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A COMPARATIVE STUDY OF ERANDA PAKA AND AJAMODADI CHURNA IN THE MANAGEMENT OF AMAVATA Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka in partial fulfillment of the regulations for the award of the degree of DOCTOR OF MEDICINE (AYU) By DEEPAK S.M., B. A. M. S. GUIDE DR.U.N. PRASAD, M.D. (AYU) Professor and H.O.D. Department of Kayachikitsa S.D.M. College of Ayurveda, Udupi CO-GUIDE DR. V.K. SRIDHAR HOLLA, M.D.(AYU) Assistant Professor Department of Kayachikitsa S.D.M. College of Ayurveda, Udupi DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118. 2002 – 2003

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Page 1: Amavata kc004 udp

A COMPARATIVE STUDY OF ERANDA PAKA AND AJAMODADI

CHURNA IN THE MANAGEMENT OF AMAVATA

Dissertation submitted to the Rajiv Gandhi University of Health Sciences,

Bangalore, Karnataka in partial fulfillment of the regulations for the award of the

degree of

DOCTOR OF MEDICINE (AYU)

By

DEEPAK S.M., B. A. M. S.

GUIDE

DR.U.N. PRASAD, M.D. (AYU) Professor and H.O.D.

Department of Kayachikitsa S.D.M. College of Ayurveda, Udupi

CO-GUIDE

DR. V.K. SRIDHAR HOLLA, M.D.(AYU) Assistant Professor

Department of Kayachikitsa S.D.M. College of Ayurveda, Udupi

DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA

S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118.

2002 – 2003

Ayurmitra
TAyComprehended
Page 2: Amavata kc004 udp

DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA

S.D.M. COLLEGE OF AYURVEDA, UDUPI – 574 118

CERTIFICATE

This is to certify that the dissertation entitled “A comparative

study of Eranda Paka and Ajamodadi Churna in the management of Amavata” is the record of the research work conducted by Deepak S.M.

under my direct supervision and guidance in S. D. M. College of

Ayurveda, Udupi.

The candidate has put in sincere effort in both the conceptual and

clinical studies.

This title has not been awarded Degree, Diploma, Associateship,

Fellowship or similar honors from this University.

I recommend and forward the same for being submitted for

evaluation to the adjudicators.

Place : Udupi Date :

Dr. U. N. Prasad, M.D. (Ayu) Professor and Head of the Department of

Post graduate studies in Kayachikitsa

S. D. M. College of Ayurveda, Udupi.

Page 3: Amavata kc004 udp

DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSA

S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118

CERTIFICATE

This is to certify that the dissertation entitled “A comparative

study of Eranda Paka and Ajamodadi Churna in the management of Amavata” is the record of the research work conducted by Deepak S.M

under my direct supervision and guidance.

The candidate has put in sincere effort in both the conceptual and

clinical studies.

I recommend the same for being submitted for evaluation to the

adjudicators.

Place : Udupi Date :

Dr. U. N. Prasad, M.D. (Ayu) Professor and Head of the Department of

Post graduate studies in Kayachikitsa

S. D. M. College of Ayurveda, Udupi.

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ACKNOWLEDGEMENTS

I am Ever Indebted To Lord Almighty,

My Venerated Parents,

Respected Teachers And

Affectionate Friends

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Dedicated to

My Beloved Father

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CONTENTS LIST OF CHARTS

LIST OF TABLES

LIST OF GRAPHS

LIST OF ABBREVIATIONS

Page No

PART - I: INTRODUCTION 1

PART - II: CONCEPTUAL STUDY Chapter I - Historical Review 5

Chapter II - Vyutpatti of Amavata 11

Ama and Vata 12

Nidana 30

Samprapti 35

Poorvaroopa 41

Bheda 43

Roopa 46

Upadrava 55

Investigations 58

Upashaya Anupashaya 62

Sadhyasadhyata 65

Sapeksha Nidana 67

Chikitsa 69

Pathya-Apathya 76

Chapter III - Drug Review 79

PART - III: CLINICAL STUDY

Materials and Methods 87

Observations 99

Results 104

PART – IV: DISCUSSION 128

PART –V: SUMMARY AND CONCLUSION 145

BIBLIOGRAPHY

APPENDIX-CASE SHEET

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LIST OF GRAPHS

Graph No. Contents

1. Age groupwise distribution of patients

2. Percentage of patients of different sex

3. Percentage of patients of different religion

4. Incidence of Literacy

5. Percentage of patients of different marital status

6. Incidence of socio-economical status of patients

7. Occupation wise distribution of patients

8. Distribution of patients according to their habits

9. Prakriti wise distribution of patients

10. Vikruti wise distribution of patients

11. Percentage of patients according to Satva

12. Percentage of patients according to Sara

13. Percentage of patients according to Samhanana

14. Percentage of patients according to Satmya

15. Percentage of patients according to Abhyavaharana Shakti

16. Percentage of patients according to Aahara-Jarana Shakti

17. Percentage of patients according to Vyayama Shakti

18. Percentage of patients according to Vaya

19. Effect of Eranda Paka on cardinal symptoms of Amavata

20. Improvement in general symptoms recorded in patients treated with

Eranda Paka

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21. Over all effect of Eranda Paka on general symptoms of Amavata

22. Effect of Eranda Paka on symptoms of Ama

23. Effect of Eranda Paka on total symptom score of Ama

24. Effect of Eranda Paka on different clinical parameters

25. Effect of Eranda Paka on TLC

26. Effect of Eranda Paka on Hb%

27. Effect of Eranda Paka on ESR

28. Over all effect of treatment in 10 patients of Amavata

29. Effect of Ajamodadi Churna on cardinal symptoms of Amavata

30. Effect of Ajamodadi Churna on general symptoms of Amavata

31. Total effect of Ajamodadi Churna on general symptoms of Amavata

32. Effect of Ajamodadi Churna on symptoms of Ama

33. Total effect of Ajamodadi Churna on symptoms of Ama

34. Effect of Ajamodadi Churna on different clinical parameters

35. Effect of Ajamodadi Churna on TLC

36. Effect of Ajamodadi Churna on Hb%

37. Effect of treatment on ESR

38. Overall effect of Ajamodadi Churna in patients of Amavata

39. Comparison of the effect of treatment on the cardinal symptom of

Amavata

40. Comparison of effect of treatment on general symptom in two

groups

41. Comparison of effects on symptoms of Ama in two groups

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42. Comparison of effects on range of joint movement

43. Comparison of effects on foot pressure between the groups

44. Comparison of the effect on hand grip power

45. Comparison of effect on body weight

46. Comparison of effect on haemoglobin percentage

47. Comparison of effect on erythrocyte sedimentation rate

48. Comparison of overall effect of the treatments in both the groups

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LIST OF TABLES

Table No. Contents

1. Lakshanas of Amavata according to different authors

2. Properties and therapeutic effect of the individual drugs in Eranda

Churna

3. Properties and therapeutic effect of the individual drugs in

Ajamodadi Churna

4. Properties and therapeutic effect of the individual drugs in

Panchakola Phanta

5. Age Group of Patients

6. Sex Incidence of Patients

7. Religion of patients 20 patients of Amavata

8. Literacy incidence in patients of Amavata

9. Marital status of Amavata patients

10. Socio-economic status of patients

11. Incidence of occupation in Amavata patients

12. Study of Habit incidence

13. Study of patients Prakriti in the study

14. Incidence of Vikriti

15. Incidence of Satva in the Study

16. Study of Saratah Incidence in the Study

17. Study of patients Samhanana in the study

18. Satmya Incidence

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19. Study of patients Ahara-Abhyavaharana Shakti

20. Study of Patients Ahara-Jarana Shakti the Study

21. Study of patients Vyayama Shakti in the study

22. Vaya incidence

23. Effect of Eranda Paka on cardinal symptoms of Amavata

24. Effect of Eranda Paka on general symptoms of Amavata

25. Overall effect of Eranda Paka on general symptoms of Amavata

26. Effect of Eranda Paka on the symptoms of Ama

27. Overall effect of Eranda Paka on symptoms of Ama

28. Effect of Eranda Paka on circumference of limbs

29. Effect of Eranda Paka on different clinical parameters

30. Effect of treatment on body weight of patients of Amavata

31. Effect of Eranda Paka on different hematological values

32. Over all effect of treatment in 10 patients of Amavata

33. Effect of Ajamodadi Churna on cardinal symptoms of Amavata

34. Effect of Ajamodadi Churna on general symptoms of Amavata

35. Total effect of Ajamodadi Churna on general symptoms

36. Effect of Ajamodadi Churna on symptoms of Ama

37. Total effect of Ajamodadi Churna on symptoms of Ama

38. Effect of Ajamodadi Churna on circumference of the limbs

39. Effect of Ajamodadi Churna on different clinical parameters

40. Effect of Ajamodadi Churna on body weight of patients of Amavata

41. Effect of Ajamodadi Churna on different hematological parameters

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42. Over all effect of treatment in 10 patients of Amavata

43. Comparison of effect of treatments on cardinal symptoms of

Amavata

44. Comparison of effect on general symptoms

45. Comparison of effect on symptoms of Ama between the groups

46. Comparison of effect on different clinical parameters

47. Comparison of the effect on body weight in both the groups

48. Comparison of effect on different haematological values

49. Comparison of overall effect of treatment in two groups

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LIST OF CHARTS

Chart no. Contents

1. Schematic representation of Nidana of Amavata

2. Schematic representation of Samprapti in the light of Kriyakalas

3. Schematic representation of the evolution of Poorvaroopa

4. Schematic representation of the evolution of Roopa

5. Schematic representation of the evolution of Upadrava

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LIST OF ABBREVIATIONS

1. A.H. : Ashtanga Hridaya

2. A.P.I. : A.P.I.Text Book Of Medicine

3. A.S. : Ashtanga Sangraha

4. A.K. : Amarakosha

5. A.V.S. : Atharvaveda Sayana Bhashya

6. Basa : Basavarajeeyam

7. B.P. : Bhava Prakasha

8. B.R. : Bhaishajya Rathnavali

9. C.S. : Charaka Samhita A

10. C.D. : Chakra Datta

11. Ckr. : Chakrapani.

12. D.P.P.M. : Davidson’s Practice and Principles of Medicine

13. Dl. : Dalhana

14. D.N. : Dhanvantari Nighantu

15. D.G. : Dravya Guna Vijnana

16. E.M.P. : Essentials Of Medical Pharmacology

17. G.N. : Gada Nigraha

18. H.P.I.M. : Harrison’s Principle Of Internal Medicine

19. H.S. : Harita Samhita.

20. K.S. : Kashyapa Samhita

21. K.K. : Kalyanakaraka

22. K.N. : Kaiyadeva Nighantu

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23. M.K.A. : Malavikagnimitra

24. Madhu. : Madhukosha

25. M.N. : Madhava Nidana

26. M.P.N. : Madanapala Nighantu

27. R.P.B.D. : Robbin’s Pathologic Basis Of Disease

28. R.R.S. : Rasa Ratna Samucchaya

29. R.N. : Raja Nighantu

30. R.V. : Rugveda

31. S.N. : Saligrama Nighantu Bhushana

32. S.K.D. : Shabda Kalpa Druma

33. Sh.S. : Sharangadhara Samhita

34. S.S. : Sushruta Samhita

35. T.B.P. : Text Book Of Pathology By Harsh Mohan

36. Vag. : Vagbhata

37. Vang. : Vangasena

38. W.I. : The Wealth Of India

39. Y.R. : Yogaratnakara

ABBREVIATIONS OF STHANAS AND KHANDAS

1. Chi. : Chikitsa Sthana

2. Ind. : Indriya Sthana

3. Ka. : Kalpa Sthana

4. Ma.Kha. : Madhyama Khanda

5. Ni. : Nidana Sthana

Page 16: Amavata kc004 udp

6. Po.Kha. : Poorva Khanda

7. Sha. : Shareera Sthana

8. Si. : Siddhi Sthana

9. Su. : Sutra Sthana

10. Ut. : Uttara Tantra

11. Vi. : Vimana Sthana

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Introduction

INTRODUCTION

“Necessity is the mother of invention”, true to this sermon the invention:

“Ayurvedo Ayam” and the necessity “Rogastasysa Apahartaraha” Kasya?

“Shreyaso Jeevitasya cha”. Roga was hence the research problem, which led to

dawn of a philosophy, a religion, a science and the second important milestone

after the birth of man away from the land of immortals.

“Jignyasa Nama Pareksha” is a virtue that develops as a response to the

stimulus of a problem, which haunts a human being to restrict him in his

pursuits. Inventions like the microscope by Robert Koch, penicillin by Alexander

Fleming are examples of such responses from the recent past.

The history of medical science hence begins with the advent of Ayurveda

and takes many twists and turns gifting the modern world with awesome

discoveries and inventions enough to create a revolution. The revolution in

medical science has been progressing a lot since then as rightly put below.

“We can put it down as one of the principles learned from the history of

science that a theory is only overthrown by a better theory, never merely by

contradictory facts. Attempts are first made to reconcile contradictory facts to

the existing conceptual scheme by some modification of the concept. Only the

combination of a new concept with facts contradictory to old ideas finally brings

about a scientific revolution and when this has taken place then in short years

1

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Introduction

discovery follows upon discovery and the branch of science in question

progresses by leaps and bounds”.

-James B. Somnant

The process of research hence continues with renewed momentum

whenever a medical problem is encountered especially that which becomes

more knotty and mysterious each time attempts are made to decipher it. Ama

Vata or Rheumatoid arthritis (Y.N. Upadyaya) as perceived in modern parlance

is one such medical problems that cripples a man to an extent to render him

unfit for independent living. The patient experiences pain, which is so miserable

as to promote a statistical study on the suicide rates in Rheumatoid Arthritis

(RA) patients.

Leave alone the articular manifestation the extra articular effects on the

other systems are even more deleterious. In the musculoskeletal system it

causes skeletal muscle atrophy and osteoporosis, pleuropulmonary

manifestation of respiratory system, the vasculitis phenomenon of the vascular

system peripheral neuropathies of nervous system, scleritis and other

manifestation of opthalmic system, haematological manifestation like anaemia

and splenomegaly are the common complications of the disease. R.A. effects

approximately 0.8% of the population without race bias. Females are affected

three times more than males. Interestingly, studies indicate that climate and

urbanization have a major effect on the incident and severity of R.A. studies to

discover the mechanism of etiology, pathogenesis and treatment have been

2

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Introduction

inconclusive at best and the disease continues to elude the modern researches

in all perspectives of objectivity.

In this situation, the Ayurvedic viewpoint on the disease assumes

significant relevance, according to which Ama the toxic byproduct of a

transformative error in body’s metabolic homeostasis conjugates with Vata the

supreme controller of homeostasis and the prime Dosha to manifest the

symptoms of Ama Vata.

Ama is produced whenever the factors governing mechanisms that

render the gross nutrients assimilable and compatible to the body elements are

overwhelmed both at the digestive and metabolic levels. Though the major

sources of Ama is from the Adishtana of Jatharagni initiated by Prakupita

Doshas, it is also produced at the Dhatwagni level when the inherent

compatibility of an equilibrium of contradictions in the Gunas of Doshas are

disrupted, a concept consistent with the description of autoimmunity in modern

medicine.

The Ayurvedic approach to the treatment is the need of the hour as no

system is successful in providing the complete cure to this disease. A

comprehensive Ayurvedic management with Langhana-a concept over sighted

by the modern scientists as accidental and inconsequential, promises to make a

significant difference in the management of R.A. Among the Ayurvedic drugs

Eranda and Ajamoda are among the best Amapachakas and their effects in

3

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Introduction

Amavata has been hailed in Yogaratnakara. A well-organized clinical study

comparing the effect of Eranda Paka and Ajamodadi Churna is another attempt

to search an effective remedy for Amavata.

4

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Conceptual Study

HISTORICAL REVIEW

An offshoot of Atharva and Rigveda, this science of medicine is without

beginning, but Ayurveda saw throughout many people, who organized it into

beautifully woven treatises, incorporating newer diseases and their treatment

which cropped up during their times. It is evident in the Samhitas that the most

prevalent and deadly diseases have been devoted separate chapters were

included as secondary diseases under the major category.

Amavata might not have been widely prevalent and severely crippling as

it was during the time of Madhava Nidana, as we see only passing references

to the disease have been made in the Bruhatrayees. Madhava was the first

person to devote separate chapter for Amavata. Thus the birth of this disease

and its formative years can be glanced, starting from Vedic period.

Vedic period (5000 BC to 1000 BC):

Clear cut explanations of Amavata are not available in Vedic Samhitas,

but disease caused by Kapha have been more or less described under the

major heading Balasa, but the diseases of joints are not included here. Few of

references indicating arthritic syndromes have been quoted by Sayana. Such

as

Rapasi1: Disease arising due to sin (Rigveda) characterized by pain in

multiple joints also referred to as Papa. Yakshma and treatment with Jala, Vayu

Yava, Kushta have been indicated.

5

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Conceptual Study

Jayanya1: This disease is said to effect the bones cervical vertebrae

and arise from women through Sanga. Whether the disease refers to

rheumatoid arthritis is still not clear.

Grahi1 (Rigveda and Atharvaveda): This has been described as the

disease of joints but characteristic features have not been clearly mentioned.

Treatment of this disease with Dashavruksha has been mentioned.

Vatikrut1: This disease has been described as a serious ailment caused

by Vata and treatment with Pippali and Vishanashaka has been mentioned.

Sandhivikruti1 (Atharvaveda): This disorder is caused by Sleshma and

can be treated with prayers.

Samhita period (1000 BC TO 600 AD):

Charaka Samhita: Charaka has described in detail Ama and Ama

Pradoshaja Vikara and their treatment with Langhana and Ullekhana.2

Charaka had described treatment for Amavata while dealing with

Avarana Chikitsa in Vatavyadhi3 which indicate Pramehahara and Medohara

Vidhi. Amavata finds a mention in the list of therapeutic indication of Kamsa

Hareetaki4 in Shwayathu Chikitsa and Vishaladi Phanda in Pandu Chikitsa.5

The treatment of Shariragata Ama in Grahani Chikitsa by Charaka6 is

similar to the description of Amavata Chikitsa by Bhava Mishra i.e. Langhana,

6

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Conceptual Study

Pachana and oral administration of Panchakola Phanta7, same is the case with

Amavata Chikitsa of Chakrapani in Chakradatta7.

Sushruta Samhita: The description of Amavata in Sushruta Samhita is

conspicuous by its absence.

Bhela Samhita: The tenth chapter in Sutra Sthana deals with Ama

Pradosha. This description has some resemblance with that of Amavata.

Harita Samhita: A complete chapter on Amavata finds a mention in

Harita Samhita9. The classification of Amavata is quite unique and not followed

by any of the later works in this field.

Anjana Nidana: This work is claimed to be written by Acharya

Agnivesha, contains detailed description about etiology, premonitory symptoms,

clinical manifestations, complications.

Sangraha Kala (600AD-1600AD):

Astanga Sangraha and Astanga Hridaya have ignored the disease

though the word Amavata is included in the therapeutic index of compounds

Vatsakadi Yoga10 and Vyoshadi yoga10.

Madhava Nidana11: Madhavakara accorded this disease the status of a

independent disease and has dealt the topic threadbare.

Chakradutta: Chakrapanidutta has described the treatment for

Amavata8.

7

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Conceptual Study

Vangasena12 and Vrinda Madhava followed Madhava with few additions

in the treatment aspect. Works like Bhava Prakasha13, Yogaratnakara14 and

Bhaishajya Ratnavali15 have only corroborated the descriptions with additional

principles of treatment.

Adhunika Kala (1600AD onwards):

Mahopadhyaya Acharya Gananath Sen has coined the term Rasavata

for Amavata.

In Yoga Shastra the practice of Shushka Basti for improving Jatharagni

and treating Amavata has been mentioned16. Y.N.Upadhyaya (1955) has

corelated the disease with rheumatoid arthritis. Later research workers have

agreed with Y.N.Upadhyaya.

Modern History of Rheumatoid Arthritis:17

First Century AD: The rheumatoid/rheumatology is derived from the root

‘Rheuma’, which refers to a substance that flows and probably was derived

from phlegm, an ancient primary humor, which was believed to originate from

brain and flow to various parts of the body causing ailments.

1642 A.D.: The word rheumatism is introduced into the literature by the French

physician Dr.G.Baillou who emphasized that arthritis could be a systemic

disorder.

8

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Conceptual Study

1800 A.D.: Landre Baervier a physician from Salta Petruver in Paris, seemed to

have described the disease for the first time he called it Gartte Asthanique

Primitivae.

1857 A.D.: Sir Garrod proposed the name Rheumatoid Arthritis, Bannatyne

also in 1959 published his pathological observations on the disease but he

could differentiate it from Osteoarthritis only in his later edition.

1928 A.D.: The American committee for the control of rheumatism is

established in U.S. by Dr.R.Pemberton, renamed American Association for the

study and control of rheumatic disease (1934), then American Rheumatism

Association (1937) and finally American college of Rheumatology (ACR) (1988).

1940 A.D.: The terms Rheumatology and Rheumatologist are first coined by

Drs. Hollander and Comroe respectively.

1948 A.D.: Roses identified some criteria for diagnosis of RA.

1958 A.D.: American Rheumatic Association suggested uniform criteria for

diagnosis.

1987 A.D.: The criteria were revised.

In the beginning it was thought to be an infective condition especially in

early 20th century. French scientists thought it to be due to tuberculosis.

9

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Conceptual Study

Hench and Kendell introduced steroids in the management of

rheumatoid arthritis described paediatric onset, juvenile RA in 1896. Later Felty

A.R. described Felty’s syndrome.

Recent advancement in immunology have opened new vistas in the

management of RA. Unfortunately till date the etiology of RA is unknown the

pathogenesis is speculative, the treatment is only palliative and there is no cure

to this disease.

10

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History

REFERENCES:

1. History of Indian Medicine. P.V.Sharma

2. C.S.Vi. 2/13

3. C.S.Chi. 28/195

4. C.S.Chi. 12/51, 52

5. C.S.Chi. 16/162

6. C.S.Chi. 15/75-80

7. B.P.Madya.Kha. Amavata, Chi./14-16

8. Chakradutta 25/1

9. H.S.Tri.Stha. 21

10. A.H.Chi. 21/47

11. M.N. 25

12. Vang. Amavata Rogadhikara

13. B.P. 26

14. Yr.Po. Amavata Chikitsa

15. B.R. 29

16. Gheranda Samhita 1/49

17. Rheumatology Secrets.

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Conceptual Study

AMAVATA

In our classics depending upon the permutation and combination of

Doshas, involved Dhatus, Vedana, Adishtana, Avayava, Gati, specefic

symptoms and so on, naming of the disease is done.

The disease Amavata is named after the involvement of pathological

factors – Ama and Vata. These two are the central phenomenon of the disease.

Vyutpatti of Amavata:

1. Amam Cha Vatam Cha Amavatam:1 The word Amavata comprises of two

meaningful terms Ama and Vata which form the pathogenic basis of the

disease.

2. Amena Sahito Vata Amavata:2 This derivation highlights the propulsion of

Ama by Vata to produce Amavata.

3. Amo Apaaka Hetuh Vataha Swanaama Khyaata Rogavisheshaha:3 That

which is the result of improper digestion is Ama and with Vata the disease is

popularly known as Amavata.

Definition:

Yugapath Kupithavantaha Trikasandhi Praveshakau

Stabdham Cha Kuruthe Gatramamavathaha Sa Uchyate4

Amavata is a condition where Stabdhata of the body occurs due to

lodging of vitiated Ama and Vata in the Trika Sandhi.

11

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Conceptual Study

From the above definition it is clear that for well understanding of the

disease Amavata, it is necessary to know the role of Ama and Vata in detail.

AMA:

The first twin of the pathological duo of Amavata, Ama is the root cause

of all Vikaras more so in Amavata and it prompts a detailed study as discussed

below.

Etymology:

1. “Am+Nich”: ‘Am’ Dhathu with ‘Nich’ Pratyaya constitutes the word Ama.7

2. Amyate Gamyate Pakadyartham Iti Amah:7 The substance which goes into

the process of digestion is Ama.

3. Amyate Ishath Pachyathe:3 It means substance which is incompletely

digested or uncooked is Ama.

4. Amyate Peedyate Srotas Samooho Anena Iti Ama:7 Substance which harms

a group of Srotas is Ama. This etymology of Ama is nearer to the disease

Amavata.

Definition of Ama:

In Samhitas various definitions of Ama are available. Some of them are:

1. Usmano Alpa Balatvena Dhatumadyamapachitam

Dushtam Amashaya Gatam Rasamamam Prachakshyate8

Due to hypo-functioning of Ushma (Agni), the first Dhatu - the Rasa is

not properly formed; instead the Annarasa undergoes Fermentation or

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Conceptual Study

putrefaction (Dushta) and remains in Amashaya. It is this state of Rasa which is

spoken of as Ama.

2. Amasayasthaha Kayagnerdourbalyadavipachita

Adya Ahara Dhathuryaha Sa Ama Iti Keerthithaha9

This quotation gives the same meaning as above.

3. Avipakvam Asamyuktam Dourgandhyam Bahu Picchilam

Sadanam Sarvagatranam Amam Ityabhideeyate9

The substance which has not undergone Vipaka giving rise to foul

smelling and slimy substance causing Gatra Stabdhata in the body is termed as

Ama.

4. Aharasya Rasaha Shesho Yo Na Pakvo Agni Laghavat

Samoolam Sarvaroganam Ama Ityabhideeyate9

Because of Mandagni, the residue of Ahara Rasa which is immature,

forming the root cause of all diseases is labeled as Ama.

5. Amam Anna Rasam Kechit Kechit Malasanchayam

Prathamam Dosha Dushtim Cha Kechit Amam Prachakshate9

Here, the 3 different opinions about Ama are compiled by Vijaya

Rakshita. First view is about the improperly digested food and the second

describes the accumulation of Malas in the different parts of the body.

According to the third view, the first stage of Dosha Dushti is Ama.9

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ETIOLOGY OF AMA:

The causative factors of Ama are described detailed in Charaka

Samhita10,11. These can be classified into Aharaja, Viharaja, Manasika and

Anya Hetuja.

Aharaja Hetu:

Abhojana (not taking food), Atibhojana (excessive consumption of food)

Ajeerna Bhojana (taking food before the previous food gets digested), Asatmya

Bhojana (taking unwholesome food), Viruddha Bhojana (simultaneous

consumption of food having antagonistic properties). Consumption of Dwishta

(unpalatable), Ashuchi Ahaara (unclean food), Rooksha, Sheeta, Shushka,

Vishtambhi Vidahi Bhojana.

Viharaja Hetu:

Improper administration of Samshodhana and Snehana, Vega

Vidharana, Prajaagara and Dukhashayya (sleeping on uneven mattress) can

also initiate production of Ama.

Manasika Hetu:

Food consumed by a person in the state of Bhaya, Krodha, Shoka also

leads to Ama Utpatti.

Anya Hetu:

Desha, Kaala, Rutuvaishamya, Vyaadhikarshana are mentioned as the

causative factors for Ama.

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LAKSHANAS OF AMA:12

The following explains the generalized symptoms with their

etiopathogenesis of manifestation which may be later modified by individual

Doshas to show its specific presentations.

Symptoms Etiopathogenesis

Srotodushti Picchila and Snigdha Guna of Ama

Balabramsha Mandagni causing lack of nutrients

Gourava Snigdha, Picchila, Guru Gunas of Ama

Alasya Snigdha, Picchila, Guru Gunas of Ama

Malasanga Disturbance to Vata by Srotorodha

Anila moodhata Disturbance to Vata by Srotorodha

Apakti The qualities of Ama in turn leads to

Agnimandya forming a vicious cycle

Nishteeva Madagni causing Kaphotklesha

Aruchi As a result of Ajeerna

Klama Due to Dhatvagnimandya

Above said symptoms are the general symptoms produced by Ama.

Further, when this Ama comes in contact with Dosha, Dushya and Mala it is

termed as Sama Dosha, Sama Dushya and Sama Mala. Assessment of Sama-

Nirama is very much helpful for the treatment.

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SAAMA DOSHA LAKSHANAS:5

If Ama combines with the Vayu then it gives rise to Vibandha

(constipation), Mandagni (impaired digestion), Stambha (stiffness), Antra

Kujana (gurgling sound). Further, Vedana (pain), Shopha (edema), Nistoda (pin

prick sensation) gradually affects the body parts one after the other. The

Lakshanas will aggravate during morning hours, night hours, during cloudy

days, and by Snehana. Sama Pitta is durgandhayukta, Amlarasa, Harita-shyava

Varna and is Guru Sama Kapha is Durgandhayukta, Avila, Tantula, there by

sticks to Kanta Pradesha, prevents Udgara.

NIRAMA DOSHA LAKSHANAS:5

Nirama Vayu shows Alpa Vedana, Nirvibandha and has Ruksha and

Vishada qualities, Vedana subsides on Snehana. Nirama Pitta is of Tamra or

Peeta Varna, Ushna, Katu Rasa, Sara, Vigandha and improves the Agni and

Ruchi. Nirama Kapha is Phenavat, Pindita, Nirgandhi and has Pandu Varna,

Vaktra Shuddhi will be there as it comes out easily. Separate symptomatology

of Sama Dushya has not been mentioned as the manifestations are similar to

the Dhatu Pradoshaja Vikaras itself.

CONCEPT OF AMA:

In other words, Ama reflects the products of deranged homeostatic

mechanisms in the body. This clogs the controlling centers and pathways of

normal physiologic functions marking the beginning of pathogenesis in the form

of Sammurcchana of Nidana, Dosha and Dushya.

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In Ashtanga Hridaya Doshopakramaniya Adhyaya, Acharya Vagbhata

has described in length about the treatment of vitiated Doshas in the form of

Vatasyopakrama, Pittasyopakrama, and Kaphasyopakrama. Later, he highlights

the formation of Ama and its treatment. He has given equal importance to Ama,

as that to Dosha. The presence or absence of Ama i.e. Sama Avastha and

Nirama Avastha decides the line of treatment of disease.5

MECHANISM OF PRODUCTION OF AMA - A PERSPECTIVE:13

Physiology:

A normal homeostatic function involves input from the food, processing

by the action of Agni at the levels of Amasaya, Mahabhoota and Dhatus,

transformation of the raw materials in to the vital elements (Sara) consistent

with tissue compatibility and waste products (Kitta or Malas) warranting

expulsion. This process affects the nourishment of Dhatus, development and

maintenance of Vyadhikshamatva (the capacity of the body to resist the disease

onslaught) initiated by Kshut (appetite), Trit (thirst) and Malavisarjana

(excretion).

Hence, the total body homeostasis is the augmented effect of non-

defective functioning of the multiple organizations called Srotases. Each Srotas

has a feeding point, a target point, a controlling center (Srotomula) and a

pathway (Srotas) and its function is appropriate transformation of the input raw

material in to a finished product with elimination of the waste product, effected

by the transformative principle Agni.

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Pathology:

The Vikara or Dhatu Vaishamya is hence a defective transformation,

giving rise to a morbid finished product. The cause for which may exist in the

raw material provided, the Srotomula, the Srotas or in the target tissue, in the

backdrop of impaired Vyadhikshamatva, effected by vitiated Agni and inflicted

by Doshas.

The resulting incompletely transformed product or Ama exhibits certain

characteristic features, it is neither suitable for absorption nor is the body

capable of excreting it. It is toxic and hence hinders the normal functions of the

Srotases. The severity of morbidity is directly proportional to its accumulation.

LEVELS OF EXISTENCE OF AMA:

As mentioned above, the Ama exists at three levels in the body.

A) Ama at Jatharagni level: Amashaya is the substratum of Jatharagni, when

the vitiated Agni acts upon the Ahara, it fails to completely transform Ahara into

nourishing moieties. The resulting Ahara Rasa is a mixture of formed and

unformed elements called Ama, which is thrown out of the Amashaya through

the Urdhwamarga by the Chardi (vomiting) and through the Adhomarga

(diarrhoea), or it may get displaced into the Grahani to remain stagnant. Due to

prolonged stagnation, it may assume the properties of Visha. Further, Ama may

associate with the Doshas, Dhatus and Malas after getting absorbed from

Amashaya and manifest symptoms related with each of them.

Dietetic indiscretions and emotional stresses may between them impair

the functioning of the neurohumoral mechanisms responsible for ensuring

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proper secretion of the digestive juices, the disturbances of the pH in the

gastro-intestinal environment and more often sluggish and sometime hyper-

motility of the stomach and intestine, thus leading to Shuktata or Shuktapaka

where food will be Avipakva, Asamyukta, Bahupicchila and Durgandha, due to

fermentation and putrefaction of the carbohydrate, fat and protein components.

Thus causes the toxic state - Visharupatvam.

This pathogenesis may cause the following metabolic disturbances

• Toxic states:

1. Intermediate toxic byproducts of metabolism

2. Superadded microbial action

• Malnutritional states

Intermediate toxic by products of metabolism: It is clear from the texts that

Sama Ahara Rasa induces the production of various deranged metabolites like,

i. Sama Dosha: In Avasthapaka, there will be Udeerana of the Doshas i.e.

Madhura Avasthapaka – Kapha (Amashaya),

Amla Avasthapaka – Pitta (Pittashaya)

Katu Avasthapaka – Vata (Pakvashaya)

But, due to Apakva Ahara produced by Mandagni, there will be

Udeerana of Dushita Dosha called as Samadosha. Further in Nishthapaka, due

to affliction of Rasa and Rakta Dhatu, there will be further increase of vitiated

Kapha and Pitta in the form of Mala thus contributing to Sama Dosha.

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ii. Bhutagni and Dhatvagni Mandya: Jatharagnimandya will lead to

Bhutagni and Dhatvagni Mandya also. Jatharagni is the Poshaka to the

different Agni of the body, but Bhutagni and Dhatvagni can even get

vitiated independently i.e. irrespective of Jatharagnimandya. Apakva

Ahara from Avasthapaka when gets treated by Manda Bhutagni and

Dhatvagni further causes Vikrita or Dushita Nishthapaka.

a) Sama Dhatu: With affliction of both Avastha and Nishthapaka, the Dhatu

Poshaka Rasa produced is Vikruta. Thus, with production of Sama Rasa

Dhatu, succeeding Dhatu will also get vitiated producing Dhatu

Pradoshaja Vikara. Sama Dhatu Utpatti is due to Bhutagni and

Dhatvagni Mandya but it can even be independent of Jatharagni status.14

b) Sama Mala: The word Mala includes 2 entities.

• Mala of Ahara Rasa i.e. Pureesha, Mutra and Sweda and also the

other Dhatugata Malas.

• Dushita Dosha and Dhatu are also called Mala

Superadded microbial action: Toxins in the intestines in the present days are

greatly attributed to the action of different microbes, thus leading to different

manifestations like:

• Infective gastro-enteritis

• Toxic gastro-enteritis

• Botulism

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Intestinal flora in the human body exists in the state of symbiosis; these

can be very well compared with Sahaja Krimi. Chakrapanidatta15 explains them

as the one which exists within the body without causing diseases. Intestinal

flora breaks the complex molecule which are not broken by the body,

metabolises them into simple molecules by 2 kinds of actions. They are

Fermentation and Putrefaction.

Putrefaction is similar to fermentation but it specifically refers to

conversion of protein substances to smaller molecules with the liberation of

various gases viz. Indol, Skatole, Phenol, Hydrogen sulphate and Ammonia that

are characteristically pungent in odour. Fermentation is related to the

Carbohydrate and fat metabolism by the microbes. Microbe’s metabolism

releases few of the waste products vital for the body like Vit. B groups.

Among these microbes, there are some in borderline populations which

under circumstances become parasitic. There are other groups of virulent

organisms which invade body through food and drinks, producing abnormalities

in the body. e.g.: Salmonella, Staphylococcus, B. botulinus, B. typhosus and

coma bacillus of Koch. Hence, the normal food metabolism also includes the

metabolism by Intestinal flora (Sahaja Krimi).

The following are circumstances which make the body susceptible to the

infection.

• Irradiation, metabolic abnormalities, emotional stress, overstrain, intense

treatment with anti-microbial agents

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• Tissue produces an anti-microbial substance called Properdin. It has

been shown that a low concentration of this substance in an area

coincides with the highest susceptibility to the invasion of the tissue even

by otherwise friendly intestinal flora causing bacteremia.

• Experiments carried out at the Rockfeller institute and other research

centers in U.S.A. have shown that susceptibility to microbial disease can

be caused by manipulation of metabolism. e.g.: with such simple

measures as temporary deprivation of food or feeding an unbalanced

diet rich in Citrate. The resistance was again seen to have been restored

back to normal within 2-3 days by the correction of nutritional errors.

• But in case of epidemics and pandemics the microbes strike human

irrespective of body strength, constitution and other predisposing factors.

Interestingly, this phenomenon is observed when a microbe is newly

introduced in a susceptible population which serves as a virgin soil.

Ama is the immediate cause of most human affliction, exposure to

disease causing microbes results in the disease only in those people where

internal conditions are ripe for colonization. Louis Pasteur and Claude Bernard

argued for years over the primacy of infective agents versus internal conditions,

and it was only on his deathbed that Pasteur finally admitted that Bernard was

right and that the milieu interior is more important than exposure to a pathogen.

This is especially true of diseases in which no pathogen can be detected.6

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Hence, different microbial infection occur in the body when it is made

susceptible by predisposing factors like metabolic abnormalities, emotional

stress, overstrain and other Agnimandyakara and Amotpattikara Nidana.

Malnutritional states:

In chronic disorders, due to Agnimandya or Amotpatti, there will be

predominant manifestation of Dhatukshaya as it is told in Vatavyadhi context

that the Avarana will cause Rasadi Dhatu Kshaya. Depending on the speed of

manifestation, disease can be

• Acute

• Sub-acute and Chronic

Acute conditions include Visuchika, Jwara, Atisara, Pravahika and so on.

Sub-acute and chronic conditions include Grahani Dosha, Udara roga, Pandu,

Amavata, Prameha and so on.

B) Dhatvagni level:

The Ama at Dhatvagni level occurs due to vitiated Dhatvagni first as a

result of a direct influence from Jatharagni as the Dhatvagnis are derivatives of

Jatharagni and Jatharagni hyperfunction or hypofunction results in respective

derangements of Dhatvagnis too16. Secondly, as a result of Dhatvagni

malfunction independent of Jatharagni. The hypofunction of Dhatvagni leads to

morbid increase of the Dhatu involved and hyperfunction leads to its morbid

decrease. The Ama hence formed gets associated with these morbid Dhatus to

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form Sama Dhatus resulting in manifestation of symptoms explained under

Dhatupradoshaja Vikara17.

C) Bhutagni level:

The Ama at the Bhutagni level occurs as a result of Bhutagnimandya, the

mechanism of formation is similar to that mentioned under Dhatvagni level. The

symptoms produced are Shosha, Vrana, Vidradhi and similar diseases18.

Ama as a result of Malasanchaya:9

The Malas (waste products) produced at various levels in the body, when

accumulates beyond tolerable limits also constitutes Ama. The Mutra and

Pureesha are the Malas of Ahara, Kapha that of Rasa, Pitta of Rakta, Vasa and

Khamala of Mamsa, Sweda of Medas, Loma, Asthi and Tvacha Sneha and

Akshi Vit of Majja19. The Shukra is the essence of all Dhatus and it does not

have any Malas. The excessive accumulation of these Malas (Mala Sanchaya)

therefore gets to be called Ama as they are harmful to the normal physiology of

the body.

Production of Ama independent of influence of Agni – as a result of Dosha

Anyonya Sammurcchana:

Strangely, the Doshas exist in the body in an equilibrium of mutually

paradoxical Gunas of Doshas; this equilibrium is inherent and compatible with

the normal bodily functions. This has been called as “Sahajasatmya”32 by

Charaka. This unique coexistence has been compared to the existence of fatal

poison in a serpent without harming it, by Vagbhata. Nevertheless this

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equilibrium sometimes may get disturbed due to excessive aggravation of

Doshas, and the Doshas start affecting each others’ Gunas resulting in the

production of Ama. This process is on the analogy of the production of toxic

material when the grains like Kodrava are kept in water for a long time, this

Ama is highly virulent and can cause incurable diseases. The schematic

representation of the same is given in the chart no. 1.

An interesting feature of this concept is its close resemblance to the

concept of auto immunity in the modern parlance. The Major Histocompatibility

Complex determined by Human Leukocyte Antigens marks the surface proteins

of all the cells of the body. This helps the T cells (responsible for Cell mediated

immunity) to recognize the self antigens from the non-self. When this

mechanism fails, the immune system starts secreting antibodies against body’s

self proteins producing crippling and fatal diseases. They are called Auto

immune diseases and Rheumatoid arthritis is one among them.

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VATA:

The second of the duo Vibhu as it is called Vata in its Prakruta Avastha

sustains the human body. When it becomes Vimarga is responsible for fatal

ailments. The pathogenic sequence of Vatic vitiation requires a comprehensive

background as discussed below.

Nirukti:20

The Nirukti of Vata is as follows, the term Vata is derived from the root

“Va” with “Tan” Pratyaya, it forms the word Vata. The root Vata summerises the

essential Karma of Vata-Gati and Gandhana.

Guna:

Ruksha, Sheeta, Laghu, Sukshma, Chala, Vishada, Daruna and Khara.21

Bheda:

There are five classification of Vata Dosha based on the location and

function. They are Prana, Udana, Samana, Vyana and Apana.22

Karma:23

Vata Dosha has complex psycho somatic integrative function. They are:

Tantra Yantra Dhara (upholds the structure and function of body), Chesta

Pravartaka (motivates the movements), Praneta Niyanta Cha Manasa

(controller and conductor of Mana), Sarvendriyanam Udyojaka (stimulates all

sensory function), Sarvendriya Artha Abhivoda (carrier of all sensory impulses),

Dhatu Vyoohakara (integrator of body elements), Shareera Sandhanakara

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(integrates of bodily structure and function), Vak Pravartaka (stimulator of

speech), Shabda Sparsha Prabrith (cause of feeling and audition), Srota

Sparshayoho mula (primary source of auditory and tactile sensation), Harsha

Utsahayoho Yoni (originator of excitement and animation), Agni Sameerana

(stimulator of Agni), Dosha-Samshoshana (desicator of morbid Dosha), Mala

Kshepta (cleanses the body channels), Garbha Akriti Karta (gives shape to the

fetus), Ayushya Anuvritti (sustainer of life).

Importance:

Following opinions shows the importance and supremacy of Vata:

Charaka opines that the Vayu in its abode with unimpaired functions in

its normalcy, facilitates the Ayus of an individual to be hundred years.24

The Pitta, Kapha, Mala and Dhatus are inert (Pangu) until mobilized by

Vata, which takes them to get localized in specific location and cause disease,

hence Vata controls all other Doshas Dhatus and Malas.25

Vata, Pitta and Kapha are circulating all over the body, Vata the subtle

among them provokes Kapha and Pitta and causes them to lodge in various

places from where the disease originates. The Pitta and Kapha hence occludes

the channels of Vata, thus vitiating Vata; it also gets vitiated by diminution of

tissue elements which may be an independent cause or an effect of occlusion.26

Etiological factors of vitiation of Vata:

Etiological factors which vitiate Vata can be brought under Aharaja,

Viharaja, Manasika and Anya Hetuja.

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Ahara:

Ruksha Ahara (dry food) Sheeta Ahara (cold foods) Alpa Ahara

(subnormal quantity), Laghu Ahara (light food).27

Vihara:

Vyavaya (excessive indulgence in sex), Atiprajagara (night vigil),

Vishama Upachara (improper nourishment), Rakta Atisravana (removing Dosha

and Rakta in excess), Langhana (excessive fasting), Plavana (excessive

swimming), Atyadva (walking excessively),27 Atichesta (excessive improper

body movement), Dukhashayya Asana (uneven mattresses), Divaswapna (day

sleep), Abhighata (trauma), Marmaghata (injury to vital organs), Patana (falls).28

Manasika Karanas:

Includes Chinta (depressive episode), Shoka (depression), Krodha

(excessive anger) and Bhaya (fear).28

Anyahetuja:

Dhatu Sankshaya (depletion of tissue elements) and Rogatikarshya

(emaciation due to disease).28

Symptoms of Vata Prakopa:

Parva Sankocha (contractures), Stambha (immobolity), Asthi Parva

Bheda (painful bones), Lomaharsha (piloerrection), Pralapa (irrelevant speech),

Pani Prishta Shirograha (stiffness of hands, hip, joints of head), Kanja Pangu

(disability of lower limbs), Kubjata (loss of normal lumbar curvature), Anga

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Shosha (wasting), Anidrata (insomnia), Garbha Shukra Rajonasha (disease of

reproductory system), Spandana (involuntary movements), Gatra Suptata

(sensory system abnormality), Shiro Hundana (disorders of scalp), Nasa

Hundana (disorders of olfaction), Jatru Hundana (cervical ankylosis), Griva

Hundana (stiffness of neck), Moha (altered consciousness), Alasya (lethargy)

and Akshepa (convulsive fits).29

Symptoms of Vata Kshaya:

Kshaya of Vata leads to Manda Cheshta (decreased activity), Alpavak

(decreased speech), Apraharsha (erectile dysfunction) and Mudha Samjnyata

(altered consciousness).30

Chikitsa:

Sneha (fatty substance), Swadu, Amla Lavana, Ushna Bhojana (food of

sweet, saline and hot properties), Paishtika or Goudika (types of Madhya),

Abhyanga (external oleation), Mrudu Samshodana (light eliminative therapies),

Mardana (massage), Veshtana (tying clothes), Trasana (supportive

psychotherapy), Seka (stream of oil over the body) and Snigda Ushna Basti

(enemas having Snigda Ushna properties).31

In Amavata, Ama formed will be circulated through out the body by

vitiated Vata, this Sama Vata is responsible for vitiating other two Doshas. So

understanding of Vata is essential in treating Amavata.

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REFERENCES:

1. M.N. 25/2-5

2. M.N. 25/2

3. S.K.D.

4. M.N. 25/5

5. A.H.Su. 13/27-28

6. Ayurveda Life Health and Longevity, RE Svoboda, Pg.162

7. A.K.

8. A.H.Su. 13/25

9. M.N. 25/1-5, Madhu

10. C.S.Chi. 15/42-43

11. C.S.Vi. 2/8

12. A.H.Su. 13/23-24

13. Introduction to Kaya Chikitsa, Dwarakanath

14. S.S.Su. 15/13

15. C.S.Vi. 7/9

16. C.S.Chi. 15/39

17. C.S.Su. 28/8-22

18. Atanadarpana, M.N. 6/22

19. C.S.Chi. 15/18-19

20. S.S.Su. 21/5

21. C.S.Su. 12/4

22. S.S.Ni. 1/11-12

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23. C.S.Su. 12/8

24. C.S.Chi. 28/4

25. Sh.S.Po.Kha. 5/25

26. C.S.Chi. 28/60, 61

27. S.S.Su. 21/19

28. C.S.Chi. 28/15-18

29. C.S.Chi. 28/20-23

30. S.S.Su. 15/7

31. A.Hr.Su. 13/1-3

32. C.S.Chi. 26/293

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NIDANA

The word creation is a neologue. It should be actually called as

evolution. Similarly destruction is called involution, because something can

come from something not from nothing.

Circumstances favoring the evolution of a existence is the cause. The

effect can be useful or harmful. Man’s indulgence governs the good or bad

effects he has to enjoy. If his indulgence is Hita, leads to peace. If it is Ahita,

leads to commotion. Besides, the contents of ahita are highly disease specific.

Though being common to quite a few diseases, they lead only to Amavata.

Identifying the causative factors and understanding the role of these

causative factors in the manifestation of the disease is utmost important to

make a proper diagnosis, to predict prognosis and to plan treatment.

Invariably two factors are responsible for the manifestation of the disease

Amavata. As the name indicates, Ama and Vata are those two factors. The

Anjana Nidana author opines Ama and Vata get vitiated due to their own

respective causes to promote disease. Hence, individual etiological factors

responsible for the vitiation of Vata and those etiological factors which produce

Ama may also be considered as etiological factors of Amavata.

Madhavakara has explained following Nidanas for Amavata.1

1. Viruddha Ahara (incompatible diet)

2. Viruddha Cheshta (Erroneous habit)

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3. Mandagni (diminished digestive fire)

4. Nischalata (Sedentary habits)

5. Vyayama soon after Snigdha Ahara.

Besides this, Harita opines that a person consuming Guru Ahara, Kanda

Shaka (tubers) in excess and indulging in excessive Vyavaya is the Nidana of

Amavata.2

To sum up, the causative factors of Amavata can briefly be classified in

to two.

1) Viruddha Ahara- unwholesome diet.

2) Viruddha Cheshta- erroneous habit.

Now it is very important to know what is Viruddha, as Viruddha itself is

the root cause of the disease Amavata. The factors which cause Dosha

Utklesha (vitiation) but do not have the capacity to eliminate those Doshas out

of the body are considered as Viruddha.3

Charaka has elaborately mentioned regarding Viruddha Ahara and

categorized these into 18 types.4 They are Desa (Habitat) Viruddha, Kala

(season) Viruddha, Agni (digestive power) Viruddha, Matra (dose) Viruddha,

Satmya (compatibility) Viruddha, Dosha Viruddha, Samskara (processing)

Viruddha, Veerya (potency) Viruddha, Koshta (bowels) Viruddha, Parihara

(proscription) Viruddha, Avastha (state of health) Viruddha, Krama (order)

Viruddha, Upachara (prescription) Viruddha, Paka (cooking) Viruddha,

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Samyoga (combination) Viruddha, Hrit (palatability) Viruddha, Sampath (quality)

Viruddha, Vidhi (rules of intake) Viruddha.

Besides Charaka also considers the Brashta Niyama of Ashta Vidha

Ahara Vidhi Vishesha Ayatana5 as unwholesome. These Ashta Vidha Ahara

Vidhi Vishesha Ayatana are Prakriti (Natural food habits), Karana (Method of

processing), Samyoga (Combination), Rashi (Quantity), Desha (Habitat), Kala

(Time), Upayoga Samstha (Rules governing intake of food), Upayoktru (The

person who is taking the food).

Viruddha Cheshta includes a wide variety of causative factors. They are

consumption of Snigdha Ahara and doing Vyayama immediately, Sheetoshna

Vyatyasa (alternative use of Sheeta and Ushna), use of Sheetodaka at once

during Bhaya Shrama and so on, Vega Vidharana (suppression of natural

urges), Vega Udeerana (provoking of natural urges), Diva Swapna (day sleep),

Ratri Jagarana (night vigil), Sahasa (act beyond capacity), Karma Kalatipata

(avoidance of medication).

The causative factors of a disease operate in varied patterns in the body

to cause the disease. This depends upon the level of predisposition, in other

words the extent to which the environment is made favorable for the interaction

of Nidana, Dosha and Dushya.6

The capacity of the body to resist this interaction is called Vikara Vighata

Bhava or Pratyaneeka Bala. This Bala differs from person to person. That is

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why we see that inspite of exposure to Nidanas, some people do not develop

the disease and some develop severe disease with negligible exposure. Further

it is also seen that a single causative factor leads to development of many

diseases and many Nidanas are needed for the manifestation of a single

disease.7

Hence, not withstanding the list of Nidanas implicated to cause the

disease Amavata, it is ultimately the Vyadhikshamatva which renders a patient

vulnerable.

Thus Viruddha Ahara and Cheshta are accepted as the causative factors

of disease Amavata. But Viruddha Ahara and Viruddha Cheshta need not

cause same disease in everyone i.e. all the unwholesome diet and erroneous

habits may not vitiate the same Dosha and also vitiation need not be of same

grade as every individual do not have the same Vyadhikshamatva (immunity).8

Schematic representation of Nidana is given in the chart no. 2.

Etiology of Rheumatoid Arthritis:10

The disease Amavata is best compared with Rheumatoid arthritis in the

modern parlance.9 Rheumatoid arthritis (RA) is a chronic multisystem disease

of unknown cause. It has been suggested that RA might be a manifestation of

the response to an infectious agent in a genetically susceptible host. Because

of the worldwide distribution of RA, it has been hypothesized that if an infectious

agent is involved, the organism must be ubiquitous. A number of possible

causative agents have been suggested, including Mycoplasma, Epstein-Barr

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virus (EBV), cytomegalovirus, parvovirus, and rubella virus, but convincing

evidence that these or other infectious agents cause RA has not emerged. The

process by which an infectious agent might cause chronic inflammatory arthritis

with a characteristic distribution also remains a matter of controversy. Recent

work has focused on the possible role of "superantigens" produced by a number

of microorganisms, including staphylococci, streptococci and M. arthritidis.

Superantigens are proteins with the capacity to bind to HLA-DR molecules and

particular Vb segments of the heterodimeric T cell receptor and stimulate

specific T cells expressing the Vb gene products. The role of superantigens in

the etiology of RA remains speculative. Of all the potential environmental

triggers, the only one clearly associated with the development of RA is cigarette

smoking.

Sero positive RA aggregates in families Genetic factors versus their

interaction with environmental facilitators is unclear HLA DR4 is found in 70% of

causascian sero positive patients compared to 25% of controls. Increased

relative risk of 4-5 times for the DR4 positive persons, although a minority are

affected African Americans tend not to exhibit this predilection.11

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Chart No. 1-Schematic representation of Nidana of Amavata:

kashaya, tikta, katu ruksha laghu, sheeta, shushka shaaka vallura, uddalaka, kora dusha, shamaka, vishamashana, adhyashana

Aharatah

Vataja nidana

AtimRuShVisVidVirAka

A

Viharatah

manasika ati shoka, chinta, bhaya, krodha, kshobha,

Shareerika Ativyayama, prapatana, bhagna, ratrijagarana, vegadharana, ativyavaya, raktati sravana.

SVVcRAVVS

NIDANA

atra, Guru ksha, Sheeta ushka, Dvishta htambhi ahi, Aruchi uddha la annapana

haratah

Amaja nidana

Viruddha ahara Shaka Katu ahara Guru ahara Mandagnikaraka

Aharatah

Amavataja nidana

Viharatah Viharatah

hareerika egavarodha, iruddha heshta, atri jagarana, yoga of amana, irechana and nehana

Manasika Kama, Krodha, Lobha, Moha, Irshya, Hree, Shoka, Mana, Udvega Bhaya, Bhojana with these Upatapta manas.

Viruddha Cheshta- Nischalata,Vyayama, Mandagni Karaka.

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REFERENCES:

1. M.N. 25/1

2. H.S. 21/1, 2

3. A.Hr. 7/45

4. C.S.Su. 28/86-89

5. C.S.Vi. 1/21

6. C.S.Ni. 4/4

7. C.S.Ni. 8/24

8. C.S.Su. 28/7

9. Y.N. Upadhyaya

10. H.P.I.M., 14th edition, pg.1880

11. CIMS, 5Min, Clinical Assistance, pg.88

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SAMPRAPTI

The pathology of a disease is not always simple; rather it involves

various intricate and sequential mechanisms. This has to be unraveled for the

proper understanding of the disease and then to plan successful treatment.

Intricate mechanisms of the disease process are best understood by means of

Samprapti of the disease.

As elaborated under the title Nidana it is clear that the illness Amavata is

basically caused by the Viruddha Ahara as well as Cheshta. More over this

phenomenon of Viruddha Ahara may not be similar in every patients rather it is

individual specific. This etiology of Viruddha Ahara in the form of Bahya Nidana

is said to be incriminatory in three distinct ways ultimately resulting in the

establishment of the disease. On exposure to Viruddha Ahara it may cause

morbidity of Dosha, impair the functioning of the Jataragni or else it may lead to

the formation of more virulent Amavisha.1

Dosha Dushti:

Consumption of Viruddha Ahara precipitates morbidity of Doshas.2 Due

to the deleterious effect of the Viruddha Ahara, any Dosha may get vitiated or

else any combination of the two Doshas or all the three together. These vitiated

Doshas in turn afflicting the specific Dushya manifests as illness, pertaining to

Amavata. By the deleterious effect of the Viruddha Ahara, there occurs the

morbidity of the Vata Dosha. The clinical manifestations like Anaha, Antrakuja,

Vibandha, Sandhi Sula, Sandhi Jadyata etc are suggestive of vitiation of Vata

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Dosha at different levels. By definition, this Viruddha Ahara only influences the

generation of morbid Doshas, and is incapable of its removal from the body.

Agni Mandya and Amotpatti:

Intake of Viruddha Ahara has detrimental effect on the functioning of the

Jataragni. As mentioned by Acharya Charaka, intake of Viruddha Ahara leads

to Agnimandya which in turn generates the virulent Ama in the body.3 Invariable

involvement of Ama is characteristic of the disease Amavata. Both Koshtagata

as well as Shareeragata Ama are the hallmarks of the pathogenesis of

Amavata. Reduction in the Abhyavaharana Shakti and Jarana Shakti,

symptoms like Praseka, Aruchi, Apakti, Malasanga and similar other symptoms

are indicative of Koshtagata Ama5. Shareeragourava, Alasya, Klama, Sandhi

Shotha, Staimitya are the other common clinical features of Amavata

suggestive of Shareeragata Ama5,6. Moreover, the symptom complex of

Amavata is more indicative of combined effect of Ama as well as morbid Vata

and is popularly known as Samavata4 state. Progressive involvement of the

joints in the form of severe pain and swelling, worsening of the symptoms by

the application of the oil, more severity of the symptoms at the time of sunrise,

as well as on appearance of the clouds in the sky4, all are the typical features

indicative of Samavata state in the disease Amavata.

The Ama and morbid Vata, stemming out from Amashaya circulates in

the whole body. The properties of the Samavata being similar to that of the

Kapha Dosha, Ama and morbid Vayu exhibits an affinity to get lodged in the

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Kapha Sthana. More particularly the vitiated Vata Dosha along with Ama tend to

get localized in the joint. With in the joint, these two pathological factors

undergo a pathological union with the naturally present Doshas in the joints. It is

said that by the interaction with the naturally present Doshas in the joint the

Ama and morbid Vata acquires further virulence and then manifests as

Amavata. Here, the interaction with in the joint causes the generation of

Amavisha1. Perpetuation of the illness for a long duration destroying the joints

is analogous to the effect of Garavisha12 in the body. Progressive damage that

occurs for long is very characteristic of Garavisha. Similarly the pathological

interaction between normal Doshas present in the joint and the morbid Vata as

well as Ama getting localized in the joint, is akin to the damaging effect of the

Garavisha, and hence is named as Amavisha. Thus relating this to the

causation of the illness, indulgence of Viruddha Ahara ultimately culminates in

the generation of Amavisha. Similar to Garavisha, this Amavisha gradually

causes destruction of the body. Later, during the course of the disease,

permanent destruction of the joints results in the Anga Sankocha8, Jadyata8,

Anga Vaikalya10 etc, totally incapacitating the patients and restricting him to the

bed.

Dhatu Dushti:

Deleterious effect of the Viruddha Ahara is not restricted to the Dosha

and Agni, rather it badly influences the Dhatu even. This nature of the Viruddha

Ahara is described as Dhatupratyanika13 effect. It is worth mentioning here that

the Viruddha Ahara is considered as an etiology of Majjavaha Sroto Dushti14

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and the Mula of the Majjavaha Srotas17 being Asthi and Sandhi, this implies the

detrimental effect of the Viruddha Ahara on the Asthi and Sandhi wherein the

disease Amavata manifests. The symptoms like Sandhi Shotha, Sandhi Shoola,

Bhedanavat Shoola in Asthi and Parva Pradesha, Mamsa Kshaya, Sandhi

Sankocha etc. are suggestive of Asthimajja Gata Vata15 and Sandhi Gata

Vata16 in the disease Amavata.

So to say, the indulgence of Viruddha Ahara causes morbidity of Vata

Dosha, generates the Ama, afflicts the Dhatu Asthi and Sandhi, and in all the

pathology perpetuates and destructs the body in the form of Amavisha.

Viruddha produces some alteration in the humoral activity of the body

and results in the production of Ama. This Ama is antagonistic to the bodily

tissues (Dhatu Virodhi). Effect of this may be rapid or gradual. Viruddha has

Dhatu Virodhi Karma by way of producing Ama as a intermediate product in

case of Amavata. Because of Dhatuvirodhi quality of Ama it can be correlated

with autoimmunity in modern parlance.

Madhavakara18 has explained the Samprapti of Amavata as follows in

the presence of Mandagni, if one is exposed to Nidana then Ama is formed in

the Amashaya along with vitiation of Vata Dosha. This Ama circulates in the

body propelled by the vitiated Vata exhibiting an affinity to get lodged in the

Shleshma Sthana i.e. Sandhi. Further, this circulating Ama in the Dhamanis

interact with the normally present Vata Pitta and Kapha Dosha giving rise to

variegated color to the virulent Ama. It becomes qualitatively heavy and

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viscous, facilitating Sroto Abhishyandana and Srotorodha. Alteration in the

Srotas endures Sthana Samshraya leading to the manifestation of symptoms

like Hrutgourava, Dourbalya, Sandhi Shotha and Shoola etc.11

Samprapti Ghataka:

Dosha: Vata predominant Tridosha.

Dhatu: Rasa, Mamsa, Asthi, Majja.

Upadhatu: Snayu, Sandhi.

Srotas: Annavaha, Rasavaha, Asthivaha, Majjavaha, Udakavaha,

Purishavaha, Mutravaha.

Srotodushti: Sanga, Vimargagamana.

Udbhavasthana: Amashaya, Pakvashaya.

Adhishtana: Sarvashareera

Vyakta Sthana: Sarva Shareera more particularly Sandhi

Avayava: Sandhi

Vyadhisvabhava: Chirakari.

Roga Marga: Madhyama

Pathogenesis of Rheumatoid Arthritis:19

In contemporary medical science, Amavata can be best correlated to

Rheumatoid Arthritis (Y.N.Upadhyaya). It is described as an autoimmune

disorder. The propagation of Rheumatoid Arthritis is an immunologically

mediated event, although the original initiating stimulus has not been clear. One

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view is that the inflammatory process in the tissue is driven by T4 helper cells

infiltrating the synovium. Evidence for this includes,

• The predominance of T4 cells in the synovium

• The local production of lymphokines by these infiltrating T cells

• Amelioration of the disease by removal of T cells by thoracic duct

drainage or suppression of their function by total lymphoid irradiation

Since T lymphocytes produce a variety of cytokines that promote B cell

proliferation and differentiation into antibody forming cells. T cell activation may

also produce local B cell stimulation. The resultant production of

immunoglobulin is rheumatoid factor that can lead to immune complex

formation. With consequent compliment activation there will be exacerbation of

inflammatory process by the production of anaphylatoxins and haemostatic

factors. This tissue inflammation is reminiscent of delayed type of

hypersensitivity reaction occurring in response to soluble antigens or micro

organisms. It is how ever unclear that whether this represents a response to

persistent exogenous antigens or to altered auto antigen such as collagen or

immunoglobulins.20

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Chart No. 2-Schematic representation of Samprapti in the light of

Kriyakalas:

Nidana-Viruddha

Vata Prakopa Agnimandya Dhatu Virodhi

Vata Dushti Ama (Koshta) Majjavaha Srotas

Dhamani

Trika Sandhi

Saruja Shotha (in multiple joints)

Sankocha Adi Upadrava

Bheda

Vyakta

Sthana Samshraya

Sanchaya Prakopa Prasara Samavata Dosha

(Amavisha/Garavishatulya)

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REFERENCES:

1. C.S.Chi. 15/44

2. A.H.Su. 7/45

3. C.S.Vi. 2/9

4. A.H.Su. 13/27

5. A.H.Su. 13/23,24

6. A.H.Su. 13/26

7. A.H.Su. 13/27

8. M.N. 25/7-10

9. H.S.Tri. 21/4

10. M.N. 25/7

11. A.H.Su. 7/29

12. A.S.Su. 9/7

13. C.S.Vi. 5/18

14. C.S.Chi. 28/33

15. S.S.Ni. 1/28

16. C.Vi. 5/8

17. M.N. 25/1

18. H.P.I.M. 14th edition, pg.1881

19. A.P.I. 5th edition, pg-1118

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POORVA ROOPA

Poorva Roopa are alarms signaling the onset of an ambush, like clouds

indicate the arrival of rain. They sometimes simulate the symptoms of actual

disease and sometimes not, but in any case they indicate occurrence of an

ailment.

Though the Poorva Roopa of Amavata is not explained in the Samhitas,

we can consider few of the Samanya Amavata Lakshanas as its Poorva Roopa.

It is understood from Ayurvedic classics that some of the Poorva Roopa may

continue as Samanya Lakshana of any disease.1

In Amavata before the onset of disease, Ama is formed. The symptoms

produced when Ama only gets involved with Vata before getting lodged in the

Shleshma Sthana, can be considered as Poorva Roopa. The Samanya

Lakshanas2 of Amavata though not very disease specific to Amavata, like

Agnimandya, Aruchi, Angamarda and Gourava can be considered as Poorva

Roopa.

Agnimandya: Nidana Sevana effects the normal functioning of Agni.

Aruchi: Vitiation of Rasa Dhatu and Bodhaka Kapha impairs the

functioning of Rasanendriya.

Anga Marda: Inadequate nourishment of Dhatu and presence of Ama leads to

feeling of aching pain in the body.

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Gaurava: Ama and vitiated Kapha causes feeling of heaviness in the body.

Also Sama Rasa and vitiated Kapha generates Hritgourava, i.e.

subjective feeling of heaviness in chest.

The production of Ama is the central phenomenon in Amavata, hence all

the Ama Lakshana can be considered as Poorva Roopa of this disease.

Prodromals of Rheumatoid Arthritis:

Onset of rheumatoid arthritis in approximately two thirds of patients is

insidiously with, fatigue anorexia, generalized weakness and vague

musculoskeletal symptoms until the appearance of synovitis becomes apparent.

This prodrome may persist for weeks or months and defy diagnosis.3

REFERENCES:

1. A.H.Ni. 1/5

2. M.N. 25/6

3. H.P.I.M. 14th edition, pg.1883

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Chart No. 3-Schematic representation of the evolution of Poorvaroopas:

Nidana-Viruddha

Vata Prakopa Agnimandya Dhatu Virodhi

Vata Dushti Ama (Koshta) Majjavaha Srotas

Dhamani

Trika Sandhi

Saruja Shotha (in multiple joints)

Agnimandya Aruchi Angamarda Gaurava

Sankocha Adi Upadrava

Samavata Dosha (Amavisha/Garavishatulya)

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BHEDA

For a better understanding, the disease Amavata can be broadly

classified into two categories, the first, on the basis of clinical manifestation and

the second, on the basis of prognosis, with sub classification existing in each

category. The details are as follows;

1. Based on clinical manifestations it is divided into:

A) Dosha Bhedena:

In Amavata, the Pradhana Dosha is invariably Vata. Due to some

supportive factors other two Doshas also get involved; accordingly, we can

observe the symptoms. Madhavakara has explained seven type of Amavata on

the basis of Dosha Pradhanyata1. They are as follows:

1. Vataja: In Vataja type of Amavata, Shoola will be the predominant

symptom. This can be well correlated to the Sheeta and Chala Guna of

Vayu. In Amavata, the path of the Vata is obstructed due to Ama. Hence

the characteristics feature of Vata-shoola will be more.

2. Pittaja: Symptoms Raga and Daha are indicative of Pittaja Amavata.

These are due to the Teekshna, Ushna Guna of Pitta.

3. Kaphaja: Symptoms Sthaimitya, Guruta, Kandu indicate the dominance

of Kapha. Sthaimitya is produced due to Picchila, Sthira and Sheeta

Guna of vitiated Kapha. As Ama and Kapha have similar qualities,

Guruta and Kandu are seen in the Sandhis.

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4. Vatapittaja: Symptoms of Vata and Pitta are seen together in Vatapittaja

type of Amavata.

5. Vatakapha: Here the symptoms of Vata and Kapha are seen together.

6. Pittakapha: Here the symptoms of Pitta and Kapha predominate.

7. Sannipatika: In Sannipatika type of Amavata, symptoms of all the three

Doshas are profoundly seen.

B) Avastha Bhedena:2

Based on the different stages of the disease, Madhavakara has broadly

classified Amavata into two varieties they are,

1. Samanya

2. Pravruddha.

The symptomatology of this has been discussed in chapter Roopa.

C) Lakshana Bhedena:3

Acharya Harita’s classification of Amavata has been unique. According

to him, Amavata is of four types.

1. Vishtambhi: This type of Amavata presents with Shareera Guruta,

Adhmana, and Basti Shoola.

2. Gulmi Amavata: Amavata having Jatara garjana, Gulmavat peeda

and Kati jadata is called as Gulmi.

3. Snehi: Here Gaatra snigdhata, Jadhya, Mandagni and excretion of

Vijala and Snigdha ama are characteristic.

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4. Pakva ama: This variety of Amavata presents with excretion of

Shyava vijala pitta and Pakva ama along with Shrama and Klama.

D) Based on prognosis:

Based on the general principle of Sadhyasadhyata, Amavata can be of

two types.

1. Naveena: If the duration of disease is not more than one year, it is called

Naveena Amavata which is Sadhya.

2. Purana: If the duration of Amavata is more than one year, it is called

Purana Amavata which is difficult to treat.

REFERENCES:

1. M.N. 25/11

2. M.N. 25/6-10

3. H.S.Tri.Sth. 21/5-6

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ROOPA Specific signs and symptoms of a disease when manifested distinctly is

considered as Roopa Avastha1 or Lakshana of a disease. Roopa is one of the

key tool in arriving at the diagnosis. Of course this is also helpful in assessing

the Sadhyasadhyata and to plan the treatment.

The Lakshanas of Amavata have been explained in length in the classics

and are listed in the Table No. 1

On keen observation and assessment of Lakshanas, they can be broadly

classified into 3 categories.

1. Lakshana specific to involvement of Sandhi.

2. Lakshana specific to involvement of Ama.

3. Lakshanas produced as a consequence of the disease process. They

are elaborated below:

Lakshana specific to involvement of Sandhi:

The Lakshanas such as Shoola and Shotha in Hasta, Pada, Shira,

Gulpha, Trika, Janu2 and so on are very specific to involved Sandhi. Further

Lakshanas like Shunata Anganam3 (swelling in Sandhi) Sashabdha Sandhi4

(crepitation in joints) also indicates the same.

Gatrasthabdhata (immobility of Sandhi), Jadyata (unable to do the

physical work due to Vedana in the Sandhi Pradesha) Sandhi Vikunchana,

Sankocha, Kanja and so on deformities in the limbs further shows involvement

of Sandhi4.

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As seen in the Samprapti, the vitiated Dosha and Ama will move to the

Kaphasthana9 i.e. Sandhi Pradesha. The involvement of the Asthi and Sandhi is

very much pathognomonic of the disease.

Hence, it can be said that Sandhi Shoola and Shotha2 is one of the

cardinal features of this disease. But keeping in mind the narration of multiple

joints involvement in other diseases in the text, we should consider multiple joint

involvement with Ama Lakshana only as the cardinal symptom of the disease

Amavata.

Lakshana specific to involvement of Ama:

Most of the Lakshanas other than Lakshana related with the Sandhi will

refer to Ama Dosha in the body. If we scrutinize these Lakshanas some of them

are specific to Ama in the Annavahasrotas6, where as some other refer to effect

of Ama on the Rasavahasrotas6.

Chardi, Arochaka and so on are the features suggestive of

Annavahasrotodushti6 specifically by Ama. The symptoms produced due to

Rasavahasrotodushti6 can be considered at two dimensional levels, the

Sthanika and Sarvadaihika Lakshanas3. Aruchi3, Anaha3 and so on are the

Sthanika Lakshanas suggestive of Ama, where as Angamarda3, Alasya3 are

Sarvadaihika Lakshanas suggestive of Ama.

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Lakshanas produced as a consequence of the disease process:

Remaining few symptoms such as Nidraviparyaya4, Bhrama2 Murcha2,

are neither the cardinal features nor the Ama Lakshanas. Basically they are the

effect of pathological process in the body. Shoola is the culprit behind

Nidraviparyaya, where as Bhrama and Murcha point towards the involvement of

Majjavahasrotas10.

Though in this disease is Vata predominant, involvement of Ama is

invariable. Hence, we see Sama Vata Lakshanas7 in the patients of Amavata.

This might be the reason for not mentioning the disease Amavata separately by

Charaka.

Doshanubandha Lakshanas:

(1) Vatanubandha8 : Sasulam

(2) Pittanubandha8 : Sadaha, Saraga

(3) Kaphanubandha8 : Stimitatam, Guru, Kandu

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Table No. 1-Lakshanas of Amavata according to different authors:

LAKSHANA M.N B.P Y.R R.R.S G.N BRJ HS VGA TRA1. Angamarda + + + - + - - + - 2. Aruchi + + + - + - - + - 3. Trushna + + + - + - - + - 4. Hrillasa + + + - + - - + - 5. Gourava + + + - + - - + - 6. Jwara + + + - + - + + - 7. Apaka + + + - + - - + - 8. Angasoonata + + + - + - - + - 9. Sa Ruk Shotha Hasta + + + - + - - + - 10. Sa Ruk Shotha Pada + + + - + - - + - 11. Sa Ruk Shotha Shira + + + - + - - + - 12. Sa Ruk Shotha Gulpha + + + - + - - + - 13. Sa Ruk Shotha Trika + + + - + - - + - 14. Sa Ruk Shotha Janu + + + - + - - + - 15. Sa Ruk Shotha Uru + + + - + - - + - 16. Agnidourabalya + + + - + - - + - 17. Praseka + + + - + - + + - 18. Utsaha Hani + + + - + - - + - 19. Vyrasya + + + - + - - + - 20. Daha + + + - + - - + - 21. Bahumutrata + + + - + - - + - 22. Kushikadhinata + + + - + - - + - 23. Kukshishoola + + + - + - - + - 24. Nidraviparyaya + + + - + - - + - 25. Trut + + + - + + - + - 26. Chardi + + + - + + - + - 27. Brama + + + - + - - + - 28. Moorcha + + + - + - - + - 29. Hrutgraha + + + - + - - + - 30. Vitvibhandha + + + - + - - + - 31. Jadyata + + + - + - - + - 32. Antrakoojana + + + - + - - + - 33. Anaha + + + - + - - + - 34. Vikunchana of Manya - - + - + - - - - 35. Vikunchana of Prushata - - + - + - - - - 36. Vikunchana of Kati - - + - + - - - - 37. Vikunchana of Janu - - + - + - - - - 38. Vikunchana of Trika - - + - + - - - - 39. Sashabda Gatra - - + - + - - - - 40. Srasta Gatra - - + - + - - - - 41. Kati Vyadha - - - + - - - - -

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42. Sandhi Shotha - - - + - - + - - 43. Uthana Asamartha - - - + - - - - - 44. Deha Pandura - - - - - + - - - 45. Mootra Pandura - - - - - + - - - 46. Peta and Ushna Netra - - - - - + - - - 47. Peeta and Ushna Chardi - - - - - - + - - 48. Jangha Vyadha - - - - - - - - + 49. Uru Vyadha - - - - - - - - + 50. Trika Vyadha - - - - - - + - + 51. Hrut Vyadha - - - - - - - - + 52. Nabhi Vyadha - - - - - - - - + 53. Pada Vyadha - - - - - - - - + 54. Prushta Vedana - - - - - - + - - 55. Manya Vedana - - - - - - + - - 56. Ama Atisara - - - - - - + - - 57. Anga Vaikalya - - - - - - + - - 58. Shosha - - - - - - - - + 59. Visuchika - - - - - - - - +

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Clinical Manifestations of Rheumatoid Arthritis

Articular manifestations:

Rheumatoid arthritis is characterized by chronic polyarthritis. It begins

insidiously – the earliest manifestations being fatigue, anorexia, generalized

weakness and vague musculoskeletal symptoms and the later symptom being

the appearance of synovitis. Specific symptoms usually appear gradually and

symmetrically as several joints, especially those of the hands, wrists, knees,

and feet, become affected. In approximately 10% of individuals, there is acute

onset, with a rapid development of polyarthritis, often accompanied by

constitutional symptoms, mainly fever, lymphadenopathy, and splenomegaly.

Symptoms may initially be confined to one or a few joints in nearly a third of the

patients. Although a symmetric pattern is more typical, the pattern of joint

involvement may remain asymmetric in a few patients.

Initially, pain, swelling, and tenderness may be poorly localized to the

joints. The most common manifestation of established Rheumatoid Arthritis is

pain in affected joints, aggravated by movement. The pain corresponds to the

joint involvement in pattern but does not always correlate with the degree of

apparent inflammation. Generalized stiffness is frequent and is usually greatest

after periods of inactivity. Morning stiffness of greater than 1 hour duration is an

almost invariable feature of inflammatory arthritis and may serve to distinguish

it from various non-inflammatory joint disorders. The majority of patients will

experience constitutional symptoms such as weakness, easy fatigability,

anorexia, and weight loss. Temperature in excess of 38°C is unusual; on

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occasion the temperature may rise to 40°C, but this may suggest an

intercurrent problem such as infection.

Clinically, synovial inflammation results in swelling, tenderness, and

limitation of motion. Warmth is usually found on examination, especially of large

joints such as knee, but erythema is infrequent. Joint swelling is caused by

accumulation of synovial fluid, hypertrophy of the synovium, and thickening of

the joint capsule. Initially, motion is limited by pain. The inflamed joint is usually

held in flexion as this position provides maximum joint volume and minimum

distention of the capsule. Later, fibrosis or bony ankylosis or soft tissue

contractures form, ultimately leading to fixed deformities.

Although inflammation can affect any diarthrodial joint, Rheumatoid

arthritis most often causes symmetric arthritis, characteristically involving

certain specific joints such as the proximal interphalangeal and

metacarpophalangeal joints. Involvement of the distal interphalangeal joints is

rare. Synovitis of the wrist joints is a nearly uniform feature of RA and may lead

to limitation of motion, deformity, and carpal tunnel syndrome (median nerve

entrapment). When synovitis effects the elbow joint, flexion contractures often

develop, early in the disease. The knee joint is commonly involved with synovial

hypertrophy, chronic effusion, and frequently ligamentous laxity. Baker’s cyst,

caused by the extension of the inflamed synovium into the popliteal space, may

cause pain and swelling behind the knee. Arthritis in the forefoot, ankles, and

subtalar joints can produce severe pain with ambulation as well as a number of

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deformities. Axially, involvement is usually limited to the upper cervical spine.

Lower back pain cannot be ascribed to rheumatoid inflammation, as

involvement of Lumbar spines is not seen. Occasionally, inflammation from the

synovial joints and bursae of the upper cervical spine leads to atlantoaxial

subluxation. This usually presents as pain in the occiput and rarely, may lead to

compression of the spinal cord.

Persistent inflammation can lead to a variety of characteristic joint

changes. These can be attributed to a number of pathologic events, including

laxity of supporting soft tissue structures; damaged or weakened ligaments,

tendons, and the joint capsule; cartilage degradation; muscle imbalance; and

unopposed physical forces associated with the use of affected joints.

Characteristic changes of the hand include (1) radial deviation at the wrist with

ulnar deviation of the digits, often with palmar subluxation of the proximal

phalanges ("Z" deformity); (2) hyperextension of the proximal interphalangeal

joints, with compensatory flexion of the distal interphalangeal joints (swan-neck

deformity); (3) flexion contracture of the proximal interphalangeal joints and

extension of the distal interphalangeal joints (boutonniere deformity); and (4)

hyperextension of the first interphalangeal joint and flexion of the first

metacarpophalangeal joint with a consequent loss of thumb mobility and pinch.

Typical joint changes may also develop in the feet, including eversion at the

hindfoot (subtalar joint), plantar subluxation of the metatarsal heads, widening

of the forefoot, hallux valgus, and lateral deviation and dorsal subluxation of the

toes.

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Extra-articular Manifestations:

Rheumatoid arthritis is a systemic disease with various extra-articular

manifestations.

In 20 to 30% of persons with Rheumatoid arthritis, rheumatoid nodules

develop, usually found on periarticular structures, extensor surfaces, or other

areas subjected to mechanical pressure; but they can develop elsewhere,

including the pleura and meninges. Other common locations include the

olecranon bursa, the proximal ulna, the Achilles tendon, and the occiput. The

nodules are of differing size and consistency and are rarely symptomatic, but

on occasion they break down as a result of trauma or become infected. They

are found almost invariably in individuals with circulating rheumatoid factor.

Clinical weakness and atrophy of skeletal muscle are common. Muscle

atrophy may be evident within weeks of the onset of Rheumatoid arthritis and is

usually most apparent in musculature approximating affected joints

Another associated pathological event, rheumatoid vasculitis, can affect

nearly any organ system, and is seen in patients with severe Rheumatoid

arthritis and high titers of circulating rheumatoid factor. When in severe form,

rheumatoid vasculitis can cause polyneuropathy and mononeuritis multiplex,

cutaneous ulceration and dermal necrosis, digital gangrene, and visceral

infarction. Such widespread vasculitis is very rare, but more limited forms are

not uncommon, especially in white patients with high titers of rheumatoid factor.

Limited forms of vasculitis may present as Neurovascular disease either with

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mild distal sensory neuropathy or mononeuritis multiplex as the only sign.

Cutaneous vasculitis usually presents as crops of small brown spots in the nail

beds, nail folds, and digital pulp. Large ischemic ulcers may develope,

especially in the lower extremity. Myocardial infarction secondary to rheumatoid

vasculitis has been reported, as has vasculitic involvement of lungs, bowel,

liver, spleen, pancreas, lymph nodes, and testes. Renal vasculitis is rare.

Pleuropulmonary manifestations, which are more commonly observed in

men, include pleural disease, interstitial fibrosis, pleuropulmonary nodules,

pneumonitis, and arteritis. Presence of pulmonary fibrosis can impair the

diffusing capacity of the lung. Single or clusters of pulmonary nodules may

appear. Associated with pneumoconiosis, the nodules can cause a diffuse

nodular fibrotic process (Caplan's syndrome). In other cases, pulmonary

nodules may cavitate and produce a pneumothorax or bronchopleural fistula. ,

Pulmonary hypertension, secondary to obliteration of the pulmonary

vasculature, is a rare occurrence. In addition to pleuropulmonary disease,

upper airway obstruction from cricoarytenoid arthritis or laryngeal nodules may

develop.

Clinically apparent heart disease attributed to the rheumatoid process is

rare, but autopsy studies have revealed evidence of asymptomatic pericarditis

in 50% of cases. Pericarditis may be asymptomatic, or on rare occasions death

has occurred from tamponade. Chronic constrictive pericarditis may also occur.

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Rheumatoid arthritis tends to spare the central nervous system directly,

although vasculitis can cause peripheral neuropathy. Neurologic manifestations

may also result from atlantoaxial or midcervical spine subluxations. Nerve

entrapment secondary to proliferative synovitis or joint deformities may produce

neuropathies of median, ulnar, radial (interosseous branch), or anterior tibial

nerves.

Rheumatoid arthritis involving the eye is seen in fewer than 1% of

patients. Affected individuals usually have long-standing disease and nodules.

The two principal manifestations are mild and transient episcleritis and scleritis.

Felty's syndrome is most common in individuals with long standing

disease. It consists of chronic Rheumatoid arthritis, splenomegaly, neutropenia,

and, on occasion, anemia and thrombocytopenia. These patients frequently

have high titers of rheumatoid factor, subcutaneous nodules, and systemic

manifestations of rheumatoid disease.

Secondary osteoporosis, following rheumatoid involvement, is common

and may be aggravated by glucocorticoid therapy. Osteopenia in Rheumatoid

arthritis involves both juxta-articular bone and long bones distant from involved

joints.

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Chart No. 4-Schematic representation of the evolution of Roopa:

1. Angamarda 2. Daha 3. Sashabda Gatra 4. Aruchi 5. Bahumutrata 6. Srasta Gatra 7. Trushna 8. Kushikadhinata 9. Kati Vyadha 10. Hrillasa 11. Kukshishoola 12. Sandhi Shotha 13. Gourava 14. Nidraviparyaya 15. Uthana Asamartha 16. Jwara 17. Trut 18. Deha Pandura 19. Apaka 20. Chardi 21. Mootra Pandura 22. Angasoonata 23. Brama 24. Peta and Ushna Netra 25. Sa Ruk Shotha Hasta 26. Moorcha 27. Peeta and Ushna Chardi 28. Sa Ruk Shotha Pada 29. Hrutgraha 30. Jangha Vyadha 31. Sa Ruk Shotha Shira 32. Vitvibhandha 33. Uru Vyadha 34. Sa Ruk Shotha Gulpha 35. Jadyata 36. Trika Vyadha 37. Sa Ruk Shotha Trika 38. Antrakoojana 39. Hrut Vyadha 40. Sa Ruk Shotha Janu 41. Anaha 42. Nabhi Vyadha 43. Sa Ruk Shotha Uru 44. Vikunjana of Manya 45. Pada Vyadha 46. Agnidourabalya 47. Vikunjana of Prushata 48. Prushta Vedana 49. Praseka 50. Vikunjana of Kati 51. Manya Vedana 52. Utsaha Hani 53. Vikunjana of Janu 54. Ama Atisara 55. Vyrasya 56. Vikunjana of Trika 57. Anga Vaikalya 58. Shosha 59. Visuchika

Vata Prakopa Agnimandya Dhatu Virodhi

Vata Dushti Ama (Koshta)

Dhamani

Trika Sandhi

Saruja Shotha (in multiple joints)

Sankocha Adi Upadrava

Samavata Dosha (Amavisha/Garavishatulya)

Majjavaha Srotas

Nidana-Viruddha

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REFERENCES:

1. A.H.Ni. 1/5

2. M.N. 25/7-10

3. M.N. 25/6

4. Y.R.Po. Amavata Nidana/1, 2

5. A.H.Su. 13/23,24

6. C.S.Vi. 5/8

7. A.H.Su. 13/27

8. M.N. 25/11

9. M.N. 25/1-5

10. C.S.Su. 28/17

11. H.P.I.M. 14th edition, pg.1883, 1884.

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UPADRAVA

Among the different scholars of Ayurveda, there is a wide range of

difference in relation to Amavata Upadrava.

Yogaratnakara1 has included all the advanced stage manifestations as

its complications whereas Vachaspati includes all Vatavyadhis as its

Upadravas. But, other Acharyas differentiate symptoms of Amavata from its

complications. Vijayarakshita mentions Sankocha and Khanja2 specifically.

Bhavaprakasha3 includes Kalaya Khanja. Anjana Nidana4 includes Jadya,

Antrakujana, Anaha, Trushna, Chardi, Bahumootrata, Shoola, Shayananasha

as Upadrava of Amavata.

Following are the Upadravas which are elaborated;

1. Granthi

2. Angavaikalya

3. Vatavyadhi

4. Sankocha

5. Khanja

Granthi (Rheumatoid nodules):

Granthi is one of the feature of Snayu Dushti5. Develops in 20-30% of

persons with RA. They are usually found on the peri-articular structures,

extensor surfaces and other areas subjected to mechanical pressure, but are

also seen in pleura and meninges. Common locations include Olecranon bursa,

Proximal ulna and so on. Nodules vary in size and consistency.6

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Angavaikalya:7

Angavaikalya, one of the Lakshana mentioned by Harita can be

considered as an Upadrava of Amavata as most of the different deformities of

the body parts are produced in the later part of the disease RA.

Deformity of joints:6

• Swan neck deformity

• Boutonniere deformity

• Ulnar deviation

• Eversion at the hind foot, plantar subluxation of the metatarsal heads,

widening of the forefoot, hallux vulgus, lateral deviation and dorsal

subluxation of the toes.

• Z-Deformity of wrist and fingers.

Vatavyadhi:

Vachaspati mentions Vatavyadhi to manifest in the Upadravavastha of

Amavata. But, Vijayarakshita mentions Khanja, Sankocha.

Different neurological manifestations in RA are:

• The subluxation of Atlantoaxial joint is a severe complication and may

lead to compression of spinal cord by the Odontoid process producing

symptoms like bladder dysfunction, sphincter laxity, circummonal

hypesthesia, and long tract signs may occur. It may even lead to sudden

death due to the laceration of the cord by the Odontoid process.

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• Affliction of Crico-arytenoid joints leads to hoarseness of voice and even

life threatening upper airway obstruction.

• Tenosynovitis in wrist causes Carpal tunnel syndrome due to median

nerve compression.

• Vasculitis vasonervorum cause motor and sensory type of neuropathy.

• Autonomic nervous system dysfunction cause cold and damp

extremities.

Sankocha:

Inability to extend the limbs or normal fixed state of limb in flexion is

Sankocha.8 Sankocha is due to the affliction of Snayu, Sira and Khandara9.

Yogaratnakara has used the term Vikunchana of different Sandhis.

Inflamed joint is usually held in flexion to maximize joint volume and

minimize distension of the capsule. Later, fibrous and bony ankylosis or soft

tissue contractures lead to fixed deformities.6

Khanja:2

Patients gait gets altered because of Akshepana of Khandara. Gayadasa

clarifies Akshepana as reduced Gati10. This is usually due to painful joints,

contractures and stiffness.6

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Chart No. 5-Schematic representation of the evolution of Upadrava:

Vata Prakopa Agnimandya Dhatu Virodhi

Vata Dushti Ama (Koshta)

Dhamani

Trika Sandhi

Saruja Shotha (in multiple joints)

Sankocha Adi Upadrava

Granthi AngavaikalyaVatavyadhi Sankocha Kanja

Samavata Dosha (Amavisha/Garavishatulya)

Majjavaha Srotas

Nidana-Viruddha

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REFERENCES:

1. Y.R.Amavata Chi. 3-6

2. M.N. 25/7-10

3. B.P.M. Madhu 26/11

4. Anjana Nidana

5. C.S.Su. 28/21

6. H.P.I.M. 14th edition, pg.1883

7. H.S.Tri. 21/4

8. A.H.Su. 12/49 (Hemadri)

9. C.S.Su. 28/29

10. Gay-M.N. 25/7-10

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INVESTIGATIONS

Immunological assay:1,2

No tests are specific for diagnosing RA. However gamaglobulins with

demonstrable antigamma globulin activity have long been called Rheumatoid

factor (RF) because of their occurrence in serum of over 80% of patients. The

presence of Rheumatoid factor is not specific to RA. It is found in 15% healthy

people and frequency of RF in general population increases with age. It does

not establish the diagnosis of RA but can be of high value in prognosis because

patients with high titers tend to have more severe progressive disease. In

addition a number of conditions like systemic lupus erythematosis, Sjogren’s

syndrome, chronic liver diseases, sarcoidosis, intestinal pulmonary fibrosis,

infective mononeucleousus, hepatitis B, TB, Syiphilis, subacute bacterial

endocarditis, schistosomiasis and malaria.

Blood picture:2

Normochromic, normocytic anaemia is frequently present in RA. Large

iron stores in bonemarrow are usually noted. In general anaemia and

thrombocytosis correlate with disease activity. The WBC count is ususlly

normal. But a mild leucocytosis may be present.

ESR:2

The erythrocyte sedimentation rate is increased in nearly all patients with

active RA. In few patients, the ESR may be continuously elevated even after

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the disease activity subsides which may be attributed to elevation of serum

globulin level.

Biochemical investigations

Antinuclear antibodies (ANA):1

Higher titers of ANA are usually associated with highly expressed RA,

but attempts to differentiate SLE from RA is a key in diagnosing RA precisely.

Anti DNA Antibodies (anti n DNA):1

Though higher levels of anti n DNA are associated with SLE, in about

20% of RA patients the levels anti n DNA are usually found increased.

C-reactive proteins and ceruloplasmin levels:1

The C-reactive protein and ceruloplasmin levels are elevated and

gradually such elevations correlate with disease activity and likely hood of

progressive joint damage.

Synovial fluid analysis:2

The fluid is usually turbid with reduced viscosity, increased protein

content and slightly decreased or normal glucose concentration. The white cell

count varies between 5-50,000 cells per microlitre, polymorphoneuclear

leukocytes dominate. A synovial fluid WBC count of more than 2,000 cells per

microlitre with more than 75% polymorphoneuclear leucocytes is highly

characteristic of inflammatory arthritis. The total haemolytic complement C3 and

C4 are markedly diminished in synovial fluid relative to total protein

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concentrations as a result of activation of classic compliment pathway by locally

produced immune complexes.2

Cellular morphology:1

In about 95% of patients, both phase and ordinary light microscopy

reveals small dark cytoplasmic granules or 0.5-2.0 µ diameter within 5-100% of

neutrophils. Such neutrophils are called RA cells. A given RA cell may contain

1-20 granules in its cytoplasm. RA cells are not specific fro RA but also occur in

other conditions such as gout and septic arthritis (Scott 1975).

Radiographic evaluation:2

Roentgenograms of the affected joints early in the disease are usually

not helpful in establishing a diagnosis they reveal only that which is apparent

from physical examination namely evidence of soft tissue swelling and joint

effusion. As disease progresses abnormality becomes more pronounced

diagnosis is supported by a characteristic pattern of abnormality including the

tendency towards the systemic involvement. Juxta articular osteopenia may

become apparent within weeks of onset. Loss of articular cartilage and bone

erosion develop after months of sustained activity. The primary value of

radiography is to determine the extent of cartilage destruction and bone erosion

produced by the disease.

Other means of imaging bones and joints including 99mTC biphosphonate

bone scanning2 and magnetic resonance imaging2 may be capable of detecting

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early inflammatory changes that are not apparent from standard radiography

but are rarely necessary in routine evaluation of patients with RA.2

REFERENCES:

1. Clinical Diagnosis of Laboratory Methods, Bernard Hennry, pg.477, 478,

932.

2. H.P.I.M. 14th edition, pg.1884.

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UPASHAYA ANUPASHAYA

Oushadha, Ahara and Vihara which are responsible for relief from the

symptoms of Vyadhi are known as Upashaya and that which aggravate are

known as Anupashaya1. As said in the Amavata treatment2, Langhana, Tikta,

Katu Deepana and Ushna Ahara Viharas are the Upashaya measures of this

disease, since they carry out Ama pachana thereby giving relief from symptoms

like Jwara, Sandhi Vedana, Angamarda and Gourava and so on.

Ruksha Guna of Ruksha Sweda employed in Amavata is opposite to

Ama Gunas. viz. Snigdha, Picchiladi. It is Srotovishodhakara and Pachaka

hence effectively reduces pain. Besides, Ushna Jala suppresses symptoms of

the disease as it is Pathya3. In brief Ruksha Sweda, Langhana, Ushnakala and

Sayamkala are the Upashaya in Amavata.

Anupashaya:

On the contrary, Sheeta Guru Snigdha Ahara Meghodaya Kala, Pratah

Kala and Snigdha Sweda are considered as Anupashaya4 in this disease.

Snigdha Sweda supports the formation of Ama in early morning hours, cloudy

and rainy days because Sheeta Guna enhances the Vata and Ama. Hence

considered as Anupashaya.

This characteristic feature helps to differentiate Amavata from other

closely related diseases of Sandhi. When the symptoms of two diseases are so

similar as to confuse the physician (“Bhishak Mohakara”), the classics suggest

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the use of the concept of Upashaya and Anupashaya to bring out the occult

symptoms (Guda Linga) to diagnose the disease5. When application of oil

relieves the pain, the disease is free from Ama.

REFERENCES:

1. A.H.Ni. 1/67

2. Chakradutta 25/1

3. B.R. 21/232-234

4. A.Hr.Su. 13/27 footnote

5. C.S.Vi. 5/7

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SADHYASADHYATA

Physician who wants to be successful should have clear knowledge of

curable and incurable disease, and start treatment in time with well

understanding of various aspects of the disease. This will help in

accomplishing his goal of curing diseases. Physician treating incurable

diseases would loose wealth, fame and earn bad reputation. He will become

victim of legal sanctions.1

Generally Amavata is a Krichrasadhya Vyadhi as it includes Madhyama

Rogamarga2. It is also difficult to treat because of opposite nature of Ama and

Vata. Diseases accompanied by Upadrava becomes Asadhya the same is

applicable to Amavata.

Ekadoshaja Amavata3 caused by minimum Nidana, with few

Lakshanas, of recent origin2 is Sadhya and Harita adds Pakwama type of

Amavata is Sukhasadhya4. When the disease is Dwidoshaja3, having many

Nidanas and Lakshanas, then it become Yapya. Disease becomes

Krichrasadhya by the involvement of Tridosha and when associated with

Sarvangashotha.3 Snehi ama, Vistambi, Gulmi types of Amavata are

Kashtasadhya.4

Shopha anana, Jadya, Ghana udara, Aruchi and Amathisarayuktha

Snehi Amavata is Asadhya according to Harita.5

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PROGNOSIS OF RHEUMATOID ARTHRITIS:6

In Rheumatoid arthritis prognosis is variable. Life expectancy is reduced

by 25%. 10-15 yrs mortality is increased in patient with functional impairment.

The overall prognosis is much better in patients whose symptoms are not of

such severity as to require admission to hospital. Poor prognosis may be

associated with high titer of Rheumatoid Factor, insidious onset of disease,

more than a year of active disease without remission, early development of

nodules and erosion, extra articular manifestation, severe functional

impairment.

REFERENCES:

1. C.S.Su. 7/8

2. C.S.Su. 10/18

3. M.N. 25/12

4. H.S.Tritiya sthana 21/21

5. H.S.Tritiya sthana 21/14

6. Davidson’s PPM 18th edition. pg. 848

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SAPEKSHA NIDANA

For the diagnosis of any disease physician should have clear knowledge

of other conditions which mimic particular condition. This can avoid the

physician from embarrassment and prevents the patient from taking the

unwanted pain and complications. Therefore for the accurate diagnosis of

Amavata the disease having similar feature has to be excluded. Following are

few conditions which have to be differentiated from Amavata.

1. Vata Shonita:

In the disease process of Vata Shonita, Rakta Dushti plays an important

role. Vata and Shonita1 get vitiated due to each others own causative factors.

Though this disease presents with Shotha in Parshva Sandhi and big joints

also, it classically begins with affliction of big toe2 with skin manifestations unlike

Amavata.

2. Kroshtuka Sheersha:

This is a disease of the knee joint and the question of involvement of

other joints does not arise. Swollen Knee has the appearance of head of a

jackal (Jambuka Shira)3. Here too Vata and Shonita are the two factors

involved.

3. Sandhigata Vata:

Sandhigata Vata typically presents with swelling of the joint that gives a

feeling of a bag inflated with air.8 Notably, use of oil here results in improvement

of symptoms rather than aggravation.

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4. Sandhiga Sannipata Jwara:11

In this disease the joint manifestations are secondary to Jwara which is

the cardinal symptom. Besides, excessive mucoid secretion from mouth,

Insomnia and Saruja Kasa differentiates this condition from Amavata

Along with the above mentioned diseases, Shotha and Shoola in Sandhi,

like in Amavata can be seen in Vataja Atisara4, Grahani5, Kshayaja Kasa6,

Vatodara7, Arsha9, Antarvega Jwara10. But these can be differentiated from

Amavata by their own characteristic features.

REFERENCES:

1. C.S.Chi. 29/4

2. C.S.Chi. 29/4

3. A.S.Ni. 15/35 (Indu)

4. C.S.Chi. 19/5

5. C.S.Chi. 15/54

6. B.P. 11/35

7. A.S.Ni. 12/14

8. C.S.Chi. 28/37

9. A.S.Ni. 7/16

10. C.S.Chi. 3/39, 40

11. B.P.Mady.Kha. Sandhiga Sannipata Jwaradhikar/500

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CHIKITSA

The treatment modalities for Amavata listed by Chakradatta1 can be

organized into three groups, to be administered in the following order.

1. The treatment aimed at Amapachana - Langhana, Swedana, Tikta, Katu,

Deepana drugs.

2. Shodhana - Virechana and Basti

3. Shamana - Snehapana.

Amapachana:

The first step in the management of Amavata is Amapachana, as it is the

first step in the general management of all the diseases and as Ama is the

prime pathogenic factor in Amavata.

The modalities for Amapachana in the Chakradatta’s Chikitsa Sootra are,

1. Langhana

2. Swedana

3. Tikta, Deepana, Katu Oushadhis to be administered in order.

Langhana:

In the management of Amavata, Upavasa is the ideal line of treatment.

Bhavaprakasha in the context of Jwara, considers Langhana as Upavasa.2 As

both Jwara and Amavata are Amashayotha diseases, Upavasa3 can be

considered as the ideal method of Langhana in Amavata also. This is also

because of unsuitability of the other methods of Langhana, analysed below.

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o Chatushprakara samshudhi, cannot be employed because

Samshodhana is contraindicated in the Samavastha of a disease.4

o Pipasa cannot be employed because in morbid patients Jala is

Pranadharaka5.

o Maruta and Atapa Sevana are less efficient for Jatharagni impairment

when compared to Upavasa.

o Deepana, Pachana cannot be employed as Agni affected by Ama is

incapable of Dosha, Ahara and Oushadha Pachana.6

o Vyayama is incompatible in the disease Amavata.

For these reasons, Upavasa is the ideal method of achieving Langhana

in Amavata, which can be achieved by Anashana or Alpabhojana. The

Langhana thus achieved will have Amapachaka effects at the Koshta level as

well as Sarvadaihika level.7

Swedana:

The definition of Sweda8 includes its benefits, viz. Stambha, Gourava

and Sheetagna. Since these are antagonistic to the qualities of Kapha and

Ama, Swedana has an important role to play in the treatment of Amavata.

Snigdha Sweda, Ruksha Sweda and Ekangasweda, Sarvangasweda are

the two fold classifications of Sweda9 and in Amavata, the Ruksha type of

Sweda should be administered for the following reasons;

1. The pathogenesis of Amavata involves spread of Ama and Vata to the

Sleshmasthana, specifically Amashaya and Sandhi.10

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2. In all conditions of Amashayagata vata, Ruksha sweda should be

administered.11

As disease is localized in Sandhipradesha, Ekangasweda is ideal. The

Rukshasweda can be advised to the affected Sandhi using Valukapottali or

Rukshopanaha.12

Tiktam Deepanani Katuni Cha:

Administration of Tikta, Katu Deepana oushadhis in Ama achieves

Amapachana both at the Koshta level and Sarvadaihika level. The methods

used for Ama Pachana are potentially Vataprakopaka. But as Langhana is

indicated in Sama Vata condition the danger of Vata Prakopa is minimal

because,13 the Amapachana methods of Langhana, Swedana and Tikta Katu

Deepana drugs are administered only until Niramavastha is achieved. After this,

Nirama Doshas have to be eliminated from the body by Shodhana. The

Shodhana methods which can be employed are Virechana and Basti.

Virechana:

Virechana is the best preferred form of Shodhana in Amavata because

Vamana (Ullekhana),14 though indicated by Charaka in Amachikitsa is

unsuitable here as it aggravates the symptoms of Amavata caused by

Pratilomagati of Vayu like Anaha, Vibandha and Antrakoojana. They can best

be relieved by Virechana. Besides, the production of Ama involves the Avarana

of the Pachaka Pitta by Kledaka Kapha. Virechana administered here provides

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dual benefits of removing the Avarana produced by Kledaka Kapha and acting

on the Sthanika Pitta Dosha.

Basti:

Basti forms the second method of Shodhana. Both Niruha and

Anuvasana Bastis should be employed here. The Niruha Basti does the

Shodhana of the Doshas brought to Pakvashaya and the Anuvasana Basti

alleviates Prakupita vata as a consequence of Niruha Basti.

Shamana Snehapana:

This is a third component in the plan of management of Amavata. The

objective of Snehapana here is Shamana. It is important to administer Sneha

only after the disease has become Nirama. Shamana Snehapana in Amavata

provides the following benefits;

o Snehapana prevents the aggravation of Vata and Rukshata as a result of

the previously employed therapeutic measures.15

o It helps in increasing the Bala of the patient who has been debilitated as

a result of previously employed therapeutic measures.15

o Shamana Sneha stimulates the Agni16 which is an important component

in the treatment of Amavata.

o Since the Snehapana has been prescribed in Asthi Majja Gata Vata, it

can be comfortably used in Amavata.

o Vataharana is the inherent property of Sneha, an essential requirement

in the treatment of Amavata.

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General principles in treatment of Rheumatoid Arthritis:17

The goals of therapy of RA are;

1. Relief from pain

2. Reduction of inflammation

3. Protection of articular structures

4. Maintenance of function

5. Control of systemic involvement

The therapy of RA remains empirical and palliative since the etiology,

pathogenesis and mechanism of therapeutic action is speculative till date. The

interdisciplinary approach in the management of RA includes both physical and

medical modalities.

Physical therapy and education:

This includes rest, splinting to reduce unwanted motion of inflamed

joints, exercise to maintain muscle strength and joint mobility, arthrotic and

assistive devices for support and alignment of deformed joints to reduce pain

and improve joint function, patient and family education to give the insight of the

disease and make necessary life style changes to minimize stress on the joints.

Medical management:

This includes four approaches

I. First line of treatment with non steroidal anti-inflammatory drugs (NSAIDs):

Besides aspirin, the new generation NSAIDs have shown to act by

inhibiting cycloxygenase II pathways which is responsible for the inflammatory

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activity. They have analgesic anti inflammatory, and anti pyretic properties.

Though non aspirin agents are lesser gastric irritants, the NSAIDs in general

are associated with following side effects

1. Gastric irritation,

2. Azotemia

3. Platelet dysfunction

4. Rash

5. Liver function abnormalities

6. Bone marrow depletion

7. Toxicity in elderly on diuretic therapy.

The NSAIDs have minimal effect on disease progression.

II. Second line of treatment with disease modifying anti rheumatic drugs

(DMARD):

The DMARDs include Gold, Depencillamine, Antimalarials and

Sulphasalazine. They have the capacity to decrease elevated levels of acute

phase reactants, like RA factor, C-reactive protein and ESR. Thus, they modify

the destructive capacity of the disease. They have been shown to induce

remission, but have minimal anti inflammatory activity. Hence, NSAIDs must be

continued during DMARD therapy.

The Folic acid antagonist Methotrexate is currently a frequently utilized

DMARD as its onset of action is more rapid than others. The toxicity of

DMARDs include GIT upset, oral ulceration, hepatic fibrosis and pneumonitis.

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Concurrent administration of folic acid may diminish the frequency of the side

effects.

III. Third line of treatment with glucocorticoids:

Low dose (less than 7.5 mg/day) Prednisolone has been advocated as a

useful additive therapy to control symptoms and retard progression of bone

erosions.

IV. Fourth line of treatment with immuno suppressants:

Drugs like Azathioprim and Cyclophosphamide have same effects like

the DMARDs and are used when the DMARD therapy has completely failed. In

higher doses the toxic effects include predisposition to malignant neoplasms.

Recent trials have found that high dose cyclosporine therapy may induce rapid

improvement but are associated with renal and gastrointestinal toxicity.

Cyclosporine has still not been approved for use in RA.

V. Surgery:

Surgery helps patients with severely damaged joints. Surgeries like

Arthroplasty, total joint replacement (especially of hip and knees.), Arthroscopic

synovectomy and Tensosynovectomy can be adopted to give the patient relief

from pain and deformity.

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REFERENCES:

1. Chakradutta 25/1

2. C.S.Chi. 3/142

3. B.P.Madhy.kha.Prathambhaga.1/9 (AnashanamUchyate)

4. A.H.Su. 13/28

5. B.P. 1/14

6. A.H.Su. 8/18

7. C.S.Chi. 15/75

8. C.S.Su. 22/4

9. C.S.Su. 14/66

10. M.N. 25/2 – Madhu

11. C.S.Su. 14/9

12. B.P. Madhya 26/14-15

13. C.S.Chi. 3/283 - Chakrapani

14. C.S.Vi. 2/13 (Ullekhana)

15. C.S.Chi. 28/81

16. C.S.Chi. 15/201

17. H.P.I.M. 14th edition, pg. 1885-1888

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PATHYAPATHYA

Pathyapathya plays vital role in crushing the disease process as well as

in the recurrence of the disease. Success of treatment depends upon the

practice of Pathyapathya. Vaidyakiya Subhashita quotes,” there is no need to

take the medicine for the one who follows the Pathya properly, contrarily there

is no need to take the medicine for the one who does not follow the Pathya, as

it will be of no use”. Purusha has been carved out of nature itself. That is why

there exists little difference between the constituents of his make and that of his

environment. The dimensions of man’s interaction with his environment include

Ahara, Vihara and Oushadha. A beneficial interaction is termed Hita and a

harmful one is called Ahita, this leads to homeostasis and homeostenosis

respectively. The factors governing this aspect of treatment constitutes the

concept of Pathya and Apathya.

By definition, Pathya means “Patho Anapetam” and “Manasaha Priyam”1

which can be interpreted as “Manoshareera Anupaghati”2. That which is

harmless to both to Shareera and Manas is Pathya. On the contrary, Apathya

means otherwise. Among the Pathya Varga, the methods involved in

administration of Oushadha have been dealt in the chapter of Chikitsa. The

details of Ahara and Vihara are discussed here. Raja Nighantu has listed the

following Hitakara Dravya Samooha3. i.e. which are in general are Pathya for all

diseases. Ghrita, Saindhava, Dhanyaka, Jeeraka, Ardraka, Tanduleeyaka,

Patola, Alabu, Godhuma, Jeerna shali, Gokshura, Hamsodaka and Mudga.

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In Amavata, the Ahara and Vihara which are Vatahara, Kaphahara,

Amapachaka, Agnideepaka and Rasaprasadaka are considered as Pathya. So,

the diet and the Oushada having Katu, Tiktarasa, Ushna, Tikshna guna are

considered as Pathya. They are as follows,

Shuka Dhanya - Purana Shali, Purana Shastika Shali, Yava5

Shami Varga - Chanayusha, Kalayayusha, Kulatta, Kodrava5

Shakha Varga - Nimba Patra, Gokshura, Varuna, Sigru, Ardraka, Lashuna,

Karavellaka, Patola5

Mamsa Varga - Jangala mamsa, Lava mamsa processed with Takra4

Paniya Varga - Ushna Jala, Panchakola siddha jala, Madhya4

Ksheera Varga - Takra4

Mutra Varga - Gomutra4

Harita opines that all the Pathya which are mentioned in Jwara

Rogadikara should be considered in Amavata also6.

Apathya:

The Ahara and Vihara which compliment or supplement the Prakruti of

the Vyadhi are called as Apathya. In Amavata, to be a Apathya it should be

Amakaraka and Vatakaraka. It should cause Mandagni and vitiate the Rasa

Dhatu.

Aharatah Apathya:

Shami Dhanya - Masha Pistaka4,5,7,8 Dvidala dhanya6

Mamsa Varga - Matsya, Anupa4,5,7,8

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Ksheera Varga - Dhadhi, Ksheera, Guda9,5,7,8,10

Mutra Varga - Gomutra9,11

Jala Varga - Dushta jala9,11

Anna - Viruddha, Asatmya, Vishamashana9,11

Guru7,9,11 Picchila Abhishyandi7,9,10,11, Ushna, Drava, Goulya6

Viharatah Apathya:

Poorva Vata, Vegavarodha, Jagarana, Vishamashana9,11

Harita opines that all the Nidana which are Atisarakaraka are Apathya in

Amavata.6

REFERENCES:

1. C.S.Su. 25/45

2. Chakrapani on C.S.Su. 25/45

3. Ra Ni 11/126

4. B.R.Amavata 21/232-234

5. Y.R. Amavata.1,2

6. H.S.Tritiya stana 21/47-49

7. B.P Ma.Amavata.26/129

8. G.N.Kaya chikitsakhanda.22/38.

9. B.R.Amavata 21/235-236

10. Vang.Amavata/123

11. Y.R. Amavata.3,4

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79

DRUG REVIEW

The therapeutic effect of any drug combination in the patients of

Amavata depends upon its ability to pacify the Ama and Vata Dosha, correction

of Rasa Dhatu abnormality, rectifying the Agni, correcting the structural

abnormality in Sandhis, ability to pacify and bring out reduction in pain,

softening the stiff Sandhis, reducing morning stiffness and such measures.

The drugs used in the clinical trial have been reviewed below:

1. Eranda Paka1

2. Ajamodadi Churna2

3. Panchakola Phanta3

4. Eranda Taila.4

ERANDA PAKA: Contents

Name of the drug Latin Name Quantity

1. Eranda Ricinus communis 750 grams

2. Ksheera Milk 6 liters

3. Ghrita Ghee 375 grams

4. Khandasharkara Sugar candy 1500 grams

5. Pippali Piper longum Linn. 12 grams

6. Maricha Piper nigrum Linn. 12 grams

7. Shunti Zingiber officinale 12 grams

8. Twak Cinnamomum zeylanicum 12 grams

9. Ela Elettaria cardamomum 12 grams

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80

10. Patra Cinnamomum tamala 12 grams

11. Nagakesara Mesua ferrea 12 grams

12. Pippalimoola Piper longum Linn. 12 grams

13. Chitraka Plumbago zeylanica 12 grams

14. Chavya Piper retrofractum 12 grams

15. Shatapushpa Anethum sowa 12 grams

16. Shati Hedychium spicatium 12 grams

17. Bilwamoola twak Aegle marmelos 12 grams

18. Yavani Trachyspermum ammi 12 grams

19. Jeeraka Cuminum cyminum 12 grams

20. Krishna jeeraka Carum bulbocastanum 12 grams

21. Haridra Curcuma longa 12 grams

22. Daruharidra Berberis aristata 12 grams

23. Aswagandha Withania somnifera 12 grams

24. Balamoola Sida cordifolia 12 grams

25. Patha Cissampelus pereira 12 grams

26. Hapusha Juniperus communis 12 grams

27. Vidanga Embelia ribes 12 grams

28. Pushkaramoola Inula racemosa 12 grams

29. Goshura Tribulus terrestris 12 grams

30. Kushta Saussurea lappa 12 grams

31. Amalaki Embelica officinalis 12 grams

32. Haritaki Terminalia chebula 12 grams

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81

33. Vibheetaki Terminalia bellirica 12 grams

34. Devadaru Cedrus deodara 12 grams

35. Baboola twak Acacia arabica 12 grams

36. Satavari Asperagus racemosus 12 grams

Method of Preparation:

Eranda Paka is herbal compound mainly contains Eranda Beeja, Milk,

Ghee and 33 Prakshepaka Dravyas, tabled above. A special preparation

method, mentioned in Yogaratnakara was followed in preparing Eranda Paka.

Initially Eranda Beeja are collected and its outer covering is removed. Heat

these Eranda Beeja with milk on Mandagni till it turns to pasty consistency. This

paste is grinded well and fried in ghee on an Iron pan. Then 33 Prakshepaka

Dravyas are added, mixed well till it gets granule form.

Dose: Orally in a dose of 15 gms, thrice a day with hot water after food.

Duration: For a duration of 30 days in patients of Group EP.

Eranda is one of the main ingredient in Eranda paka. Eranda is Tikta,

Kashaya and Madhura Rasatmaka, Ushna veerya and Madhura vipaka. Thus

with Madhura rasa and Madhura vipaka contradicts Vata and with Tikta rasa

and Ushna veerya counters Ama. In Amavata, Vedanasthapana and

Shothahara properties plays an important role, which are also the main action

of the Eranda as Eranda is Vata Anulomana, Vedanasthapaka and Shothahara

in nature. The rest 33 Prakshepaka drugs are added in very minute quantity.

Most of them are Deepaka, Pachaka and Vata anulomaka in nature. The

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82

different properties and therapeutic effect of the individual drugs are shown in

the table below5 (Table No. 2)

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Table no. 2-Properties and therapeutic effect of the individual drugs in Eranda Paka:

Sl.

No.

Name of the

Drug

Latin Name Rasa Guna Veerya Vipaka Doshaghnata Karmukata

1.

Eranda Beeja Ricinus

Communis

Madhura

Katu

Kashaya

Guru

Snigdha

Teekshna

Sookshma

Ushna Madhura Vatakapha

Prashama

Swedopaga

Shothahara

Rasayana, Vedana

Shamaka

2.

Milk Madhura Shigdha,

Mrudu

Sheeta

Guru

Shlaksna

Picchila

Madhura Vata Pittahara Jeevaniya

Rasayana

Vajikara

Balya

Bruhmana

3.

Ghee Madhura Shigdha,

Guru

Sheeta Madhura Vata Pittahara Dhatuvardhaka

4. Kanda Sharkara Madhura Sara

Snigda

Sheeta Madhura Vata Pittahara Vrishya

Bruhmana

5. Nagara Zingiber officinale Katu Laghu

Snigdha

Ushna Madhura Kaphavata

Shamaka

Deepaka, Pachaka

Shoolaprashamana

Vatanulomana

6. Pippali Piper nigrum Katu Laghu

Teekshna

Ushna Katu Vatakapha

Shamaka

Deepana,

Triptighna,

Vatanulomana,

Mrudureehana,

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Balya, Rasayana

7. Maricha Piper nigrum Katu Laghu,

Teekshna

Ushna Katu Kaphavata

Shamaka

Deepana,

Pachana,

Vatanulomana

Pramathi

8. Twak Cinnamomum

Zeylanica

Katu Tikta

Madhura

Laghu

Rooksha

Teekshna

Ushna Katu Vatakapha hara Deepana Pachana

Vedanashamaka

9. Ela Elettaria

cardamomum

Katu

Madhura

Laghu

Rooksha

Sheeta Madhura Tridosha hara Deepana Pachana

Vedanashamaka

10. Patra Cinnamomum

tamala

Katu Ushna

Laghu

Ushna Katu Kaphaghna Deepana Pachana

Vedanashamaka

11. Nagakeshara Mesua ferrea

Kashaya

Tikta

Laghu

Rooksha

Ushna Katu Kaphapitta

Shamaka

Deepana Pachana

Vedanashamaka

12. Pippali moola Piper longum Katu Laghu

Snigdha

Teekshna

Anushna Madhura Kaphavata

Shamaka

Deepana,

Triptighna,

Vatanulomana,

Balya, Rasayana

13. Chitraka Plumbago

Zeylanica

Katu Teekshna

Laghu

Rooksha

Ushna Katu Kapha hara Deepaka, Pachaka

Shoolaprashamana

Vatanulomana

14. Chavya Piper

retrofractum

Katu Laghu

Rookhsa

Ushna Katu Kaphavata

Shamaka

Deepaka, Pachaka

Shoolaprashamana

Vatanulomana

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15. Shatapushpa Anethum sowa Katu

Tikta

Laghu

Rooksha

Teekshna

Ushna Katu Kaphavata

Shamaka

Rochana,

Deepana,

Pachana,

Anulomana,

Shothahara

16. Shati Hedychium

spicatium

Katu Tikta

Kashaya

Laghu

Teekshna

Ushna Katu Kaphavata

Shamaka

Deepana Rochana

Shoolaprashamana

17. Bilwamoola

Twak

Aegle marmelos

Kashaya

Tikta

Laghu

Rooksha

Ushna Katu Kapha Shamaka Vedana Shamaka

18. Yavani Trachyspermum

ammi

Katu Tikta Laghu

Rooksha

Teekshna

Ushna Katu Kaphavata

Shamaka

Rochana Deepana

Vatanulomana

Shoolaprashamana

19. Jeeraka Cyminum

cuminum

Katu Laghu

Rooksha

Ushna Katu Kaphavata

Shamaka

Deepana, Pachana

Vatanulomana

Shoolaprashamana

20. Krishna Jeeraka Carrium carvi

Katu Laghu

Rooksha

Ushna Katu Kaphavata

Shamaka

Deepana Pachana

Vedanashamaka

21. Haridra Curcuma longa

Tikta Katu Rooksha

Laghu

Ushna Katu Kaphavata Nashaka Vedanashamaka

Varnya Deepana

Anulomana

22. Daruharidra Berberis aristata

Tikta

Kashaya

Rooksha

Laghu

Ushna Katu Kaphapitta hara Shothahara

Vedanashamaka

Anulomana

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23. Ashwaganda Withania

somnifera

Madhura

Kashaya

Tikta

Laghu

Snigdha

Ushna Madhura Kaphavata

Shamaka

Shothahara,

Vedanashamaka

Rasayana

24. Balamoola Sida codifolia

Madhura Guru

Snigdha

Picchila

Sheeta Madhura Vata Shamaka Vedanahara

Shothahara

25. Patha Cissampelos

Pereira

Tikta Laghu

Teekshna

Ushna Katu Tridosha Nashaka Anulomana

Vedanashamaka

Deepana pachana

26. Hapusha Juniperus

communis

Katu Tikta Guru

Rooksha

Teekshna

Ushna Katu Kaphavata

Shamaka

Deepana Pachana

27. Vidanga Embelia ribes Katu

Kashaya

Laghu

Rooksha

Teekshna

Ushna Katu Kaphavata

Shamaka

Deepana, Pachana

Anulomana

Krimighna

28. Pushkaramoola Inula recemosa

Tikta Katu Laghu

Teekshna

Ushna Katu Kaphavata

Shamaka

Shothahara

Vedanasthapaka

29. Gokshura Tribulus terestris

Madhura Guru

Snigdha

Sheeta Madhura Vatapitta Shamaka Balya anulomaka

Vedanasthapaka

30. Kushta Saussurea lappa Tikta

Katu

Madhura

Laghu

Rooksha

Teekshna

Ushna Katu Kaphavata

Shamaka

Deepana, Pachana

Anulomana

31. Amalaki Emblica

officinalis

Amla

Pradhana

Guru

Rooksha

Sheeta Madhura Tridosha hara Rochana, Deepana

Anulomana

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Pancharasa

Lavana

Rahita

Sheeta Rasayana

32. Haritaki Terminalia

chebula

Kashaya

Pradhana

Pancha Rasa

Laghu

Rooksha

Ushna Madhura Tridosha Shothahara,

Vedanasthapaka,

Anulomana,

Mruduvirechaka,

Deepana, Pachana

33. Vibhitaki Terminalia

bellerica

Kashaya Laghu

Rooksha

Ushna Madhura Tridosha hara Shothahara

Vedanasthapaka

34. Devadaru Cedrus deodara Tikta Laghu

Snigdha

Ushna Katu Kaphavata

Shamaka

Shothahara

Vedanasthapaka

Deepana pachana

35. Babbula Twak Acacia arabica

Kashaya Guru

Rooksha

Sheeta Katu Kaphapitta

Shamaka

Dahasamaka,

Vrushya

36. Shatavari Asperagus

recemosus

Madhura

Tikta

Guru

Snigdha

Sheeta Madhura Kaphapitta

Shamaka

Vedana sthapana

Balya rasayana

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83

AJAMODADI CHURNA: Contents

Name of the drug Latin Name Quantity

1. Ajamoda Carum roxburghianum 1 part

2. Vidanga Emblia ribes 1 part

3. Saidhava Sodium cloride 1 part

4. Pippalimoola Piper longum Linn. 1 part

5. Chitraka Plumbago zeylanica 1 part

6. Devadaru Cedrus deodara 1 part

7. Pippali Piper longum Linn. 1 part

8. Maricha Piper nigrum Linn. 1 part

9. Shatapushpa Anethum sowa 1 part

10. Haritaki Terminalia chebula 5 part

11. Vrudhadaru Argyreia speciosa 10 part

12. Nagara Zingiber officinale 10 part

Ajamodadi churna, a compound preparation contains above mentioned

12 ingredients.

Method of preparation:

The first 9 drugs mentioned above are taken 1 part each, where as

Hareetaki is 5 parts, Nagara and Vruddhadaru are taken 10 parts each. These

above mentioned drugs are taken as per classics and made into Churna.

Dose: 5 gms thrice a day with hot water before food.

Duration: For 30 days in patient of group AC.

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First 9 ingredients are used commonly in both Ajamodadi Churna and

Eranda Paka preparation. These drugs are Deepaka, Pachaka and Vata

Anulomana in nature.5 Details of which are explained in Table No. 3.

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Table no. 3-Properties and therapeutic effect of the individual drugs in Ajamodadi Churna: Sl. No.

Name of the Drug Latin Name Rasa Guna Veerya Vipaka Doshagnata Karmukata

01 Ajamoda Carumroxburghianum

Katu, Tikta Laghu Rookshna Teekshna

Ushna Katu KaphavataNashaka

Vedanasthapaka, Deepana, Pachana, Vidahi, Vatanulomana,

02

Vidanga Embelia ribes KatuKashaya

Laghu Rooksha Teekshna

Ushna Katu KaphavataShamaka

Deepana, Pachana, Anulomana

03 Saindhava Sodiumchloride

Lavana SnigdhaTeekshna Laghu Sookshma

Sheeta Lavana DeepanaPachana Vatanulomana Tridoshahara

Deepana, Pachana, Vatanulomana

04 Devadaru Cedrusdeodara

Tikta Laghu Snigda

Ushna Katu KaphavataShamaka

Deepana, Pachana Anulomana

05 Chitraka Plumbago zylanicum

Katu, Tikta Teekshna Laghu Rookshna

Ushna Katu KaphavataShamaka

Vedanastapaka Deepana Pachana

06 Pippali moola Piper longum Katu Laghu, Snigdha, Teekshna

Anushna Madhura Kaphavata Shamaka

Deepana, Triptighna, Vatanulomana, Balya, Rasayana

07 Pippali Piper longum Katu Laghu,Snigdha,

Teekshna

Anushna Madhura Kaphavata Shamaka

Deepana, Triptighna, Vatanulomana, Balya, Rasayana

08 Shatapushpa Anethum sowa KatuTikta

Laghu Rooksha Teekshna

Ushna Katu KaphavataShamaka

Rochana, Deepana, Pachana, Anulomana, Shothahara

09 Maricha Piper nigrum Katu Laghu, Teekshna

Ushna Katu KaphavataShamaka

Deepana, Pachana Vatanulomana

10 Nagara Zingiberofficinale

Katu Laghu, Snigdha

Ushna Madhura Kaphavata Shamaka

Triptighna, Rochana, Deepana, Pachana, Vatanulomana, Shothahara

11 Vriddhadaru Argeriaspeciosa

Tikta Laghu,Snigdha

Ushna Katu KaphavataShamaka

Vedanasthapana, Deepana, Pachana

12 Haritaki Terminaliachebula

Kashaya Pradhana Pancha Rasa

Laghu Rooksha

Ushna Madhura Tridosha Shothahara, Vedanasthapana,Anulomana, Mruduvirechana, Deepana, Pachana

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Drug Review

85

PANCHAKOLA PHANTA:3

This yoga contains 5 ingredients which are taken in equal quantity and

made into coarse powder. Phanta is prepared according to the Phanta Vidhi. In

both the group patients’, Panchakola Phanta 20 ml thrice daily administered

before food for a period of three days. The list of ingredients is given below:

Ingredients Proportion

Pippali 1part

Pippali moola 1part

Chavya 1part

Chitraka 1part

Nagara 1part

As discussed earlier Agni Deepana and Ama Pachana holds its

supremacy in treating the disease Amavata Deepana-Pachana helps in

Sampraptivighatana by virtue of its qualities. In Panchakola phanta, most of the

drugs are having Tikshna guna and Ushna veerya. Because of these qualities

it, does the Dosha Niramata and prevents further production of Ama6 (Table No.

4). This in turn brings vitiated Dosha to Koshta so that later it can be removed.

Hence the Panchakola Phanta is opted.

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Table no. 4-Properties and therapeutic effect of the individual drugs in Panchakola Phanta:

Sl.No. Name LatinName

Rasa Guna Veerya Vipaka Doshagnata Karmukata

01 Pippali Piperlongum

Katu Lagu,Snigdha, Teekshna

Anushnasheeta Madhura Kaphavata Deepana, Triptigna, Vatanulomana, Mruduvirechana, Balya, Rasayana

02 Pippalimoola

Piper longum

Katu Lagu,Snigdha, Teekshna

Anushnasheeta Madhura Kaphavata Deepana, Triptighna,Vatanulomana, Mruduvirechana, Balya, Rasayana

03 Chavya Piper chaba Katu Lagu,Rooksha

Ushna Katu Kaphavata Deepaka, PachakaShoolaprashamana Vatanulomana

04 Chitraka Plumbagozeylanicum

Katu Lagu,Rooksha Teekshna

Ushna Katu Kaphavata Deepaka, PachakaShoolaprashamana Vatanulomana

05 Nagara Zingiberofficinale

Katu Lagu,Snigdha

Ushna Katu Kaphavata Deepaka, PachakaShoolaprashamana Vatanulomana

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Eranda Taila:

Action of Eranda Taila in the management of Amavata has been

compared to the supremacy of the lion in the rivalry between lion and elephant4.

Eranda has Madhura rasa, Katu, Kashaya Anurasa; Snigdha, Tikshna,

Sukshma are its Gunas. It undergoes Madhura vipaka and has Ushna veerya7.

Due to the above said qualities, it does Vata and Kapha Shamana. It is

said that it does Srotovishodhana and thus can be employed in Samavata

condition. For the above said reasons, Taila has been selected for Koshta

Shodhana7.

After the Deepana, Pachana by administering Panchakola phanta for 3

days, Eranda Taila administered 10 ml once in morning hours on empty

stomach for 3 days.

REFERENCES:

1. Y.R. Poorva Kha. Vatavyadhi Chi 1-5

2. Y.R. Poorva Kha. Amavata Chi. 1-3

3. B.R. 5/193

4. B.R. 28/23

5. D.G. vol. II by P.V.Sharma

6. B.P. Madhya Kha. 26/49

7. S.S.Su. 45/114

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Materials and Methods

MATERIALS AND METHODS

MATERIALS TAKEN FOR THE STUDY:

Eranda Paka: Prepared according to the prescribed method in S.D.M.

Ayurvedic Pharmacy.

Ajamodadi Churna: Prepared according to the prescribed method in S.D.M.

Ayurvedic Pharmacy.

Panchakola Phanta: Prepared using Panchakola phanta churna procured from

S.D.M. Ayurvedic Pharmacy.

Eranda Taila: Procured from S.D.M. Ayurvedic Pharmacy.

METHODS:

Objective of the study:

1) To evaluate effect of Eranda Paka in the management of Amavata

2) To study the efficacy of Ajamodadi Churna in Amavata

3) To compare the efficacy of Eranda Paka and Ajamodadi Churna in Amavata.

Source of data:

20 patients diagnosed as Amavata (Rheumatoid arthritis) from IPD and

OPD of S.D.M. Ayurveda Hospital, Udupi. The patients were randomly grouped

into two groups of 10 each which were called Group EP (Eranda Paka group)

and Group AC (Ajamodadi Churna group)

Study design: Single blind comparative clinical study with pre-test and post-

test design.

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Inclusion criteria:

• Patients aged between 16 – 70 years age

• Signs and symptoms of Amavata

• Criteria for diagnosis of Rheumatoid Arthritis as approved by American

Rheumatism Association (ARA),1987 revision

Exclusion criteria:

• All connective tissue disorders other than Rheumatoid arthritis.

• Systemic Lupus Erythematosus

• With any other systemic disorder

Diagnostic criteria:

Patients were diagnosed on the basis of signs and symptoms of

Amavata and the criteria as approved by ARA, 1987 revision

• Morning stiffness* (Stabdata) (>1hour)

• Arthritis of three or more joints* (Shoola and Shotha in three or more

joints)

• Arthritis of hand joints.*

• Symmetrical arthritis.*

• Rheumatoid nodules.

• Rheumatoid factor.

• Radiological changes.

.

* - Duration of 6 weeks or more.

N.B. Diagnosis of R.A. made with four or more criteria

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Assessment criteria:

The patients were observed on the weekly basis and the change in

subjective signs and symptoms assessed by suitable scoring method and

objective signs using appropriate clinical tools. Details of which are given below.

A. Subjective criteria:

1. Pain in the joints:

Symptom Grading

No pain 0

Mild (on motion only) 1

Moderate (at rest) 2

Severe (wakes patient from sleep) 3

2. Morning stiffness (duration in hours):

Symptom Grading

0-5 min. 0

5 min. - 2 hrs. 1

2 - 8 hrs. 2

8 hrs. or more 3

3. Swelling in the joints:

Symptom Grading

Absent 0

Mild 1

Moderate 2

Severe 3

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4. Redness:

Symptom Grading

Absent 0

Mild 1

Moderate 2

Severe 3

5. Warmth:

Symptom Grading

Absent 0

Mild 1

Moderate 2

Severe 3

6. Tenderness in the joints:

Symptom Grading

No tenderness 0

Says tender 1

Patient winces 2

Winces and withdraws 3

Not allowed to be touched 4

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7. Alasya:

Symptom Grading

Fully active 0

Mild laziness, slow initiative in work 1

Initiative in some works, absent in others 2

Absolute lack of initiative even though capacity for work exists 3

8. Dourbalya:

Symptom Grading

No feeling of weakness 0

Slight weakness 1

Feeling of weakness but ability unimpaired 2

Ability to do duties affected 3

9. Knuckle swelling:

Jewellers rings were used to measure the knuckle swelling. The ring

which passes through knuckle with least resistance was noted. Any change in

the number of the ring after the treatment was recorded.

10. Muscle wasting:

The circumference of arm, fore arm, thigh and calf were measured in

cms using a measuring tape both before and after treatment to have an

objective view of muscle wasting.

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11. Malabaddhata/Vibandha (Constipation):

Symptom Grading

Absent 0

Slight with one motion per day 1

Marked constipation with one motion after two days or more 2

12. Jwara (in degree Fahrenheit):

Symptom Grading

No fever 0

Mild (990 F-1010 F) 1

Moderate (1010 F-1030 F) 2

Severe (>1030 F) 3

13. Sadana - fatigue:

Symptom Grading

No fatigue 0

Works full-time despite some fatigue 1

Patient must interrupt to rest 2

Fatigued at rest 3

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14. Bahumootrata (frequency of micturition per 24 hours):

Symptom Grading

Absent (less than 4 times/24 hrs) 0

Mild (upto 6 times/24 hrs) 1

Moderate (6-10 times/ 24 hrs) 2

Severe (> 10 times/ 24 hrs) 3

15. Chardi (frequency of bouts per 24 hours):

Symptom Grading

Absent 0

Mild (upto 2 vegas/24 hrs) 1

Moderate (2-4 vegas/24 hrs) 2

Severe (4 vegas/24 hrs) 3

16. The other symptoms like Angamarda, Aruchi, Gourava, Brama,

Kukshishoola, Hrithgraha, Anaha, Praseka, Trishna, Hasta pada daha, Kandu

are scored as mentioned below.

Grading

No symptoms 0

Mild symptoms 1

Moderate symptoms 2

Severe symptoms 3

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B. Functional assessment:

To assess the objective improvements following functional assessments

were carried out in patients of Amavata.

1. Grip strength: The patient’s ability to compress the inflated ordinary

sphygmomanometer cuff under standard conditions to assess the functional

capacity of effected upper limb, both before and after treatment.

2. Foot pressure: Foot pressure was recorded both before and after treatment

by the ability of the patient to press a weighing machine, to an objective view of

functional capacity of lower limb.

3. Range of joint movement: By using the Goniometer the range of movement

of all effected joints was noted both before and after treatment.

4. General functional capacity:

• Complete ability to carry on all usual duties without handicap 1

• Adequate normal activity despite handicap of discomfort or limited joint

movement 2

• Limited only to little or none of the usual occupation or self care 3

• Bedridden or confined to wheel chair, little or no self care 4

C. Investigations:

To assess the general condition and to confirm the diagnosis following

investigation were conducted before after the treatment

1. Hemoglobin percentage (Hb% using Sahli’s method)

2. Total Leukocyte count (TC using Neubauer’haemocytometer)

3. Differential Leukocyte count (DC using Neubauer’haemocytometer)

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4. Erythrocyte sedimentation rate (ESR using Westergren’s method)

5. Rheumatoid arthritis factor (using immunoglobulin agglutination method)

6. If required other investigations to rule out other pathologies.

D. Disease activity degrees:

On basis of criteria laid down by American rheumatism association

(1967) the degree of disease activity was estimated for the diagnosis and

therapeutic purpose. Details are as follows:

Grade 0 1 2 3

Morning

stiffness

5 minutes or

less

5 minutes to 2

hours

2 to 8 hours 8 hours or

Fatigue None Works full time

despite some

fatigue

must interrupt

work to rest

Fatigue at rest

Pain None only on

movement

At rest Wakes patient

from sleep.

Patients

estimation

Fine Almost well Pretty good Pretty bad

General

function

Full activity

without difficulty Most activities

but with difficulty

Few activities

cares for self

Little self care

mainly chair and

bed

Grip strength 200mm/Hg or

more 195 to 120

mm/Hg

115 to 70

mm/Hg

under 70mm/Hg

Spread of joint

Involvement

None 0to50 51to100 Over 100

Westergren

ESR

0to20mm 20to35 35to50 above 50

Haemoglobin 12.5gms% 12.4to11gms% 10.9to9.5gms% Less than

9.5gms%

Physicians

estimate

Inactive Minimal active moderately

active

severely active

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E. Overall assessment of the treatment:

The overall effect of the therapies assessed on the basis of criteria laid

down by ARA (1967) was adopted. The results are classified as four groups as

listed below.

Grade I: Complete remission

• No systemic signs of rheumatoid activity.

• No sign of inflammation.

• No evidence of activity in any extra articular process, including nodules,

tino-vaginitis and iritis.

• No lasting impairment of joint mobility other than that associated with

irreversible changes.

• No elevation of erythrocyte sedimentation rate.

• Articular deformity or extra articular involvement due to irreversible

changes may be present.

Grade II: Major improvement

• No systemic sign of rheumatoid activity, with the exception of an

elevated sedimentation rate and vasomotor imbalance.

• Major signs of inflammation resolved, such as heat, redness of joint

structures.

• No new rheumatoid process of intraarticular or extraarticular structures.

• Minimum joint swelling may be present.

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• Impairment of joint mobility associated with minimum residual activity

may be present.

• Articular deformity or extra articular involvement due to irreversible

changes may be present.

Grade III: minor improvement

Any decrease in the signs of rheumatoid activity inadequate to fulfill the

criteria of grade II.

• Diminution of systemic signs of rheumatoid activity.

• Signs of joint inflammation only partially resolved.

• No evidence of extension of rheumatoid activity into additional articular

or extra articular structures.

• Decreased but not minimum joint swelling present.

• Impairment of joint mobility may be present.

• Articular deformity or extraarticular involvement due to irreversible

changes may be present.

Grade IV: Unimprovement or progression

• Undiminished signs of rheumatoid activity, regardless of functional

capacity.

• Exacerbation of any previously involved joint or joints, or development of

sites of rheumatoid activity.

• Roentgenologic changes indicative of progression of the rheumatoid

process, excepting hypertrophy changes.

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• In the presence of one or more of the aforesaid criteria, involvement in

other features, including a normal or lowered ESR, not significant.

• Items which must be present.

INTERVENTION:

Deepana Pachana and Koshta Shodhana:

• Patients were randomly divided into two groups of minimum 10 patients

each.

• Before administration of medication, all patients of both groups were

given Panchakola phanta 20 ml thrice daily before food for first three

days for Deepana - Pachana.

• All patients of both groups were then given Eranda Taila 10ml on empty

stomach in the morning for next three days for Koshta Shodhana.

Eranda Paka and Ajamodadi Churna:

• Patients of Group EP were given Eranda Paka 15 gms three times daily

after food with warm water for 30 days.

• Patients in group AC were given Ajamodadi Churna 5 gms three times

daily after food with hot water for 30 days.

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Observations

OBSERVATIONS

In both the Eranda Paka and Ajamodadi Churna group, a total of 20

patients suffering from Amavata fulfilling the inclusion criteria were studied. The

observation and the results as well as statistical analysis of these are

elaborated as mentioned below.

• Descriptive statistical analysis.

• Assessment of the effect of Eranda Paka and Ajamodadi Churna in

patients of Amavata, and the assessment of the significance of the

treatment by adapting the paired ‘t’ test.

• Comparison of the effects of treatment between the Eranda Paka group

and Ajamodadi Churna group, and statistical analysis of the comparison

by performing unpaired ‘t’ test.

Descriptive statistical analysis:

Age group of patients: Out of 20 patients of Amavata studied in this work,

maximum number of 6 (30%) patients belonged to the age group of 50 to 60

years, against a minimum of 1 (5%) patient was in the age group of 10 to 20

years. The details are given in the Table No. 5 and Graph No. 1.

Sex incidence of patients: 15 (75%) of patients of Amavata were females as

against only 5 (25 %) of males in the present study. The details are elaborated

in the Table No. 6 and Graph No. 2.

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Incidence of Religion: As shown in the Table No. 7 and Graph No. 3 (65%) of

patients were Hindus, 5 (25%) were Muslims and only 2 (10%) of patients were

Christians.

Incidence of Literacy: Prevalence of literates was recorded in the present

study involving 20 patients of Amavata. 45% of the patients were illiterates and

the remaining 55% of patients had education, as detailed in the Table No. 8 and

Graph No. 4.

Incidence of Marital status: Among the 20 patients of Amavata taken for this

study, a maximum of 16 (80%) patients were married as against mere 4 (20 %)

of unmarried people. The details are shown in the Table No. 9 and Graph No. 5.

Socio-economical status of patients: The study revealed that most of the

patients belonged to either poor (35%) or lower middle socio-economical status

(35%) category. None of the patients were either from rich socioeconomic

status or from very rich socioeconomic status. Very poor percentage of patients

were from the middle class socioeconomic status (5%) and the upper middle

class socioeconomic status (5%) category. The details are given in the Table

No. 10 and Graph No. 6.

Incidence of Occupation: It is observed that 12 (60%) of the females in this

study were house wives by their occupation. Also, this formed the largest

category of patients leaving behind the patients engaged in other occupations.

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Observations

No patients from the business or student category were recorded in any of the

groups. Details are given in the Table No. 11 and Graph No. 7.

Incidence of Habits: Large percentage of patients in this study did not have

any addiction. Only 6 (30%) patients reported addiction to tobacco chewing as

against 14 (70%) of the non addicts. Table No. 12 and Graph No. 8 show the

details of the habits of patients.

Prakriti of patients: All the patients in the present study belonged to the

Dvandaja Prakriti. 6 (30%) patients were of Vatapitta and Vatakapha each. The

maximum 8 (40%) patients were of Pittakapha Prakriti Table No. 13 and Graph

No. 9.

Severity of the Vikriti: The degree of Vikriti was assessed to be Madhyama, in

a maximum of 16 (80%) patients in the present study followed by Avara in 3

(15%) patients and Pravara Vikriti in 1 (5%) patient. Details of the distribution of

the patients according to their degree of Vikriti is given in the Table No. 14 and

Graph No. 10.

Satva of patients: Majority of 14 (70%) patients belong to Madhyama Satva, 3

(15%) were of Pravara Satva and Avara Satva each in this study. The details

are shown in Table No. 15 and Graph No. 11.

Sara of patients: The assessment of Sara in 20 patients of Amavata showed

maximum number of patients having Madhyama Sara 19 (95%) and remaining

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Observations

1 (5%) patient belong to Avara Sara. Incidence of patients according to their

Sara is detailed in the Table No. 16 and Graph No. 12.

Samhanana of patients: Samhanana of every patient was assessed before

the treatment, and it was observed that among the 20 patients 17 (85%) of the

patients had Madhyma Samhanana. Pravara Samhanana was recorded in just

1 (5%) of the patients. Remaining 2 (10%) of the patients showed characters of

the Avara Samhanana. The detail of the same are given in the Table No. 17

and Graph No. 13.

Satmya of patients: Observation of 20 patients of Amavata revealed that only

1 (5%) of the patients had Pravara Satmya, and the remaining 19 (95%) of

patients showed Madhyama Satmya. Table No. 18 and Graph No. 14 show the

details.

Ahara Abhyavaharana Shakti in patients of Amavata: Interrogation of the 20

patients of Amavata revealed that 12 (60%) of the patients had Madhyama

Abhyavaharana Shakti and 4 (20%) each patients had either Pravara or Avara

Abhyavaharan Shakti. Details are given in the Table No. 19 and Graph No. 15.

Ahara Jarana Shakti of patients: Jarana Shakti of 20 patients suffering from

amavata revealed that majority 12 (60%) had Madhyama Jarana Shakti. 4

(20%) each patients had the Avara and Pravara Jarana Shakti. The same is

shown in the Table No. 20 and Graph No. 16.

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Observations

Vyayama Shakti of patients: Madhyama Vyayama Shakti is recorded in 13

(65%) of patients. 5 (25%) of the patients had Avara Vyayama Shakti and the

remaining 2 (10%) patients had Pravara Vyayama Shakti. The same is given in

the Table No. 21 and Graph No. 17.

Vaya of the patients: All the 20 patients in this study belonged to Madhyama

Vaya. This has been shown in Table No. 22 and Graph No. 18.

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Observations

Table No. 5-Age Group of Patients:

Total Age in years

No %

10-20 1 5

20-30 4 20

30-40 5 25

40-50 4 20

50-60 6 30

Graph No. 1-Age groupwise distribution of patients:

5%

20%

25%

20%

30%

0%

5%

10%

15%

20%

25%

30%

20ـ10 20-30 30-40 40-50 50-60

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Observations

Table No. 6-Sex Incidence of Patients:

Total Sex

No %

Male 5 25

Female 15 75

Graph No. 2-Percentage of patients of different sex:

25%

75%

0%

10%

20%

30%

40%

50%

60%

70%

80%

Male Female

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Observations

Table No. 7-Religion of patients 20 patients of Amavata:

Total Religion

No %

Hindu 13 65

Muslim 5 25

Christian 2 10

Others 0 0

Graph No. 3-Percentage of patients of different religion:

65%

25%

10%

0%

10%

20%

30%

40%

50%

60%

70%

Hindus Muslims Christian

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Observations

Table No. 8-Literacy incidence in patients of Amavata:

Total Education

No %

Illiterate 9 45

Literate 11 55

Graph No. 4-Incidence of Literacy:

55%

45%

0%

10%

20%

30%

40%

50%

60%

Literate Illiterate

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Observations

Table No. 9-Marital status of Amavata patients:

Total Marital Status

No %

Single 4 20

Married 16 80

Widowed 0 0

Graph No. 5-Percentage of patients of different marital status:

80%

20%

0%

10%

20%

30%

40%

50%

60%

70%

80%

Married Unmarried

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Observations

Table No. 10-Socio-economic status of patients:

Total S.E.Status

No %

Poor 7 35

Lower Middle 7 35

Middle 5 25

Upper Middle 1 5

Rich 0 0

Very Rich 0 0

Graph No.6-Incidence of Socio-economical status of patients:

35% 35%

25%

5%

0% 0%

0%

5%

10%

15%

20%

25%

30%

35%

Poor L.Middle Middle U.Middle Rich Very Rich

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Observations

Table No. 11-Incidence of occupation in Amavata patients:

Total Occupation

No %

Manual Laborer 6 30

House Wife 12 60

Student 0 0

Business 0 0

Others 2 10

Graph No.7-Occupation wise distribution of patients:

30%

60%

0% 0%

10%

0%

10%

20%

30%

40%

50%

60%

Laborer House-Wife Student Buisness Others

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Observations

Table No. 12-Study of Habit incidence:

Total Habit

No %

Alcohol 0 0

Tobacco 6 30

Smoking 0 0

None 14 70

Graph No. 8- Distribution of patients according to their habits:

0%

30%

0%

70%

0%

10%

20%

30%

40%

50%

60%

70%

Alcohol Tobacco Smoking None

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Observations

Table No. 13-Study of patients Prakriti in the study:

Total Prakriti

No %

Vata 0 00

Pitta 0 00

Kapha 0 00

Vata-Pitta 6 30

Pitta-Kapha 6 30

Vata-Kapha 8 40

Sama 0 00

Graph No.9- Prakriti wise distribution of patients:

0% 0% 0%

30% 30%

40%

0%

0%

5%

10%

15%

20%

25%

30%

35%

40%

Vata Pitta Kapha V-P V-K P-K Sama

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Observations

Table No.14-Incidence of Vikriti:

Total Vikriti

No %

Pravara 1 5

Madhyama 16 80

Avara 3 15

Graph No. 10-Vikruti wise distribution of patients:

5%

80%

15%

0%

10%

20%

30%

40%

50%

60%

70%

80%

Pravara Madhyama Avara

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Observations

Table No.15-Incidence of Satva in the Study:

Total Satva

No %

Pravara 3 15

Madhyama 14 70

Avara 3 15

Graph No. 11-Percentage of patients according to Satva:

15%

70%

15%

0%

10%

20%

30%

40%

50%

60%

70%

Pravara Madhyama Avara

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Observations

Table No.16-Study of Saratah Incidence in the Study:

Total Saratah

No %

Pravara 0 0

Madhyama 19 95

Avara 1 5

Graph No. 12- Percentage of patients according to Sara:

0%

95%

5%

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Pravara Madhyama Avara

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Observations

Table No. 17-Study of patients Samhanana in the study:

Total Samhanana

No %

Pravara 1 5

Madhyama 17 85

Avara 2 10

Graph No.13. Percentage of patients according to Samhanana:

5%

85%

10%

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

Pravara Madhyama Avara

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Observations

Table No. 18-Satmya Incidence:

Total Satmya

No %

Pravara 1 5

Madhyama 19 95

Avara 0 0

Graph No. 14- Percentage of patients according to Satmya:

5%

95%

0%

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Pravara Madhyama Avara

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Observations

Table No. 19- Percentage of patients according to Abhyavaharana Shakti:

Total Ahara-Abhyavaharana Shakti

No %

Pravara 4 20

Madhyama 12 60

Avara 4 20

Graph No. 15-Percentage of patients of different Abhyavaharana Shakti:

20%

60%

20%

0%

10%

20%

30%

40%

50%

60%

Pravara Madhyama Avara

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Observations

Table No. 20-Study of Patients Ahara-Jarana Shakti the Study:

Total Ahara-Jarana Shakti

No %

Pravara 4 20

Madhyama 12 60

Avara 4 20

Graph No. 16- Percentage of patients according to Aahara-Jarana Shakti:

20%

60%

20%

0%

10%

20%

30%

40%

50%

60%

Pravara Madhyama Avara

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Observations

Table No. 21-Study of patients Vyayama Shakti in the study:

Total Vyayama Shakti

No %

Pravara 2 10

Madhyama 13 65

Avara 5 25

Graph No. 17- Percentage of patients according to Vyayama Shakti:

10%

65%

25%

0%

10%

20%

30%

40%

50%

60%

70%

Pravara Madhyama Avara

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Observations

Table No.22-Vaya incidence:

Total Vaya

No %

Bala 0 0

Madhyama 20 100

Vruddha 0 0

Graph No. 18- Percentage of patients according to Vaya:

0%

100%

0%

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

Baala Madhyama Vruddha

Page 161: Amavata kc004 udp

Results

RESULTS

Eranda Paka group

Effect on cardinal signs and symptoms:

The oral administration of Eranda Paka had resulted in remission of all

the cardinal symptoms of Amavata as elaborated in the following paragraph.

Effect on Stabdhata:

Patients treated with Eranda Paka marked remission of the symptom

Stabdhata was recorded. 2.3 was the mean initial score of Stabdhata in 10

patients of Amavata came down to 1.1 after the treatment. The improvement to

the tune of 52% is found to be statistically highly significant (P≤0.001) as shown

in the Table No. 23 and Graph No. 19.

Effect on Sandhi Shoola:

Sandhi Shoola, one of the cardinal symptoms of Amavata relieved by

65% as the initial score of Sandhi Shoola which was 2.3 reduced to 0.8 after the

treatment with Eranda Paka. This improvement when analyzed by the paired ‘t’

test found to the highly significant (P≤0.001). Table No. 23 and Graph No. 19

provides the details.

Effect on Sandhi Shotha:

69% of improvement was observed in the symptom Sandhi Shotha.

1.353 was the initial mean score of Sandhi Shotha recorded in the 10 patients

of Amavata in this group. This was brought down to 0.418 after the

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administration of Eranda Paka. This improvement after the treatment is found to

be highly significant (P≤0.002) as per the paired ‘t’ test. The detail of the

different statistical values are shown in the Table No. 23 and Graph No. 19.

Effect on tenderness:

1.649 was the mean initial score of tenderness before the treatment in

patients of Eranda Paka group. This initial mean score came down to 0.439

after the treatment. The improvement to the tune of 73% was highly significant

(P≤0.001) as revealed by the paired ‘t’ test. Details of the same are given in the

Table No. 23 and Graph No. 19.

Effect on Crepitation:

Crepitation is another cardinal symptom of Amavata. None of the

patients in this Eranda Paka group presented this symptom. Therefore, the

effect of the Eranda Paka in relieving this symptom could not be assessed.

Details of the same are represented in the Table No. 23 and Graph No. 19.

Effect on general symptoms:

Complete cure of the symptom Jwara was observed in all the patients

treated with Eranda Paka. The initial mean score of Jwara was 0.6, and it

became 0 after the treatment. 91% remission of the symptom Aruchi was

recorded in patients of Amavata. The initial mean score of Aruchi which was 2.2

was reduced to 0.2 after the treatment with Eranda Paka. A minimal mean initial

score of 0.5 was observed in the symptom trit. Complete remission of trit was

recorded after the treatment with Eranda Paka. 76% of the improvement was

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noted in the symptom Alasya. The initial mean score of 2.10 was reduced to 0.5

after the treatment. Before the institution of the treatment the initial mean score

of the symptom Apaka was 2.3. This came down to 0.2 after the treatment. The

improvement by the treatment recorded was 91%. Marked improvement was

observed in the symptom Angamarda also. The initial mean score of

Angamarda was 2.3 and was reduced by 57% after the treatment. The

symptoms like Angasunata, Raga, Staimitya, Angagourava, Kandu and

Antrakujana was not found in any of the 10 patients studied in this group. The

initial mean score of 1.3 of the symptom Daha was reduced by 92% after the

treatment. The mean score of Daha was 0.1 after the treatment. Complete

remission of the Hrillasa was observed in all the patients treated with Eranda

Paka. The initial mean score of 0.1 came down to 0 after the treatment. The

initial mean score of Chardi was 0.10. Cent percent remission of this symptom

was observed after the treatment. Complete remission of the symptom Anaha

was noted in all the patients. The initial mean score of Anaha, which was 1.0

became zero after the employment of the treatment. 0.5 was the initial mean

score of the symptom Praseka in patients treated with Eranda Paka. The

symptom got completely cured after the treatment. The initial mean score of the

symptom Kukshi Shoola was found to be 0.3. This initial score reached to zero

after the treatment releaving 100% cure. 50% of improvement was observed in

patients complaining of disturbed sleep. The initial mean score of the symptom

Nidralpata was 1.0 and that dropped to 0.5 after the treatment. The details of

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the effect of the Eranda Paka on different general symptoms of Amavata are

given in the Table No. 24 and Graph No. 20.

Effect on total score of general symptoms:

The mean of the total score of general symptoms showed marked

improvement in these symptoms. Initially before the treatment the total score of

general symptom was 18.6 and was reduced to 3.3 after the administration of

the Eranda Paka. An over all improvement of 82% in general symptoms was

recorded in this group. The improvement after the treatment is also statistically

highly significant (P≤0.001) as revealed by the paired ‘t’ test. The details are

given the Table No. 25 and Graph No. 21.

Effect of Eranda Paka on symptoms of Ama:

Significant improvement was noticed in all the symptoms indicative of

Ama by the administration of Eranda Paka. Bala of the patients was improved

by 64% as suggested by the change in the symptom score to 0.80 after the

treatment from the initial score of 2.20. The symptom Gaurava was not

observed in any patients studied in this group. The initial mean score of Alasya,

which was 2.1 before the treatment dropped down to 0.50 after the treatment.

Thus the treatment showed a reduction of Alasya by 76 %. Complete remission

of the symptom Apaka was recorded in patients of Amavata treated with Eranda

Paka. The initial score before the treatment was 1.10, and which came down to

zero after the treatment. The initial mean score of Nistiva was 0.5, which came

down to zero after the treatment recording complete remission of the symptom.

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91% of the improvement was recorded in the symptom Aruchi. The initial score

of 2.20 reduced to 0.2 after the treatment with Eranda Paka. Proper bowel habit

was restored after the medication with Eranda Paka in patients of Amavata.

Before the treatment the severity score of Vibanda was 1.1, and it became zero

after the treatment suggesting the complete remission. Impaired taste in the

mouth was reduced by the treatment with Eranda Paka to the tune of 64%. The

mean score of Aruchi was reduced by 2.0 from the initial score of 2.2 before the

treatment. Patients felt more comfortable after the treatment as the severity of

the Klama was reduced by the treatment. 2.2 was the initial score of Klama

before the treatment. This score dropped down to 0.8 following the treatment.

Analysis of the symptoms of the Ama before and after the treatment is

elaborated in the Table No. 26 and Graph No. 22.

Statistical analysis of effect on symptoms of Ama:

Before the treatment the total score of symptoms of Ama was 12.7. After

the treatment with Eranda Paka this reduced to 2.4. The total improvement was

to the tune of 81%. This improvement after the treatment was found to be

statistically highly significant (P≤0.001) as assessed by the paired ‘t’ test. The

details of the same is given in the Table No. 27 and Graph No. 23.

Effect on clinical parameters

Effect on circumference of the limbs:

The circumference of the limbs that was assessed before and after the

treatment showed that there was neither increase nor decrease in the

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circumference after the medication with Eranda Paka. The details of the same

is given in the Table No. 28.

Effect on the range of joint movement:

Range of joint movement was increased after the treatment with Eranda

Paka in patients of Amavata. Initially an average range of 61.98 degree of joint

movement was recorded. This range of joint movement was increased to

78.864 after the treatment. The paired ‘t’ test revealed that this change after the

treatment was not because of the chance factor. The improvement of joint

movement was highly significant. The details are given in the Table No. 29 and

Graph No. 24.

Effect on foot pressure:

Improvement in the foot pressure was recorded in patients of Eranda

Paka group. Before the treatment the average foot pressure of the patients was

30.4 kgs. And this was increased to 38.95 kgs after the treatment. This marked

change after the treatment was also statistically highly significant according to

the paired ‘t’ test. Table No. 29 and Graph No. 24 shows the detail of the

statistical values.

Effect on hand grip power:

After the treatment with Eranda Paka the hand grip power of the patients

was significantly increased. The average hand grip power before the treatment

was 62.000 mm of hg. After the administration of the Eranda Paka it increased

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to 85.950 mm of hg. This increase in hand grip power after the treatment was

found to be statistically highly significant (P≤0.001). Table No. 29 and Graph

No. 24 shows the detail.

Effect on general functional capacity:

Treatment with Eranda Paka has shown favorable effect on functional

ability of patients of Amavata. The functional disability score before the

treatment was estimated as1.700. And this score came down to 0.800 recording

an improvement by 52%. Statistical analysis by adapting paired ‘t’ test revealed

that this change after the treatment is highly significant (P≤0.001). Details are

given in the Table No. 29 and Graph No. 24.

Effect on body weight:

The body weight of the patients recorded before and after the treatment

showed marginal change. There was very little increase of body weight by

0.100 kg after the treatment. This change following the treatment is statistically

insignificant (P=0.343) as determined by the paired ‘t’ test. The details are given

in the Table No. 30.

Effect on hematological values

Effect on total leukocyte count:

There was marginal decrease in total leukocyte count after the treatment.

The initial TC was 10345.000 cu.mm and this came down to 8759.000 cu.mm.

after the treatment. The details are shown in the Table No. 31 and Graph

No.25.

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Effect on differential count of WBC’s:

Minimal change was also observed in the differential count of white blood

corpuscles. The statistical analysis by adapting the paired ‘t’ test revealed that

these changes after the treatment are insignificant. The details are given in the

Table No. 31.

Effect on haemoglobin percentage:

Before the treatment the initial haemoglobin percentage was 10.175

gm%. This was then increased to 10.970 gm% after the treatment. This

increase of hemoglobin by 0.795 gm% is statistically insignificant as shown by

the paired ‘t’ test. The details of the same are shown in the Table No. 31 and

Graph No. 26.

Effect on erythrocyte sedimentation rate:

The erythrocyte sedimentation showed a marginal decrease. Before the

treatment the average ESR in patients of Amavata studied in this group was

82.0 mm at 1st hour. A reduction by 38.400 mm at 1st hour was recorded after

the treatment with Eranda Paka. This decrease in the ESR was also statistically

highly significant (P=0.006). Table No. 31 and Graph No. 27 shows the detail.

Over all effect of treatment in 10 patients of Amavata:

The assessment of the overall effect of the treatment revealed that 40%

of the patients recorded complete remission. 30% of the patients showed major

improvement. And an equal percentage of the patients also responded with

minor improvement. All the patients studied in this Eranda Paka group showed

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Results

different degrees of remission. The details are given in the Table No. 32 and

Graph No. 28.

From the foregoing observations, it is clear that the patients who are

treated with Eranda Paka have shown favorable response in regards to cardinal

symptoms of Amavata, general symptoms of Amavata, clinical parameters,

hematological investigations and overall effect of the medication. Most of these

improvements are found to be statistically highly significant as per the paired ‘t’

test except the few parameters like circumference of the limbs, body weight.

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Table No. 23-Effect of Eranda Paka on cardinal symptoms of Amavata:

Mean score Paired ‘t’ test Signs and

symptoms B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

Stabdata 2.3(0.483) 1.1 (0.316) 52 0.632 0.20 6.0 ≤0.001

Sandhi

Shoola 2.3 (0.675) 0.8 (0.422) 65 0.527 0.167 9.00 ≤0.001

Sandhi

Shotha

1.353

(0.574)

0.418

(0.498) 69 0.702 0.222 4.214 ≤0.002

Tenderness 1.649

(0.317)

0.439

(0.277) 73 0.269 0.0849 14.249 ≤0.001

Crepitation 0 0 - - - - -

Graph No. 19-Effect of Eranda Paka on cardinal symptoms of Amavata:

2.3

1.1

2.3

0.8

1.35

0.42

1.65

0.44

0 00

0.5

1

1.5

2

2.5

Stabdata S Shoola S Shotha Tenderness Crepetation

B T A T

Page 171: Amavata kc004 udp

Results

Table No. 24-Effect of Eranda Paka on general symptoms of Amavata:

Mean score Symptoms

Initial After treatment

Percentage of

relief.

Jwara 0.600 0.000 100

Aruchi 2.200 0.200 91

Trit 0.500 0.000 100

Alasya 2.100 0.500 76

Apaka 2.300 0.200 91

Angamarda 2.300 1.000 57

Anga Sunata 0 0 0

Daha 1.300 0.1000 92

Raga 0 0 0

Staimitya 0 0 0

Gaurava 0 0 0

Kandu 0 0 0

Hrillasa 0.1000 0.000 100

Chardi 0.1000 0.000 100

Anaha 1.000 0.000 100

Praseka 0.500 0.000 100

Antrakujana 0 0 0

Kukshi Shoola 0.300 0.000 100

Vibanda 1.100 0.000 100

Shrama 2.200 0.800 63

Bahumutra 0.500 0.000 100

Bhrama 0.1000 0.000 100

Hridgraha 0.500 0.000 100

Nidralpata 1.000 0.500 50

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Results

Graph No. 20-Improvement in general symptoms recorded in patients

treated with Eranda Paka:

0.60

2.20.2

0.50

2.10.5

2.30.2

2.30.1

1.30.10.1

00.1

01

00.5

00.3

01.1

02.2

0.80.5

00.1

00.5

01

0.5

0 0.5 1 1.5 2 2.5

Jwara

Aruci

Trit

Alasya

Apaka

Angamarda

Daha

Hrillasa

Chardi

Anaha

Praseka

Kuksi sula

Vibandha

Shrama

Bahumutra

Bhrama

Hridgraha

Nidralpata

B T A T

Page 173: Amavata kc004 udp

Results

Table No. 25-Overall effect of Eranda Paka on general symptoms of

Amavata:

Mean score Paired ‘t’ test Criteria

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

General

symptoms

18.600

(3.406)

3.300

(2.312) 82 2.946 0.932 16.424 ≤0.001

Graph No. 21-Overall effect of Eranda Paka on general symptoms of

Amavata:

18.6

3.3

0

5

10

15

20

B.T. A.T.

Page 174: Amavata kc004 udp

Results

Table No. 26-Effect of Eranda Paka on the symptoms of Ama:

Mean score Symptoms

Initial After treatment Percentage of relief

Balabhramsa 2.200 0.800 64

Gaurava 0 0 -

Alasya 2.100 0.500 76

Apakthi 1.100 0.000 100

Nistiva 0.500 0.000 100

Malasanga 1.100 0.000 100

Aruchi 2.200 0.200 91

Klama 2.200 0.800 64

Graph No. 22-Effect of Eranda Paka on symptoms of Ama:

2.2

0.8

0 0

2.1

0.5

1.1

0

0.5

0

1.1

0

2.2

0.2

2.2

0.8

0

0.5

1

1.5

2

2.5

Scor

e

Bala

bram

sha

Gou

rava

Alas

ya

Apak

ti

Nis

htiva

Mal

asan

ga

Aruc

hi

Klam

a

B T A T

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Results

Table No. 27-Overall effect of Eranda Paka on symptoms of Ama:

Mean score Paired ‘t’ test Criteria

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

Symptoms

of Ama

12.700

(2.406)

2.400

(2.221) 81 2.111 0.667 15.431 ≤0.001

Graph No. 23-Effect of Eranda Paka on total symptom score of Ama:

12.7

2.4

02468

101214

Tota

l sco

re

B.T. A.T.

Table No. 28-Effect of Eranda Paka on circumference of limbs:

Mean score Paired ‘t’ test Circumference

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

Arm 24.625

(2.698)

24.625

(2.698) - - - - -

Fore arm 23.425

(2.249)

23.425

(2.249) - - - - -

Thigh 44.700

(4.894)

44.700

(4.894) - - - - -

Leg 32.350

(3.859)

32.350

(3.859) - - - - -

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Results

Table No. 29-Effect of Eranda Paka on different clinical parameters:

Mean score Paired ‘t’ test Parameters

B.T.(S.D.±) A.T.(S.D.±)

Difference

in mean S.D.± S.E.± ‘t’ P

Range of

joint

movement

in degrees

61.980

(26.315)

78.864

(37.491) 27.24 14.267 4.512 3.742 =0.005

Foot

pressure in

kgs

30.400

(9.216)

38.950

(9.290) 28 2.640 0.835 10.242 ≤0.001

Hand grip

in mm of hg

62.000

(16.700)

85.950

(22.47) 39 13.475 4.261 5.620 ≤0.001

General

functional

disability

1.700

(0.483)

0.800

(0.632) 52 0.568 0.180 5.014 ≤0.001

Graph No. 24-Effect of Eranda Paka on different clinical parameters:

61.98

78.86

30.4

38.95

62

85.95

1.7 0.80

10

20

30

40

50

60

70

80

90

J motion F pressure H grip F disability

B T A T

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Results

Table No. 30-Effect of treatment on body weight of patients of Amavata:

Mean score Paired ‘t’ test Criteria

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

Body

weight

51.000

(11.235)

51.100

(11.140)

0.100 0.316

0.1000 1.000 =0.343

Table No. 31-Effect of Eranda Paka on different hematological values:

Mean score Paired ‘t’ test Investigation

B.T.(S.D.±) A.T.(S.D.±)BT-AT

S.D.± S.E.± ‘t’ P

TC /cu.mm. 10345.000

(1977.857)

8759.000

(1828.882)1586.000 1850.064 585.042 2.711 =0.024

DC-

neutrophils-%

68.800

(7.843)

56.100

(14.594) 12.700 18.343 5.800 2.189 =0.056

Lymphocytes 26.100

(8.020)

36.500

(13.534) -0.400 16.748 5.296 -1.964 =0.081

Eosinophils 4.600

(0.966)

6.100

(2.601) -1.500 2.838 0.898 -1.671 =0.129

Monocytes 0.400

(0.516)

0.700

(0.483) -0.300 0.483 0.153 -1.964 =0.081

Basophils 0.1000

(0.316)

0.000

(0.000) 0.1000 0.316 0.1000 1.000 =0.343

ESR – I hour 82.000

(35.640)

43.600

(28.702) 38.400 34.069 10.774 3.564 =0.006

Haemoglobin 10.175

(1.728)

10.970

(1.259) 0.795 1.362 0.431 1.846 =0.098

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Results

Graph No. 25-Effect of Eranda Paka on TLC:

10345

8759

7500

8000

8500

9000

9500

10000

10500

TLC

B T A T

Graph No. 26-Effect of Eranda Paka on Hb%:

10.175

10.97

9.6

9.8

10

10.2

10.4

10.6

10.8

11

Hb%

B T A T

Graph No. 27-Effect of Eranda Paka on ESR:

82

43.6

0

20

40

60

80

100

ESR

B T A T

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Results

Table No. 32-Over all effect of treatment in 10 patients of Amavata:

Treatment effect No of patients Percentage

Complete remission 4 40

Major improvement 3 30

Minor improvement 3 30

No change 0 00

Graph No. 28-Over all effect of treatment in 10 patients of Amavata:

40

3030

005

10

15

2025

30

35

40

complete Major Minor No change

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Results

Ajamodadi Churna group

Effect on cardinal signs and symptoms:

The oral administration of Ajamodadi Churna has resulted in remission of

all the cardinal symptoms of Amavata as elaborated in the following

paragraphs.

Effect on Stabdhata:

69% of improvement was observed in the symptom Stabdhata. 2.200

was the initial mean score of Stabdata recorded in the 10 patients of Amavata

in this group. This was brought down to 1.000 after the oral administration of

Ajamodadi Churna. This improvement after the treatment is found to be

statistically highly significant (P≤0.002) as per the paired ‘t’ test. The detail of

the different statistical values are shown in the Table No. 33 and in Graph No.

29.

Effect on Sandhi Shoola:

Reduction in the severity of the Sandhi Shoola was noted after the

medication. 2.200was the initial mean score of Sandhi shoola recorded in the

10 patients of Amavata in this group. This symptom score then reduced to

1.200 after the administration of Ajamodadi Churna. This improvement after the

treatment is found to be statistically highly significant (P≤0.001) and is assessed

by the paired ‘t’ test. The related statistical values are depicted in the Table No.

33 and in Graph No. 29.

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Effect on Sandhi Shotha:

Sandhi Shotha, one of the cardinal symptom of Amavata was relieved by

58% as the initial score of Sandhi Shotha which was 1.377 then reduced to

0.565 after the treatment with Ajamodadi Churna. This improvement when

analyzed by the paired ‘t’ test found to the highly significant (P≤0.001). Table

No. 33 and the Graph No. 29 provides the detail.

Effect on tenderness:

1.884 was the mean initial mean score of tenderness before the

treatment in patients of Ajamodadi Churna group. This initial mean score came

down to 0.897 after the treatment. The improvement to the tune of 52% was

highly significant (P≤0.001) as revealed by the paired ‘t’ test. The related

statistical values are shown in the Table No. 33 and in the Graph No. 29.

Effect on crepitation:

None of the patients in this Ajamodadi Churna group presented with this

symptom. There fore the effect of the Ajamodadi Churna on this symptom could

not be assessed. Table No. 33 and in Graph No. 29 shows the details.

Effect on general symptoms:

Best improvement was observed in all the general symptoms of Amavata

in patients treated with Ajamodadi Churna. Following lines elaborate the exact

percentage of improvement. Marked improvement was observed in the

symptom Angamarda. The initial mean score of Angamarda was 2.3 and then

was reduced by 48% after the treatment. The mean symptom score after the

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treatment was 1.2. By the administration of Ajamodadi Churna the fever came

down significantly in patients of Amavata. The initial score of Jwara was 0.500

and that came down to 0.1000 after the treatment recording 80% of

improvement. 91% remission of the symptom Aruchi was recorded in patients of

Amavata. The initial mean score of Aruchi which was 1.200 then reduced to

0.1000 after the medication. A minimal mean initial score of 0.5 was observed

in the symptom trit. This score came down to 0.200 after the treatment with

Ajamodadi Churna. This means 60% of improvement in the symptom Aruchi by

the medication. 58% of the improvement was noted in the symptom Alasya. The

initial mean score of 1.900 was reduced to 0.800 after the treatment. Before the

institution of the treatment the initial mean score of the symptom Apaka was

1.400. This came down to 0.2 after the treatment. The improvement by the

treatment recorded was 86%. The symptoms like Angashunata, Raga,

Staimitya, Angagourva, Kandu Hrillasa Chardi and Antrakujana was not found

in any of the 10 patients studied in this group. The initial mean score of 1.100 of

the symptom Daha was reduced by 73% after the treatment. The mean score of

Daha was 0.300 after the treatment. Marked remission of the symptom Anaha

was noted in all the patients. The initial mean score of Anaha, which was 1.100,

became 0.200 after the employment of the treatment indicating 90% of

improvement. 0.400 was the initial mean score of the symptom Praseka in

patients treated with Ajamodadi Churna. This reduced to 0.1000 after the

treatment. Thus an improvement by 75% was recorded by the treatment. The

initial mean score of the symptom Kukshi Shoola was found to be 0.500. This

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initial score reached to zero after the treatment releaving 100% cure. The initial

mean score of Vibandha was 0.600, and this came down to 0.1000 after the

administration of Ajamodadi Churna. Thus 83% of improvement was recorded

in this symptom. The symptom Shrama was reduced by 55% by the treatment

with Ajamodadi Churna. The initial mean score of Shrama was 2.000 and which

reduced to 0.900 after the treatment. 25% of the improvement was recorded in

the symptom Bahumutra after the treatment. The initial mean score of

Bahumutrata was 0.4 and that came down to 0.3 after the treatment. Complete

remission of the symptom was noted in patients treated with Ajamodadi Churna

in relation to the symptoms, Bhrama and Hridgraha. 57% of improvement was

observed in patients complaining of disturbed sleep. The initial mean score of

the symptom Nidralpata was 0.700 and that dropped to 0.300 after the

treatment. The details of the effect of the Ajamodadi Churna on different

general symptoms of Amavata is given in the Table No. 34 and Graph No. 30.

Total effect on general symptoms:

The study showed that after the administration of the Ajamodadi Churna

marked remission of the symptoms was observed. Initially before the treatment

the total score of general symptom was 15.2 and was reduced to 4.9 after the

administration of the Ajamodadi Churna. An over all improvement of 68% in

general symptoms was recorded in this group. The improvement after the

treatment is also statistically highly significant (P≤0.001) as revealed by the

paired ‘t’ test. The details are given in the Table No. 35 and in Graph No. 31.

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Effect of Ajamodadi Churna on symptoms of Ama:

Symptoms indicative of Ama showed marked remission by the

administration of Ajamodadi Churna. Bala of the patients was improved by 55%

as suggested by the change in the symptom score to 0.900 after the treatment

from the initial score of 2.000. Significant remission of the symptom Gourava

was seen in patients treated with Ajamodadi Churna. Before the treatment the

symptom score of Gourava was 2.300. This reduced to 1.100 after the

treatment. The initial mean score of Alasya, which was 1.900 before the

treatment dropped down to 0.800after the treatment. Thus the treatment

showed a reduction of Alasya by 57%. Marked remission of the symptom Apaka

was recorded in patients of Amavata treated with Ajamodadi Churna. The initial

score before the treatment was 1.400, and which came down to 0.200 after the

treatment. The initial mean score of Nistiva was 0.400, which came down to

0.1000 after the treatment recording 75% remission of the symptom. 92% of the

improvement was recorded in the symptom Aruchi. The initial score of 1.200

reduced to 0.1000 after the treatment with Ajamodadi Churna. Good restoration

of the bowel habit was recorded after the medication with Ajamodadi Churna in

patients of Amavata. Before the treatment the severity score of Vibandha was

0.600, and it became 0.1000 after the treatment suggesting 83% of remission.

Patients felt more comfortable after the treatment as the severity of the Klama

was reduced by the treatment. 2.100 was the initial score of Klama before the

treatment. This score dropped down to 1.000 following the treatment. Analysis

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of the symptoms of the Ama before and after the treatment is elaborated in the

Table No. 36 and Graph No. 32.

Statistical analysis of effect on symptoms of Ama:

Before the treatment the total score of symptoms of Ama was 11.9. After

the treatment with Ajamodadi Churna this reduced to 4.3. The total

improvement was to the tune of 64%. This improvement after the treatment was

found to be statistically highly significant (P≤0.001) as assessed by the paired ‘t’

test. The details of the same is given in the Table No. 37 and in Graph No. 33.

Effect on clinical parameters

Effect on circumference of the limbs:

The circumference of the limbs that was assessed before and after the

treatment showed that there was neither increase nor decrease in the

circumference after the medication with Ajamodadi Churna. The details of the

same is given in the Table No. 38.

Effect on the range of joint movement:

Range of joint movement was increased after the treatment with

Ajamodadi Churna in patients of Amavata. Initially an average range of 79.690

degree of joint movement was recorded. This range of joint movement was

increased to 94.200 after the treatment. The paired ‘t’ test revealed that this

change after the treatment was not because of the chance factor. The

improvement of joint movement was highly significant. The details are given in

the Table No. 39 and in Graph No. 34.

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Effect on foot pressure:

Improvement in the foot pressure was recorded in patients of Ajamodadi

Churna group. Before the treatment the average foot pressure of the patients

was 32.800 kgs. And this was increased to 40.050 kgs after the treatment. This

marked change after the treatment was also statistically highly significant

according to the paired ‘t’ test. Table No. 39 and Graph No. 34 shows the

details of the statistical values.

Effect on hand grip power:

After the treatment with Ajamodadi Churna the hand grip power of the

patients was significantly increased. The average hand grip power before the

treatment was 71.750 mm of hg. After the administration of the Ajamodadi

Churna it increased to 98.500 mm of Hg. This increase in hand grip power after

the treatment was found to be statistically highly significant (P=0.005). The

Table No. 39 and Graph No. 34 shows the details.

Effect on general functional capacity:

Treatment with Ajamodadi Churna has shown favorable effect on

functional ability of patients of Amavata. The functional disability score before

the treatment was estimated as 1.900. And this score came down to 1.000

recording an improvement by 0.90 score. Statistical analysis by adapting paired

‘t’ test revealed that this change after the treatment is highly significant

(P≤0.001). Details are given in the Table No. 39 and in Graph No. 34.

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Effect on body weight:

The body weight of the patients recorded before and after the treatment

showed minimal change. There was mere an increase of 100 gms in the mean

body weight after the treatment. Also this change is statistically insignificant (P=

0.343) as revealed by paired ‘t’ test. The details are given in the Table No. 40.

Effect on hematological values

Effect on total leukocyte count:

There was marginal decrease in total leukocyte count after the treatment.

The initial TC was 9245.000 cu.mm and this came down to 8425.000 cu.mm

after the treatment. This change is found to be statistically insignificant. Table

No. 41 and the Graph No. 35 show the details.

Effect on differential count of WBC’s:

Minimal change was also observed in the differential count of white blood

corpuscles. The statistical analysis by adapting the paired ‘t’ test revealed that

these changes after the treatment are insignificant.

Effect on haemoglobin percentage:

Before the treatment the initial haemoglobin percentage was 11.00 gm%.

This was then increased to 11.63 gm% after the treatment. This increase of

hemoglobin by 0.625 gm% is statistically insignificant as shown by the paired ‘t’

test. The details of the same is shown in the Table No. 41 and the Graph No.

36.

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Effect on erythrocyte sedimentation rate:

The erythrocyte sedimentation showed a marginal decrease. Before the

treatment the average ESR in patients of Amavata studied in this group was

40.6 mm 1st hour. A reduction by 18.00 mm was recorded after the treatment

with Ajamodadi Churna. This decrease in the ESR was also statistically highly

significant (P=0.001). Table No. 41 and Graph No. 37 shows the details.

Overall effect of treatment in 10 patients of Amavata:

The assessment of the overall effect of the treatment revealed that 10%

of the patients recorded complete remission. 30% of the patients showed major

improvement. And 60% of the patients responded with minor improvement. All

the patients studied in this Ajamodadi Churna group showed different degrees

of remission.

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Table No. 33-Effect of Ajamodadi Churna on cardinal symptoms of

Amavata:

Mean score Paired ‘t’ test Signs and

symptoms B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D± S.E± ‘t’ P

Stabdata 2.200

0.422

1.000

0.667 54 0.422 0.133 9.000 ≤0.001

Sandhi

Shoola

2.200

0.422

1.200

0.422 45 0.000 0.000 >1e20 ≤0.001

Sandhi

Shotha

1.377

0.501

0.565

0.399 58 0.173 0.0549 14.795 ≤0.001

Tenderness 1.884

0.299

0.897

0.354 52 0.226 0.0715 13.805 ≤0.001

Crepetation 0 0 - - - - -

Graph No. 29-Effect of Ajamodadi Churna on cardinal symptoms of

Amavata:

2.2

1

2.2

1.2 1.377

0.569

1.884

0.897

0 00

0.5

1

1.5

2

2.5

Sco

re

Stabdata S Sula S Sotha Tenderness Crepetation

B T A T

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Table No. 34-Effect of Ajamodadi Churna on general symptoms of

Amavata:

Mean score Symptoms

Initial After treatment Percentage of relief.

Angamarda 2.300 1.200 48

Jwara 0.500 0.1000 80

Aruchi 1.200 0.1000 91

Trit 0.500 0.200 60

Alasya 1.900 0.800 58

Apaka 1.400 0.200 86

Angasunata 0 0 -

Daha 1.100 0.300 73

Raga 0 0 -

Staimitya 0 0 -

Gaurava 0 0 -

Kandu 0 0 -

Hrillasa 0 0 -

Chardi 0 0

Anaha 1.100 0.200 90

Praseka 0.400 0.1000 75

Antrakujana 0 0 -

Kukshi Shoola 0.500 0.000 100

Vibanda 0.600 0.1000 83

Shrama 2.000 0.900 55

Bahumutra 0.400 0.300 25

Bhrama 0.300 0.000 100

Hridgraha 0.300 0.1000 66

Nidralpata 0.700 0.300 57

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Results

Graph No. 30-Effect of Ajamodadi Churna on general symptoms of

Amavata:

0.50.1

1.20.1

0.50.2

1.90.8

1.40.2

2.31.2

1.10.3

0000

1.10.2

0.40.1

0.50

0.60.1

20.9

0.40.30.3

00.3

0.10.7

0.3

0 0.5 1 1.5 2 2.5

Jvara

Aruci

Trit

Alasya

Apaka

Angamarda

Daha

Hrillasa

Chardi

Anaha

Praseka

Kuksi sula

Vibandha

Shrama

Bahumutra

Bhrama

Hridgraha

Nidralpata

B T A T

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Results

Table No. 35-Total effect of Ajamodadi Churna on general symptoms:

Mean score Paired ‘t’ test Criteria

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

General

symptoms

15.200

(4.022)

4.900

(2.132) 68 4.620 1.461 7.050 ≤0.001

Graph No. 31-Total effect of Ajamodadi Churna on general symptoms of

Amavata. 15.2

4.9

02468

10121416

Sco

re

B.T. A.T.

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Results

Table No. 36-Effect of Ajamodadi Churna on symptoms of Ama:

Mean score Symptoms

Initial After treatment

Percentage of relief.

Balabhramsa 2.000 0.900 55

Gaurava 2.300 1.100 52

Alasya 1.900 0.800 57

Apakthi 1.400 0.200 86

Nistiva 0.400 0.1000 75

Malasanga 0.600 0.1000 83

Aruchi 1.200 0.1000 92

Klama 2.100 1.000 52

Graph No. 32-Effect of Ajamodadi Churna on symptoms of Ama:

2

0.9

2.3

1.1

1.9

0.8

1.4

0.20.4

0.1

0.6

0.1

1.2

0.1

2.1

1

0

0.5

1

1.5

2

2.5

Sco

re

Bal

abra

msh

a

Gou

rava

Ala

sya

Apa

kti

Nis

htiv

a

Mal

asan

ga

Aru

chi

Kla

ma

B T A T

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Results

Table no. 37-Total effect of Ajamodadi Churna on symptoms of Ama:

Mean score Paired ‘t’ test Criteria

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

Symptoms

of Ama

11.900

(1.524)

4.300

(2.312) 64 2.221 0.702 10.820 P=<0.001

Graph No. 33-Total effect of Ajamodadi Churna on symptoms of Ama:

11.9

4.3

0

2

4

6

8

10

12

Scor

e

B.T. A.T.

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Results

Table No. 38-Effect of Ajamodadi Churna on circumference of the limbs:

Mean score Paired ‘t’ test Circumference

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

Arm 26.775

(3.566)

26.775

(3.566) 0 - - - -

Fore arm 24.350

(2.404)

24.350

(2.404) 0 - - - -

Thigh 45.050

(4.036)

45.050

(4.036) 0 - - - -

Leg 31.375

(7.400)

31.375

(7.400) 0 - - - -

Table No. 39-Effect of Ajamodadi Churna on different clinical parameters:

Mean score Paired ‘t’ test Parameters

B.T.(S.D.±) A.T.(S.D.±)

improve

ment S.D.± S.E.± ‘t’ P

Range of joint

movement in

degrees

79.690

(25.072)

94.200

(29.662) -14.510 8.256 2.611 5.558 ≤0.001

Foot pressure

in kgs

32.800

(7.220)

40.050

(7.228) 7.250 3.729 1.179 6.149 ≤0.001

Hand grip in

mm of Hg

71.750

(30.278)

98.500

(40.624) 26.750 23.035 7.284 3.672 =0.005

Functional

disability

1.900

(0.316)

1.000

(0.667) 0.900 0.568 0.180 5.014 ≤0.001

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Results

Graph No. 34-Effect of Ajamodadi Churna on different clinical parameters:

79.69

94.2

32.840.05

71.75

98.5

1.9 10

10

20

30

40

50

60

70

80

90

100

Sco

re

J motion F pressure H grip F disability

B T A T

Table No. 40-Effect of Ajamodadi Churna on body weight of patients of

Amavata:

Mean score Paired ‘t’ test Criteria

B.T.(S.D.±) A.T.(S.D.±)BT-AT

S.D.± S.E.± ‘t’ P

Body

weight

55.500

(10.721)

55.400

(10.741) 0.1000 0.316 0.1000 1.000 =0.343

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Table No. 41-Effect of Ajamodadi Churna on different hematological

parameters:

Mean score Paired ‘t’ test Investigation

B.T.(S.D.±) A.T.(S.D.±)

% of

relief S.D.± S.E.± ‘t’ P

TC /cu.mm 9245.000

(2472.791)

8425.000

(2085.965) 820.000 1413.074 446.853 1.835 =0.100

DC-

neutrophils-%

63.700

(7.394)

64.900

(5.238) 1.200 5.051 1.597 -0.751 =0.472

Lymphocytes 31.600

(7.106)

30.600

(5.232) 1.000 4.876 1.542 0.649 P=0.533

Eosinophils 4.100

(2.132)

4.800

(2.348) 0.700 2.359 0.746 0.938 P=0.373

Monocytes 0.500

(0.527)

0.600

(0.966) 0.1000 0.876 0.277 -0.361 P=0.726

Basophils 0 0 - - - - -

ESR – I hour 40.600

(15.116)

22.600

(13.794) 18.000 10.995 3.477 5.177 P=<0.001

Haemoglobin 11.000

(0.825)

11.625

(0.981) 0.625 0.835 0.264 2.366 =0.042

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Graph No. 35-Effect of Ajamodadi Churna on TLC:

9245

8425

8000

8200

8400

8600

8800

9000

9200

9400

Cel

ls p

er c

ubic

mm

TLC

B T A T

Graph No. 36-Effect of Ajamodadi Churna on Hb%:

11

11.63

10.610.710.810.9

1111.111.211.311.411.511.611.7

gm %

Hb%

B T A T

Graph No. 37-Effect of treatment on ESR: 40.6

22.6

0

5

10

15

20

25

30

35

40

45

mm

afte

r 1st

hou

r

ESR

B T A T

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Table No. 42-Overall effect of treatment in 10 patients of Amavata:

Treatment effect No of patients Percentage

Complete remission 1 10

Major improvement 3 30

Minor improvement 6 60

No change 0 00

Graph No. 38-Overall effect of Ajamodadi Churna in patients of Amavata:

10

30

60

00

10

20

30

40

50

60

% o

f pat

ient

s

complete Major Minor No change

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COMPARISON

Comparison of effect on cardinal signs and symptoms:

By observing the response to the treatments in both the group it is clear

that both the medicines are effective in relieving the cardinal symptoms of the

Amavata. Comparison of the efficacy of the treatments is detailed in the

following paragraphs.

Effect on the symptom Stabdhata:

The effect of the treatment in both the group on the symptom Stabdhata

appears to be equal. In both the groups the difference in the mean symptom

score before and after the treatment is 1.2. This explains equal efficacy of the

treatment in both the groups. Table No. 43 and Graph No. 39 represents the

same.

Effect on Sandhi Shoola:

The difference in means of Sandhi Shoola score before and after the

treatment in the Eranda Paka group was 1.5 as against1.0 in the Ajamodadi

group. This difference proves the better efficacy of the Eranda Paka in relieving

the symptom Sandhi Shoola in comparison to the relief obtained by the

Ajamodadi Churna. Table No. 43 and Graph No. 39 gives the detail.

Effect on Sandhi Shotha:

Favourable response was obtained in both the groups in regards to

effect of the treatment on the symptom Sandhi Shotha. Also, comparatively a

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better response was observed in the Eranda Paka group. The difference in

mean symptom scores before and after the treatment was 0.935 in the Eranda

Paka group, and is just higher than the one noted in the Ajamodadi Churna

group. In patients treated with Ajamodadi Churna, the difference in mean

scores before and after the treatment was 0.812. Though the statistical analysis

of the same by adapting the unpaired ‘t’ test does not rule out the chance factor

for such a difference between the groups, the efficacy is marginally better in

Eranda Paka group. Details are given in Table No. 43 and Graph No. 39.

Effect on joint tenderness:

Severity of tenderness was reduced in both the groups after the

treatment. The difference in mean scores before and after the treatment in two

groups when compared reveals that the Eranda Paka is better in relieving the

sign joint tenderness. In the Ajamodadi group the difference in mean scores

before and after the treatment was 0.987, and is lesser than the one noted in

Eranda Paka group. Here in patients treated with Eranda Paka the difference in

mean symptom score before and after the treatment was 1.21. Here also the

difference observed between these groups could be due to chance. Statistically

this difference was insignificant (P=0.060). Table No. 43 and Graph No. 39

show the details.

Joint crepetation another cardinal symptom of the illness was not present

in both the groups.

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Effect on general symptoms:

In patients treated with Eranda Paka a difference of 15.3 was recorded in

the sum total of different scores of general symptoms before and after the

treatment. The value of the same in the Ajamodadi Churna group was 10.3.

This difference in values states that the oral administration of Eranda Paka is

more efficacious in relieving the general symptoms of Amavata. But the

unpaired ‘t’ test could not prove the statistical significance of the variations seen

between the groups. Table No. 44 and Graph No. 40 represents the same.

Effect on Ama:

Comparison of effects on symptoms of Ama in two groups reveals that,

better improvement was found in patients treated with Eranda Paka. The

variance of symptom score before and after the treatment in Eranda Paka

group was 10.3 and the same in Ajamodadi group was 7.6, confirming the

better efficacy of the Eranda Paka in relieving the symptoms of Ama. The

change observed between the groups was also statistically significant according

to unpaired ‘t’ test. Same is represented in Table No. 45 and in Graph No. 41.

Effect on clinical parameters

Effect on circumference of the limbs:

The circumferences of the arm, fore arm, thigh and legs were noted

before and after the treatment in both the Eranda Paka group as well as

Ajamodadi group. Both the group showed no variation in the circumferences

after the treatment.

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Effect on the range of joint movement:

In an average the range of joint movement was increased by 16.884

degrees in Eranda Paka group as against the increase by 14.51 degrees in

Ajamodadi group. This implies a better improvement in the range of joint

movements in patients treated with Eranda Paka though the statistical analysis

by adapting the unpaired ‘t’ test does not justify the significance of variation

between the groups. Table No. 46 and Graph No. 42 shows the details.

Effect on foot pressure:

Comparison of effects of treatments on foot pressure indicates that

Eranda Paka has an edge over the Ajamodadi Churna in improving the foot

pressure after the treatment. The difference in the mean foot pressure in the

Eranda Paka group was 8.55 kgs as against 7.25 kgs in Ajamodadi group.

Statistical analysis by unpaired ‘t’ test could not rule out the possibility of

chance factor in causing such a variance between the groups. Table No. 46 and

Graph No. 43 gives the detail.

Effect on hand grip power:

Ajamodadi Churna was found to be more efficacious in improving the

hand grip power in comparison to the Eranda Paka. After the treatment in

Eranda Paka group the increase in the mean hand grip power was 23.95 mm of

Hg as against 26.75 mm of Hg in Ajamodadi Churna group. Of course this

variation between the groups was statistically insignificant (P=0.744). Details

are given in the Table No. 46 and Graph No. 44.

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Effect on general functional capacity:

The analysis of the functional disability in both the groups showed that

functional capacity of the patients has increased following the treatment. The

functional disability score reduced to the tune of 0.9 in both the groups,

recording no difference in the efficacy of two treatments when compared. Table

No. 46 represents the same.

Effect on body weight:

Marginal improvement in body weight was observed in Eranda Paka

group and marginal decrease in body weight was recorded in Ajamodadi group

after the treatment. However the difference is statistically insignificant

(P=0.174). Table No. 47 and Graph No. 45 provides the details.

Effect on haematological values:

Haematological examinations carried out before and after the treatment

in both the groups showed that there was marginal change in TLC and DC. The

changes also found to be statistically insignificant. Details are in Table No. 48.

Better improvement of Hb% was noted in the Eranda Paka group in

comparison to the Ajamodadi group. The average increase of Hb% following

the medication with Eranda Paka was 0.795 gm%. And the same in Ajamodadi

group was just 0.625 gm%. This explains the Eranda Paka has an edge over

the Ajamodadi Churna in improving the Hb%. The variation noted in the two

groups when compared showed statistically insignificant change (P=0.740).

Table No. 48 and Graph No. 46 shows details.

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Reduction in the ESR following treatment was recorded in both the

groups. However the Eranda Paka group patients showed a better fall in ESR

level. The average fall in ESR after the treatment with Eranda Paka was 38.4

mm after1st hour, as against 18.0 mm after1st hour in Ajamodadi group. Also

statistical significance of this variation noted could not be confirmed by the

unpaired ‘t’ test. Table No. 48 and Graph No. 47 shows the details.

Over all effect of treatment in 20 patients of Amavata:

Comparison of the overall effects of the treatment in both the groups

reveals that Eranda Paka is more efficacious. Complete remission of the illness

was observed in 40% of the patients in Eranda Paka group as against mere

10% of the patients in Ajamodadi group. 30% of the patients in each group

recorded major improvement. In patients treated with Eranda Paka, 30% of the

patients showed minor improvement as against 60% of patients showing this

response in Ajamodadi Churna group. In both the groups no patients were

observed in the “no change” category. Details of comparison are given in the

Table No. 49 and Graph No. 48.

In a nutshell, almost all the parameters of assessment have shown

improvement in both the groups following treatment. In most of these

assessment criteria the Eranda Paka group has shown a better response in

comparison to the Ajamodadi group. The better improvement in the cardinal

symptoms and general symptoms was also statistically significant where as the

clinical parameters as well as laboratory investigations have shown insignificant

change between the groups.

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Table No. 43-Comparison of effect of treatments on cardinal symptoms of

Amavata:

Unpaired ‘t’ test Symptoms Group

No. of

patients

BT -

AT

Difference

in mean S.D. S.E.M. ‘t’ P

EP 10 1.2 0.632 0.200 Stabdata

AC 10 1.2 0.000

0.422 0.133 - -

EP 10 1.5 0.527 0.167 Sandhishoola

AC 10 1 0.500

0.000 0.000 3.000 P=0.008

EP 10 0.935 0.702 0.222 Sandhishotha

AC 10 0.812 0.123

0.173 0.0547 0.538 P=0.597*

EP 10 1.21 0.269 0.0851 Tenderness

AC 10 0.987 0.223

0.226 0.0715 2.007 P=0.060*

EP 10 0 - - Crepetation

AC 10 0 -

- - - -

Graph No. 39-Comparison of the effect of treatment on the cardinal

symptom of Amavata:

1.2 1.2

1.5

1

0.9350.812

1.21

0.987

0 00

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

Des

iffer

e in

eaor

n sc

Stabdata S Sula S Sotha Tenderness Crepetation

EPAC

mnc

e

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Results

Table No. 44-Comparison of effect on general symptoms:

Unpaired ‘t’ test Symptoms

Group No. of

patients

BT-AT Difference

in mean S.D. S.E.M. ‘t’ P

EP 10 15.300 2.946 0.932 General

symptoms AC 10 10.3005.000

4.620 1.461 2.886 P=0.010

Graph No. 40-Comparison of effect of treatment on general symptom in

two groups:

15.3

10.3

02468

10121416

Diff

eren

ce in

mea

n sc

ores

EP AC

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Results

Table No. 45-Comparison of effect on symptoms of Ama between the

groups:

Unpaired ‘t’ test Symptoms Group

No. of

patientsBT-AT

Difference

in mean S.D. S.E.M. ‘t’ P

EP 10 10.300 2.111 0.668 Ama

AC 10 7.600 2.700

2.221 0.702 2.786 P = 0.012

Graph No. 41-Comparison of effects on symptoms of Ama in two groups:

15.3

10.3

0

2

4

6

8

10

12

14

16

Diff

eren

ce in

mea

n sc

ores

EP AC

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Results

Table No. 46-Comparison of effect on different clinical parameters:

Unpaired ‘t’ test Parameters Group

No. of

patients BT-AT

Difference

in mean S.D. S.E.M. ‘t’ P

EP 10 16.884 14.267 4.512 Range of

joint

movement AC 10 14.51 2.374

8.256 2.611 0.455 P=0.654*

EP 10 8.55 2.640 0.835 Foot

pressure AC 10 7.25 1.300

3.729 1.179 0.900 P=0.380

EP 10 23.95 13.475 4.261 Hand grip

AC 10 26.75 -2.800

23.035 7.284 0.332

P=0.744

EP 10 0.9 0.568 0.180 Functional

capacity AC 10 0.9 0.000

0.568 0.180 - -

Graph No. 42-Comparison of effects on range of joint movement: 16.884

14.51

13

13.5

14

14.5

15

15.5

16

16.5

17

Diff

eren

ce in

rang

e of

jt

mov

emen

t

EP AC

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Results

Graph No. 43-Comparison of effects on foot pressure between the groups:

8.55

7.25

6.6

6.8

7

7.2

7.4

7.6

7.8

8

8.2

8.4

8.6

Diff

eren

ce in

foot

pre

ssur

e in

Kg

EP AC

Graph No. 44-Comparison of the effect on hand grip power:

23.95

26.75

22.523

23.524

24.525

25.526

26.527

Diff

eren

ce in

han

d gr

ip p

ower

in

mm

of H

g

EP AC

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Results

Table No. 47-Comparison of the effect on body weight in both the groups:

Unpaired ‘t’ test Criteria Group

No. of

patients BT-AT

Difference

in mean S.D. S.E.M. ‘t’ P

EP 10 0.100 0.316 0.1000 Body

weight AC 10 -0.1000 0.200

0.316 0.1000 1.415 P=0.174

Graph No. 45-Comparison of effect on body weight: 0.1

-0.1

-0.1-0.08-0.06-0.04-0.02

00.020.040.060.08

0.1

Diff

eren

ce in

bod

y w

eigh

t in

Kgs

EP AC

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Results

Table No. 48-Comparison of effect on different haematological values:

Unpaired ‘t’ test Investigations Group

No. of

patients BT-AT

Difference

in mean S.D. S.E.M. ‘t’ P

EP 10 1586.000 1850.064 585.042 TLC

AC 10 820.000 766.000

5.051 1.597 1.309 P=0.207

EP 10 12.700 18.343 5.800 Neutrophil

AC 10 1.200 11.500

5.051 1.597 1.911 P=0.072

EP 10 10.400 16.748 5.296 Lympthocyte

AC 10 1.000 9.400

4.876 1.542 1.704 P=0.106

EP 10 -1.500 2.838 0.898 Eosinophil

AC 10 0.700 -2.200

2.359 0.746 1.885 P=0.076

EP 10 -0.300 0.483 0.153 Monocyte

AC 10 0.1000 -0.400

0.876 0.277 1.264 P=0.222

EP 10 0.1000 0.316 0.1000 Basophil

AC 10 0 0

- -

EP 10 0.795 1.362 0.431 Hb %

AC 10 0.625 0.170

0.835 0.264 0.337 P=0.740

EP 10 38.400 34.069 10.774 ESR

AC 10 18.000 20.400

10.995 3.477 1.802 P=0.088

Graph No. 46-Comparison of effect on haemoglobin percentage:

0.795

0.625

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

Diff

eren

ce in

hem

oglo

bin

perc

enta

ge

EP AC

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Results

Graph No. 47-Comparison of effect on erythrocyte sedimentation rate: 38.4

18

0

5

10

15

20

25

30

35

40

Diff

eren

ce in

ES

R in

mm

/1st

ho

ur

EP AC

Table No. 49-Comparison of overall effect of treatment in two groups:

Percentage of patients Treatment effect

Group EP Group AC

Complete remission 40 10

Major improvement 30 30

Minor improvement 30 60

No change 00 00

Graph No. 48-Comparison of overall effect of the treatments in both the groups:

40

10

30 3030

60

0 0

0

10

20

30

40

50

60

Ove

rall

impr

ovem

ent i

n %

Completeremission

Majorimprovement

Minorimprovement

No change

Group EP

Group

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DISCUSSION

The name of the disease Amavata represents Ama and Vata as the two

predominant pathological factors involved in the Samprapti of the disease.

Vitiated Vata Dosha in association with Ama circulating ubiquitously in the body,

gets lodged in the Sandhi, one among the Kaphasthana producing the

symptoms like Sandhi Stabdata, Sandhi Shoola, Sandhi Shopha and other local

and generalized symptoms. Though the literature related to the disease is

restricted to the mentioning of the word Amavata in Brihatrayi, an elaborate

description is found in Chakradatta and Madhava Nidana. All the diseases

affecting the locomotor system are elaborated under the single name Vatarakta

in Charaka, Sushruta and Vagbhata Samhita. Another distinct clinical entity of

the locomotor system, named as Amavata, and its clear clinical presentation is

given in Madhava Nidana. Acharya Chakradatta has given the full account of

the effective treatment of the same in his best work Chakradatta.

Severely disabling as well as perpetuating nature of the illness is

attributed to the unique pathogenesis of the illness. The specific etiological

factors in the form of unwholesome diet and regimen, causes generation of

Ama, as well as morbidity of the Vata Dosha in the Abhyantara Roga Marga.

Trivial involvement of Pitta and Kapha Dosha is also contended as pathological

factors. Ama along with morbid Vata Dosha circulated in the whole body more

particularly in the Madhyama Roga Marga, and tend to get localized in the joint

producing the typical clinical signs and symptoms. During the course of the

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pathogenesis the morbid Dosha afflicts the Sandhi, and in turn its Dhatu

structure viz. Mamsa, Snayu, Asthi, and Majja. Symptoms related to the joints

like Sandhi Shotha, Stabdhata and Shoola are the initial manifestations. And in

the later stages of the disease deformities like Sandhi Sankocha, Sandhi

Jadhyata and Angavaikalya are the hall marks of the disease. In addition to the

symptoms related to the joints, patients are likely to suffer from certain other

symptoms like Sthaimitya, Dourbalya, Agnimandya, Apaka, Vibanda,

Antrakujana, etc. Needless to say the disease cripples the patients in the long

run.

Amavata in modern parlance:

Rheumatoid arthritis a systemic disease, though it involves the

cardiovascular, nervous respiratory and similar other systems, mainly affects

the locomotor system is analogous to Amavata in terms of Ayurveda. The

effective curative medical management of the illness is doubted by the chronic

lingering nature of the illness as well as the risk of disabling deformities in

patients suffering from rheumatoid arthritis. In spite of continuous extensive

research works for years in this regard, ambiguity about the aetio-pathogenesis

of the illness still persists. Autoimmune mechanism related to the connective

tissue more particularly the sinovium is mostly accepted as the pathology of the

illness. The ambiguity in most aspects of the disease has impeded the

exploration of effective and curative treatment for this dreaded illness.

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The abnormal activity of the immune system is said to be initiated by the

exogenous or endogenous antigens. Probably these antigens are either viral or

bacterial in origin. The presence of these antigens in the body causes the

formation of RA factors and other antibodies. The combined activity of the

antigen and antibody with in the connective tissues including the joint resulting

in the inflammatory changes is the prime pathological event of the rheumatoid

arthritis. This inflammatory response is always destructive. This unique

pathological process of Rheumatoid arthritis is analogous to the Samprapti of

Amavata in many respects as expounded in Ayurvedic literature. Unwholesome

diet and regimen, mostly in the Vairodhika form causes the initiation of the

illness by the production of Ama as well as morbidity of Vata Dosha. Propelled

by the vitiated Vata Dosha the virulent Ama circulates in the body, and tends to

localize in Sandhi. With in the Sandhi, in combination with the Doshas naturally

present in the joint, the Amadosha and vitiated Vata Dosha acquires still more

virulence and thus produces the perpetuating and disabling illness. This typical

sequence of Samprapti may be compared to the aetiopathogenesis of

Rheumatoid arthritis, beginning from the exogenous or endogenous antigens.

Samprapti Vighatana and there by remission or cure of the illness is

achieved by advocating the different therapeutic procedures. Deepana,

Pachana, Shodhana and Shamana are the procedures said to be efficacious in

patients suffering from Amavata. Ama is the one among the predominant

pathological factor in the Samprapti of Amavata, and is initially treated by

Deepana and Pachana. Thus at the outset of the Samprapti Vighatana an

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attempt is made to eliminate the effect of Ama. As the morbid Dosha acquire

the Pakwa stage by these procedures, this renders ideal stage for the

purificatory procedures. Virechana or the Ksharabasti when employed in

patients of Amavata eliminates the excessive accumulation of vitiated Dosha

further causing the remission of the illness. To complete, Shodhana treatment is

followed by Shamana procedure. Based on these principles of treatment the

present study is planned to evaluate the efficacy of Eranda Paka in patients of

Amavata that constitutes both Shodhana and Shamana treatment. A control

group treated with Ajamodadi Churna is also maintained to prove the efficacy of

the Eranda Paka.

Selection of the regimen:

In the present study, the Eranda Paka and Ajamodadi Churna is taken to

treat the patients of Amavata and to explore the efficacy of these in bringing

about cure of the illness.

Pancha Kola Phanta is administered initially for the purpose of achieving

Amapachana. This herbal combination is said to possess Katu rasa, Katu

vipaka and Ushna veerya and therefore likely to render Amapachana in patients

suffering Amavata. More over, Amapachana is considered to be an essential

procedure before administering the Shodhana treatment. With this rationality

Pancha Kola Phanta was opted to bring about Ama Pachana in the present

study.

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In the classics, Eranda Taila is considered as best among the

medications for the Snigdha Virechana. Following the Deepana and Pachana

the elimination of the excessive accumulation of the Dosha is the treatment of

choice. This is made possible by the oral administration of the Eranda Taila in

prescribed dose. For the same purpose this oil is taken for the study in the

present work.

Eranda is a unique herb having both Shodhana as well as Shamana

effect in patients of Amavata. Also, it is claimed that this is the best drug in

Amavata and efficacious in bringing about the cure of the illness. It is argued

that by virtue of the Snigdha property it alleviates the Vata Dosha. Vyadhihara

property of this drug is also contended. Drugs like Pippali, Chitraka, Sati, etc

are efficacious in rectifying the Amadosha. With this idea Eranda Paka is opted

for this study.

Ajamodadi Churna is an herbal combination containing drugs that render

Amapachana as well as alleviate the morbid Vata Dosha. Pippali, Pippali Moola

Chitraka and similar other drugs in Ajamodadi Churna are efficacious in

achieving the Amapachana. In addition to this the drugs like Devadaru, Bilva

moola, etc., are effective in alleviating the Vata Dosha. This is the rationality of

selecting the Ajamodadi Churna for treating the patients of Amavata in this

study.

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Discussion

Plan of the study:

20 patients suffering from Amavata are taken for the study and all

completed the course of the treatment. The disease is mainly diagnosed on the

basis of signs and symptoms Amavata as mentioned in the Ayurvedic texts,

aided by the A.R.A. criteria (Hollander et al, 1967). RA test was also carried out

to confirm the diagnosis. To assess the general health status of the patients as

well as to rule out other possible pathologies routine haematological and urine

examination was carried out in all the patients. Routine blood examination was

repeated after the course of the treatment.

These 20 patients of Amavata selected for the study are randomly

segregated in to two groups irrespective of age, sex or creed as well as severity

of the illness. In the first Eranda Paka group Deepana Pachana Shodhana and

Shamana treatment is carried out. Deepana and Pachana are achieved by

administering the Pancha Kola Phanta in a dose of 20 ml thrice a day for three

days. This was followed by Kostasodhana for another three days by oral

administration of Eranda taila in a dose of 10 ml in the morning in empty

stomach. For the next one month course of treatment, Eranda Paka was given

orally in a dose of 15 gms thrice a day with warm water after food.

In the second Ajamodadi Churna group also Deepana Pachana

treatment is initially carried out by the oral administration of Pancha Kola

Phanta for first three days in a dose of 20 ml thrice a day.

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Discussion

This was followed by the Koshta Shodhana by Eranda Taila given orally

in a dose of 10 ml in the morning in empty stomach for the next three days. For

the next 30 days regimen, patients were orally treated with Ajamodadi Churna

in a dose of 5 gms thrice a day with warm water after food.

Descriptive statistical analysis of patients:

In this study involving 20 patients of Amavata showed majority of the

patients belonged to the age group of 50 to 60 years. Though the illness

rheumatoid arthritis is said to be more common during the 3rd and 4th decade of

the life, this study of 20 patients of Amavata being small could not represent this

general observation. 75% of the patients were females among the 20 recorded

in this study. This observation represents the general observation of prevalence

of the illness in females. Majority of the patients were Hindus in the present

series. The religion has nothing to do with the causation of the illness, and the

predominance of Hindus accounting 65% in this study only represent the

population in around Udupi, which is dominated by Hindus. Most of the patients,

females in particular revealed house hold as their occupation, once again

reflecting the usual occupation of females in this area. As per the socio-cultural

status of this geographical area females usually will not have any addiction. In

the present study involving majority of females showed only 30% of the patients

were addicted and is true to the socio-cultural status of the general population

here. Majority of patients accounting 80% were married as against remaining 20

% of the patients who were unmarried. This only represents the adult age group

of the patients that is taken for the study, and further the illness is more

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Discussion

common in the later decades of adult age group which is also the marriageable

age of general population. More number of poor and lower middle class people

were recorded in this study, and the poor socio-economic status of the patient

has nothing to do with the causation of the illness, more over this incidence only

represents the socio-economic status of the patients in and around Udupi. 45%

of the patients were illiterates, and 35% of the patients had primary education.

Once again education has no role in the predisposition of the illness, and this

only correspond to the educational status of population at large from which the

present sample is selected.

Ekadoshaja Prakriti as well as Sama Prakriti was not observed in any

patients of Amavata. All the patients belonged to the Dvandvaja Prakriti, and in

that 40% of the patients had Pitta Kaphaja Prakriti. It is said that, diseases due

to morbidity of Vata is common in Vata Prakriti people and also such an illness

is severe in them. This nature of the incidence of the illness is not reflected in

this small sample of 20 patients of Amavata. To substantiate the preponderance

of Amavata in patients having Vata Prakriti a study of larger sample is needed.

The study of the degree of the severity of the illness revealed that 80% of the

patients had Madhyama Vikriti. Interrogation of the patients revealed that 70%

of the patients had Madhyama Satva as against 15 % of patients having Avara

Satva. It is understood that, mental tension and anxiety has some role to do

with the severity of the illness, and the present observation in this sample

showing majority of the patients with either Madhyama or Avara Satva bear the

same understanding. Analysis of the Sara in 20 patients of Amavata revealed

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Discussion

that 95% of the patients had Madhyama Sara and the remaining 5% had Avara

Sara. None of the patients showed the features of the Pravara Sara. In the

pathogenesis of the Amavata it is clear that morbid Vata Dosha is

predominantly involved. And this morbid Vata has a tendency to cause

depletion of the body elements and that may be reason the patients of Amavata

showing Madhyama or Avara Sara in their physique. In addition to this, most of

the patients belonging to the poor or lower middle socioeconomic status in this

study may have poor nutrition. This further affects the Sara of the patients.

Analogous to Sara of the patients, assessment of the Samhanana of the

patients showed the higher incidence of Madhyama Samhanana. 85% of the

patients had Madhyama Samhanana out of 20 patients of Amavata. Morbid

Vata Dosha has a role in reducing the excellency of the Samhanana of the

patients and poor physical activity due to sever joint pain may further contribute

in the same line. Madhyama Satmya was observed in 95% of the patients of

Amavata. Satmya of the patients has direct bearing with the Sara and

Samhanana, predominance of Madhyama Satmya also explains preponderance

of Madhyama Sara as well as Madhyama Samhanana. Assessment of the Agni

was also carried out in all the patients suffering from Amavata. It was observed

that majority of 60% of the patients had Madhyama Abhyavaharana as well as

Madhyama Jarana Shakti. 20% of the patients had Avara Abhyavaharana and

Jarana Shakti. Impairment of the Agni is a common phenomenon of Amavata.

Impaired functioning leads to impaired ability to consume food as well as

reduced digestive ability. The same is reflected in the present sample with a

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Discussion

minimum 20% of patients showing good functioning of the Agni. Functional

ability of the patients will be affected either due to the Sandhi Shoola or

Stabdata. Physical strength is likely to be reduced as the depletion of the body

element is a regular phenomenon in patients suffering from Amavata.

Corroboratory to this phenomenon, in the present study also majority of the

patients had reduced ability to do the physical exercise.

The therapeutic effect of the treatments in both the groups was assessed

methodically in regards to the salient features of Amavata, general symptoms of

Amavata, symptoms of Ama, functional disability of the patients, degrees of

disease activity and haematological investigations. Overall effect of the

treatments was also analyzed. The results of the treatments in both the groups

are discussed in the following pages.

Therapeutic effect of the treatments:

The signs and symptoms of Amavata, both cardinal and general

symptoms were scored depending upon the degree of severity of these

symptoms, and the same is elaborated in the chapter on clinical study. The

change in these initial scores of the symptoms after the treatment was noted to

know the therapeutic benefit of these treatments.

Effect on the symptom Stabdhata:

The effect of the treatment in both the group on the symptom Stabdhata

appears to be equal. In both the groups the difference in the mean symptom

score before and after the treatment is 1.2. This explains equal efficacy of the

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Discussion

treatment in both the groups. And the improvement recorded after the treatment

was statistically highly significant.

Effect on Sandhi Shoola:

The difference in means of Sandhi Shoola score before and after the

treatment in the Eranda Paka group was 1.5 as against 1.0 in the Ajamodadi

group. This difference proves the better efficacy of the Eranda Paka in relieving

the symptom Sandhi Shoola in comparison to the relief obtained by the

Ajamodadi Churna.

Effect on Sandhi Shotha:

Favorable response was obtained in both the groups in regards to effect

of the treatment on the symptom Sandhi Shotha. Also, comparatively a better

response was observed in the Eranda Paka group. Though the statistical

analysis of the same by adapting the unpaired ‘t’ test does not rule out the

chance factor for such a difference between the groups, the efficacy is

marginally better in Eranda Paka group.

Effect on joint tenderness:

Severity of tenderness was reduced in both the groups after the

treatment. The difference in mean scores before and after the treatment in two

groups when compared reveals that the Eranda Paka is better in relieving the

joint tenderness. In the Ajamodadi group the difference in mean scores before

and after the treatment was 0.987 and is lesser than the one noted in Eranda

Paka group. Here in patients treated with Eranda Paka the difference in mean

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Discussion

symptom score before and after the treatment was 1.21. Here also the

difference observed between these groups could be due to chance. Statistically

this difference was insignificant (P = 0.060).

Joint crepitation another cardinal symptom of the illness was not present

in both the groups.

In patients treated with Eranda Paka a difference of 15.3 was recorded in

the sum total of different scores of general symptoms before and after the

treatment. The value of the same in the Ajamodadi Churna group was 10.3.

This difference in values states that the oral administration of Eranda Paka is

more efficacious in relieving the general symptoms of Amavata. But the

unpaired ‘t’ test could not prove the statistical significance of the variations seen

between the groups.

Effect on Ama:

Comparison of effects on symptoms of Ama in two groups reveals that,

better improvement was found in patients treated with Eranda Paka. The

variance of symptom score before and after the treatment in Eranda Paka

group was 10.3. And the same in Ajamodadi group was 7.6, confirming the

better efficacy of the Eranda Paka in relieving the symptoms of Ama. The

change observed between the groups was also statistically significant according

to unpaired ‘t’ test.

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Discussion

Effect on clinical parameters

Effect on circumference of the limbs:

The circumferences of the arm, fore arm, thigh and legs were noted

before and after the treatment in both the Eranda Paka group as well as in

Ajamodadi churna group. Both the groups showed no variation in the

circumferences after the treatment.

Effect on the range of joint movement:

In an average the range of joint movement was increased by 16.884

degrees in Eranda Paka group as against the increase by 14.51 degrees in

Ajamodadi churna group. This implies a better improvement in the range of joint

movements in patients treated with Eranda Paka though the statistical analysis

by adapting the unpaired ‘t’ test does not justify the significance of variation

between the groups.

Effect on foot pressure:

Comparison of effects of treatments on foot pressure indicates that

Eranda Paka has an edge over the Ajamodadi Churna in improving the foot

pressure after the treatment. The difference in the mean foot pressure in the

Eranda Paka group was 8.55 kgs as against 7.25 kgs in Ajamodadi Churna

group. Statistical analysis by unpaired ‘t’ test could not rule out the possibility of

chance factor in causing such a variance between the groups.

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Discussion

Effect on hand grip power:

Ajamodadi Churna was found to be more efficacious in improving the

hand grip power in comparison to the Eranda Paka. After the treatment in

Eranda Paka group the increase in the mean hand grip power was 23.95 mm of

Hg as against 26.75 mm of Hg in Ajamodadi Churna group. Of course this

variation between the groups was statistically insignificant (P=0.744).

Effect on general functional capacity:

The analysis of the functional disability in both the groups showed that

functional capacity of the patients has increased following the treatment. The

functional disability score reduced to the tune of 0.9 in both the groups,

recording no difference in the efficacy of two treatments when compared.

Effect on body weight:

Marginal improvement of body weight was observed in the Eranda Paka

group after the medication. Contrary to this marginal decrease in body weight

was recorded in the Ajamodadi group after the treatment. However the

difference noted in these groups when compared, is statistically insignificant

(P=0.174).

Effect on haematological values:

Haematological examinations carried out before and after the treatment

in both the groups showed that there was marginal change in TLC and DC. The

changes were also found to be statistically insignificant.

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Discussion

Better improvement of haemoglobin % was noted in the Eranda Paka

group in comparison to the Ajamodadi group. The average increase of Hb%

following the medication with Eranda Paka was 0.795 gm%. And the same in

Ajamodadi Churna group was just 0.625 gm%. This explains the Eranda Paka

has an edge over the Ajamodadi Churna in improving the haemoglobin %. The

variation noted in the two groups when compared showed statistically

insignificant change (P=0.740)

Reduction in the ESR following treatment was recorded in both the

groups. However the Eranda Paka group patients showed a better fall in ESR

level. The average fall in ESR after the treatment with Eranda Paka was 38.4

mm after 1st hour, as against 18.0 mm after 1st hour in Ajamodadi Churna

group. Statistical significance of this variation noted could not be confirmed by

the unpaired ‘t’ test.

Over all effect of treatment in 10 patients of Amavata:

Comparison of the overall effects of the treatment in both the groups

reveals that Eranda Paka is more efficacious. Complete remission of the illness

was observed in 40% of the patients in Eranda Paka group as against mere

10% of the patients in Ajamodadi Churna group. 30% of the patients in each

group recorded major improvement. In patients treated with Eranda Paka, 30%

of the patients showed minor improvement as against 60% of patients showing

this response in Ajamodadi Churna group. In both the groups no patients were

observed in the “no change” category.

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Discussion

From the foregoing it is clear that both Eranda Paka as well as

Ajamodadi Churna are very effective in the patients suffering from Amavata.

The sequential administration of Pancha Kola Phanta, Koshtashodhana by

Eranda Taila and Shamana Chikitsa by Eranda Paka is found to be very

effective in alleviating signs and symptoms of the disease. Eranda is said to be

very effective as Vata Kaphahara and is helpful in the disease Amavata. Eranda

is described as drug of choice in patients of Amavata. The present clinical data

justifies the Vata Kaphahara as well as Vyadhihara effect of the drug Eranda.

The complete or partial remission of the cardinal symptoms of Amavata proves

the Vyadhihara effect of the herb. The alleviation of the symptoms like Shoola,

Antrakujana, Vibandha, etc., explains the Vatahara effect of the Eranda Paka.

Further the alleviation of the symptoms like Agnimandya, Praseka and similar

other symptoms of Kapha Dosha corroborates the Kaphahara effect of the drug.

Ama is one of the predominant pathological factor in Amavata, the alleviation of

the symptoms of Amavata like Balabramsha, Alasya, Apakti, Malasanga etc.,

prove the therapeutic effect of the Eranda Paka as Amapachaka.

Ajamodadi Churna consists of herbs that render Amapachana and that

pacify Vata Kapha Dosha. The herbs like Pippali, Chavya, Chitraka etc., are

said to improve the digestive ability rendering Amapachana. In patients treated

with Ajamodadi Churna, the remission of the symptoms like Apakti, Praseka,

Hrillasa, Chardi, Malasanga etc., prove the efficacy of the drug in alleviating the

Ama. The herbal combination Ajamodadi Churna also contains herbs like

Devadaru that has proven efficacy to pacify Vata Dosha. Reduction in the

143

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Discussion

symptom score of Shoola, Stabdata, Sandhi Sankocha, Balakshaya in patients

treated with Ajamodadai Churna as observed in the clinical data justifies the

efficacy of the drug in this regard. Kaphahara effect of the herbal combination is

proved by the remission of the symptoms like Aruchi, Praseka, Hrillasa, Chardi,

etc., in patients treated with Ajamodadi Churna.

The comparison of the two treatments clearly showed that the Eranda

Paka has an edge over the Ajamodadi Churna in the remission of cardinal

symptoms of Amavata, general symptoms of Amavata, symptoms of Ama,

activity of the disease, functional disability, improvement in the laboratory

investigation findings, hand grip and foot pressure, etc. This corroborates the

textual reference in Bhavaprakasa :

Amavata gajendrasya shareeravana charinaha |

Eka eva nihantyaashu eranda taila keshari || (B.P. Madh. Kha. 26/50)

144

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Summary and Conclusion

SUMMARY AND CONCLUSION

This dissertation work entitled “A Comparative Study of Erandapaka and

Ajamodadi Churna in the Management of Amavata” comprises of five parts, viz.

Conceptual study, Clinical study, Discussion and Conclusion.

Introduction:

In the first part, brief introduction to the disease Amavata and to

Rheumatoid arthritis in the modern parlance is given.

Conceptual part:

Conceptual the second part includes 3 chapters. The first chapter deals

with a brief historical review of the disease Amavata starting from Vedic period

to this age. Second chapter includes etymology of Amavata, the concepts of

Ama and Vata in Amavata, Nidana, Poorvaroopa, Roopa, Chikitsa, Upadrava

and Sadhyasadhyata. Along with that description of Rheumatoid arthritis is also

given. In the third chapter under the heading drug review, drug compound and

ingredients there in are described.

Clinical study:

The third part titled ‘Clinical study’ where in a detailed description of

materials and methods are given. Subsequently the results obtained were

subjected to statistical analysis and are given in the form of tables and graphs.

145

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Summary and Conclusion

Discussion:

The fourth part entitled as ‘discussion’ includes logical interpretation of

results obtained. The conclusion drawn from those are given below:

1. Among the patients studied in this work maximum of 6 patients (30%)

belonged to age group of 50-60 years. Predominance of females (75%),

Hindus (65%) and domestic workers (60%) was observed in this study.

Addiction to tobacco is seen in 30% of patients and a majority of 45% of

illiterates. Most of the patients were married (80%) and dominant part of

the patients were economically poor (35%), lower middle class (35%).

Predominance of patients using mixed diet (80%) was seen.

2. 40% of patients registered in the study belonged to Pittakapha Prakriti.

Dominance of Madhyama Satwa (70%) along with Madhyama Saara

(95%) and Madhyama Samhanana (95%).

3. Majority of patients showed Madhyama Satmya (95%)

4. Regarding Agni Abhyavarana Shakti and Jarana Shakti was Madhyama

in most of the patients (60%)

5. Statistically insignificant improvement was seen on the symptom

Stabdata in both the groups.

6. Highly significant relief in Sandhi Shoola is observed in Eranda Paka

group against Ajamodadi Churna group.

7. Marginally better results were observed in Eranda Paka group in

reducing the Sandhi Shotha and joint tenderness.

8. Joint crepitations were not observed in both group patients

146

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Summary and Conclusion

9. Eranda Paka has shown edge over Ajamodadi Churna in reducing the

general symptoms of Amavata.

10. Statistically significant change is obtained in Eranda Paka group in

reducing the symptoms of ama against Ajamodadi Churna group.

11. No change observed in circumference of arm, forearm, thigh and calf in

both groups before and after treatment.

12. The range of movement increased by 16.884 degrees in Eranda Paka

group against Ajamodadi Churna group (16.51 degrees). The difference

was statistically insignificant.

13. Comparatively better improvements in foot pressure test (8.55 kgs)

observed in Eranda Paka group where as in Ajamodadi Churna group

improvement of 7.25 kgs was seen. Chance factor could not be ruled

out. Improvement in hand grip power was observed in Ajamodadi group

but statistical analysis could not rule out chance factor. Efficacy in

improving the general functioning capacity observed is equal in both the

groups. Marginal improvement in body weight in Eranda Paka group

contrary to marginal decrease in body weight in Ajamodadi Churna group

was observed. But the difference is statistically insignificant.

14. Average reduction of E.S.R. was more in Eranda Paka group against

Ajamodadi Churna group (38.4mm in first hour, 18.0mm in first hour

respectively). Marginal change observed in TLC and DC values in both

groups. Better improvement in Hb% noted in Eranda Paka group.

147

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Summary and Conclusion

15. Complete remission is observed in 40% patients belonging to Eranda

Paka group and 10% of patients in Ajamodadi Churna group.30% of

patients in each group, recorded major improvement. Where as 30% of

patients in Eranda Paka group showed minor improvement against 60%

of patients in Ajamodadai Churna group.

To brief, the Eranda Paka group patient showed comparatively better

improvement. Eranda Paka found more efficacious in relieving the cardinal

signs and symptoms and general symptoms of Amavata, symptoms of Ama

improvement in functional ability. Deduction in above said signs and symptoms

comparatively less in Ajamodadi Churna group. Hence it can be said as Eranda

Paka has an edge over Ajamodadi Churna in the management of Amavata.

148

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Case Proforma

DEPARTMENT OF KAYACHIKITSA S.D.M. COLLEGE OF AYURVEDA

KUTHPADY, UDUPI

RESEARCH PROFORMA FOR STUDIES ON AMAVATA

Guide: Prof. U. N. Prasad Co-Guide: Dr. Sridhar Holla

Researcher: Dr. Deepak S. M.

Name : Serial No : Age : Group : Sex : M / F OPD No : Religion : H / M / C / O IPD No : Education : UE / P / M / MS / GR / PG DOA : Marital Status : UM / M / D / W DOD : Social Status : VP / P / LM / M / UM / RVR Diagnosis : Occupation : Result : Postal Address :

MAIN COMPLANTS:

OTHER SYMPTOMS

Duration BT AT 1

AT 2

AT 3

AT 4

Jwara Stabdatha Aruchi Mala Bhaddatha Angamarda Sadana Alasya Hrutgraha Anaha Preseka Trushna Hasta-Pada Daha Bahumootrata Kukshi Shoola Chardi Bhrama Shareera Bhara Antrakoojana Kandu

Page 243: Amavata kc004 udp

Case Proforma

HISTORY OF PRESENT ILLNESS:

Onset: insidious / gradual / sudden

Sequence of joint involvement:

1……Since……2……Since……3……Since……4……Since……

5……Since……6……Since……7……Since……8……Since……

Course: Progressive / receding / relapsing / stationery

Aggravating factors:

Relieving factors:

Symmetry of joint involvement: 1 2 3 4 5

HISTORY OF PAST ILLNESS:

FAMILY HISTORY: TREATMENT HISTORY:

Drugs Dosage Duration Details NSAID’S STEROIDS OTHERS

PERSONAL HISTORY:

Vyasana: Coffee/Tea…… Alcohol…… Cigarette…… Tobacco Chewing……

Others……

Duration: Since………Occational / Regular / Stopped / Reduced / Continued

Ahara: Veg / Mixed Samasana / Visamasana / Adyasana / Anasana Dominant Rasa - M / A / L / K / T / Ka Dominant Guna – R / S / U / Sh / G / L

Nature of work: Manual /Sedentary / Labour / Traveling / Walking / Studying / Sitting/

Day/Night.

Vishrama: ……Hours Proper / Less / Excessive

Vyayama: No / Proper / Excessive / Irregular

Nidra: Sound / Disturbed Night …… Day ……

Difficulty in falling Asleep / Staying Asleep

Bowel: Frequency ……… Consistency ………… Colour

Micturation: ………Frequency………quantity………

Page 244: Amavata kc004 udp

Case Proforma

OBSTETRIC HISTORY:

No. of delivery ……. Normal…… Surgical Intervention……

Abortions …… Miscarriages …… Last Delivery ……

Years Back……

GYNAECOLOGICAL HISTORY:

Menstrual cycle: …… Regular / Irregular / Menarche …… years

Bleeding ….. days Menorrhagia / Metrorrhagia / Dysmenorrhoea / Leucorrhoea

Menopause since……years

GENERAL EXAMINATION: DASHAVIDHA PARIKSHA

Pulse …… / min Prakrutitah:V/P/K/VP/VK/PK/KP/KV/PV/VPK B.P …… mm / Hg Vikrutitah: P / M / A Temperature……F Satwatah: P / M / A Respiratory rate…… / min Saratah: P / M / A Nourishment: G / F / P Satmyatah: P / M / A Built: Samhanatah: P / M / A Nails: Ahara Shaktitah: Abyavaharana: P / M / A Conjunctiva: JaranaShaktitah: P / M / A Sinuses: Vyayama Shaktitah: P / M / A Lymph nodes: Pramanatah: P / M / A Deformities: Height …… cms Contractures: Weight …… Kgs Nodules: Y / N Vayataha; Bala / Madya / Vradha Others: SYSTEMIC EXAMINATION:

CNS : CVS : RS : GUS : P/A :

ASSESSMENT CRITERIA FUNCTIONAL TEST

BT 1 2 3 4 Joint Motion Rt Lt Rt Lt Rt Lt Rt Lt Rt Lt

Flexion Extension Abduction Adduction Lat. Rot.

Shoulder

Medi. Rot. Flexion Elbow Extension Supination Forearm Pronation

Page 245: Amavata kc004 udp

Case Proforma

Uln. Devi. Radi. Devi. Flexion

Wrist

Extension Flexion Extension Abduction Adduction Lat. Rot.

Hip

Medi. Rot Extension Knee Flexion Plant. Flex. Ankle Dorsi. Flex. Inversion Foot Eversion

MCP1 Flexion Extension Abduction Adduction

MCP2 Flexion Extension Abduction Adduction

MCP3 Flexion Extension

MCP4 Flexion Extension Abduction Adduction

MCP5 Flexion Extension Abduction Adduction

PIP1 PIP2 PIP3 PIP4 DIP1 DIP2 DIP3 DIP4

Flexion TOE Extension

Spine Flexion Extension Lat. Bend.

Neck

Rotation

Page 246: Amavata kc004 udp

Case Proforma

RING TEST BT 1 2 3 4 No.

Rt Lt Rt Lt Rt Lt Rt Lt Rt Lt 1 2 3 4 5

BT 1 2 3 4 TEST

Rt Lt Rt Lt Rt Lt Rt Lt Rt Lt Grip Test Foot Pressure Gen. Functions

BT 1 2 3 4 Circumference Rt Lt Rt Lt Rt Lt Rt Lt Rt Lt

Arm Forearm Thigh Calf INVESTIGATION:

Test BT 1 2 3 4 HB% T.L.C D.C / N D.C / L D.C / E D.C / B D.C / M E.S.R RA Factor Others

RADIOLOGICAL EXAMINATIONS: TREATMENT: OBSERVATION:

Page 247: Amavata kc004 udp

Pain Swelling Stiffness Tenderness Warmth RednessJoints Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4 Du BT 1 2 3 4Rt DIP Lt Rt PIP Lt Rt MCP Lt Rt WRI Lt Rt ELB Lt Rt SH Lt Rt DIP Lt Rt PIP Lt Rt MTP Lt Rt ANK Lt Rt KN Lt Rt HIP Lt Rt JAW Lt Rt STC Lt Rt ARC Lt

Spine C/T/L/S