pakshaghata kc012 hyd

A STUDY OF THE EFFECT OF VATA RAKSHASA RAS WITH

BHRINGADI TAILA NASYA IN THE MANAGEMENT OF

PAKSHAGHATA

DISSERTATION SUBMITTED IN PARTIAL FULFILLMENT FOR THE

DEGREE OF

DOCTOR OF MEDICNE (AYURVEDA)

IN KAYACHIKITSA

BY

DR.G.RANGA NADH

CO-GUIDE GUIDE

Dr. VIJAYA LAKSHMI Dr. V.VIJAYA BABU

M.D (Ayu) M.D (Ayu)

/LECTURER READER

POST GRADUATE TRAINING AND RESEARCH UNIT

DEPARTMENT OF KAYA CHIKITSA

DR. B.R.K.R.Govt. AYURVEDIC COLLEGE AND HOSPITAL

HYDERABAD

FACULTY OF AYURVEDA

N.T.R. UNIVERSITY OF HEALTH SCIENCES

VIJAYAWADA, A.P., INDIA

2007-2008.

created by technoayurveda.wordpress.com of Dr.KSRPrasad

Ayurmitra

TAyComprehended

DR.N.T.R.UNIVERSITY OF HEALTH SCIENCES

VIJAYAWADA, A.P.

DEPARTMENT OF KAYACHITIKSA

POST GRADUATE UNIT

DR. B.R.K.R. Govt.Ayurvedic College/Hospital

Erragadda, Hyderabad, Andhra Pradesh

INDIA.

Date:

Place: Hyderabad

CERTIFICATE

This is to certify that the present study titled “A STUDY OF

THE EFFECT OF VATARAKSHASA RAS WITH BHRINGADI TAILA

NASYA IN THE MANAGEMENT OF PAKSHAGHATA” was carried out by

Dr.G.Ranga Nadh under our direct supervision and guidance for the award of

Doctor of Medicine in Ayurveda in the speciality of kaya chikitsa.

A continuous effort has been done not only in compiling the

relevant information and also in conducting the clinical study sincerely and

carefully.

Hence we recommend this work for accept

CO - GUIDE GUIDE

Dr. VIJAYA LAKSHMI, Dr. V.VIJAYA BABU

M.D. (Ay) M.D. (Ay)

LECTURER READER


DR.N.T.R UNIVERSITY OF HEALTH SCIENCES

VIJAYAWADA, A.P

DEPARTMENT OF KAYACHIKITSA

POST GRADUATE UNIT

DR. B.R.K.R.Govt. Ayurvedic College / Hospital

Erragadda, Hyderabad, Andhra Pradesh.

INDIA

Place : Hyderabad

Date :

C E R T I F I C A T E

This is to certify that Dr. G.Ranga Nadh a student of

M.D.(Ayu) Kayachikitsa, has worked for his thesis on the topic ‘A STUDY OF

THE EFFECT OF VATARAKSHASA RAS WITH BHIRNGADI TAILA

NASYA IN THE MANAGEMENT OF PAKSHAGHATA’ as per requirements

of the ordinance laid down by NTR university of health sciences, Vijayawada

for the purpose. The Hypothesis submitted by him in the first year M.D. is one

and the same to that of the dissertation submitted.

I am fully satisfied with this original work and here by

forward the thesis for the evaluation of the adjudicators.

DR.PRAKASH CHANDER

M.D.(Kayachikista)

PROFESSOR &

Head of the Department of K.C.

Post graduate unit

Dr.B.R.K.R.Govt.AyurvedicCollege/ Hospital

Hyderabad.


ACKNOWLEDGEMENTS

I convey my heartful gratitude and respect towards my beloved

parents

It gives me great pleasure to express my profound sense of

gratitude and deep respect to my guide Dr. V.Vijaya Babu, Reader K.C.Department,

P.G.Unit, Dr. B.R.K.R. Govt. Ayurvedic Medical College / Hospital, Erragadda,

Hyderabad, for his valuable guidance constructive advises and whole hearted co-

operation which enabled me to present this thesis in its present form.

I am very highly indebted to my co-guide Dr. Vijaya Lakshmi

Gaxetted Lecturer, K.C. Department, P.G. Unit, Dr.B.R.K.R. Govt. Ayurvedic

Medical College / Hospital. It is only due to his constant encouragement, wise

advises, stimulating discussions and admirable affection inspired me to bring out

this heavy work.

It is pleasure to convey my thanks to former co-guide Dr.

Ramalingeshwara Rao, Gaz. Lecturer, Dept. of K.C., P.G.Unit, for his suggestions.

My sincere regards to Dr. Prakash Chander Reader, Professor,

Head of the department, K.C., P.G.Unit, Dr. B.R.K.R. Govt. Ayurvedic Medical

College / Hospital, Erragada, Hyderabad, for his valuable suggestions during my

couse of study.

I am highly thankful to the College principal Dr. Sadashiva Rao

for providing my necessary equipment.

I am thankful to the hospital Superintendent Dr. L.R.K.Murthy

for his cooperation for allowing me to do work on his patients and providing

necessary requirements.


I acknowledge sincere gratitude to Dr. Anantha Sena Chary,

Professor, Head of the Department of Shalya, Dr. V.L.N.Sastry, Dr. Philip Anand,

Dr. Jeevaratnam for their valuable suggestions.

I am thankful to Dr. Ramakrishna, adviser of Annapurna Herbal

Industry for his contribution towards preparing the Thesis Drugs.

The assistance received from Dr. P.Yoshada, Lecturer of Govt.

Ayuverdic College, Hyderabad, Dr. Parumallu, Dr. Priya, Dr.Vinod Singh, Dr.

Sivannaryana, Dr. Lavanya for their valuable suggestions and co-operation.

I am thankful to my friends Dr. Ravi, Dr. Padmaja, Dr.

Venkateshwarulu, Dr. Nagaraju, Dr. Kavitha, Dr. Nageshwara Rao, Dr. Samba

Shiva Rao, Dr. Sirisha, Dr. Karnate, Dr. Jha, Dr. Shivarama Krishna, Dr. Namratha,

Dr. Kandagadla, Dr. Rajalakshmi and all of my classmates for their wholehearted

co-operation during my education.

It becomes impossible to complete Thesis work without the co-

operation of my Sister K.Rama Devi, Brother In-law K.Raghavendra Rao. Wife

G.Tulasi Devi, my Parents G.Sanjeeva Rao & G.Bhagya Lakshmi and my father in-

law M.V.V.Kumar Babu.

.

My thanks are also due to college library and P.G.Dept, Libraray

staff for providing necessary books for the literary work of this thesis.

I am highly thankful to my patients and their attendars for

allowing me to conduct clinical trails and their co-operation through out my clinical

studies.

My respects to all those who helped me directly and indirectly in

completing the present thesis work smoothly.

Date :

Place : Hyderabad DR.G.Ranganadh


INDEX

––––––––––––––––––––––––––––––––––––––––––––––––––––––––––

Topic Page No.

–––––––––––––––––––––––––––––––––––––––––––––––––––––––––––––––––––

Section I.

(1) Introduction

(2) Historical Ascept

Section II

SHAREERA

(1) Sareera – Ayurvedic Aspect

(2) Sareera – Modern Aspect

Section III

VYADHI SAMEEKSHA

(1) Definition & Classification

(2) Nidana - Etiology

(3) Poorva Roopa – Prodromal Symptoms

(4) Roopa - Symptoms

(5) Samprapti - Pathology

(6) Upadravas

(7) Arishta Lakshanas

(8) Sashyasadhyata

section IV

CHIKITSA YOJANA

(1) Chikitsa


(2) Pakshaghata Chikitsa – Modern Aspect

(3) Nasya Treatment

(4) Pathya – Apathya

Section V

DRUG REVIEW

(1)Vatarakshasaras

(2) Bhirngadi Taila Nasya

Section VI

CLINICAL STUDY

(1) Criteria

(2) Parameters

(3) Materials and Methods

(4) Observations

(5) Results

Section VII

(1) Discussion

(2) Conclusion

(3) Summary

Section VIII

APPENDIX

1) Bibliography

2) Case – Sheet


1

INTRODUCTION

Ayurveda is a science of life. AYU – LIFE, VEDA – SCIENCE,

covering the interrelation of body. It is said that this science is a part of Vedas

mainly Atharvana veda. In ancient India it developed and advanced and was divided

into 8 main branches i.e. (1) Kaya chikitsa, (2) Salakya, (3) Salya (4) Visha

Chikitsa, (5) Bhuta vidya, (6) Kowmara bhritya, (7) Rasayana chikitsa and (8)

Vajeekarana chikitsa.

Out of these Ashtangas Kaya chikitsa occupies prominent place in

Ayurveda. Kaya chikitssa deals with numerous internal diseases. Vataja vikaras

outnumber other doshic vikaras. Pakshaghata is one such Vataja nanatmaja vyadhi,

where in Ayurvedic line of treatment gives encouraging results. Rasoushadhas will

give more encouraging results, because no need of panchakarmas (shodhana). It was

fast acting therapy and has been found effective in smaller doses. It is said to be

more of Rasayana in nature, which in practice prevents Jara (old age or the ageing

process) and vyadhis (disease), rejuvenates body and prolongs life span.

We know that 50% of Indian population is above the age group of 50

years and one out of 10 suffer from vata vikaras and a majority of them suffer from

Pakshaghata The incidence of pakshaghata is alarming. It occurs mostly as a

complication of Diabetes mellitus and Hypertension. If a study on Rasoushadhis like

Vatarakshasa Ras is made, which is said to be useful, it will be more helpful in the

present day.

Along with vatarakshasa ras Bhringadi taila nasya is taken for the

Treatment.


2

HISTORICAL ASPECT

Ithihasa is an essential aspect ot know about the diseases, drugs, the

mode of treatment and the life style of the people starting from the prevedic period.

VEDAKALA:

Atharvana veda(4.13.4) is considered as the main source of Ayurvedic

knowledge among the four Vedas the four Vedas but the first and the fore most veda

i.e. Rigveda(8.20.23-26) also contributed much for Ayurvedic therapeutics.

In Rigveda(11.7.6) there are some references which directly or

indirectly indicate the existence of a disease like pakshaghata. The derailment of

‘panchavidha vatas’ takes place in the disease pakshaghata. Yajurveda mentions

about the different types of vatas.

Ayurveda is considered as the Upa veda of Atharvana Veda((s.s.su.1.6)

because of the existence of many pharmacological, anatomical, physiological and

therapeutic aspects, The word ‘vata vyadhi’ is noted first in Atharvana veda.

According to Atharvana veda there are hundreds of ‘Hirah’ (sira) and thousands of

‘Dhamanis’ in which the blood flows like river. The vessels are of different colours

ranging from ‘aruna’, ‘dhoomra’ directed upwards and downwards. These words are

simulating the Susruta’s pakshathata samprapti.

SAMHITA KALA:

Atreya samhita : called as Charaka samhita, the first samhita grantha

explains the nidana, samprapti, chikitsa and sadhyaaasadhyata of pakshaghata. The

other synonyms used in this are pakshagraha and pakshavadha.


3

Susruta samhita: Mentioned the detailed description of the samprapti,

types, sadhyaasadhyata, chikitsa and the duration of chikitsa. The treatment

procedures like mastishkya, sirovasti, abhyanga, parisheka and anuvasana vasti with

specific dravyas is described.

But the contemporars and co-scholars of Agnivesa i.e. Bhela and

Hareetha have not used the word Pakshaghata. They mentioned vatavyadhi prakopa

nidana and lakshanas. Kasyapa is the only authority who mentioned pakshaghata

among the ‘Asheethi Vata Vikaras’. Other information is not seen regarding the

disease but vata prakopa nidanas etc. are described.

SANGRAHA KALA :

Vagbhata mentioned the samprapti of Susruta and the chikitsa of

Charaka Samhita.

Shamana Chitisa : formulae are newly added in :-

Chakradatta (11th Century)

Sarangadhara samhita (13th century)

Basava Rajeeyam (15th century)

Vaidya chintamani (16th century)

Bhava prakasha (16th century)

Yoga Ratnakaram (17th century)

Bahishajya Ratnavali (18th century)

The contribution of Madhavakara is the parakopa lakshanas of vata

in association with pitta and kapha. In this way he explained the “Samsarga doshas”

given by Susrutha while explaining the sadhyasadhyata of pakshaghata.


4

The sources of information are mainly Charaka Samhita, Susruta

Samhita and its commentaries – Nibandha snagraha, Nyaya Chandrika, Madhava

nidana and its madhukosa commentary.

Based on the information available in different snagraha granthas, it

can be stated that there is gradual development in chikitsa.

History of Pakshaghataa in Allopathic system of medicine :

The word “stroke’ is synonym to pakshaghata. Stroke indicates

cerebrovascular disease which came into existence in 19th century. Till then the

word “Apoplexy” is used.

Hippocrates : He used the term “Apoplexy” and described the features of sudden

loss of consciousness.

Galen (130 – 200 A.D.) : he concluded that apoplexy involved brain matter. It was

he who first proved that arteries contain and carry blood. He was the first to describe

the cranial nerves and the sympathetic system. He made the first experimental

bisection of the spinal cord and proved that it caused paraplegia.

Gabriel Falopius (1523 – 1562 A.D.) : He was the first to describe the trigeminal,

auditory and glossopharyngeal nerves.

Romberg M.M. (1795 – 1873) observed paralysis of the body in the opposite side of

the hemispheric lesion

Virchow R.L.K (1821 – 1902 A.D.) : Proposed the concept of ‘thrombosis’ and

‘embolism’, which lead to infarction.

J.M.Charcot (1825 – 1893 A.D.) : He acquainted with the ankle clonus.


5

The world Health Organization has introduced a clinical and research

classification of stroke which is as follows:

1. Transient Cerebral ischemic attack

2. Completed stroke

3. Minor stroke

4. Major stroke

5. Progressing stroke or stroke in evolution.


6

SHAREERA

INTRODUCTION

The Importance of Vata is explicit by the fact that charaka

has allotted one seperate chapter (Chraka Sutra 12) for discussion on this dosha.

A few references from the Ayurvedic classes will indicate the

vata is the most important and powerful of the three doshas.

So long as vata lasts in the body as long as thus life exists.

Bhe.sam. su.16.2

It is indicative of the continuity of the life.

Vata is powerful and important because of:

Its control over the functions of the body its capacity to spread

throughout the body.

There it is capable of swift action

Powerful and

Capable to Vitiate other factors.

Independent movements and

Its vitation causes a large number of diseases.

The term ‘VATA’ is derived from the root ‘VAA GATHI

GANDHANA YOH1’ means to move, to enthuse, to make known, to

become aware of, induction, effort and to enlighten.Co-incidence of all these

factors is called ‘VATA’.


7

According to Vyakarana shastra the dhatu which gives the ‘GATI’

and jaanartha bodhana is called vata2.

GATHI – To move

GANDHANA- To make known, to enthuse

VAA GATHI – presence of movement, knowledge and enthusiasm.

The movements in the body are manifested by the action of all the muscles,

i.e., the motor functions of the cognitive organs; i.e. the sensory functions.

Therefore for a humour or a factor which is capable of conducting both

motor and sensory functions is called vata.

Vata is the combination of AKAASHA MAHA BHUTA and VAYU

MAHABHUTA.

The properties of Akaasha bhuta are Shabda, sense of hearing

(Sravanendriya – KARANA), porosity, power of differentiation. According

to Dalhana VIVIKTATHA means individualization of srothases also; and

the properties of Vayu bhuta are Sparsha, sparshanendriya (the sense of

perception – TWACHA). All functional activities of organism, and all

vibrations (spandana) and lightness.

Vata will have both the properties as it is the combination of akaasa

and vayu mahabhutas with the predominance of vayu mahabhuta.

Moolam shareeram is dosha dhatu and malas. We find elaborate

description about them in Ayurveda3. They are,

1) DOSHAS : VATA, PITTA AND KAPHA

2) DHATUS : RASA, RAKTA, MAMSA, MEDAS, ASTHI &

SHUKRA.

3) MALA : SWEDA, MOOTRA AND PUREESHA.


8

Doshas in normal state also said as dhatus in which condition they

bear the body. ‘DOSHA’ means the factor which is capable of vitiating certain other

factors or (tissues) dushyas of the body is known as DOSHA. Since tridoshas are

capable of getting vitiated due to the respective causes and modify and disturb the

physiological functions of the doshas to initiate the process of onset of disease. They

are known as Doshas. In chetana shareera above three doshas are there .

Vata, Pitta and Kapha pervade the whole body, but special seats in

the normal state are lower, middle and upper portion of the body respectively4. Thus

as three pillars can support and maintain the building, these three doshas support

and maintain the body. That’s why they are called as “TRISTHUNA” or three

pillars5.

Doshas in our body are of two varieties, namely sukshma and sthoola

doshas. Vata is sukshma dosha; by its performance only we will infer its existence.

It shows vata is invisible6 and this is produced in kostha itself7.

Tridoshas in their state of equilibrium working as complementary to

each other perform and control all physiological processes of the body and mind

maintaining the health, therefore these three doshas are also known as “Tridhatus”.

The word dhatu is defined as a factor which supports the body, here with reference

to the Tridhatus, the physiological processesof the body. In Rigveda we will find

‘Tridhatus’. Shayana the commentrator of Vedas explains the term ‘Tridhatu’ as a

synonym of vata, pitta and Kapha8.

SWAROOPA:

Vata is termed as Bhagavan. Because as it is Swayambhu, Swatantra

and Nitya. Some people worship it as God, due to its presence in Pranis as Prana

swaroopa, the complete human machinery is controlled by Vata, because it is

‘TANTRA YANTRA DHARA’9, means the upholder of both structures and the


9

functions of the body, the Vata maintains this machinery and keeps it in good order

as it is swayambhu performs the srushti karya but it never is visible, that’s why Vata

swaroopa is not visible but it’s actions and functions only are experienced by the

sensory organs10.

The Roukshya, Shaitya, Laghava, Vaishadya, Gati, Amoortatva and

Anavasthitha are all swaroopas described by Acharyas in Ayurvedic treatises11.

GUNAS:

According to Charaka Vata is Anavasthita, Asanghata and

Amoortatva (incorporeal). This word has been explained by Chakrapani as

Adrishyata i.e. invisibility and Rooksha (dryness), Laghu (lightness), Daruna, Khara

(roughness), Vishada (clearness) and Sookshma (penetrative) and Chalatva

(mobility)12. Chakrapani the commentator interprets Daruna as Chalatva but

according to others darunatva is ‘Kathinaya’ meaning the vata can make a substance

hard by drying it up. Which means to be a better interpretation. The sookshmatva

quality is the capacity to penetrate through the smallest orifices of the body. 13 The

Chalatva or mobility has been qualified to be very swift.14

Susrutha said it is also Asukari, Neta or commander of dosha. Roga

samrat or emperor of diseases and will have Achintya veerya.

Therefore the earlier stated qualities of vata appeared to be based on

inferential reasoning. Both Shareera vata and loka vayu are invisible. Therefore the

description of the physical attributor of these two can only be used on Anumana

Pramana which is relied on the facts of observation the presence of both can be

recognized by the functions they perform.

Another important observation for the inference of the qualities of

vata is related to the influence of AHARA, OUSHADHA and VIHARA. The

constant use of the Abharaoushadhas possessing the Rookshadi guans is associated


10

with the abnormal states of functioning of vata and the use of Aharaoushadhas

possessing opposite gunas like snigdhadis is associated with the alleviation of the

signs and symptoms of the vitiated vata and restoration to its normal states of

functioning these observation leads to conclusion that the qualities of the shareera

vata must comprise of the former group of qualities viz. Rookshadi gunas, the main

principle on which this conclusion is based is the application of the postulate

‘Samanya’ is the cause of an increase in all things at all times.15

It also stated that Vata is ‘YOGAVAHI’ that is a medium which

when associated with other substances projects their qualities also without losing its

own qualities when vata induces the other pitta, kapha doshas into activity. It

identifies itself with the; when associated with pitta produces a feeling of Ushna,

Daha and Daha and when with Kapha produces a feeling of Sheeta.16

Susrutha states thata vata will have Rooksha, Sheeta, Laghu, Khara.

Has movement in all directions is possessed of the two qualities of Shabda, Sparsha

and has the Rajo guna in predominant degree.17

SITES OF VATA:

Vata, Pitta and Kapha pervade the whole body, their general seats

being the lower, middle and upper portions of the body respectively. But particular

parts of the body where the normal doshas are generally located are mentioned

below.

According to Charaka the seats of vata are Vasthi, Pureeshadhanam,

Kati, Uru, Pada, Asthi and Pakwashaya. The Pureeshadhana has been interpreted by

Chakrapani as Pakwashaya but Pureeshadhanam, should be taken as that portion of

the intestines where it is located the Pureeshadhara Kala of these, the Pakwasaya is

the special seat of the Vata.18


11

In addition, locations of vata as stated by Vagbhata are the ears and

skin.19 It is a fact that the perception by those two sensory organs is mediated

through changes in the air.20

GENERAL FUNCTIONS OF VATA:

Functions related to Emotions and Mind:

1. Utsaha

2. Harsha

3. Control of the mind from indulging in undesirable

arthas and Direct it towards desireable arthas.

Vata capable of actually shutting down the pathways

connecting the Manas with undesirable Arthas and open up the pathways towards

desirables.

I. Motor Functions:

1. Activity of Skeletal muscles.

2. Action of Involuntary muscles like Heart, Intestines,

muscle fibres present in blood vessels and also respiratory

muscles (both voluntary and involuntary).

3. Secretory functions.

II. Sensory Functions:

1. Vata Stimulatory all sensations.

2. The information about the Artha from sense organ is

carried to the Mangas and Buddhi (Cortical centers) for

Nischyatmkajnana.


12

The receptive impression of the Artha on the sense organ is

transformed in to the nerve impulse in the organ and carried through the

Samjnavaha srotas via the Manas to Indriya Buddhi ( Respective Cortical centers) .

III. Integration of Motor and sensory Functions:

The “Tantra – Yantra Dharah’ Function of vata signifies this

integration. This function incorporates the maintenance of equilibrium of the body

and also the kinesthetic sense (perception of One’s own body parts, weight and

movement). This integration of gate and gandhana is executed in the Manas which

is ubhayatmaka, to make the movements co-ordinated and purposeful. Therefore an

emphasis is given on relation of vata with the srota and spanyanandnya.

IV. Biochemical Functions:

Even though the chemical relations in the body are conducted by the

respective pitas the planning is managed by vata.

1. Dhatuvyuhakana sign thesis of the dhatus from the nutrients present

in the Rejadhatu / Ahevarafa in to definite structures according to the

plan of requirement of the body.

2. Regulation of the functions of the dhatas.

V. Division and Differentiation of the Cells:

1. Vata is the main force for the union and division of the Para manus.

“Samyoga Vilshaga Paramanunam karanam vayuh” Here the

“paramanus “are to be understood as cells (or) Jeevapanamanus.

2. Development of the Garbhakfi is through the differentiation of cells

during the development according to the requisite specialized

functions.


13

3. The first four of the above stated functions are related to the

Mastishka and Vatavaha Srotasas (CNS) and the last two to the

genetic material, affected by the stimulation by vata present in each

cell.

TYPES OF VATA:

Vata has been classified into five types according to sites and

functions viz. Prana, udana, Samana and Apana.21In Vedic treatises aiso we will

find five types of vata, NAGA, KURMA, KRUKARA, DEVA DATTA

ANDDHANUNJAYA VATAS.22

Charaka has given complete description of five types of vata and left

other two doshas. In tridoshas only vata is swatantra as other two are dependents of

it.23

PRANA VATA:

Shiras is stated to be the seat of Prana vata by Charaka and Vagbhata.24, and this is stated to be the transverse in the region of the oral cavity, ears, neck

and chest for the proper control and the discharge of its functions.

Stheevana, Kshavathu (sneezing), Udgara, Uchwasa, Nisswasa,

control over Hridaya, Buddhi, Indritas and Manas; these are all functions of Prana

vata. 25

UDANA VATA:

Nabhi, Uras, Kantha desha 26 Susruta has not mentioned any

particular seat of Udanavata but states that the most important of the vayus which

courses upwards is called Udana 27 and Vagbhata explains its seat is Uras and

moves in the regions of Throat, Nose and Nabhi. 28


14

Vakpravruthi, Praytna, Urja, Bala, Varna and Smrithi are the

functions of this vata. 29 Susruta mentions only Vakpravrithi, while Vagbhata added

functions – nourishment or soothing effect of srotases and arousal of the mind,

intellect, will and memory.30

VYANA VATA:

Charaka, Susruta have not mentioned any specific place regarding

the location of the vyana vata except that it pervades swiftly throughout the body31

but Vagbhata says vyana vata stays in Hridaya but traverses throughout the body

very swiftly.32

Gathi, Prasarana, Akunchana, Utkshepana, Apakshepana, Nimesha

and regulation of circulation of Rasa dhatu through out the body.33 In addition to it

Susruta saya outflow of sweda and raktha from body. Five kinds of movements –

extension, flexion upwards, downward movements and lateral thrust are observed,

by Susruta as functions of Vyana vata.34

While Vagbhata says Jrumba, recognizing the taste of food,

cleansing of the srotases, effecting the outflow of the srotases and bloof from the

body, depositing, the semen inside the vaginal cavity. Separating the essence of

food from the waste matter and nourishing the dhatus and all movements of the

body are conducted by the vyana vata.

SAMANA VATA:

Charaka says Samana vata is located in the neighbourhood of the seat

of Agni.36 Here the word Agni is understood as ‘ANTARAGNI’ or Pachakagni

(Pachaka pitta), one of the five kinds of pitta, which is capable of digesting Asitadi

four varieties of food ingested by man located in the Amashaya and Pakwashaya.

Susruta has only stated that Samana vata courses in the Amashaya

and Pakwashaya 37 while Vagbhata states that this is located near the Antaragni and


15

courses through Amashaya and Pakwashaya and also the channels carrying doshas,

malas, shukra, artava and ambu.38

Main function of samana vata is stimulation or initiation of the

pachakagni (pitta). It also regulates the srotases carrying sweda, dosha (waste

matter) and ambu (water) 39, and helps anaragni to digest the food taken in proper

dose and at proper time which leads to the increase of the life40 and after the

digestion is completed, it helps in the saara kitta vibhajana 41. As Vagbhata says that

this will receive the food (into anna vaha srotas), retains it till the digestion is

completed is completed, separates the saara from kitta and finally propels the kitta

to the later part of the vaha srotas.42

APANA VATA:

The vata which has a special tendency to move downward is called

‘APANA VATA’. According to Charaka the seat of this is two tests, the urinary

bladder, the penis, the umbilicus, the thigh, the groin, the rectum and the lower part

of the antrum.43 Susruta states that Apana vata is located in the pakwadhanam44

means the receptacle of the fully digested food.

Vagbhata states the apana vata resides in the region of sroni which may be

interpreted as the pakwadhana (colon and rectum) and moves through the regions of

urinary bladder, hips, penis, tests, groin and thighs.45

There is no different opition among all authorities regarding

functions of apana vata.They are to facilitate excretion of faeces and urine, ejection

of semen, to bring down the menstrual flow, to bear down the foetus at the time.


16

Shariravata and Nerve Phenomenon:

It has often been asked if vata as indeed the tridoshas can be

quantitatively determined and experimentally demonstrated the available

descriptions of tridoshas mentioned in the books are essentially qualitative and

functional. Thils is particularly so in the case of vata. It may however; vata that is

very closely resembles that of the nerve impulse, which has been described as a self

– prorogated disturbance in the nerve fibre. In other words, the energy for the

transmission of the impulse is stated to be derived from the nerve fibre over which it

passes.

The Similarities between the Phenomenon of vata and nerve impulse can be noticed

from the following table.

VATA NERVE IMPULSE

1. Amurta – invisible no corporeal form .

It is energy

1. Invisible not perceived by Sense

organs.

2. Anavasthita / Chalaswabha It is

mobile

2. It is conducted in one direction from

the neuron through axon to its

termination.

3. Swamyambhu self originate and self

propagated

3. Self originated in the neurons of cells

and self propagated in nerve fibre

4. Sukshma capable of passing through

small channels

4. Pass through a nerve fibre of even of

one micron in diameter

5. Seegraghati Swift movement 5. Moves in a nerve fibre some times at

a velocity of 100 mts / second

6. Avyahatagata 6. Obstruction in its movement leads to

Pathalogical condition.

7. Functions of gati and gandhana 7. Motor and sensory functions.


17

References:

1. Ch. Su.21/4; Su.Su 21/5

2. Panimi 27. Su. ni. 1/14

3. Su.su. 15/3 and A.H.Su 11/1 28. A.San.su.20/4

4. A.Hru.su.1/7 29. A.Hru.su.12/5

5. Su.su. 12/3 Ch.chi.28/1

6. Ch.su. 12/3 30. As.San.Su.20/4

7. A.San. Ni.6 31. Ch.chi. 28/9

8. Rigveda 1-3-6 Su.ni1/17

9. Ch.su.12/25 32. A.Hru.su.12/6

10. Ch.Vi.1 A.San.su. 20/4

11. Ch.Su.20 33. Chi. 15/36

12. Ch.su. 12/4; Su.ni.4 34. A.Hru.su.12/7

13. Su.su. 46/24 35. A.Hru.su.12/7

14. Ch.vi. 8/98 A.San.su. 20/4

15. Ch.su. 1/9 36. Ch.chi.28/8

16. Ch.chi.3/38 37. Su.ni.1/16

17. Su.ni. 1/7-8 38. A.San.su. 20/4

18. Tridosha theory by V.V.Subrahmanya sastry

19. A.Hru. su. 12/11 39. Ch.chi. 28/6

20.Ch.chi.28 40. Ibid 15/17

21. A.San.su. 20 Su.ni. 1/16

22. Agni Purana 41. Ibid

23. Ch.chi. 28/6 ; A.Hru.su. 12/4 42. A.San.su. 20/4

24. Ch.chi 28/6 ; A.Hru.su. 12/4 A.Hru.su. 12/8

25. Su.ni.1/3 ; A.Hru.su. 12/45 43. Ch.chi. 28/20

A.San.su.20/4

44. Su.ni. 1/19 A.Hru.su.12/1

45. A.San.su. 20/4 A.Hru.su. 12/4

46. Ch.chi. 28/10 Su.ni. 1/19 A.San.su. 20/4 A.Hru.su. 12/9


18

STRUCTURAL & FUNCTIONAL ASPECTS OF

NERVOUS SYSTEM

The nervous system is the body’s control centre and communications net

work. In human being the nervous system serves three broad functions.

First it senses changes within the body and in the outside environment,

second it interprets the changes, third it responds to the interpretation by initiating

action in the form of a muscular contractions or glandular secretions.

Through sensation, integration and response, the nervous system represents

the body’s most rapid means of maintaining homeostasis.

ORGANISATION:

The nervous system may been divided into two principal divisions. The

Central Nervous System (C.N.S) and the Peripheral Nervoua System (P.N.S) and

several subdivisions.

The C.N.S is the common centre for the entire system and consists of the

BRAIN & SPINAL CORD. The various nerve processes that connect the brain and

spinal cord with preceptors, muscles and glands constitute the peripheral nervous

system. The P.N.S may be divided into AFFERENT and EFFERENT system.

The Afferent System consists of nerve cells that convey information from

receptors in the periphery of the body to the C.N.S.

The efferent system consists of nerve cells that convey information from the

C.N.S. to muscles and glands.


19

The efferent system is subdivided into a SOMATIC NERVOUS SYSTEM

(S.N.S) and an AUTONOMIC NERVOUS SYSTEM (A.N.S). the S.N.S. consists of

efferent neurons that conduct impulses from the C.N.S to skeletal muscle tissue. The

A.N.S by contrast contains efferent neurons that convey impulses from the C.N.S to

smooth muscle tissue, cardiac muscle tissue and glands with few exceptions. The

viscera receive nerve fibers from the two divisions of the A.N.S the

SYMPATHETIC DIVISION, and the PARA SYMPATHETIC DIVISION.

HISTOLOGY:

Despite the organizational complexity of the nervous system it consists of

only two principal kinds of cells NEURONS & NEUROGLIA.

NEUROGLIA:

The cells of the nervous system that perform the functions of support and

protection are called neuroglia (Neuro = Nerve, Glia = Glue) or glial cells. About

50% of the all brain cells are neuroglial cells. See table No.1 for description and

functions of neuroglia of central nervous system.


20

TABLE NO.1

NEUROGLIA OF CENTRAL NERVOUS SYSTEM

TYPE DESCRIPTION FUNCTION

Astrocytes Star shaped cells with numerous

processes. Proto plasmic

astrocytes are found in the gray

matter of the C.N.S. and fibrous

astrocytes are found in the white

matter of the C.N.S

Twine around nerve cells to

form supporting net work in

brain, and spinal cord, attach

neurons to their blood

vessels.

Oligo dendroytes Resemble astrocytes in some

way but processes are fewer and

shorter

Give support by forming semi

rigid connective tissue rows

between neurons in brain and

spinal cord; produce a myelin

sheath around axons of

neurons on central nervous

system.

Microglia Small cells with few processes,

derived from monocytes;

normally stationay jbut may

migrate to site of injury; also

called brain macro phages.

Engulf and destroy microbes

and cellular debris; may

migrate to area of injured

nervous tissue and function as

small macrophages.

Ependyma Epithelial cells arranged in

single layer and ranging in

shape from squamus to

columnar; many are ciliated.

Form a continuous epithelial

lining for the ventricles of the

brain (spaces that form and

circulate cerebro spinal fluid)

and the central canal of the

spinal cord.


21

NEURONS:

Nerve cells are called neurons are responsible for conducting impulses from

one part of the body to another. They are the structural and functional units of the

nervous system.

Structure of Neurons:

The neuron consists of 3 distinct portions 1.Cell body 2.Dendrites and

3.Axon.

The cell body or soma or perikaryon contains a defined nucleus and

nucleolus surrounded by a granular cytoplasm. Within the cytoplasm are typical

organells such as lysosomes, mitochondria and golgi complexes. Many neurons also

contain cytoplasmic inclusions such as LIPOFUSCIN. It may be a by product of

lysosomal activity. Although its significance is un-known, lipofuscin is related to

ageing. Also located in the neurons Nissl body’s and Neurofibrils. Nissl bodies are

orderly arrangements or granular (rough) endoplasmic reticulum, whose function is

protein synthesis. Neuro fibrils are long thin fibrils composed of microtubules.

The cytoplasmic processes of neurons generally depend on the direction in

which they conduct impulses. There are two kinds of dendrites and Axons (Dendro

= Tree).

Dendrites are highly branched, thick extensions of the cytoplasm of the cell

body.

They typically contain Nissl bodies, Mitochondria and other cytoplasmic

organelles. A neuron usually has several main dendrites. Their function it to conduct

an impulse towards the cell body.


22

The second type of cytoplasmic process, celled as an Axon (Axis =

Cylinder) is a single, highly specialized, long, thin process that conducts impulses

away from the cell body to another neuron or tissue. It usually originates from the

cell body as a small conical elevation called the AXON HILLOCK. An Axon

contains mitochondria and Neurofibrils but no Nissl bodies. Thus it does not carry

on protein synthesis. It’s cytoplasm, cells or axoplasm is surrounded by a plasma

membrane known as the anolemma (Lemm = Sheath or husk). Along the coarse or

an axon there may be side branches called Axon collaterals. The Axon and its

collaterals terminate by branching into many fine filaments called TELODENDRIA.

The distal ends of telodendrial are expanded into bulb like structures called synaptic

knobs (end feet) which are important in nerve impulse conduction. They contain

membrane enclosed sacs called synaptic muscles that store chemicals that determine

whether impulse conduction occurs or not. The cell body of a neuron it essential for

the synthesis of many substances that sustain the life of the nerve cell. Many axons

are surrounded by a segmented covering called MYELIN SHEATH. The function of

the myelin sheath is to increase the speed of nerve impulse conduction and to

insulate and maintain the axon. Myelin is responsible for the colour of the white

matter in the nerves, brain and spinal cord.

The myelin sheath or axons of the peripheral nervous system is produced by

flattened cells called Schwann Cells located along the axons. The inner portion

consisting of several layers of schwann cell membrane is the myelin sheath. The

peripheral nucleated cytoplasmic layer of the schwann cell (The ouer layer that

encloses the sheath) is called the NEUROLEMMA (Sheath of Schwann). The

neurilemma is peripheral nervous system. Its function is to assist in the regeneration

of injured axons. Between the segments of the myelin sheath are unmyelinated gaps

called NODES OF RANVIER. The amount of myelin increases from birth to

maturity.


23

Classification of Neurones:

The different neurons of the body may be classified by structure and

function. The structural classification is based on the number of processes extending

from the cell body.

Multipolar neurons have several dendrites and one axon.

Eg. : Mostly in brain and spinal cord.

Bi-polar neurons have one dendrite and one axon.

Eg. : Found in retina of the eye, the inner ear and the olfactory area.

uni-polar neurons have only one process extending from the cell body.

Eg. : Found in posterior root ganglia or spinal nerves.

PHYSIOLOGY OF THE NERVOUS SYSTEM:

The functions of the nervous tissue are:-

i. Limited ability to regenerate

ii. Highly developed ability to produce and transmit electrical messages

called nerve impulses.

REGENERATION:

Unlike the cells of epithelial tissue, neurons have only limited powers for

regeneration. Around the time of birth the cell bodies or most developing nerve cells

loose their mitotic apparatus and their ability to reproduce. Thus when a neuron is

damaged or destroyed it cannot be replaced by the daughter cells of the other

neurons. A neuron destroyed is permanently lost and only some types of damage

may be repaired.

Damage to some types of myelinated axons often can be repaired it the cell

body remains intact and if the cell that performs the myelination remains active.


24

Axons in the peripheral nervous system are myelinated by schwann cells.

Schwann cells proliferate follwing axonal damage and their neurilemmas form a

tube that assists in regeneration, axons in the brain and spinal cord are myelinated

by OLIGODENDROGLIAL CELLS. These cells do not from neurilemmas to assist

in regeneration and do not survive following axonal damage and the affected region

is rapidly converted into a special form of scar tissue by ASTROGLIAL

PROLIFERATION. The scar tissue from s barrier to regeneration. Thus an injury to

the brain and spinal cord is also permanent because axonal regeneration is blocked

by rapid scar tissue formation. An injury to a nerve in the arm (P.N.S i.e.

pheripheral nervous system) may repair itself before scar tissue forms and so some

nerve function may be restored.

FUNCTIONS OF THE NERVOUS SYSTEM:

The nervous system carries out a complex ara of tasks such as

sensing various smells, producing speech, remembering signals that control body –

movements and regulating the operation of internal organs. These diverse activites

can be grouped in to three basic functions. Sensory integrative and motor.

Sensory Function:

Sensory receptors detect internal stimuli such as increase in

blood acidity and external stimuli landing on your arm. The nervous that carry

sensory information from spinal and cranial nerves in to the brain and spinal card or

from a lower to higher level in the spinal card and brain are sensory (or0 afferent

nervous.


25

Integrative Funcion:-

The Nervous system integrates (process), sensory information

by analyzing and storing some of it and by making decisions for appropriate

response. Many of the nurons that participate in integration are interring neurons,

who axons exterd only for a short distance and contact near by neurouns in the brain

spinal card or ganglion. Inter neurons comprise the vast variety of neurons in the

brain.

Motor Function:

The nervous system’s motor function involves responding to

integration decisions. The neurons that serve this function are motor or different

neurons. Motor neurons carry information from to brain towards the spinal card (or)

out of the brain and spinal card in to cranial (or) spinal nerves.The cells and organs

contacted y motor – neurons in cranial and spinal nerves are termed effectors

muscle – fibers and glandular cells are examples of effectors.

NERVE IMPULSE:

1. The nerve impulse is the body’s quickest way of controlling and maintaining

homeostasis.

2. The membrane of a non-conduction neuron is positive outside and negative

inside due to the operation of the sodium potassium pump. This difference in

charge is called a resting potential and the membrane is said to be polarized.

3. When a stimulus causes the inside of the cell membrane to become positive

and the outside negative, the membrane is said to have an action potential,


26

which travels from point to point along the membrane. The traveling action

potential is a nerve impulse. The ability of a neuron to respond to a stimulus

and convert it in a nerve impulse is called excitability.

4. Restoration of the resting potential is called repolarisation. The period of

time during which the membrane recovers is called the refractory period.

5. According to the all-or-none principle, if a stimulus is strong enough to

generate an action potential, the impulse travels at a constant and maximum

strength for the existing conditions.

6. Nerve impulse conduction in which the impulse jumps from node to node is

called SALTATORY CONDUCTION.

7. Fibers with larger diameters conduct impulses faster than those with smaller

diameters.

8. Conduction across synapses:

a. Impulse conduction can occur from one neuron to another or from a

neuron to effecter.

b. The junction between neurons is called a synapse.

c. At a synapse there is only one way. Impulse conduction from a pre-

synaptic axon to a post synaptic dendrite, cell body or axon hillock.

d. An excitatory transmitter receptor interaction is one that can lower

(make less negative) the post synaptic neurons membrane potential.

So that a new impulse can be generated across the synapse.


27

e. A inhibitory transmitter or receptor interaction is one that can raise

(make more negative) the post synaptic neurons membrane potential

and they inhibit an impulse at a synapse.

f. It is through that the transmitter that causes excitation in a major

portion of the C.N.S is ACETYL CHOLINE. An enzyme called

ACETYL CHOLINESTERASE it activates acetylcholine. The

probable transmitters that lead to excitation are NOREPINEPHRINE,

SEROTONIN, DOPAMINE, HISTAMINE and GLUTAMATE.

Transmitters that are probably inhibitory are GAMMA AMINO

BUTYRIC ACID (G.A.B.A.) and CLYCINE.

g. The post synaptic neuron is an integrator. It receives signals

integrates them and then responds accordingly.

ORGANISATION OF NEURON SYNAPSES:

1. Neurons in the C.N.S. are organized into definite patterns called NEURAL

POOLS. Each pool differs from all others and has its own role in regulating

homeostasis.

2. Neuronal pools are organized in to circuits. These include simple series,

diverging, converging, reverberating and parallel after discharge circuits.

TRANSMITTER SUBSTANCES IN THE BRAIN:

1. Over 40 different substances are known or suspected transmitter substances

in the brain that can facilitate i.e. exite or inhibit postsynaptic neurons.

2. Examples of transmitter substances include acetylocholine (ACH)

norepinephrine (NE), dopamine (DA), serotonin (5-HT) glutamine acid,

aspartic acid, gamma amino-butyric acid (GABA) and glycine.


28

3. Peptide chemical messengers that act as natural pain killers in the body are

encephalins, endorphins and dynorphin.

4. Other peptides serve as hormones or other regulators of physiological

responces. Examples include angiotensis cholecystokinin, neurotensin and

regulating factors produced by the hypothalamus.

ANATOMY

The Encephalon (or) brain and the medulla Spinals (or)

Spinal Card together from the central nervous system. Extended from this in pairs

are 12 pairs of cranial nerves and 31 pairs of Spinal nerves constituting a Peripheral

nervous system. This itself includes not only all the ramificationsof these merves,

which mediate Sanatic sensory and motor functions, but also the entire complex of

visceral (or) Splanchanic nerves, Connected to the CNS through somatic Channels,

Thus forming a peripheral autonomic nervous system.

DIVISIONS OF THE BRAIN

Brain:-

I. Rhombencecephalon (Hind Brain)

a. Myelencaphalon (Medulla Oblongata)

b. Metencephalon (Pons)

c. Cerebellum

II.Mesencephalon (Mid Brain)

III.Prosencephalon (Fore Brain)

a. Diencephalon (Between brain)

b. Telencephalon (Cereberal Hemispheres – Cerebrum)


29

The diencephalon which is central connecting part of the brain,

corresponding approximately to the thalamus and hypothalamus and telencephalon.

which comprises the two so called cerebral hemispheres (or) cerebrum.

Blood flows to the brain mainly via the internal carotid anteries and

vertebral anteries. The internal singular veins retum blood from the head to the

heart.

In an admit the brain represents only 2% of total body weight, but it

consumes only about 20% of the oxygen and glucose at rest. Neurons synthize ATP

almost exclusively from glucose via reactions that use O2 (Oxidative

Phosphorylationin mitochondria). When activity of neurons and neunoglia increase

in a region of the brain, blood flow to that area also increases. Even a brief slowing

of brain boold flow may cause unconscousness. Typically, are interruption in blood

flow for 1 or 2 minutes impares neuronal function, and total deprivation of 02 for

about 4 minutes causes permanent injury. Because no glucose is stored in the brain,

the supply of glucose also must be continous. If blood entering the brain has a low

level of gluose mental confusions, dizziness, convulsions and loss of consciousness

may occur.

The existence of a blood – brain barrier (BBB) protects brain cells from

harmful substances and pathogens by reventing panage of many substances from

blood in to the brain tissue.

Protective coverage of the brain:-

The cranium and the cranial meninges surround and protect the brain

the cranial menings are continous with the spinal menings have the same stratus the

Outer-duramatter

Middle-arachoid matter

Inner-piameter


30

There extensions of the durameter separate parts of the brain

1. the falx cerebri – separates two hemispheres of cerebrum

2. the balxcerebelli - separates two hemispheres of cerebellum

3. the tentorium cerebella – separates cerebrum from the

cerebellum.

Cerebrospinal fluid (CSF):-

CSF is a char, colourless liquid that protects the brain and spinal cord

against chemical and physical injuries.It also carries O2, glucose and other neeed

chemical;s from the blood to nervous and neurogla.CSF continuously circulates

through cavities in the brain and spinal cord and around the brain and SC in the sub-

arachnoid space.

THE BRAIN STEM

The brainstem is the part of the brain between the spinal cord and the

diencepnaton.It consists of three structurally and functionally connected regions.

1. the medulla oblongata

2. pons

3. mid-brain

Extending through the brain stem the reticular formation. a net like region of

interspersed grey and white – matter.


31

Medulla oblongata :-

The Medulla oblongata begins at the foramen magnum and extends

to the inferior border of the pons, a distance of about –3cm.

It contains both motor and sensory axons contains nuclei that are

reflex centres for regulation of heart rate, swallowing, respiratoray,

vasoconstriction, coughing, vomiting and sneezing.

It also contains nuclei associates with cranial nerves VIII through

XII.

PONS :-

It connects the spinal cord with the brain and links parts of the brain

with one another by way of tracks.

Pontine nuclei relay nerve impulses related to voluntary skeletal

muscles from the cerebral catex to the cerebellum.

The Pons contain the pneumotaxic and apneustic centres which help

control breathing. It contains nuclei associated with cranial nerves. V – VII and the

vestibular branch of cranial nerve VIII.

MID – BRAIN:

The mid brain is between pons and diencephalon and surrounds the

cerebral duct.

It conveys motor – impulses from the cerebrm to the cerebellum and

spinal cord sends sensory impulses from the S.C. to Thalamus and mediates

auditory and visual refuxes.


32

It also contains nuceli associated with cranial nerves. III & IV.

A large part of the brain stem consists of small areas of grey – matter

and white – matter called the reticular formation. It helps maintain consciousness,

causes awaking from sleep and contributes to regulating muscle tone.

THE CEREBELLUM:-

The cerebellum occupies the inferior and posterior aspects of the

cranial – cavity. It consists of two lateral – hemispheres and a medial constricted –

vermis.

It connects to the brain – stem by 3 pairs of cerebral – penduncles. The

cerebellum functions to co – ordinate movements and to maintain normal muscle

tone, posture and balance.

THE DIENCEPTHALON:-

The diencephalon surrounds the third ventricle and consists of the

thalamus, , hypothalamus, epithalamus and sub – thalamus.

The thalamus is superior to the mid – brain and contains nuclei that

relay sensory impulses to the cerebral cortex. It also allows crude appreciation of

painful, thermal and pressure sensations and mediates some motor activites.

The Hypothalamus is inferior to the thalamus. It controls the

autonomic nervous system, secretes harmones, functions in the rage and aggression,

governs body temperature, regulates food and fluid intake and establishes greadian

rhythms.


33

The epithalamus consists of the pineal gland and the habecular

nuclei. The pineal gland seeretes melatonin which promotes sleep and helps set the

body’s biological clock.

The sub – thalamus connects to motor – areas of the cerebrum.

Circum vetricular organs (CVO’s) can monitor chemical changes in the blood

because they lack the blood – brain barrier.

CEREBRUM:-

The cerebrum is the largest part of the brain. Its contex contains gyri

(convulutions). Fissures and sulci.The cerebral lobes are named frontal, parietal,

temoporal, and occipital.

Which matter is deep to the cortex and consists of myelinated and

unmyelinated axons exending to other regions as association, commissural and

projection tracts.

The basal – ganglia are several groups of nuclei in each cerebral

hemisphere. They help automatic movements of skeletal muscles and helps regulate

muscle tone.

The linbic – system encircles the upper part of the brain – stem and

the corpus – callosum. It functions in emotional aspects of the behaviour and

memory.

BLOOD SUPPLY OF THE BRAIN:

Arteries supplting the brain

The arteries supplying the brain are the internal carotid and vertebral

arteries and their branches. Which lie in the sub – arachonoid space.


34

Cerebral part of I.C.A. and its branches:-

After piereing the duramater forming the roof of the cavernous sinus

the I.C.A gives off 3 large branches. These are the

1. Opthalmic artery - Which supplies the orbit and

2. Anterior and

3. Middle cerebral anteries of the brain.

It also gives off two smaller branches that take part in supplying the

brain these are the posterior communicating antery and the anterior choroidal artery.

Anterior Cerebral Artery:-

It arises from the I.C.A below the anterior perforated substance,

lateral to the optic – chaisma from here it runs forwards and medially crossing

above the opticnerve to reach the longitudinal tissure separating the two cerebral

hemispheres. Here the artery of the two sides lie close together and are linked to

each other by the anterior communicating antery. The antery now turns sharply to

reach the genu of the corpos callosum. It winds round the front of the genu and then

runs backwords just above the body of carposum callosum, ending man its posterior

part. The distribution of the artery is considered.

The recurrent branch of the anterior cerebral artery (artery of

heubner).This artery runs backwords and laterally to enter other anterior perforted

substance.


35

Middle cerebral artery:-

After its origin form the I.C.A. the middle cerebral artery runs

laterally in the depth of the stem of the lateral sulus. It curves on to the superolateral

surface and runs backward in depth of the posteiror rami to lateral sulcus. The main

stem of the artetry can be seen only by artificially seperating the lips of the suclus.

Posterior communicationg Artery:-

The artery runs backwards and anastomoses with the posterior

cerebral artery, helping to complete the circulus arteriors.

Cranial part of Vertebral Arteris:-

It gives of the anterior and posterior spinal arteries and the posterior

inferior cerebbral artery to the spinal cord and brain.

Basilar artery and its branches:-

The basilar artery is formed by the union of the right and left

vertebral arteries at the lower border of the pons. It ascends in the midline ventral to

the pons, and ends at its upper border by dividing in to the right and left posterior

cerebral arteries. It gives off the following branches:

Cerebellar

Pontine

labryn thine

Anterior inferior cerebellar.


36

The Circulus Arteriosus (of Willis):-

A considerable part of the brain is supplied by the two

vertebral arteries and a remarkable anastomoses, the circulus arteriosus exists

between these and the two internal carotid arteries. This circle (which is really more

polygonal than circular), is situated in the cisterna interpeduncularis at the base of

the brain and encloses the optic- chaisma and the structures in the interpenducular

fossa.

It is formes as follows:

Infornt the two anterior cerebral arteries are joined to each

other by the anterior communicating artery behind the basilar artery divides in to the

two posterior cerebral arteries each of which is joined to the internal carotid artery

of the same side by posterior communicating artery.

CRANIAL NERVES

1. Twelve pairs of cranial nerves originate from the brain.

2. The pairs are named primarily on the basis of distribution and numbered by

order of attachment of the brain.


37

CRANIAL NERVES LOCATION AND FUNCTIONS

CRANIAL

NERVE

LOCATION FUNCTION AND

CLINICAL APPLICATION

OLFACTORY

NERVE

Arises in olfactory mucosa,

passes through olfactory bulb

and olfactory tract and

termineates in primary

olfactory areas of cerebral

cortex

Smell:

Loss of the sense of smell, called

anosmia, may result from head

injuries in which the cribrifrom

plate of the ethmoid bone is

fractured and from lesions along

the olfactory pathway.

OPTIC NERVE Arises in retina of the eye,

forms optic chiasma passes

through optic tracts, lateral

geneculate nucleaus in

thalamus, and terminates as

in visual areas of cerebral

cortex.

Vision:

Fractures in the orbit, lesion

along the visual pathway, and

diseases of the nervous system

may result in visual field defects

and loss of visual acuity. A

defect of vision is called anopsia.

OCULOMOTOR

NERVE

Motor portion:

Originates in mid brain and

is distributed to levator

palpebrae superioris of upper

eye lid, four extrinsic eye

ball muscles (superior rectus,

rectus, inferior rectus and

inferior ciliory muscles of

eye ball and sphincter muscle

of iris.

Sensory protion:

Motor:

Movement of eye lid and eye

ball, accommodation of lens for

near vision and constriction of

pupil.

Sensory:

Muscles sense (Proprioception).

A lesion in the nerve causes

strabismus (sqinting), ptosis

(drooping) of the upper eye lid,

pupil dilation, the movement of


38

Consists of afferent fibers

from proprioceptors in eye

base muscles and terminates

in mid brain.

the eye ball down wards and out

ward on the damaged side, loss

of accommodation for near

vision and double vision.

(Diplopia)

TROCHLEAR

NERVE

Motor portion:

Originates in mid brain and

is distributed to superior

oblique muscle, and extrinsic

eye ball muscle.

Sensory portion:


from proprioceptors in

superior oblique musclces

and terminates in mid brain.

Motor:

Movement of eye ball

Sensory:

Muscle sense (proprioception).

In trochlear nerve paralysis, the

head is tilted to the affected side

and diplopia and strabismus

occurs.

TRIGEMINAL

NERVE

Motor portion:

Originates in pons and

terminates in muscles of

mastication.

Sensory portion:

Consists of three branches:

1. Opthalmic: Contains

sensory fibers from

skin over upper eye lid,

eye ball, lacrimal

glands, nasal cavity,

side of nose, fore head

and anterior half of

scalp.

Motor: Chewing

Sensory: Conveys sensations for

touch pain and temperature from

structures supplied. Muscles

sense (Proprioception). Injury

results in paralysis of the

muscles of mastication and a

loss of sensation of touch, and

temperature. Neuroglia pain of

one or more branches of

trigeminal nerve is called

Trigeminal neuralegia

(ticdoulareux)


39

2. Maxillary: Contains

sensory fibers from

mucosa of nose, palate

parts of pharynx upper

teeth, upper cheek and

lower eye lid.

3. Mandibular: Contains

sensory fibers from

anterior two thirds of

tongue, lower teeth,

skin over mandible and

side of head in front of

ear. The three branches

terminates in pons.

Sensory portion also

consists of afferent

fibers from

proprioceptors in

muscles of mastication.

ABDUCENT

NERVE

Motor Portion:

Originates in pons and is

distributed to lateral rectus

musclean, extrinsic eye ball

muscle.

Sensory Protion:


from proprioceptors in lateral

rectus muscle and terminates

in pons.

Motor: Movement of eye ball

Sensory: Muscle sens

(Proprioception). With damage

to this nerve, the affected ball

cannot move laterally beyond the

midpoint and the eye is usually

directed medically.


40

FACIAL NERVE Motor Portion:

Originates in pons and

distributed to facial, scalp,

and neck muscles, and to

lacrimal, sublingual, sub

mandibular, nasal and

palatine glands.

Sensory Protion:

Arises from taste buds on

anterior two-thirds of tongue,

passes through geniculate

ganglion a nuleus in pons

that sends fibers to thalamus

for relay to gustatory areas of

cerebral cortex. Also consist

of afferent fibers from

proprioceptors in muscles of

face and scalp.

Motor: Facial expression and

secretion of saliva and tears.

Sensory: Taste, muscle sense

(Proprioception). Injury

produces paralysis of the facial

muscles, called Bell’s pasly, loss

of taste and the eye remain open,

even during sleep.

VESTIBUL

COCHLEAR

NERVE

Cohlear branch:

Arises in spiral organ, forms

spiral ganglion, passes

through a nucleus in the

medullar, and terminates in

thalamus. Fibers synapse

with neurons that relay

impulses to auditory areas of

cerebral cortex.

Vestibular branch:

Arises in semicircular canals,

Cochlear branch:

Conveys impulses associated

with hearing.

Vestibular branch:

Conveys impulses associated

with equilibrium. Injury to the

cochlear branch may cause.

Tinnitus (Ringing) or deafness.

Injury to the vestibular branch

may cause vertigo (a subjective

feeling of rotation), ataxia, and


41

saccule, and utricle, and

forms vestibular ganglion;

fibers pass through medullar

and pons and terminate in

thalamus.

nystagmus (Involutary rapid

movement of the eye ball).

GLOSSO

PHARYNGEAL

NERVE

Motor protion:

Originates in medullar and is

distributed to swallowing

muscles of pharynx and to

parotid gland.

Sensory protion:

Arises from taste buds on

posterior one-third of tongue

and from cartid sinus and

terminates in the tongue also

consists to afferent fibers


swallowing muscles

supplied.

Motor: Swallowing movements

and secretion of saliva.

Sensory: Taste and regulation of

blood pressure; muscle sense

(proprioception). Injury results

in pain during swallowing,

reduced secretion of saliva, loss

of sensation in the throat, and

loss of taste.

VAGUS NERVE Motor portion:

Originates in medullar and

terminates in muscles of

pharynx, bronchus,

respiratory passage ways,

lungs, esophagus, heart,

stomach, small intestine,

most of large intestine and

gallbladder.

Sensory Portion:

Motor: Visceral muscle

movement and swallowing

movements.

Sensory: Sensations from organs

supplied; muscle-sense

(proprioception). Severing of

both nerves in the upper body

interferes with swallowing,

paralyzes vocal cords, and

interrupts sensations from many


42

Arises from assentially same

structures supplied by motor

fibers and terminates in

medullar and pons. Also

consists of alterent fibers


muscles supplied.

organs. Injury to both nerves in

the abdominal area has little

effect, since the abdominal

organs are also supplied by

autonomic fibers from the spinal

cord.

ACCESSORY

NERVE

Motor portion:

Consists of a bulbar portion

and a spinal portion. Bulbar

portion originates from

medullar and supplies

voluntary muscles of

pharynx, larynx and soft

palate. Spinal portion

originates from anterior gray

horn of first five cervical

segments of spinal cord and

supplies sternocleido mastoid

and trapezius muscles.

Sensory portion:



muscles supplied.

Motor:

Bulbar portion mediates

swallowing movements spind

portion mediates movements of

heads.

Sensory:

Muscle sense (proprioception). If

damaged the ster

nocleidomastoid and trapezius-

muscles become paralysed, with

regulating inability to turn the

head or raise the shoulders.

HYPOGLOSSAL

NERVE

Motor Portion:

Originates in medullar and

supplies muscles of tongue.

Sensory portion:

Consists or fibers from

Motor:

Movement of tongue during

speech and swallowing.

Sensory:

Muscle sense (proprioception).


43

proprioceptors in tongue

muscles that terminate in

medullar.

Injury results in difficulty in

chewing, speaking and

swallowing, the tongue when

protruded curls towards the

affected side and the affected

side becomes atrophied,

shrunken and deeply furrowed.

GROUPING OF NEURAL TISSUE:

1. White matter is an aggregation of myelinated axons and associated

neuroglia.

2. Gray matter is a collection of nerve cell bodies and dendrites of

unmyelinated axons along with associated neuroglia.

3. A nerve is a bundle of nerve fibers outside the central nervous system.

4. A ganglion is a collection of cell bodies outside the CNS.

5. A tract is a bundle of fibres of similar function in the CNS.

6. A nucleus is a mass of nerve cell bodies and dendrites in the gray matter of

the brain and spinal cord.

7. A horn or column is an area of gray matter in the spinal cord.


44

SPINAL CORD-GENERAL FEATURES:

1. The spinal cord begins as a continuation of the medullar oblongata and

terminates at about the second lumbar vertebra.

2. It contains cervical lumbar enlargements which serve as points of origin for

nerves to the extremities.

3. The tapered portion of the spinal cord is the conus medularis from which

arises the filum terminal and cauda equine.

4. The spinal cord is partially divided into right and left sides by the anterior

median fissure and posterior median sulcus.

5. The gray matter in the spinal cord is divided into horns and the white matter

into funiculi or columns.

6. In the center of the spinal cord is the central canal which runs the length of

the spinal cord and contains CSF.

7. There are ascending (sensory) tracts and descending (motor) tracts.

PROTECTION AND COVERINGS:

1. The spinal cord is protected by the vertebral canal, meninges, CSF and

vertebral ligaments.

2. The meninges are three coverings that run continuously around the spinal

cord and brain; dura mater, arachnoid and pia mater.


45

3. Removal of CSF from the subarachnoid space or ventricle is called a spinal

(lumbar) puncture. The procedure is used to diagnose pathologies and to

introduce antibiotics.

STRUCTURE IN CROSS SECTION:

1. Parts of the spinal cord observed in cross section are the gray commissure:

central canal: anterior, posterior and lateral gray horns; anterior, posterior

and lateral white columns and ascending and descending tracts.

2. The spinal cord conveys sensory and motor information by way of the

ascending and descending tracts respectively.

FUNCTIONS:

1. A major function of the spinal cord is to convey sensory impulses from the

periphery to the brain and to conduct motor impulses from the brain to the

periphery.

2. Another function is to serve as a reflex center. The posterior root, posterior

root ganglion and anterior root are involved in conveying and impulse.

3. A reflex is the shortest route that can be taken by an impulse from a receptor

to an effector. Its basic components are a receptor, a sensory neuron a center,

a motor neuron and an effector.

4. A reflex is a quick, involuntary response to a stimulus that passess along a

reflex arc. Reflexes represent the body’s principal mechanism for responding

to changes in the internal and external environment.


46

5. Somatic spinal reflexes include the stretch reflex, flexor reflex and crossed

extensor reflex.

6. A two-neuron or monosynaptic reflex arc contains one sensory and one

motor neuron. A stretch, such as the patellar reflex is an example.

7. A polysynaptic reflex arc contains a sensory association and motor neuron.

A withdrawal or flexor reflex and a crossed extensor reflex are examples.

8. Stretch and flexor reflexes are ipsilateral. The crossed extensor reflex is

contralateral.

9. The flexor and crossed extensor reflexes illustrate reciprocal innervation of

muscles.

10. Among clinically important somatic reflexes are the patellar reflex, the

Achilles reflex, the babinski sign and the abdominal reflex.

SPINAL NERVES:

Names: The 31 pairs of spinal nerves are named and numbered according to the

region and level of spinal cord from which they emerge.

COMPOSITION AND COVERINGS:

1. Spinal nerves are attached to the spinal cord by means of a posterior root and

an anterior root. All spinal nerves are mixed.

2. Spinal nerves are covered by endoneurium, perineurium and epineurium.

DISTRIBUTION:


47

1. Branches of a spinal nerve include the dorsal ramus, ventral ramus,

meningeal branch and rami communications.

2. The ventral rami of spinal nerves except for T2-T11 from networks of nerves

called plexus.

3. Emerging from the plexuses are nerves bearing names that are often

descriptive of the general regions they supply or the course they take.

4. The principal plexuses are called the cervical, branchial, lumbar and sacral

plexuses.

5. Nerves T2-T11 do not form plexuses and are called intercostals nerves. They

are distributed directly to the structures they supply in intercostals spaces.

DERMATOMES:

1. All spinal nerves except C1 innervate specific, constant segments of the skin.

The skin segments are called dermatomes.

2. Knowledge of dermatomes helps a physician to determine which segment of

the spinal cord or spinal nerve is malfunctioning.

SENSATIONS:

Definition:

1. Sensation is a state of awareness of external and internal conditions of the

body.

2. The prerequisites for sensation are reception of a stimulus, conversion of the

stimulus in to a nerve impulse by receptor, conduction of the impulse to the

brain and translation of the impulse into a sensation by a region of the brain.


48

CHARACTERISTICS:

1. Projection occurs when the brain refers a sensation to the points of

stimulation

2. Adaptation is the loss of sensation even though the stimulus is still applied.

3. An attennamage is the persistence of a sensation even through the stimulus is

removed.

4. Modality is the property by which one sensation is distinguished from

another.

CLASSIFICATION OF RECEPTORS:

1. According to location, receptors are classified as exteroceptors,

vesceroceptors and proprioceptors.

2. On the basis of type of stimulus detected, receptors are classified as

mechanoreceptors, thermoreceptors, nociceptors, electromagnetic receptors

and chemo receptors.

In terms of simplicity or complexity, simple receptors are associated with general

senses and complex receptors are associated with special senses

Somatic Efferent and Autonomic Nervous System:

1. The ANS or visceral efferent nervous system, regulates visceral activities

that is activities of smooth muscle, cardiac muscle and glands.


49

2. It usually operates without conscious control.

3. It is regulated by centers in the brain, in particular by the cerebral cortex the

hypothalamus and the medulla oblongata.

4. The somatic efferent nervous system produce conscious movement in

skeletal muscles.

Structure of the Autonomic Nervous System:

See Table No.4 for structural featurea of sympathetic and para sympathetic

divisions.

1. The ANS consists of visceral efferent nerves organized into nerves, ganglia

and plexuses.

STRUCTURAL FEATURES OF SYMPATHETIC & PARA SYMPATHETIC

DIVISIONS.

SL.NO SYMPATHETIC PARA SYMPATHETIC

1 Forms Thoraco lumber outflow Forms cranio sacral outflow

2 Contains sympathetic trunk and

pre vertebral ganglia.

Contains terminal ganglia

3 Ganglia are close to the C.N.S.,

and distant from visceral effectors

Ganglia are nearer or within

visceral effectors.

4 Each pre ganglionic bifre

synapses with many post

ganlionic neurones that pass to

many visceral effectors.

Each pre ganglionic fibre usually

synapses with four to five post

ganglionic neurones tht pass to a

single visceral effector.

5 Distributed through out the body,

including the skin.

Distribution limited primarily to

head and viscera of thorax,

abdomen and pelvis.

2. It is entirely motor. All autonomic axons are efferent fibers.


50

3. Efferent neurons are preganglionic (with myelinated axons) and

postganglionic (with unmyelinated axons).

4. The autonomic system consists of two principal divisions. Sympathetic

(Thoracolumnbar) and parasympathetic (Craniosacral).

5. Autonomic ganglia are classified as sympathetic thrunk ganglia (on sides of

spinal column), prevertebral ganglia (anterior to spinal column) and terminal

ganglia (near or inside the visceral effectors).

PHYSIOLOGY:

1. Autonomic fibers release chemical transmitters at synapses on the basis of

the transmitter produced. These fibers may be classified as cholinergic or

adrenergic.

2. Cholinergic fibers release acetylcholine (ACH) Adrenergic fibers produce

norepinephrine (NE).

3.


51

ACTIVITIES OF AUTONOMIC NERVOUS SYSTEM

VISCERAL

EFFECTOR

EFFECT OF

SYMPATHETIC

STIMULATION PARA

SYMPATHETIC

EYE

Iris

Ciliary muscle

Contraction of dilator muscle

that results in dilation of pupil.

No innervation

Contraction of sphincter

muscle that result in

constriction of pupil.

Contraction that results in

lens accommodation for

near vision.

GLANDS

Sweat

Lacrimal (tear)

Salivary

Gastric

Intestinal

Adrenal medulla

Stimulates secretion

Vaso constriction, which inhibits

secretion.

Vaso constriction, which

decreases secretion.


secretion.


secretion.

Promotes epinephrine and nor

epinephrine secretion.

No innervation.

Normal or excessive

secretion.

Stimulates secretion and

vaso dilation.

Stimulates secretion.

Stimulates secretion

No innervation


52

Adrenal cortex Promotes glycocorticoid

secretion

No innervation

LUNGS

Bronchial tubes Dilation Constriction.

HEART Increases rate and strength of

contraction; dilates coronary

vessels that supply blood to

heart muscle cells.

Decreases rate and strength

of contraction; constricts

coronary vessels.

BLOOD

VESSELS

Skin

Skeletal muscle

Visceral organs

(Exc.Heart & lungs)

Constriction

Dilation

Constriction

No innervation for most

No innervation

No innervation for most

LIVER Promotes glycogenolysis,

decreases bile secretion

Promotes glycogenolysis,

increases bile secretion.

GALL BLADDER Relaxation Contraction.

STOMACH Decreases motility Increases motility

INTESTINES Decreases motility Increases motility

GASTRO

INTESTINAL

SPHINCTERS

Increases tone Relaxation

KIDNEY Constriction of blood vessels

that results in decreased urine

volume

No innervation.

PANCREAS Inhibits secretion Promotes secretion

SPLEEN Contraction and discharge of No innervation


53

stored blood in to general

circulation

URINARY

BLADDER

Relaxation of muscular wall;

increases tone in internal

sphincter

Contraction of muscular

wall; relaxation of internal

sphincter.

ARRECTOR PILI

OF HAIR

FOLLICLES

Contraction that results in

erection of hairs.

No innervation

UTERUS Inhibits contraction if non

pregnant. Stimulates contraction

if pregnant

Minimal effect.

SEX ORGANS In male, vaso constriction of

ductus deferences, seminal

veside. Prostate results in

ejaculation. In female reverse

uterine peristalsis.

Vaso dilation and erection

in both sexes. Secretion in

female.

4. Sympathetic responses are widespread and in general concerned with energy

expenditure. Parasympathetic responses are restricted and are typically

concerned with energy restoration and conservation.

VISCERAL AUTONOMIC REFLEXES:

1. A visceral autonomic reflex adjusts the activity of a visceral effector.

2. A visceral autonomic reflex consists of a receptor, efferent neuron,

associateion neuron, visceral efferent preganglionic neuron, visceral efferent

postganglionic neuron and visceral effector.


54

CONTROL BY HIGHER CENTRES:

1. The hypothalamus controls and integrates the automonic nervous system. It

is connected to both the sympathetic and the parasympathetic divisions.

2. Biofeedback is a process in which people learn to monitor visceral functions

and to control them consciously. It has been used to control hearth rate to

alleviate migraine headaches and to make childbirth easier.

REFERENCE:

1. Principles of Anatomy and Physiology by TORTORA

2. Bbrain and banister clinical neurology

3. API Text book of medicine


55

DEFINITION & CLASSIFICATION

Definition

Pakshagata comprises of two words paksha and agatham

a) paksha means- a part of bird or any thing

b) Agahatam means- injury

According to charaka the vata disorder which will paralyse one side of

the total body i.e., paksham is denoted as pakshaghata

Acharya Susruta quotated Pakshavadha and pakshaghata synonymously.

However its description about clinical pictures appears to be more

relavent interms of the contralateral hemiplegia.

The chief complaints being complete loss of motor and sensory

functions of either one side of the body i.e., Hemiplegia. In general terms

Pakshagraha, Pakshaghata and Pakshavadha are in practice for the comparision of

hemiparesis, hemiplegia and absolute paralysis respectively.

From the modern perspectives it appears that the entity of vata

disorder containing ekanga vata, sarwanga vata and pakshaghata etc will come

under either cerebro vascular accident (CVA) or other degenerative changes of

central nervous system. Mere loss of function of one limb, both limbs or all four

limbs may occurred due to vata dushti which can be explained in the following

terms. Loss of function of one limb monoplegia, lose of function of two limbs

(either upper or lower limbs) Paraplegia, all four limbs quadriplegia. Lose of

function of upper and lowe limbs ( either right or left) is hemiplegia.


56

Classification :

In madhava nidanam pakshaghata is classified into three groups:

1) Keval vataja pakshaghata.

2) Pitta lakshana yukta pakshaghata i.e. daha, santapa,

moorcha.

3) Kaphaja lakshana yukta i.e. sotha (oedema), Guruthva

(heaviness), and Saithilya.

When the above clinical conditions are compared with the modern

medicine they are upper motor neuron lesions, thalamic, hypothalamic lesions and

lower motor neuron lesions respectively.

Reference: Madhava nidanam vata vyadhi chikasta.

In Ayurvedic system of medicine the disease aspect in general and

particularly pakshaghata was mentioned under the following headings i.e.

a. Nidana aspect (Aetiology)

b. Samprathi aspect (Pathogenesis)

c. Poorvaroopa aspect (Prodromata)

d. Roopa aspect (Clinical features)

e. Upasaya and anupasya aspect (Therapeutic trials)

f. Upadrava and Arista lakshanas ( Complications and morbid signs)

g. Sadhya and Asadhyatha (Prognosis)


57

NIDANA

The aetiological factors of vatavyadhi in general have been

described in Charaka, Susrata and Vagbhata Samhitas, but there is no separate

description of Nidanic factors for the pakshagata.

Pakshagata is one of the varieties of vata vyadhis

All Nidanic factors of Vata vyadhis can be taken as nidanas

of Pakshagata hence the Nidanas of Vata vyadhis are discussed below.

Generally the term Nidana explains the causative factors of a disease.

Therefore the Nidanas of any disease can be studied under the following headings:

1. Ahara rupa nidana

2. Vihara rupa nidana

3. Manasika

4. Agantuja

5. Chikitsa Kruta

6. Atmsopheric and Kala Karanas

7. Anya Karanas.


58

NIDHA

NA

KARAN

AS

CHARAKA SUSRUTHA VAGBHATA MADHA

VA

NIDHAN

A

BHAVA

PRAKASHA

AHARA

RUPA

NIDANA

1.Rookshabh

ojana

2.SeetaannaP

ana

3.AlpaAhara

4.Laghuanna

Sevana

5.Abhojana

1.Excessive

Inake of

KatuRasa,ti

kta rasa &

Kashaya

rasas.

2.Laghu anna

Sevana

3.Seeta

Veerya

Annapana

4.Vishamajee

rna &

Adhyasana

1.TiktA Rasa

2.Ushna Ahara

3.Kashaya

Rasa

4.Alpa Ahara

5.Ruksha

Ahara

6.Pramita

Bhojanat

1.Rooksh

a

Bhojan

a

2.Seeta

Anna

Pana

3.AlpaAh

ara

4.Laghu

annasev

ana

5.Abhoja

nat

1. Excestiv

e intake of

Katu, Tikta

and Kashaya

Rasas.

2. Pramita

Bhojanam

3. Ruksha

Ahara

4. Laghu

Ahara

VIHARA

RUPA

NIDANA

1.Langhana

2.Vyavaya

3.Ati

Prajagaranam

4.Plavana

5.Aatyadva

6.Vyayama

7.Dukha

Saaya Asanat

8.Gaja, Ustra,

1.

BalavadhwaG

rahati

2. Vyayama

3. Vyavaya

4. Adhyayana

5. Prapatna

6. Pradhavana

7. Prapeedana

8. Plavana

1. Nisa

Jagaranam

2. Uccha

Bashayam

3. Vyayama

4. Maidhnnam

5. Grishma

6. Ahooratram

1.Langhan

a

2.Vyavaya

3.Ati

Prajagaran

am

4.Plavana

5.Aatyadv

a

1. Mala Dhirya

2. Hina Vihara

3. Adhanra

Vihara


59

Aswa, Sigra

Yanam A

Patamaynat

9. Vega

Dharana

10. Diva

Swapnat

9. Langhana

10. Pratarana

11. Ratri

Jagarana

12. Bara

harana

13. Gaja,

Turaga,

Radha Padhati

14. Viga

Dharana

6.Vyayam

a

7.Dukha

Saaya

Asanat

8.Gaja.Ust

ra, Aswa,

Sigrayara

m,

Apatamay

anat

9. Vega

Dharana

10.Diva

Swapnat

MANASI

KA

NIDANA

S

1. Chinat

a

2. Soka

3. Bhaya

m

4. Kodat

Pittam

1. Chinta

2. Soka

4.Chin

ta

5.Soka

1. Soka

2. Chinta

3. Bhayam

4. Manm

Madhana

CHIKITS

A

KRUYT

A

1. Visha

mad

Uppac

harcha

2. Excess

ive

Sravan

1. Kriya Ati.

Yoga

1.

Visham

ad

Uppach

eracha

2.

Excessi

1. Excessive

Sodhana

Therapies


60

as of

Kapha

, Pitta

and

Rakta

3. Ati

Vische

shtha

ve

Sravana

s of

Kapha,

Pitta

and

Radta

3. Ati

Vischesht

ha

AGANT

UJA

KARAN

AS

1. Abhighata

in Marma

Sthana

1.Abhigata 1.

Abhigata

in Marma

Sthana

ATMOS

PHERIC

& KALA

KARAN

AS

1. Ahoorat

ri

2. Bhuktan

te

1 Dina

Kshnadya

2. Tritiya

Amasaye

3. Atisita

4. Sisira

5. Snanja Kala

6. Arja

7. Amatigata

ANYA

KARAN

AS

1. Ama

Dosha

1. Dhatu

Kshay

a

1. A

ma

Du

sha

2. Dh

1. Ati Krushata

2. Ati Manya

Kshaya

3. Dhatu

Kshayata


61

2. Chira

Kahin

aRuga

Pudita

3. Ati

Kmus

hata

atu

Ks

ha

ya

3. Ch

iya

kal

ina

4.

Ati

Krushate

Reference:

1. Charaka Chikitsa 28th Chapter / 15-18

2. Susruta Sutra Sthana 21th Chapter / 19

3. Astanga Hridaya Nidana 1st Chapter / 14-15

4. Madhava Nidana vata vyadhi chikitsa 21 chapter

5. Bhava Prakasa Madhyama Kanda.


62

ETIOLOGY OF

CEREBROVASCULAR DISEASES

The term ‘stroke’ is defined as rapidly developed clinical signs of a focal

disturbance of cerebral function of presumed vascular origin and of more than 24

hours duration. Stroke is not a diagnosis, but a clinical syndrome with numerous

causes mainly.

A. Cerebral ischemic disease of arterial origin.

1. TIA’S with total recovery.

2. Progressive stroke (or) stroke in evaluation.

3. Completed stroke - established cerebral infarct from

(a) Thrombosis (b) Embolism

B. Venous infarct

C. Subarachnoid haemorrhage.

Main risk factors for stroke:

Hypertension

Cardiac disease – ischemic heart disease atrial fibrillation

Transient ischemic attacks

Cigarette smoking

Alcohol

Hyperlipidemia

Oar contraceptives

Obesity

Sedentary life


63

Associated risk factors:

Diabetis mellitus

Previous stroke

Raised Haemotocrit

High Plasma fibrinogen

Anti-phospholid antibodies (APLA)

Asymptomatic carotid lesions (Carotid bruits)

CAUSES:

A. Ischemic stroke

1. Transient Ischemic attack (TIAs):

Episodes of focal neurological symptoms of less than 24 hrs duration

occurring as a result of reduced flow to a vessel from fall in perfusion

pressure (e.g. Cardiac arrythmia is associated with localized stroke

cerebrovascular disease). (or) blockage of flow by embolism arising from

plaques in aorticarch or extracranial vessels or from heart. If flow is restored

within the critical period, ischemic symptoms reverse themselves, otherwise

infarction may occur.

Since there is no serious persisting disability the term

“REVERSIBLE ISCHEMIC NEUROLOGIC DEFICIT” is used in such

cases.

2. Developing (Progressive) Stroke:

Sometimes paralysis progresses. Slowly commensurate with

increasing deprivation of blood due to successive emboli (or)

extension of thrombus further occluding the lumen. It evolves

gradually over several hours.


64

3. Completed stroke:

Caused by infarction of the cerebral hemisphere is the most common

cause of an acute cerebrovascular disease. A completed stroke reaches its

peak in less than one hour leaving considerable residual deficit.

B. VENOUS INFARCTION:

Thrombosis of cortical veins and / or dural sinuses is less common

than central arterial occlusion.

Causes: Dehydration, pyogenic middle ear or sinus infection, pregnancy,

and puerperial polycythemia, hyper viscosity syndromes, septicemia,

neccrative editis, severe iron deficiency anemia, head injury, extra cranial

malignancy.

C. Sub arachnoid haemorrhage:

1. Haemorrhage from intra cranial aneurysm.

2. Haemorrhae from arterio venous malformation.

3. Cerebral or cerebellar haemorrhage leading in to the ventricles of

sub-arachnoid space.

Less common causes of stroke:

Haematological abnormalitics:

That promote thrombosis eg: Polycythemia and thrombocythemia.

Anticardiolipin antibodies may cause acquired abnormalities of thrombolysis

and are associated with stroke in younger patients.

Thrombophilia may cause Cerebral venous thrombosis. Low dose

oestrogen containing oral contraceptives do not increase risk of stroke

significantly in healthy woman, but may do so in those with vascular risk

factors.


65

Sub-clavian steal: is an uncommon cause of haemodynamic symptoms. If

the sub-clavian artery is occluded (or) stenosed before the origin of

vertebral-artery. Arm exercise may cause retrograde flow down the

vertebral artery at the expense of the vertibrobasilar circulation, resulting in

brain stem TIA.

Migraine:

is rare cause of cerebral – infarction. Headache is common in ischemic –

stroke and may be caused by collateral vasodilation (or) carotid dissection

arising from plaques in aortic arch, (or) extracranial vessels (or) from heart.

It flow is restored with in the critical period, ischemic symptoms reverse

themselves, otherwise infarction may occur. Since there is no serious

persisting disability, the term reversible ischemic neurological deficit

(RIND) is used in such cases.

Vasculitis:

is a rare cause of both haemorrhagic and ischemic stroke. Systemic

features of the underlying vasculitis usually suggest the diagnosis in SLE,

Polyarteritis nodosa and gaint-cell arteritis, but absent in isolated (or)

granulomatous angitis of the CNS. Cardiac embolism from endocarditis

and acquired thrombophilia with anticardiolipin antibodies are other possible

causes of stroke in SLE.

Watershed infarction:

During transient circulatory arrest (or) profound anoxia, infarction

can occur between arterial territorities, particularly in parieto-occipital

region which is the water-shed between middle, anterior and posterior

cerebral arteries. Usual picture is of usual disorientation (or) cortical

blindness. Often associated with visual field defect and sensory impairment.


66

Multi infarct dementia:

A succession of minor vascular events can lead to dementia may also

result from diffuse small vessel disease which leads to ischemia of deep

white matter and basal Ganglia (Binswanger’s disease (or) sub-cortical

arteriosclerotic encephalopathy). There may not be a clear history of stroke

but dementia it usually marked by step-wise deterioration with periods of

improvement. CT (or) MRI shows patchy (or) diffuse abnormalities in the

periventricular regions. (Leukoaraiosis).

Differential diagnosis of vascular causes of Hemiplegia

Embolism Thrombosis Haemorrhage

Age Young Middle age or old Middle age or

old

Nature of onset Instantaneous Sudden or

progressive

Catastrophic

Premonitory

absent

symptoms

Absent Difficult in

speaking or

weakness of arm

or leg may be

present

Usually absent

Common cause Mitral steinosis

with atrial

fibrialation and

carotid stenosis

Arteriosclerosis

with or without

hypertension

Hypertension

almost invariable

Reference:

1. Current medical diagnosis and treatment by Golwalla

2. Brain and Banniester clinical neurology

3. Principles of Anatomy and Physiology by Torotora


67

POORVA - ROOPA

The Lakshanas of Poorva - roopa are not mentioned specially not

only for Pakshaghata but also for Vata Vyadhis.

Poorvarupavastha is an investigation of a disease next to nidana.

These Prodromal features occur before the beginning of the Clear Manifestation of a

disease.

The Unmanifested Symptoms of the Vata Disorders are known as

Poorva roopa (Prodromal Symptoms). When the same are manifested they represent

the own entity of disorders.1

So, the Alpalakshanas of Vatavyadhess are:

1. Sramsa - Seperation

2. Bhramsa - Dislocation

3. Vyasa - Division

4. Sanga - Obstruction/ attachment

5. Bheda - Tearing pain in organs

6. Sada - Emaciation / Malaise

7. Harsha -

8. Tarsha - Thirst

9. Varta - Circumvention

10. Marda -

11. Kampa - Tremors

12. Chala - Loosenes

13. Thoda - piercing Pain

14. Vikruta

Chesta - Unwanted Works (Pain Movement)

15. Kara - Coarseness

16. Parusha - Roughness


68

17. Visada - Non. Sliminess

18. Sushira - Raucousness’

19. Arunarama - Reddish Lusture

20. Keshaya Ursa

Mukatwa - Astringent taste and Tastelessness

21. Sankochana - contractures

22. Sosha - Wasting

23. Soola - Pain

24. Supti - Numbness

25. Sthambhana - Stiffness

26. Kharjatha - Limping

When these Symptoms appear they indicate the prodromal

symptoms of Vata vyadhi.2

In Modern medicine the transient ischaemic attacks (TIA’S)

may considered as Poorvaroopas for Cerebrovascular disorders.

Transient ischemic attack:

Transient ischemic attack is brief episodes of

neurological dysfunction with recovery but with a tendency to reoccur. They might

be distinguished from other brief attacks due for example to migrane or epilepsy.

They may be due to inadequate flow. Emboli or Spasm or a combination of these

factors.3

Most transient strokes are due to transient cerebral ischemia

but a occasionally reveals a small intracranial hemorrhage, which arterial territory

was involved can be determined from the history of the attack. Approximately 80%

occur in the carotid artery vertebro basilar attack are recognizable from a history of

transient hemianopia (or) brainstem features such as diplopia (or) vertigo. If these

are not present, a transient hemiplegia, hemi sensory loss and, if the dominnant


69

hemisphere is affected dysphasia can be assumed to arise from carotid territory

ischemic.

Most Transient Stokes are caused by atherosclerotic thromboembolic disease of

the major extracranial vessels. The risk of a disabling stroke or death after a TIA

(Stroke) can be reduced by 20-30% with aspirin, if patients have a major stenosis

(more than 70%) of their carot

id artery. Carotid edarterectomy is of proven benefit.4

Completed stroke

Caused by infarction of the Cerebral hemisphere is the most common

cause of an acute cerebrovascular disease. A completed stroke reaches its peak in

less than one hour leaving considerable residual deficit.

Therefore TIA’S are considered to be Poorvarupas (Prodromal

symptoms).

Reference:

1. Cha. Chi. 28th Chapter / 19.

2. Cha. Sutra. 20th Chapter / 16.

3. Brain & Bannister’s Clinical Neurology. Page no. 255

4. Davidson’s Principles of Medicine Page no. 1164-1165.


70

ROOPA

“Pradhurbhuta Lakshanam Punarlingam”1

In the Roopavastha Complete Establishment of Disease

Process appears. The Total Symptomatology will be observed in this stage.

The Pakshaghata included in aseethi vata vyadhis.

Therefore some of the Samnya Lakshanas of Vata vyadhis are also

observed in most of the cases of Palshaghata, apart from the impairement of the half

of the body. The most frequently associated Samanya Lakshanas of Vata Vyadhis in

Pakshagata are described as follows.

1. Sankocha – Contractures

2. Parwa Sthambha – Stiffness in joints

3. Asthi Bhudha – Tearing in bones

4. Parva Bhudha – Tearing in joints

5. Pralapa – Delerium

6. Panigraham – Stiftness in Hands

7. Pristagraham – Stiffness in Back

8. Sirograha – Stiffness in Head.

9. Lomaharsha - Horripilation

10. Khanjatwa – Limping

11. Pangutwa – Crippledness

12. Kubhjatwa- Humpedness

13. Angasosha – Drying of Organs

14. Anidrata – Sleeplessness

15. Grabha Nasa – Destruction of Foetus

16. Sukra Nasa – Destruction of Sperms


71

17. Raju Nasa – Destruction of Ovum.

18. Spandanam – Pulsatiom

19. Gatra Suptatha – Numbness in Organs

20. Siro Hundana – Crookedness of Head

21. Nasa Hundana - Crookedness of Nose

22. Akshi Hundana - Crookedness of Eyes

23. Greeva Hundana - Crookedness of Neck

24. Jatru Hundana - Crookedness of Clavicular Region

25. Bheda – Tearing Pain

26. Thoda – Peircing Pain

27. Aarthi – Distress

28. Akshepam – Convultions

29. Moha – Mental Confusion

30. Ayasam – Exhaustion. 2

Charaka said that a person whose half of the body either left (or)

right side becomes function less both in activities of Samnjavaha and Chestavaha

Vyaparas along with ruk and Vaksthamaba can be called as Pakshagatha Rogi.3

In view of Susrutha the vitiated vata enters in to adho, urdhva and

Thiryak dhamanis, excessive on either part of the body causes saithilyata of sandhis,

Due to it the functions of the concened parts are Paralysed. This is termed as

Pakshaghata.4

Vagbhata Mentions that Prakupita Vata expands in the half part of

the body causing soshana (Atrophy) of siras, snayus and Saithilyatha of Sandhi

bandhanas. Due to this, the part which was affected is unable to do its normal

functioning. Herefore it can be called as “Nischestavastha” in the organs of the body

or exactly half portion of the body either to the left or to the right. This condition is

called as Pakshagata.5


72

The signs and symptoms which are manifested specially can be considered

as roopa.

1. Chestanrivuthi of a Paksha - This may be dakshina or Vama

1. Vaksthambha

2. Sandhi Bhandha Vimokshona

3. Sirasnayu Vishoshna

4. Diva ratra Shira Pada Ardhanga Shoola

5. Akarmanya Vichestanam

6. Rujam

Reference:

1. Cha-Ni-1st Chapter / 8

2. Cha. Chik 28th / 20-23

3. Cha. Chik 28th / 53-55

4. Su. Ni. Chapter / 60-61

5. A.H. Nidana 15th Chapter / 38-39


73

SYMPTOMS OF CEREBRO VASCULAR DISORDERS

Symptoms of atheromatous ischaemic and Infarction:

A patient who is suffering from atheromatous ischaemia is likely to

be middle aged or older. The onset of symptoms may be sudden and not

uncommonly occurs during sleep so that the patient awakens in the morning

to discover the disability. On the other hand, prodromal transitory

disturbances of cerebral function of vascular origin one common. The

symptoms may increase in seventy for 24 or 48 hours after the onset. They

will sometimes present a clear-cut picture of obstruction of one particular

cerebral artery or there may be an incomplete picture of this, the lesion

falling with in the domain of a single vessel but not involving the whole area

of its supply. Frequently consciousness is preserved or there is merely some

confusion profound loss of consciousness is rare except when there is a large

area of infarction or the lesion involves the brain-stem.

Hypertensive encephalopathy:

The onset is usually subacute, the patient complaining of headaches

of increasing severity, which often associated with vomiting of a cerebral

type. Epileptic form convulsions are common and may be followed either

by mental confusion or coma. Impairment of vision on even complete

blindness may occur. Other focal disturbances include aphasia and

hemiparesis.

Artrial hypertension is present in every case, but the blood pressure may not

be greatly raised in acute nephritis and eclampsia. The retinae may he

normal or there may be bilateral papilloedema, depending up on the casual

condition. Both renal function and the composition of the urine may be


74

normal except when the encephalopathy complicates acute or chronic renal

damage. The pressure of the CSF is often increased and it may be normal in

composition or show a raised protein count.

Cerebral embolism:

The onset of symptoms of Cerebral Embolism with blood clot is

extremely sudden, the lodgement of the embolus producing symptoms more

rapidly than either cerebral haemorrhage or thrombosis. Loss of

consciousness is not very common unless the carotid artery is blocked, but

the patient is usually some what confused. A convulsion may occur at the

onset and there is usually headache. The nature of the focal symptoms

depends on the vessel to which the embolus becomes impacted. After the

onset of embolism, there may be a gradual increase in the severity of the

symptoms due to spasm of the vessel, the development of edema or the

extension of thrombosis.

Intracranial Haemorrhage:

Symptoms of sub arachnoid haemorrhage:

The main feature of the headache due to a sub-arachnoid

haemorrhage from an intracranial aneurysm is its suddenness and its

severity. Sometimes being likened to being hit over back of the head. It

usually occurs with out previous warning, but in a small proportion of cases

there are focal symptoms produced by the aneurysm before rupture. There

may be a history of headaches. Sub-arachbnoid haemorrhage from a

cerebral angioma may occur without previous warning, but is more often

preceded by symptoms and signs of the cerebral lesion.


75

At one extreme SAH may lead to immediate coma associated with

profound shock and cause death in a few hours. While at the other extreme

it may cause only a headache which it not severe enough to interfere with

the patient’s occupation, and the cause of which is established only by

examination of the CSF. Loss of consciousness occurs rapidly when the

leakage is considerable and vomiting is not uncommon at the onset. Unless

severe cases the patient may not lose consciousness completely, but may

pass in to a semi-stuporose stage lying in an attitude of general flexion

resenting interference, and confused and imitable when aroused. Headache

is severe and the presence of blood in the sub-arachnoid space produces

signs of meningeal imitation. Such a cervical rigidity and kernig’s sign.

Moderate pyrexia is common at this stage.

Changes are sometimes found in the fundus of the eye. Papilloedema

is sometimes present, though slight in amount. Unilateral or bilateral retinal

haemorrhages occur in same cases, and may accompanied by sub-hyaloid or

vitreous haemorrhages changes are most likely to be seen in the fundi when

the SAM is near the optic nerve.

Other signs of SAH include diminution or loss of the tendon reflexes,

and of the abdominal reflexes and extensor plantar responses in the absence

of gross muscular weakness Albiminuria and glycosuria occasionally occur.

Focal symptoms are due to compression of neighbouring cranial

nerves by blood clot or to invasion of the cerebral hemisphere by the

haemorrhage. Lateral is likely to produce a crossed hemiplegia and

increases the tendency to or the depth of come.


76

SAH originating in the posterior fossa is likely to cause a degree of cervical

rigidity disproportionate to the rest of the symptoms and may cause focal

signs from disturbance of function of the cerebellum or one or more of the

cranial nerves leaving the pons and medulla.

Cerebral haemorrhage:

Symptoms:

The onset of a cerebral haemorrhage is always sudden. The actual

rupture of the vessel may be brought about by mental excitement or physical

efforts or may occur during rest or sleep usually patient complains of sudden

severe headache and may vomit. He becomes dazed and in all but the

mildest cases lose consciousness in a few minutes. Convulsions may occur

at the onset, but are exceptional. The physical signs produced by a cerebral

haemorrhage depend up on its situation and its size.

CLINICAL PICTURE OF HEMIPLEGIA

Mode of onset: Catastrophic in haemorrhage progressive in thrombosis /

instantaneous in embolism.

Transient hemiplegia or cellular transient focal neurological disturbance may be

due to transient cerebral ischemia, embolism from the heart, migranine epilepsy

structural intracranial disorders such as tumour chronic subdural haematoma,

giant aneurysm or angioma; polycythemia, thrombocytopenia or sickle cell

disease, Anaemia, hyper viscosity syndromes. Hypo glycemia, hypertensive

encephalopathy. Hesteric paroxysmal symptoms in multiple sclerosis.

Congestive attacks or GPI.

1. Head ache: In cerebral haemorrhage the headache is intense with

accompanying stiffness of neck.


77

In carotior insufficiency the headache is temporal and usually in the side

of the ischemia.

In basilar artery insufficiency the headache is occipital or suboccipital.

Sever headache is felt in subarachnoid haemorrhage at the onset.

Headache and vomiting may occur in cerebral tumour or abscess and sub

dural haematoma.

Vomiting preceding a stroke follows a diagnosis of haemorrhage. Chest

pain suggests associated myocardial infarction

Symptoms suggestive of hysterical hamiplegia:

1. Onset after emotional shock

2. Hysterical type of rigidity

3. Plantars never extensors.

4. Hoovers contra lateral leg sign is negative – when patient attempts to rise the

paralysed leg, the opposite heel does not make counter pressure backwards.

In the palm of the examiners hand as in organic hemiplegia.

5. Contraction of platysma present on affector side

6. Hysterical gait.

7. COMA sudden or rapid loss of consciousness at onset, common in

subarachnoid haemorrhage, intra cerebral haemorrhage, and brain stem

strokes. In sub dural heamatoma increasing drousyness and spontaneous

variations in coma like the patient may pass the consciousness in to coma

and back again in a few hours.

8. Jacksonian fits occur in turnovers

9. Fever more common in haemorrhagic conditions and in infection like

manengitis, encephalitis and cerebral abscess.


78

10. Involuntary movements occurs in encephalitis and chorea. In chorea usually

upper limb alone is paretic.

11. Mental symptoms : In dementia paralytica, encephalitis and sometimes

tumours.

12. Abdominal pain and melena suggest gastro intestinal beldding as the

precipitating cause.

13. Histology of acute infections: Hemiplegia may rarely be a complication of

Typhod, pneumonia, typhus and diphtheria etc.

CLINICAL FEATURES

Headache Variable Slight or absent Seveare

Vominting on

onset

Rare Rare Common

Convulsions Common Rare Common

Coma Rarely deep Rare, varies with

the extent of

thrombosis.

Deep in

consciousness.

Cheyne stokes

respiration

Not common Seldom Common

Stiff neck Rare Rare Frequent

Conjugate

deviation of eyes

Rare Seldom Frequent

Bilateral

extensor plantar

Rare May be present Frequent

Reaction of pupil

to light

No change May be impaired Commonly

impaired

Blood pressure Normal May be high Usually high

C.S.F Usually normal

pleocytosio if

Clear C.S.F.

pressure elightly

Usually bloody

pressure is


79

infector emboius increases increased.

C.T.Scan Infarction may

not appear for 2

to 4 days

May not appear

for 2 to 4 days

Can be confirmed

with in minutes of

onset.

Termination Recovery usual Recovery often High mortality

References:

1. Brain and Bannisters clinical neurology

2. Principles of Anatomy and Physiology by Toratora

3. Medicine by Golwala


80

SAMPRAPTHI

The Samprapthi of a disease explains the Process by which the

altered doshas reach the body elements (Dushyas) and produces the anatomical and

physiological variations in the target avayavas leading to the expression as a

disease.1

The Samprapthi (or) Pathogenesis of Pakshagata under the

vatavyadhi has been described in all the samhitas of Ayurveda.

The different views explained by Brihattrayees regarding the

samprapthi of Pakshahata is as follows.

According to Charaka tha Pathogenesis or Samprapthi of

pakshaghata is as explained: the vata which is vitiated (or) provoked by its own

nidanic factors leads to the seizing of dhamanis controlling the functions of the side

of the body and constricting the siras afflicts dakshina or vama ardha bhagas of the

body resulting in the impairement of movements of urdhwa (or) adhobhaga (or)

both. It also causes loss of sensation, pain and Some times loss of Speech. 2

In view of Susrutha the Disease in which the vitiated vata affects the

dhamanis, which spreads either in the vamabhaga (or) in the dakshinabhaga of the

body in other terms it may affect the urdhwabhaga, adhobhaga and thiryak disha and

making them, resulting in abnormal state (or) condition known as pakshagata,

Further he stressed lax and vigourless in which the sandhis of either side of the body

become useless and inoperature both in motor and sensory functions. 3

Vagbhata Mentions that the prakupita vata lodges (or) occupies a part

of the body causing loosening of the sandhis and further affects one side of the body

making useless, both the functions of karmendriyas and Gnanendriyas and functions

of affected parts of the body resultling in a condition producing inability in

performing karmas of affected parts.4


81

The Views of Bhavamisra in Madhyama Kanda and

Madhavakara in Vata Vyadhi Nidana Cahpters appear to coincide with above

mentioned options of Acharyas.

1. Amaya – Pakshagata {hemiplegia}

2. Udbahava Sthana – Masthiska

3. Sanchara – Dhamanees

4. Adhistana – Dhamaness of Masthiska, Sira and Snayus

5. Vyakti – Ardhs Sareera (Half of the body)

6. Srotases – Rasavaha, Raktavaha, Chestavaha and Sanjnavaha

Srotases

7. Avayava – hasta, Pada,Muka, Netra and Swara Yantra

8. Dosha Dusti – Vata

9. Dushyas – Rasa, Rakta, mamsa, Meda, Asthi ,Majja, Dhamani

,Sira and Snayu.

10. Vyadhi Swabhava – Asukari in most of the cases, Chirakari in

some cases.

Charaka Stated that the dhatukshaya and obstruction of the vata

channels due to kapha and pitta is the main cause in vata Prakopa. 5

He indicated that the obstruction as the prime cause of vata rogas. He

further stated that when aggrevated vata forcibly filled in the empty srotases of the

body than vata disorders occur. 6

Susrutha mentioned more clearly that the involvement of cerebral -

vessels it self is the samprapti of Pakshagheta using the word “Dhamaneerurdwa

Dehaga” 7


82

REFERNCE

1. A.H.N. / Chapter / 8

2. Cha. Chikitsa 28th Chapter / 53-55

3. Susruta Nidana 1st Chapter / 61-62

4. A.H.N. 15th Chapter / 38-39

5. Cha. Chikitsa 28th Chapter / 59

6. Cha. Chikitsa 28th Chapter / 18

7. Susruta Nidana 1st Chapter / 61-62


83

CEREBRAL ISCHAEMIA

Pathology and Pathological Physiology:

There is a group of disorders in which the symptoms are due to

insufficiency of the blood supply to the brain. The commonest of these is

atheroma of the arteries, supplying the brain. The Pathology of atheroma is

the same in the cerebral vessels as in other parts of the body. As, elsewhere,

for example in the coronary circulation infarction of the brain may occur of

the result of narrowing of an artery by atheroma without its complete

occlusion or as the result of its occlusion by thrombosis (or) embolism. The

vessel affected may be large (or) small and the larger vessels may be

affected at any point between their intrathoracic and their intracranial course.

Moreover, the symptoms may be due predominantly to narrowing of

one vessel or the result of diffuse changes involving a number of small –

vessels. The presence of atheroma in collateral channels often plays an

important part in influencing the effects of a more advanced degree of

atheroma in a single large vessel.

The Pathological effects of cerebral ischemia due to atheroma

therefore range from a massive area of cerebral infraction produces by

obstruction of one internal carotid (or) one middle cerebral artery to small

areas in the cerebralcortex (or) white matter due to an impaired circulation

through the smaller arteries and arterioles following occlusion of a cerebral

artery there may be zones of over perfusion and under perfusion determined

by the degree of damage to auto regulatory function in adjacent regions of

the circulation.


84

After an acute ischaemic infarct, causing cerebralvasomotor

paralysis, flow is profuse and if pressure is maintained is in excess of

metabolic demand. So called ‘Luxury’ profusion. The use of vasodilator

drugs can precipitate a ‘steal’ by adjacent areas, whereas vasoconstrictors

may cause an inverse ‘steal’ effect. In a large area of infarction there is wide

spread destruction of nerve cells, nerve fibres and the glial tissues except the

microglia. The cortex presents a hemorrhagic appearance and the white

matter, which is pale, undergoes ischemic necrosis. Infarction of a large

area of one cerebral hemispehere may cause so much swelling that it leads to

symptoms of increased intracranial pressure.

Generalised atheroma without occlusion of any single large vessel

leads to diffuse atrophy of the brain with multiple small patches of softening

of various ages.

Lacunar-infarcts are among the commonest cerebrovascular lesions

recognized at post-mortem and represent healed ischemic infarctions after

occlusion caused by a lipohyaline change in small – vessels. There are

small cavities about 5-10 mm in diameter non commonly in the deep nuclei

of the brain, especially the putamen. Because of their small size many are

not recognized clinically but the larger ones may be shown on CT (or) MRI

SCANS. Other syndromes of ischaemic-brain disease are white matter

lesions in hypertensive (binswanger’s disease (or) progressive sub-cortical

encephalopathy), and infarctions in border zones of arterial territories. Often

bilaterally following hypotension, especially in the parietal cortex where the

territories of anterior middle and posterior cerebral arteries meet.

Since the cerebral circulation depends directly up on the adequacy of

the blood pressure , a fall of blood pressure from any cause especially

myocardial infarction (or) paroxysmal arrythmia, may render temporarily


85

inadequate the circulation throuth a narrowed atheromatous vessel which

may become adequate, when the blood pressure rises again.

Local vascular spasm, associated with hypertension is another

possible cause of temporary ischaemic symptoms.

Small emboli, probably arising from atheromatous plaques on the

walls of extracerebral vessels, may pass into the cerebral circulation and

cause ischaemic symptoms. These emboli, which are occasionally seen in

the retinal circulation, are sometimes highly refractile and contain

cholesterol material. It has been shown that rotation of the head may cause

temporary ischaemia of the brain stem in subjects who have both

cervicalspondylosis and atheroma of the vertebral arteries.

Other forms of cerebrovascular disease which may lead to cerebral

ischaemia include endarterisis due to meningovascular syphilis or

tuberculous meningitis and three are rare disorders thrombo-angitis,

polyarteritis nodosa and giant celled arteritis (cranial arteries). Cerebral

embolism is also a cause of cerebral ischaemia. There is a three fold risk of

cerebral thrombosis in women taking oral-contraceptives particularly a high

dose oestrogen-progesterone combination.

Hypertensive Encephalopathy:

, Pathology and Pathological Physiology:

The term “Hypertensive Encephalopathy” is used to describe the

form of cerebral disturbance occurring in disorders which differ in their

Pathology but posses a common tendency to cause arterial hypertension.

This and the fact the onset of the encephalopathy is not uncommonly

preceded by a rapid raise in the blood pressure suggest that the disturbance


86

of function is closely related to the hypertension. Additional rise of blood

pressure occurring in a patient already hypertensive in many cases results in

focal arterial spasm, with anoxic damage to the neurons and to the capillary

walls. The commonest pathological finding is oedema of the brain, but this

is not always present and seems likely to be a by-product of the pathological

process and not the cause of symptoms.

In hypertensives the lower level of auto regulation or maintenance of

unchanged flow is reset from 60 mm Hg to 110 or

higher, causing a higher threshold at which ischaemic symptoms occur on

lowering blood pressure. In severe hypertension the cerebral blood flow

paradoxically increase thus suggesting that the symptoms in malignant

hypertension may be over distension of vessels rather than spasm. After a

stroke CBF studies have shown ischaemic foci, hyperaemic foci, and

sometimes global loss of auto regulation in different parts of the lesion. The

rate of resolution of these changes that resolving obstruction by thrombolysis

is present in many cases of TIA’s rather than haemodynamic crisis has

formerly assured.

During an epileptic seizure the CBF is increased up to three fold. In

coma, the CBF may become immeasurably small, though without

irrecoverable brain damage necessarily have occurred.

The age incidence of hypertensive encephalopathy is that of casual

disorders. Acute glomerulonephritis is commonest in childhood,

adolescence and early adult life. Chronic glomerulonephritis in second and

third decade; eclampsia during the early part of child bearing period; and

malignant hypertension in the thirties and forties, though it may occur in


87

childhood or late middle age. Lead encephalopathy in some respects

resembles hypertensive encephalopathy.

Cerebral embolism:

Pathology:

Cerebral embolism is a variety of ischaemic cerebral disease in

which the ischaemia develops acutely as a result of some substance, usually

blood clot, being carried in the circulation to lodge in one or more of the

blood vessels.

A now much rares of cerebral embolism is mitral stenosis, and in

most cases there is atrial fibrillation, the clot coming from the paralysed

atrium. A clot may form on the mural endocardium after myocardial

infarction or in association with the brady-tachycardia syndrome or a

prolapsed mitral valve. Clots may also form in the heart after operation on

one of the valves. Infected vegetations may become detached from the

mitral or aortic valve in sub-acute bacterial endocarditis. Sterile emboli

occur in “marantic” endocarditis in severe debilitating diseases. The source

of thrombus may be in the lung, infected emboli from the lungs are the cause

of cerebral abscess complicating pulmonary-infarction and tumour cells may

pass in the same-way from the lung to the brain.

The arteries of the left side of the brain are the site of embolism more

frequently than those of the right and the left middle cerebral is the vessel

more often affected. After the lodgement of an embolus the vessel usually

goes into spasm and thrombosis may occur in it. When the embolus is

infected, cerebral abscess may subsequently develop or when the infection is

of low virulence embolism may be followed by infective softenings of the

vessel wall and aneurysm formation- mycotic aneurysm.


88

Intracranial Haemorrhage:

Intracranial Haemorrhage may be classified according to its

anatomical site in to 4 varieties, namely:

1. extradural

2. Sub-dural

3. sub-arachnoid

4. intracerebral

Extradural and sub-dural haemorrhage are of great importance

and almost invariably traumatic.

SAH and ICH though anatomically distinct, overlap pathologically

because the same haemorrhage may involve both the brain substance and the

sub-arachnoid space.

Sub arachnoid haemorrhage:

Pathology:

Sub-arachnoid haemorrhage may occur as the result of any condition

in which there is rupture of one or more blood vessels that the extravasated

blood can reason the sub-arachnoid space. Massive sub-arachnoid

haemorrhage is usually due either to rupture of an intracranial aneurysm or

bleeding from cerebral angioma or the extension of an intracerebral

haemorrhage in a hypertensive patient in to the sub-arachnoid space either

directly or more often through the ventricular system.

Intracranial aneurysm which may single or multiple is often due to a

congenital weakness in the media at the point of junction of two of the


89

components of the circle of willis or at a bifurcation of one of the cerebral

arteries. Though the aneurysm may itself be congenital it is probable that it

may develop at any period of life on the basis of the congenital structural

deficiency.

Recent reviews have shown that atheroma is probably as important

as congenital weakness in the media as a cause of the development of

intracranial aneurysms and sub-arachnoid bleeding. Whenever hypertension

plays a part in its causation is doubtful, but it may certainly contribute to its

rupture. Congenital aneurysms may be single or multiple and one most

frequently encountered on the intracranial course of the internal carotid

artery. On the middle cerebral artery, and the junction of the anterior

communicating artery with the anterior cerebral artery.

The usual sites are either supraclinoid at the origin of the posterior

communicating artery in which there is usually pain behind the eye and a

third nerve palsy or infraclinoid causing pressure on the occulomoter nerves

and a sympathetic paralysis because of involvement of the sympathetic

plexuses around the carotid artery. They range in size from smaller than

pin’s size of a pea. They may be found at any age, and may even rupture in

childhood, but more than half first cause symptoms between the ages 40 and

50 and females suffer more often than males.

A less common form of intracranial aneurysm which is now days

becoming even rarer is a mycotic aneurysm caused by softening of the wall

of an artery around an infected embolus which has reached it from the heart

in sub-acute infective-endocarditis. Such aneurysm may also cause sub-

arachnoid haemorrhage.


90

Sub-arachnoid haemorrhage from a cerebral angioma is considulably

less common than one from a ruptured aneurysm.

Sub-arachnoid haemorrhage from any cause spreads at first

throughout the sub-arachnoid space from its point of origin and so extends in

to sub arachnoid space of the spinal cord. The haemorrhage may also invade

the brain, which is especially common in the frontal lobe after rupture of an

aneurysm at the junction of the anterior cerebral and anterior communicating

arteries. There may also be only of cerebral-infarction. A cerebral angioma

may also bleed simultaneously in to the brain substance and in to the sub-

arachnoid space. Among the rare causes of massive sub-arachnoid

haemorrhage are the haemorrhagic diseases and haemorrhage from an

angioma of the spinal cord in a small proportion of cases the source of

haemorrhage cannot be discovered.

CEREBRAL HAEMORRHAGE:

Pathology:

The commonest cause of cerebral haemorrhage is hypertension

and the associated changes in the vessel walls. These have been much

discus sed and probably are not the same in every case. The most

important are probably lipohyaline changes in the muscle cells and atheroma

with medial degeneration, both caused by microaneurysms. Cerebral

haeorrhage is most likely to occur in the neighbourhood of the internal

capsule in the cerebellum or in the pons. A capsular haemorrhage may last

in to one lateral ventricle or much less frequently sub-arachnoid space.

After a large intracerebral haemorrhage the affect hemisphere is larger than

the opposite one and the convulsions are flattened. The site of haemorrhage


91

is occupied by a red clot, and the surrounding tissues are compressed and

may be oedematous. Later if the patient survives, the clot is absorbed and

may be replaced by a neurological scar, or by a cavity containing yellow

serous fluid multiple haemorrhages sometimes occur.

Hypertensive cerebral haemorrhages usually occurs in late

middle life. It is comparatively rare in younger hypertensives, and the

vascular changes of old age more often that to ischaemic cerebral infarction

male sufferer from cerebral haemorrhage more often than females and a

familial incidence is common.

Cerebral haemorrhage occurring in the first half of the adult life is

likely to be the result of a congenital vascular abnormality, either an

angioma or aneurysm. Other causes of cerebral haemorrhage include trauma

and thrombocytopenic purpura, petechial haemorrhages occur in the brain in

toxic and inflammatory states.

*Flattening of the noso-labial furrow may be evident on the paralysed side,

and the cheek is usually disturted more on the paralysed than on the normal

side during expiration.

It the patient is not too deeply comatose it may be observed that the

moves the limbs spontaneously on the normal but not on the paralysed side.

At first, after haemorrhage the limbs on the paralysed side are hypotonic and

the arm and leg, if lifted up fall on the bed inertly whereas even in deep

coma the normal arm and leg subside much more gradually.

Pricking with a pin even in unconscious patient usually causes

contraction of the muscles of the face and movements of withdrawl of the


92

limb which is pricked. These movements do not occur on the paralysed side.

The loss of such movements may be due to hemianalgesia. The tendon

reflexes are variable. They may be much diminished or abolished on the

paralysed side but sometimes they are exaggerated. The plantar reflux on

that side is extension. On the other side if may be flexor, or in deep coma

extensa. Retention or inconvineous of urine and facas is the rule as long as

patrent is unconscious.*

Haemorrhage in the region of internal capsule:

The patient is usually unconscious and there is often slight pyrexia.

The pulse – rate is generally slow 50-60 and the pulse full and bounding.

The respirations are deep and stertorous and the respiratory rate may be

either slow or quickened or there may be cheyne stroke syndrome. The head

is usually rotated and the eyes are deviated towards the side of lesion. This

is due to the paralysis of rotation of the head and conjugate deviation of the

eyes to the opposite side as a consequence of unbalanced action of the

undamaged cerebral hemisphere. The optic discs are usually normal though

slight papilloedema is not uncommon, and may or may not be accompanied

by hypertensive retinopathy. The pupils may be unequal but react to light

unless the patient is very deeply comatose. A divergent squint is common.

The corneal reflex is often lost on the side opposite to the lesion and will he

lost on both sides when coma is profound.

A capsular haemorrhage cause paralysis of the opposite side of the

body, but the comatose patient cannot be asked to carry out voluntary

movements, so it is necessary to resort to indirect methods of demonstrating

paralysis.


93

Haemorrhage in to the ventricles:

If a haemorrhage in the region of internal capsule bursts in to the

lateral vertical, coma deepens and the signs of pyramidal lesion are usually

present on both side of the body. There is often tendency for the upper-

limbs to exhibit a posture of rigid extension and conical rigidity is likely to

occur. The temperature frequently exhibits a marked terminal rise.

Pontine haemorrhage:

If the patient is seen soon after the onset of a pontaine haemorrhage

the signs may be those of unilateral lesion of the pons, namely facial

paralysis on the side of the lesion with flaccid parasysis of the limbs on the

opposite side. Owing to paralysis of conjugate ocular deviation and rotation

of head to the side of the lesion of the patient with his eyes and head turned

towards the side of the paralysed limbs. Even when the signs at the outset

are those of a unilateral lesion of the pons, extention of the haemorrhage

soon involves the opposite side or the signs may be bilateral from the

beginning. When both sides of the pones are thus affected , there is paralysis

of the face and limbs on both sides with the bilateral extensor plantar

reflexes.

Marked contraction of the pupils – ‘pinpoint-pupils’ – the result of a

bilateral distruction of the occular symphatetic fibres, is characteristic of a

pontine haemorrhage and there is often a terminal hyperpyrexia.

Cerebellar haemorrhage:

This is usually sudden with occipital headache and vomiting and

sooner or later, loss of consciousness. Localising signs are often absent.


94

The cerebrospinal fluid:

Red blood cells are likely to be present in the clued and visible blood

if the haemorrhage has ruptured in to a ventricle or sub-arachnoid space. As

in a case of S.A.H., lumbar – puncture may be hazardous.

SYNDROMES

Internal carotid syndrome:

The cervical portion of the internal carotid artery near the carotid

sinus is a common site for the athero-stenosis and about 60% of all

thrombotic lesions are located here. Often, these lesions may be silent

(asymptomatic) because of collateral anastomoses (external carotid

ophthalmic anastomosis or from superficial and deep cervical anastomoses

or from the opposite carotid artery through the anterior – segment of circle

of willis). Warning symptoms precede a major ichs in nearly 50% of the

subjects. Such symptoms include brief episodes of confusion. With speech

difficulty (aphasia, dysarthia, dyslexia) sensory parasythesia with or without

motor weakness of the opposite side. Ipsilateral aurourosis fugax

(transient mono-ocular blindness) fleeting or semi-permanent, alternating

with or accompanied by the contralateral hemiplegia or sensory deficiet, is

pathognomic of carotid artery syndrome, however these events occur on

only 15 to 20% of the subjects.

The clinical manifestations of acute carotid artery occlusion are

almost indistinguishable from those of middle cerebral syndrome. Feeble

internal carotid or superficial temporal artery pulsations, dilated pupil and

poorly pulsating retinal vessels on the side of the suspected carotid-lesion

and ocular or cortical bruits on the ipsilateral side may suggest the correct


95

diagnosis. Carotid duplex Doppler sonography and angiography are helpful

in defining the extent and degree of stenosis.

In subjects with an old or silent occlusive carotid artery lesion on one

side, a new lesion on the opposite side may prove catastrophic. Here the

physical findings of bilateral hemiplegia (quadriplegia) with coma can be

mistaken for basilar artery syndrome.

Asymptomatic Cervical Bruit:

A carotid bruit may be heard in the neck is about 5% of

asymptomatic elderly subjects (55-80 years). Unless haemodynomically

significant, it is very difficult to correlate the mere presence of a bruit with

subsequent TIA or stroke in that territory. The role of prophylactic

endarterectomy to prevent a future stroke (estimated at 6% with in next 3

years) has not been established by clinical trails. In such cases antiplatelet

therapy may be prescribed.

Middle cerebral syndrome:

The cortical branches supply lateral surface of the cerebral-

hemisphere, except for the regions supplied by the anterior and posterior

cerebral arterics. The area of the supply include the sensory-motor cortex,

the motor and sensory speech centres, auditory area and optic-radiation. The

penetrating branches (lenticulo-striate arteries) supply the putamen, globus

pallidus, genu and posterior limb of internal capsule.

The clinical picture of middle cerebral artery occlusion is variable.

Contralateral hemiplegia, hemianaesthetia with or without homonymous

hemianopia and aphasia (dominant hemisphere) are common manifestations

. Occlusion of the superior division presents as contralateral hemiparesis

with sensory deficit and expressive aphasia (Broca’s aphasia), whereas


96

wernicke’s aphasia (sensory aphasia) is frequent with inferior division of

dominant side. Monoplegic symptoms with lesion of single cortical

branches are not uncommon.

Occlusion of penetrating branches (lenticulo – striate arteries) has

been repeatedly blamed for a dense sensory – motor hemiplegic syndrome

(capsular – hemiplegia ), but significant sensory loss seldom occurs with

such a lesion and “pure motor hemiplegia” is common..

Anterior cerebral syndrome:

The cortical branches mainly supply the medial superior surface of

frontal lobe and parietal lobe up to the para central lobule. The penetrating

branches supply the anterior limb of the internal capsule and part of the head

of the caudate nucleus.

An anterior cerebral artery occlusion proximal to the anterior

communicating artery in subjects with a symmetrical circle of willis is

frequently asymptomatic. Occlusion distal to the anterior communicating

artery manifests itself by a sensory motor parlysis of the opposite lower

extremity. With mild weakness of the opposite shoulder. Mental changes

ictal and urinary incontinence gait disturbances. Apraxia, grasp and sucking

reflexes may accompany the above findings.

Occlusion of a unpaired cerebral artery (supplyings both the

hemispheres) results in cubical type of paraplegia with sphincter

incontinence and a mental state is which the patient is alert but mute

(akinetic mutism). Aphasia and hemianopia are never seen.

Occlusion of the penetrating branches of the heubner’s artery

frequently blamed for ataxic tremours of the contralateral limbs (frontal


97

ataxia). Aphasias idiomotor dysphasia of limbs and gait may also be

present.

Posterior cerebral syndrome:

This artery supplies the middle and inferior aspects of the occipital

and temporal lobes. Its branches also supply the mid brain, cerebral

peduncle most of the thalamic and sub-thalamic regions.

Embolic occlusion of the posterior cerebral arteries is not

uncommon. Contralateral homonymous hemianopia is significant finding

and this results from infarction of the primary visual area (calcarine cortex)

the central vision is frequently spared even in cases with bilateral disease

(gun-barrel vision other manifestations of visual dysfunction include illusory

or distorted vision. Visual object agnosia and various forms of dyslexia

without dysgraphia. The papillary reflexes are well preferred. Contral

hemiphagia from lesion of cerebral peduncle (Peduncular hemiplegia) and

thalamic-syndrome (dejerine roussy syndrome) may also be present. In the

varying degree of sensory loss to all the modalities and spontaneous burning

or agonizing pain are frequent canalgia dolorosa . Memory loss (amnesia)

suggests upon of the medial temporal cortex. Contralateral involuntary

choreoathetosis or ataxic tremors are rarely observed.

Vertebro-basilar Syndrome:

After traversing through the bony vertebral canals both vertebral

arteries unite intracranially to form the basilar trunk . Their short para

median and long circumferential branches supply the entire brainstem.

Cerebellum and vestibular apparatus. Ischaemic attacks (TIA) manifest as

episodes of vertigo dizziness, diplopia, dysarthia, dysphasia, inco-ordination

of gait and limbs and bilateral signs of sensory motor deficiect. Occipital


98

headaches may be present . Ipsilateral IIIrd nerve palsy with contralateral

hemiplegia (weber’s syndrome) or with cerebellar ataxia (claude’s

syndrome) is diagnostic of mid-brain location. Homolateral parlysis of VII

th nerve with contralateral hemiplegia and hemianaephesia (Millard Gulbler

Syndrome) is suggestive of pontine lesion. Palatal paralysis with ataxia of

limbs with impairment of posterior column sensation on same side of the

body accompanied by diminution of pain and thermal sense on the opposite

side (wallenberg’s syndrome) indicate lateral medullary infarction from a

distal vertebral artery lesion.

Quadriplegia with bilateral conjugate lateral gaze palsy and mute

state with fully preferred consciousness has been described (locked-in

syndrome) in infarction of the basis pontis (sparing the tegmentum ) from a

mid-basilar occlusion.

Occlusion of isolated cerebellar branches may produce dizziness,

nausea, vomiting, nystgamus and appendicular or truncal ataxia without

sensory motor deficit in any limb. Such a syndrome should be differentiated

from cerebellar haemorrhage where emergency surgical decompression may

prove life saving.

Aortic Arch Syndrome:

The intriguing clinical syndrome is characterized by diminution or

absence of arterial pulsation in the vessels of the arms and the neck, the seat

of the disease, irrespective of its aetiology being located near the origins of

the great vessels arising from the aortic arch.

Several aetiological factors (congenital anomalies, trauma with or

without aneurysm, chronic dissecting aneurism, mediastinal tumours,


99

thrombophilia). Syphilitic aortitis rather than athromatotis, appeared to be

one of the common causes of this syndrome and that an arteritis of

undetermined origin was responsible for a good number of female cases.

Likewise, it has been a prevalent infraction that nearly all syphilitic cases of

aortic arch syndrome related from India are a form of arteritis of rheumatic

syphilitic or undetermined origin. It has now been appreciated that the

primary lesion in such cases. Particularly in men may not always be an

arteritis.

Reference:

1. Brain and Bannisters Clinical Neurology

2. Medicine by Golwala

3. API text book of Medicine

4. Harrison Medicine.


100

UPADRAVAS AND ARISTA LAKSHANAS

There is no specific description of upadravas of Pakshagata, hence

the upadravas of Vatavyadhess may be taken be taken for this context.

According to Madhavakara the following are the upadravas of

Vatavyadhis.

1. Visarpa

2. Daha

3. Shoola

4. Moorcha

5. Aruchi

6. Agnimandhya

7. Bala Mamsa Kshaya

8. Shodha

9. Sparsa Sunyatha 1.

Upadrvas of Vatavyadhi according to Susrutha

1. Bala Kshaya

2. Mamsa Kshaya

3. Sosha

4. Trishana

5. Chardi

6. Jwara

7. Atisara

8. Swasa

9. Moorcha

10. Hikka


101

11. Bhagna

12. Kampa

13. Adhmana

14. Srama due to disease.2.

The body which has kshaya of balamamsa and

pakshagata

Like diseases along with the above said upadravas wills troubles the patient.3

ARISTA

Arista Lakshana is pioneering indicationof Predictable death

which occur both in the ailing and non – ailing persons.4

This should be carefully observed by the physicians in case of

treating the patients otherwise he is giving up his credit and profit.

Charaka says that just as the blossom is the harbinar of the

coming fruit so is the exit of the symptoms known as fatal prognosis the herbiniran

of death of patients.5

Vagbahta and Susrute also explained similar view. 6

Arista Lakshanas more or less appear before the death in

every patient, but it is difficult to explain some of the aristas why and how they

appear. No death can take place with out fatal symptoms and nobody is seen

escaping from the death after exhibiting such symptoms though the death is

inevitable. After manifestation of arishtalakshanas still there are some measures

such as Rasayana, Japa etc, which can resist the death of the patient.


102

According to susrutha Arishtas can be divided into 2.

1. Niyata – can be cured with Rasayana, Japa etc

2. Aniyata - which cannot be cured. 7

Vagbhata divided the arishtas in to 2 types.

1. The Asthayee – which occur due to the predominance of doshas.

2. The Sthayee Aristhtes – Certainly kill the patients 8

According to Charaka the prakupita vata enters in pindikas

(Calf Muscles) causes Shaithilya. If it enters in nose causes deviation of nose and

manya sthamba along with dhatu sosha of Patient results into death.9

Vagbhata also have the same opinion 10

Rakta, Mamsa, Balakshyam, takes place in a Pakshaghata

rogi leads to death. 11

According to Susruta in a person if the following conditions

arise it is said to be definite death of a patient.

1. Soonatha

2. Supta Twacham

3. Bhagnam

4. Kampa

5. Adhamana

6. Rujartha Manthescha.12


103

References:

1) M.N.22nd Chapter / 76.

2) Su. Suthra. 33rd Chapter / 4-5.

3) Madhava Nidhana 22nd Chapter / 76-77

4) Cha. Ind. 11th Chapter / 29

5) Cha. Ind. Sthara 2nd Chapter / 3.

6) A.H.Sarena. 5th chapter /1

Su.Sutra. 28th Chapter / 2.

7) Su. Sutra. 28th Capter / 3-4.

8) A.H.Sarie. 5th Chapter / 3.

9) Cha. Ind. Sthan.10th Chapter / 5

10) A.H.Saree. 5th Chapter / 104.

11) A.H.Saree.5th Chapter / 101.

12) SU. SU. 33rd Chapter /6.


104

SADHYA SADHYATHA

Sadhyasadhyatha of the disease is generally depends

on three factors. They are

1. Duration of the onset of the disease.

2. Place of origin

3. Seveirety of Lakshanas.

Charaka says that Pakshagata is Kashtasadhya (or) asadhya

because it is deep seated in the body. Charaka also mentioned “Navan

Balavarthastroetan Sadhayennirupadravan”. It denotes the good prognosis of the

disease, provided the disease is free of upadravas. The onset of disease is recent and

more over the victim is strong enough i.e., Balavan rogi.1

According to Susrutha the Pakshaghata caused due to Suddha

Vata is Kashta Sadhya but if it is associated with either Kapha or Pitta it can be

taken as Sadhya and Pakshagata developed due to Dathu Kshya is taken as

Asadhya.2

Acharya Susrutha says in Sootrasthana that the Vatavyadhi in

general is “MAHA ROGA” having incurable nature and suggest that the physicians

not to treat when the patient is afflicts with serious upadravas.3

Astanga Hridyakara Says that the Pakshaghata is due to

Suddha Vata Janya can be considered as Asadhya and if the disease is associated

with Pitta or Kapha is said to be Kricchra Sadhya and Pakshaghata due to Dhatu

Kshaya is Asadhya.4

According to Susrutha if the Pakshaghata patient is unware of

Sparsa (Sensation & loss of Functions) that can be treated as asadhya. Sometimes

the patient may fall in death. 5


105

Pakshaghata caused to Garbhini, perpeurial woman, children

and senile objects is asadhya. Pakshaghata cause due to Adhika Raktasrava is

Asadhya. 6

References:

1) Cha. Chi.28 th Chapter / 72-74.

2) Su.Nid. 1st Chapter / 63.

3) Su. Sutra. 33rd Chapter / 2-3.

4) A.H.N.15th Chapter / 41.

5) Su.Nid. 1st Chapter / 62.

6) Su.Nid. 1st Chapter


106

CHIKITSA

As Pakshagatha is mainly as “Nanatmaja Vata Vyadhi” mostly the

samnya vata hara chitiksa will be suitable to it along with the specific line of

treatment. Hence it will be appropriate to discuss samnya vata hara chikitsa

(General) line of treatment for vata in the beginning and then to proceed to specific

line of treatment.

SAMANYA VATA ROGA CHIKITSA

1. Diets and Drugs:

The Diets and drugs possessing Madhura, Amla ,Lavana,

Ushna Vrishya and Balya properties be adopted. Liquid diet processed with

vatahara drugs and mamsayushas be given.

2. Sneha Karmas:

Snehas obtained from different sources which include ghrita

(ghee), Taila (oils), Vasa (Musclelfat) and Majja (bone marrow) should be

processed with drugs possessing deepana, pachana, vatahara and

virechaneeya properties should be administered in different routes i.e.,

orally, nasya ,abhyanga and vasthi etc.

3. Sweda Karma:

Swedana karma may be adopted along with swedhana, nadi-

sweda, prasthra sweda, sankara, pinda etc. are to be adopted to suit

individual cases.


107

4. Samsodhana:

Mridhu Shodhana Karmas particularly virechana should be

adopted proceded by appropriate sneha, swedas. The virechana drugs also

should be mixed with snehas possessing ushna, madhura, amla, lavana

properties, virechana will cause annulomana of vata, there by relieves

obstruction in the srotoses.

After Sodhana when agni becomes good again sneha, sweda,

swadhu, amla, Lavana, Snighu, Aharas, Navanas and dhooma panas all can

be repeated as per necessity which will be useful in relieving the vata vyadhi

as quickly as possible.

5. External measures:

unmardhana, Samvahana, (pressing and massaging). Peedana

(Pressing),Parisheka (affusion) avagahana (tub bath)be adopted.

References:

1. Cha. Chi. 28th Chapter / 75-78, 104.105

2. Su. Chi. 4th Chapter / 21-26

3. A.H. Chi. 21st Chapter / 1-3

In Pakshaghata cases associated with excessive doshaprakopa

and not alienated by Sneha, Sweda, Mridhu sodhana therapies should be

adopted in the patient is suitable to undergo them.1

Sneha and Swedas should be done before the patient

should be taken for shodhana theraphy.


108

1. Sneha Karma (oleation theraphy):

It is the best therapy for elevating vata.

It should be administered both internally and externally. Ghritha, Taila, vasa and

majja should be used for snehana.

The patient who had fatigued due to snehana should

be given some rest they should be thoroughly oleated with payah. 2

Charaka States that there is no other medicine which

can mitigate vata as effective as taila. The Tailas which are processed with vata hara

drugs will mitigate vata more effectively. Hence if the tailas are processed with

vatahara drugs l00 to 1000 times they can reach the minute channels (Srotases) and

mitigate the unease caused by vata in the minute channels.3

Sweda Karma (Fomentation or Suddation Therapy):

Swedanam is useful in all disease of vata, Kapha (or)

vatakapha origin.4

In pakshaghata the swedana should be adopted with snigdha

drugs

Nadi, Prastara, Sankara Sweda etc. are prescribed specially

for pakshaghata, stabdhata (Spasticity), Vakrata (Contraction) of the muscles are the

main components of various disabilities of the pakshaghta. The Swedna is a

treatment of choice too alleviate the above two conditions.

Importance of Sneha Swedas:

Sneha Sweda accomplish mridutva (or) softness at the

site of origin of vata i.e., kosta which facilitates the movement of vata to normalcy. 5


109

The appropriate adoption of sneha swedas alleviate

the vakrata and sthadhata of impaired hasta and padas of the patient and

accomplishes mridutva and restoration of the movements in the similar manner of a

dry stick which can be moulded as desired after applying oil and heat without

getting it damaged. 6

Virechana Therapy:

Vasthi Karma is regarded as the important therapy for vata

vyadhis in general .charaka and vagbhata indicated virechana karma it self as

specific shodhana karma for pakshaghata.

Virechana is particularly indicated when Kapha is settled in

Pakwasaya, when pitta get provoked in the entire body.

Virechana karma acts as vatanulomaka measure also when

the channels of vata got occluded due to accumulation of malas.7

Vasthi Therapy:

Vasthi Karma is main treatment for the vata disorders

because vasthi oushada immediately after entering in to the pakwasya strike at the

very root of the vitiated vata.

In the similar manner as the water given at the root of plants

leads to growth of the tree with tender leaves. Flowers and fruits the niruhavasthi

and anuvsana vasthi also causes enhancement of strength complession and

appropriate functioning of Vata. 8


110

Vamana Therapy:

In Pakshagata there will be no necessity of vamana in

general.

In Pakshagata when vata followed by Kapha in and when

kapha is accumulated in Amashaya and ready to expel. In that condition vamana

holds good.

Nasya Therapy:

On Pakshagata Various types of Nasyas are indicated like

Bhingadi, Mashadi Nasya etc.

Siro Vasthi:

Sirovasthi is the most potent of moordha taila described by

vagbhata. Pichu, Sirasheska and sirobyanga the other three forms of moordha taila

are less potent than one other in order.

Sustutha indicated sirovasthi particularly for Pakshagata and

generally for all vata disorders.

General shamana chikitsa in pakshaghata

1. Guggulu Preparations

a) Maha Yogaraja Guggulu (Shrangadhara)

b) Yogaraja Guggulu (S.S)

c) Trayodashang Guggulu (CD)

d) Shadaseethi Guggulu (Y.R)

e) Panchamrita loha Guggulu (B.N.R)


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f) Shadanga Guggulu(R.R.S)

g) Shadanga Guggulu(R.R.S)

h) Dhatrishathi Guggulu (Y.R)

2. Rasona yogas

a) Rasona panda (B.R)

b) Rasona Kalka (B.R)

c) Lashuna vati (Y.R)

3. Ghritas

a) Dashamooladi Ghritam (Charaka)

b) Chitrakadi Ghritam (Charaka)

c) Chagalyadi Ghritam (Charaka)

d) Trivrut Ghritam (Susruta)

e) Tilwaka Ghritam (Susruta)

f) Sauvarchaladi Ghritam (A.H)

g) Rasnadi Ghritam (A.H)

4. Tailas

a) Nirgundi Tailam (Charaka)

b) Pancha mulyadi Tailam (Charaka)

c) Yavadi Tailam (Charaka)

d) Sachacharadi Tailam (Charaka)

e) Swadamshtradi Tailam (Charaka)

f) Amrita Tailam (Charaka)

g) Bala Tailam (Charaka)


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h) Rasnadi Tailam (Charaka)

i) Moolakadi Tailam (Charaka)

j) Vrishamooladi Tailam (Charaka)

k) Prasarini Tailam (A.H)

l) Nimbasi Tailam (A.H)

m) Maha masha Tailam (Ch.D)

n) Maha naraya Tailam (Bha. Pra)

o) Vijaya Bhairava Tailam (R.R.S)

5. Churnas

a) Vaishwanara Churnam (G.N)

b) Sigrumooladi Churnam(G.N)

c) Rasnadi Churnam(B.R.)

d) Shaddharana Churnam(B.R.)

6. Guti and Vati

a) Gaganadi Vati (Bhai. Ra)

b) Rasnadi Gutika (Bhai.Ra)

c) Agnitundi Vati (R.T.S.S.P.S )

7. Quathas

a) Baladi Quatham (Bhai.Ra)

b) Erandadi Quatham (Bhai.Ra)

c) Simhasyadi Quatham (Bhai.Ra)

d) Rasna saptaka Quatham (Bhai.Ra)

e) Gokshuradi Quatham (Bhai.Ra)

f) Masha Baladi Quatham (Bhai.Ra)

g) Rasna dasha mooladi Quatham (Bhai.Ra)


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8. Rasoushadhis

a) Brihat vata chintamani ras (Bhai.Ra)

b) Swacchanda Bhairava ras (Vai.Chi)

c) Vata Rakshasa Ras (Y.R)

d) Vatari Ras (Bahi.Ra)

e) Vata Gajankusha Ras (Vai.Chi)

f) Kala Kantha Ra (Vai.Chi)

g) Kanaka Sundara Ra (Vai.Chi)

h) Ekanga veera Ras (Bhai. Ra)

i) Rasa Raja Ras

j) Yogendra Ras (Bhai.Ra)

k) Lakshmi Vilas Ras (Bhai.Ra)

9. Arishtas

a) Balarishta (V.C)

b) Ashwagandharishta (G.N)

c) Dashamoolarishta (B .R.)

10. Bhasmas

a) Malla sindur (R.T.S.S.P.S)

b) Roupya bhasma (R.T.S.S.P.S)

c) Abharaka bhasma (R.T.S.S.P.S)

d) Swarna bhasma (R.T.S.S.P.S)

11. Lavana Yogas

a) Sneha Lavanam (G.N)

b) Kalyanaka Lavanam (G.N.)


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12. Eranda Yogas

a) Eranda Tailam (Bhai.Rat)

13. Naimithika Rasayanam

a) Bhallataka Rasayanam (G.N)

b) Guggulu and Rasna (B.R

References:

1) Cha. Chi. 28th Capter / 83.

2) Cha. Chi. 28/75-77

3) Cha. Chi. 28th Chapter /181-182.

4) Cha. Su. 14th Chapter / 8.

5) Cha. Chi. 28th Capter / 82.

6) Cha.Chi. 28th Capter/79.

7) Cha. Chi. 28th Capter/85.

8) Cha. Siddhi. 1st Chapter / 30-31.

9) Cha. Chi. 28th Capter/88.


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LINE OF THE TREATMENT OF PAKSHAGHATA:

The specific therapies described for pakshagata by various

acharayas are as follows.

According to Charaka:

“Swedonam Sneha Samyuktam Pakshagate Virecainam”.1

The line of treatment is Swedanam and Sneha Yukta Virechanam.

Vagbhabata in he stated same as that of charaka.2

“Swedanam Sneha Samyukutam Pakshagata Virechenem”

Susruta:

Tatra prarega sneha.--------------------------------------

----------------------------------------------Vidhana

Upachanat. 3

Here we can see an eleberate description of different

aspects of treatment along with the routine type of treatment like sneha, sweda,

mriduvirechava. Anuvasana, as therefore and sirovasthi. Anutaila abhyangam,

Salvanaswedanam, as special treatment and should to have continue the intense

treatment up to 3 to 4 months.

Dalhana States that vomiting should be performed

first it necessary. Then vireechana, Anuvasyana vasthi should be given.After

appearance of Sneha Lakshanas as therefore vasti can be given. Immediate after

asthapana, anuvasanam should be adopted. 4

Astanga Sangrahakena described Pkshagata in similar

manner to susruta. He also indicated the therapies of akshepaka in pakshagata. 5


116

References:

1) Cha. Chi. 28th Chapter / 100.

2) A.H.Chi. 21st Chapter / 135

3) Su. Chi. 5th Chapter / 43.

4) Dalhana on Su. Chi. 5th Chapter / 19.

5) A.S. Chi. 23/30


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CEREBRAL ISCHAEMIA:-

TREATMENT ASPECT OF CVA’s:

Treatment:

This requires a knowledge of its natural history. Angiography may

be contraindicated because a patient is over 60 with coronary disease or

diabetis and in other patients it is reasonable to consider if surgery would be

undertaken if a lesion were demonstrated before embarking on angiography.

Large surveys have shown that approximately two thirds of strokes are the

result of atheromatous thrombosis one-sixth the result of embolism and one-

sixth are associated with intracerebral haemorrhage. The major cause of

death in patient with transient cerebral ischaemic attack is ischaemic heart

disease.

Trasient ischaemic attacks (TIA’s):

Since the aim of treatment in CVA’s is the prevention of a major

stroke, the management of TIA’s is considered first.

TIA’s are brief episodes of neurological disfunction with recovery

but with a tendency to recur. They might be distinguished from other brief

attacks due some examples to migraine or epilepsy. They may be due to

inadequate flow emboli or spasm or combination of these factors.

The aim of medical treatment in the TIA’s is to try to stop embolism

from fibrin platelet emboli on atheroma in arteries, which is likely to cause

further ischaemic attacks or strokes. After many controlled trails. It seems

that Aspirin is effective in reducing the incidence of strokes at least in men


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though the best dose to be given is uncertain. Usually a dose between 300

mg and 1 gm a day is prescribed though smaller doses may have a protective

benefit. Aspirin inhibits platelet function by irreversibly inhibiting the

enzyme cyclo-oxeggenase which catalyses the synthesis of thromboxane A2

which has procoagulant and platelet aggregation properties. In conjuction

with aspirin other drugs which are likely to reduse platelet adhesiveness and

platelet release include dipyridamole (50mg slowly) and sulphin Pyrazole

(Afaran) (200 to 400mg doses), Ticlopidine is a platelet anti aggregate,

proved to be effective but it is expensive and neutropenia. Skin rashes and

diarrohoea may limit its use.

Heparin may be given as 1,00,000 units every 6 hours. The usual

anticoagulant given after a short term heparin is the coumarin derivative

warfarin.

The completed stroke :

Angiography may be necessary to exclude other than vascular causes

but demonstration of a stenosis or occlusion and surgical treatment of it will

be too late to be benefit acute disabling symptoms.

A group of patients in whom a CT scan is particularly indicated is

those in whom the stroke is complete in less than 2 hours and intracranial

bleeding may have occurred.

The size of a infarct is affected by many factors which include

metabolic changes occurring with Calcium influx, excitotoxin release and

the formation of free radicals all of which affect the extent of oedema and

neuronal death.


119

Specific treatment may influence the outcome and drugs used have

included thrombolytic agents (such as urokinase and the use of Calcium

channel blockers (nimodipine) ) and prostaglandin-analogues as well as

usual methods reducing the oedema.

It has been proposed that there is a place for agents which reduce

erythrocyte deformability and inhibit their aggregation such as the propriety

drug pentoxifylline.

It must however be added to so far none of these drugs has been

proved o improve the prognosis significantly after a complete stroke.

Surgical treatment:

The place of cartoid endartectomy in patients with TIA’s represents a

balance of risk between the expected stroke rates with out surgery.

Cerebral Embolism:

Treatment:

The prophylactic value of anticoagulants in patients liable to cerebral

embolism now seems established. When definite repeated emboli occur

from an uncorrectable source. Anti-coagulants should be used but not when

infarction is thought to have occurred because the risk of causing

haemorrhages in the infracted area. Treatment of the cerebral lesion is the

same as that of cerebral infarction from any other cause though in view of

the risk of further embolisation a good case can be made in the immediate

use of heparin followed by a coumarine derivative. Alternatively anti-

coagulants may be delayed for 3 weeks as their prior use may run the risk of

causing haemorrhage in the infracted areas. Rest for several weeks is

essential in order to diminish the risk of further emboli occurring.


120

Hypertensive encephalopathy:

Treatment:

Since the arteriolar spasm upon which the symptoms depend is

secondary to the hypertension, the object of treatment is in general is to

lower the hypertension, and for this purpose hypertensive drugs such as the

calcium channel anatgonist nifedipine can be used. If the patient is

unconscious then hydralezine or labatelol should be considered first. Too

rapid a reduction has led to blindness. Morphine may also be given and

barbiturates and diazepam if convolutions occur. If necessary cerebral

oedema can be dealt with by administering hypertonic solutions.

Intracranial haemorrhage:

Sub-arachnoid haemorrhage:

Treatment:

The most urgent question is the suitability of the patient for surgery,

which must be considered in the light of the angiographic findings if he has

been considered suitable for angiography. The object of surgical treatment

is to occlude the aneurysm by a clip or ligation if the aneurysm is accessible.

So far aneurysms of the middle cerebral artery aneurysms are usually

tackled directly. Preferably by clipping the neck of the aneurysm.

Aneurysm of the anterior cerebral artery have proved least easy to treat

surgically.

If the patients level of consciousness deteriorates gradually watch

must be kept for the development of communicating hydrocephalus which

may need shunting.


121

Hyponatremia due to inappropriate antidiuretic harmone (ADH)

secretion is a recognized complication of SAH and can also leads to coma

and fits.

Controlled trails have shown nimodipine, which controls the entry of

calcium in to ischaemic cells to be beneficial in the acute management of

SAH and it is now in general use. Postoperative blood pressure and fluid

balance may be difficult to control so a central line is usually used. After the

operation steroids, if they have been given can be rapidly withdrawn and

Nimodipine can be stopped after some weeks and anticonvulsants more

slowly.

If comatose the patient should be treated along the usual lines.

Headache will require analgesics and if very troublesome may respond to a

second lumbar puncture carried out a few days after the first. The patient

should be kept completely at rest in bed for 3 weeks, and then if there has

been no evidence of recurrence allowed to move about in bed and begin to

get up out the end of another week. He most be advised to lead a quiet life

as far as possible and avoid any activity likely to raise the blood pressure.

The bowels should be regulated to prevent straining.

Cerebral Haemorrhage:

Treatment:

The rational treatment of a cerebral haemorrhage would be the

evaluation of the clot and control of the bleeding point, but the scope of

surgery in treatment is still limited.

The age of most patients the extent of damage caused by the haemorrhage

together with the aedema of neighbouring tissues. The condition of the rest

of the cerebral circulation and of the cardio vascular system generally all


122

militate against successful surgery. Nevertheless when the conditions are

more favourable especially when cerebral haemorrhage occurs before middle

life and many come from a congenital vascular abnormality or may be

cerebellar in site, surgery should always be considered. Lumbar puncture

should be avoided. Cerebellar haemorrhage is potentially treated surgically.

The diagnosis is made on CT Scan and rapid referral to the neurosurgeons

should be made. If unconscious he should be treated as usual. After

recovery from the immediate effects of the haemorrhage, physiotheraphy

should be began. Special stress should be laid upon passive movements of

all joints. Orthopedic supports for the affected limbs may be required as for

a haemiparesis from any cause


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NASYA KARMA

Definiition:

The administration of either medicine (drug) or medicated oil

through the nose is known as nasyakarma.1

Nasyakarma is also known as sirorechana, Siro – Vireka and

moordhavirechana. Charaka has also used the word “Nastah Prachardenam” for the

same. 2

Similary the words “Navan” and “Nasthah Karma” also are

found indicating the same kriyas.

Classification of Nasya:-

I. Charaka explained 5 varieties of Nasya Karma.3

Navana nasya :- This is again of 2 types

a. Snehana and

b. Sodhana.

2. Avapidaka Nasya:- This of is of 2 varities

a. Sodhana and

b. Sthambana.

3. Dhoomapana Nasya.

4. Dhooma nasya:- This it 3 varieties

a. Prayogika

b. Vairechanika

c. Snaihika

5. Pratimarsa nasya:- This is 2 varieties

a. Snehana and


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b. Virechana.

The nasya may de divided in to 3 varieties according to its

action.

1. Rechana

2. Tarpana and

3. Shamana.

II. According to Susruta, Nasya is mainly of two varieties 4

1. Sirovirechana

2. Snehana.

Eventhough it is of two varieties, it is again classified into 5

varieties.

1. Nasyam

2. Sirovirechana

3. Pratimarsa

4. Avapidaka

5. Pradhamana.

III. According to Vagbhata, Nasya is of 3 varieties.

1. Virechana Nasya

2. Brimhana Nasya

3. Shamana Nasya.

IV. Sarangadhara divided nasya into 2 varieties

1. Rechana – Which acts as Karshana

2. Snehana - Which acts as Brimhana.


125

Utility of Nasya Karma:-

The Nasya Karma is essentially useful in the diseases of the

neck and head. The conditions in which the nasyakarma is contra – indicated are

given below.

Contra – Indications:

1. Indigestion

2. Person who have just taken their meals (or) an oleacious portion.

3. Those who are thirsty for water

4. Who have bathed their head.

5. Those who are going to take their bath.

6. Hungry.

7. Fatigued

8. Fainted

9. Injured

10. Exhausted by Sex – act, Exercise (or) drink

11. Suffering from acute Fever (Short in duration)

12. Afflicted with grief

13. Who had purgation or other langhana Kriyas

14. Who were given unctuous enema

15. Pregnant lady (or) just delivered

16. Afflicted with Coryza

17. Who just had a drink

18. Afflicted with poison

19. Stopped natural urges.


126

The conditions in which the Nasyakarma is indicated:-

Except in the conditions in which the Nasya Karma is Contra

indicated in all other conditions it may be administered and more so in the

following:-

1. Sira Sthamba

2. Manya Sthamba

3. Danta Sthamba – Soola

4. Galagraha

5. Hanugraha

6. Peenasa

7. Galasundika

8. Galasaluka

9. NetragataSukraroga

10. Timira

11. Vartmaroga

12. Vyanga

13. Upajihvika

14. Arthavabhedaka

15. Greeva SkandhaMukharoga

16. Karnashoola

17. Nasashoola

18. Akshishoola

19. Sirashoola

20. Ardita

21. Apatantraka

22. Apatanaka.

23. Galaganda


127

24. Danta Shoda, Harsha etc

25. Akshiruja

26. Arbuda

27. Swarabheda

28. Vakgraha

29. The Vata diseases of the head and neck:-

It can be noticed that in the above stated

indications of Nasyakarma, the vitation of Kapha and / or Vata is

clearly discerbable.

Nasya Vidhi:-

The actual method of Nasya Karma may be divided in to 3 parts:

1. Poorva Karma

2. Pradhana Karma

3. Paschat Karma

Poorva Karma:-

There should be separate room for conducting the

nasyakarma, and it should have good and concealed ventilation and impereable to

smoke, dust and sunlight but good lighting should be available.

The Patient should be made to sit or lie down as desired by

the physician. The head and face are to be applied with our oil like Ksheerabala

Taila, Dhanvantari taila or any other which the physician considers suitable. The

Mridusweda is to be applied on the face, head, throat and neck. This Swedakriya

melts and liquefies the doshas from the nose and head. After the Sweda kriya, Light

massage with hands is given to these areas.


128

Pradhana Karma:-

The Patient should be made to take the correct posture, and

the nasal administration of the medicine. In the posture the head will be in a slightly

hanging position but resting on the head rest attached to the seat or bed. So that the

nares are directed upwards for easy administration of the medicine. The eyes and

brows are covered with a clean cloth to avoid the medicine accidentally falling in

the eyes. After lifting the tip of the nose with the index finger, the Luke warmed

medicine is admimistered in to the nostrils as drops in the prescribed dose. The

drops should be put in as continous manner in each nostril separately, but not very

fast or very slow an even with a break in between.

After the administration of the medicine in to nostrils, mridu

Swedana is given to the throat, cheeks and brows and then light massage is applied

on the shoulders and palms and soles. The patient is asked to spit the medicine

which gets in to the throat in to the spitions arranged near by. The lacrimation is

regularly wiped by clean cloth. The physician has to observe the patient clearely for

any complications etc. The medicine that reached the throat from the nose should by

spit only but not swallowed.

Paschat Karma:-

Just after the administration of the medicine. The patient

should lay down for about 5 minutes. Then tapasweda is done on the forehead,

cheeks and throat, and light message on the neck and shoulder region and soles of

the feet. The medicine that has flown in to the throat and mucus which is seeveting

should be spit out. Gorgling with hot water is essential.


129

References:

1) Su. Chi. 40-21

2) Su. Chi. 1-85

3) Cha. Si. 9-95

4) Shu. Chi. 40-21


130

PATHYA APATHYA

“Pathona Apetam Pathyam”

The drugs and diets which are useful to Srotas are called Pathyas.

The Pathya and Apathyas of Vatavyadhis i.e., Pakshaghata are as follows:

1. Rasas:

Pathyam : Madhura, Amla, Lavana.

Apathyam: Katu, Tikta, Kashaya

2. Pulses & Grains:

Pathya : Purana Rakta Sali, Masha, Wheat, Horse gram and

blackgram

Apathaya: Green Gram, Sharshapa, Mudga, Navadhanya,

Yava.

3. Gunas:

Pathya : Ushna, Mridhu, Snigdha, vrishya, Poushitka aharas

and oushadas.

Apathya: Langanam, Ruksha, Seetala, Laghu, Abhishyanda

kara, Dravyas

4. Sakas:

Pathya : Kushmanda, Brinjal, Karela, Snake Guard, Drum

stick, Raddish.

Apathya: Bimbi, Alabu, Cucumber, Kandasakas, Kosatakii.

5. Phalam:

Pathya : Dadima, Badara, Amra, Draksha

Apathya : Jambu


131

6. Mamsa:

Pathya : Aaja, Kukkuta, Aavi

Apathya : Mastya, Anupamamsa, Bilasaya.

7. Vihara:

Pathya : Abhyanga, Ustadana, Snanem, all snehas,

Nivatha Sthanam, Soft bed, Warm Clothes.

Apathya : Ati Vyavaya, Ati Vyayama, Vegadharana,

Jagarana, Udvega, Seetala Jala, Seetala Phala

References:

Vaidya chintamani vatavyadhi chikitsa chapter


132

VATA RAKSHASA RAS

The drug Vatarakshasa Ras is indicated in vata disorders along with

Pakshaghata in books like Yoga Tarangini. Vaidya Chinta Mani Basava Rajeeyam.

It contains

Abhraka Bhasma - ¼ Kg

Rasa Bhasma - ¼ Kg

Tamra Bhasma - ¼ Kg

Kantaloha Bhasma -¼ Kg

Suddha Gandhaka -¼ Kg

At first Rasabhasma & Suddha Gandhakam was finely grounded &

mixed and all the remaining bhasmas and churnas are added one by one and made

bhavana and mardhana for 3 days with Punarnavamoola Swarasa. Guduchi

Kashaya, Chitramoola swarasa, Tulsipatra Swarasa and with Trikatu Kashaya then

dried and put in Saravam and seel it made swangaseetale take it out and paste it with

water and made pills.

Vatarakshasa ras is vatahara, srotosodhana and deepana, along with

pakshaghata it is indicated in Urusthamba, Vatarakata, Amavata, Dhanurvata and in

Sandhivata.


133

AUSHADA SAMEEKSHA:

1. ABHRAKA (Mica)

Synonyms ------------- Gagana, vyoma, Kha, Antariksha,

Pharmacological and therapeutic properties ---

Rasa – Kashaya , Madhura

Guna – Snigdha

Veerya – Seeta

Vipaka – Madhura.

Karma – Deepana, balya, vrushya, Ayushya, sutendra bhandi, soukya

janana, pachana, Roghaghna, Mrityuharana, Shareera Dardhyakara, veerya stambha

kara, Veeryaviddhikara, smrutikara, sadyo Prana vardhana, yogavahi, pumstvakara,

santanakara, Rasayana, Dhatu Vruddhikara, Pragna bhodhi, prasamitaruja,

Kshayashara, Paramamamrutam.

Dosha Prabhava – Vata Pittaghna. Kaphagna.

Vyadhi Prabhava - Kshaya, Jara, Valipalitha, Pandu, Grahani,

Amashoola, , Jwara, swasa, Prameha,. Aruchi, Kasa, Mandagni, Mootra krichrra,

Shoola roga, unmada, shophaamaya, kamala, pancha vidha gulma, udara, roga,

Mrutyunasha.

Rasa Bhasma (Rasa Sindhura):

Pharmacological and therapeutic properties of Rasa Sindhura

Rasa – Madhura, Tikta

Guna - Snigdha, Guru

Veerya – Seeta

Vipaka- Madhura

Karma –Rasayana


134

Dosha Prabhava – Tridoshaghana.

Vyadhil Prabhava – Prameha, Pandu, Purana Jwara,

Apsmara.

TAMRAM (Copper)

Synonyms – Ravi Priya, Nepaliya, Surya loha, Lohitasaya,

Trayambaka.

Pharmacological and Therapeutic Properties m-

Rasa - Kashaya, Tikta, Madhura, Amla

Guna - Seeta, Laghu, Sara

Veerya - Ushna

Vipaka - Katu

Karma – Lekahana, Alpa Brimhana, Hrudvishodhana, Krimighana, Shodhanna,

Garahra, Rasayana, Ropana, Netrya.

Dosha Prabhava – Vata Kapha hara

Vyadhi Prabhava – Pandu, udara roga, Arsha, Pleeha roga, Gulma,

yakrut roga, krimi, shotha, shoola, udara shoola, Asta Vidha shoola, Amla Pitta.

Jwara, Kasa, Swasa, Kshaya, Kushta, Peenasa, Agnimandya, Kshaya, Prameha,

Grahani Roga, Mootra Krichra, Jeerna Jwara, Arochaka, Murcha, Amadosha,

Amavata, Vruddhi, Sthonla, Jara and Mrutya hara, Vishadosha hara.

KANTHA LOHAM:

Synonyms:-

Varieties:- Bramakam, Chumbakam, Karshakam, Dravakam,

Romakam,.

Pharmacological and Therapeutic Properties.

Rasa - Tikta


135

Guna - Tikshana, Ushna

Veerya - Seeta

Vipaka - Madhura

Karma - Rasayana, AyurvriddhikarA.

Dosha Prabhava - Tridosha Samaka

Vyadhi Prabhava -Soola, Amahara, Moolaroga, Gulma, Pandu, Yakrut,

Kshya,Udara.

GUNDHAKA (Sulphur):

Synonyms – Gandha Pashanam, Sougandhikam, Bali, Balivasa.

Pharmacological and Therapeutic Properties.

Rasa - Katru, Tikta, Kashaya.

Guna - Sara, Snigdha

Veerya - Ushna

Vipaka - Madhura (R.Chi) Katu (Ay. Pr)

Karma – Deepana, Pachana, Vishahara, Jantughna, Krimihara, Agnikaraka,

Amashoshana, Rasayana, Suta Moorchana, Baleveerya Vardhana,

Deergaayush Kara, Drushti Shakti vardhaka, Rasa veerya janana.

Dusha Prabhava – Kapna vata hara, pittahara.

Vyadhi Prabhava – Kandu, kushta, Visarpa, Dadru, twak dusha, Ama dosha,

visha dosha, Bhoota Dosha, Krimidosha, Pleeha roga, kshaya

roga, Jara roga, Netra roga, Jwaradi roga, kasa, Amajirna,

Mandagni, Balakshaya.


136

The above mentioned bhasmas are to be made bhavana in the swaras / quathas of

the following dravyas, one by one for 3 days:

1. Punarnava Quatha

2. Guduchi Kashaya

3. Chitramoola Swarasa

4. Tulasi Patra Swarasa and

5. Trikatu Kashaya


137

Bhringadi Taila Nasya

Bhringadi Taila Nasya is indicated in Pakshagata along with Aardita

Vata in Vaidya Chintamani

It contains

1. Bringaraja - Swarasa 4 times to Taila

2. Erranda - Swarasa 4 times to Taila

3. Nirgundi - Swarasa 4 times to Taila

4. Mastchyakshi - Swarasa 4 times to Taila

5. Arkapatram - Swarasa 4 times to Taila

6. Maricha Churnam – ¼ th to Taila

7. Tila Tailam - 3 Liters

Bhringaraj:-

Sanskrit Name: Bhringaraj

Latin Name : Eclipta Alba

Family : Asteraceae

Telugu : Gunta Galagara Aaku.

Synonyms:- Markava, Kesaraja, Kesaranjana.

Gunas:-

Rasa : Katu, Tikta

Gunam : Ruksha, Laghu

Veeryam : Ushna

Vipaka : Katu

Karna:- Kaphavatahara, Balya, Rasayana, Kesya, Chekshushya.


138

Indications:- Kushta, Krimi, Kasa, Swasa, Sodha, Pandu, Netraroga, Siroruja,

Hridroga.

Useful part:- Panchanga.

Eranda:-

Sanskrit Name: Eranda

Latin Name : Ricinus Communis

Family : Euphorbiaceae

Telugu : Amudam

Synonyms:- Eranda, Gandharwa, Hasta, Panchangula, Vyagrapuccha, vatari,

urubuka.

Gunas:-

Rasa : Madhura,Katu, Kashaya

Gunam : Snighda, Tikshna, Sookshma

Veeryam : Ushna

Vipaka : Madhura

Karna:- Kaphavatasamaka, rechana, twachyam, vrishyam (Moolam).

Indications:- Glulma, Anaha, Soola, Jwara, Vata Sleshmaharam, Yakrut

Pleehodaram, Arsas, Krimi, Pravahika, Amavatem, Sodha, Swasa,

Mritakriccheram, Vriddhi.

Useful part:- Moolam, Patram, Beejam, Tailam.


139

NIRGUNDI:

Sanskrit Name : Nirgundi

Latin Name : Vitex Nirgundo

Family : Verbenaceae

Telugu : Vavili

Synonyms:- Nirgundi, Saphalika, Suvaha, Sindhuvara, Sindhuka.

Gunas:-

Rasa : Katu, Tikta

Gunam : Laghu, Ruksha

Veeryam : Ushna

Vipaka : Katu

Karna:- Vatasleshaharam, Kesyam, Chekshusyam.

Indications:- Sodha, Amavata, Krimi, Soola, Kushtam, Vranam, Kasam, Pradaram

Useful part:- Patram, Moolam, Beejam.

MASTYAKSHI

Sanskrit Name: Mastchyakshi

Latin Name : Altenranthera Sessilis

Family : Amaranthaceae

Telugu : Ponnaganti Kura

Synonyms:- Bahlika, Mastyagandha, Mastyadani.


140

Gunas:-

Rasa : Katu

Gunam : Laghu

Veeryam : Seeta

Vipaka : Madhura

Karna:- Kapha Pittahara, Satnya Vardaka, Agni Deepaka.

Indications:- Grahani, Atisara, Kushta, Charmaroga.

Useful part:- Whole Plant.

ARKA

Sanskrit Name: Arka

Latin Name : Calotropis Gigentaea / C. Procera

Family : Asclepidaceae

Telugu : Jeeladu.

Synonyms:- Sweta Arka: Sadapusha, Mandara, Alarka,

Rakta Arka: Arkaparna, Suklaphala, Vikarna, Raktapushpa,

Asphota.

Gunas:-

Rasa : Katu, Tikta

Gunam : Laghu, Ruksha, Tikshna

Veeryam : Ushna

Vipaka : Katu

Karna:- Vatahara, Deepana, Rechana, Vishahara, Vrishyam (Pushpam).


141

Indications:- Kushta, Kandu, Pureeshajakrimi, Udara, Pleehavriddhi, Arsas, Swasa,

Kasa, Sodha.

Useful part:- Mool Twak, Ksharam, Pushpam,Patram.

MARICHAM

Sanskrit Name : Maaricham

Latin Name : Piper Nigrum

Family : Piperaceae

Telugu : Mireyalu

Synonyms:- Vellaja, Ushana, Krishna, Dharma Pattana.

Gunas:-

Rasa : Katu

Gunam : Laghu, Tikshna

Veeryam : Ushna

Vipaka : Katu

Karna:- Kashavatehara, Deepana, Avrishya

Indications:- Pravahika, Kasa, Peenasa, Hridroga.

Useful part:- Phalam.


142

TILA Sanskrit Name: Tila

Latin Name : Sesamum Indicum

Family : Pedaliaceae

Telugu : Nuvuulu

Gunas:-

Rasa : Madhura, Kashaya

Gunam : Guru, Snigdha

Veeryam : Ushna

Vipaka : Madhura

Karna:- Vatahara, Kaphapittahara, Kesya, Twachya, Balya, Grahi, Sukrala, Vrana

Prakshalana

Indications:- Agnimandhya, Grahani, Vataroga.

Useful part:- Beejam, Tailam.


143

CRITERIA

Criteria selection and admission of patients-

Thirty patients suffering from pakshaghata are selected randomly for

the present

Study from the bulk of patients coming for the treatment for the treatment at the

Kayachikitsa

Department of Post-graduate Training and research Centre at Govt. Ayurvedic

Hospital, Erragadda, Hyderabad (A.P) during 2006-2008.

The patients were selected after conducting a screening test to exclude the

following type of patients.

1. Patients with Cerebral Haemorrhage

2. Patients below the age of 20 years and above the age of 70 years.

3. Pregnant women

4. Pakshaghata patients with dislocation of joints

5. Comatose patients

6. Pakshaghata caused due to the mechanical injury. Known causes of

Granthi and Arbuda.

These points are excluded from the present study. After excluding all theses

types of patients, finally 30 patients were selected to study the treatment with

vatarakshasaras and bhringadi taila nasya.


144

PARAMETERS-

Subjective and objective parameters are taken into consideration. The

clinical improvement in the relief of symptoms of like-

1. Impaired walking

2. Impaired movements of upper limbs

3. Dysphagia / dysarthria (Vakgraham / Vakstambha)

4. Loss of appetite and digestion

5. Sleeplessness (Nidra nasha)

6. Anxiety (Krodha / soka)

Objective parameters-

1. Blood pressure

2. Tendon reflexes : Grading

0 – Absent

1 – Positive

2 – Brisk

3 – Very Brisk

4 – Clonus

3. Muscle power grading –

0 – No contractions

1 – Flicker or trace of contractions

2 – Active movement with gravity eliminated

3 - Active movement with gravity

4 - Active movement with gravity and resistance

5 – Normal


145

MATERIALS AND METHODS

Thirty patients suffering from Pakshaghata are selected randomly for

the present study. To study the treatment Vatarakshasa Ras and with Bhringadi

Taila Nasya.The drugs and their quantity are mentioned belowVatarakshasaras 1BD

for 60 days with hot water andBhringadi taila nasya 8 drops in each nostril for 5-7

days.

OBSERVATION

The patients are studied based on the Darsana, Sparsana, and Prasna

parikshas.

These include Dasavidha Pariksha and Astasthana Pariksha. Every day

the condition of the patients is observed and the treatment procedure is adopted. The

total observations of every day are summed up after twenty days of duration of

treatment.

The patients are classified based on different categories

1) Linga

2) Nidana

3) Lakshana

4) The ‘Paksha’ affected

5) Dosha involvement

6) Hypertension and Madhumeha

7) Age

8) Muscle Power

9) Tendon reflex


146

Table 1 Classsification of patients according to sex

LINGA (SEX) NO. OF PATIENTS PERCENTAGE

MALE 22 73%

FEMALE 8 27%

22 (73.3%)

8 (26.7%)

0

5

10

15

20

25

No.

ofpa

tine

ts(%

)

Male Female

Showing Sex wise classifcation of patients


147

Table 2 Affected side of pakshaghata on patient’s body

S.No.AFFECTED

SIDE

NUMBER OF PATIENTS

TOTAL MALE FEMALE

PERCEN

TAGE

1 RIGHT SIDE 15 14 1 50%

2 LEFT SIDE 15 8 7 50%

14 (46.7%)

1 (3.3%)

8 (26.7%)

7 (23.3%)

0

2

4

6

8

10

12

14

No.

ofpa

tien

ts(%

)

Right side Left side

Showing Affected Attacked side of the patients

MaleFemale


148

Table 3 Age wise classification of patients

S.No. AGE GROUP MALE FEMALE TOTAL PERCENTAGE

1 20-30 2 1 3 10.0%

2 30-40 4 2 6 20.0%

3 40-50 6 1 7 23.4%

4 50-60 5 3 8 27.6%

5 60-70 5 1 6 20.0%

2

1

4

2

6

1

5

3

5

1

0

1

2

3

4

5

6

7

8

No

.o

fp

atie

nts

(%)

20--30 30--40 40--50 50--60 60--70

Age (in yrs.)

Showing Age wise classification of patients

FemaleMale

3 (10%)

6 (20%)

7 (23.4%)

8 (27.6%)

6 (20%)


149

Table 4 Dictary classification of the total number of patients

S.No. DIET NUMBER OF PATIENTS PERCENTAGE

1 Veg 4 13.3%

2 Non-veg 26 86.7%

4 (13.3%)

26 (86.7%)

0

5

10

15

20

25

30

No

.o

fp

atie

nts

(%)

Vegetarian Nonvegetarian

Showing Dietary habits of the patients


150

Table 5 Classification of Nidanas (Male Patients):-

S.No. AGE MP DP Katu Tikta Kashya Amla Lavana Ruksha ADP

1 52 - - + - - + + + +

2 63 + + + - - + + + +

3 37 + + + + + + + + +

4 48 + + + + + - + + -

5 41 + - - - - + + + +

6 66 + + + + + + - + +

7 65 - - + + + - - - +

8 43 + + + + - + + + +

9 55 + + + + + + + + +

10 41 + - + + + + + + +

11 35 + + - + + + + + +

12 62 - - + + + + + + +

13 59 + + + + + + + + +

14 57 + + + + + + + + +

15 35 + + - - - + + + +

16 26 + + + + + + + + +

17 28 - - + + + + + + +

18 48 + + + + + + + + +

19 68 - - + + + + + + +

20 45 + + + + + + + + +

21 32 - - + + + + + + -

22 52 + + + + + + + + +

Key:- MP = Madya Pana

DP = Dhooma Pana

ADP = Adhika Deha Parisrama


151

Table 6 Classification of Nidanas (Female Patients):-

S.No. Age MP DP Katu Tikta Kashaya Amla Lavana Rukdha ADP

1 36 - - - - - + + + +

2 56 - - + + + + + + -

3 52 - - + + + + + + -

4 35 - - + + + + + + +

5 68 - - + + + + + + +

6 48 - - + + + + + + +

7 22 - - - + - + - + -

8 53 - - - - + + + - -

Among the thirty patients, who are indulged in

Madyapana ------------------- 16

Dhoomapana ------------------- 14

Adhika Katu Rasa ------------------- 27

Adhika Tikta Rasa ------------------- 23

Adhika Kashaya Rasa ------------------- 27

Adhika Amal Rasa ------------------- 28

Adhika Lavana Rasa ------------------- 29

Adhika Ruksha ------------------- 23

Ahika Deha Parisrama------------------- 23


152

Table 7 Clinical features of Male Patients :-

S.No. Age UL LL DP DA AP SD ADD CON IC AN

1 28 + + - - - - - - - +

2 41 + + + - - + + + - -

3 33 + + + + - + + + - +

4 48 + + - + - + + + - +

5 66 + + - - + + + + - -

6 52 + + - + - - + - - +

7 41 + + - - - + + - - -

8 26 + + - + - - - - - -

9 48 + + + + - + + + - -

10 57 + + - - - + + + - +

11 65 + + + - - - + + - +

12 35 + + + + - - - - - +

13 35 + + + - - - - - - -

14 63 + + + + - + + + - -

15 45 + + - - - + - + - +

16 55 + + + + - + - + - +

17 32 + + + - - - + + - +

18 37 + + - - + + + - - -

19 68 + + + + - + - + + -

20 62 + + + + - + + + - -

21 59 + + + - - + - + - -

22 52 + + + + - + + + - -


153

Table 8 Clinical features of Female Patients:-

S.No. Age UL LL DP DA AP SD ADD CON IC AN

1 53 + + + + - + - - - -

2 48 + + + + - + + - - +

3 35 + + + - - + + + - -

4 56 + + - + - + + + + +

5 36 + + - - - + + + - -

6 22 + + + - - - - + - +

7 52 + + - + - + + + - -

8 68 + + + + - + - + + -

Key:-

UL - Involvement of Upper Limb

LL - Involvement of Lower Limb

DP - Dysphasia

DA - Dysarthria

AP - Aphasia

SD - Sleep Disturbances

ADD - Disturbances of Appetite & digestion

CON - Constipation

IC - Urinary Incontinence

AN - Anxiety


154

Table 9 Patients having sufferes in the family and which are associated with

CAD

S.No. Sex Patients having Sufferers in

family

Associated with

CAD

1 Male 10 5

2 Female 4 6

10

4

5

6

0

1

2

3

4

5

6

7

8

9

10

No

.of

pa

tie

nts

(%)

Sufferers in family Associated with CAD

Showing Patients having Sufferers in Family and association withCAD

MaleFemale


155

Table 10 Pakshaghata with Hypertension and Madhumeha

Sex Hypertension and

Madhumeha

Hypertension Madhumeha None

1 Male 16 13 0 3

2 Female 2 2 2 2

13

2

0

2

6

2

3

2

0

2

4

6

8

10

12

14

No

.of

patie

nts

(%)

Hypertension Madhumeha Both None

Showing Pakshaghata with Hypertension and Madhumeha

Male

Female

Hypertension

13

2


156

Table 11 Patients with Addiction of Madyapana and Dhoomapana

S.No. Sex Madyapana and

Dhoomapana

Madyapana Dhoomapana None

1 Male 14 2 0 6

2 Female 0 0 0 8

2

0

00

14

0

6

8

0

2

4

6

8

10

12

14

No

.of

pat

ient

s(%

)

Madhyapana Dhoomapana Both None

Showing addiction of Madyapana and Dhoomapana

Female

Male


157

Table 12 Showing Dosha predominance of patients

S.No. Sex Vata Vata

Pitta

Vata

Kapha

Vata Pitta

Kapha

1 Male 6 7 3 3

2 Female 4 2 2 3

6

4

7

2

3

2

3 3

0

1

2

3

4

5

6

7

No

.of

patie

nts

(%)

Vata Vata Pitta Vata Kapha Vata Pitta Kapha

Showing Dosha predominance of patients

Male

Female


158

RESULTS

The difference in the condition of the patients after the completion of

duration of 60 days was observed. The results are categoriezed based on the

improvement they got as good, moderate, and mild. Subjective and objective

parameters were followed while assessing the results. The results are considered the

linga (sex), Vayah (Age), Paksha involved (affected side), Dosha, Muscle power,

Tendon reflexes, Hypertension and Madhumeha.

Clinical Features:

1. Movements of the limbs improved actively in 11 patients in 60

days treatment and they have started walking.

2. 12 Patients started walking with some support and 5 patients were

started walking with great difficulity and two of them not able to

walk.

3. Gripping power, Holding power improved in 23 of the patients and

7 patients showing mild improvement.

3. Speech is improved to good extent in almost all vakvikruti patients.

4. There are no noticeable changes observed in hypertension and

madhumeha.

5. The patients suffering with Malabaddaka (Constipation) are

relived. Chinta, Soka are decreased and patients manasika avastha

improved.


159

Muscle power Grading (Male)

BEFORE TREATMENT

Grading 0 1 2 3 4 5

Total Number

of Patients

1 5 10 5 1 0

After 20 days of Treatment

AFTER 20 DAYS OF TREATMENT

Grading 0 1 2 3 4 5

Total Number

of Patients

1 4 9 4 3 1



Grading 0 1 2 3 4 5

Total Number

of Patients

1 2 5 5 4 5



Grading 0 1 2 3 4 5

Total Number

of Patients

0 0 5 10 6 9


160

1

0

5

0

10

5 5

10

1

6

0

9

0

1

2

3

4

5

6

7

8

9

10

No.

ofp

atie

nts

Grade-0 Grade-1 Grade-2 Grade-3 Grade-4 Grade-5

Showing Power grading before and after treatment in male

B.T.

A.T.


161

Muscle power Grading (Female)

BEFORE TREATMENT

Grading 0 1 2 3 4 5

Total Number

of Patients

0 0 5 3 0 0



Grading 0 1 2 3 4 5

Total Number

of Patients

0 0 3 2 1 2



Grading 0 1 2 3 4 5

Total Number

of Patients

0 0 2 2 2 2



Grading 0 1 2 3 4 5

Total Number

of Patients

0 0 1 3 1 3


162

0 0 0 0

5

1

3 3

0

1

0

3

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

5

No

.o

fpa

tien

ts


Showing Power grading before and after treatment in female

B.T.

A.T.


163

Tendon Reflexes Grading (Male)

Before Treatment

Grading 0 1 2 3 4

Total Number

of Patients

1 2 2 5 12



Grading 0 1 2 3 4

Total Number

of Patients

1 6 6 5 4



Grading 0 1 2 3 4

Total Number

of Patients

1 8 6 3 3



Grading 0 1 2 3 4

Total Number

of Patients

1 11 7 2 2


164

1

0

2

11

2

7

5

2

12

2

0

2

4

6

8

10

12

No

.of

pat

ien

ts

Grade-0 Grade-1 Grade-2 Grade-3 Grade-4

Showing Tendon reflexes grading before and after treatment in male

B.T.

A.T.


165

Tendon Reflexes Grading (Female)

Before Treatment

Grading 0 1 2 3 4

Total Number

of Patients

0 2 0 4 1



Grading 0 1 2 3 4

Total Number

of Patients

1 3 1 2 1



Grading 0 1 2 3 4

Total Number

of Patients

1 3 2 2 0



Grading 0 1 2 3 4

Total Number

of Patients

0 5 2 1 0


166

0 0

2

5

0

2

4

1 1

0

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

5

No

.of

pat

ien

ts


Showing Tendon reflexes grading before and after treatment infemale

B.T.

A.T.


167

TABLE SHOWING SUB-SIDE OF SYMPTOMS AFTER TREATMENT

S.

No

Name Age Sex Prakruthi Side

affect

ed

Vak

vikruthi

B A

Sleep

Disturbances

B A

Appetite &

Digestion

disturbances

B A

Constipa

tion

B A

Urinary

Incontin

ence

B A

Anxi

ety

B

A

1 Sita Maha

Lakshmil

53 F KV LT ++ - + - - - - - - - - -

2 Venkatama 48 F PV LT ++ + + + + - + + - - + +

3 Indira 35 F VK LT ++ - + - + - + - - - - -

4 Swaroopa 56 F KV RT ++

+

+ + + + - + - + + + +

5 Raja

Lakshmi

36 F PV LT - + - + - + - - - - - -

6 Kranthi 22 F KV LT + - + - - - + - - - + -

7 Naresh 28 M KV RT - - - - - - - - - - + -

8 Narsing Rao 41 M VK RT ++ - + + + + + + - - - -

9 Sanjeev 43 M VK LT ++

+

+ + - ++

+

+ + - - - + +


168

10 Narshimulu 48 M VP RT ++ - - - ++ - + - - - + +

11 Pochaiah 66 M VP RT ++

++

- + + ++ + + + - - - -

12 Narshima

Reddy

52 M VK RT ++ + - - + + - - - - + -

13 Lakshman 41 M VP RT - - + - ++ - - - - - - -

14 Rajesh 26 M VP RT + - - - - - - - - - - -

15 Mahamood 48 M VP RT + - + - ++ + + + - - - -

16 Tirupathiah 57 M KV RT - - + - ++ + + + - - + +

17 Venkat

Reddy

65 M KP RT ++ - - - + - + - - - + +

18 Narshima 35 M VK RT ++ - - - - - - - - - + -

19 Prasad 35 M VP LT ++

+

+ - - - - - - - - - -

20 Rammulu 63 M VK LT ++ + + - + + + - - - - -

21 Ramaiah 52 M KV LT ++ - + - ++ - + - - - - -

22 Rajeshwara

Rao

45 M VP LT - - + - + + + - - - + +

23 Bhumaiah 55 M VK LT ++ + + + + + + - - - + -

24 Lakshmi 32 M KV LT ++ - - - + - + - - - + -


169

Narayana

25 Mallesh 37 M VK RT - - + - + - - - - - - -

26 Chinni Rao 68 M VK LT ++

+

+ + - + + + - + + - -

27 Patel 62 M VK RT ++

++

+ + + - - + - - - - -

28 Saraswathi 52 F KV LT ++ - + - + - + - - - - -

29 Rama Rao 59 M VP RT ++ - + - - - - - - - - -

30 Karunama 68 F VK LT + - + - - - + + + + - -


170

24

3

5

16

23

0

9

14

21

3

8

10

3 3

13

4

8

0

5

10

15

20

25

No

.o

fpa

tien

ts

B.T A.T B.T A.T B.T A.T B.T A.T B.T A.T

Speech difficulty Sleepdisturbances

Apetite andDigestive

Urinaryincontinence

Anxiety

Showing subside of Signs & symptoms after treatment

Good

Moderate

Mild

No response

Present


171

S.

No.

Name Ag

e

Se

x

Prak

ruti

Side

Affected

UL LL Date

of

Admi

ssion

Date of

Dischar

ge

When

treatm

ent

stared

after

attack

Duratio

n of

Treatm

ent

Vak

Vikruti

B A

Powe

r

B A

Refle

xes

B A

Result

s

1 Sita Maha

Lakshmil

53 F KV LT + + 3/7/07 15/10/07 1

Year

60 days

5-7-

days

++ - 2 5 1 1 Good

2 Venkatam

a

48 F PV LT + + 29/7/7 30/12/07 15

days

60 days

5-7-

days

++ + 0 2 0 2 Mild

3 Indira 35 F VK LT + + 12/3/0

7

28/7/07 18

month

s

60 days

5-7-

days

++ - 2 3 3 3 Mod

4 Swaroopa 56 F KV RT + + 6/5/07 8/10/07 15

days

60 days

5-7-

days

++ + 2 3 4 1 Mod

5 Raja

Lakshmi

36 F PV LT + + 12/2/0

7

26/6/07 1 year 60 days

5-7-

- - 3 5 3 1 Good


172

days

6 Kranthi 22 F KV LT + + 8/4/07 12/9/07 1

month

60 days

5-7

days

+ - 3 5 1 1 Good

7 Naresh 28 M KV RT + + 25/9/0

7

9/12/07 2

month

s

60 days

5-7-

days

- - 3 5 1 1 Good

8 Narsing

Rao

41 M VK RT + + 18/4/0

7

25/8/07 1 year 60 days

5-7-

days

++ - 1 3 3 2 Mod

9 Sanjeev 43 M VK LT + + 3/2/07 5/6/07 4

month

s

60 days

5-7-

days

++

+

+ 2 4 4 1 Mod

10 Narshimul

u

48 M VP RT + + 6/9/07 12/12/07 10

month

s

60 days

5-7-

days

++ - 1 3 2 1 Mod

11 Pochaiah 66 M VP RT + + 3/8/07 12/11/07 1 year 60 days

5-7-

days

++

++

+ 2 3 4 3 Mild

12 Narshima 52 M VK RT + + 5/7/07 15/11/07 2 60 days ++ + 1 3 3 2 Mod


173

Reddy years 5-7-

days

13 Lakshman 41 M VP RT + + 7/5/07 16/9/07 1 year 60 days

5-7-

days

- - 2 3 4 2 Mod

14 Rajesh 26 M VP RT + + 3/8/07 6/12/07 3

years

60 days

5-7-

days-

+ - 1 5 1 1 Good

15 Mahamoo

d

48 M VP RT + + 10/9/0

7

27/12/07 10

days

60 day-

s 5-7- -

days

+ - 2 3 4 1 Mod

16 Tirupathia

h

57 M KV RT + + 9/06/0

7

24/10/07 10

month

s

60 days

5-7-

days

- - 3 4 4 2 Mod

17 Venkat

Reddy

65 M KP RT + + 13/10/

07

5/1/08 18

month

s

60 days

5-7-

days

++ - 2 2 0 2 Mild

18 Narshima 35 M VK RT + + 14/3/0

7

12/7/07 5

month

s

60 days

5-7-

days

++ - 3 5 4 1 Good


174

19 Prasad 35 M VP LT + + 15/5/0

7

27/9/07 18

month

s

60 days

5-7-

days

++

+

- 3 5 4 1 Good

20 Rammulu 63 M VK LT + + 20/8/0

7

27/12/07 1

month

60 days

5-7-

days

++ + 2 3 4 3 Mild

21 Ramaiah 52 M KV LT + + 12/9/0

7

21/9/07 3

month

s

60 days

5-7-

days

++

+

+ 2 4 3 1 Mod

22 Rajeshwar

a Rao

45 M VP LT + + 11/5/0

7

11/12/07 15

days

60 days

5-7-

days

- - 1 2 4 4 Mild

23 Bhumaiah 55 M VK LT + + 12/6/0

7

29/12/07 1

month

60 days

5-7-

days

++

+

+

+

2 2 4 2 Mild

24 Lakshmi

Narayana

32 M KV LT + + 30/7/0

7

26/11/07 15

days

60 days

5-7-

days

++ - 3 5 3 1 Good

25 Mallesh 37 M VK RT + + 17/7/0

7

8/12/07 15

days

60 days

5-7-

- - 4 5 3 1 Good


175

days

26 Chinni

Rao

68 M VK LT + + 3/5/07 15/9/07 2

month

s

60 days

5-7-

days

--- + 2 4 4 2 Mod

27 Patel 62 M VK RT + + 12/2/0

7

30/8/07 3

month

s

60 days

5-7-

days

++

+

+ 0 2 4 4 Mild

28 Saraswath

i

52 F KV LT + + 1/9/07 12/1/08 15

days

60 days

5-7-

days

++ - 2 4 3 1 Good

29 Rama Rao 59 M VP RT + + 6/6/07 10/11/07 15

days

60 days

5-7-

days

++ - 2 4 2 1 Good

30 Karunama 68 F VK LT + + 16/9/0

7

28/12/07 1 year 60 days

5-7-

days

+ - 3 3 3 2 mod


176

Showing the therapeutic response

Mild response7 (24.3%)

Moderate response12 (40%)

Good response11 (36.7%)


177

56.5 + 22.0

0

10

20

30

40

50

60

Mea

n%

resp

on

se

Mean response

Showing Mean percent response of patients


178

S.No B.T. A.T Diff

1 60 10 50 83.33333

2 100 60 40 40

3 70 45 25 35.71429

4 75 45 30 40

5 60 10 50 83.33333

6 50 10 40 80

7 50 10 40 80

8 80 45 35 43.75

9 75 35 40 53.33333

10 75 45 30 40

11 75 60 15 20

12 80 40 40 50

13 75 35 40 53.33333

14 70 10 60 85.71429

15 75 35 40 53.33333

16 65 30 35 53.84615

17 80 55 25 31.25

18 65 10 55 84.61538

19 65 10 55 84.61538

20 75 50 25 33.33333

21 85 65 20 23.52941

22 70 30 40 57.14286

23 75 50 25 33.33333

24 60 10 50 83.33333

25 50 5 45 90 B.T, A.T. P<0.01

26 75 30 45 60 Mean 70.83 32.5 significant

27 95 60 35 36.84211 S.D 11.68 19.02

28 70 15 55 78.57143


179

29 65 20 45 69.23077

30 60 40 20 33.33333

Mean 70.83333 32.5 38.33333 56.49407 56.5

S.D. 11.67692 19.0167802 11.69537 21.99315 22

Count 30

t-test 17.95243

In this present clinical study the mean percent response of the patients is 56 + or –22.

The mean of this is 56.5% and standard diviation is 22%.

The T test of this present study is 17.9%

The P Value of this clinical trial is P< 0.01 which is significant


180

DISCUSSION

Vata Vyadhi is one of the “Maha rogas” described out of the Asta

Maharogas described by susruta.

Pakshaghata is a variety of Vata Vyadhi and in Pakshaghata the main

clinical feature is Akarmanyate of Hasta & Pada. Its Separate entity was observed

by the ancient acharyas and its description is explained in vatavyadhi chapters in the

classics.

Vata disorders are caused to the dhatu kshaya and avarantwa,

Pakshaghata also caused due to the above said two factors in general vata disorders

are difficult to cure and when it is associated with Upadravas and aristalakshanas

they are asadhya.

Pakshagata caused predominantly by vata dosha even though all the

three doshas also take part besides its dushyas namely siras, snayus, dhamanis.

Sandhis and mamsa resulting in to this disease.

Present clinical study comprises of the effect of vata rakshasaras along

the bhrungadi taila nasya.

The drug vatarakshasa Ras is indicated in vata disorders along with

Pakshagata in books like yoga tarangini, vaidya chintamani, Basava Rajeeyam.

It contains Abhraka Bhasma, Rasabhasma, Tamrabhasma, Kantaloha

and Suddha Gandhakam.


181

Abharakam has the properties like tridoshahara and dhatuvriddhi,

Rasabhasma has Tridoshahara, Rasayana, Yogavahi, Balaprade, Tamra has

Rasayana, and Lekhana.

Kanta Loha Bala, Veerya, Dhatupushte, Agnivardhana and

Gandhaka Vatekaphahae and Rasayana.

Rasaoushadas has properties like

- Alpamatra (Smaller dose)

- Arucheraprasangatha (Palatable)

- Kshipramarogya Dayitwa (Fast Acting)

Vata rakshasa Ras is Rasaousadha posses the above said 3 qualities and

having the drugs that are vatahara and Rasayana properties. So, Vatarakshasa Ras is

the drug of choice for Pakshaghata.

Bhringadi Tailam:

It contins Bhringaraja, which is the one of the best rasayana drug –

Pakshaghata is caused due to dhatukhasaya, so rasayana is indicated along with it

contains erranda which is vatanlumona, which is indicated because in Pakshagata

avarantwa is another cause. Bhringaditaila also contains nirungdi and other drugs

which are vatahara properties.

Taila itself is the best remedy for Vatavyadhi moreover the “Nasa” is

the external opening of the Masthiska therefore by applying Nasya it directly

stimulates the siras, Snayus dhamanis of masthiska.

So, Bhuringadi Taila nasya is selected for the clinical trail.

Dose:

- Vatarakshasa ras – 125 mg -2 X BD – 60 days

- Bhringadi Taila Nasya – 8 drops in each nostril -5 to 7 days.


182

30 patients are selected from the hospital out of 30, 15 are suffered

from Dakshina Pakshaghata and other 15 are from Vama Pakshaghata.

Hypertension and Mahdumeha are observed in 8 patients. Only

Hypertension in 15 patients only Madhumeha in 2 patients, without HTN &

Madhumeha in 5 patients.

Carotid atheroma and transient cerebral ischaemic are more common in

hypertensive patients. The next risk after hypertension is Madhumeha.

In this clinical study cerebral haemorrhagic patients are excluded,

because sometimes Nasya may futher provokes the bleeding tendency.

14 Patients are habituated to madhyapana and dhoomapana and 2 are

habituated to Madhyapana and 14 are not habituated.

No, Female patient is habituated to dhoomapana (or) Madhyapana in

this trial.

Madhya possess Kashya, Tikta, Katu, Amlarasas, Amlavipaka and

Laghu, ushna gunas.

Dhoomapana Gunas are ushna, Teekshna, Rooksha and laghugunas.

Adhika Kashaya Rasa Sevana, Laghu, Ruksha gunas vitiates vata

which are causative factors for their disease.

According to the modern system of medicine high alcohol intake is the

risk factor for stroke. Cerebral haemorrhage, dementia, cerebellar degeneration etc.,

are the physical effects of alcohol abuse.


183

Smoking is the risk factor in stroke. It is responsible for hypertension,

myocardial infexetion, ischaemic heart disease, peripherial arterial disease etc.

These are the aetiological factors for stroke.

Interestingly, the patients with dysarthria, dysphasia and also with

Aphasia are responding well to the treatment after nasya speech improvement is

very good in almost all of the vak - vikruti patients.

Patients which are non-diabetic young and posse’s good strength

respondes well to the treatment compared to diabetic and older patients.

Out of 30 patients 11 patients responds well to the treatment, 12

patients show moderate response and 8 patients show minimal response.


184

CONCLUSION

An attempt has been made to study the effect of Vatarakshasa Ras with

Bhringadi Taila Nasya in the management of Pakshaghata. A clinical trail has been

conducted on 30 patients selected from IPD of Govt.Ayurvedic Hospital, Erragadda,

Hyderabad.

Approximately about 11 patients were recovered completely, 12

patients were left with some disability or deformity, 7 patients left with persistent

deformity, either chesta vaha (motor) or Sangana vaha (Sensory) through out the

life.

In Ayurveda Charaka maharshi said that the history of Pakshaghata

with short duration of onset and without complications and moreover if the

pakshaghata patient is balavan (strong enough) such type of cases can be easily

caurable and it has been proved in the present clinical study.

Patients with diabetis, oldage having other complications are not

responding well to the treatment which confirms the Apatha vachana.

Now a day’s the present life is very fast and competitive. So the

patients are also seeing for immediate cure .Though number of techniques and

remedies are available most of the people are preferring ayurvedic treatment mainly

for pakshaghata.

So taking all these observations and views of the people inspired me to

prepare this fast acting Rasaoushada like Vatarakshasa Ras along with rasayana

nasya like Bhringadi Taila Nasya.


185

Vatarakshasa Ras is a drug which acts very fast and showed the

curative results to the patients with in short period. After giving nasya there is a

good improvement in speech in almost all of the vakvikruti patients.

During the period of treatment no complications are unwanted effects

were observed. This shows the non toxic effect of vatarakshasa ras. Vatarakshasa

Ras can be used in krichra sadhya and Asdhya vyadhis because of presence of

Rasaoushadhis like Rasabhasma, Tamra Bhasma etc.

Rasaoushadhi is comparatively best than the Kashthoushadhis

because as mentioned in the text that Rasaoushadhis will not lose there potency

forever. So, vatarakshasa Ras along with rasayana Bhringadi Taila Nasya is selected

for this clinical trail in the management of pakshaghata.


186

SUMMARY

The present dissertation entitled “A STUDY OF THE EFFECT OF

VATARAKSHASA RAS WITH BHRINGADI TAILA NASYA IN THE

MANAGEMENT OF PAKSHAGHATA” is summarized as below:

The entire thesis is mainly divided in to eight sections.

Section I : Introduction & Historical aspect

Section II : Sareera

Section III : Vyadhi Sameeksha

Section IV : Chikitsa Yojana

Section V : Oushadha Sameeksha

Section VI : Clinical Study

Section VII : Discussion, Conclusion & Summary

Section VII : Bibliography

INTRODUCTION

1. Definition of Ayurveda and concept of disease has been discussed.

2. Causes of vyadhi and its consequences have been discussed.

3. The Rasoushadha action and its importance have been discussed.

4. Itihasa tells that there is gradual evolution in the treatment pattern from

prevedic period to sangraha kala. It also states that Ayurvedic system was

much advanced than the Allpothic system of medicine in diagnosis and

treatment aspects.

SHAREERAM

5. Definition of vata and its importance has been discussed.

6. Utpatthi of vata and its relationship to panchamahabhutas, and properties of

akasha and vayu mahabhutas have been explained.


187

7. Dosha dhatu sambandha and their functions when they are in normal state

have been discussed.

8. Swaroopa of vata has been stated.

9. Gunas of vata according to different Acharyas have been explained.

10. Sites of vata and types of vata according to Brihattrayee, sthanas and

karmas of five sub-divisions of vata have been tabulated.

11. The cerebral blood flow is an essential aspect in the disease process. Carbon

dioxide, hydrogen, oxygen concentrations have potent effected in controlling

the cerebral blood flow.

12. The human brain normal functions are dependent on constant supply of

oxygen and other nutrients derived from blood perfusing it. Two internal

carotids, two vertebrals and their branches perfuse the brain tissue.

VYADHI SAMEEKSHA

13. The Nidana has been classified and types have been discussed.

14. The basic aetiology involved in the disease has been summarized.

15. Aetiology of Vata vyadhis have been discussed because of a fact that

pakashaghata is one among the vata vyadhis.

16. The expression of poorvaroopa and meaning of poorvaroopa are discussed in

detail.

17. The generalized lakshanas of the disease has been stated according to

different Ayurvedic Acharyas.

18. The role of nidana, doshas and dushyas in the process of samprapti were

explained in detail.

19. The meaning of samprapti in general with special references to kriya kalas

has been discussed.

20. The samprapti of the disease pakshaghata has been discussed in detail

according to Brihattrayees.

21. The samprapti of pakshaghata has been made elaborately in terms of utbhava

sthana, sanchara, dosha, dushyas and srothases etc.


188

22. Pakshaghata is synonymus to ‘Stroke’ in Allopathic system. It is a

cerebrovascular disease. It signifies thrombosis, embolism and haemorrhage.

These are responsible for ischaemia and there by infarction.

23. The upadrvas in general of vata vyadhis are discussed in detail

24. The arishta lakshanas, general concept of arista lakshanas has been

discussed along with the disease pakshaghata arista lakshanas as mentioned

in Ayurvedic classics in detail as far as possible.

25. General information of sadhya asadhyata of disease has been discussed in

detail with special reference to pakshaghata.

CHIKITSA YOJANA

26. In chikitsa aspect treatment of pakshaghata, shodhana chikitsa and shamana

chikitsa were explained clearly.

27. Pathya apathya of pakshaghata have been discussed.

AUSHADHA SAMEEKSHA

28. Composition of Vatarakshas Ras and Bhringadhi Taila Nasya explained in

detail.

CLINICAL STUDY

29. Parameters, criteria and method and materials have been explained.

30. Obsevations and Results: Dakshina part of the body is affected same as that

of vama bhaga. Hypertension is commonly associated with the disease than

the madhumeha.

31. Obsevations of linga, nidana, lakshana, the paksha effected dosha

involvement, hypertension, madhumeha, age, muscle power and Tendon

reflexes are tabulated.

32. The results of clinical trial are tabulated.

33. The results are tabulated as good– 11 patients, moderate – 12 patients and

mild – 7 patients.


189

34. Discussion. The observations and results are discussed.

35. Total study on the disease pakshaghata. The drug and the clinical work have

been revived in a brief discussion.

36. Conclusion. Vata Rakshasa Ras and Bhringadi Taila Nasya have been

adopted for treatment in the present study. As anticipated the results were

encouraging. This once again proves the validity of aptavachana


190

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Dr.B.R.K.R.GOVT.AYURVEDIC COLLEGE / HOSPITAL

(Affiliated to ATR University of Health Sciences)

POST GRADUATE TRAINING AND RESEARCH UNIT

Department of Kaya Chikitsa

Erragadda, Hyderabad – 500038.

__________________________________________________________________

Atura Pariksha Patra - Pakshaghata

Name of the patient : Bed No. :

Age / Sex : Regd.No. :

Occupation : Date of Admission :

Caste / Religion : Date of discharge :

1. Chieg Complaint & Duration:

2. Associated Symptoms:

3. History of present illness:

4. History of previous illness:

a) Hridroga: + /- d) Pakshagraha / Pakshaghata: +/-

b) Hypertension: +/- e) Sastrakrma: +/-

e) Prameha / Madhumeha: +/- f) Sanjanasha: +/-

5. History of treatment taken :

Ayurvedic :

Allopathic :

Any other :


198

6. Personal History : Ahara: Mamsa / Saka / ruksha snigdha

Dhoomapana / Madyapana / Tambula / Tea /

Cofee

Vihara: Deha Parisrama : Adhika / Madhyama

7. Family History:

Sufferers of Pakshaghata : Mother/Father/Grandmother/grandfather/any

other

DASAVIDHA PARIKSHA:

Prakruti Satwa

Vikruti Ahara Sakti

Samhanana Vyayama Sakti

Pramana Vayah

ASTHA STHANA PARIKSHA:

a) Nadi

Gati: Blood pressure:

b) Mala : Sama / Nirama Vibandha:

c) Mootra: Varna:

Pramana : Alpa / Madhyama / Avara

d) Jihwa : Sama / Nirama Rasajnana : +/-

e) Sabda : Sravana sakti – Pravara /Madhyama / Avara.

f) Sparsa : Sparsa jnana : +/-

g) Drik : Samanya / Madhyama / Alpa / Andhya

h) Akriti : Ksheena / Dourbalya / Krisha / Sthoola

SROTAS INVOLVED:

Vata vaha / Chesta vaha / Sanya vaha

SROTO DUSTI:

Atipravritti / Sangha / Siragrandhi / Vimarga gamana

ROGI PARIKSHA:


199

Paksha of sareera affected : Dakshina / Vama

Mukha involved : Dakshina / Vama

Vaksthambha / Vaghraha : +/-

Roga avadhi : Dina / Masa / Samvatsara

Gamana Sakthi : Prakruta / Pangulya

Sadhana sahita / Sadhanasahita aswatantra

Sanjana : Sasamjana / Nisamjna

Rogaprarambha vega : Manda / Kshipra

Rogaprarambha kala : Dina/ Ratri / Nidravastha / Gamanavastha/

Krodhavastha

Sanjna nasha avadhi :

CRANIAL NERVOUS SYSTEM:

VII – Facial

SENSORY SYSTEM: Sensations : +/-

MANASIKA AVASTHA: Prakruta / Dainya / Pralepa / Shoks / Anavasthitha

chesta

Nidra- Alpa / Adhika / Nasa / Prakruta

MOTOR SYSTEM :

a) Bulk of muscles – Normal / Contractures / Atrophy / Hupertrophy

b) Tone of muscles – Normal / Hypertonia / Hypotonia

c) Muscle power – Grading : 0 / 1 / 2 / 3 / 4 / 5

d) Tendon reflexes – Grading : 0 / 1 / 2 / 3 / 4 / 5

e) Coordination of muscles : +/-

f) Gati :

g) Involuntary movements: +/-


200

INVESTIGATION:

Radiological: Biochemistry: a) CBP: Others

CT Scan brain b) CUE: Carotid Doppler

MRI – BRAIN c) Lipid Profile 2D ECHO

d) Renal Profile:

Serum creatinine

Blood urea

e) FBS:

RBS:

PLBS:

Urilne sugar:

NIDANA PANCHAKA:

Nidana :

Poorva Rupas :

Rupas :

Upashaya / Anupashaya :

VYADHI VINISCHAYA:

Vyadhibala – Balavattara / Madhyama / Alpabal

RESPONSE TO THE TREATMENT:

Duration Changes Observed Remarks

After 20 days

After 40 days

After 60 days

Response Observed After 30 Days of Treatment – Pravara / Madhyama / Avara

Signature of the Co-guide

Signature of the Guide Signature of the patient


A CLINICAL STUDY OF THE EFFECT OF VATA RAKSHASA RAS WITHBHRINGADI TAILA NASYA IN THE MANAGEMENT OF

PAKSHAGHATA

ByDr. G. RANGA NADH

B.A.M.S

GuideDr. V.VIJAYA BABU

M.D (Ayu)


INTRODUCTIONINTRODUCTION

AyurvedaAyurveda is a science of life. AYUis a science of life. AYU –– LIFE, VEDALIFE, VEDA –– SCIENCE, covering theSCIENCE, covering theinterrelation of body. It is said that this science is a part ofinterrelation of body. It is said that this science is a part of Vedas mainlyVedas mainlyAtharvanaAtharvana vedaveda. In ancient India it developed and advanced and was divided int. In ancient India it developed and advanced and was divided intoo8 main branches i.e. (1)8 main branches i.e. (1) KayaKaya chikitsachikitsa, (2), (2) SalakyaSalakya, (3), (3) SalyaSalya (4)(4) VishaVisha ChikitsaChikitsa,,(5)(5) BhutaBhuta vidyavidya, (6), (6) KowmaraKowmara bhrityabhritya, (7), (7) RasayanaRasayana chikitsachikitsa and (8)and (8) VajeekaranaVajeekaranachikitsachikitsa..

Out of theseOut of these AshtangasAshtangas KayaKaya chikitsachikitsa occupies prominent place inoccupies prominent place in AyurvedaAyurveda.. KayaKayachikitssachikitssa deals with numerous internal diseases.deals with numerous internal diseases. VatajaVataja vikarasvikaras outnumber otheroutnumber otherdoshicdoshic vikarasvikaras.. PakshaghataPakshaghata is one suchis one such VatajaVataja nanatmajananatmaja vyadhivyadhi, where in, where inAyurvedicAyurvedic line of treatment gives encouraging results.line of treatment gives encouraging results. RasoushadhasRasoushadhas will givewill givemore encouraging results, because no need ofmore encouraging results, because no need of panchakarmaspanchakarmas ((shodhanashodhana). It was). It wasfast acting therapy and has been found effective in smaller dosefast acting therapy and has been found effective in smaller doses. It is said to bes. It is said to bemore ofmore of RasayanaRasayana in nature, which in practice preventsin nature, which in practice prevents JaraJara (old age or the ageing(old age or the ageingprocess) andprocess) and vyadhisvyadhis (disease), rejuvenates body and prolongs life span.(disease), rejuvenates body and prolongs life span.

We know that 50% of Indian population is above the age group ofWe know that 50% of Indian population is above the age group of 50 years and50 years andone out of 10 suffer fromone out of 10 suffer from vatavata vikarasvikaras and a majority of them suffer fromand a majority of them suffer fromPakshaghataPakshaghata The incidence ofThe incidence of pakshaghatapakshaghata is alarming. It occurs mostly as ais alarming. It occurs mostly as acomplication of Diabetes mellitus and Hypertension. If a study ocomplication of Diabetes mellitus and Hypertension. If a study onn RasoushadhisRasoushadhislikelike VatarakshasaVatarakshasa RasRas is made, which is said to be useful, it will be more helpful inis made, which is said to be useful, it will be more helpful inthe present day.the present day.

Along withAlong with vatarakshasavatarakshasa rasras BhringadiBhringadi tailataila nasyanasya is taken for the Treatment.is taken for the Treatment.


HISTORICAL ASPECTHISTORICAL ASPECT

ItihasaItihasa is an essential aspectis an essential aspect otot know about the diseases, drugs, the modeknow about the diseases, drugs, the modeof treatment and the life style of the people starting from theof treatment and the life style of the people starting from the prevedicprevedic period.period.

VEDAKALA:VEDAKALA:

AtharvanaAtharvana veda(4.13.4) is considered as the main source ofveda(4.13.4) is considered as the main source of AyurvedicAyurvedic knowledgeknowledgeamong the four Vedas the four Vedas but the first and the fore mamong the four Vedas the four Vedas but the first and the fore mostost vedaveda i.e.i.e.Rigveda(8.20.23Rigveda(8.20.23--26) also contributed much for26) also contributed much for AyurvedicAyurvedic therapeutics.therapeutics.

SAMHITA KALA:SAMHITA KALA:

AtreyaAtreya SamhitaSamhita :: called ascalled as CharakaCharaka samhitasamhita, the first, the first samhitasamhita granthagrantha explainsexplainsthethe nidananidana,, sampraptisamprapti,, chikitsachikitsa andand sadhyaaasadhyatasadhyaaasadhyata ofof pakshaghatapakshaghata. The other. The othersynonyms used in this aresynonyms used in this are pakshagrahapakshagraha andand pakshavadhapakshavadha..

SusrutaSusruta SamhitaSamhita:: Mentioned the detailed description of theMentioned the detailed description of the sampraptisamprapti, types,, types,sadhyaasadhyatasadhyaasadhyata,, chikitsachikitsa and the duration ofand the duration of chikitsachikitsa. The treatment procedures. The treatment procedureslikelike mastishkyamastishkya,, sirovastisirovasti,, abhyangaabhyanga,, parishekaparisheka andand anuvasanaanuvasana vastivasti with specificwith specificdravyasdravyas is described.is described.


SANGRAHA KALASANGRAHA KALA::

VagbhataVagbhata mentioned thementioned the sampraptisamprapti ofof SusrutaSusruta and theand the chikitsachikitsa ofof CharakaCharaka SamhitaSamhita..

ShamanaShamana ChitisaChitisa:: formulae are newly added in :formulae are newly added in :--

ChakradattaChakradatta (11th Century),(11th Century), SarangadharaSarangadhara samhitasamhita (13th century),(13th century),BasavaBasava RajeeyamRajeeyam (15th century),(15th century), VaidyaVaidya chintamanichintamani (16th century),(16th century),BhavaBhava prakashaprakasha (16th century),(16th century), YogaYoga RatnakaramRatnakaram (17th century),(17th century),BahishajyaBahishajya RatnavaliRatnavali (18th century).(18th century).

History ofHistory of PakshaghataPakshaghata in Allopathic system of medicinein Allopathic system of medicine ::

The wordThe word ““strokestroke’’ is synonym tois synonym to pakshaghatapakshaghata. Stroke indicates. Stroke indicates cerebrovascularcerebrovascular diseasediseasewhich came into existence in 19th century. Till then the wordwhich came into existence in 19th century. Till then the word ““ApoplexyApoplexy”” is used.is used.

Hippocrates :Hippocrates : He used the termHe used the term ““ApoplexyApoplexy”” and described the features of sudden loss ofand described the features of sudden loss ofconsciousness.consciousness.

The world Health Organization has introduced a clinical and reseThe world Health Organization has introduced a clinical and research classification of strokearch classification of strokewhich is as follows:which is as follows:

Transient Cerebral ischemic attackTransient Cerebral ischemic attack Completed strokeCompleted stroke Minor strokeMinor stroke Major strokeMajor stroke Progressing stroke or stroke in evolution.Progressing stroke or stroke in evolution.


SHARRERASHARRERA


The Importance ofThe Importance of VataVata is explicit by the fact thatis explicit by the fact that charakacharaka has allotted onehas allotted one seperateseperatechapter (chapter (ChrakaChraka Sutra 12) for discussion on thisSutra 12) for discussion on this doshadosha..

A few references from theA few references from the AyurvedicAyurvedic classes will indicate theclasses will indicate the vatavata is the mostis the mostimportant and powerful of the threeimportant and powerful of the three doshasdoshas..

So long asSo long as vatavata lasts in the body as long as thus life exists.lasts in the body as long as thus life exists.Bhe.samBhe.sam. su.16.2. su.16.2

It is indicative of the continuity of the life.It is indicative of the continuity of the life. VataVata is powerful and important because of:is powerful and important because of:

Its control over the functions of the body its capacity to spreaIts control over the functions of the body its capacity to spread throughout the body.d throughout the body.

There it is capable of swift action Powerful and Capable to VitiThere it is capable of swift action Powerful and Capable to Vitiate other factors.ate other factors.Independent movements and ItsIndependent movements and Its vitationvitation causes a large number of diseases.causes a large number of diseases.

The termThe term ‘‘VATAVATA’’ is derived from the rootis derived from the root ‘‘VAA GATHI GANDHANA YOHVAA GATHI GANDHANA YOH’’ means tomeans tomove, to enthuse, to make known, to become aware of, induction,move, to enthuse, to make known, to become aware of, induction, effort and toeffort and to enlighten.Coenlighten.Co--incidence of all these factors is calledincidence of all these factors is called ‘‘VATAVATA’’..

According toAccording to VyakaranaVyakarana shastrashastra thethe dhatudhatu which gives thewhich gives the ‘‘GATIGATI’’ andand jaanarthajaanartha bodhanabodhana isiscalledcalled vatavata..GATHIGATHI –– To moveTo moveGANDHANAGANDHANA –– To make known, to enthuseTo make known, to enthuseVAA GATHIVAA GATHI –– presence of movement, knowledge and enthusiasm. The movements ipresence of movement, knowledge and enthusiasm. The movements in then thebody are manifested by the action of all the muscles, i.e., thebody are manifested by the action of all the muscles, i.e., the motor functions of the cognitivemotor functions of the cognitiveorgans; i.e. the sensory functions. Therefore for aorgans; i.e. the sensory functions. Therefore for a humourhumour or a factor which is capable ofor a factor which is capable ofconducting both motor and sensory functions is calledconducting both motor and sensory functions is called vatavata..

VataVata is the combination of AKAASHA MAHA BHUTA and VAYU MAHABHUTA.is the combination of AKAASHA MAHA BHUTA and VAYU MAHABHUTA.


GENERAL FUNCTIONS OF VATA:GENERAL FUNCTIONS OF VATA:

Functions related to Emotions and Mind:Functions related to Emotions and Mind:

1.1. UtsahaUtsaha2.2. HarshaHarsha3. Control of the mind from indulging in undesirable3. Control of the mind from indulging in undesirable arthasarthas and Direct it towardsand Direct it towards

desireabledesireable arthasarthas..

VataVata capable of actually shutting down the pathways connecting thecapable of actually shutting down the pathways connecting the ManasManas withwithundesirableundesirable ArthasArthas and open up the pathways towards desirables.and open up the pathways towards desirables.

I.I. Motor Functions:Motor Functions:

1. Activity of Skeletal muscles.1. Activity of Skeletal muscles.2. Action of Involuntary muscles like Heart, Intestines, mus2. Action of Involuntary muscles like Heart, Intestines, musclecle fibresfibres present in bloodpresent in blood

vessels and also respiratory muscles (both voluntvessels and also respiratory muscles (both voluntary and involuntary).ary and involuntary).3.3. SecretorySecretory functions.functions.

II.II. Sensory Functions:Sensory Functions:

1.1. VataVata Stimulatory all sensations.Stimulatory all sensations.2. The information about the2. The information about the ArthaArtha from sense organ is carried to thefrom sense organ is carried to the MangasMangas andand

BuddhiBuddhi (Cortical centers) for(Cortical centers) for NischyatmkajnanaNischyatmkajnana..

The receptive impression of theThe receptive impression of the ArthaArtha on the sense organ is transformed in to the nerveon the sense organ is transformed in to the nerveimpulse in the organ and carried through theimpulse in the organ and carried through the SamjnavahaSamjnavaha srotassrotas via thevia the ManasManas toto IndriyaIndriyaBuddhiBuddhi (Respective Cortical centers) .(Respective Cortical centers) .


III.III. Integration of Motor and sensory Functions:Integration of Motor and sensory Functions:

TheThe ““TantraTantra –– YantraYantra DharahDharah’’ Function ofFunction of vatavata signifies this integration. This functionsignifies this integration. This functionincorporates the maintenance of equilibrium of the body and alsoincorporates the maintenance of equilibrium of the body and also the kinesthetic sensethe kinesthetic sense(perception of One(perception of One’’s own body parts, weight and movement). This integration of gates own body parts, weight and movement). This integration of gate andandgandhanagandhana is executed in theis executed in the ManasManas which iswhich is ubhayatmakaubhayatmaka, to make the movements co, to make the movements co--ordinatedordinated and purposeful. Therefore an emphasis is given on relation ofand purposeful. Therefore an emphasis is given on relation of vatavata with thewith the srotasrota andandspanyanandnyaspanyanandnya..

IV.IV. Biochemical Functions:Biochemical Functions:

Even though the chemical relations in the body are conducted byEven though the chemical relations in the body are conducted by the respective pitas thethe respective pitas theplanning is managed byplanning is managed by vatavata..

1.1. DhatuvyuhakaraDhatuvyuhakara sign thesis of thesign thesis of the dhatusdhatus from the nutrients present in thefrom the nutrients present in theRasadhatu/AhararasaRasadhatu/Ahararasa in to definite structures according to the plan of requirementin to definite structures according to the plan of requirementof the body.of the body.

2. Regulation of the functions of the2. Regulation of the functions of the dhatusdhatus..

V.V. Division and Differentiation of the Cells:Division and Differentiation of the Cells:

1.1. VataVata is the main force for the union and division of the Para manus.is the main force for the union and division of the Para manus. ““SamyogaSamyoga VilshagaVilshagaParamanunamParamanunam karanamkaranam vayuhvayuh”” Here theHere the ““paramanusparamanus ““are to be understood as cells (or)are to be understood as cells (or)JeevapanamanusJeevapanamanus..

2.2. Development of theDevelopment of the GarbhakrutiGarbhakruti is through the differentiation of cells during theis through the differentiation of cells during thedevelopment according to the requisite specialized functions.development according to the requisite specialized functions.

3.3. The first four of the above stated functions are related to theThe first four of the above stated functions are related to the MastishkaMastishka andand VatavahaVatavahaSrotasasSrotasas (CNS) and the last two to the genetic material, affected by the(CNS) and the last two to the genetic material, affected by the stimulation bystimulation by vatavatapresent in each cell.present in each cell.


ShariravataShariravata and Nerveand NervePhenomenon:Phenomenon:

It has often been asked ifIt has often been asked if vatavata asasindeed theindeed the tridoshastridoshas can becan bequantitatively determined andquantitatively determined andexperimentally demonstrated theexperimentally demonstrated theavailable descriptions ofavailable descriptions of tridoshastridoshasmentioned in the books are essentiallymentioned in the books are essentiallyqualitative and functional.qualitative and functional. ThilsThils isisparticularly so in the case ofparticularly so in the case of vatavata. It. Itmay however;may however; vatavata that is very closelythat is very closelyresembles that of the nerve impulse,resembles that of the nerve impulse,which has been described as a selfwhich has been described as a self ––prorogated disturbance in the nerveprorogated disturbance in the nervefibrefibre. In other words, the energy for. In other words, the energy forthe transmission of the impulse isthe transmission of the impulse isstated to be derived from the nervestated to be derived from the nervefibrefibre over which it passes.over which it passes.

The Similarities between theThe Similarities between thePhenomenon ofPhenomenon of vatavata and nerveand nerveimpulse can be noticed from theimpulse can be noticed from thefollowing table.following table.

7.Motor and sensory7.Motor and sensoryfunctions.functions.

7.Functions of7.Functions of gatigati andandgandhanagandhana

6.Obstruction in its6.Obstruction in itsmovement leads tomovement leads toPathalogicalPathalogical condition.condition.

6.6. AvyahatagataAvyahatagata

5. Moves in a nerve5. Moves in a nerve fibrefibresome times at a velocitysome times at a velocityof 100of 100 mtsmts / second/ second

5.Seegraghati Swift5.Seegraghati Swiftmovementmovement

4. Pass through a nerve4. Pass through a nervefibrefibre of even of oneof even of onemicron in diametermicron in diameter

4.Sukshma capable of4.Sukshma capable ofpassing through smallpassing through smallchannelschannels

3.Self originated in the3.Self originated in theneurons of cells and selfneurons of cells and selfpropagated in nervepropagated in nerve fibrefibre

3.Swamyambhu self3.Swamyambhu selforiginate and selforiginate and selfpropagatedpropagated

2. It is conducted in one2. It is conducted in onedirection from thedirection from theneuron through axon toneuron through axon toits termination.its termination.

2.Anavasthita/Chalaswabha2.Anavasthita/ChalaswabhaIt is mobileIt is mobile

1. Invisible not perceived1. Invisible not perceivedby Sense organs.by Sense organs.

1.1. AmurtaAmurta –– invisible noinvisible nocorporeal form . It iscorporeal form . It isenergyenergy

NERVE IMPULSENERVE IMPULSEVATAVATA


STRUCTURAL & FUNCTIONAL ASPECTS OFSTRUCTURAL & FUNCTIONAL ASPECTS OFNERVOUS SYSTEMNERVOUS SYSTEM

The nervous system is the bodyThe nervous system is the body’’s control centre and communicationss control centre and communicationsnet work. In human being the nervous system serves three broad fnet work. In human being the nervous system serves three broad functions.unctions.First it senses changes within the body and in the outside envirFirst it senses changes within the body and in the outside environment,onment,second it interprets the changes, third it responds to the intersecond it interprets the changes, third it responds to the interpretation bypretation byinitiating action in the form of a muscular contractions or glaninitiating action in the form of a muscular contractions or glandular secretions.dular secretions.

Through sensation, integration and response, the nervous systemThrough sensation, integration and response, the nervous systemrepresents the bodyrepresents the body’’s most rapid means of maintaining homeostasis.s most rapid means of maintaining homeostasis.

ORGANISATION:ORGANISATION: The nervous system may been divided into two principalThe nervous system may been divided into two principaldivisions. The Central Nervous System (C.N.S) and the Peripheraldivisions. The Central Nervous System (C.N.S) and the Peripheral NervouaNervouaSystem (P.N.S) and several subdivisions.System (P.N.S) and several subdivisions.

HISTOLOGY:HISTOLOGY: Despite the organizational complexity of the nervous system itDespite the organizational complexity of the nervous system itconsists of only two principal kinds of cells NEURONS & NEUROGLIconsists of only two principal kinds of cells NEURONS & NEUROGLIA.A.

NEUROGLIA:NEUROGLIA: The cells of the nervous system that perform the functions ofThe cells of the nervous system that perform the functions ofsupport and protection are calledsupport and protection are called neuroglianeuroglia ((NeuroNeuro = Nerve,= Nerve, GliaGlia = Glue) or= Glue) orglialglial cells. About 50% of the all brain cells arecells. About 50% of the all brain cells are neuroglialneuroglial cells. See table No.1cells. See table No.1for description and functions offor description and functions of neuroglianeuroglia of central nervous system.of central nervous system.


NEUROGLIA OF CENTRAL NERVOUS SYSTEMNEUROGLIA OF CENTRAL NERVOUS SYSTEM

TYPETYPE DESCRIPTIONDESCRIPTION FUNCTIONFUNCTION

AstrocytesAstrocytes Star shaped cells with numerousStar shaped cells with numerousprocesses. Protoprocesses. Proto plasmicplasmic astrocytesastrocytes arearefound in the gray matter of the C.N.S.found in the gray matter of the C.N.S.and fibrousand fibrous astrocytesastrocytes are found in theare found in thewhite matter of the C.N.Swhite matter of the C.N.S

Twine around nerve cells to formTwine around nerve cells to formsupporting net work in brain, andsupporting net work in brain, andspinal cord, attach neurons to theirspinal cord, attach neurons to theirblood vessels.blood vessels.

OligoOligo dendroytesdendroytes ResembleResemble astrocytesastrocytes in some way butin some way butprocesses are fewer and shorterprocesses are fewer and shorter

Give support by forming semi rigidGive support by forming semi rigidconnective tissue rows betweenconnective tissue rows betweenneurons in brain and spinal cord;neurons in brain and spinal cord;produce a myelin sheath around axonsproduce a myelin sheath around axonsof neurons on central nervous system.of neurons on central nervous system.

MicrogliaMicroglia Small cells with few processes, derivedSmall cells with few processes, derivedfromfrom monocytesmonocytes; normally; normally stationaystationay jbutjbutmay migrate to site of injury; also calledmay migrate to site of injury; also calledbrain macro phages.brain macro phages.

Engulf and destroy microbes andEngulf and destroy microbes andcellular debris; may migrate to areacellular debris; may migrate to areaof injured nervous tissue and functionof injured nervous tissue and functionas small macrophages.as small macrophages.

EpendymaEpendyma Epithelial cells arranged in single layerEpithelial cells arranged in single layerand ranging in shape fromand ranging in shape from squamussquamus totocolumnar; many are ciliated.columnar; many are ciliated.

Form a continuous epithelial liningForm a continuous epithelial liningfor the ventricles of the brain (spacesfor the ventricles of the brain (spacesthat form and circulatethat form and circulate cerebrocerebro spinalspinalfluid) and the central canal of thefluid) and the central canal of thespinal cord.spinal cord.


FUNCTIONS OF THE NERVOUS SYSTEMFUNCTIONS OF THE NERVOUS SYSTEM

The nervous system carries out a complexThe nervous system carries out a complex araara of tasks such as sensing various smells,of tasks such as sensing various smells,producing speech, remembering signals that control bodyproducing speech, remembering signals that control body –– movements and regulating the operationmovements and regulating the operationof internal organs. These diverse activities can be grouped in tof internal organs. These diverse activities can be grouped in to three basic functions. Sensoryo three basic functions. Sensoryintegrative and motor.integrative and motor.

Sensory Function:Sensory Function:

Sensory receptors detect internal stimuli such as increase in blSensory receptors detect internal stimuli such as increase in blood acidity and external stimuli landingood acidity and external stimuli landingon your arm. The nervous that carry sensory information from spion your arm. The nervous that carry sensory information from spinal and cranial nerves in to thenal and cranial nerves in to thebrain and spinal card or from a lower to higher level in the spibrain and spinal card or from a lower to higher level in the spinal card and brain are sensory (or0nal card and brain are sensory (or0afferent nervous.afferent nervous.

Integrative Function:Integrative Function:

The Nervous system integrates (process), sensory information byThe Nervous system integrates (process), sensory information by analyzing and storing someanalyzing and storing someof it and by making decisions for appropriate response. Many ofof it and by making decisions for appropriate response. Many of the neurons that participate inthe neurons that participate inintegration are interring neurons, who axons extend only for a sintegration are interring neurons, who axons extend only for a short distance and contact near byhort distance and contact near byneurons in the brain spinal cord or ganglion. Inter neurons compneurons in the brain spinal cord or ganglion. Inter neurons comprise the vast variety of neurons inrise the vast variety of neurons inthe brain.the brain.

Motor Function:Motor Function:

The nervous systemThe nervous system’’s motor function involves responding to integration decisions. Ts motor function involves responding to integration decisions. Theheneurons that serve this function are motor or different neurons.neurons that serve this function are motor or different neurons. Motor neurons carry information fromMotor neurons carry information fromto brain towards the spinal card (or) out of the brain and spinato brain towards the spinal card (or) out of the brain and spinal card in to cranial (or) spinal nerves.l card in to cranial (or) spinal nerves.The cells and organs contacted y motorThe cells and organs contacted y motor –– neurons in cranial and spinal nerves are termed effectorsneurons in cranial and spinal nerves are termed effectorsmusclemuscle –– fibers and glandular cells are examples of effectors.fibers and glandular cells are examples of effectors.


VYADHI SAMEEKSHAVYADHI SAMEEKSHA


DefinitionDefinition

PakshagataPakshagata comprises of two wordscomprises of two words pakshapaksha andand agathamagatham

1.1. PakshaPaksha meansmeans-- a part of bird or any thinga part of bird or any thing2.2. AgahatamAgahatam meansmeans-- injuryinjury

According toAccording to charakacharaka thethe vatavata disorder which willdisorder which will paralyseparalyse one side of the totalone side of the totalbody i.e.,body i.e., pakshampaksham is denoted asis denoted as pakshaghatapakshaghata.. AcharyaAcharya SusrutaSusruta quotatedquotated PakshavadhaPakshavadhaandand pakshaghatapakshaghata synonymously.synonymously.

However its description about clinical pictures appears to be moHowever its description about clinical pictures appears to be morere relaventrelavent intermsintermsof theof the contralateralcontralateral hemiplegiahemiplegia..

The chief complaints being complete loss of motor and sensoryThe chief complaints being complete loss of motor and sensory functions of eitherfunctions of eitherone side of the body i.e.,one side of the body i.e., HemiplegiaHemiplegia. In general terms. In general terms PakshagrahaPakshagraha,, PakshaghataPakshaghata andandPakshavadhaPakshavadha are in practice for theare in practice for the comparisioncomparision ofof hemiparesishemiparesis,, hemiplegiahemiplegia and absoluteand absoluteparalysis respectively.paralysis respectively.

From the modern perspectives it appears that the entity ofFrom the modern perspectives it appears that the entity of vatavata disorder containingdisorder containingekangaekanga vatavata,, sarwangasarwanga vatavata andand pakshaghatapakshaghata etc will come under eitheretc will come under either cerebrocerebro vascularvascularaccident (CVA) or other degenerative changes of central nervousaccident (CVA) or other degenerative changes of central nervous system. Mere loss ofsystem. Mere loss offunction of one limb, both limbs or all four limbs may occurredfunction of one limb, both limbs or all four limbs may occurred due todue to vatavata dushtidushti whichwhichcan be explained in the following terms. Loss of function of onecan be explained in the following terms. Loss of function of one limblimb monoplegiamonoplegia, loss of, loss offunction of two limbs (either upper or lower limbs) Paraplegia,function of two limbs (either upper or lower limbs) Paraplegia, all four limbs quadriplegia.all four limbs quadriplegia.Loss of function of upper andLoss of function of upper and lowelowe limbs ( either right or left) islimbs ( either right or left) is hemiplegiahemiplegia..


Classification :Classification :

InIn madhavamadhava nidanamnidanam pakshaghatapakshaghata is classified into three groups:is classified into three groups:

KevalaKevala vatajavataja pakshaghatapakshaghata.. PittaPitta lakshanalakshana yuktayukta pakshaghatapakshaghata i.e.i.e. dahadaha,, santapasantapa,, moorchamoorcha.. KaphajaKaphaja lakshanalakshana yuktayukta i.e.i.e. sothasotha ((oedemaoedema),), GuruthvaGuruthva (heaviness), and(heaviness), and

SaithilyaSaithilya..

When the above clinical conditions are compared with the modernWhen the above clinical conditions are compared with the modernmedicine they are upper motor neuron lesions, thalamic, hypothalmedicine they are upper motor neuron lesions, thalamic, hypothalamic lesionsamic lesionsand lower motor neuron lesions respectively.and lower motor neuron lesions respectively.

InIn AyurvedicAyurvedic system of medicine the disease aspect in general andsystem of medicine the disease aspect in general andparticularlyparticularly pakshaghatapakshaghata was mentioned under the following headings i.e.was mentioned under the following headings i.e.

a)a) NidanaNidana aspect (aspect (AetiologyAetiology))b)b) SamprathiSamprathi aspect (Pathogenesis)aspect (Pathogenesis)c)c) PoorvaroopaPoorvaroopa aspect (aspect (ProdromataProdromata))d)d) RoopaRoopa aspect (Clinical features)aspect (Clinical features)e)e) UpasayaUpasaya andand anupasyaanupasya aspect (Therapeutic trials)aspect (Therapeutic trials)f)f) UpadravaUpadrava andand AristaArista lakshanaslakshanas ( Complications and morbid signs)( Complications and morbid signs)g)g) SadhyaSadhya andand AsadhyathaAsadhyatha (Prognosis)(Prognosis)


NIDANANIDANA

TheThe aetiologicalaetiological factors offactors of vatavyadhivatavyadhi in general have been described inin general have been described inCharakaCharaka,, SusrataSusrata andand VagbhataVagbhata SamhitasSamhitas, but there is no separate description, but there is no separate descriptionofof NidanicNidanic factors for thefactors for the pakshagatapakshagata..

PakshagataPakshagata is one of the varieties ofis one of the varieties of vatavata vyadhisvyadhis

AllAll NidanicNidanic factors offactors of VataVata vyadhisvyadhis can be taken ascan be taken as nidanasnidanas ofof PakshagataPakshagatahence thehence the NidanasNidanas ofof VataVata vyadhisvyadhis are discussed below.are discussed below.

Generally the termGenerally the term NidanaNidana explains the causative factors of a disease.explains the causative factors of a disease.

Therefore theTherefore the NidanasNidanas of any disease can be studied under the followingof any disease can be studied under the followingheadings:headings:

1.1. AharaAhara ruparupa nidananidana2.2. ViharaVihara ruparupa nidananidana3.3. ManasikaManasika4.4. AgantujaAgantuja5.5. ChikitsaChikitsa KrutaKruta6.6. AtmsophericAtmsopheric andand KalaKala KaranasKaranas7.7. AnyaAnya KaranasKaranas..


NIDHANANIDHANAKARANASKARANAS

CHARAKACHARAKA SUSRUTHASUSRUTHA VAGBHATAVAGBHATA MADHAVAMADHAVANIDHANANIDHANA

BHAVA PRAKASHABHAVA PRAKASHA

AHARAAHARARUPARUPANIDANANIDANA

1.1. RookshabhojanaRookshabhojana2.2. SeetaannaPanaSeetaannaPana3.3. AlpaAharaAlpaAhara4.4. LaghuannaLaghuanna SevanaSevana5.5. AbhojanaAbhojana

1.1. ExcessiveExcessive InakeInakeofof KatuRasaKatuRasa,,tiktatikta rasarasa &&KashayaKashaya rasasrasas..

2.2. LaghuLaghu annaannaSevanaSevana

3.3. SeetaSeeta VeeryaVeeryaAnnapanaAnnapana

4.4. VishamajeernaVishamajeerna&& AdhyasanaAdhyasana

1.1. TiktATiktA RasaRasa2.2. UshnaUshna AharaAhara3.3. KashayaKashaya RasaRasa4.4. AlpaAlpa AharaAhara5.5. RukshaRuksha AharaAhara6.6. PramitaPramita BhojanatBhojanat

1.1. RookshaRookshaBhojanaBhojana

2.2. SeetaSeeta AnnaAnnaPanaPana

3.3. AlpaAharaAlpaAharaLaghuLaghuannasevanaannasevana

4.4. AbhojanatAbhojanat

1.1. ExcestiveExcestive intakeintakeofof KatuKatu,, TiktaTikta andandKashayaKashaya RasasRasas..

2.2. PramitaPramita BhojanamBhojanam3.3. RukshaRuksha AharaAhara4.4. LaghuLaghu AharaAhara

VIHARAVIHARARUPARUPANIDANANIDANA

1.Langhana1.Langhana2.Vyavaya2.Vyavaya3.Ati3.Ati PrajagaranamPrajagaranam4.Plavana4.Plavana5.Aatyadva5.Aatyadva6.Vyayama6.Vyayama7.Dukha7.Dukha SaayaSaaya AsanatAsanat8.Gaja,8.Gaja, UstraUstra,, AswaAswa,,

SigraSigra YanamYanam AAPatamaynatPatamaynat

9. Vega9. Vega DharanaDharana10. Diva10. Diva SwapnatSwapnat

1.BalavadhwaGrahati1.BalavadhwaGrahati2.2. VyayamaVyayama3.3. VyavayaVyavaya4.4. AdhyayanaAdhyayana5.5. PrapatnaPrapatna6.6. PradhavanaPradhavana7.7. PrapeedanaPrapeedana8.8. PlavanaPlavana9.9. LanghanaLanghana10.Pratarana10.Pratarana11.Ratri11.Ratri JagaranaJagarana12.Bara12.Bara haranaharana13.Gaja,13.Gaja, TuragaTuraga,,

RadhaRadha PadhatiPadhati14.Viga14.Viga DharanaDharana

1.1. NisaNisa JagaranamJagaranam2.2. UcchaUccha BashayamBashayam3.3. VyayamaVyayama4.4. MaidhnnamMaidhnnam5.5. GrishmaGrishma6.6. AhooratramAhooratram

1.Langhana1.Langhana2.Vyavaya2.Vyavaya3.Ati3.Ati

PrajagaranamPrajagaranam4.Plavana4.Plavana5.Aatyadva5.Aatyadva6.Vyayama6.Vyayama7.Dukha7.Dukha SaayaSaaya

AsanatAsanat8.Gaja.Ustra,8.Gaja.Ustra,

AswaAswa,,SigrayaramSigrayaram,,ApatamayanatApatamayanat

9.Vega9.Vega DharanaDharana10.Diva10.Diva

SwapnatSwapnat

1.1. MalaMala DhiryaDhirya2.2. HinaHina ViharaVihara3.3. AdhanraAdhanra ViharaVihara


MANASIKAMANASIKANIDANASNIDANAS

1.1. ChinataChinata2.2. SokaSoka3.3. BhayamBhayam4.4. KodatKodat PittamPittam

1.1. ChintaChinta2.2. SokaSoka

1.Chinta1.Chinta2.Soka2.Soka

1.1. SokaSoka2.2. ChintaChinta3.3. BhayamBhayam4.4. ManmManm MadhanaMadhana

CHIKITSACHIKITSAKRUYTAKRUYTA 1.1. VishamadVishamad

UppacharchaUppacharcha2.2. ExcessiveExcessive

SravanasSravanas ofofKaphaKapha,, PittaPittaandand RaktaRakta

3.3. AtiAtiVischeshthaVischeshtha

1.1. KriyaKriya AtiAti. Yoga. Yoga 1.1. VishamadVishamadUppacherachaUppacheracha2. Excessive2. Excessive

SravanasSravanas ofofKaphaKapha,, PittaPittaandand RadtaRadta

3.3. AtiAtiVischeshthaVischeshtha

1. Excessive1. Excessive SodhanaSodhanaTherapiesTherapies

AGANTUJAAGANTUJAKARANASKARANAS

1.1. AbhighataAbhighata ininMarmaMarma SthanaSthana

1.Abhigata1.Abhigata 1.1. AbhigataAbhigata ininMarmaMarmaSthanaSthana

ATMOSPHATMOSPHEE

RIC &RIC &KALAKALAKARANASKARANAS

1.1. AhooratriAhooratri2.2. BhuktanteBhuktante

1 Dina1 Dina KshnadyaKshnadya2.2. TritiyaTritiya AmasayeAmasaye3.3. AtisitaAtisita4.4. SisiraSisira5.5. SnanjaSnanja KalaKala6.6. ArjaArja7.7. AmatigataAmatigata

ANYAANYAKARANASKARANAS

1.1. AmaAma DoshaDosha1.1. DhatuDhatu KshayaKshaya2.2. ChiraChira

KahinaRugaKahinaRugaPuditaPudita

3.3. AtiAti KmushataKmushata

1.1. AmaAma DushaDusha2.2. DhatuDhatu

KshayaKshaya3.3. ChiyakalinaChiyakalina4.4. AtiAti

KrushateKrushate

1.1. AtiAti KrushataKrushata2.2. AtiAti ManyaManya KshayaKshaya3.3. DhatuDhatu KshayataKshayata


ETIOLOGY OF EREBROVASCULAR DISEASESETIOLOGY OF EREBROVASCULAR DISEASES

The termThe term ‘‘strokestroke’’ is defined as rapidly developed clinical signs of a focal distuis defined as rapidly developed clinical signs of a focal disturbancerbanceof cerebral function of presumed vascular origin and of more thaof cerebral function of presumed vascular origin and of more than 24 hours duration.n 24 hours duration.Stroke is not a diagnosis, but a clinical syndrome with numerousStroke is not a diagnosis, but a clinical syndrome with numerous causes mainly.causes mainly.

A.A. Cerebral ischemic disease of arterial originCerebral ischemic disease of arterial origina)a) TIATIA’’S with total recovery.S with total recovery.b)b) Progressive stroke (or) stroke in evaluation.Progressive stroke (or) stroke in evaluation.c)c) Completed strokeCompleted stroke -- established cerebral infarct fromestablished cerebral infarct from

a.a. ThrombosisThrombosis b. Embolismb. EmbolismB.B. Venous infarctVenous infarctC.C. SubarachnoidSubarachnoid haemorrhagehaemorrhage..

Main risk factors for strokeMain risk factors for stroke:: HypertensionHypertension Cardiac diseaseCardiac disease –– ischemic heart diseaseischemic heart disease atrialatrial fibrillationfibrillation Transient ischemic attacksTransient ischemic attacks Cigarette smokingCigarette smoking AlcoholAlcohol

Associated risk factorsAssociated risk factors:: DiabetisDiabetis mellitusmellitus Previous strokePrevious stroke RaisedRaised HaemotocritHaemotocrit High Plasma fibrinogenHigh Plasma fibrinogen


CAUSESCAUSES::A.A. Ischemic strokeIschemic stroke

1.1.Transient Ischemic attack (Transient Ischemic attack (TIAsTIAs):):Episodes of focal neurological symptoms of less than 24 hrs duraEpisodes of focal neurological symptoms of less than 24 hrs duration occurring as ation occurring as a

result of reduced flow to a vessel from fall in perfusion pressuresult of reduced flow to a vessel from fall in perfusion pressure (e.g. Cardiacre (e.g. Cardiac arrythmiaarrythmia isisassociated with localized strokeassociated with localized stroke cerebrovascularcerebrovascular disease). (or) blockage of flow bydisease). (or) blockage of flow byembolism arising from plaques inembolism arising from plaques in aorticarchaorticarch oror extracranialextracranial vessels or from heart. If flowvessels or from heart. If flowis restored within the critical period, ischemic symptoms reversis restored within the critical period, ischemic symptoms reverse themselves, otherwisee themselves, otherwiseinfarction may occur.infarction may occur.

2.2.Developing (Progressive) Stroke:Developing (Progressive) Stroke:Sometimes paralysis progresses. Slowly comSometimes paralysis progresses. Slowly commensurate with increasingmensurate with increasing

deprivation of blood due to successive emboli (or) extension ofdeprivation of blood due to successive emboli (or) extension of thrombus further occludingthrombus further occludingthe lumen. It evolves gradually over several hours.the lumen. It evolves gradually over several hours.

3.3.Completed strokeCompleted stroke::Caused by infarction of the cerebral hemisphere is the most commCaused by infarction of the cerebral hemisphere is the most common cause of anon cause of an

acuteacute cerebrovascularcerebrovascular disease. A completed stroke reaches its peak in less than onedisease. A completed stroke reaches its peak in less than one hourhourleaving considerable residual deficit.leaving considerable residual deficit.

B.B. Venous Infarction:Venous Infarction:Thrombosis of cortical veins and / orThrombosis of cortical veins and / or duraldural sinuses is less common than centralsinuses is less common than central

arterial occlusion.arterial occlusion.

C.C. SubSub arachnoidarachnoid haemorrhagehaemorrhage::1.1. HaemorrhageHaemorrhage from intra cranial aneurysm.from intra cranial aneurysm.2.2. HaemorrhaeHaemorrhae fromfrom arterioarterio venous malformation.venous malformation.3.3. Cerebral orCerebral or cerebellarcerebellar haemorrhagehaemorrhage leading in to the ventricles of subleading in to the ventricles of sub--arachnoidarachnoid

space.space.


Differential diagnosis of vascular causes ofDifferential diagnosis of vascular causes of HemiplegiaHemiplegia

EmbolismEmbolism ThrombosisThrombosis HaemorrhageHaemorrhage

AgeAge YoungYoung Middle age or oldMiddle age or old Middle age or oldMiddle age or old

Nature of onsetNature of onset InstantaneousInstantaneous Sudden or progressiveSudden or progressive CatastrophicCatastrophic

Premonitory absentPremonitory absentsymptomssymptoms

AbsentAbsent Difficult in speaking orDifficult in speaking orweakness of arm or leg mayweakness of arm or leg maybe presentbe present

Usually absentUsually absent

Common causeCommon cause MitralMitral steinosissteinosis withwith atrialatrialfibrialationfibrialation and carotidand carotidstenosisstenosis

Arteriosclerosis with orArteriosclerosis with orwithout hypertensionwithout hypertension

Hypertension almostHypertension almostinvariableinvariable


POORVAPOORVA -- ROOPAROOPA

TheThe LakshanasLakshanas ofof PoorvaPoorva -- rooparoopa are not mentioned specially not only forare not mentioned specially not only forPakshaghataPakshaghata but also forbut also for VataVata VyadhisVyadhis.. PoorvarupavasthaPoorvarupavastha is an investigation of a diseaseis an investigation of a diseasenext tonext to nidananidana. These. These ProdromalProdromal features occur before the beginning of the Clearfeatures occur before the beginning of the ClearManifestation of a disease.Manifestation of a disease.

TheThe UnmanifestedUnmanifested Symptoms of theSymptoms of the VataVata Disorders are known asDisorders are known as PoorvaPoorva rooparoopa((ProdromalProdromal Symptoms). When the same are manifested they represent the ownSymptoms). When the same are manifested they represent the own entity ofentity ofdisorders. So, thedisorders. So, the AlpalakshanasAlpalakshanas ofof VatavyadhessVatavyadhess are:are:

1.1. SramsaSramsa -- SeperationSeperation2.2. BhramsaBhramsa -- DislocationDislocation3.3. VyasaVyasa -- DivisionDivision4.4. SangaSanga -- Obstruction/ attachmentObstruction/ attachment5.5. BhedaBheda -- Tearing pain in organsTearing pain in organs6.6. SadaSada -- Emaciation / MalaiseEmaciation / Malaise7.7. HarshaHarsha --8.8. TarshaTarsha -- ThirstThirst9.9. VartaVarta -- CircumventionCircumvention10.10. MardaMarda --11.11. KampaKampa -- TremorsTremors12.12. ChalaChala -- LoosenesLoosenes13.13. ThodaThoda -- piercing Painpiercing Pain14.14. VikrutaVikruta

ChestaChesta -- Unwanted Works (Pain Movement)Unwanted Works (Pain Movement)15. Kara15. Kara -- CoarsenessCoarseness


ROOPAROOPA““PradhurbhutaPradhurbhuta LakshanamLakshanam PunarlingamPunarlingam””. In the. In the RoopavasthaRoopavastha CompleteComplete

Establishment of Disease Process appears. The TotalEstablishment of Disease Process appears. The Total SymptomatologySymptomatology will be observed inwill be observed inthis stage. Thethis stage. The PakshaghataPakshaghata included inincluded in aseethiaseethi vatavata vyadhisvyadhis..

Therefore some of theTherefore some of the SamnyaSamnya LakshanasLakshanas ofof VataVata vyadhisvyadhis are also observed in mostare also observed in mostof the cases ofof the cases of PalshaghataPalshaghata, apart from the, apart from the impairementimpairement of the half of the body. The mostof the half of the body. The mostfrequently associatedfrequently associated SamanyaSamanya LakshanasLakshanas ofof VataVata VyadhisVyadhis inin PakshagataPakshagata are described asare described asfollows.follows.

SankochaSankocha –– ContracturesContractures ParwaParwa SthambhaSthambha –– Stiffness in jointsStiffness in joints AsthiAsthi BhudhaBhudha –– Tearing in bonesTearing in bones ParvaParva BhudhaBhudha –– Tearing in jointsTearing in joints PralapaPralapa –– DeleriumDelerium PanigrahamPanigraham –– StiftnessStiftness in Handsin Hands PristagrahamPristagraham –– Stiffness in BackStiffness in Back SirograhaSirograha –– Stiffness in Head.Stiffness in Head. LomaharshaLomaharsha -- HorripilationHorripilation KhanjatwaKhanjatwa –– LimpingLimping

The signs and symptoms which are manifested specially can be conThe signs and symptoms which are manifested specially can be considered assidered as rooparoopa..

1.1. ChestanrivuthiChestanrivuthi of aof a PakshaPaksha -- This may beThis may be dakshinadakshina oror VamaVama2.2. VaksthambhaVaksthambha3.3. SandhiSandhi BhandhaBhandha VimokshonaVimokshona4.4. SirasnayuSirasnayu VishoshnaVishoshna5.5. DivaDiva ratraratra ShiraShira PadaPada ArdhangaArdhanga ShoolaShoola6.6. AkarmanyaAkarmanya VichestanamVichestanam7.7. RujamRujam


CLINICAL PICTURE OF HEMIPLEGIACLINICAL PICTURE OF HEMIPLEGIA

CLINICAL FEATURESCLINICAL FEATURES

HeadacheHeadache VariableVariable Slight or absentSlight or absent SeveareSeveare

VomintingVominting on onseton onset RareRare RareRare CommonCommon

ConvulsionsConvulsions CommonCommon RareRare CommonCommon

ComaComa Rarely deepRarely deep Rare, varies with the extentRare, varies with the extentof thrombosis.of thrombosis.

Deep in consciousness.Deep in consciousness.

CheyneCheyne stokes respirationstokes respiration Not commonNot common SeldomSeldom CommonCommon

Stiff neckStiff neck RareRare RareRare FrequentFrequent

Conjugate deviation of eyesConjugate deviation of eyes RareRare SeldomSeldom FrequentFrequent

Bilateral extensor plantarBilateral extensor plantar RareRare May be presentMay be present FrequentFrequent

Reaction of pupil to lightReaction of pupil to light No changeNo change May be impairedMay be impaired Commonly impairedCommonly impaired

Blood pressureBlood pressure NormalNormal May be highMay be high Usually highUsually high

C.S.FC.S.F Usually normalUsually normal pleocytosiopleocytosioif infectorif infector emboiusemboius

Clear C.S.F. pressureClear C.S.F. pressureelightlyelightly increasesincreases

Usually bloody pressure isUsually bloody pressure isincreased.increased.

C.T.ScanC.T.Scan Infarction may not appearInfarction may not appearfor 2 to 4 daysfor 2 to 4 days

May not appear for 2 to 4May not appear for 2 to 4daysdays

Can be confirmed with inCan be confirmed with inminutes of onset.minutes of onset.

TerminationTermination Recovery usualRecovery usual Recovery oftenRecovery often High mortalityHigh mortality


SAMPRAPTHISAMPRAPTHITheThe SamprapthiSamprapthi of a disease explains the Process by which the alteredof a disease explains the Process by which the altered doshasdoshas reachreach

the body elements (the body elements (DushyasDushyas) and produces the anatomical and physiological variations in) and produces the anatomical and physiological variations inthe targetthe target avayavasavayavas leading to the expression as a disease.leading to the expression as a disease.

TheThe SamprapthiSamprapthi (or) Pathogenesis of(or) Pathogenesis of PakshagataPakshagata under theunder the vatavyadhivatavyadhi has beenhas beendescribed in all thedescribed in all the samhitassamhitas ofof AyurvedaAyurveda. The different views explained by. The different views explained by BrihattrayeesBrihattrayeesregarding theregarding the samprapthisamprapthi ofof PakshahataPakshahata is as follows.is as follows.

According toAccording to CharakaCharaka thatha Pathogenesis orPathogenesis or SamprapthiSamprapthi ofof pakshaghatapakshaghata is asis asexplained: theexplained: the vatavata which is vitiated (or) provoked by its ownwhich is vitiated (or) provoked by its own nidanicnidanic factors leads to thefactors leads to theseizing ofseizing of dhamanisdhamanis controlling the functions of the side of the body and constrictcontrolling the functions of the side of the body and constricting theing thesirassiras afflictsafflicts dakshinadakshina oror vamavama ardhaardha bhagasbhagas of the body resulting in theof the body resulting in the impairementimpairement ofofmovements ofmovements of urdhwaurdhwa (or)(or) adhobhagaadhobhaga (or) both. It also causes loss of sensation, pain and(or) both. It also causes loss of sensation, pain andSome times loss of Speech.Some times loss of Speech.

In view ofIn view of SusruthaSusrutha the Disease in which the vitiatedthe Disease in which the vitiated vatavata affects theaffects the dhamanisdhamanis,,which spreads either in thewhich spreads either in the vamabhagavamabhaga (or) in the(or) in the dakshinabhagadakshinabhaga of the body in otherof the body in otherterms it may affect theterms it may affect the urdhwabhagaurdhwabhaga,, adhobhagaadhobhaga andand thiryakthiryak dishadisha and making them,and making them,resulting in abnormal state (or) condition known asresulting in abnormal state (or) condition known as pakshagatapakshagata, Further he stressed lax, Further he stressed laxandand vigourlessvigourless in which thein which the sandhissandhis of either side of the body become useless andof either side of the body become useless andinoperatureinoperature both in motor and sensory functions.both in motor and sensory functions.

The Views ofThe Views of BhavamisraBhavamisra inin MadhyamaMadhyama Kanda andKanda and MadhavakaraMadhavakara inin VataVata VyadhiVyadhiNidanaNidana CahptersCahpters appear to coincide with above mentioned options ofappear to coincide with above mentioned options of AcharyasAcharyas..


AmayaAmaya –– PakshagataPakshagata {{hemiplegiahemiplegia}}UdbahavaUdbahava SthanaSthana –– MasthiskaMasthiskaSancharaSanchara –– DhamaneesDhamaneesAdhistanaAdhistana –– DhamanessDhamaness ofof MasthiskaMasthiska,, SiraSira andandSnayusSnayusVyaktiVyakti –– ArdhaArdha SareeraSareera (Half of the body)(Half of the body)SrotasSrotas–– RasavahaRasavaha,, RaktavahaRaktavaha,, ChestavahaChestavaha andandSanjnavahaSanjnavaha SrotasesSrotasesAvayavaAvayava –– hastahasta,, Pada,MukaPada,Muka,, NetraNetra andand SwaraSwaraYantraYantraDoshaDosha DustiDusti –– VataVataDushyasDushyas –– Rasa,Rasa, RaktaRakta,, mamsamamsa,, MedaMeda,, AsthiAsthi ,,MajjaMajja,,DhamaniDhamani ,,SiraSira andand SnayuSnayu..VyadhiVyadhi SwabhavaSwabhava –– AsukariAsukari in most of the cases,in most of the cases,ChirakariChirakari in some cases.in some cases.

CharakaCharaka Stated that theStated that the dhatukshayadhatukshaya andandobstruction of theobstruction of the vatavata channels due tochannels due to kaphakapha andand pittapitta is theis themain cause inmain cause in vatavata PrakopaPrakopa..


UPADRAVAS AND ARISTA LAKSHANASUPADRAVAS AND ARISTA LAKSHANAS

There is no specific description ofThere is no specific description of upadravasupadravas ofof PakshagataPakshagata, hence the, hence the upadravasupadravas ofof VatavyadheesVatavyadheesmay be taken be taken for this context. According tomay be taken be taken for this context. According to MadhavakaraMadhavakara the following are thethe following are the upadravasupadravas ofofVatavyadhisVatavyadhis..→→ VisarpaVisarpa→→ DahaDaha→→ ShoolaShoola→→ MoorchaMoorcha→→ AruchiAruchi→→ AgnimandhyaAgnimandhya→→ BalaBala MamsaMamsa KshayaKshaya→→ ShodhaShodha→→ SparsaSparsa SunyathaSunyatha

UpadrvasUpadrvas ofof VatavyadhiVatavyadhi according toaccording to SusruthaSusrutha

1.1. BalaBala KshayaKshaya2.2. MamsaMamsa KshayaKshaya3.3. SoshaSosha4.4. TrishanaTrishana5.5. ChardiChardi6.6. JwaraJwara7.7. AtisaraAtisara8.8. SwasaSwasa9.9. MoorchaMoorcha10.10. HikkaHikka11.11. BhagnaBhagna12.12. KampaKampa13.13. AdhmanaAdhmana14.14. SramaSrama due to disease.due to disease.

The body which hasThe body which has kshayakshaya ofof balamamsabalamamsa andand pakshagatapakshagata Like diseases along with the aboveLike diseases along with the abovesaidsaid upadravasupadravas wills troubles the patient.wills troubles the patient.


ARISTAARISTA

AristaArista LakshanaLakshana is pioneering indication of Predictable death which occur bothis pioneering indication of Predictable death which occur both in thein theailing and nonailing and non –– ailing persons.ailing persons.

This should be carefully observed by the physicians in case of tThis should be carefully observed by the physicians in case of treating the patientsreating the patientsotherwise he is giving up his credit and profit.otherwise he is giving up his credit and profit.

CharakaCharaka says that just as the blossom is thesays that just as the blossom is the harbinarharbinar of the coming fruit so is theof the coming fruit so is theexit of the symptoms known as fatal prognosis theexit of the symptoms known as fatal prognosis the herbiniranherbiniran of death of patients.of death of patients.

According toAccording to susruthasusrutha ArishtasArishtas can be divided intocan be divided into

1.1. NiyataNiyata –– can be cured withcan be cured with RasayanaRasayana,, JapaJapa etcetc2.2. AniyataAniyata -- which cannot be cured.which cannot be cured.

VagbhataVagbhata divided thedivided the arishtasarishtas in to 2 types.in to 2 types.

1.1. TheThe AsthayeeAsthayee –– which occur due to the predominance ofwhich occur due to the predominance of doshasdoshas..2.2. TheThe SthayeeSthayee AristhtesAristhtes –– Certainly kill the patientsCertainly kill the patients

According toAccording to SusrutaSusruta in a person if the following conditions arise it is said to bein a person if the following conditions arise it is said to bedefinite death of a patient.definite death of a patient.

SoonathaSoonatha SuptaSupta TwachamTwacham BhagnamBhagnam KampaKampa AdhamanaAdhamana RujarthaRujartha MantheschaManthescha..


SADHYA SADHYATHASADHYA SADHYATHASadhyasadhyathaSadhyasadhyatha of the disease is generally depends on three factors. They areof the disease is generally depends on three factors. They are

Duration of the onset of the disease.Duration of the onset of the disease. Place of originPlace of origin SevieretySevierety ofof LakshanasLakshanas..

CharakaCharaka says thatsays that PakshagataPakshagata isis KashtasadhyaKashtasadhya (or)(or) asadhyaasadhya because it is deep seated inbecause it is deep seated inthe body.the body. CharakaCharaka also mentionedalso mentioned ““NavanNavan BalavarthastrostanBalavarthastrostan SadhayennirupadravanSadhayennirupadravan””. It. Itdenotes the good prognosis of the disease, provided the diseasedenotes the good prognosis of the disease, provided the disease is free ofis free of upadravasupadravas. The onset. The onsetof disease is recent and more over the victim is strong enough iof disease is recent and more over the victim is strong enough i.e.,.e., BalavanBalavan rogirogi..

According toAccording to SusruthaSusrutha thethe PakshaghataPakshaghata caused due tocaused due to SuddhaSuddha VataVata isis KashtaKashta SadhyaSadhya butbutif it is associated with eitherif it is associated with either KaphaKapha oror PittaPitta it can be taken asit can be taken as SadhyaSadhya andand PakshagataPakshagata developeddevelopeddue todue to DathuDathu KshyaKshya is taken asis taken as AsadhyaAsadhya..

AcharyaAcharya SusruthaSusrutha says insays in SootrasthanaSootrasthana that thethat the VatavyadhiVatavyadhi in general isin general is ““MAHA ROGAMAHA ROGA””having incurable nature and suggest that the physicians not to thaving incurable nature and suggest that the physicians not to treat when the patient is afflictsreat when the patient is afflictswith seriouswith serious upadravasupadravas..

AstangaAstanga HridyakaraHridyakara Says that theSays that the PakshaghataPakshaghata is due tois due to SuddhaSuddha VataVata JanyaJanya can becan beconsidered asconsidered as AsadhyaAsadhya and if the disease is associated withand if the disease is associated with PittaPitta oror KaphaKapha is said to beis said to be KricchraKricchraSadhyaSadhya andand PakshaghataPakshaghata due todue to DhatuDhatu KshayaKshaya isis AsadhyaAsadhya..

According toAccording to SusruthaSusrutha if theif the PakshaghataPakshaghata patient ispatient is unwareunware ofof SparsaSparsa (Sensation & loss of(Sensation & loss ofFunctions) that can be treated asFunctions) that can be treated as asadhyaasadhya. Sometimes the patient may fall in death.. Sometimes the patient may fall in death.

PakshaghataPakshaghata caused tocaused to GarbhiniGarbhini,, perpeurialperpeurial woman, children and senile objects iswoman, children and senile objects isasadhyaasadhya.. PakshaghataPakshaghata cause due tocause due to AdhikaAdhika RaktasravaRaktasrava isis AsadhyaAsadhya..


CHIKITSA YOJANACHIKITSA YOJANA


CHIKITSACHIKITSA

AsAs PakshagathaPakshagatha is mainly asis mainly as ““NanatmajaNanatmaja VataVata VyadhiVyadhi”” mostly themostly the samnyasamnya vatavata harahara chitiksachitiksawill be suitable to it along with the specific line of treatmentwill be suitable to it along with the specific line of treatment. Hence it will be appropriate to discuss. Hence it will be appropriate to discusssamnyasamnya vatavata harahara chikitsachikitsa (General) line of treatment for(General) line of treatment for vatavata in the beginning and then to proceed toin the beginning and then to proceed tospecific line of treatment.specific line of treatment.

SAMANYA VATA ROGA CHIKITSASAMANYA VATA ROGA CHIKITSA

1.1. Diets and Drugs:Diets and Drugs:The Diets and drugs possessingThe Diets and drugs possessing MadhuraMadhura,, AmlaAmla ,,LavanaLavana,, UshnaUshna VrishyaVrishya andand BalyaBalya propertiesproperties

be adopted. Liquid diet processed withbe adopted. Liquid diet processed with vataharavatahara drugs anddrugs and mamsayushasmamsayushas be given.be given.

2.2. SnehaSneha Karmas:Karmas:SnehasSnehas obtained from different sources which includeobtained from different sources which include ghritaghrita (ghee),(ghee), TailaTaila (oils),(oils), VasaVasa

((MusclelfatMusclelfat) and) and MajjaMajja (bone marrow) should be processed with drugs possessing(bone marrow) should be processed with drugs possessing deepanadeepana,, pachanapachana,,vataharavatahara andand virechaneeyavirechaneeya properties should be administered in different routes i.e., oraproperties should be administered in different routes i.e., orally,lly, nasyanasya,,abhyangaabhyanga andand vasthivasthi etc.etc.

3.3. SwedaSweda Karma:Karma:SwedanaSwedana karma may be adopted along withkarma may be adopted along with swedhanaswedhana,, nadinadi-- swedasweda,, prasthraprasthra swedasweda,,

sankarasankara,, pindapinda etc. are to be adopted to suit individual cases.etc. are to be adopted to suit individual cases.

4.4. SamsodhanaSamsodhana::MridhuMridhu ShodhanaShodhana Karmas particularlyKarmas particularly virechanavirechana should be adoptedshould be adopted procededproceded by appropriateby appropriate

snehasneha,, swedasswedas. The. The virechanavirechana drugs also should be mixed withdrugs also should be mixed with snehassnehas possessingpossessing ushnaushna,, madhuramadhura,,amlaamla,, lavanalavana properties,properties, virechanavirechana will causewill cause annulomanaannulomana ofof vatavata, there by relieves obstruction in the, there by relieves obstruction in thesrotosessrotoses..

5.5. External measures:External measures:unmardhanaunmardhana,, SamvahanaSamvahana, (pressing and massaging)., (pressing and massaging). PeedanaPeedana ((Pressing),ParishekaPressing),Parisheka ((affusionaffusion))

avagahanaavagahana (tub(tub bath)bebath)be adopted.adopted.


LINE OF THE TREATMENT OF PAKSHAGHATALINE OF THE TREATMENT OF PAKSHAGHATA

The specific therapies described forThe specific therapies described for pakshagatapakshagata by variousby various acharayasacharayas are as follows.are as follows.

According toAccording to CharakaCharaka::““SwedanamSwedanam SnehaSneha SamyuktamSamyuktam PakshagatePakshagate VirecainamVirecainam””. The line of treatment is. The line of treatment is

SwedanamSwedanam andand SnehaSneha YuktaYukta VirechanamVirechanam..

VagbhabataVagbhabata in he stated same as that ofin he stated same as that of charakacharaka.. ““SwedanamSwedanam SnehaSneha SamyukutamSamyukutamPakshagataPakshagata VirechenemVirechenem””

SusrutaSusruta::TatraTatra praregaprarega sneha.sneha.----------------------------------------------------------------------------------------------------------------------------------------------------------

--------------VidhanaVidhana UpachanatUpachanat..

Here we can see anHere we can see an eleberateeleberate description of different aspects of treatment alongdescription of different aspects of treatment alongwith the routine type of treatment likewith the routine type of treatment like snehasneha,, swedasweda,, mriduvirechavamriduvirechava.. AnuvasanaAnuvasana, as, astherefore andtherefore and sirovasthisirovasthi.. AnutailaAnutaila abhyangamabhyangam,, SalvanaswedanamSalvanaswedanam, as special treatment and, as special treatment andshould to have continue the intense treatment up to 3 to 4 monthshould to have continue the intense treatment up to 3 to 4 months.s.

DalhanaDalhana States that vomiting should be performed first it necessary. ThStates that vomiting should be performed first it necessary. Thenen virechanavirechana,,AnuvasyanaAnuvasyana vasthivasthi should beshould be given.Aftergiven.After appearance ofappearance of SnehaSneha LakshanasLakshanas as thereforeas therefore vastivastican be given. Immediate aftercan be given. Immediate after asthapanaasthapana,, anuvasanamanuvasanam should be adopted.should be adopted.

AstangaAstanga SangrahakaraSangrahakara describeddescribed PkshagataPkshagata in similar manner toin similar manner to susrutasusruta. He also. He alsoindicated the therapies ofindicated the therapies of akshepakaakshepaka inin pakshagatapakshagata..


NASYA KARMANASYA KARMA

The administration of either medicine (drug) or medicated oil thThe administration of either medicine (drug) or medicated oil through the nose isrough the nose isknown asknown as nasyakarmanasyakarma..

NasyakarmaNasyakarma is also known asis also known as sirorechanasirorechana,, SiroSiro –– VirekaVireka andand moordhavirechanamoordhavirechana..CharakaCharaka has also used the wordhas also used the word ““NastahNastah PrachardenamPrachardenam”” for the same.for the same.

SimilarySimilary the wordsthe words ““NavanNavan”” andand ““NasthahNasthah KarmaKarma”” also are found indicating thealso are found indicating thesamesame kriyaskriyas..

Utility ofUtility of NasyaNasya Karma:Karma:TheThe NasyaNasya Karma is essentially useful in the diseases of the neck and heaKarma is essentially useful in the diseases of the neck and head. Thed. The

conditions in which theconditions in which the nasyakarmanasyakarma is contrais contra –– indicated are given below.indicated are given below.

ContraContra –– Indications:Indications: IndigestionIndigestion Person who have just taken their meals (or) anPerson who have just taken their meals (or) an oleaciousoleacious portion.portion. Those who are thirsty for waterThose who are thirsty for water Who have bathed their head.Who have bathed their head. Those who are going to take their bath.Those who are going to take their bath. Hungry.Hungry. FatiguedFatigued FaintedFainted InjuredInjured Exhausted by SexExhausted by Sex –– act, Exercise (or) drinkact, Exercise (or) drink


The conditions in which theThe conditions in which the NasyakarmaNasyakarma is indicated:is indicated:Except in the conditions in which theExcept in the conditions in which the NasyaNasya Karma is Contra indicated in all otherKarma is Contra indicated in all other

conditions it may be administered and more so in the following:conditions it may be administered and more so in the following: SiraSira SthambaSthamba ManyaManya SthambaSthamba DantaDanta SthambaSthamba –– SoolaSoola GalagrahaGalagraha HanugrahaHanugraha PeenasaPeenasa GalasundikaGalasundika GalasalukaGalasaluka NetragataSukrarogaNetragataSukraroga TimiraTimira

NasyaNasya VidhiVidhi::The actual method ofThe actual method of NasyaNasya Karma may be divided in to 3 parts:Karma may be divided in to 3 parts:

PoorvaPoorva KarmaKarma PradhanaPradhana KarmaKarma PaschatPaschat KarmaKarma

PoorvaPoorva Karma:Karma:There should be separate room for conducting theThere should be separate room for conducting the nasyakarmanasyakarma, and it should have good and concealed, and it should have good and concealed

ventilation andventilation and impereableimpereable to smoke, dust and sunlight but good lighting should be availabto smoke, dust and sunlight but good lighting should be available.le.PradhanaPradhana Karma:Karma:

The Patient should be made to take the correct posture, and theThe Patient should be made to take the correct posture, and the nasal administration of the medicine. In thenasal administration of the medicine. In theposture the head will be in a slightly hanging position but restposture the head will be in a slightly hanging position but resting on the head rest attached to the seat or bed. So thating on the head rest attached to the seat or bed. So thatthethe naresnares are directed upwards for easy administration of the medicine. Tare directed upwards for easy administration of the medicine. The eyes and brows are covered with a cleanhe eyes and brows are covered with a cleancloth to avoid the medicine accidentally falling in the eyes.cloth to avoid the medicine accidentally falling in the eyes.

PaschatPaschat Karma:Karma:Just after the administration of the medicine. The patient shoulJust after the administration of the medicine. The patient should lay down for about 5 minutes. Thend lay down for about 5 minutes. Then tapaswedatapasweda

is done on the forehead, cheeks and throat, and light message onis done on the forehead, cheeks and throat, and light message on the neck and shoulder region and soles of the feet.the neck and shoulder region and soles of the feet.The medicine that has flown in to the throat and mucus which isThe medicine that has flown in to the throat and mucus which is seevetingseeveting should be spit out.should be spit out. GorglingGorgling with hot water iswith hot water isessential.essential.


PATHYA APATHYAPATHYA APATHYA

““PathonaPathona ApetamApetam PathyamPathyam”” The drugs and diets which are useful toThe drugs and diets which are useful to SrotasSrotas arearecalledcalled Pathyas.ThePathyas.The PathyaPathya andand ApathyasApathyas ofof VatavyadhisVatavyadhis i.e.,i.e., PakshaghataPakshaghata are as follows:are as follows:

RasasRasas::PathyamPathyam :: MadhuraMadhura,, AmlaAmla,, LavanaLavana..ApathyamApathyam:: KatuKatu,, TiktaTikta,, KashayaKashaya

Pulses & Grains:Pulses & Grains:PathyaPathya :: PuranaPurana RaktaRakta SaliSali,, MashaMasha, Wheat, Horse gram and, Wheat, Horse gram and blackgramblackgramApathayaApathaya: Green Gram,: Green Gram, SharshapaSharshapa,, MudgaMudga,, NavadhanyaNavadhanya,, YavaYava..

GunasGunas::PathyaPathya :: UshnaUshna,, MridhuMridhu,, SnigdhaSnigdha,, vrishyavrishya,, PoushitkaPoushitka aharasaharas andand oushadasoushadas..ApathyaApathya:: LanganamLanganam,, RukshaRuksha,, SeetalaSeetala,, LaghuLaghu,, AbhishyandaAbhishyanda karakara,, DravyasDravyas

SakasSakas::PathyaPathya :: KushmandaKushmanda,, BrinjalBrinjal,, KarelaKarela, Snake Guard, Drum stick,, Snake Guard, Drum stick, RaddishRaddish..ApathyaApathya:: BimbiBimbi,, AlabuAlabu, Cucumber,, Cucumber, KandasakasKandasakas,, KosatakiiKosatakii..

PhalamPhalam::PathyaPathya :: DadimaDadima,, BadaraBadara,, AmraAmra,, DrakshaDrakshaApathyaApathya :: JambuJambu

MamsaMamsa::PathyaPathya :: AajaAaja,, KukkutaKukkuta,, AaviAaviApathyaApathya :: MastyaMastya,, AnupamamsaAnupamamsa,, BilasayaBilasaya..

ViharaVihara::PathyaPathya ::AbhyangaAbhyanga,, UstadanaUstadana,, SnanemSnanem, all, all snehassnehas,, NivathaNivatha SthanamSthanam, Soft bed, Warm Clothes., Soft bed, Warm Clothes.ApathyaApathya ::AtiAti VyavayaVyavaya,, AtiAti VyayamaVyayama,, VegadharanaVegadharana,, JagaranaJagarana,, UdvegaUdvega,, SeetalaSeetala JalaJala,, SeetalaSeetala PhalaPhala


DRUG REVIEWDRUG REVIEW


VATA RAKSHASA RASVATA RAKSHASA RAS

The drugThe drug VatarakshasaVatarakshasa RasRas is indicated inis indicated in vatavata disorders along withdisorders along with PakshaghataPakshaghata ininbooks like Yogabooks like Yoga TaranginiTarangini.. VaidyaVaidya ChintaChinta ManiMani BasavaBasava RajeeyamRajeeyam..

It containsIt contains AbhrakaAbhraka BhasmaBhasma RasaRasa BhasmaBhasma TamraTamra BhasmaBhasma KantalohaKantaloha BhasmaBhasma SuddhaSuddha GandhakaGandhaka

At firstAt first RasabhasmaRasabhasma && SuddhaSuddha GandhakamGandhakam was finely grounded & mixed and all thewas finely grounded & mixed and all theremainingremaining bhasmasbhasmas andand churnaschurnas are added one by one and madeare added one by one and made bhavanabhavana andand mardhanamardhanafor 3 days withfor 3 days with PunarnavamoolaPunarnavamoola SwarasaSwarasa.. GuduchiGuduchi KashayaKashaya,, ChitramoolaChitramoola swarasaswarasa,,TulsipatraTulsipatra SwarasaSwarasa and withand with TrikatuTrikatu KashayaKashaya then dried and put inthen dried and put in SaravamSaravam andand seelseel ititmademade swangaseetaleswangaseetale take it out and paste it with water and made pills.take it out and paste it with water and made pills.

VatarakshasaVatarakshasa rasras isis vataharavatahara,, srotosodhanasrotosodhana andand deepanadeepana, along with, along with pakshaghatapakshaghata ititis indicated inis indicated in UrusthambaUrusthamba,, VatarakataVatarakata,, AmavataAmavata,, DhanurvataDhanurvata and inand in SandhivataSandhivata..

The above mentionedThe above mentioned bhasmasbhasmas are to be madeare to be made bhavanabhavana in thein the swarasswaras // quathasquathas ofofthe followingthe following dravyasdravyas, one by one for 3 days:, one by one for 3 days: PunarnavaPunarnava QuathaQuatha GuduchiGuduchi KashayaKashaya ChitramoolaChitramoola SwarasaSwarasa TulasiTulasi PatraPatra SwarasaSwarasa andand TrikatuTrikatu KashayaKashaya


BhringadiBhringadi TailaTaila NasyaNasya

BhringadiBhringadi TailaTaila NasyaNasya is indicated inis indicated in PakshagataPakshagata along withalong with AarditaAardita VataVata inin VaidyaVaidyaChintamaniChintamani

It containsIt containsBringarajaBringarajaErrandaErrandaNirgundiNirgundiMastchyakshiMastchyakshiArkapatramArkapatramMarichaMaricha ChurnamChurnamTilaTila TailamTailam


CLINICAL STUDYCLINICAL STUDY


CRITERIACRITERIA

Criteria selection and admission of patientsCriteria selection and admission of patients--

Thirty patients suffering fromThirty patients suffering from pakshaghatapakshaghata are selected randomly for theare selected randomly for thepresent Study from the bulk of patients coming for the treatmentpresent Study from the bulk of patients coming for the treatment at theat theKayachikitsaKayachikitsa Department of PostDepartment of Post--graduate Training and research Centre atgraduate Training and research Centre atGovt.Govt. AyurvedicAyurvedic Hospital,Hospital, ErragaddaErragadda, Hyderabad (A.P) during 2006, Hyderabad (A.P) during 2006--2008.2008.

The patients were selected after conducting a screening test toThe patients were selected after conducting a screening test to excludeexcludethe following type of patients.the following type of patients.

1.1. Patients with CerebralPatients with Cerebral HaemorrhageHaemorrhage2.2. Patients below the age of 20 years and above the age of 70 yeaPatients below the age of 20 years and above the age of 70 years.rs.3.3. Pregnant womenPregnant women4.4. PakshaghataPakshaghata patients with dislocation of jointspatients with dislocation of joints5.5. Comatose patientsComatose patients6.6. PakshaghataPakshaghata caused due to the mechanical injury. Known causes ofcaused due to the mechanical injury. Known causes of GranthiGranthi andand

ArbudaArbuda..

These points are excluded from the present study. After excludinThese points are excluded from the present study. After excluding allg alltheses types of patients, finally 30 patients were selected to stheses types of patients, finally 30 patients were selected to study thetudy thetreatment withtreatment with vatarakshasarasvatarakshasaras andand bhringadibhringadi tailataila nasyanasya..


PARAMETERS-Subjective and objective parameters are taken into consideration.

The clinical improvement in the relief of symptoms of like-Impaired walkingImpaired movements of upper limbsDysphagia / dysarthria (Vakgraham / Vakstambha)Loss of appetite and digestionSleeplessness (Nidra nasha)Anxiety (Krodha / soka)Objective parameters-Blood pressureTendon reflexes : Grading

0 – Absent1 – Positive2 – Brisk3 – Very Brisk4 – Clonus

3. Muscle power grading –0 – No contractions1 – Flicker or trace of contractions2 – Active movement with gravity eliminated3 - Active movement with gravity4 - Active movement with gravity and resistance5 – Normal


MATERIALS AND METHODSMATERIALS AND METHODS

Thirty patients suffering fromThirty patients suffering from PakshaghataPakshaghata are selected randomly for the presentare selected randomly for the presentstudy. To study the treatmentstudy. To study the treatment VatarakshasaVatarakshasa RasRas and withand with BhringadiBhringadi TailaTaila Nasya.TheNasya.Thedrugs and their quantity are mentioneddrugs and their quantity are mentioned belowbelow’’.Vatarakshasaras.Vatarakshasaras 1BD for 60 days with1BD for 60 days withhot water andhot water and BhringadiBhringadi tailataila nasyanasya 8 drops in each nostril for 58 drops in each nostril for 5--7 days.7 days.

OBSERVATIONOBSERVATION

The patients are studied based on theThe patients are studied based on the DarsanaDarsana,, SparsanaSparsana, and, and PrasnaPrasna parikshasparikshas..

These includeThese include DasavidhaDasavidha ParikshaPariksha andand AstasthanaAstasthana ParikshaPariksha. Every day the. Every day thecondition of the patients is observed and the treatment procedurcondition of the patients is observed and the treatment procedure is adopted. The totale is adopted. The totalobservations of every day are summed up after twenty days of durobservations of every day are summed up after twenty days of duration of treatment.ation of treatment.

The patients are classified based on different categoriesThe patients are classified based on different categories

LingaLinga NidanaNidana LakshanaLakshana TheThe ‘‘PakshaPaksha’’ affectedaffected DoshaDosha involvementinvolvement Hypertension andHypertension and MadhumehaMadhumeha AgeAge Muscle PowerMuscle Power Tendon reflexTendon reflex


ClasssificationClasssification of patients according to sexof patients according to sex

LINGA (SEX)LINGA (SEX) NO. OF PATIENTSNO. OF PATIENTS PERCENTAGEPERCENTAGE

MALEMALE 2222 73%73%

FEMALEFEMALE 88 27%27%

22 (73.3%)

8 (26.7%)

0

5

10

15

20

25

No

.ofp

atin

ets

(%)

Male Female

Showing Sex wise classifcation of patients


Affected side ofAffected side of pakshaghatapakshaghata on patienton patient’’s bodys body

S.NoS.No.. AFFECTEDAFFECTEDSIDESIDE

NUMBER OF PATIENTSNUMBER OF PATIENTS

TOTAL MALE FEMALETOTAL MALE FEMALE

PERCENTAGEPERCENTAGE

11 RIGHT SIDERIGHT SIDE 15 14 115 14 1 50%50%

22 LEFT SIDELEFT SIDE 15 8 715 8 7 50%50%

14 (46.7%)

1 (3.3%)

8 (26.7%)

7 (23.3%)

0

2

4

6

8

10

12

14

No.

ofp

atie

nts

(%)

Right side Left side

Showing Affected Attacked side of the patients

MaleFemale


Age wise classification of patientsAge wise classification of patients

S.NoS.No.. AGE GROUPAGE GROUP MALEMALE FEMALEFEMALE TOTALTOTAL PERCENTAGEPERCENTAGE

11 2020--3030 22 11 33 10.0%10.0%

22 3030--4040 44 22 66 20.0%20.0%

33 4040--5050 66 11 77 23.4%23.4%

44 5050--6060 55 33 88 27.6%27.6%

55 6060--7070 55 11 66 20.0%20.0%

2

1

4

2

6

1

5

3

5

1

0

1

2

3

4

5

6

7

8

No.

ofp

atie

nts

(%)

20--30 30--40 40--50 50--60 60--70Age (in yrs.)

Showing Age wise classification of patients

FemaleMale

3 (10%)

6 (20%)

7 (23.4%)

8 (27.6%)

6 (20%)


DictaryDictary classification of the total number of patientsclassification of the total number of patients

S.NoS.No.. DIETDIET NUMBER OF PATIENTSNUMBER OF PATIENTS PERCENTAGEPERCENTAGE

11 VegVeg 44 13.3%13.3%

22 NonNon--vegveg 2626 86.7%86.7%

4 (13.3%)

26 (86.7%)

0

5

10

15

20

25

30

No

.ofp

atie

nts

(%)

Vegetarian Nonvegetarian

Showing Dietary habits of the patients


Classification ofClassification of NidanasNidanas (Male Patients)(Male Patients)

S.NoS.No.. AGEAGE MPMP DPDP KatuKatu TiktaTikta KashyaKashya AmlaAmla LavanaLavana RukshaRuksha ADPADP

11 5252 -- -- ++ -- -- ++ ++ ++ ++

22 6363 ++ ++ ++ -- -- ++ ++ ++ ++

33 3737 ++ ++ ++ ++ ++ ++ ++ ++ ++

44 4848 ++ ++ ++ ++ ++ -- ++ ++ --

55 4141 ++ -- -- -- -- ++ ++ ++ ++

66 6666 ++ ++ ++ ++ ++ ++ -- ++ ++

77 6565 -- -- ++ ++ ++ -- -- -- ++

88 4343 ++ ++ ++ ++ -- ++ ++ ++ ++

99 5555 ++ ++ ++ ++ ++ ++ ++ ++ ++

1010 4141 ++ -- ++ ++ ++ ++ ++ ++ ++

1111 3535 ++ ++ -- ++ ++ ++ ++ ++ ++

1212 6262 -- -- ++ ++ ++ ++ ++ ++ ++

1313 5959 ++ ++ ++ ++ ++ ++ ++ ++ ++

1414 5757 ++ ++ ++ ++ ++ ++ ++ ++ ++

1515 3535 ++ ++ -- -- -- ++ ++ ++ ++

1616 2626 ++ ++ ++ ++ ++ ++ ++ ++ ++

1717 2828 -- -- ++ ++ ++ ++ ++ ++ ++

1818 4848 ++ ++ ++ ++ ++ ++ ++ ++ ++

1919 6868 -- -- ++ ++ ++ ++ ++ ++ ++

2020 4545 ++ ++ ++ ++ ++ ++ ++ ++ ++

2121 3232 -- -- ++ ++ ++ ++ ++ ++ --

2222 5252 ++ ++ ++ ++ ++ ++ ++ ++ ++


Classification ofClassification of NidanasNidanas (Female Patients)(Female Patients)

S.NoS.No.. AgeAge MPMP DPDP KatuKatu TiktaTikta KashayaKashaya AmlaAmla LavanaLavana RukdhaRukdha ADPADP

11 3636 -- -- -- -- -- ++ ++ ++ ++

22 5656 -- -- ++ ++ ++ ++ ++ ++ --

33 5252 -- -- ++ ++ ++ ++ ++ ++ --

44 3535 -- -- ++ ++ ++ ++ ++ ++ ++

55 6868 -- -- ++ ++ ++ ++ ++ ++ ++

66 4848 -- -- ++ ++ ++ ++ ++ ++ ++

77 2222 -- -- -- ++ -- ++ -- ++ --

88 5353 -- -- -- -- ++ ++ ++ -- --

Among the thirty patients, who are indulged inMadyapana ------------------- 16Dhoomapana ------------------- 14Adhika Katu Rasa ------------------- 27Adhika Tikta Rasa ------------------- 23Adhika Kashaya Rasa ------------------- 27Adhika Amal Rasa ------------------- 28Adhika Lavana Rasa ------------------- 29Adhika Ruksha ------------------- 23Ahika Deha Parisrama ------------------- 23


Clinical features of Male PatientsClinical features of Male Patients

S.NoS.No.. AgeAge ULUL LLLL DPDP DADA APAP SDSD ADDADD CONCON ICIC ANAN

11 2828 ++ ++ -- -- -- -- -- -- -- ++

22 4141 ++ ++ ++ -- -- ++ ++ ++ -- --

33 3333 ++ ++ ++ ++ -- ++ ++ ++ -- ++

44 4848 ++ ++ -- ++ -- ++ ++ ++ -- ++

55 6666 ++ ++ -- -- ++ ++ ++ ++ -- --

66 5252 ++ ++ -- ++ -- -- ++ -- -- ++

77 4141 ++ ++ -- -- -- ++ ++ -- -- --

88 2626 ++ ++ -- ++ -- -- -- -- -- --

99 4848 ++ ++ ++ ++ -- ++ ++ ++ -- --

1010 5757 ++ ++ -- -- -- ++ ++ ++ -- ++

1111 6565 ++ ++ ++ -- -- -- ++ ++ -- ++

1212 3535 ++ ++ ++ ++ -- -- -- -- -- ++

1313 3535 ++ ++ ++ -- -- -- -- -- -- --

1414 6363 ++ ++ ++ ++ -- ++ ++ ++ -- --

1515 4545 ++ ++ -- -- -- ++ -- ++ -- ++

1616 5555 ++ ++ ++ ++ -- ++ -- ++ -- ++

1717 3232 ++ ++ ++ -- -- -- ++ ++ -- ++

1818 3737 ++ ++ -- -- ++ ++ ++ -- -- --

1919 6868 ++ ++ ++ ++ -- ++ -- ++ ++ --

2020 6262 ++ ++ ++ ++ -- ++ ++ ++ -- --

2121 5959 ++ ++ ++ -- -- ++ -- ++ -- --

2222 5252 ++ ++ ++ ++ -- ++ ++ ++ -- --


Clinical features of Female PatientsClinical features of Female Patients

S.NoS.No.. AgeAge ULUL LLLL DPDP DADA APAP SDSD ADDADD CONCON ICIC ANAN

11 5353 ++ ++ ++ ++ -- ++ -- -- -- --

22 4848 ++ ++ ++ ++ -- ++ ++ -- -- ++

33 3535 ++ ++ ++ -- -- ++ ++ ++ -- --

44 5656 ++ ++ -- ++ -- ++ ++ ++ ++ ++

55 3636 ++ ++ -- -- -- ++ ++ ++ -- --

66 2222 ++ ++ ++ -- -- -- -- ++ -- ++

77 5252 ++ ++ -- ++ -- ++ ++ ++ -- --

88 6868 ++ ++ ++ ++ -- ++ -- ++ ++ --

Key:-UL - Involvement of Upper LimbLL - Involvement of Lower LimbDP - DysphasiaDA - DysarthriaAP - AphasiaSD - Sleep DisturbancesADD - Disturbances of Appetite & digestionCON - ConstipationIC - Urinary IncontinenceAN - Anxiety


Patients having suffers in the family and which are associated wPatients having suffers in the family and which are associated withithCADCAD

S.NoS.No.. SexSex Patients having Sufferers in familyPatients having Sufferers in family Associated with CADAssociated with CAD

11 MaleMale 1010 55

22 FemaleFemale 44 66

10

4

5

6

0

1

2

3

4

5

6

7

8

9

10

No

.ofp

atie

nts

(%)

Sufferers in family Associated with CAD

Showing Patients having Sufferers in Family and association withCAD

Male

Female


PakshaghataPakshaghata with Hypertension andwith Hypertension and MadhumehaMadhumeha

S.S.NoNo..

SexSex Hypertension andHypertension andMadhumehaMadhumeha

HypertensionHypertension MadhumehaMadhumeha NoneNone

11 MaleMale 1616 1313 00 33

22 FemaleFemale 22 22 22 22

13

2

0

2

6

2

3

2

0

2

4

6

8

10

12

14

No.

ofpa

tient

s(%

)

Hypertension Madhumeha Both None

Showing Pakshaghata with Hypertension and Madhumeha

Male

Female

Hypertension

13

2


Patients with Addiction ofPatients with Addiction of MadyapanaMadyapana andand DhoomapanaDhoomapana

S.NoS.No.. SexSex MadyapanaMadyapana andand DhoomapanaDhoomapana MadyapanaMadyapana DhoomapanaDhoomapana NoneNone

11 MaleMale 1414 22 00 66


2

0

00

14

0

6

8

0

2

4

6

8

10

12

14

No.

ofp

atie

nts

(%)

Madhyapana Dhoomapana Both None

Showing addiction of Madyapana and Dhoomapana

FemaleMale


ShowingShowing DoshaDosha predominance of patientspredominance of patients

S.NoS.No.. SexSex VataVata VataVataPittaPitta

VataVataKaphaKapha

VataVata PittaPitta KaphaKapha

11 MaleMale 66 77 33 33


6

4

7

2

3

2

3 3

0

1

2

3

4

5

6

7

No

.ofp

atie

nts

(%)

Vata Vata Pitta Vata Kapha Vata Pitta Kapha

Showing Dosha predominance of patients

MaleFemale


RESULTSRESULTS

The difference in the condition of the patients after the completion of durationof 60 days was observed. The results are categoriezed based on theimprovement they got as good, moderate, and mild. Subjective and objectiveparameters were followed while assessing the results. The results are consideredthe linga (sex), Vayah (Age), Paksha involved (affected side), Dosha, Musclepower, Tendon reflexes, Hypertension and Madhumeha.

Clinical Features:

1. Movements of the limbs improved actively in 11 patients in 60 daystreatment and they have started walking.

2. 12 Patients started walking with some support and 5 patients were startedwalking with great difficulity and two of them not able to walk.

3. Gripping power, Holding power improved in 23 of the patients and 7 patientsshowing mild improvement.

4. Speech is improved to good extent in almost all vakvikruti patients.5. There are no noticeable changes observed in hypertension and

madhumeha.6. The patients suffering with Malabaddaka (Constipation) are relived. Chinta,

Soka are decreased and patients manasika avastha improved.


Muscle power Grading (Male)

BEFORE TREATMENTBEFORE TREATMENT

GradingGrading 00 11 22 33 44 55

Total NumberTotal Numberof Patientsof Patients

11 55 1010 55 11 00

AFTER 20 DAYS OF TREATMENTAFTER 20 DAYS OF TREATMENT


Total Number ofTotal Number ofPatientsPatients

11 44 99 44 33 11




11 22 55 55 44 55





00 00 55 1010 66 99

After 60 days of TreatmentAfter 40 days of Treatment


1

0

5

0

10

5 5

10

1

6

0

9

0

1

2

3

4

5

6

7

8

9

10

No.

ofp

atie

nts


Showing Power grading before and after treatment in male

B.T.

A.T.


BEFORE TREATMENTBEFORE TREATMENT



00 00 55 33 00 00




00 00 33 22 11 22




00 00 22 22 22 22




00 00 11 33 11 33

Muscle power Grading (Female) After 20 days of Treatment

After 40 days of Treatment After 60 days of Treatment


0 0 0 0

5

1

3 3

0

1

0

3

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

5N

o.o

fp

atie

nts


Showing Power grading before and after treatment in female

B.T.A.T.


Tendon Reflexes Grading (Male)

Before TreatmentBefore Treatment

GradingGrading 00 11 22 33 44


11 22 22 55 1212




11 66 66 55 44




11 88 66 33 33




11 1111 77 22 22




1

0

2

11

2

7

5

2

12

2

0

2

4

6

8

10

12

No

.of

pa

tien

ts


Showing Tendon reflexes grading before and after treatment in male

B.T.A.T.


Before TreatmentBefore Treatment



00 22 00 44 11




11 33 11 22 11




11 33 22 22 00




00 55 22 11 00

Tendon Reflexes Grading (Female) After 20 days of Treatment



0 0

2

5

0

2

4

1 1

0

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

5

No

.o

fp

ati

en

ts


Showing Tendon reflexes grading before and after treatment infemale

B.T.A.T.


TABLE SHOWING SUBTABLE SHOWING SUB--SIDE OF SYMPTOMSSIDE OF SYMPTOMSAFTER TREATMENTAFTER TREATMENT

S.S.NNOO

NameName AgeAge SexSex PrakruthiPrakruthi SideSideAffecAffec

eded

VakVakvikruthivikruthiB AB A

SleepSleepDisturbancesDisturbancesBB AA

Appetite &Appetite &DigestionDigestion

disturbancesdisturbancesB AB A

ConstipaConstipationtion

B AB A

UrinaryUrinaryIncontinIncontin

enceenceB AB A

AnxiAnxietyetyBB

AA

11 SitaSita MahaMahaLakshmilLakshmil

5353 FF KVKV LTLT ++++ -- ++ -- -- -- -- -- -- -- -- --

22 VenkatamaVenkatama 4848 FF PVPV LTLT ++++ ++ ++ ++ ++ -- ++ ++ -- -- ++ ++

33 IndiraIndira 3535 FF VKVK LTLT ++++ -- ++ -- ++ -- ++ -- -- -- -- --

44 SwaroopaSwaroopa 5656 FF KVKV RTRT ++++++++ ++ ++ ++ -- ++ -- ++ ++ ++ ++

55 RajaRajaLakshmiLakshmi

3636 FF PVPV LTLT -- ++ -- ++ -- ++ -- -- -- -- -- --

66 KranthiKranthi 2222 FF KVKV LTLT ++ -- ++ -- -- -- ++ -- -- -- ++ --

77 NareshNaresh 2828 MM KVKV RTRT -- -- -- -- -- -- -- -- -- -- ++ --

88 NarsingNarsing RaoRao 4141 MM VKVK RTRT ++++ -- ++ ++ ++ ++ ++ ++ -- -- -- --

99 SanjeevSanjeev 4343 MM VKVK LTLT ++++++++ ++ -- ++++++ ++ ++ -- -- -- ++ ++


1010 NarshimuluNarshimulu 4848 MM VPVP RTRT ++++ -- -- -- ++++ -- ++ -- -- -- ++ ++

1111 PochaiahPochaiah 6666 MM VPVP RTRT ++++++++

-- ++ ++ ++++ ++ ++ ++ -- -- -- --

1212 NarshimaNarshimaReddyReddy

5252 MM VKVK RTRT ++++ ++ -- -- ++ ++ -- -- -- -- ++ --

1313 LakshmanLakshman 4141 MM VPVP RTRT -- -- ++ -- ++++ -- -- -- -- -- -- --

1414 RajeshRajesh 2626 MM VPVP RTRT ++ -- -- -- -- -- -- -- -- -- -- --

1515 MahamoodMahamood 4848 MM VPVP RTRT ++ -- ++ -- ++++ ++ ++ ++ -- -- -- --

1616 TirupathiahTirupathiah 5757 MM KVKV RTRT -- -- ++ -- ++++ ++ ++ ++ -- -- ++ ++

1717 VenkatVenkatReddyReddy

6565 MM KPKP RTRT ++++ -- -- -- ++ -- ++ -- -- -- ++ ++

1818 NarshimaNarshima 3535 MM VKVK RTRT ++++ -- -- -- -- -- -- -- -- -- ++ --

1919 PrasadPrasad 3535 MM VPVP LTLT ++++++++ -- -- -- -- -- -- -- -- -- --

2020 RammuluRammulu 6363 MM VKVK LTLT ++++ ++ ++ -- ++ ++ ++ -- -- -- -- --

2121 RamaiahRamaiah 5252 MM KVKV LTLT ++++ -- ++ -- ++++ -- ++ -- -- -- -- --

2222 RajeshwaraRajeshwaraRaoRao

4545 MM VPVP LTLT -- -- ++ -- ++ ++ ++ -- -- -- ++ ++

2323 BhumaiahBhumaiah 5555 MM VKVK LTLT ++++ ++ ++ ++ ++ ++ ++ -- -- -- ++ --

2424 LakshmiLakshmiNarayanaNarayana

3232 MM KVKV LTLT ++++ -- -- -- ++ -- ++ -- -- -- ++ --


2525 MalleshMallesh 3737 MM VKVK RTRT -- -- ++ -- ++ -- -- -- -- -- -- --

2626 ChinniChinni RaoRao 6868 MM VKVK LTLT ++++++++ ++ -- ++ ++ ++ -- ++ ++ -- --

2727 PatelPatel 6262 MM VKVK RTRT ++++++++

++ ++ ++ -- -- ++ -- -- -- -- --

2828 SaraswathiSaraswathi 5252 FF KVKV LTLT ++++ -- ++ -- ++ -- ++ -- -- -- -- --

2929 RamaRama RaoRao 5959 MM VPVP RTRT ++++ -- ++ -- -- -- -- -- -- -- -- --

3030 KarunamaKarunama 6868 FF VKVK LTLT ++ -- ++ -- -- -- ++ ++ ++ ++ -- --

24

3

5

16

23

0

9

14

21

3

8

10

3 3

13

4

8

0

5

10

15

20

25

No.o

fpa

tients

B.T A.T B.T A.T B.T A.T B.T A.T B.T A.T

Speech difficulty Sleepdisturbances

Apetite andDigestive

Urinaryincontinence

Anxiety

Showing subside of Signs & symptoms after treatment

GoodModerate

Mild

No response

Present


S.S.No.No.

NameName AAgege

SSexex

PraPraKrutiKruti

SideSideAffectedAffected

UULL

LLLL

DateDateofof

AdmAdmIssionIssion

Date ofDate ofDischargeDischarge

WhenWhenTreatTreatmentment

StaredStaredafterafter

AttackAttack

DuratiDuration ofon ofTreatTreatmentment

VakVakVikrutiVikrutiB AB A

PowerPowerBBAA

ReflexReflexB AB A

ResultsResults

11 SitaSitaMahaMaha

LakshmilLakshmil

5353 FF KVKV LTLT ++ ++ 3/7/03/7/077

15/10/015/10/077

11YearYear

6060daysdays55--77--daysdays

++++ -- 22 55 11 11 GoodGood

22 VenkataVenkatamama

4848 FF PVPV LTLT ++ ++ 29/7/729/7/7 30/12/030/12/077

1515daysdays


++++ ++ 00 22 00 22 MildMild

33 IndiraIndira 3535 FF VKVK LTLT ++ ++ 12/3/712/3/7 28/7/0728/7/07 1818MonthMonth

ss


++++ -- 22 33 33 33 ModMod

44 SwaroopaSwaroopa 5656 FF KVKV RTRT ++ ++ 6/5/076/5/07 8/10/078/10/07 1515daysdays


++++ ++ 22 33 44 11 ModMod

55 RajaRajaLakshmiLakshmi

3636 FF PVPV LTLT ++ ++ 12/2/12/2/0707

26/6/0726/6/07 11yearyear


-- -- 33 55 33 11 GoodGood


66 KranthiKranthi 2222 FF KVKV LTLT ++ ++ 8/4/078/4/07 12/9/0712/9/07 11monthmonth

60 days60 days55--77daysdays

++ -- 33 55 11 11 GoodGood

77 NareshNaresh 2828 MM KVKV RTRT ++ ++ 25/9/025/9/077

9/12/079/12/07 22monthsmonths

60 days60 days55--77--daysdays

-- -- 33 55 11 11 GoodGood

88 NarsingNarsing RaoRao 4141 MM VKVK RTRT ++ ++ 18/4/018/4/077

25/8/0725/8/07 1 year1 year 60 days60 days55--77--daysdays

++++ -- 11 33 33 22 ModMod

99 SanjeevSanjeev 4343 MM VKVK LTLT ++ ++ 3/2/073/2/07 5/6/075/6/07 44monthsmonths


++++++++ 22 44 44 11 ModMod

1010 NarshimuluNarshimulu 4848 MM VPVP RTRT ++ ++ 6/9/076/9/07 12/12/0712/12/07 1010monthsmonths


++++ -- 11 33 22 11 ModMod

1111 PochaiahPochaiah 6666 MM VPVP RTRT ++ ++ 3/8/073/8/07 12/11/0712/11/07 1 year1 year 60 days60 days55--77--daysdays

++++++++

++ 22 33 44 33 MildMild

1212 NarshimaNarshimaReddRedd

yy

5252 MM VKVK RTRT ++ ++ 5/7/075/7/07 15/11/0715/11/07 22yearsyears


++++ ++ 11 33 33 22 ModMod

1313 LakshmanLakshman 4141 MM VPVP RTRT ++ ++ 7/5/077/5/07 16/9/0716/9/07 1 year1 year 60 days60 days55--77--daysdays

-- -- 22 33 44 22 ModMod

1414 RajeshRajesh 2626 MM VPVP RTRT ++ ++ 3/8/073/8/07 6/12/076/12/07 33yearsyears

60 days60 days55--77--daysdays--

++ -- 11 55 11 11 GoodGood


1515 MahamoodMahamood 4848 MM VPVP RTRT ++ ++ 10/9/010/9/077

27/12/0727/12/07 1010daysdays

60 day60 day--s 5s 5--77-- --

daysdays

++ -- 22 33 44 11 ModMod

1616 TirupathiahTirupathiah 5757 MM KVKV RTRT ++ ++ 9/06/09/06/077

24/10/0724/10/07 1010monthmonth

ss


-- -- 33 44 44 22 ModMod

1717 VenkatVenkatReddyReddy

6565 MM KPKP RTRT ++ ++ 13/10/13/10/0077

5/1/085/1/08 1818monthmonth

ss


++++ -- 22 22 00 22 MildMild

1818 NarshimaNarshima 3535 MM VKVK RTRT ++ ++ 14/3/014/3/077

12/7/0712/7/07 55monthmonth

ss


++++ -- 33 55 44 11 GoodGood

1919 PrasadPrasad 3535 MM VPVP LTLT ++ ++ 15/5/015/5/077

27/9/0727/9/07 1818monthmonth

ss


++++++-- 33 55 44 11 GoodGood

2020 RammuluRammulu 6363 MM VKVK LTLT ++ ++ 20/8/020/8/077

27/12/0727/12/07 11monthmonth


++++ ++ 22 33 44 33 MildMild

2121 RamaiahRamaiah 5252 MM KVKV LTLT ++ ++ 12/9/012/9/077

21/9/0721/9/07 33monthmonth

ss


++++++++ 22 44 33 11 ModMod

2222 RajeshwaraRajeshwaraRaoRao

4545 MM VPVP LTLT ++ ++ 11/5/011/5/077

11/12/0711/12/07 1515daysdays


-- -- 11 22 44 44 MildMild

2323 BhumaiahBhumaiah 5555 MM VKVK LTLT ++ ++ 12/6/012/6/077

29/12/0729/12/07 11monthmonth


++++++++

++22 22 44 22 MildMild

2424 LakshmiLakshmiNarayanaNarayana

3232 MM KVKV LTLT ++ ++ 30/7/030/7/077

26/11/0726/11/07 1515daysdays


++++ -- 33 55 33 11 GoodGood

2525 MalleshMallesh 3737 MM VKVK RTRT ++ ++ 17/7/017/7/077

8/12/078/12/07 1515daysdays


-- -- 44 55 33 11 GoodGood


2626 ChinniChinniRaoRao

6868 MM VKVK LTLT ++ ++ 3/5/073/5/07 15/9/0715/9/07 22monthsmonths


------ ++ 22 44 44 22 ModMod

2727 PatelPatel 6262 MM VKVK RTRT ++ ++ 12/2/012/2/077

30/8/0730/8/07 33monthsmonths


++++++++ 00 22 44 44 MildMild

2828 SaraswathiSaraswathi 5252 FF KVKV LTLT ++ ++ 1/9/071/9/07 12/1/0812/1/08 1515daysdays


++++ -- 22 44 33 11 GoodGood

2929 RamaRama RaoRao 5959 MM VPVP RTRT ++ ++ 6/6/076/6/07 10/11/0710/11/07 1515daysdays


++++ -- 22 44 22 11 GoodGood

3030 KarunamaKarunama 6868 FF VKVK LTLT ++ ++ 16/9/016/9/077

28/12/0728/12/07 1 year1 year 60 days60 days55--77--daysdays

++ -- 33 33 33 22 modmod

Showing the therapeutic response

Mild response7 (24.3%)

Moderate response12 (40%)

Good response11 (36.7%)


1.1. In this present clinical study the mean percent response of theIn this present clinical study the mean percent response of thepatients is 56 + orpatients is 56 + or –– 22.22.

2.2. The mean of this is 56.5% and standard deviation is 22%The mean of this is 56.5% and standard deviation is 22%3.3. The t test of this present study is 17.9%The t test of this present study is 17.9%4.4. The p value of this clinical trial is p<0.01 which is significanThe p value of this clinical trial is p<0.01 which is significant.t.

56.5 + 22.0

0

10

20

30

40

50

60

Me

an%

resp

onse

Mean response

Showing Mean percent response of patients


DISCUSSIONDISCUSSION

VataVata VyadhiVyadhi is one of theis one of the ““MahaMaha rogasrogas”” described out of thedescribed out of the AstaAsta MaharogasMaharogas described bydescribed bysusrutasusruta.. PakshaghataPakshaghata is a variety ofis a variety of VataVata VyadhiVyadhi and inand in PakshaghataPakshaghata the main clinical feature isthe main clinical feature isAkarmanyataAkarmanyata ofof HastaHasta && PadaPada. Its Separate entity was observed by the ancient. Its Separate entity was observed by the ancient acharyasacharyas and itsand itsdescription is explained indescription is explained in vatavyadhivatavyadhi chapters in the classics.chapters in the classics.

VataVata disorders are caused to thedisorders are caused to the dhatudhatu kshayakshaya andand avarantwaavarantwa,, PakshaghataPakshaghata also caused due toalso caused due tothe above said two factors in generalthe above said two factors in general vatavata disorders are difficult to cure and when it is associated withdisorders are difficult to cure and when it is associated withUpadravasUpadravas andand aristalakshanasaristalakshanas they arethey are asadhyaasadhya.. PakshagataPakshagata caused predominantly bycaused predominantly by vatavata doshadoshaeven though all the threeeven though all the three doshasdoshas also take part besides itsalso take part besides its dushyasdushyas namelynamely sirassiras,, snayussnayus,, dhamanisdhamanis..SandhisSandhis andand mamsamamsa resulting in to this disease.resulting in to this disease.

Present clinical study comprises of the effect ofPresent clinical study comprises of the effect of vatavata rakshasarasrakshasaras along thealong the bhrungadibhrungadi tailatailanasya.Thenasya.The drugdrug vatarakshasavatarakshasa RasRas is indicated inis indicated in vatavata disorders along withdisorders along with PakshagataPakshagata in books likein books likeyogayoga taranginitarangini,, vaidyavaidya chintamanichintamani,, BasavaBasava RajeeyamRajeeyam..

It containsIt contains AbhrakaAbhraka BhasmaBhasma,, RasabhasmaRasabhasma,, TamrabhasmaTamrabhasma,, KantalohaKantaloha andand SuddhaSuddha GandhakamGandhakam..AbharakamAbharakam has the properties likehas the properties like tridoshaharatridoshahara andand dhatuvriddhidhatuvriddhi,, RasabhasmaRasabhasma hashas TridoshaharaTridoshahara,,RasayanaRasayana,, YogavahiYogavahi,, BalapradeBalaprade,, TamraTamra hashas RasayanaRasayana, and, and LekhanaLekhana..

KantaKanta LohaLoha BalaBala,, VeeryaVeerya,, DhatupushteDhatupushte,, AgnivardhanaAgnivardhanaGandhakaGandhaka VatakaphaharaVatakaphahara andand RasayanaRasayana..

RasaoushadasRasaoushadas has properties likehas properties like AlpamatraAlpamatra (Smaller dose)(Smaller dose) ArucheraprasangathaArucheraprasangatha (Palatable)(Palatable) KshipramarogyaKshipramarogya DayitwaDayitwa (Fast Acting)(Fast Acting)

VataVata rakshasarakshasa RasRas isis RasaousadhaRasaousadha posses the above said 3 qualities and having the drugs thatposses the above said 3 qualities and having the drugs thatareare vataharavatahara andand RasayanaRasayana properties. So,properties. So, VatarakshasaVatarakshasa RasRas is the drug of choice foris the drug of choice for PakshaghataPakshaghata..


BhringadiBhringadi TailamTailam::ItIt continscontins BhringarajaBhringaraja, which is the one of the best, which is the one of the best rasayanarasayana drugdrug –– PakshaghataPakshaghata is caused dueis caused due

toto dhatukhasayadhatukhasaya, so, so rasayanarasayana is indicated along with it containsis indicated along with it contains errandaerranda which iswhich is vatanlumonavatanlumona, which is, which isindicated because inindicated because in PakshagataPakshagata avarantwaavarantwa is another cause.is another cause. BhringaditailaBhringaditaila also containsalso contains nirungdinirungdi andandother drugs which areother drugs which are vataharavatahara properties.properties.

Dose:Dose:-- VatarakshasaVatarakshasa rasras –– 125 mg125 mg --2 X BD2 X BD –– 60 days60 days-- BhringadiBhringadi TailaTaila NasyaNasya –– 8 drops in each nostril8 drops in each nostril --5 to 7 days.5 to 7 days.

30 patients are selected from the hospital out of 30, 15 are suf30 patients are selected from the hospital out of 30, 15 are suffered fromfered from DakshinaDakshina PakshaghataPakshaghata and other 15and other 15are fromare from VamaVama PakshaghataPakshaghata. Hypertension and. Hypertension and MahdumehaMahdumeha are observed in 8 patients. Only Hypertension in 15are observed in 8 patients. Only Hypertension in 15patients onlypatients only MadhumehaMadhumeha in 2 patients, without HTN &in 2 patients, without HTN & MadhumehaMadhumeha in 5 patients.in 5 patients.

CarotidCarotid atheromaatheroma and transient cerebraland transient cerebral ischaemicischaemic are more common in hypertensive patients. The next riskare more common in hypertensive patients. The next riskafter hypertension isafter hypertension is MadhumehaMadhumeha. In this clinical study cerebral. In this clinical study cerebral haemorrhagichaemorrhagic patients are excluded, because sometimespatients are excluded, because sometimesNasyaNasya maymay futherfuther provokes the bleeding tendency. 14 Patients are habituated toprovokes the bleeding tendency. 14 Patients are habituated to madhyapanamadhyapana andand dhoomapanadhoomapana and 2and 2are habituated toare habituated to MadhyapanaMadhyapana and 14 are not habituated.and 14 are not habituated.

No, Female patient is habituated toNo, Female patient is habituated to dhoomapanadhoomapana (or)(or) MadhyapanaMadhyapana in this trial. Madhya possessin this trial. Madhya possess KashyaKashya,, TiktaTikta,,KatuKatu,, AmlarasasAmlarasas,, AmlavipakaAmlavipaka andand LaghuLaghu,, ushnaushna gunasgunas.. DhoomapanaDhoomapana GunasGunas areare ushnaushna,, TeekshnaTeekshna,, RookshaRooksha andandlaghugunaslaghugunas.. AdhikaAdhika KashayaKashaya RasaRasa SevanaSevana,, LaghuLaghu,, RukshaRuksha gunasgunas vitiatesvitiates vatavata which are causative factors for theirwhich are causative factors for theirdisease.disease.

According to the modern system of medicine high alcohol intake iAccording to the modern system of medicine high alcohol intake is the risk factor for stroke. Cerebrals the risk factor for stroke. Cerebralhaemorrhagehaemorrhage, dementia,, dementia, cerebellarcerebellar degeneration etc., are the physical effects of alcohol abuse. Sdegeneration etc., are the physical effects of alcohol abuse. Smoking is the riskmoking is the riskfactor in stroke. It is responsible for hypertension, myocardialfactor in stroke. It is responsible for hypertension, myocardial infexetioninfexetion,, ischaemicischaemic heart disease,heart disease, peripherialperipherial arterialarterialdisease etc. These are thedisease etc. These are the aetiologicalaetiological factors for stroke.factors for stroke.

Interestingly, the patients withInterestingly, the patients with dysarthriadysarthria, dysphasia and also with Aphasia are responding well to the tre, dysphasia and also with Aphasia are responding well to the treatmentatmentafterafter nasyanasya speech improvement is very good in almost all of thespeech improvement is very good in almost all of the vakvak -- vikrutivikruti patients. Patients which are nonpatients. Patients which are non--diabeticdiabeticyoung and posseyoung and posse’’s good strengths good strength respondesrespondes well to the treatment compared to diabetic and older patients.well to the treatment compared to diabetic and older patients. Out of 30Out of 30patients 11 patients responds well to the treatment, 12 patientspatients 11 patients responds well to the treatment, 12 patients show moderate response and 7 patients show minimalshow moderate response and 7 patients show minimalresponse.response.


CONCLUSIONCONCLUSION

An attempt has been made to study the effect ofAn attempt has been made to study the effect of VatarakshasaVatarakshasa RasRas withwith BhringadiBhringadi TailaTaila NasyaNasya ininthe management ofthe management of PakshaghataPakshaghata. A clinical trail has been conducted on 30 patients selected fr. A clinical trail has been conducted on 30 patients selected from IPD ofom IPD ofGovt.AyurvedicGovt.Ayurvedic Hospital,Hospital, ErragaddaErragadda, Hyderabad. Approximately about 11 patients were recovered, Hyderabad. Approximately about 11 patients were recoveredcompletely, 12 patients were left with some disability or deformcompletely, 12 patients were left with some disability or deformity, 7 patients left with persistentity, 7 patients left with persistentdeformity, eitherdeformity, either chestachesta vahavaha (motor) or(motor) or SanganaSangana vahavaha (Sensory) through out the life.(Sensory) through out the life.

InIn AyurvedaAyurveda CharakaCharaka maharshimaharshi said that the history ofsaid that the history of PakshaghataPakshaghata with short duration of onsetwith short duration of onsetand without complications and moreover if theand without complications and moreover if the pakshaghatapakshaghata patient ispatient is balavanbalavan (strong enough) such(strong enough) suchtype of cases can be easilytype of cases can be easily caurablecaurable and it has been proved in the present clinical study. Patientsand it has been proved in the present clinical study. Patients withwithdiabetisdiabetis,, oldageoldage having other complications are not responding well to the treathaving other complications are not responding well to the treatment which confirms thement which confirms theApathaApatha vachanavachana..

Now a dayNow a day’’s the present life is very fast and competitive. So the patientss the present life is very fast and competitive. So the patients are also seeing forare also seeing forimmediate cure .Though number of techniques and remedies are avaimmediate cure .Though number of techniques and remedies are available most of the people areilable most of the people arepreferringpreferring ayurvedicayurvedic treatment mainly fortreatment mainly for pakshaghatapakshaghata. So taking all these observations and views of. So taking all these observations and views ofthe people inspired me to prepare this fast actingthe people inspired me to prepare this fast acting RasaoushadaRasaoushada likelike VatarakshasaVatarakshasa RasRas along withalong withrasayanarasayana nasyanasya likelike BhringadiBhringadi TailaTaila NasyaNasya..

VatarakshasaVatarakshasa RasRas is a drug which acts very fast and showed the curative resultsis a drug which acts very fast and showed the curative results to the patientsto the patientswith in short period. After givingwith in short period. After giving nasyanasya there is a good improvement in speech in almost all of thethere is a good improvement in speech in almost all of thevakvikrutivakvikruti patients.patients.

During the period of treatment no complications are unwanted effDuring the period of treatment no complications are unwanted effects were observed. Thisects were observed. Thisshows the non toxic effect ofshows the non toxic effect of vatarakshasavatarakshasa rasras.. VatarakshasaVatarakshasa RasRas can be used incan be used in krichrakrichra sadhyasadhya andandAsdhyaAsdhya vyadhisvyadhis because of presence ofbecause of presence of RasaoushadhisRasaoushadhis likelike RasabhasmaRasabhasma,, TamraTamra BhasmaBhasma etc.etc.

RasaoushadhiRasaoushadhi is comparatively best than theis comparatively best than the KashthoushadhisKashthoushadhis because as mentioned in the textbecause as mentioned in the textthatthat RasaoushadhisRasaoushadhis will not lose there potency forever. So,will not lose there potency forever. So, vatarakshasavatarakshasa RasRas along withalong with rasayanarasayanaBhringadiBhringadi TailaTaila NasyaNasya is selected for this clinical trail in the management ofis selected for this clinical trail in the management of pakshaghatapakshaghata..


SUMMARYSUMMARYThe present dissertation entitledThe present dissertation entitled ““A STUDY OF THE EFFECT OF VATARAKSHASA RAS WITH BHRINGADIA STUDY OF THE EFFECT OF VATARAKSHASA RAS WITH BHRINGADI

TAILA NASYA IN THE MANAGEMENT OF PAKSHAGHATATAILA NASYA IN THE MANAGEMENT OF PAKSHAGHATA”” is summarized as below:is summarized as below:The entire thesis is mainly divided in to eight sections.The entire thesis is mainly divided in to eight sections.

Section ISection I : Introduction & Historical aspect: Introduction & Historical aspectSection IISection II :: SareeraSareeraSection IIISection III :: VyadhiVyadhi SameekshaSameekshaSection IVSection IV :: ChikitsaChikitsa YojanaYojanaSection VSection V :: OushadhaOushadha SameekshaSameekshaSection VISection VI : Clinical Study: Clinical StudySection VIISection VII : Discussion, Conclusion & Summary: Discussion, Conclusion & SummarySection VIISection VII : Bibliography: Bibliography

INTRODUCTIONINTRODUCTION Definition ofDefinition of AyurvedaAyurveda and concept of disease has been discussed.and concept of disease has been discussed. Causes ofCauses of vyadhivyadhi and its consequences have been discussed.and its consequences have been discussed. TheThe RasoushadhaRasoushadha action and its importance have been discussed.action and its importance have been discussed. ItihasaItihasa tells that there is gradual evolution in the treatment patterntells that there is gradual evolution in the treatment pattern fromfrom prevedicprevedic period toperiod to sangrahasangraha kalakala. It also. It also

states thatstates that AyurvedicAyurvedic system was much advanced than thesystem was much advanced than the AllpothicAllpothic system of medicine in diagnosis andsystem of medicine in diagnosis andtreatment aspects.treatment aspects.

SHAREERAMSHAREERAM Definition ofDefinition of vatavata and its importance has been discussed.and its importance has been discussed. UtpatthiUtpatthi ofof vatavata and its relationship toand its relationship to panchamahabhutaspanchamahabhutas, and properties of, and properties of akashaakasha andand vayuvayu mahabhutasmahabhutas havehave

been explained.been explained. DoshaDosha dhatudhatu sambandhasambandha and their functions when they are in normal state have been disand their functions when they are in normal state have been discussed.cussed. SwaroopaSwaroopa ofof vatavata has been stated.has been stated. GunasGunas ofof vatavata according to differentaccording to different AcharyasAcharyas have been explained.have been explained. Sites ofSites of vatavata and types ofand types of vatavata according toaccording to BrihattrayeeBrihattrayee ,, sthanassthanas and karmas of five suband karmas of five sub--divisions ofdivisions of vatavata havehave

been tabulated.been tabulated. The cerebral blood flow is an essential aspect in the disease prThe cerebral blood flow is an essential aspect in the disease process. Carbon dioxide, hydrogen, oxygenocess. Carbon dioxide, hydrogen, oxygen

concentrations have potent effected in controlling the cerebralconcentrations have potent effected in controlling the cerebral blood flow.blood flow. The human brain normal functions are dependent on constant supplThe human brain normal functions are dependent on constant supply of oxygen and other nutrients derived fromy of oxygen and other nutrients derived from

bloodblood perfusingperfusing it. Two internal carotids, twoit. Two internal carotids, two vertebralsvertebrals and their branches perfuse the brain tissue.and their branches perfuse the brain tissue.


VYADHI SAMEEKSHAVYADHI SAMEEKSHA TheThe NidanaNidana has been classified and types have been discussed.has been classified and types have been discussed. The basicThe basic aetiologyaetiology involved in the disease has been summarized.involved in the disease has been summarized. AetiologyAetiology ofof VataVata vyadhisvyadhis have been discussed because of a fact thathave been discussed because of a fact that pakashaghatapakashaghata is one amongis one among

thethe vatavata vyadhisvyadhis.. The expression ofThe expression of poorvaroopapoorvaroopa and meaning ofand meaning of poorvaroopapoorvaroopa are discussed in detail.are discussed in detail. The generalizedThe generalized lakshanaslakshanas of the disease has been stated according to differentof the disease has been stated according to different AyurvedicAyurvedic

AcharyasAcharyas.. The role ofThe role of nidananidana,, doshasdoshas andand dushyasdushyas in the process ofin the process of sampraptisamprapti were explained in detail.were explained in detail. The meaning ofThe meaning of sampraptisamprapti in general with special references toin general with special references to kriyakriya kalaskalas has been discussed.has been discussed. TheThe sampraptisamprapti of the diseaseof the disease pakshaghatapakshaghata has been discussed in detail according tohas been discussed in detail according to BrihattrayeesBrihattrayees.. TheThe sampraptisamprapti ofof pakshaghatapakshaghata has been made elaborately in terms ofhas been made elaborately in terms of utbhavautbhava sthanasthana,, sancharasanchara,,

doshadosha,, dushyasdushyas andand srothasessrothases etc.etc.

CHIKITSA YOJANACHIKITSA YOJANA InIn chikitsachikitsa aspect treatment ofaspect treatment of pakshaghatapakshaghata,, shodhanashodhana chikitsachikitsa andand shamanashamana chikitsachikitsa werewere

explained clearly.explained clearly. PathyaPathya apathyaapathya ofof pakshaghatapakshaghata have been discussed.have been discussed.

AUSHADHA SAMEEKSHAAUSHADHA SAMEEKSHA Composition ofComposition of VatarakshasVatarakshas RasRas andand BhringadhiBhringadhi TailaTaila NasyaNasya explained in detail.explained in detail.

CLINICAL STUDYCLINICAL STUDY Parameters, criteria and method and materials have been explaineParameters, criteria and method and materials have been explained.d. ObsevationsObsevations and Results:and Results: DakshinaDakshina part of the body is affected same as that ofpart of the body is affected same as that of vamavama bhagabhaga. Hypertension is. Hypertension is

commonly associated with the disease than thecommonly associated with the disease than the madhumehamadhumeha.. The results of clinical trial are tabulated.The results of clinical trial are tabulated. The results are tabulated as goodThe results are tabulated as good–– 11 patients, moderate11 patients, moderate –– 12 patients and mild12 patients and mild –– 7 patients.7 patients. Discussion. The observations and results are discussed.Discussion. The observations and results are discussed. Total study on the diseaseTotal study on the disease pakshaghatapakshaghata. The drug and the clinical work have been revived in a brief di. The drug and the clinical work have been revived in a brief discussion.scussion. Conclusion.Conclusion. VataVata RakshasaRakshasa RasRas andand BhringadiBhringadi TailaTaila NasyaNasya have been adopted for treatment in the present study. Ashave been adopted for treatment in the present study. As

anticipated the results were encouraging. This once again provesanticipated the results were encouraging. This once again proves the validity ofthe validity of aptavachanaaptavachana


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