 5/19 4. A. San. Chi. 23/9 5. B. R. 379 6. C. D. 22/27 7. A. Sha. 23/19 8. Ch. Su. 22/11 9. Ch. Chi. 28/81 10. Ch. Su. 22/11 11. Ch. Su. 22/04 12. Su. Chi. 4/14-17 13. A. S. Su. 32/31 14. Su. Chi. 5/19 15. Ch. Chi. 28/84 16. Ch. Si. 28/84 17. Ch. Si. 1/38-40 18. Su. Chi. 14/21 19. Kastoore’s Ayurvediya Panchakarma Vignan 20. Ch. Chi 28/183,188 21. Ch. Chi.

22. A. S. Su. 15/10 23. C. D. 22/27 24. S.S. 6/19 25. S. Y. 29, 39, 80 26. ibid 316, 324, 260, 339, 279, 216, 292, 27. ibid 252, 275, 292, 321 28. A. S. Su. 29. S. Y. S. 595, 575 30. B. Y. T. 576, 594 31. B. R. 26/120 32. Walton’s Brain’s diseases of the Nervous System Page No. 251-255. 33. C. N. S. Drugs supplements Page No. 12-15

PATHYAPTHYA 1. Ch. Chi. 28/109 2. B. R. 556. 3. Y. R. 548.

DRUG REVIEW 1. A. S. Su. 46-48 2. S.Y.Tail prakaran 38 3. A.S.Su.17 4. S.Y.Tail prakaran 81.82 5. S.Y.Tail prakaran 124 6. I.M.M. P.No.1292,113, 299,35,21,65 7. A. S. S. 17 8. R. Y. S. P.N0.357 9. A. S. Su.6/86-93.

MATERIAL AND METHODS 1. S. Su. 46-48 2. S.Y.Tail prakaran 38 3. A.S.Su.17 4. S.Y.Tail prakaran 81.82 5. S.Y.Tail prakaran 124 6. I.M.M. P.No.1292,113, 299,35,21,65 7. A. S. S. 17 8. R. Y. S. P.N0.357 9. A. S. Su.6/86-93. 10. Gold Stein L. B. Barhtel’s C. Devis J. N. Interrater reliability of the NIH stroke

scale. Arch Neurol 46 : 660, 1989. 11. Mahoney FI, Barthel DW : Functional evaluation : The Barhtel Index. Md State

Med. J. 14 : 61-65, 1965. 12. Rankin J. : Cerebrovascular accidents in patients with the age of 60 : II. Prognosis.

Scott Med. J. 2 : 200-215, 1957. MODE OF ACTION OF THERAPIES

1. A. Su. 27/ Ch. Su. 20/16

2. K. Si. 2 3. Y. T. 34 4. Ch. Kal. 1/5 5. Ch. Chi. 28/100 6. Ch. Su. 13/12 7. IMM Page No. 1065

SNEHANA AND SWEDANA 1. Ch. Su. 21/11 2. Ch. Su. 13/99 3. A. Su. 25/3 4. Ch. Ch. 28/142 5. Amrut Bindu 2000

NASYA 1. Ch. Si. 2/22 2. Ch. Si. 2/12 3. Su. Su. 6/27 4. A. Su. 20/1 5. Kasture Ayurvediya Panchakarma Page No. 538

DISCUSSION ON OBSERVATIONS 1. Waltons Brain’s diseases of the Nervous System 8th Ed. Page No. 199-201 2. C. N. S. Drugs Vol. 9 1998, Page No. 3-4.

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Shri D.G.M.A.M.C, GADAG.

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147

Table No. 69 : Showing the Master chart for group A (10 patients) :

NINDS B. I. R.D.S. Sl. No.

OPD No.

IPD No.

Age Sex Occu. Rel. Chr. (in days)

T/F Sd. Pr. HTN DM BP MP D0 D90 BT AT BT AT

Rm

01. 2454 206 40 M L M 40 T Rt PK Yes Yes 160/100 V 10 05 20 40 V III Mild 02. 367 21 70 M A H 40 T Rt VK Yes - 170/110 V 15 08 20 45 V IV Mild 03. 763 51 40 M A H 60 T Rt VP Yes - 160/100 V 10 06 30 50 V III Mild 04. 1080 77 51 M A H 60 T Rt VP Yes - 170/100 V 12 08 25 45 V IV Mild 05. 1824 162 70 M B H 180 T Lt VP Yes - 170/100 V 12 08 25 45 V IV Moderate 06. 1898 178 68 M B H 120 T Rt VP Yes Yes 170/100 V 10 06 20 50 V IV Moderate 07. 1984 177 64 M H/H H 30 T Lt VP Yes - 170/110 V 14 10 20 40 V IV Moderate 08. 2068 186 65 F H/H H 30 T Rt VK Yes - 160/100 V 14 10 20 40 V III Mild 09. 2527 333 65 M H/H H 10 F Lt VK Yes - 160/100 V 12 10 20 50 V IV Moderate 10. 2673 457 66 M H/H H 30 T Rt VK Yes - 160/110 V 12 10 10 50 V III Moderate Abbreviations : Occu. – Occupation, { L – Labour, A – Agriculture, B – Business, H/H – House hold}, Rel. – Religion {H - Hindu, M –

Muslim}, Chr. – Chronicity, T/F – Treated / Fresh, Sd. – Side affected, {Rt. – Right, Lt. – Left}, Pr. – Prakrati, {PK – Pitta Kapha, VK –

Vata Kapha, VP – Vata Pitta, KP – Kapha Vata}, HTN – Hypertension, DM – Diabetes Mellitus, BP – Blood Pressure, MP – Muscles

Power, V – Grade five loss, NINDS – National Institute of Health Neurological Disorders and Stroke, B.I. – Barthel’s Index Score, R.

D. S. - Rankin’s Disability Scales, BT – Before treatment, AT – After treatment. D0 – Day, D90 – Day ninety.

148

Table No. 70 : Showing the Master chart for group B (10 patients) : NINDS B. I. R.D.S. Sl.

No. OPD No.

IPD No.



Remarks

01. 901 58 41 M L H 60 T Rt PK Yes - 180/100 V 14 10 15 30 V IV Mild 02. 972 64 70 M H/H C 20 T Rt VK Yes - 170/100 V 9 05 10 55 V IV Mild 03. 1225 92 65 F H/H H 30 T Lt VP Yes - 170/100 V 10 06 20 40 V IV Mild 04. 1322 105 70 F H/H H 20 T Rt PK Yes Yes 150/98 V 10 05 20 70 V II Marked 05. 1337 106 70 M H/H H 20 T Rt PK Yes - 110/70 V 10 05 20 60 V III Moderate 06. 2223 205 50 M A H 30 T Rt VP Yes - 170/100 V 10 04 20 60 V III Moderate 07. 2256 301 70 F H/H H 40 T Rt VP Yes - 170/98 V 10 05 20 50 V IV Mild 08. 2730 371 60 F H/H H 30 T Rt VK Yes - 160/98 V 10 05 20 60 V III Moderate 09. 958 61 55 F H/H H 20 T Rt VP Yes - 160/80 V 12 08 30 65 V IV Mild 10. 3452 460 40 M H/H H 20 T Rt VP Yes - 170/110 V 12 07 20 65 V III Moderate Abbreviations : Occu. – Occupation, { L – Labour, A – Agriculture, B – Business, H/H – House hold}, Rel. – Religion {H - Hindu, M –





149

Table No. 71 : Showing the Master chart for group C (10 patients) : NINDS B. I. R.D.S. Sl.

No. OPD No.

IPD No.



Remarks0

01. 6336 96 62 M L H 20 T Rt VP Yes I 140/80 V 10 03 10 90 V III Moderate 02. 1222 93 40 M A H 20 T Lt VP Yes - 140/80 V 11 03 15 85 V III Moderate 03. 1671 147 50 M A H 20 T Lt VPK Yes - 160/90 V 11 02 25 85 V III Moderate 04. 2071 187 65 M A M 20 T Lt VK Yes Yes 160/80 V 10 04 30 80 V III Moderate 05. 1783 160 40 F B M 15 T Lt VP Yes - 110/70 V 10 03 20 75 V III Moderate 06. 2149 199 40 M B H 15 T Lt PK Yes - 130/80 V 13 01 15 85 V II Moderate 07. 2251 208 40 M H/H M 20 T Rt KP Yes - 140/70 V 13 03 10 100 V II Marked 08. 2452 322 42 F H/H H 30 T Rt KP Yes 160/100 V 12 03 15 100 V III Moderate 09. 3153 - 60 F H/H H 40 T Rt P Yes - 160/90 V 12 03 15 85 V III Moderate 10. 3452 460 40 M H/H M 30 T Rt KP Yes Yes 170/100 V 12 03 15 85 V II Marked

Abbreviations : Occu. – Occupation, { L – Labour, A – Agriculture, B – Business, H/H – House hold}, Rel. – Religion {H - Hindu, M –





Department of Kaya Chikitsa POST GRADUATE AND RESEARCH CENTER Shri D.G.M.Ayurvedic Medical College, Gadag.

Guide : Dr. V. Varadacharyulu Co-guide : Dr. Ashok Kumar Panda

Atur Nama:

(Name of the patient)

Father name/Husband name :

Age (Vaya) : Years :

Linga : M F

(Sex)

Vyavasaya (Occupation) :

Religion :

Address :

Economical Status : Poor Middle High

Selection : Excluded Included Group A Group B

Group C

Result : Complete relief Partial relief Not relieved Defaulter

Consent :I son / daughter / wife of

excercise my free will to particiapte in the study. I have been in-

formed to my satisfaction by the attending physician that the purpose of clinical

evaluation, nature of drug & treatment. I am also

SPECIAL CASE SHEET FOR PAKSHAGHATA

Sl. No. :

O.P.D. No. :

I.P.D. No. :

Bed No. :

D.O.A. :

D.O.D. :

M. D. (Ayu)M.D. (Ayu)

aware of my right to quit at

Signature of Patient

Schedule Initiation :Schedule Completion :

Phone :

E-mail :

OthersH M C

1

any time during the schedule.

PRADHANA VEDANA: (Chief complaints) – Yes / No Kala Prakarsha

01. Akarmanyatva of half of the body vama / dakshina 02. Shakti hrasata vama / dakshina 03. Chesta kshaya 04. Vak sanga 05. Vak aspashtata 06. Shiraha shoola 07. Bhrama 08. Chardi (Vomiting) 09. Hikka (Hiccough) 10. Sparsha agnyata (Unilateral sensory symptoms) 11. Eka drishiti dosha (Homonymus hemiphonia) 12. Diplopia 13. Unsteadiness

ADHYATANA VHYADHI VRITTANTA : (History of chief complaints) – Roga prarambha vega - Kshipra (acute) Manda (Sub acute) Roga prambha kala – Prataha (morning) Dina (afternoon) Sayam (evening) Nidravastha (sleeping condition) Gamana kala (walking) Krodha avastha (angry state) Associated with - Loss of consciousness Poorva roopa POORVA VYADHI VRITTANTA : (History of past illness) –

01. HTN 02. DM1, DM2 03. Heart disease 04. Apasmara (epilepsy) 05. Sthoulya (obesity) 06. Hyperlipidaemia 07. Head injury 08. Arbuda (malignancy)

KOUTUMBIKA VRITTANTA : (Family history) – CHIKITSA VRITTNATA : (Treatment history) – Treatment taken for Pakshaghata

Ayurvedic

Current using medicines for Drug Dose Duration HTN DM Heart disease Hyperlipidaemia Primary prevention Secondary prevention Psychosis Epilepsy Oral contraceptives Ayurvedic medicine Oils Rasoushadhi Any VAYAKTIKA VRITTANTA : (Personal history) – Ahara (Food) Pure vegetarian Mixed Taste predominance Madhura Amla Lavana Katu Tikta Kashaya Smoking / Beedi / Cigaratte / Ganja - day. Alcohol brand ml / day. Tobacco chewing gm / day. Shoka Chinta Krodha Risk factors HTN DM Heart disease Hyperlipidaemia Epilepsy Alcohol Smoking Hormone therapy Jatharagni avastha Manda / Tikshana / Vishama / Sama Purisha pravritti Vibhanda / Dravamala / Frequency Mutra pravritti Frequency / Colour / Odour Nidra Sukha / Ati / Alpa / Vishama / Hinata

Arthava pravritti Regular / Irregular / Menopaused

SAMANYA PAREEKSHA : (General examination) – General condition of the patient Good / Moderate / Bad

Loss of function / weakness of Rt. U.L. & L.L.

Lt. U.L. & L.L.

Pulse / min. BP mm of Hg. Temperature 0 F

Respiration rate / min. Height cms. Weight kg.

Skeletal abnormalities General appearance & configuration of – Head Eyes Neck Chest Abdomen UL LL Lymph nodes Special examination Nadi V P K VP VK PK VPK

Prakriti V P K VP PK VK VPK

Sara Pravara Avara Madhyama

Samhana Pravara Avara Madhyama

Satmya Eka rasa Sarva rasa

Satwa Pravara Avara Madhyama

Ahar shakti Pravara Avara Madhyama

Vyayama shakti Pravara Avara Madhyama

Vaya Balya Yauvana Vardhakya

Desha Jangala Anupa Sadharana

Vata BT AT Pitta BT AT Kapha BT AT Dosha vriddhi

Dosha kshaya

Sama dhatu lakshana

Nidana

Samprapti ghatakas

Neurological Examination

Examination Yes No BT AT Higher functional test Level of consciousness – Stupor Lethargic Coma Unconsciousness

Orientation – Place Person Time

Memory – Recent Past

Emotional status Sleep Judgment Intellect Systemic examination : C.V.S. Inspection Palpation Percussion Auscultation R.S. G.I.S. Genito-urinary system Srotas pareeksha : Systemic examination of nervous system Motor function test

Rt. UL Rt. LL Lt. UL Lt. LL BT AT Strength Co-ordination of movements Involuntary movements Gait Bulk of muscle wasting Present Absent Tone of muscle wasting Hypo Hyper Reflexes Deep reflexes Superficial reflexes Before T After T Knee Papillary Biceps Corneal Triceps Ankle Plantar Abdominal Swallowing

Sensory functional test Sensation Before After Pain Touch Temperature Vibration Cortical sensation Trunk Babniski’s sign Beevor’s sign Speech

01. Handedness 02. Educational status

a. Language out put b. Reading c. Writing

03. Spontaneous speech a. Word out put b. Phase length c. Syntax d. Paraphesia - Literal

- Verbal - Neologism

e. Dysprosody f. Effort of speech

04. Comprehension a. Comprehension of spoken language b. Comprehension of written language

05. Naming 06. Reception - Words

- Sentences 07. Reading - Reading aloud

- Reading for comprehension 08. Writing - Copying

- Writing Cranial nerve examination

01. Olfactory nerve - Smell 02. Optic nerve - Vision : Right eye –

Left eye –

03. Occulomotor nerve – I) Eye ball movement – II) Ptosis – III) Papillary reflex – IV) Accomodation –

04. Trochlear nerve – Rotation of eye ball -

05. Trigeminal nerve –

Sensory test I) Scalp II) Face III) Nasal mucosa membrane

06. Abducent nerve – Lateral movement of eye ball

07. Facial nerve – Facial muscles movements – Elevation of hyoid bone – Taste – Secretion of saliva & lacrimation –

08. Vestibulocochlear nerve – Rinner’s test Webber’s test

09. Glossopharangeal nerve – Sensation of taste Deglutition Palatal reflex Gag reflex

10. Vagus nerve Swallowing Intestinal motility Cough reflex Cutaneous sensitivity

11. Accesory nerve Movement of head and shoulder

12. Hypoglossal nerve Movement of Tongue

ASSESSMENT CRITERIA : I. Rankin disability score Grade I : No significant disability Grade II : Slight disability Grade III : Moderate disability Grade IV : Moderately severe disability Grade V : Severe disability II. Stroke Scale Of National Health-National Institute Of Neurological Disorders And Stroke (NIH-NINDS) : D0 D30 D60 D90

01. Date performed 02. a. Level of consciousness: Alert ( )0

Drowsy ( )1 Stupor us ( )2 Coma ( )3

b. Level of consciousness: Answers both correctly ( )0 Answers one correctly ( )1 Incorrect ( )2 Normal ( )0

c. Level of consciousness: Obeys both correctly ( )0 Obeys one correctly ( )1 Incorrect ( )2 Normal ( )0

03. Best gaze: Partial gaze palsy ( )1 Facial deviation ( )2

04. Best visual: No visual loss ( )0 Partial hemianopia ( )1 Complete hemianopia ( )2 Bilateral hemianopia ( )3

05. Facial palsy: Normal ( )0 Minor ( )1 Partial ( )2 Complete ( )3

06. Best motor arm right: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

07. Best motor arm left: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

08. Best motor leg right: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

09. Best motor leg left: No drift ( )0 Drift ( )1 Can not resist gravity ( )2 No effort against gravity ( )3 No movement ( )4

10. Limb ataxia: Absent ( )0 Present in either upper or lower ( )1 Present in both upper and lower ( )2

11. Sensory: Normal ( )0 Partial loss ( )1 Dense loss ( )2

12. Neglect: No neglect ( )0 Partial neglect ( )1 Complete neglect ( )2

13. Dysarthria : Normal articulation ( )0 Mild to moderate dysarthria ( )1 Near unintelligible or worse ( )2

14. Best language: No aphasia ( )0 Mild to moderate aphasia ( )1 Severe aphasia ( )2 Mute ( )3

Total

III. Barthel index :

FUNCTIONAL STATUS SCALES (STROKE SEVERITY SCALE)

Function Score Description BT AT 10 Independent, able to apply to any

necessary device, eats in reasonable time

Feeding

5 Needs help 15 Movements of wheel chair 10 Minimal assistance or supervision

Wheel chair or bed transfers 5 Able to sit but needs maximal assistance

to transfer

5 Washes face, combs hair, brushes teeth, shaves

10 Independent with toilet or bedpan, handles cloths, whips, flushes, or cleans pan.

Personal toilet (grooming) toilet transfers

5 Needs help for balance, handling clothes or toilet

Bathing self 5 Able to use shower or complete sponge bath without assistance

15 Independent for 50 feet, may use assistive devices, except for rolling walker

10 Walk with for50 yards

Walking

5 Independent with wheel chair for 50 feet only if unable to walk

Stairs, ascending & descending & dressing & undressing

10 5 10 5

Independent, am use assistive devices Needs help or supervision Independent, ties shoes, Needs help but, does at least half of task within reasonable time

10 No accident, able to care for collecting devices if use

Bowel control

5 Occasional accidents or needs help with enema or suppository

10 No accidents, able to care for collecting device if used

Bladder control

5 Occasional accidents or needs help with device.

Total score

INVESTIGATIONS : Complete blood picture BT AT Hb% ESR TC DC RBS Widal test MP VDRL HIV Lipid profile Serum cholesterol Serum triglycerides HDL LDL VLDL Serum creatinin Serum urea ECG CT brain ROGA VINISCHAYA : Shuddha vataja Vata-kaphaja Vata-pittaja Dhatu kshayaja TREATMENT PROTOCOL Shodhana treatment Sneha pana, abhyanaga, swedana, Virechana, Nasya Remarks Initial day 30th 60th 90th Shamana treatment Pakshaghatari yoga Remarks Initial day 30th 60th 90th INVESTIGATOR’S NOTE :

Signature of the scholar

Signature of the Guide

Documents

Pakshaghata kc024 gdg