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A CLINICAL STUDY ON THE EFFECT OF MANJISTADI LEPAM ANDMANJISTA KWATHAM IN VYANGA ROGA

Dissertation submitted in partial fulfillment for the degree ofDoctor of Medicine (Ayurveda)

InKayachikitsa

ByDr. N. Sandhya Sundeepa

Co-Guide GuideDr.S.Ramalingeswara Rao Dr.Prakash chander

M.D (AY) M.D (A.Y)T.A / Lecturer Professor & H.O.D

P.G. Department of Kayachikitsa P.G. Department of Kayachikitsa

Dr.B.R.K.R.Govt.Ayurvedic College / HospitalHyderabad

Dr.N.T.R University of Health SciencesVijayawada.AP, India

2005-2008

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r. N.T.R UNIVERSITY OF HEALTH SCIENCESVijayawada, A.P

Post graduate Department of KayachikitsaDr.B.R.K.R.Govt. Ayurvedic College / Hospital

Erragadda, Hyderabad

C E R T I F I C A T E

This is to certify that Dr.N.Sandhya Sundeepa of M.D. (Ayu) Kayachikitsa hasworked for the thesis on the topic “A clinical study on the effect of manjistadi lepamand manjista kwatham in vyanga roga”as per the requirements of the order laid downby the Dr.N.T.R.University of Health Sciences, for the purpose. The hypothesissubmitted by her in the first year MD (Ayu) is one and the same to that of the dissertationsubmitted.

I am fully satisfied with her work and hereby forward the dissertation for theevaluation of the adjudicators.

Date : / / 2008 DR.PRAKASH CHANDERPlace : Hyderabad MD(AY)

Professor & H.O.DPost graduate Dept. of KayachikitsaDr.B.R.K.R.Govt.Ayurvedic College,

Hyderabad, A.P.

Dr.N.T.R UNIVERSITY OF HEALTH SCIENCESVijayawada, A.P

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Post graduate Department of KayachikitsaDr.B.R.K.R.Govt. Ayurvedic College / Hospital

Erragada, Hyderabad

C E R T I F I C A T E

This is to certify that Dr.N. Sandhya Sundeepa is a final year Post-graduatescholar of M.D.(Ay) in the speciality of Kaya Chikitsa of this institute. She has written thedissertation entitled “A clinical study on the effect of manjistadi lepam and manjistakwatham in vyanga roga” in partial fulfillment for the degree of Doctor of medicineunder our direct supervision and guidance. The candidate has put in all his efforts in thesuccessful completion of this thesis.

Hence this dissertation is recommended for the evaluation of the adjudicators.

Dr.S.RAMALINGESWARA RAO Dr.PRAKASH CHANDERM.D (Ay) MD(AY)

T.A / Lecturer Professor & H.O.DPost graduate Dept. of Kayachikitsa Post graduate Dept. of Kaya ChikitsaDr.B.R.K.R.Govt.Ayurvedic College, Dr.B.R.K.R.Govt.Ayurvedic College,

Hyderabad, A.P. Hyderabad, A.P.

Date : / / 2008Place : Hyderabad

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ACKNOWLEDGEMENTS

At this unforgettable moment, I prostrate my head on the feet of our Lord fordeputing me to serve the mankind.

I am deeply indebted to my honorable guide Dr.Prakash Chander, professor,and H.O.D.P.G Dept. of Kayachikitsa and my sincere thanks to him for his unendinginspiration, valuable teachings, thought provoking ideas, constructive criticism andencouragement at all levels in the progress of the work.

I express my heartful gratitude to Dr.V.Vijaya Babu, M.D.(Ayu), Reader, P.GDept. of Kayachikitsa, for his thought provoking lecturers, his constant support,guidance, encouragement and kind co-operation in all aspects.

The practical outlook, clinical experience, proficient scrutiny of my co-guideDr.S.Ramalingeswara Rao has helped me to complete my work. I fall short of words aswell as eloquence to express my gratitude but ‘Thanks”holds formal.

I express my sincere thanks to Dr.B.Venkataiah, M.D, prof(retd) for his basicguidelines, encouragement and suggestions in the selection of the topic.

I extend my thanks to the principal Dr.M.Sada Siva Rao, for providing facilitiesfor the research work.

It gives me immense pleasure to offer gratitude to my esteemed teachers,Dr.v.vijaya laxmi, Dr.C.H.Rama Devi, Dr.P.Rama Rao for their valuable teachings,suggestions, and guidance.

With deep sense of gratitude, I express my thanks to my co-scholars Dr.M.K.Jha,Dr.Namratha, Dr.V.Jaya Laxmi and all my colleagues for their kind co-operationduring my course of study.

My special thanks to Smt.C.Ratna Kumari, librarian Research library GAH,Sri.M.Ramgopal photographer Research Dept and Smt.G.C.R.Varakumari librarianand P.Sudhaker library assistant GAC, Hyderabad.

My love and gratitude to my father Sri.N.J.Divaker, Lec(retd) for the confidencehe instilled in me.

I bestow my respects to my mother Smt. N.Madhurakshi Ass.prof(retd), whohas been a source of inspiration for all my academic achievements.

I am extremely thankful to my brother N.Ronald, Sister N.Saritha Saleena fortheir co-operation by providing timely suggestions in completing the thesis work.

I am highly grateful to my unty Smt. O. Sowndarya Tilaka, sisters M.SowjanyaPriyadarshini, M.Sowmya, and M.Sowdhamini for helping me in tacking care of my son,during my course period.

It is my great pleasure to thank my husband M.Gnana Raju for his constructivecriticism, which has made me firm and dedicated to my work.

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Special thanks to my son M.Sam Dheeraj for his understanding and co-operation,with out creating any disturbance during my work.

I wish to express my special thanks to Smt.Katheeja for helping me in typingwork.

Last but not least, I thank all my patients, especially K.Sudhamani for introducingmany patients, who have co-operated with me by coming for the reviews and informingthe response periodically.

My special thanks to all my well-wishers and I lack words to express my allassociated acquitants and son on who has directly or indirectly helped me to shape thisthesis.

(Dr.N.Sandhya Sundeepa)

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ABBREVIATIONS

Ada.Veda - Adarvana vedam

Ag.Pu - Agnipuranam

A.H. - Astanga HrudhayamU.S - Utarra stanamSu.S - Sutra stanamSa.S - Shareera sthanam

A.SA - Astanga Sangraham

B.P - Bava PrakashaPo.K - Poorva KandamMa.K - Madyama Kandam

Be.S - Bhela samhita

Ch.Up - Chandogya Upanishad

C.S - Charaka SamhitaCh.S - Chikitsa StanamIn.S - Indriya StanamVi.S - Vimana StanamSu.S - Sutra StanamSa.S - Shareera Stanam

Ch.Da - Chakra Datta

M.N - Madava Nidanam

S.K.D - Shabdha Kalpa Drumam

S.S - Susrutha SamhitaSu.S - Sutra StanamSa.S - Shareera StanamNi.S - Nidana StanamCh.S - Chikitsa Stanam

S.D.S - Sharangadhara SamhitaP.K - Poova KandamU.K - Uttara Kandam

Sa.E.D - Sanskrit English Dictionary Va.Se - Vanga Sena V.P - Vachaspatyam Yo.Ra - Yoga Ratnakara

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LIST OF TABLES

1. Showing the skin layers according to Charaka

2. Showing the skin layers according to Susrutha

3. Showing skin types as per prakruthi

4. Showing skin types as per sara

5. Showing the types of ahita ahara

6. Showing classification of hyperpigmentation according to its spread

7. Showing classification according to the color of pigmentation in genetic and

naevoid factors

8. Showing classification according to the color of pigmentation in acquired

hypermelanosis

9. Showing properties of rasa

10. Showing varities of madhu

11. Showing age-wise distribution of patients

12. Showing gender-wise distribution of patients

13. Showing marital-status wise distribution of patients

14. Showing religion-wise distribution of patients

15. Showing occupation wise distribution of patients

16. Showing education wise distribution of patients

17. Showing social-status wise distribution of patients

18. Showing locality-wise distribution of patients

19. Showing diet wise distribution of patients

20. Showing prakruthi-wise distribution of patients

21. Showing Cronicity-wise distribution of patients

22. Showing the level of discoloration in patients

23. Showing hormone therapy-wise distribution of patients

24. Showing prognosis of lesion-wise distribution of patients

25. Showing type of distribution-wise incidence in patients

26. Showing nidana-wise distribution of patients

27. Showing etiological factors-wise distribution in patients

28. Showing number of patches-wise distribution of patients

29. Showing location-wise distribution of patches in patients

30. Showing the T and P Values

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31. Showing the total effect of the therapy

LIST OF FIGURES

1. Components of the integumentary system

2. Types of cells in the epidermis

3. Layers of epidermis

4. Synthesis of tyrosine from phenylalanine

5. Metabolism of tyrosine-biosynthesis of melanin

6. Diagram of a melanocyte showing dendrites and different stages of melanosomes.

7. Biochemical pathway for synthesis of melanin

8. Biochemical pathway for synthesis of phaeomelanin

9. Diffuse brown pigmentation of the cheek in chloasma

10. Root and plant of manjista

11. Dry roots of manjista

12. Madhu

13. Manjista kwatha churna

14. Fine powder of manjista and madhu

15. Handi-lens

LIST OF PLATES

1. Observation chart - 1

2. Observation chart - 2

3. Observation chart - 3

4. Photogarphs of the patients

5. Result chart

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INDEX

PART – I

SECTION – I INTRODUCTIONSECTION – II REVIEW OF LITERATURE

CHAPTER – I HISTORICAL REVIEW

CHAPTER – II SARIRA RACHANAANATOMY OF THE SKIN

CHAPTER – III SARIRA KRIYAPHYSIOLOGY OF THE SKIN

CHAPTER – IV EXAMINATION OF THE SKIN

CHAPTER – V DISEASE ASPECTNIDANAPOORVARUPAROOPASAMPRAPTHIRUGVINISCHAYAMSADYA-ASADYATAUPADRAVACHIKITSAPATHYA-APATHYA

CHAPTER – VI VYANGAM (PSYCHO PHYSIOLOGICALAPPROACH)

CHAPTER– VII DRUG REVIEW

PART - II

SECTION – III MATERIALS AND METHODSSECTION – IV OBSERVATIONS AND RESULTSSECTION – V DISCUSSIONSECTION – VI SUMMARYSECTION – VII CONCLUSIONSECTION – VIII APPENDIX

SPECIAL CASE SHEET FOR VYANGAMBIBILOGRAPHY

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Introduction

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CHAPTER: I

INTRODUCTION

The word “beauty” is derived from the French word “beau”which is used tomean “fine” and of late “beloved” too. On contrary, the word “sundara” which is theadjective of the noun soundarya is derived from the Sanskrit root “ardrikaroti chittamiti” meaning “that which melts (is pleasing to) the mind”. The difference in the conceptas well as the depth in the choice of the root denoting the suitable meaning are evident.Sayings such as “beauty lies in the eyes of the beholder” and “a thing of beauty is a joyforver” denote the subjective and objective aspects of beauty respectively. The Sanskritroot “ardrikarana” suits both these aspects ably.

In modern science papillary dilatation is taken to be the subjective reaction tosighting a pleasant or loved object. The mind automatically is more open and responsiveto the object in question, there by citing the psycho-social implications of beauty ineveryday life. This fact more than amply illustrates the effect of “ardikarana” on thechitta. This chitta or a subtle psyche cannot be pleased but in close conjunction with theatma or the eternal soul.

Swasthya and soundarya (Beauty is the essence of good health)

“samadosha samagnischa samadhathumalakriya !Prasannatmandreyamanah swasthya etyabhedeyathe” [s.s.su 15/41]

We may note that the first half of this definition points out the physical state ofhealth with accent on the balanced functioning of the doshas, dhatus, malas, and agni.The second half brings the aspect of the psyche and the eternal soul into focus which isthe inherent uniqueness of this science of life and excluding which any system of Indianphilosophy is incomplete.

Certainly, this feeling of well being, prasanna atma, indriya, and manas isimpossible without a basic sense of social acceptability and self assurance that is a resultof an appealing outward appearance. With modern concepts of health changing for everydecade, the WHO has finally settled for a definition for health as “a feeling of completewell being and not merely the absence of disease” which has a close resemblance withthe swastha concept of ancient Ayurveda no dought, re-establishing its eternity andsupremacy.

Oriental sciences such as Ayurveda prefer calling any knowledge “Anadi” that isnot having a certain origin and inherent in any life form and “Ananantam” continououslybeing improved upon. This is why the theories of Ayurveda are based on certainfundamental and eternal concepts.

This simplistic approach in the concepts of Ayurveda has not been understood bythe changing generations. Ayurvedic and allied literature like the Vedas, Artha shastra,and Kama sutra are resplendent with references on cosmetically rewarding internal and

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external remedies. The present era lacking insight into its inherent versatility, and fed oncomplicated western concepts, is looking forward for the natural herbal remedies.

Modern medicine has conquered life-threatening diseases and infections with theadvent of antibiotics. Modern cosmetology was born-albeit less than half a century ago ascompared to Ayurveda, which had a varnya concept centuries ago. Markets were floodedwith clinically approved topical applications, many of which gave satisfactory results andpeople lapped them up to rid themselves of scars, patches, spots, rashes, pimples andother skin ailments which were alarmingly on the rise especially in this century.

Then, suddenly all the euphoria died down with disturbing reports of the long-term damage caused by laboratory-created chemical formulations and the averagecosmetic-user became suddenly wary about these safe scientifically approved medicines.

As a direct result of this increased awareness, the modern cosmetic approach inrecent years has radically changed it’s hitherto attitude towards traditional medicinewhich is still largely reliant on plants. This has developed a resurgent in herbalism. Atthis juncture, with herbs ruling almost 60-70% of world market, a lot more people arewilling to use herbal products for health problems and especially for skin ailments.

Varnya and complexion

The colour and appearance of the face skin is known as complexion. Varnyaaushada’s enhance the complexion, but according to some texts

“vreeyatha ethi varna” (vachaspatyam)That which attracts or that which is selected is called varna.

“varnya varnaya hitam”(chakrapanidatta)That which is conducive to the colour or that quality of attraction is a varnya dravya.

Here, a varnya dravya is not thought of as a lightener of the complexion but as aninstrument that restores and retains the natural hue and tone of the skin.

Varnya aushadhas have roughly been translated as “cosmetics”. Some say that themodern day cosmetics has been confined to an external application on the skin, notconcerning itself with internal metabolism, while most of Ayurvedic varnya aushadahas,including manjista used in present study, aim at correcting the factors distorting skincolour from within and are to be taken orally.

Vyangam

Vyangam is one of the skin disorders described in Ayurveda under the kshudraroga prakaranam. Vyangam is the disorder which is primarily seen on the face(mukhamagatyam) according to brihat-trayi and laghu-trayi.

In this suppressed and crowded atmosphere, the most significant development isthe identity crisis and later, the exaggerated hunger for recognition otherwise known asattention seeking. This is the urge that spurs man on to gain notice by excelling in allaspects, personal appearance being the closest and immediately rewarding.

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Indian philosophers have always held that the face is a reflection of the mind.Now a days people have become more beauty conscious and are ready to spend handfulof money for cosmetic purposes. Commercializing change in the view of the people andcraze for the ayurvedic herbal products, many companies like ‘Fair and lovely’ and‘Emami’ has come up with ayurvedic fairness creams.

Vyangam is not a major disease but it may be a symptom of an underlyingdisease. People get depressed by there looks i.e.with black patches on the face, and mayend up in many psychological problems.

This is an exceedingly common problem faced by many patients afteradolescence, particularly women. The skin becomes more darkly pigmented and thepigmentation in some sites is particularly marked. Acurious pattern of uniformpigmentation may occur on certain areas of the face, the cheeks, central zone of the fore-head, the perri-ocular area, chin and temple. Skin may become pigmented to give a mask-like appearance. The darker the normal skin colour, the more marked this alteration is.

There are many factors such as the sun-light i.e., cosmic rays (photo-sensitivedermatitis), pollution, emotional upheavals, hormones, drugs and stress that may causethe above problem. Skin is subjected to various external and internal onslaughts,therefore vyangam needs special attention in view of the above factors.

Despite of rapid advancement in modern medicine there is no adequate andcomplete treatment for this disorder even today. Although the pigmented areas are noteasy to lighten there are some preparations containing monobenzone or benoquin, withside effects of dermatitis and excessive hypopigmentaton. Above medicine is reportedlyhelpful but the desired effects are not seen.

Such a situation forces the research of other system of medicine to evolve acomprehensive clinical trial of innumerable preparations prescribed for this disorder.Hence the present work titled as “A clinical study on the effect of manjistadi lepamand manjista kwatham in vyanga rogam”is undertaken.

Vyangam is caused by vitiation of pitta, the drugs selected are for pacifying pittai.e. manjista choornam with madhu for lepam and manjista kwatham internally. Manjistais the drug of choice because it is mentioned as varnyam (charaka), pittasamshamanam,raktashodhaka, (susrutha), and varnya krith (bhavamishra).

The properties of manjista are madhura, tikta, kashaya rasa, and guru,ushnagunas, it is available freely, very economical with out any controversy, hence manjista isselected along with madhu, which is in turn mentioned as yogavahi and varnyam.

The present study is aimed at establishing the efficiency of drugs/therapiesmentioned in classical literature in the management of vyangam. Manjista along withmadhu – the promising formulation are selected for lepanam and kwatha panamrespectively. Results are recorded systematically and statistically after proper follow-up.

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Historical review

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CHAPTER: II

HISTORICAL REVIEW

Charaka samhita has grouped drugs under their curative and cosmetic activity asjeevaniya, vayah stapana etc.1 apart from having an entire group of ten drugs (varnyadashaymani) with varnya property.2Many day to day activities or dina charyas have beenattributed with life-giving properties. Some of them are danta dhavana, gandusha,shirastaila tarpana, abyanga, dhumapana and nasya. These not only have an impact on thehygiene of the individual but also purify the blood, improve its supply to all the organs,and clear the skin by flushing out toxins.

Achrya charaka has also indicated the importance of diet in maintenance ofbeauty.3 The sense of normality and abnormality in appearance is reflected in theclassification of the ashtaninditiya purushas.4

The significance of beauty seems to have only grown greater by the period ofSusruta where disfiguring skin disorders has been allotted an entire chapter, kshudrarogas.5 An entire range of drugs to prevent scar formation has been formulated under thegana vaikritapaha, the upakrama for vrana.6

In the medieval period, where Rasa shastra began to dominate the proceedings,cosmetic science caught the fancy of the rulers especially during the Moghul rule, and wesee inclusion of depilatory lepas, varnya lepas, snana and udvartana aiming atimprovement of the varna and prabha of the individual in Sarangadhara samhita.7 Still,the original concept of beauty being only a part of health was retained throughout.

The description of the skin diseases are basically found from vedic period.Vedas

In Rigveda, some names of skin diseases are mentioned, but they are not described indetail.

In Adharvanaveda twak rogas have been dealt elaborately. Description of diseasesalong with the treatment aspect has been discussed.

“naktajathasyoushade ramekrushne asiknicha !edda rajani rajai kilasa palitha cha ya the”

The medicinal plants like rama, Krishna, asikini are the plants which bloom atnight times and has properties to give natural colour to the skin. By application of lepa ofabove plants white colour of kilasa and palitham can be changed.8

“shama sarupakaraneprutivya adubdbutha !edam shu pra sadaya puna rupane kalpaya”

The herb called shama has the properties to restore the natural colour of th skin.Like wise aasuri herb is also being described for the treatement of kilasa.9

After vedic period, description of twak rogas canbe seen in upanishades,puranas, samhitas and other latest Ayurvedic texts.

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Upanishads:

In chandogya Upanishad, we find a reference regarding “pama roga” which is a type oftwak roga. In this, a story about Raikwa is told in which Jaanakshuti goes to Raikwa inquest of knowledge and finds him lying underneath a cart and suffering with pama roga.10

Mahabharat:

“na rajyamarshami twak doshopahathendriya”We find a reference about twak roga in Mahabharatam. Shantanu’s elder brother Devaapiwas declared unqualified to rule the kingdom because he was suffering with twak roga.11

Puranas:“kushtinacha tadha shastham panarda khadirodakam”

1.In Agnipuranam, food regmens for khusta rogi, and use of drinks prepared from Kadiraalong with herbal compound preparations like potions and pastes are described.12

2.In Garudapuranam, the first chapter is called “sarva roga nidana” in which, we find thedescription of kusta, visarpa, pandu and shodha roga nidanas.

Samhitas: (Bruhatraye)

1.Charaka samhita: A brief description of charma rogas, as shonitaja rogas has been deltin vidhishonitheeya adyaya along with treatement.

“kandhukotapidakakustacharmadaladayha”

Kandu,kota,pidaka,kusta, and charmadala.13 Charaka mentioned some other skindiseases viz. visarpa,pidaka in trisothiya adyaya.14

“yasya prakupitta shonita prapya shushathi !Tilaka piplava vyanga neelika tasya jayathe”

When the aggravated pitta gets dried up in combination with rakta, causes skindiseases like tilaka, piplava, vyanga and neelika.15 Vyanga has been mentioned asbahirmargaja roga. 16

2.Susrutha samhita: The ‘khudra roga’ was first and foremost coined by susrutha innidana stana. In this chapter 44 kshudra rogas are described, majority of these are skindiseases. one among them is vyangam.

3.Vagbhata samhitas: Astanga sangraha has described 37 khudra rogas and Astangahrudayam has described 36 khudra rogas, vyangam is one amongst them.

Laghutraye

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1. khudra rogas were given prominence by lagutraye. Madhavakara mentioned about 43khudrarogas in 55th chapter and about vyangam in 55/38-39.

2. Sharangadhara has mentioned about 60 khudra rogas in purvakandha,about vyangamin 7/95.

3. Bavaprakasha said about vyangam in khudrarogadikara chapter 14/36 in madyamakandha chaturdha bhaga.

Finally the other Ayurvedic classical texts such as Yogaratnakara, Bhaisajyaratnavali, Vaidya chintamani, Basavarajeeyam, Chakradatta etc. have kept up the trend ofancient dermatology which is existing up to this date.

History of dermatology of other systems of medicine are as follows:-

1.The Chinese system of medicine falls in the period of 3000 to 2000 BC. In this systemthey have given more or less accurate description of leprosy, scabies, icthyosis, vitiligo,eczema, acne, carbuncles, warts, corn etc.

2.Hippocrates (460 to 375 BC) made the first attempt separating medicine from religiouscult. He described many skin diseases and divided them into two groups according totheir exogenous and endogenous causes.

3.The Roman authour Celsus mentioned about skin diseases in 8th volume of ‘Demedicine libro acts’.

4.’Dermorbus cutaneous’ is the first book of the skin diseases on this earth written by‘mercurialis’ in 1571.

References:1. C.S.Su.S 4/82. C.S.Su.S 4/103. C.S.Su.S 5/84. C.S.Su.S 21/35. S.S.Ni.S 136. S.S.Ch.S 207. Sa.S.U.K 11/9-138. Ada.Veda 1/23-19. Adar.veda 1/23-410. Ch.Up 4-1-811. Briha.Devatta 8-15612. Ag.Pu 279/11-1613. C.S.Su.S 26/1614. C.S.Su.S 18/23-2415. C.S.Su.S 18/2516. C.S.Su.S 11/55

Previous work done on the subject:

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There is no work done on internal use of manjista in the Ayurvedic side. Though somework has been done on the Ayurvedic approach to cosmetology.

1.There has been a theoretical compilation on the cosmetics of Ayurveda in the manual ofexternal diseases-Bahya Roga Nidarshaka, published by the Baidyanath AyurvedaBhavan, Nagpur in 1976.

2.A theoretical work on the correlative aspect of the Agnibala and varna has been doneby V.Shukla 1965.

3.The Ayurvedic magazine Dhanvantari had come out with an exclusive edition 1983 onsaundarya in the Ayurvedic view. Some of the papers presented are given below-

a)Tomar G. had given a note on the Ayurvedic concept of maintenance of beauty.

b)Sharma H.S had published a paper on dealing with youvanapidakas, nyacha andvyanga.

c)The role of panchakarma in the maintenance of beauty had been discussed by KastureH.S.

4.Goyal R,K had established a relation between prabha, chhaya and pratichhaya, shareeraDept Jamnagar, 1969.

5.A study on varnyakara dravyas with an appraisal of the varnya principles had beencarried out by Nair R.V, DG.Dept. Jamnagar 1971.

6.Shah L.D had conducted a study on the pathological aspects and treatments of kshudrakustas,K.C Dept, Jamnagar 1975.

7.The cosmetic approach of Ayurveda with special reference to varnya was establishedby Mitendra P.Gohil Dept of Basic Principles, Jamnagar 1987.

8.The clinical management of vyanga with manjista madhu alepana with and withoutkumkumadi taila nasyam was worked upon by Anita Lomite,S.S.P Dept,Hyderabad 1999.

9.An evaluative study on the botanical sources of tunga with special reference to itsvarnya property by Madhavi M.Chandramohan DG.Dept, Hyderabad 2002.

10.Standardisation of purification process of guggulu and evaluative study on its varnyaproperty by R.Sirisha Devi DG.Dept, Hyderabad 2007.

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Shareera rachana Shareera rachana Anatomy of the skin

CHAPTER: II

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RACHANA OF THE TWAK

NIRUKTHI:

“twacha samvarane, tanothi visthara yathiti”(S.K.D)

“twacha sparshavad dravya gocharam”“twachati mamsam veshtayathi”(V.C.P)

Twak covers muscles, bones, and all other organs, it envelopes entire body. Twakgives protection, acts as excretory and sensory organ.

PARYAYPAD:

Twak, twacham, charma, asrugdhara, indriyaveshasha 1

Sparshagrahaka, valkala, dehavyapini 2

UTPATHI OF TWAK:

► Twak forms as an upadhatu of mamsa from prasada paka during dhatu parinama. 3

► In the sixth month of gestation, twak becomes manifested. 4

► The layers of twak are formed during the development of foetus i.e, “garbhavastha”

from shukra and shonita by tridosha, during pachamanavasta as cream forms on the

boiled milk. 5

► In the panchamahabhutatmaka shareera, datwagnis are the causative factor for

formation of saptatwacha during the process of digestion (pachamanavasta) of rakta

dhatu, just as the cream gets accumulated at the top of the surface of milk after

boiling. 6

► During the pachamanavasta of asruja (blood), layers of skin forms as cream forms

on the milk, purity (twak prasada) of the skin is purity (rakta prasada) of the blood.7

► Twak and rakta are matruja bhavas i.e, entities which are particularly maternal and

are produced from mother. 8

► Twak is considered as parthiva i.e, predominant in prithvi mahabhuta. 9

► In panchbhutatmaka shareera the formation of twak and its sensory function is due

to rajoguna bahula vayubhuta. 10

SKIN LAYERS:

Skin layers according to Charaka: 11

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There are six layers of skin, which cover the shadanga shareera

Table 1.Skin layers according to CharakaNo Skin layer Description1. Udakadhara Sustains the udaka

2. Asrugdhara Sustains the rakta3. Triteya Adhistana for sidma and kilasa4. Chaturdha Dadru and kusta sambhava adhistana5. Panchama Alaji and vidradhi sambhava adhistana6. Shasti If this layer is cut, causes loss off

consciousness. Aromsika of Krishna raktavarna, appears on stoolamula, which aredifficult to cure.

Skin layers according to Susrutha: 12

There are seven layers of twak formed in garbhavasta from shukra and shonita

Table 2. Showing skin layers according to susruthaNo Name of the layer Thickness in

vreehipramanaManifesting disease

1. Avabhasini 1/18th Sidma, padmakantaka, etc2. Lohita 1/16th Tilakalaka, nyachha, vyanga3. Shweta 1/12th Charmadala, ajagalika, mashaka4. Tamra 1/8th Different kinds of kilasa, kushta5. Vedhini 1/5th Kushta, visarpa6. Rohini 1 Granthi, apachi, arbudh, galagand7. Mamsadhara 2 Bhagandhara, vidradhi, arsha

Skin layers according to Vagbhata:

In the Astanga Hridaya, Vagbhata just said that the twak consists of seven layersand did not go into further details. 13

In Astanga Sangraha, six layers of skin are mentioned and their description is doneaccording to Charaka. The sixth layer is called pranadhara (supporter of life). 14

ANATOMY OF THE SKIN:

22

fig.1 Components of the integumentary systemIntroduction:

An appreciation of the skin, of the natural variations from region to region in thesame individual of the difference that are a reflection not of pathologic changes but of race,age, occupation and above all physiologic and more specifically, endocrinologic states - anappreciation of all these variations is necessary for a proper evaluation of the abnormal.

Measurements:

The skin is the largest organ of the human body and accounts for about 16% of totalbody weight. In the average man it weighs about 4.8 kgs and in average women it weighsabout 3.2kgs. The surface area of the skin is about 0.25 square meter in the newborn, 1.85square meters in the average-sized man, and 1.6 square meters in the average-sized women.The thickness of the entire skin varies from about 0.5 mm in the eyelid to 3-6mm on thepalm or sole. Its specific gravity is about 1.25.

Embryology:

The skin is derived from both ectoderm and mesoderm. The epidermis and itsderivatives along with nerves originate from ectoderm. The remainder of the skin alongwith subcutaneous fat is mesodermal in origin. At the beginning of the eigth week afterfertilization the ectoderm consists of simple cuboidal epithelium further which is calledperiderm. By the fourth month all layers of the epidermis are formed and each layerassumes its characteristic structure.

The dermis is derived from mesodermal cells in a zone beneath the ectoderm.There they undergo a process that changes them into the connective tissues that begin toform the dermis at about 11 weeks.

23

At about the third foetal month layer of cells forms into multilayered stratumspinosum. In fourth month basophilic keratohyalin granules are seen in stratum granulosamof face. In 5th month the desquamated cells of the stratum corneum along with sebaceoussecretion constitute the vernix caseosa. Stratum lucidum is seen at the eight month.15

Microsocpic anatomy of the skin:

Structurally the skin is formed of two main parts which are cemented to each other.1. The outer thinner portion composed of epithelial tissue is called as Epidermis.2. The inner thicker part composed of connective tissue is called as Dermis.

Beneath the dermis is a subcutaneous layer also called as, superficial fascia or thehypodermis is seen.

EPIDERMIS:

fig.2 Types of cells in the epidermis

The epidermis is keratinized stratified epithelium. It contains four principal types ofcells.

a) Keratinocytes

b) Melanocytes

c) Lngerhans cells

d) Merkel cells

A. Keratinocytes:

24

Keratinocytes form the 90% of epidermal cells, which are arranged in four or fivelayers and produce the protein keratin. Being the predominant cell type in the epidermis,keratinocytes are intuitively considered to be the most important cell type for maintainingepidermal structure integrity. The keratinocyte stem cells are known to locate at the basallayer of the epidermis, from which they continuously divide in order to provide a sufficientnumber of cells for the purpose of differentiating into the upper layers of suprabasalkeratinocytes, granular keratinocytes, and then simply keratins (at the stratum corneum).These cells form a coherent structural frame by way of desmosome, an intercellularadhesion network.

Keratin is a tough, fibrous protein that helps protect the skin and underlying tissuesfrom heat, microbes, and chemicals. Keratinocytes also produce lamellar granules, whichrelease a water-repellent sealant

B. Melanocytes:

About 8% of the epidermal cells are melanocytes which produce the pigmentmelanin. Melanocytes are not original epidermal cells, but migrate into the epidermisduring embryonic development. Originating in the neural crest, melanocytes are importantpigment-producing cells in the skin. Primarily located in the basal layer, melanocytessynthesize pigments in the form of the melanosomes, which are then transferred by way oftheir dendrites to the neighboring suprabasal epidermal layer-located keratinocytes. Onceinside keratinocytes, the melanin granules cluster to form a protective veil over the nucleus,on the side towards the skin surface. In this way, they shield the nuclear DNA from beingdamaged by UV light.

C. Langerhans cells:

Langerhans cells are not original epidermal cells, but are bone marrow derived cellsthat migrate into the epidermis during embryonic development. Localized in suprabasallayers of the epithelia of skin and mucous membrane. Langerhans cells are dendritic cells,with important immune functions. Accounting for about 5% of epidermal cells, they areprofessional antigen-presenting cells that come into contact with foreign antigens passingthrough the epidermis. Upon internalizing the antigen, the Langerhans cells migrate outfrom the skin to regional lymph nodes with the help of integrin molecules, where theypresent the processed antigen to T-cells by way of their surface MHC class II molecule,and co-stimulatory molecules.

D. Merkel cells:

Merkel cells are the least numerous of the epidermal cells. They are located in thedeepest layer of the epidermis, where they contact the flattened process of a sensoryneuron, a structure called a tactile (merker) disc. Merkel cells and tactile discs detectdifferent aspects of touch sensations.16

HISTOLOGY:

25

fig3. Layers of the epidermis

The mature epidermis is composed of the following strata

1. The basal cell layer or stratum germinativum / basale

2. The prickle cell layer or stratum spinosum

3. The granular layer or stratum granulosum

4. Stratum lucidum [seen in only thick skin]

5. Stratum corneum

The term Malpighian layer or rete malpighii, as generally used, refers to theepidermis exclusive of the stratum corneum and stratum lucidum.

1. Stratum Basale:

The deepest layer of the epidermis is the stratum basale, composed of a single rowof cuboidal or columnar kerotinocytes. Some cells in this layer are stem cells that undergocell division to continually produce new keratinocytes. The cytoskeleton withinkeratinocytes of the stratum basale includes scattered intermediate filaments; calledtonofilaments. keratin protects deeper layers from injury. Melanocytes, Langerhans cells,and Merkel cells with their associated tactile discs are scattered among the keratinocytes ofthe basal layer. The nuclei of keratinocytes in the stratum basale are large, and their

26

cytoplasm contains many ribosomes, a small Golgi complex, a few Mitochondria, andsome rough Endoplasmic reticulum.

2. Stratum spinosum:

Superficial to the stratum basale is the stratum spinosum, where 8 to 10 layers ofmany-sided keratinocytes fit closely together. Cells in the more superficial portions of thislayer become somewhat flattened. These keratinocytes have the same organelles as cells ofthe stratum basale, and some cells in this layer may retain their ability to undergo celldivision. Bundles of tonofilaments are inserting into a desmosome, tightly joining the cellsto one another. This arrangement provides both strength and flexibility to the skin.Projections of both Langerhans cells and melanocytes also appear in this stratum.

3. Stratum Granulosum:

At the middle of epidermis, the stratum granulosum consists of three to five layersof flattened keratinocytes that are undergoing apoptosis. The nuclei and other organelles ofthese cells begin to degenerate, and tonofilaments become more apparent. Darkly staininggranules of a protein called keratohyalin are present in this layer, along with membrane-enclosed lamellar granules, which release a lipid-rich secretion. The lipid-rich secretionacts as a water-repellent sealant, retarding loss of body fluids and entry of foreignmaterials.

4. Stratum Lucidum:

The stratum lucidum is present only in the thick skin of the fingertips, palms, andsoles. It consists of three to five layers of flattened clear, dead keratinocytes that containlarge amounts of keratin and thickened plasma membranes.

5. Stratum Corneum:

The stratum corneum consists of 25 to 30 layers of flattened dead keratinocytes.These cells are continuously shed and replaced by cells from the deeper strata. The interiorof the cells contains mostly keratin. Between the cells are lipids from lamellar granules thathelp, to make this layer an effective water-repellent barrier. Its multiple layers of dead cellsalso help to protect deeper layers from injury and microbial invasion.17

DERMIS:

The second deeper part of the skin, the dermis, is composed mainly of connectivetissue containing collagen and elastic fibers. The few cells present in the dermis includefibroblasts, macrophages, and some adipocytes. Blood vessels, nerves, glands, and hairfollicles are embedded in dermal tissue. Based on its tissue structure, the dermis can bedivided into two regions.

1. Papillary region

2. Reticular region

1. Papillary region:

27

The papillary region is the superficial portion of the dermis is about 1/5th of thethickness of the total layer. It consists of areolar connective tissue containing fine elasticfibers. This contains dermal papillae that house capillaries, corpuscles of touch, and freenerve endings. Different free nerve endings initiate signals that give rise to sensations ofwarmth, coolness, pain, tickling and itching.

2. Reticular region:

The deeper portion of the dermis is called the reticular region. It consists of denseirregular connective tissue containing bundles of collagen and some coarse elastic fibers. Afew adipose cells, hair follicles, nerves, sebaceous glands, and sudoriferous (sweat) glandsoccupy the spaces between fibers. The combination of collagen and elastic fibers in thereticular region provides the skin with strength, extensibility, and elasticity.

HYPODERMIS:

The tissue below the dermis is called hypodermis, which is abruptly distinct fromthe upper layer dermis histologically. The hypodermis is areolar and adipose tissue-predominant region, but is functionally integrated with the upper layer dermis throughnerve, micro vascular, and lymphatic networks and the continuity of hair follicles into thehypodermis. Mesenchymally derived, the adipocyte is the predominant cell type in thislayer. The tissues in the hypodermis serve as, insulator, cushion, an energy supplier,protector of the skin and provide mobility over the underlying structures and also containnerve endings called lamellated corpuscles that are sensitive to pressure.

APPENDAGES OF THE SKIN:

The appendages of the skin are the nails, the hairs, the sebaceous and sweat glands.

Nails:The nails are flattened, elastic structures of a horny texture, placed upon the distal

parts of the dorsal surfaces of the fingers and toes. The nail itself is a greatly thickenedstratum lucidum of the skin, and beneath it lies the germinative zone which, together withthe subjacent corium, forms the nail-bed.

The nail increases in thickness from its root to the distal edge of the lunule and theremainder is of uniform thickness. On an average nails grow about 0.5mm a week. Nailsact as a rigid background for support of the digital pads of the terminal phalanges, and thusmay function in the tactile mechanism.

Hairs:Hairs vary much in length, thickness, and color in different parts of the body and in

different races of mankind. A hair consists of a root, the part implanted in the skin, and ashaft (scapus), the portion projecting from the surface. From the capillaries in the papillahair derives its nutrition. The hair-follicle consists of two coats – an outer or dermic, and aninner or epidermic.

The shaft of the hair consists, from within outwards, of the medulla, the cortex, andthe cuticle. Hairs are of three types Lanugo hairs (primary hairs), Vellus (secondary hairs),and Terminal hairs. Growth of a hair occurs at the hair bulb, where the cells capping thepapilla proliferate and form the germinal matrix of the hair.

28

Sebaceous glands:The sebaceous glands are small, sacculated, glandular organs, lodged in the

substance of the corium. They are found in most parts of the skin, but are especiallyabundant in the scalp and face, they are also very numerous around the apertures of theanus, nose, mouth and external ear, but are wanting in the palms of the hands and soles ofthe feet.

The sebaceous gland is situated in the angle which the Arrector muscle forms withthe superficial portion of the hair-follicle and contraction of the muscle thus tends tosqueeze the sebaceous secretion out from the duct of the gland.

Sweat glands:The sweat glands are found in almost every part of the skin, and are situated in

small pits on the under surface of the corium, or more frequently, in the subcutaneoustissue, surrounded by a quantity of adipose tissue. They are especially large in thoseregions where the amount of perspiration is great, as in the axillae and groin. They areplenty in palms and soles.

The ceruminous glands of the external auditory meatus are modified sweat glands.Most of the sweat glands are merocrine in nature i.e., they produce thin watery secretionwithout demonstrable changes in the gland epithelium. Apocrine glands produce thickersecretion by degeneration and shedding of the portion of the epithelial cell nearest thelumen. 18

References:1. S.K.D2. V.P (Vol-IV)3. C.S.Ch.S 15/174. A.H.Sa.S 1/575. S.S.Sa.S 4/4a6. A.H.Sa.S 3/8a7. A.SA.Sa.S 5/178. C.S.Sa.S 3/69. C.S.Sa.S 7/1610. A.H.Sa.S 3/311. C.S.Sa.S 7/412. S.S.Sa.S 4/4b13. A.H.Sa.S 3/8b14. A.SA.Sa.S 5/1715. Gray’s Anatomy16. The skin17. Animal models of Human Inflammatory Skin Diseases18. Principles of Anatomy and Physiology

29

Shareera kriyaShareera kriyaPhysiology of the skin

CHAPTER: III

SHAREER KRIYA OF THE SKIN

Twak performs a number of vital functions related to the body. Some of them areas follows

1. Twak is sparshanendriya.1 Factors known by touch and tactile faculty are

30

governed by vayu mahabhuta.2

2. Twak is moola of mamsavaha srotas.3

3. It is brajaka pitta stana.4

4. Twak acts as site for the absorption of nutrients by the foetus in garbhavastha.5

5. Paste applied in alepa, abyanga, avagaha etc enters in to hair follicles and virya(potent fraction) permeates through sweat-carrying vessels.6

6. When the body becomes hot, udaka comes out from hair follicles in the form ofsweat. Thus twak regulates the heat.7

This being a work on varna vikriti, the factors influencing the varna of the twakare analysed.

Factors influencing varna:

1. “tasya raso balavarna kara”The foetus draws nourishment from mother in the form of rasa. The rasa (nutritivefluid) promotes strength and complexion.8

2. During garbhavastha varna is formed from rasaja and satmyaja bhava.9

3. As per mythology, kanti or the glow of complexion is ruled by the Aswinikumaras.10

4. Among the mahabhutas, tejomahabhuta is the major factor influencing pitta, ushma,kanthi and rupa of the body.11

5. Varna and teja are due to agni mahabhuta.12

6. The pitta located in the skin is bhrajaka pitta, it helps in exhibition of color andcomplexion.13

7. Prakruthi and vikruthi of brajaka pitta shows effect on varna, bhaya, krodha andharsha.14

8. “udanavatasya balavarnasmruthikriya”Among five types of vata, udanavata affects the varna15

Normal and abnormal skin colourNormal skin color:

1. With the predominance of tejomahabhuta, color formation is said to take place inthe following manner

Udaka---goura varnaPrithvi---krishna varna

Prithvi + akasa---krishnashama varnaUdaka + akasa---gourashama varna16

2. Charaka has described normal colour to be of four types Krishna, krishnashama,shamavadata, avadata.17

Abnormal skin color:

1. The atikrishna, atigaura varna are mentioned under ashtanindita purushas.18

2. Charaka has described abnormal color to be of five types neela, shama, tamra,

hareetha, shukla. 19

Chhaya and prabha:

31

Chhaya and prabha are the factors having a very close relation with skin colour.Chhaya is said to mask the varna and is perceived only in close proximity whereas prabhaenhances the complexion and catches the eye from a distance itself.20

Types of chhaya:

According to panchamahabhutas chaaya are classified in to five types

1. Nabhasi chhaya – nirmala, neelavarna, snehayukta, saprabha

2. Vayavi chhaya – ruksha, shavaruna, hataprabha

3. Agneya chhaya – vishudha rakta, deeptabha, darshanapriya

4. Ambasi chhaya – shudha vaidurya, vimala, susnigdha

5. Parthiva chhaya – sthira, snigdha, Ghana, shlakshna, shama, shweta

Among the above, vayaviya alone is considered nindita (abnormal). While theothers fall under the purview of normal.21

Types of prabha:

Prabha based on color is of seven types – rakta, peeta, sita, syava, harita, pandu,and asita.

Varna is normal from birth to death except in case of arishta lakshana whereabnormal chhayas may indicate death.22

Prakriti:Prakriti is a result of, status of the parents of the individual during the

shukraartava samyoga, Kala, garbhashaya prakriti and pancha mahabhuta vikaraswabhava.23 This, coupled with the behaviour of the mother during pregnancy includingher food habits along with the atmaja bhava of the individual which he carries over fromhis previous birth, determines the complexion of the individual.24

Skin type as per prakriti: 25

Table.3 Showing skin types as per prakritiPrakriti Skin type

Vata Ruksha, parushavadana, prominent siras and kandarasPitta Susceptible to piplu, vyanga, tila, pidaka, valipalitha and kalithyaKapha Avadata gatra, prasanna, snigdha

Sara: 26

Skin types as per sara:

Table.4 Showing skin types as per saraSara Skin type

Twak sara Snigdha, shlakshna, mrudhu, prasanna, sukumara loma, saprabhaRakta sara Snigdha, raktam, brajishnuMamsa sara Guru, stira, mamsopachithaMedha sara Visheshata sneha yukta varna

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Asthi sara StiraMajja sara Snigdha varnaShukra sara Prasanna snigdha varna

Functions of Bhrajaka pitta:

The bhrajaka pitta is stated to be located in the skin and to impart its characteristiccolor and luster.

Charaka has not described this pitta as a separate entity but he has included thefunctions attributed to it among those of pitta in general. Marichi has stated that theprakruthi and vikruthi of brajaka pitta effects varna, bhaya, krodha and harsha.27

Chakrapanidatta, in his commentary on the above, has stated that the regulation ofthe body-heat and variations in the colour of the body are the functions of bhrajaka pittawhich is located in the skin.

Susrutha, Bhela, and Vagbhata have, made separate mention of this pitta, includingthe functions ascribed to it.

According to Susrutha, the pitta located in the skin is known as bhrajakagni, itenables the digestion and utilization of substances used for abhyanga, parisheka, avagaha,alepa etc. It irradiates the glow of one’s natural complexion. 28

Dalhana commenting on the above states that, bhrajaka pitta is located in thebahyatwak, named as avabhasini and causes the radiation of luster.

According to Bhela, bhrajaka pitta is that which is responsible for the manifestationof the specific characteristics of the body; it emphasizes its importance, creates differentprabha (hues) of the head, hands, feet, sides, back, abdomen, thighs, face, nails, eyes, andhair. It also brightens them.29

Vagbhata states that, bhrajaka pitta is located in the skin. It is so called because itimparts luster to the skin and makes it radiate.30

Commenting on the above, Arunadatta states that, it is known as bhrajaka pittabecause, it performes dipana and pachana of substances used for abhyanga, lepa, parishekaetc.

PHYSIOLOGY OF THE SKIN

The skin, apart from giving appearance and shape to the body, serves other importantfunctions31

1. Thermoregulation: The skin contributes to thermoregulation, the haemostaticregulation of body temperature, in two ways: by liberating sweat at its surface andby adjusting the flow of blood in the dermis.

2. Protection: Keratin in the skin protects from microbes, abrasion, heat, and chemicals

33

Lipids protect evaporation of water from the skin surface

The oily sebum contains bactericidal chemicals that kill surface bacteria

The acidic pH of perspiration retards the growth of some microbes

Melanin provides protection from UV light

Epidermal langerhans cells alert the immune system

Macrophages in the dermis phagocytize bacteria and viruses

3. Cutaneous sensations: Sensations like pain arise in the skin. These include tactilesensations – touch, pressure, vibration, and tickling; as well as thermal sensationssuch as warmth and coolness.

4. Excretion: By evaporation of sweat, water and heat are removed from the body.Sweat is also the vehicle for excretion of small amounts of salts, carbon dioxide,and two organic molecules – ammonia and urea.

5. Absorption: Certain lipid-soluble materials penetrate the skin. These include fat-soluble vitamins A, D, E and K, certain drugs, the gases oxygen and carbondioxide.

6. Synthesis of vitamin D: UV rays in the sunlight, activates precursor molecule inthe skin, to produce hormone calcitriol, which aids in the absorption of calciumfrom foods.

PIGMENTATION OF THE SKIN: 32

Normal pigment cells:The principal pigment determining skin color is melanin. The chemistry, quantity,

character, aggregation, and distribution of melanin are the major factors that determinecolor and hue of cutaneous pigmentation. Three other pigments that contribute to normalskin color are oxygenated hemoglobin, reduced hemoglobin, and carotenoids.

Embryogenesis:

All pigment cells arise from the neural crest except those of retinal pigmentepithelium, which are derivatives of the primitive forebrain. By the eighth week ofembryogenesis, pigment cells can be identified in the dermis.Distribution of pigment cells:

Most melanocytes are located in the basal layer of epidermis. They also residewithin the papilla and matrix of the hair bulb. Melanocytes are a normal cellular componentof mucous membranes in oral cavity, nasal septum, respiratory tract, larynx, andesophagus, eyes, ears, and leptomeninges.

Functions of the pigment system:

Pigment in the skin and hair protects against the harmful effects of sunlight.Primary function of melanocytes is to remove free radicals formed in the skin during avariety of inflammatory conditions. Melanocytes protect other cells of the epidermis fromdamage caused by release of radical oxygens. Large quantities of melanin are an indicator

34

of an efficient and effective protective mechanism for elimination of detrimental effects ofmany chemical and physical toxins.

Cytology of cutaneous melanocytes:

fig.4 Synthesis of tyrosin fromphenylaline

fig.5 Metabolism of tyrosine- fig.6 Diagram of melanocytebiosynthesis of melanin

Melanocytes are oval and have a smooth cytoplasmic membrane and a roundnucleus. Dendrites extend outwards from the cell body. The cytoplasm is filled with manyorganelles and a characteristic granule, the melanosome. The Golgi apparatus is prominent.Intermediate filaments and microtubules are involved in the transfer of melanosomes fromthe pigment cell into adjacent keratinocytes.

Melanosomes are formed by the fusion of several cytoplasmic suborganelles.Vesicles with lamellae called premelanosomes are formed by the rough endoplasmicreticulum. Other vesicles containing tyrosinase pinch off from the Golgi apparatus and fusewith the premelanosome to initiate the synthesis of melanin.

The formation of the melanosome has been arbitrarily divided into four stages Stage I: melanosomes are oval or spherical and contain a few filaments with

a characteristic periodic banding and the enzyme tyrosinase in an inactiveform.

Stage II: melanosomes are oval organelles with numerous filamentsorganized into a lamellar substructure in which melanin is not present.

Stage III: melanosomes are partially filled with melanin Stage IV: melanosomes are completely filled with melanin

The skin color is determined to a large degree by the number and size ofmelanosomes, i.e, the quantity of melanin produced by the melanocyte and transferred in tothe surrounding keratinocytes.

35

Melanin synthesis:33

Human melanocytes are now known to produce 2 types of melanin: eumelanin andphaeomelanin. Eumelanin is black or brown, and phaeomelanin is red. The ratio of the 2types of pigment largely determines the hue of human hair and skin.

Eumelanin:

fig.7 Biochemical path way for synthesis of melanin

Eumelanin chemically is a polymer of indoles and quinines formed by the aminoacid tyrosine. These quinines and indoles, highly reactive chemically, are toxic to mostcells. Melanin synthesis probably is restricted to prevent these compounds from injuringthe cell.

A single enzyme, tyrosinase, performs 3 different catalytic functions in the melaninpathway. This enzyme catalyzes the oxidation of tyrosine to dopa, the dehydrogenation ofdopa to dopaquinone, and the conversion of dihydroxyindole to melanochrome. Tyrosinaseis the best-characterized enzyme involved in melanin synthesis. Two other factors –dopachrome conversion factor and indole blocking factor – seem to be involved inregulating the rate of melanin formation. Dopachrome conversion factor is now wellcharacterized as the enzyme dopachrome oxidoreductase.

Phaeomelanin:

36

fig.8 Biochemical pathway for synthesis of phaeomelanin

Phaeomelanin is formed from 2 amino acids: tyrosine and cysteine. In the formationof phaeomelanin, dopaquinone condenses with the amino acid cysteine to form cysteinyldopa. Cysteinyl dopa is oxidized into cysteinyl indoles, which condense to form a redpolymer, phaeomelanin. The melanosome in which phaeomelanin is formed is structurallydifferent from that of the eumelanosome. The phaeomelanosome is round, not oval, andlacks the organized lamellar substructures characteristic of eumelanosomes.

Factors that stimulate melanin formation:34

Many physical and chemical agents like metabolic, endocrine, nutritional, andmiscellaneous systemic causes stimulate pigment formation.

Short wave ultraviolet light (UVB; 290-320 nm), which is abundant in sunlight,causes epidermal pigment cells to increase melanin formation. This process takesseveral days to a week to be noticeable chemically.

Long wave ultraviolet light (UVA; 320-400 nm) rapidly alters the melaninpolymer, causing it to become darker.

Prostaglandin E2, estrogens, and other hormones also increase the amount ofpigment produced by pigment cells.

Some chemotherapeutic drugs, eg, bleomycin, darken the skin by inducingmelanin formation.

Ingested metals such as arsenic and silver also darken the skin by depositing inthe dermis.

Psoralens are tricyclic organic compounds fond in many plants such as limes,celery, and parsnips.in combination with UVA, psoralens stimulate formation ofmelanin.

Melanocyte-stimulating hormones (MSH) are the best-characterized stimulants ofmelanin formation. Four different MSH peptides have been identified, eachformed in the pars intermedia of the pituitary gland. These different MSHpeptides probably have a variety of functions other than causing an increase inskin color.

Specific receptors for MSH are present on the surface of the pigment cell. Whenattached to a receptor, MSH activates the enzyme adenylate cyclase to form cAMP, whichis one intracellular messenger involved in activating a protein kinase and initiatingformation of tyrosinase in the Golgi apparatus. The active enzyme is transported from theGolgi to the premelanosome and synthesizes melanin. MSH also accelerates the movementof melanosomes through the dendrites and their transfer into keratinocytes.

37

REFERANCES:

1. C.S.Sa.S 5/52. C.S.Sa.S 7/163. C.S.Vi.S 5/7-84. A.H.Su.S 12/145. C.S.Sa.S 6/236. S.S.Su.S 18/47. C.S.Sa.S 7/158. C.S.Sa.S 6/239. S.S.Sa.S 3/22-2410. C.S.Sa.S 5/511. C.S.Sa.S 7/1612. A.S.Sa.S 5/613. A.H.Su.S 12/1414. C.S.Su.S 12/1115. A.H.Su.S 12/516. S.S.Sa.S 2/3617. C.S.In.S 1/818. C.S.Su.S 21/319. C.S.In.S 1/820. C.S.In.S 7/16-1721. C.S.In.S 7/10-1322. C.S.In.S 7/14-1523. C.S.Vi.S 8/9724. C.S.Sa.S 2/2925. C.S.Vi.S 8/96-9826. C.S.Vi.S 8/103-10927. C.S.Su.S 12/1128. S.S.Su.S 21/1329. Bhela samhita30. A.H.Su.S 12/1431. Principles of Anatomy and Physiology32. Dermatology a Lange medical book33. Biochemistry of skin in health and disease34. Essentials of Biochemistry

38

Examination of the skin

39

CHAPTER: IVEXAMINATION OF THE SKIN

INTRODUCTION:

The skin is the outer layer of the human body, which forms a major interfacebetween man and his environment. The structure of human skin is complex, consisting ofa number of layers and tissue components with many important functions. Reactions mayoccur in any of the components of human skin and their clinical manifestations reflect,among other factors, the level in the skin in which they occur.

Accurate diagnosis of most skin lesions requires an adequate history, carefulexamination of the patient and occasionally laboratory investigations.

HISTORY:

Detailed information should be sought concerning the present skin condition. Thisshould include the site of onset, mode of spread and duration of the disorder. Anypersonal history or family history of skin disease, including atopy, is important. Previousmedical conditions should be noted, and a full drug history obtained, including any use ofover-the-counter preparations. The social and occupational history should be noted and insome circumstances, details of recent travel may be important.

EXAMINATION:

The whole skin, including hair, nails and assessable mucosae, should be fullyexposed, preferably in natural light. Some times a magnifying lens is useful.

Four basic features of any cutaneous lesion must be noted and considered in theexamination of the skin like, the distribution of the eruption, the types of primary lesion,the shape of individual lesions, and the arrangement of the lesions. The most importantabnormalities in the skin relevant to general examination are pallor, yellowness,pigmentation, cyanosis and cutaneous eruptions. In dehydration the skin is dry andinelastic, so that it can be pinched up into a ridge. The skin is atrophied by age andsometimes after treatment with glucocorticoids. It is thickened, greasy and loose inacromegaly.

Pallor depends on the thickness and quality of the skin and the amount and quality of theblood in the capillaries.

Yellowness a pale lemon-yellow tint is characteristic feature of haemolytic jaundice, inobstructive jaundice; there will be dark yellow or orange tint.

Pigmentation is most commonly racial or actinic. Mostly increased pigment is due toincreased melanin content or due to some other pigment. Generalized melanin hyperpigmentation is seen in Addison’s disease, nelson’s syndrome, pregnancy, acanthosisnigrican etc. Localized pigmentation are seen in melanocytic naevi, Mongolian spots,naevus of ito etc.

Cyanosis is a bluish colour of the skin and mucous membranes due to the presence ofreduced haemoglobin in the blood. Two physiological types are central and peripheral.

40

Central cyanosis results from imperfect oxygenation of blood, as in heart failure andsome lung diseases and admixture of blood from venous-arterial shunts in the heart.Peripheral cyanosis is due to excessive reduction of oxyhaemoglobin in the capillarieswhen the flow of blood is slowed. This may happen on exposure to cold, when there isvenous obstruction, or in heart failure.

Cutaneous eruptions and lesions should be examined with special reference to theirmorphology, distribution and arrangement, color, size, consistency, configuration,margination and surface characteristics should be noted.

MOPHOLOGY OF SKIN LESIONS:

A.INSPECTION AND PALPATION:

Assessment of morphology requires visual and tactile examination.

b) Lesions should be felt

c) Smooth or rough, thin or thick

d) Dry or moist

e) Any visible sweating, either general or local

f) The elasticity of the skin

B.DISTRIBUTION OF SKIN LESIONS:

a) Symmetrical – often implies an internal causation

Asymmetrical – may imply external factors

b) Centrifugal – erythema multiforme, eryhema nodosum

Centripetal – chicken pox, pityriasis rosea

c) Flexor bias – Atopic eczema in childhood

Extensor bias – psoriasis in adults

d) Localised distribution may be due to contact

CASE HISTORY:

A complete history should be obtained to emphasize the following features

1. Evolution of lesions

a) Site of onset

b) Manner in which eruption progressed or spread

c) Duration

d) Periods of resolution or improvement in chronic eruptions

2. Symptoms associated with eruptions

41

a) Itching, burning, pain, numbness

b) If anything, has relieved symptoms

c) Time of day when symptoms are most severe

3. Current or recent medications

4. Associated systemic sysmptoms (eg-malaise, fever etc)

5. Ongoing or previous illnesses

6. History of allergies

7. Presence of photosensitivity

8. Review of systems

DIAGNOSTIC TECHNIQUES:

A) Tzanck preparation

This technique is useful for rapid diagnosis of vesicular infections or blistering

eruptions such as pemphigus.

B) Microscopical examination

This is useful in the diagnosis of scabies, pediculosis and fungal infection

(tinea and candidiasis)

C) Wood’s light

Wood’s light lamp emits long-wave ultraviolet light at a peak of 360nm.

Wood’s light examination is performed in a darkened room, it is useful in identifying

fluorescence of fungi and corynebacterial infection (erythrasma), in the localization of

pigmentary abnormalities.

D) Patch testing

This is an important and valuable tool for diagnosis of suspected allergic

dermatitis due to contact.

E) Skin biopsy

Biopsy is used to identify the nature of expanding or inflammatory lesions, in

diagnosis and in assessing the progress of skin diseases.

REFERANCES:

1.Hutchison’s clinical methods

42

Disease aspect nidana poorvarupa roopa samprapthi rugvinischayam sadya-asadyata upadrava chikitsa pathya-apathya

43

CHAPTER: V

DISEASE ASPECT

Description:

The disease vyangam is described under kshudra roga prakarana.Kshudra roga = swalpa vyadhi (S.K.D)

Kshudra roga prakarana includes all those diseases whose dosha, dushya, etc,have not been described in detail. Hence all the diseases in the kshudraroga prakarana arein concise form.

Kshudra rogas have a simple hetu, lakshana and chikitsa. So, they are called askshudra rogas.

Some of the skin diseases are mentioned under kshudrarogas. Vyangam is oneamongst them.

There is difference of opinion regarding the total number of kshudrarogas.According to Susrutha – 44, Vagbhata – 36, Madhavakara – 43, Sharangadara – 60,Yogaratnakara - 44

The hyperpigmented patches effecting the face is called as vyangam. This can becorrelated with melasma or chloasma.

Nirukthi:

“Vikruthani vyangani yasya” (S.K.D)“vigata vikala vangha pradhikarma” (V.P)

The meaning of vyangam is deformity, dark spots on the cheek.(San-Eng Dictionary)

Nidana:

“yasya prakupitah pittah shonitah prapya shushati” 1

“krodhayasaprakupitho vayuh pittana samyuta” 2

“shokha krodhadhikupitadvathapittanmukkha” 3

vata, pitta, rakta, krodha, shoka and ayasa are the main etiological factors whichcause the vyangam.

Vyangam is a skin disease, so any skin disorder would have the same nidanakaranas as for kusta, therefore the nidana kranas for kusta are being considered.

Ahara:Importance of ahara:

Ahara is moola for bala, varna and oojas.4

The food taken in proper quantity and quality, provides certainly strength,complexion and happy life to the person

Ahita ahara:

44

Viruddha ahara have been mentioned to be the direct cause for the kusta rogas.Charaka has mentioned some types of ahita ahara which are to be avoided.6

Table.5 Showing types of ahitaharaAhara dravya Ahita aharraCereals YavakaPulses MashaDrinking water River water during the monsoonSalt UsharaMeat of animals Young pigeon, frogFat of animals Mahisha,kumbhira, chataka, hastiVegetable oil KusumbhaGhee AvikaLeafy vegetable SarshapaFruit NikuchaRhizome AlukaSugarcane preparation phanita

The consumption of drava, snigdha, guru, nava anna pana, dhadhi,mathsya and excessive intake of lavana, masha, mula, tila, kshira, guda are said to becauses for skin diseases.7

Vihara:Vegadharana, especially chardivega dharana, vyayama after consuming heavy

food, not observing any regular regimen of diet, taking hot and cold foods in succession,exposure to intense heat, not observing the regulations during fasting, consuming coldwater immediately after exertion, improer performance of panchakarma, sleeping duringthe day etc.

Achara:Apart from the above, certain antisocial activities or alakshmikara chesta like

disrespecting elders, holy men, places of worship are also responsible in accumulatingpapa, which is a direct nidana for skin diseases.8

Rakta as an etiological factor: Pure blood imparts strength, complexion, and happy life to the persons.9

When aggravated doshas attain stanasamsraya in the skin and blood, they produceskustha and kshudra rogas.10

Vyangam is caused due to the vitiation of rakta dosha and is mentioned under theraktajavyadhi.11

Charaka has mentioned vaivarna under the shonitaja roga.12

Rakta prakopa karana:Asruk undergoes aggravation by the same causes which aggravates pitta. Frequent

use of drava, snigdha, guru ahara, divaswapna, krodha, anala, atapa sevanam, shrama,abhigatha, ajeerna virudha and adyashana causes rakta prakopa.13

Manovikaras:

45

Krodha, shoka are the psychological disorders.14These psychological problemsarise when faced with non-fulfilment of desires and facing the undesired events.15

Aayasa:

“shokaharshatayayasah sarva snehat pravathathe” (V.P)Exertion, Fatigue, Weariness (S.E.Dic)

Synonymas: shrama, klama, parisrama, prayasa, vyayama, klesha (S.K.D)

Defenition: Tiredness without doing any work, with improper perception of senseorgans and without rise of respiratory rate, this state is called as klama.16

Too much of shrama causes vitiation of rakta.17

Above all factors vitiate vata with pitta, & rakta causing shava varna mandalah onface and manifests in to vyangam.

The etiological factors can be divided into bhahya hetu and abyantara hetu. In thiscontext shoka, krodha and aayasa are the bahya hetus where as vata, pitta and raktadoshas are the abhyantara hetus.

Poorvarupa:

Poorvarupa of vyangam are not mentioned in any Ayurvedic classics. Infact theword ‘sahasa’ was used during the description of the disease, which means that lakshanaof vyangam appears suddenly or abruptly with out poorvarupa.

Roopa:“sahasa mukhamagatya mandalah visrujatyatha

neeruja tanukah shavah mukhe vyanga thamadishet”(S.S)The cardinal symptom of vyangam is the appearance of mandala, which is tanu,

neerujam and shava varna on the face.18

As per Vagbhata, vyangam is classified in to 4 types19

1. Vataja2. Pittaja3. Kaphaja4. Raktaja

1. Vataja vyangam : Skin is rough with parusha sparsha and shava varna2. Pittaja vyangam : The edges of the mandala are in tamra varna, with neela varna in the

central area.3. Kaphaja vyangam: The edges are of shweta varna associated with kandu.4. Raktaja vyangam: The edges has rakta varna with tamra varna in the central part

associated with tigling and burning sensation.

Samprapti:

On account of all causative factors, either independently or together, the pitta andvata get vitiated and in turn vitiates rasa, and rakta dhatu along with manovaha srotas.Chiefly the agni (brajaka pittam) gets vitiated here and the function of agni which is tomaintain varna is disturbed. When these dosha hetus are sustained, the dosha-dushya

46

sammurchana takes place and the morbid factors get lodged at the level of the stana i.e,facial skin.

By the above measures, the samprapti ghattakas may be enumerated as below1. Dosha : pitta, vata2. Dushya : rasa, rakta, manas3. Marga : bahya4. Srotas : rasavaha, raktavaha, manovaha srotas5. Adhistana : twak6. Mala : sweda7. Vyakti : vaivarna

Rugvinischayam:

1. Nyacha: Broad or small, shava or asita varna, painless patches on the skin of the bodyis called Nyacha.20

2. Nilika: Similar black patches as vyangam appearing in other parts of the body isknown as Nilika.21

3. Jatumani: A congenital, slightly elevated, even, slakshna, slightly rakta Varna andpainless patch on the skin caused by kapha and rakta is known asJatumani.22

4. Masaka: Painless, immovable, black, round nodules on the skin resembling blackgramcaused by vata is called Masaka.23

5. Tilakalaka: Black, painless spots resembling sesamum seeds, not raised above thelevel of the skin, caused by vata, pitta and kapha together is known asTilakalaka.24

Sadya – Asadyata:According to Bhavamisra, vikrits occurring in the twak and mamsa are

sukhasadya. According to all other Ayurvedic texts vyangam is a sadya vyadhi.

Upadrava:Vyanga roga does not have any upadrava, but if this appears suddenly in the

diseased patient, it is considered as arista.25

Chikitsa sutra:“shiravedhaih pralepascha tatha abyangarupachareth vyanga”

The treatment indicated for vyangam is siravadham, lepam, and abyangam.26

In addition to these Vagbhata has indicated navana nasyam with markava swarasa, kshiraand thoya.27

Siravyadam:The nearest vein, should be cut, then the paste of bark and sprouts of trees having

milky-sap made with milk should be applied.28

Siravyadam should be done near the ‘lalata pradesha’ accordingly with thepractice and method. After the vyadana karma, the affected area should be rubbed withsamudraphena etc, and filled with the paste of the ksheerivruksha bark.29

Lepam:

47

Lepam is of three types’ pralepa, pradeha, and alepa. Alepam normalizes therakta and vata, cleans the skin and blood.30 Alepa again is of three types doshagna,vishagna and varnya. Varnya Kara alepa is used in vyanga roga.31

Abyangam:Abyangam is the process in which the person’s body is oleated with medicated oil

with specific pressures and movement (gati). Uses of abhyangam are shareramardavakara, kapha, vata nirodhaka, dhatu phustikara, Varna and bala vrudhi kara.32

Vadana abyangam with kumkumadhi tailam is said in Bavaprakasha.33 Katutailaabyangam in Chakradatta.34Tribhuvanadhi churna udvartanam is mentioned inYogaratnakara.35

Pathya – Apathya:Pathyam: phanita, madhu, navanita, raktashali, yava, rasona, matulunga etc,

Nutritional, and timely diet in proper quantity.

Apathyam: pitta and rakta aggravating ahara and vihara. Drava, snigdha guru and navaanna pana. Dhadhi, mathsya and execessive intake of lavana, masha, mula, tila kshira,and guda.

MELASMA; CHLOASMA

fig.9 Diffuse brown pigmentation of the cheekin cholasma

Essentials of diagnosis: 36

Mottled macular pigmentation, usually on the face Painless skin level hyperpigmentation

General considerations:

48

Melasma develops on the face of some women who are pregnant or taking birthcontrol pils. Estrogens may cause melasma by accelerating the formation of melanin andalso cause darkening of the nipples and areolas and the linea nigra on the abdomen, adarkened line extending from the pubis to the umbilicus.

Melasma is not restricted to pregnant women. Many women who have neitherbeen pregnant nor received estrogen-contaning meducations have melasma, as do somemen.

Clinical findings:

A. Symptoms and signs: Melasma is a brown gray mottled discoloration mostprominent on the forehead, malar eminences, and cheeks anterior to the ears. Sometimesit affects the upper lip and the chin.

B. Laboratory findings: the epidermis appears normal. The amount of melanin inthe darkened skin is increased compared to the normal skin. The number of pigment cellsis normal. Melanin may also be present in dermal macrophages (pigment incontinence)and causes the gray-brown discoloration observed in some patients.

Complications:Although there are no biologic complications from melasma, some patients are

markedly distressed emotionally by the cosmetic defects.

Differential diagnosis:Other pigmented lesions that commonly occur on the face are nevus of ota,

freckles, solar lentigo, and post inflammatory hyperpigmentation.

Nevus of ota: This is a blue to gray-brown pigmented patch located on the face, usuallywithin the distribution of the ophthalmic and maxillary branches of the trigeminalnerve.discoloration may be limited to the zygomatic arch or forehead or may cover halfthe face.

Freckles: These are pigmented macules, usually with reddish tan, observed in sun-exposed area on the skin. Seen mostly in children scattered across their cheeks and nose,and macules darken following exposure to ultraviolet light.

Solar lentigo: Patients with history of chronic sun exposure develop solar lentigines,usually after puberty and after age of 40 years. These are called liver spots or old-agespots.lentigens are moderately dark brown and large. With irregular borders.they occuron chronically sun exposed surfaces, on the face, and dorsum of hand.

Post inflammatory hyperpigmentation: This is caused due to a variety of inflammatoryconditions and infections of the skin. Eg, psoriasis, acne, lichen simplex, lichen planus,trauma, herpes zoster, tinea versicolor and chicken pox.

Examination:

49

Epidermal forms of hyperpigmentation usually respond to treatment. In contrast,dermal hyperpigmentation (Mongolian spots or nevus of Ito and Ota) and dermalmelanosis do not respond to any medical treatments and usually is permanent.

It is important, therefore, to determine whether the pigmentation has mainly anepidermal or dermal component. Examination of the patient with Wood’s lamp (“blacklight”) in a totally dark room can facilitate this evaluation. Epidermal melanin turnsalmost black when viewed with Wood’s lamp. In contrast, dermal pigmentation, whenobserved with Wood’s lamp, will not be visible to the examiner, and the blemishes on thepatient’s skin will disappear.

Treatment:Prevention of further hyperpigmentation is paramount. Patients with sun-induced

pigmentatory disorders must avoid habitual sun exposure. Sunscreens or sun blocksshould be applied prior to any outdoor activities.

The goal of therapy is to decrease the production of melanin without killingmelanocytes. Various bleaching medications must be applllied conscientiously 2 or 3times every day, often for 6-12 months, to achieve optimal results.

Cream containing hydroquinone in 3-4% concentration, applied twice daily to thedark areas – may decrease the production of melanin by blocking the activity ofthyrosinase, the enzyme that is primarily involved in melanin synthesis. A side effectfrom hydroquinone is mild skin irritation. At higher concentrations, colloid milia ordermal pigmentation has been reported

The addition of a corticosteroid cream increases the effectiveness of thehydroquinone and perhaps reduces the frequency of skin irritation. Caution must beexercised when prescribing corticosteroids for prolonged periods. On the face,steroids can cause telangiectases, atrophy, or acneiform lesions.

The more potent fluorinated corticosteroids should not be used on the face exceptunder special circumstances.

Tretinoin cream (Retin-A) can also be used in conjunction with hydroquinone or mild

corticosteroids, to decrease epidermal hyperpigmentation. Tretinoin can be veryirritating to the skin and cause erythema, desquamation, and soreness.

Gentle freezing with the liquid nitrogen can decrease the amount of color.Melanocytes are particularly susceptible to destruction by this treatment and maycause necrosis of the skin or blistering and permanent depigmentation in dark-skinnedpatients.

Trichloroacetic acid, is effective in light-skinned patients. It must be used with great

caution, as it is extremely reactive chemically, and higher concentrations can causeinstantaneous necrosis of the epidermis that can leave severe scarring.

50

References:

1.C.S.Su.S 18/252. S.S.Ni.S 13/453. A.H.U.S 31/284. S.S.Su.S 1/285. C.S.Su.S 5/86. C.S.Su.S 25/397. C.S.Ch.S 7/4-88. C.S. Ni.S 5/69. C.S.Su.S 24/4

10. S.S.Su.S 21/3311. S.S.Su.S 24/9, A.H.Su.S 11/8-9, A.SA.Su.S 19/412. C.S. Su.S 24/1313. S.S.Su.S 21/2514. C.S Su.S 7/4215. C.S.Su.S 1/5716.S.D.S.P.K 6/7417. C.S Su.S 24/1018. S.S.Ni.S 13/45-4619. A.H.U.S 31/29-3020. S.S Ni.S 13/43,21. S.S.Ni.S 13/47,22. S.S Ni.S 13/4023. S.S.Ni.S 13/4124. S.S.Ni.S 13/4225. C.S.In.S 1/2126. B.P.M.K 61/39, Va.Se Ks.Ro/4327. A.H.U.S 32/33a28. A.H.U.S 32/1529. S.S.Ch.S 20/33-3430. S.S.Su.S 18/831. S.D.S.U.K 11/1-232. S.S.Ch.S 24/3033. B.P. M.K Ks.Ro/4934. Ch.Da 55/5035.Yo.Ra VOL-II Ks.Ro.N/12336.Dermatology a Lange Medical

51

Vyangam(psycho physiological

approach)

52

CHAPTER. VI

VYANGAM (PSYCHO PHYSIOLOGICAL APPROACH)

MANOVIGNANAM

A brief description of manas:

Nirukthi:“manyathe budyathe anenathi mana”(S.K.D)

The functional unit which is responsible for percessiving knowledge and itsrecollection is known as manas.

Conjunction of boby, sense organs, manas and atma is termed as Ayuvu.1Manas isubayatmakam (karmendriya and gyanendriya) 2

Object of mind:“manasasthu chintyamartha”

The object of mind is that which can be thought of (chintyam).3

Synonyms:Athindriya, manah, satvasangyaka4

Seat of manas:1. Hridayam5

2. Shirastalvantara gatam6

Manovishayas:Chintyam, vicharyam, oohyam, dheyam, sankalpam are perceived by the manas

are known as manovishayas.7

Manoguna:Anutva, Ekatva are mano gunas.8

Mano lakshana:Gyana abhava and Gyana bhava are considered as mano lakshan.9

Mano kruthya:Mano kruthyas are Indriyabhigraham, Swanigraham, Ooha, Vicharyam, and

beyond that is the jurisdiction of buddhi (intellect).10

Mano doshas:Rajas and tamas are the two manodhoshas.11

Mano vikara:Psychological disorders like, Ersha, Shoka, Bhaya, Krodha, Maana, Dwesha etc

are caused due to pragnyaparadha.12

53

Causes for manovikara:1. Perverted, negative and excessive use of kala, bhudhi, indriyardha are the threefold

cause of both psychic and somatic disorders.13

2. Mano vikaras are caused due to, manodhoshas – rajas and tamas.14

3.Psychological problems arise when faced with non-fulfilment of desires and by facingthe undesired situations.15

4.For both shareera and mano dhoshas, the three aggravating factors are astamendriyardhasamyogam, pragnyaparadam and parinamam.16

5.Pragnyaparadam is the unwholesome activities performed by a person due to Dhi,Druthi, and Smruthi bramsham, and this is an intellectual error.17

Manovaha srotas:Manas and bhuddhi are the moolas for manovaha srotas. Charaka has described

about this srotas in Unmada and Apasmara nidanam.

Description of krodha and shokha:Krodha and shokha are considered as psychological disorders.18

KRODHA:

Nirukthi: “prathikula sathi thaikshgamya prabhodha” (V.P)Anger, wrath (S.E. Dic)

Synonyms: kopa, rosha, rudhra, krutha, krudha, rusha (S.K.D)

Lakshana: Injurious and destructive behaviour towards others, development ofinconsiderate violence and distress towards living creatures are the lakshnas of krodh.19

Causes: Krodha is caused due to rajo guna.20

When pitta dosha invades the sira, it produces the angry mind and irrelavent talk.21

Abnormal state of sadaka pittam results in krodha.22

Dhusta shonita causes klama and krodha.23

Pitta prokopa causes krodha.24

Effects: Krodha causes redness of face, increase in respiration and heart beat, and this leads to

hypertension and heart diseases.

Excessive anger and exertion causes the vitiation of rakta dhosha, which in turn

causes the skin diseases.25

SHOKHA:Nirukthi:

“bandhadhi viyoghajanitha manah peeda”(V.P)Sorrow, grief, distress, deep anguish (S.E.Dic)

54

Synonyms:Shuk, manyu, ityamara, shucha, neshama, khedh, shochanam (S.K.D)

Causes: Shokha is caused due to tamo guna 26

Vata prakopa causes shoka 27

Effects: Shokha causes emaciation of the body.28

Shokha leads unto sever diseases 29 like shokhatisara.

Shokha causes the vitiation of vata30

When krodha, ayasa, shokha inflict the manas, dhoshas are aggravated causingother diseases like abhishanga jwara, unmade, apasmara etc31

Effect of krodha and shokha on dhoshas:

“krodhashokhabhayaayaso……pittam prakopamapadyathe”Krodha, shokha and ayasa are the factors which causes the pitta prakopam.32

“kamashokhabhayadyauh, krodhatpittam……..”Shokha causes vata prakopam and krodha causes pitta prakopam33

Both body and mind effect each other in causing the diseases.34

Psychic and somatic diseases sometimes continuing together are associatedmutually35

The sparshanendriya alone pervades all the sense organs and it is also associatedinherently with manas.36

PSYCHOPHYSIOLOGICAL STRESS:

Psychosocial stress may be an important factor in understanding skin problems.No controlled study has been carried out which has examined relation betweenpsychophysiological stress and skin complaints. Potential role of psychophysiologicaland organizational factors in the etiology and clinical course of skin diseases is to beevaluated.37

A comprehensive assessment of physiological, occupational and psychosocialfactors were performed, blood and urine samples were tested for the determination of thelevels of stress hormones (serum cortisol, prolactin, oestradiol, testosterone, thyroxin andgrowth hormone and urinary concentration of adrenalin and noradrenalin). Rise in stresshormone levels as well as subjective feelings of stress indicate the effect of stress on theskin complaints. Physiological changes characterized by elevated metabolism andincreased dermal blood flow, may act as unconditioned stimulus.38

There were no systematic differences noted refarding age, sex, distribution, jobfunctions, personality, socioeconomic factors, marital status, alchohol or coffeeconsumption, or smoking habits and pigmentation ability. Further- more, for the persons

55

with skin complaints, a conditioning mechanism arising from a fear of health hazards isprobably of importance.

References:

1. S.S.Su.S 1/422.B.P.Po.K 1/106, S.S.Sa.S 1/63.C.S.Su.S 8/164.C.S.Su.S 8/45.C.S.In.S 5/416.Be.S.Ch.S 8/27.C.S.Sa.S 1/208.C.S.Sa.S 1/199.C.S.Sa.S 1/18

10.C.S.Sa.S 1/2111.C.S.Su.S 1/5712.C.S.Su.S 7/4213.C.S.Su.S 1/5414.C.S.Su.S 1/5715.C.S.Su.S 11/4516.C.S.V.S 6/6, C.S.Su.S 11/4317.C.S.Sa.S 1/102, C.S.N.S 7/2118.C.S.V.S 6/5, S.S.Su.S 1/2419.S.D.S.P.K.5/11720.A.SA.Sa.S 5/1321.A.SA.Su.S 19/1922.ON C.S.Su.S 12/11 Cakrapani commentary23.C.S.Su.S 24/1424.A.SA.Su.S 19/3a25.C.S.Su.S 24/9-1326.A.SA.Sa.S 5/1427.A.SA.Su.S 19/3b28.C.S.Su.S 25/4029.S.S.Su.S 15/3330.C.S Ch.S 3/11531.C.S.Su.S 24/3132.S.S.Su.S 21/2133.C.S.Ch.S 3/11534.C.S.Su.S 1/5535.C.S.V.S 6/836.C.S.Su.S 11/3837.Endocrine and dermatological concomitants of mental stress38.Report published by ‘National Institute for Psychosocial Factors and Health’ Sweden.

56

Disorders ofhyperpigmentation

57

CHAPTER: VIIDISORDERS OF HYPERPIGMENTATION:

Hyperpigmentation is a common problem, especially in patients with dark skin.Most cutaneous irritants cause an increase in pigmentation. However, patients of any racecan suffer significant cosmetic disfigurement from ocalised or generalizedhyperpigmentation. Hyperpigmentation may be a cutaneous sign of a serious metabolic ornutritional disorder. Fortunately, most types of hyperpigmented lesions are benign. Someare malignant eg-melanomas. Usually one thinks of hyperpigmentation as affecting onlythe skin. However, it can also affect the nails or mucous membranes.

Abnormality of pigmentation can be subdivided in to

a) Melanocyte population densities (increased or decreased)

b) Melanin production (enhanced or diminished)

c) Melanosomal packing and distribution

d) Miscellaneous abnormalities (usually nonmelanotic)

The depth of pigmention deposition in the skin, whether in the epidermis or abnormallyin the dermis, also affects the overall perceived color. These vroad groupsofclinicopathologic disorders are further divided into

a) Congenital or genetic diseases

b) Acquired diseases

A. CONGENITAL OR GENETIC HYPERPIGMENTATION DUE TO AN EXCESSNUMBER OF MELANOCYTES

1. Lentigo simplex

Onset during infancy or early childhood Small brown macules Not limited to sun-exposed areas Low malignant potential

3.Multiple lentigines syndrome or leopard syndrome

Lentigines Electrocardiographic abnormalities Ocular hypertelorism Pulmonary stenosis Abnormalities of the genitalia Deafness There are increased number of melanocytes in the basal layer and

increased melanisation. The melanosomal contents is expanded, and gaintmelanosomal complexes are noted.

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3. Nevus spilus

Present at birth or occasionally early infancy Light brown patch speckled with dark brown macules, usually is a

congenital The usual location is the trunk or proximal extremity

4. Mongolian spot

Blue-black pigmentation of the sacrogluteal region Present at birth Spontaneous resolution Bipolar melanocytes filled with melanin are scattered in the papillary and

reticular dermis

5. Nevi of ota

Blue to gray-brown pigmented patches Facial location Permanent Pigmented patch located, usually within the distribution of the ophthalmic

and maxillary branches of the trigeminal nerve

6. Nevi of ito

Blue to gray-brown pigmented patches Unilateral location on shoulders and neck Permanent It occurs along the distribution of the supraclavicular and brachial nerves

B. ACQUIRED HYPERPIGMENTATION DUE TO AN EXCESS NUMBER OFMELANOCYTES

1. Solar lentigo (senile lentigo) Onset after puberty and usually after age 40yrs History of chronic exposure to solar radiation Lesions confined to sun-exposed areas Solar lentigines are moderately dark brown and large, often 1cm or more in

diameter with irregular borders

2. Ultraviolet-induced hyperpigmentation (suntan) Light brown or golden brown coloration of exposed skin Sharp demarcation lines between exposed and normal skin

B. CONGENITAL HYPERPIGMENTATION DUE TO MELANOSOMALDEFECTS

Neurofibromatosis ( Recklinghausen’s disease)

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Neurofibromas: Usually soft, pedunculated, flesh colored papules and nodules,“buttonhole” deformity

Café-au-lait macules Axillary freckles Lisch nodules: Yellow or brown papules on the iris Neurofibromatosis is one of a group of disorders of neural crest-derived cells, the

neurocristopathies. They include pheochromocytoma, neuroblastoma, and othersyndromes

D. CONGENITAL HYPERPIGMENTATION DUE TO ABNORMALITIES OFTYROSINASE

1. Familial progressive hyperpigmentation Dark-skinned individuals only Reticulated, deeply pigmented patches on the skin, present at birth

3. Hereditary hyperpigmentation in blacks

Futcher’s line is a sharply demarcated line of pigmentation visible on theanterolateral side of the deltoid and the upper part of the arm

In others hyperpigmented line extending across the nose from one nasolabial foldto the other is seen

4. Periorbital hyperpigmentation Darkened rings around the eyes, seems to vary with stress or lack of sleep.

This may be due to vascular changes. The trait is transmitted as an antosomaldominant defect

5. Peutz-jegher’s syndrome Brown or black macules, especially on the lips and buccal mucosa Polyps of the intestines Autosomal dominant inheritance

6. Incontinentia pigmenti (Bloch-sulzberger syndrome) Female predominance (X-linked dominant) First stage :- streaks of vesicles Second stage :- streaks of verrucous papules Third stage :- streaks of whorled hyperpigmentation Associated with multiple defects of the central nervous system Streaks develop most commonly over the extremities and trunk

D. ACQUIRED HYPERPIGMENTATION DUE TO ABNORMALITIES OFT YROSINASE

1. Freckles (ephelides) Tan or red macules 1-5mm in diameter in sun exposed areas Especially in fair-skinned people Freckles scatter across cheeks and nose in children

2. Melasma (chloasma)

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Mottled macular pigmentation, usually on the face Most commonly during pregnancy (‘mask of pregnancy’)

3. Becker’s nevus Light brown patch usually on the unilateral shoulder and back Male predominance Hypertrichosis within the pigmented patch

4. Postinflammatory hyperpigmentation Patchy distribution following pattern of original dermatoses Very common in dark-skinned patients

5. Systemic causes of hyperpigmentation

a) Metabolic Porphyria cutanea tarda Advanced liver cirrhosis Hemochromatosis Chronic renal failure Gaucher’s disease Niemann-pick disease

c) Endocrine Addison’s disease ACTH and MSH producing tumors Pregnancy Oral estrogen therapy Acromegaly

d) Nutritional Pellagra (niacin deficiency) Pernicious anemia (Vit B12deficiency) Kwashiorkor

e) Miscellaneous Scleroderma Inflammatory bowel disease Cronkhite-canada syndrome Bleomycin therapy Fluorouracil therapy Busulfan therapy Arsenical ingestion Fixed drug reaction

5. Adrenal insufficiency (Addison’s disease) Generalized brown hyperpigmentation Accentuation in creases, sun-exposed sites and genitalia Excessive ACTH and MSH production

7. Drug-induced hyperpigmentation

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a) Heavy metals Silver :- blue-gray color called argyria Bismuth and arsenic :- brown hyperpigmentation

c) Tetracycline Minocycline Methacycline (blue-grey hyperpigmentation is seen, melanin may also be present

in epidermis)

d) Cytotoxic agents Bleomycin :- Skin becomes deeply tanned Cyclophosphamide Melphalan (hyperpigmentation in nails)

e) Miscellaneous drugs Antimalarial drugs Chlorpromazine Clofazimine (reddish-brown hue)

Table.6 Showing classification according to the color of pigmentation in genetic and naevoid factorsGENETIC AND NAEVOID FACTORS

BROWN COLOR GREY, SLATE OR BLUE COLOR

1. Ephelides (freckles)

2. Lentigines

3. Multiple lentigines syndrome

4. Peutz-jegher’s syndrome

5. Cafe-au-lait and freckle-like macules in

Albright’s syndrome

6. Acanthosis nigricans (juvenile type)

7. xeroderma pigmentosum

8. Fanconi’s syndrome

9. Dyskeratosis congenital

10. Familial progressive hyperpigmentation

1. Mongolian spot

2. Naevus of ota

3. Naevus of ito

4. Blue naevus

5. Diffuse melanocytosis

6. Incontinentia pigmenti ( Bloch-

sulzberger)

7. Naegelli-franceschetti-jadassohn

syndrome

Table.7 Showing classification according to the color of pigmentation in acquired hypermelanosis

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ACQUIRED HYPERMELANOSISCAUSATIVE FACTOR BROWN COLOR GREY, SLATE OR BLUE

COLORA. Endocrine 1. ACTH and MSH

producing pituitary andother tumours2. Addison’s disease3. ACTH therapy4. Pregnancy5. Contraceptive pills andoestrogens6. Melasma (chloasma)

B. Chemical 1. Arsenic2. Busulphan3. Bleomycin4. Cyclophosphsmide5. Adriamycin6. Psoralens7. Berloque dermatitis8. Phytophotodermatitis

1. Minocycline2. Fixed drug eruptions3. Barbiturates4. Phenolphthalein5. Phenothiazines6. Chlorpromazine

C. Physical 1. UV light2. Ionising radiation3. Trauma

D. Nutritional 1. Kwashiorkor2. Pellagra3. Sprue4. Vit B12 deficiency

Chronic nutritionaldeficiency

E. Post inflammatory 1.Eczema2. Lichen planus3. Lupus erythematosus4. Lichen and macularamyloidosis5. Systemic sclerosis6. Morphoea

1.Pinta2. Erythema dischromium3. Perstans

F. Tumours 1. Malignant melanoma2. Acanthosis nigricans withadenocarcinoma3. Malignant tumours

Metastatic melanoma withmelanogenuria

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CLASSIFICATION OF HYPERPIGMENTATION ACCORDING TO ITS SPREAD

Table.8 showing classification of hyperpigmentation according to its spreaGENERALIZEDHYPERPIGMENTATION LOCALISED HYPERPIGMENTION

1. Addison’s disease2. Nelson’s disease3. Pregnancy4. Acanthosis nigricans5. Primary

haemochromatosis6. Secondary

haemosiderosis7.Hepatic cirrhosis

(particularly biliarycirrhosis)

8. Chronic renal failure9. Glycogen storage

disease10. Gaucher’s disease11. Vagabond’s disease12. Heavy metal

intoxication(Arsenic ingestion,silver, bismuth andgold preparations)

13. Modern drugs(Minoxycycline,Amiodarone,phenothiazines,chlorpromazineetc)

14. Carotenaemia15. Canthexanthin16. Methaemoglobinaemia17. Sulpha

emoglobinaemia

6. Melanocytic naevi7. Mongolian spots8. Naevus of ota9. Naevus of ito10. Neurofibromatosis11. Peutz-jegher’s syndrome12. Albright’s syndrome13. Chloasma14. Post-inflammatory hyperpigmentation10. Lichen planus11. Fixed drug eruption12. Atopic dermatitis

Referances:

1. Roxburgh’s common skin diseases2. Histopathology of the skin3. Dermatology

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HYPERPIGMENTATION DISORDERS IN AYURVEDA

1. Vidhradhi1

Vataja vidhradhi – Krushna, aruna varna Pittaja vidhradhi – Shava varna Raktaja vidhradhi – Krushna, shava varna

2. Vataja vrana – Shava varna2

3. Kushta3

Kapala kushta – Krushna, aruna varna Ruhyajihva kusta – Raktaparyantam, Antashyavam Kitiba kusta – Shavavarna kina Vispota kusta – Shava, aruna basa Shataru kusta – Rakta, shava Vicharchika – Shava

4. Kshataja visarpa – Shavashonitam4

5. Kshudra rogas5

Jatumani – Krushna Mashaka – Krushna, mutsanna Tilakalaka – krushna Vyanga – Shava Nyacha(lanchana) – Shava Nilika – Krushna

6. Vataja pandu – black red discoloration of skin6

7. Asadhya madatyaya – Black or blue discoloration of lips, teeth, gums7

8. Haleemaka – blackish yellow discoloration of skin8

9. Vishaja unmade – Shava 9

10. Krimija hridroga - Shava 10

11. Vatodara – bluish or brownish discoloration of skin11

12. Vataja sleepada – Blackish swelling is seen12

Referances

1. M.N 40 /4,5,102. M.N 42 /23. M.N 49 /10,13,18,21,224. M.N 52 /235. M.N 55 /346. M.N 8/47. M.N 18/228. M.N 8/239. M.N 20/1510. M.N 29/611. M.N 35/712. M.N 39/9

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Drug review

66

CHAPTER: VIII

DRUG REVIEW

CRITERIA FOR SELECTION OF THE DRUGThe drug selected for the present clinical study is manjista kwatha internally and

manjista madhu lepam externally.The administration of manjista kwatha for varnya vikaras is mentioned in charaka

samhita sutrastana 5/8The use of manjista madhu lepam is described in Susrutha samhita, Vagbhata

samhita, Bavaprakasha and in many classical Ayurvedic texts.The preparation is non controversial, easily available, easy to prepair and free

from toxic effects.“ manjista madhura tikta kashaya swaravarna krut !

Raktatisara kustasavesarpa vrana mehanut”1

Manjista has madhura, tikta, kashaya rasa and it has varnya, kustagna, andraktashodaka properties.

“sowkumaryam sukshmam param srotovishodanamKashanurasam lady prasadajanakam param” Varnyam,Yogavahe 2

Madhu has madhura, tikta as anurasa. It bestows suppleness, enters into minutepores and cleanses the srotas. It has varnya and yogavahi properties.

Properties of rasa

Table.9 Showing the properties of rasaRASA PROPERTIES SAMHITA

Twachya C.S.Su 26/62Madhura Varnya A.H.Su10/8,B.Pr.Po.k 5/155Kustaprashamana C.S.Su 26/70Kusta, pitta kapha jayate A.H.Su 10/14-15TiktaKusta, raktagadapaha B.Pr.Po.k 5/199Shleshma, rakta pitta prashamana C.S.Su 26/72Pitta, kapha vishodhana, twak prasadana A.H.Su 10/19-20KashayaCapa, rakta, pittagna twak prasadana B.Pr.Po.k 5/203

Because of brajaka pitta avabasini twak layer has its normal complexión .pitta vikruthicauses rakta dhusti resulting in varna vikaras of the skin. Along with these if vitiation ofvata and kapha occurs, theye will cause disturbances in brajaka pitta functions resultingin shava, aruna and shukla varna of the skin.3

Vyanga roga is caused due to psyco-somatic disturbances, and it being a skindisease, rakta dhatu dhusti is also seen and more-over this is a varnya vikara.

Manjista has the varnya, kustagna and raktashodaka properties. When it is giveninternally it has tranquilizing effect on the brain.

Madhu is also a varnya dravya and it pacifies vata and pitta dhoshas.4 when honeyis mixed with various formulations it alleviates many diseases as it is an excellentsynergist, because of being composed of, number of factors.5 madhu is yogavahi- thatwhich exerts action similar to that of the drugs in combination.

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Keeping in view all the facts mentioned above manjista, madhu are selcted for thepresent trial.

FORMULATIONSA review of formulations employed in the study1. Manjista, madhu lepam (B.P.M.K.4A.14/39)2. Manjista kwatham (C.S.Su 4/8)

The above mentioned preparations are selected for present clinical study

Review of ingredients

1. Manjista fig.10 Root and plant of manjista

Botanical name: Rubia Cordifolia

Family: Rubiaceae

Synonyms: manjistha, vikasa, samangi, Kalameshika, manduka parni, yojanavalli,rasayana, raktangi, raktayastika, manjusha, vastra ranjani.6

Vernacular names: 7

Sanskrit : ManjistaHindi : ManjitEnglish : Indian madderTelugu : Tamravalli

GanaVarnya, Jwarahara, Vishagna (Charaka)Priyangvadhi, Pittasamshamana (Susrutha)Varnya gana (A.H.S)

Parts used; Roots

Botanical description:

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A perennial climbing herb; roots long, cylindric, with a thin red bark; stem very long,rough, grooved; Branches scandent, quadrangular, often prickly on angles. Leaves inwhorl of 4, ovate, 4-9 + 1.5-3.5cm, lower leaves longer than the upper, scabrous above,margins with minute prickles, all 5-(rarely 7-) nerved from the base; Flowers small,greenish, in terminal, panicled cymes; Fruits didymous or globose, 4-6mm in diameter,purplish black when ripe.

Distribution:

It is found through out India, ascending to an altitude of 3750 from North-WestHimalayas eastward.

Actions:

The roots are astringent, alterative, anti-inflammatory, anodyne, antiseptic,carminative, anthelmintic, depurative, vulnerary, emmenagogue, diuretic, ophthalmic,febrifuge, rejuvenating, tonic and it has tranquilizing effect on the brain.

Uses:

The roots are useful in dropsy, paralysis, rheumatoid arthritis, neuralgia, cephalalgia,dyspepsia, flatulence, leucoderma, pruritus, wounds, ulcers, upper respiratory infections,menstrual disorders, discolouration of the skin, tubercular condition of the skin andmucosal tissue, spleen and liver disorders, pectoral diseases and general debility.

Properties:8

Rasa : Madhura, Tikta, Kashaya

Guna : Guru, Ruksha

Veerya : Ushna

Vipaka : Katu

Doshaghnata : Kaphapitta shamaka

Karma : Swara varna krut, Shothahara, Vranaropana, Kushthaghna,Deepana, Pachana, Stambhana, Raktashodhaka, Pramehaghna,Balya, Rasayana and Vishaghna.

Amayika : Shota, Vrana, Charmaroga, Agnimandha, Amadhosha, Raktaprayoga Atisara, Yoni, Akshi, Karna ruk, Visarpa, Kusta, Prameha, Jwara,

Varnavikara, Daurbalya, Vishavikara.

Dose : Kwatha :- 50-100ml, Powder :- 1-3 gmsPharmacognosy of roots:

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fig.11 Roots of manjista

Root is long, cylindric, fexuose, smooth and reddish. In transverse section, theroot is circular in out line. Outer 5-7 layers of cells form the cork tissue, occasionallycontaining tannin. Secondary cortical cells are thin walled and polygonal in shape. Manyof these cells contain tannin. Phloem cells are thin walled, some of them contain tannin.Cambium is 2-3 layered. Secondary xylem consists of vessels and tracheids. Primaryxylem is triarch.

Chemical constituents:Roots contain resinous and extractive matter, gum, coloring matter and salts of

lime. Free alizarin and its glucoside, purpurin, xanthopurpurin, munjistin, glucose,sucrose, ruberythric, acid, pseudo purpurin, 1,4-dihydroxy-2-methyl anthraquinone,physcion, nordamnacanthal, scopoletol, ten fatty acids with saturated long chains,anthraquinones, naphthohydroquinones, mollugin, furomollugin and dehydro-alpha-lapchone.9

Pharmacological activities:Antioxident, antibacterial, anticancer, anti-inflammatory, antitumour, antiviral,

haemostatic, anti-lipid peroxidative activity, and hypoglycaemic.

Therapeutic evaluation:1. 45 patients suffering from scabies with secondary infection were treated with theAragwadha kwatham, for external application Pamari ointment( paranthimoola,dinesavalli, manjista) was used. About 51% cases were completely relived within 20-50days.

2. 32 cases prescribed with Alstonia scholaris bark extract (60ml twice a day) internallyand Pinda taila (manjista and shariva) applied externally showed relief from minor skindiseases in 10-30 days.

3. A paste made with manjista roots and honey is a valuable application for the frecklesand other skin discolorations, in external inflammation, ulcers and skin diseases such aspityriasis, versicolor etc, roots are said to act against staphylococcus. (Wealth of IndiaCSIR)

References:

1. B.P.Po.K.Ashta varga 5/178

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2. B.P.Po.K.Madhu varga 5/1-53. Chakrapani comentary on C.S.Su 4/84. S.S.Su 45/1325. S.S.Su 45/1426. B.P.Po 5/176-1777. Dravyaguna vignanam Vol II8. Danvantari negantu9. Data base on medicinal plants in Ayurveda(Vol - V)

MADHU

fig.12 MadhuBiological source

Honey is the sugary substance produced from the nectar of flowers by the workerbees and deposited by them in the cells of the honey comb. Honey dew, a secretion of theleaves of various trees and plants, is also gathered by bees.

Scientific name : Apis mellifica and A.dorsata and other species of ‘apis’Family : ApidaeOrder : Hymenoptera

Vernacular names:Sanskrit : MadhuHindi : ShahadhTelugu : Thene

Synonyms

Madhu, maksika, madhvika, ksaudra, saragha, maksika vanta, varati vanta,bhrngavanta, pusparasodbhava.1

Characters:

Honey is thick, syrupy, translucent liquid. The colour varies from almostcolourless to nearly black according to its botanical source and to conditions ofprocessing and storage it has undergone. The difference in the aromatic constituentsaltering the taste and aroma of the honey varies, according to the plants from which thenectar is obtained.

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At normal temperature honey is frequently supersaturated with respect to glucoseand exists as clear syrup mainly preferred by consumers. However on storage, coarsegranulation or crystallization can occur, which may lead to fermentation, in some cases.The tendency to granulate depends on, number of factors, some of which remainunknown. The ratio of sugar components and moisture have a major effect in granulation,e.g- glucose and water ratio of 2:1 or more granulate rapidly.2

Charecters of madhu according to Ayurvedic texts:

Madhu has sheeta veerya, it is easily digestable, sweet, causes dryness, grahi,sacrificant, good for eyes, kindles digestive fire, good for voice, cleanses and healsulcers. Bestows suppleness, enters into minute pores, cleanses the srotas, has astringentas secondary taste, bestows contentment, improves complexion and intelligence, isaphrodisiac, removes tastlessness, cures leprosy and other skin diseases, good in piles,cough, bleeding diseases, diabetes of kapha origin, exhaustion, worms, obesity, thirst,vomiting, dyspnoea, hiccup, diarrhea, constipation, feeling of burning sensation, woundsin the lungs, is yogavahi (enhances the effect of the drug with which it combines) andaggravates vata slightly.4

Composition:The main constituents of honey are moisture, glucose (dextrose), fructose,

maltose, sucrose, dextrine, formic acid, volatile oil and mineral matter. In addition tothese, traces of enzymes, vitamins (Vit B), proteins, aminoacids are also present in honey.Pollen is invariably present in comb honey, but may be absent in some honeys whichhave been very finely strained. Enzymes present cause changes in the proportions of theoriginal sugars present and the sucrose may disappear completely on storage.

Chemical constituents: 4

Water (%) : 15 – 22Nitrogen (%db) : 0.05 – 0.38Ash (%db) : 0.04 – 0.93Reducing sugars(%db) : 85 – 94.9Dextrin (%db) : 1.70 – 5.22Proteins : > 1%Free acid (ml 0.1m : 12.9 – 58

NaOH/100g)PH : 3.6 – 5.6

Carbohydrates in honey:The principle sugars present in honey are fructose and glucose together with

maltose, a little sucrose and dextrin. ‘Dextrin’ fraction includes a mixture of at least 22di-tri and higher oligosaccharides. Ratio of fructose to glucose in pure honey is 106-119:100.

Varieties of Madhu:

Table.10 Showing varities of madhuCHARAKA5 SUSRUTHA6 BHAVA PRAKASHA7

1. Makshika 1. Pauttika 1. Maksika

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2. Bhramara 2. Bhramara 2. Bhramara3. Ksaudra 3. Ksaudra 3. Ksaudra4. Pauttika 4. Maksika 4. Pauttika

5. Chatra 5. Chatra6. Arghya 6. Arghya7.Auddalaka 7. Auddalaka8. Dala 8. Dala

Varga:Madhu is mentioned among the Madhura varga, Kashaya varga (A.H.Su.S 10/24&31)

Pharmacological and therapeutic properties: 8

Rasa : Kashaya, Madhura(Caraka)Madhura, Kashaya anurasa (Ba.Pr)

Guna : Guru, Sheeta, Ruksha (Caraka)Laghu, Sheeta, Ruksha (Ba.Pr)

Veerya : SheetaVipaka : KatuDoshagnata : Tridosha prashamanaAction and uses: Slightly aggravates vata, alleviates rakta, pitta and kapha, grahi,

Lekhana, deepana, swarya, sowkumarya kara, srotovishodhana,Varnya, kusta hara, yogavahi.

Specific properties of madhu:1. Madhu pacifies vata and pitta due to madhura, kashaya and picchila bhavas.9

2. Madhu is composed of many factors, when it is mixed with various formulations, italleviates many diseases as it is an excellent synergist.10

3. Old (pakva) honey is tridhosha haram, where as new honey is tridhosha karam.11

Madhu after one year is considered as purana madhu.12

References:1. Ba.Pr.Po.K. 6(mv)/12. Pearson’s chemical analysis of food3. Ba.Pr.Po.K 6(mv)/1-54. AIDS to analysis of food and drugs5. C.S.Su.S 27/243-2446. S.S.Su.S 45/1337. Ba.Pr.Po.K 6(mv)/68. Madhu ke upayog9. S.S.Su.S 45/13210. S.S.Su.S 45/14211. S.S.Su.S 45/14312. Ba.Pr.Po.K 6(mv)/126

METHOD OF PREPARATION OF THE MANJISTA KWATHA:

A brief description of kwatha:

Kwatha:

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1. Definition: The preparation, prepaired by boiling a drug on fire is known as kwatha orsrutha.1

2. Kwatha is one of the panchavidha kashaya kalpanas viz swarasa, kalka, kwatha, himaand phant.2

Synonyms:Srutha, kashaya, niryuha, kadha 3

Preparation:One pala (4 tola) of coarsely powdered drug is boiled with 16 parts (64 tola) of

water in an earthen pot over a mild fire till the liquid is reduced to 1/8th of the originalquantity. Thus obtained liquid is known as kwatha.4

Administration:1. In vata and kapha pradhana vyadhis ushna kwatha and in pitta pradhana vyadhissheeta kwatha should be administered.5

2. Ancient, physicians advise administration of kwatha after the digestion of food.6

Dose:4 tola in slightly warmed media

kwatha churna:

fig.13 manjista kwatha churna

1. Kwatha churna are compounded coarse powders which are intended for usagewhenever a particular type of decoction is required.2. Churna should not be powdered finely. If the powder is very fine, the decoction isnot easily filtered into a clear liquid, this is due to the fine particles passing through thefilter.3. The kwatha churna is potent for nearly one year, if protected from moisture andinsect

Preparation of manjista kwatha :Manjista is cleaned, dried, powdered coarsely, and stored in glass jars. 30gms of

coarse powder of manjista is washed in water and taken in clean and dry vessel. Vessel isthen filled with 480ml of water and then kept on mild fire, with out covering it with thelid, and stirring the contents till the liquid reduces to 60ml (1/8 th of the total content).

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Then the decoction is filtered and used, when it is warm. Thus prepared kwatha should beused with in 12hrs.8

Dose: 30ml Twice DailyMANJISTA MADHU ALEPAM

Brief description of lepam:

Nirukti:“lipyathe anenathilepa”“turushka nama gandha dravyam”

Classification:Lepas are of three types, Pralepa, Pradeha, Alepa

1. Pralepa: This is cold, thin layer, moist or dry (sheeta, tanu) and should not beapplied in the nights eg.chandana lepam

2. Pradeha: This may be ushna or sheeta, thick layer (bahala) and moist, pacifies vataand kapha, cleanses, heals and alleviates inflammatory swelling and pain, it is used inopen and closed wounds, and can be applied in day and night times.

3. Alepa: This cleans skin and normalise blood and muscle. Its thickness is of mediumcharacter, normalizes rakta and pitta.1

Alepa types:

Alepa is of three types doshagna, vishagna and varnya based on the action. This is alsotermed as mukhalepa.

1. Doshagna: It is applied in vata, pitta dhosha and shotadi conditions. Applied in 1/4th

angula pramana (app 0.175 inch)

2. Vishagna: It is applied for the vanaspati, prani and kanija visha effect in 1/3rd angulapramana (app 0.205 inch)

3. Varnya: It is applied in vyanga, charmakeela, kshudraroga in ½ angula pramana (app0.325 inch)

As per susrutha, the thickness of alepa should be equal to moist skin ofbuffalo (mahisha ardha charma) 3

Indications and contraindications:1. The lepa on skin should be applied always in pratiloma direction i.e down to

upwards. By applying romabhimuka, the medicine is adequately absorbedthrough siramukha and romakupa. Where it shows its effect.4

2. Lepa should be applied warm for vata and kapha, for pitta it should be appliedvery cold. 5

3. The lepa applied over is removed when it is wet and never allowed to drybecause it becomes nirveerya and causes harmful effects. 6

4. Lepa should not be applied in the night, to avoid complications arise due to non-exit of heat suppressed by coldness.7

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5. one should never apply stale paste nor additional applications over a pasteapplied, due to thickness, it might cause, vedana, daha and ushma.8

6. After application of lepa, the person should avoid day sleep, speaking for longhours, exposure to fire and sunlight, sorrow and anger. 9

7. Lepa should not be administered to persons suffering from peenasa, ajeerna,dattanasya (who has received nasya), hanugraha, arochaka and has doneratrijagarana. 10

Absorption of lepa:

In Dalhana commentary on susrutha samhita, during the description of abyanga,Dalhana commented that the sneha takes 400 matrakala to reach the skin (S.S.Chi.S24/30 Dalhana vyakya). Since the procedure of lepanakarma can be compared to someextent with abyanga, the time factor can also be taken as the same, therefore the lepaapplied on the face should be kept for 5 minutes or more, and then washed away.

Action of lepa:1. If lepa is done properly, it cures akala palitha, vyanga, vali, timira and neelika.11

2. For those who apply mukhalepa the vision becomes keen and the face smooth,resembling a lotus flower. 12

Procedure adapted for application of manjista madhu alepam:

fig14.Fine powder of manjista and madhu

In this trial, patient is instructed to mix madhu with manjista choorna in a bowland to apply it with right hand middle finger upon the effected part from medial tolateral side 2-3 times a day for 5 to 10 minutes. Then patient is asked to wash away thelepa and instructed not to expose to sun-light and heat for a period of 1/2hr. In this way,the medicine is applied regularly for a period of eight weeks.

References:

1. S.S.Su.S 18/8

2. Sha,S.U.K 11/1-2 & A.H.Su.S 22/14

3. S.S.Su.S 18/10

76

4. Sha.S.U.K 11/73

5. A.H.Su.S 22/14

6. Sha.S.U.K 11/74

7. S.S.Su.S 18/12

8. S.S.Su.S 18/13

9. A.H.Su.S 22/16

10. A.H.Su.S 22/17

11. A.H.Su.S 22/18

12. A.H.Su.S 22/22

77

Materials and methodas

78

PART IISECTION III : MATERIALS AND METHODS

1. Selection of the patient: Thirty patients attending the OPD of Kaya chikitsadepartment of GAH, Hyderabad presenting with features of vyangam are selected for theclinical study irrespective of gender, age, occupation, chronicity etc.,. Patients withnotable systemic disorders are excluded. Special attention is made to notice the incidenceof gender, age, occupation, social status, diet, prakruthi, chronicity in relation to thediseases.

2. Selection of the drugs: Manjista kwatham (ref C.S.Sutrastanam) is selected forinternal use and manjista madhu alepam (ref B.Pr.Madyama Kanda) is selected forexternal use.

3. Method of preparation of the drug: Manjista roots are purchased by the reliableperson from the market, then cleaned, dried, and powdered coarsely for kwatha churnam,and fine powder is obtained to use for alepam. Madhu from reliable manufacturingcompany is taken.

4. Method of administration of drugs: Thirty patients are selected for clinical study,and treated with manjista kwatham and manjista madhu alepam daily for a period of 60days. Manjista madhu alepam is applied on the hyperpigmented patches on the face, 2-3times a day, kept for 5 to 10 minutes. Manjista kwatham is taken in the dose of 30mltwice a day.

5. Criteria for diagnosing the disease: The clinical features mentioned in the text are asfollows:

1. Tanu (thin/less in quantity)

2. Neeruja (painlessness)

3. Shyava (dark brown or dark dusky)

4. Mandala (circular patches)

These are the symptoms on the face, which are considered for the diagnosis of thecondition, but in practice, itching is an added symptom observed in some patients.

6. Critera for the assessment of results: The changes in the signs and symptoms suchas, color variation of hyperpigmented patch, size reduction of the patch, andimprovement of the associated symptoms such as itching are the chief parameters forassessing the results.

a) Color: The color of the hyperpigmented patch, before and after the treatment isrecorded based on the fairness meter.

79

fig15. Fairness meterScoring / grading:

1. Mild discoloration : 1-8 shades2. Moderate discoloration : 9-16 shades3. Severe discoloration : 17-24 shades

b) Size: The size of the discolored patchs is measured before and after the treatment byusing handi-lens, length and breadth of the patch is recorded in cms. Any reduction in thesize is considered as a positive sign.

fig16.Handi-lens

c) Number of patches: The numbers of hyperpigmented patches on the face werecounted before the treatment. Any reduction in the number was considered as animprovement.d) Associated symptoms: Before treatment any associated symptoms such as itching,oozing, scaling, etc., are noted. Relief from these symptoms is considered asimprovement.e) Assessment of the treatment: Effect of the therapy on the selected abnormality isassessed on the basis of three categories responded, partially responded, not responded.

1. Good result: The color of the hyperpigmentd patch fading to 1-3 shades on thefairness meter is considered as good result.

2. Moderate result: The color of the hyperpigmented patch fading to 4-6 shades onthe fairness meter is considered as moderate result.

3. Mild result: The color of the hyperpigmented patch fading above the 6 th shade onthe fairness meter is considered as mild result.

f) Follow up: Variations of color, size, and relief from associated symptoms are recordedevery week till the completion of treatment, later once in a month upto three months.

Type of study: The type of study opted here is single blind .

80

Observations and results

81

SECTION IV : OBSERVATIONS AND RESULTS

OBSERVATIONS

The clinical management of vyangam with manjista kwatham along with manjistamadhu alepam was conducted at GAH, Hyderabad. 30 cases were selected at random,irrespective of gender, age, occupation, religion, diet, social-status, prakruthi, level ofdiscoloration, and cronicity.

The patients who have left the treatment and who did not turned up for the followup have been excluded from the study. The data of the regular patients who continued thetreatment is being presented here.

Table 11. Age-wise distribution:S.No Age No of patients Percentage

1 15-24 4 13%

2 25-34 8 27%

3 35-44 9 30%

4 45-54 8 27%

5 55-64 1 3%

There is a peak evidence of discoloration in the age group 35-44 suggesting eitherthe use of oral contraceptives, or the pregnancy factor, stress and strain in females andstress at the working place and over exposure to the pollution and sun might be the resonfor the disease occurring in males. And the pitta dhosha is predominant in the middleaged persons.

Table 12. Gender-wise distribution:S.No Gender No.of Patients Percentage

1 male 7 23%2 female 23 77%

Females outnumbered the males in the case of discoloration, suggesting excess mentaland physical stress and strain in daily life and role of hormonal imbalance.

Table 13. Marital status-wise distribution:S.No Marital status No of patience Percentage

1 Married 26 87%2 Unmarried 4 13%

From observing the cases it is clear that married persons has the highest level ofdiscoloration, this may be due to responsibilities, stress and strain.

Table14. Religion-wise distribution:S.No Religion No.of patients Percentage

1 Hindhu 21 70%2 Muslim 5 17%3 Christian 4 13%

Out of 30 cases visited the GAH 70% patients are Hindhus, 17% are Muslims and13% are Christians.

Table 15. Occupation-wise distribution:

82

S.No Occupation No of patience Percentage1 Students 3 10%2 Working 10 33%3 House wifes 17 57%

More number of house wifes are affected with this disease, because of mental andphysical stress and strain due to house hold activities, next affected are working class dueto exposure to sunlight, pollution, and stress due to work load.

Table 16. Education-wise distribution:S.No Education No of patients percentage1 Uneducated 7 23%

2 1st-10th class 13 43%

3 Intermediate 2 7%

4 Graduation 5 17%

5 Post-graduation 3 10%

More number of patients are in basic education group (1st-10th), with loweconomic background prone to more stress and strain and low standerded of living. Nextis the uneducated group who does strenuous work and are exposed to pollution and sun.Other groups are affected with the disease due to mental stress at work place andimproper dietry habits.

Table 17. Social-status wise distribution:S.No Social status No of patients Percentage

1 Upper middle class 11 37%2 Lowere middle class 16 53%3 Lower class 3 10%

Lower middle class people are more prone to the disease due to there standered ofliving with more mental stress and strain with high responsibilities and low income.Lower class people are least affected, suggesting their sathmya with the surroundings andthus having vyadhikshamatva. Average occurance in upper middle class indicates theiraffordability to avoid some of the etiological factors.

Table 18. Locality-wise distribution:S.No Area No of patience Percentage

1 Urban 28 93%2 rural 2 7%

More number of patients are from urban are due to pollution and exposure to sunand demanding city life habits. Rural area people are less affected with the disease due tothere way of living with out tensions.

Table 19. Diet-wise distribution:S.No Diet No of patients Percentage

83

1 mixed 22 73%2 Vegetarians 8 27%

People with mixed diet are more in number suggesting that derangement of pittais caused in them due to non vegetarian food stuffs are cooked with high chilly and spicycontent.

Table 20. Prakruthi-wise distribution:S.No Prakruthi No of patients Percentage

1 V 8 27%2 P 17 56%3 K 5 17%

Pitta prakruthi persons are affected more in number as vyangam occurs in pittaprakruthi persons due to predominance of pitta dhosha.

Table 21. Cronicity-wise distribution:S.No Cronicity range No of patients Percentage

1 Upto one year 10 33%2 Upto two years 11 37%

3 Upto three years 4 13%

4 Upto four years 2 7%

5 Above four years 3 10%

More number of patients are in the chronicity range between 1-2 yrs shows thatpeople are more conserned about there looks.

Table 22. Level of discoloration:S.No Discoloration No of patients Percentage

1 Moderate 21 70%2 severe 9 30%

More number of patients are having moderate discoloration which shows that disease isless cronic.

Table 23. Hormone therapy-wise distribution:S.No Hormone therapy No of patients Percentage

1 Not used 21 70%2 Used 7 23%3 Using 2 7%

From the observation the harmone therapy is not an major etiological factor inproducing the the disease.

Table 24. Prognosis of lesion-wise distribution:S.No Prognosis of lesion No of patients Percentage1 Progressive 21 70%

2 Non-Progressive 9 30%

Progressive hyperpigmented lessions are seen in more number of patients.

Table 25.Type of Distribution-wise incidence:S.No Distribution No of patients Percentage

1 Diffuse 14 47%

84

2 Localised 16 53%Localized hyperpigmented patches are seen in more number of patients.

Table 26. Nidana-wise distribution:S.No Nidana No of patients percentage

1 Ayasa 14 47%

2 Krodha 7 23%

3 Shoka 6 20%

4 Ayasa & Krodha 1 3%

5 Ayasa & Shoka 2 7%More number of patients are affected with the disease due to nidana karana, ayasa

followed by krodha and shoka.

Table 27. Etiological factors-wise distribution:S.No Etiological factors No of patiences Percentage

1 Melasma 20 67%

2 Ultra-Voilet radiation 4 13%

3 Drug inducedhyperpigmentation 3 10%

4 Hormonal therapy 2 7%

5 Post inflammatoryhyperpigmentation

1 3%

More number of patiences are effected by the etiological factor melasma, followed byultra-voilet radiation, drug induced hyperpigmentation, hormonal therapy, postinflammatory hyperpigmentation.

Table.28 Number of patches-wise distributionS.No No of patches No of patients Percentage

1 1-2 14 47%2 3-4 12 40%3 5-6 3 10%4 7-8 0 0%5 9-10 1 3%

Only one patient has nine patches, majority of patients has 1-2 patches on thereface followed by the patients with 3-4 patches on the face.

Table.29 Location of patch-wise distributionS.No Area Location of patch No of patients Percentage

1 Area – II Around the rt.eye 2 2%

85

2 Area - III Around the lt.eye 2 2%3 Area - IV Rt.Temporal region 4 4%4 Area – V Lt.temporal region 4 4%5 Area – VI Rt.cheek 27 29%6 Area – VII Lt.cheek 27 29%7 Area – VIII Nose 11 12%8 Area – IX Around mouth 5 5%9 Area - X Fore head 12 13%

Peak level of hyperpigmentation in Area – VI and Area – VII shows that, cheeks are themore susceptible areas to develop vyangam, and we can see the similarity in both rightand left side of the face, followed by fore head, nose, temporal region and around eye.

RESULTSTable.30 Showing T and P values of the parameters

parameter MeanB.T | A.T

PercentageOf relief

S.D S.E T-value P-value Chi-square testB.T | A.T

Color variation 15.7 4 74.5% 2.76 0.50 23.22 0.001 12.46 20measurments 18.75 16.06 14.35% 1.99 0.36 7.4 0.001 1.73 2.4

Table.31 Effect of treatment

S.no Effect of therapy No of patients Percentage

1 Good result 19 63%2 Moderate result 8 27%3 Mild result 3 10%

86

MASTER CHART

S.No RegdNo

Age/Sex Occup Diet Prakriti Color Variation% of

BT AT relief

Measurement% of

BT AT relief

Result

1 6728 29y/F H-W Mix K 10 2 80% 7.75 5.25 32% Good.R2 6930 40y/F H-W Mix V 17 5 71% 26.2 21.5 18% Mode-R3 7170 48y/F H-W Veg P 13.5 3.5 74% 18.2 14.5 20% Good.R4 7718 35y/M Wor Mix P 14 6.5 70% 13.6 11.3 17% Mode-R5 8122 50y/F H-W Mix P 14 2 85% 39 35.86 8% Good.R6 11198 23y/M Stud Mix P 10 2 80% 2 1.6 20% Good.R7 11442 26y/F H.W Mix P 15 2 87% 6.66 5.23 21% Good.R8 29964 40y/F H.W Mix V 17 2 88% 15.6 12.2 22% Good.R9 30131 28y/F H.W Veg V 15 5 67% 39 33.6 14% Mode-R

10 31609 40y/F H.W Veg K 20 3 85% 23.36 19 19% Good.R11 32911 25y/M Stud Mix P 14 2 86% 5.25 4.75 10% Good.R12 33220 24y/F Wor Mix V 15 6 60% 5.13 4.4 14% Mode-R13 33231 35y/F H.W Mix P 14 5 64% 30.5 29 5% Mode-R14 33261 45y/F Wor Veg P 22 13 41% 10 8.7 13% Mild-R15 33412 35y/F H.W Mix V 12 1 92% 3.65 3 18% Good.R16 33533 32y/F H.W Mix P 16 3 81% 52.92 48.67 8% Good.R17 19521 40y/F Wor Mix V 15 5 67% 10.38 9 13% Mode-R18 21433 30y/F Wor Mix K 10 2 80% 7.75 5.75 26% Good.R19 21441 50y/F H.W Veg P 15 1 93% 27.5 21.86 21% Good.R20 21649 32y/F H.W Veg K 16 2 88% 16 12.5 22% Good.R21 21997 43y/F H.W Mix V 16 6 63% 25.25 22.5 11% Mode-R22 22685 45y/F Wor Mix P 23 12 48% 49.75 47 6% Mild-R23 23249 35y/F Wor Mix V 12 1 92% 3.25 2 38% Good.R24 23132 28y/M Wor Mix P 17 3 82% 29 22.33 23% Good.R25 23154 48y/F H.W Veg K 14 1 93% 2.28 1.8 21% Good.R26 23588 51y/M Wor Mix P 20 3 85% 43.5 36.5 16% Good.R27 23812 49y/F H.W Mix P 16 4 75% 17 14.36 16% Mode-R28 24036 23y/M Stud Veg P 13 2 85% 8.75 7.17 18% Good.R29 24880 60y//F H.W Mix P 21 3 86% 21.56 18.5 14% Good.R30 25111 18y/M Wor Mix P 24 13 46% 1.67 1.65 2% Mild-R

87

OBSERVATION CHARTS

0

2

4

6

8

10

No

of

pa

tien

ts

15-24 25-34 35-44 45-54 55-64

Age in years

Age-wise distribution

02468

101214

un-e 1-10t inter grad p.gra

education

Education-wise distribution

02468

1012

no

of

pat

ien

ts

upto1

upto2

upto3

upto4

abov4

cronicity range in years

cronicity-w ise distribution

02468

101214161820

No

of

pat

ien

ts

D-I-H Hor Mel P-I-H U-R

Etiological factors

Etiological factors-w ise distribution

0

5

10

15

No

of

pat

ien

ts

Ay Kr Sh A-k A-s

Nidana

Nidana-wise distributionGender-w ise distribution

male23%

female77%

male

female

Plate no.1

88

Religion-w ise distribution

Hindu70%

Muslim17%

Chirstian13%

Hindu

Muslim

Chirstian

Occupation-w ise distribution

Housew ifes57%

Working33%

Students10% House w ifes

Working

Students

Social status-wise distribution

Uppermiddleclass37%

Low ermiddleclass53%

Low erclass10%

Upper middleclass

Low er middleclass

Low er class

Marital-status distribution

Married87%

Unmarried

13%Married

Unmarried

Diet-w ise distribution

Mixed73%

Vegitarian27%

Mixed

Vegitarian

Locality-w ise distribution

Urban93%

Rural7%

Urban

Rural

Level of discoloration

Moderate70%

Severe30% Moderate

Severe

Prakruthi-w ise distribution

Vata27%

Pitta56%

Kapha17%

Vata

Pitta

Kapha

Plate no.2

89

Hormone therapy-w ise distribution

Not used70%

Used23%

Using7% Not used

Used

Using

Prognosis-w ise distribution

Nonprogressi

ve30%

Progressive

70%

Nonprogressive

Progressive

Distribution

Localised53%

Diffuse47%

Diffuse

Localised

Number-wise distribution

47%

40%

10% 0%3% 1-2

3-4

5-6

7-8

9-10

05

1015202530

no

of

pa

tien

ts

AreaII

AreaIV

AreaVI

AreaVIII

AreaX

location

location-wise distribution

Plate no.3

90

Effect of the drug

Plate no.4

91

Plate no.5

92

SECTION:V DISCUSSION

Vyangam is a disorder in which hyperpigmented patches are noticed on cetainareas of the face. By considering the symptomology, it is comparable to Melasma /Chloasma. Vyangam is one among the ‘44’ kshudra rogas, Charaka has mentioned it inbahirmargaja rogas and Susrutha has described in kshudra roga prakarana. In vyangamincreased pigmentation is seen, particularly affecting the skin of the face. The studyentitled “A clinical study on the effect of manjistadi lepam and manjista kwatham invyanga rogam”was conducted at Govt. Ayurvedic Hospital, Hyderabad. Total 30 caseswere selected at random and were treated with manjista madhu alepana and manjistakwatham 30ml twice daily for 60 days.

From observations female population (77%) is more effected than males (23%)with this disorder. This may be due to mental and physical stress and atrain in daily lifeand role of hormonal imbalance. More over, the disorder has cosmetic significance, sothe female gender is more concerned and approach for the treatment.

There is a peak incidence of this disease in the age group of 35-44 years. Out of30 cases, 30% were in this age group, they belong to pre-menopausal phase, there is ahigh alteration of hormonal balance in this age group. Equal number of cases wasmoderately affected in 25-34 and 45-54 (27%) age groups. Least effected patients are inthe age groups of 15-24 and 55-64.

More number of patients was under the married group (77%), this may be due tothe responsibilities, stress and strain.

It is observed that out of 30 cases, 21patients (70%) were Hindus, 5 patients(17%) were Muslims and 4 patients (13%) were Chirstians, this can be emulated to theirreligious customs and beliefs pratcised.

Occupational status reveals that 57% are house-wifes, 10% are working, and 3%are students. More number of house-wifes are effected with this disease, because ofmental and physical stress and strain due to house hold activities, next effected areworking class due to exposure to sunlight, pollution and stress due to work load.

Among 30 cases 43% are among basic education group (1st-10th class), 23% areuneducated, 17% are graduates, 10% are post graduates, and 7% are of intermediateeducation. More number of patients are in basic education group, with low economicbackground prone to more stress and strain and low standered of living. Next is theuneducated group who does strenuous work and are exposed to pollution and sun. othergroups are effected with the disease due to mental stress at work place and improperdietry habits.

According to the social status out of 30 cases 53% are of lower middle class, 37%are of upper middle class and 10% are of lower class. Lower middle class people aremore prone to the disease due to there standered of living with more mental stress andstrain with high responsibilities and low income. Lower class people are least effected,suggesting their sathmya with the surroundings and thus having vyadhikshamatva.Average occurance in upper middle class indicates their affordability to avoid some ofthe etiological factors.

93

It is observed that 93% patients were from the urban area, due to pollution andexposure to sun and demanding city life habits. Rural area patients were 7% due to theirway of living with out tensions.

Among 30 cases, 22 patients (73%) have mixed dietary habits, most of themprefer non-vegetarian food. Generally these food items are hot and spicy, so vitiation ofpitta dosha is suspected.

When prakruthi of the patients was taken into consideration 56% belonged to pittaprakruthi, 27% belonged to vata prakruthi, 17% belong to kapha prakruthi. Fromobservation it is clear that pitta prakruthi people are more susceptible to vyangam.

About range of chronicity of these pigmentary changes- out of 30 cases, 37%cases fall under cronicity range of upto 2 years, 33% upto1 year, 13% upto 3years, 10%above five years and 7% upto 4 years. From this it is clear that the disease is moderatelychronic, despite of rapid progress in modern medicine, there is lack of satisfactorytreatment for this disorder. Further, chronic use of various drugs may precipitate theproblem.

Level of discoloration among 30 cases, moderate level of discoloration is noted in70% of patients and severe level of discoloration is noted in 30% of patients. This showsthat 70% of patients has less cronic disease.

Taking in to consideration, prognosis of the hyperpigmented patch among 30cases, 70% patients has progressive lesion and 30% patients has non-progressive lesion.

Regarding the type of distribution of the hyperpigmented patch, among 30 cases,47% has diffuse type of lesion and 53% has localized type of lesion.Nidana wise distribution of 30 cases shows that, 47% patients has ayasa as nidana karana,23% has krodha as nidana karana, 20% has shoka as nidana karana, 7% has ayasa &shoka as nidana karana and 3% of patients has ayasa & krodha as nidana karana

Taking in to consideration of the etiological factor among 30 cases, 67% patientshas melsama as etiological factor, 13% has exposure to ultra-voilet radiation, 10% hasdrug induced hyperpigmentation, 7% has hormonal therapy as etiological factor and 3%has post inflammatory hyperpigmentation.

According to the number of patches in 30 cases, 47% of patients has 1-2 patches,40% of patients has 3-4 patches, 10% has 5-6 patches and 3% of patients has 9-10patches on the face.

It is observed that among the 30 cases around Rt. and Lt. eye 2+2 patches (4%),on Rt. and Lt. temporal region 4+4 patches (8%),on Rt. and Lt. cheeks 27+27 (58%), onnose 11 patches (12%), around mouth 5 patches 5%, and on fore head 12 patches (13%)are present. Cheeks are the more effected areas on the face, followed by fore head, nose,mouth, temporal region and eyes.

It has been observed that there was no spread of lesion in the patients who hastaken the treatment.

94

The results were divided into good result, moderate result and mild result groups.They were assessed on the basis of color variation and measurement of the lesion beforeand after treatment. Out of 30 cases 19 patients (63%) showed good result, 8 patients(27%) showed moderate results and 3 patients (10%) showed mild results. This scoringhas been obtained by taking color fading level scoring on fairness meter. From any shadeif the color fades to 1-3 levels on the fairness meter, it is considered as good result. Fromany shade if the color fades to 4-6 levels on the fairness meter, it is considered asmoderate result. From any shade if the color fades to, above 7th shade on the fairnessmeter it is considered as mild result.

From the results obtained we can observe that there is marked variation in thecolor but only one or two centimeters of lesion is reduced.

Manjista kwatham is given 30ml twice daily along with manjista madhu alepamon the hyperpigmented patches for 60 days. Manjista mentioned as varnyam and pittashamanam by Charaka and Susruta respectively, having the properties such as madhura,tikta, kashaya rasa pacifies the pitta which is one of the etiological factors of vyangam.This pitta can be stated as bhrajaka pitta- asper the claim of Ayurveda, there exists in theavabhasini layer of the skin, a pitta known as bhrajaka which is responsible for providingthe skin with that pigment which imparts to it its normal color. This pigment can becalled as ‘melanin’ which is metabolically produced by specialised cells in the skin by theenzyme tyrosinase. The roots of manjista contains coloring matter such as purpurin,manjistin, xanthine etc., which may be effective in restoring the normal skin color andcomplexion of the face by acting as a skin bleaching agent and inhibiting melaninsynthesis in the melanocytes of the skin.

Madhu or makshika, with its tridosha prashamana property may effect vata andpitta which are vitiated in the disorder vyangam. Madhu is described as ‘varnyam’ hence,bestows color or complexion. The topical drug treatment (lepana karma) aims atproviding high concentrations of the drug at the site of application. Madhu with its“yogavahi” guna is taken as base or vehicle and it enhances the properties of manjista.Madhu may function as a reservoir for manjista, allow local release of suitable amountsof the active drug, assist in the absorption and provide a reasonably safe in infra-structurefor practical application. In addition to these, it has lubricating effects. The paste ofmanjista and madhu also protect the skin from external irritants and from sunlight.

Thus it can be concluded that the manjista kwatham and the manjista madhualepam had good effect on vyangam.

95

summary

96

SECTION: VI

SUMMARY

1. The present clinical study entitled ‘A clinical study on the effect of manjistadilepam and manjista kwatham in vyanga rogam’ was conducted at GAH,Hyderabad in 30 patients presenting with the features of vyangam.

2. The disorder vyangam has close resemblance with Melasma / Chloasma.

3. Vyangam has no systemic effects but it is of cosmetic significance and concernedwith the beauty of the face.

4. Vyangam occurs due to psycho-physiological changes caused due to krodha,shoka and ayasa. Other etiological factors like, ahitahara sevana, pittaprakopakara ahara sevana cause pitta prakopa along with vata, which manifests asvyanga roga on the face.

5. Females (77%) are more effected than males (23%). This is due to improper diethabits, stress and strain due to excess work and high responsibilities inmaintaining the family.

6. Localised hyperpigmentation is seen as a side effect of several of several systemicmedications and also due to the photosensitivity of the skin.

7. Results were assessed on the bases of signs and symptoms before and after thetreatment.

8. Drugs used in the clinical trial were varnyakara and has pittashamana properties.

9. Manjista, and madhu has coloring matter, hence they proved to be good skinbleaching agents.

10. Lepana karma was effective, because the drug entered the skin in adequateconcentration from the site of application.

11. Manjista has pitta shamana properties so it also pacifices rakta dosha as well.

12. Results are found to be encouraging, they are compiled and analyzed statistically.

97

conclusion

98

SECTION: VIICONCLUSION

1. Manjista madhu alepam and manjista kwatham is proved to be an effective drugin the disorder vyangam.

2. Irrespective of the cause of the hyperpigmentation i.e., hormones; drug inducedhyperpigmentation; photosensitivity; and combination of the above the treatmentproved to be effective.

3. it is advisable to conduct the clinical trial on more number of patients and on alltypes of discolored patches on the face.

4. It is also advisable to have more effective parameters or investigations like biopsy(scrapings of patches) / melanin assessment / hormonal assays.

5. It is also advisable to assess the role of manjista as coloring agent locally on theface as well as all over the body.

6. It is proved that the disorder vyangam is comparable to hyperpigmented patchescaused by either exposure to ultra-voilet radiations or drug reactions or allergy tocertain chemicals and cosmetics or hormonal imbalances or oral contraceptives.

7. From observation fading of patch takes place more than two months, so treatmentmay be continued for four to five months.

99

RESEARCH CASE SHEET FOR VYANGA

P.G.DEPARTMENT OF KAYA CHIKITSADR.B.R.K.R.AYURVEDIC GOVERNMENT COLLEGE/HOSPITAL

S.R.NAGAR, HYDERABAD-38

PARTICULARS OF PATIENTS:

Name : Occupation :

Age : Marital status :

Sex : Date :

Address : S.No :

Religion : OP/IP No :

Education : Ward/Bed No :

Social Status : Probable Diagnosis :

PRADANA VEDANA (CHIEF COMPLAINT):

ANUBANDA VEDANA (ASSOCIATED COMPLAINTS):

ADYATANA VEDANA VRITTANTA (HISTORY OF PRESENT ILLNESS):

POORVA VYADHI VRITTANTA (HISTORY OF PREVIOUS ILLNESS):

KULA VRITTANTA (FAMILY HISTORY):

100

VAIYAKTIKA VRITTANTA (PERSONAL HISTORY)Ahara(Food): Agni(Apetite):

Vihara(Activities): Mala Pravritti( Bowel):

Nidra(Sleep): Mootra Pravritti(Micturition):

Vyasana(Addictions):

ATURA PAREEKSHA (EXAMINATION OF THE PATIENT):A. SAMANYA PAREEKSHA(GENERAL EXAMINATION):

Prakriti : Nadi:

Height: Temp:

Weight: B.P:

B. VESHASHA PAREEKSHA( LOCAL EXAMINATION OF SKIN):a) LOCATION OF THE LESION:

101

b)TWAKGATA STANIKA PAREEKSHA:1. Prograssive/Nonprograsive :2. Localised/Diffuse :3. Colour :4. Size :5. Shape : Irregular/Flat Round/Oval/Rectangular

NIDANA (ETIOLOGICAL FACTORS):1. a)Krodha b)Ayasa c)Shoka2. Ultra-Violet radiation(Exposure to sunlight)3. Melasma / Chloasma4. Drug induced hyperpigmentation5. Hormonal therapy6. Allergy to chemicals7. Post-Inflammatory hyperpigmentation8. Allergy to certain cosmetics9. Systemic causes of hyperpigmentation

LEVEL OF VAIVARNYATA-SCORING:

1. MILD DISCOLORATION

2. MODERATE DISCOLOURATION

3. SEVERE DISCOLOURATION

SAMPRAPTI GHATAKAS:

Dosha : Udbhbava stana :

Dooshya : Sanchara stana :

Srotas : vyakta stana :

Prakara : Rogamarga :

Agni : Swabhava :

VYADHI VINISCHAYA (DIAGNOSIS):

CHIKITSA (TREATMENT):

Dravya (Drug): Matra (Dose): Kala(Duration):

Upayoga vidhi(Mode of Administration):

Dietary advice: Pathya—

102

Apathya---

PROGNOSIS:

Observation chart:Lakshana Before

Treatment9th

Day18th

Day27th

Day36th

Day45th

Day52nd

Day60th

Day Remarks

Vaivarnyata

MeasurementOf lesion

Other signs &symptoms

RESULTS:1. Good result2. Moderate result3. Mild result

Signature of the scholar Signature of the Supervisor

INFORMED CONSENT

I -----------------son/daughter/wife of -----------------am exercising my freewill to participate in the above study as a subject. I have been informed to my satisfactionby the attending physician the purpose of clinical evaluation and the nature of the drug-treatment. I am also aware of my right to opt out of the treatment schedule at any timeduring the course of the treatment.

Patient signature

My commitment increases my level of energy. My energy increases my level of action. Myaction increases my level of success. My success increases my level of commitment.

Research in any field is the most important section of development. Ayurveda is inservice is for ages to the needy mankind to relieve their ailments and recording the factsfor the future generations. At present the Ayurveda research scholar, developing theAyurveda and understanding under the limelight of contemporary scientific backgrounds.The plagiarism is more and more now a day in the scientific community. This ishappening as the researches of the various institutions are not available for the commonresearcher. We wish to control this plagiarism by contributing the dissertations forscientific community. If you find any thesis is a copy of the previous publication, we takethis issue to the university authorities for proper action. The solution to prevent copy catsis … http://ayurvedaresearch.wordpress.com/

Dr. Shiva Rama Prasad Kethamakka

technoayurveda@gmail.com,