Scientific Basis for Ayurvedic Therapies -15

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

TABLE 11.1 (continued)

Formulations Used in Therapy of Sciatica, Monoplegia, and Paraplegia

No. Name (Manufacturer*) Doses, Vehicle, and Duration Ref.

28 Mahamash taila (a, b, c, d, e, f) Apply to the affected parts of the leg 16

29 Narayan taila (c, d, e, f) Apply to the affected parts of the leg 35

30 Prasarini taila (a, f) Apply to the affected parts of the leg 34

31 Prabhanjan vimardanam taila (d) Apply to the affected parts of the leg 20

32 Saindhavadya taila (a, b) Apply to the affected parts of the leg 13

33 Erand phal payas Oral, once/day (12 g/day) for 1 month (Note:

Payas made of 30 to 50 uncoated cooked castor

seeds in 350 ml cow’s milk)

13, 33

34 Vrihachhagaladya ghrit (d) Oral (12 g/day) 31

35 Gunja phal/gunja pistadi lepa Apply once/day 13, 35

36 Ekang vir ras (a, c, e, f) 125 mg three times/day for 60 days with milk 37

37 Khanjanikari ras (a) 250 mg three times/day for 90 days 33

38 Lashun ksheer pak made of Rason

kalk (15 g) in cow’s milk (200 ml)

200 ml/day 4

* (a) Baidyanath Pharmaceuticals;

(b) Indian Medicines Pharmaceutical Corporation Ltd. (IMPCL);

(c) Unjha Pharmaceuticals;

(d) Indian Medical Practitioners Co-operative Pharmacy & Stores (IMPCOPS);

(e) Zandu Pharmaceuticals;

(f) Dabur Pharmaceuticals.

11.12 Scientific Basis for the Use of Ayurvedic Drugs in Sciatica

11.12.1 Clinical Studies

1. In one study, 52 sciatica patients were given Trayodashang guggul (2 g) and vistinduk

vati one tab three times/day for 3 weeks. The patients were also treated with

Nirgundi taila massage and poultice for 3 weeks.17 In another study, 60 sciatica

patients were given Yograj guggul (1 g) three times/day plus purified Nuxvomica

seed powder (100 mg) in one capsule twice/day for 15 days. The patients were

also treated with Mahavisgarbha taila massage and steam fomentation of Rasnasaptak

decoction.18 The criteria for assessment of the results were based on pricking

and pulling pain, stiffness, tenderness over sciatic nerve, SLR, knee and ankle

jerks, plantar reflexes, muscle wasting, pressing power, walking speed, sensory

impairment, and posture, as per global score method. In both studies, results were

significant (p < 0.05) in more than 70% of the patients in terms of relief from the

symptoms.

2. Nirgundi oil and dehydrated butter prepared as per the Ayurvedic Formulary of

India were administered classically under purification therapy on 66 sciatica

patients along with purified guggul (1 g) and Vitex negundo decoction (60 ml) three

times/day for 45 days. The results showed complete cure in 76% of sciatica

patients.19

3. Sixty-eight sciatica patients were distributed equally in four groups at random:

(1) palliation, (2) placebo, (3) purification, and (4) purification with palliation. They

were given Prabhanjan vimardanam taila as per classical schedule. Although the

results of treatment were highly encouraging in both purification and purification

cum palliation groups, the results were better in the purification cum palliation

than the purification group.20

4. In a clinical trial conducted on 80 patients with paraplegia, a group of 40 patients

received panchakarma therapy with Moorchhit Sesamum indicum (til) oil as per

classical schedule, and the other group was treated with one tablet of Gorochanadi

gutika (250 mg) after Ashwagandha decoction (60 ml) three times/day. Both groups

were given massage with 50 ml of bala ashwagandha lakshadi taila for 60 days.

Results of both the groups were quite significant (p < 0.001). The group with

panchakarma therapy showed better results than did the ashwagandha group, even

after a 6-month follow-up. The progress in relief was judged on the basis of pain,

bladder control, rectum control, sensory changes, muscle powers, fasciculations,

deep tendon reflexes, plantar reflexes, wasting, and walking speed, as per global

score method.21

11.12.2 Animal Studies for Anti-Inflammatory Activity

11.12.2.1 Yograj Guggul and Rasnasaptak Decoction

The aqueous extract of yograj guggul and rasnasaptak decoction were administered intraperitoneally

(i.p.) in albino rats 30 min prior to carrageenin challenge, in combination and

alone at the doses of 1 g/kg. Test drugs produced significant inhibition of paw edema.

Phenylbutazone was taken for standard comparison in the study.22

11.12.2.2 Commiphora mukul (Hook. ex stocks) (Burseraceae)

Phenylbutazone (100 mg/kg), hydrocortisone acetate (20 mg/kg i.p.), ibuprofen (50 mg/

kg orally), acetylsalicylic acid (300 mg/kg orally), or steroidal compound from C. mukul

(100 mg/kg i.p.) were given 1 h before the carrageenin challenge to groups of 6 rats. No

treatment was given to a control group of six rats. The steroid isolated from C. mukul

showed a pronounced anti-inflammatory (p < 0.001) in paw edema as compared to phenylbutazone

(p < 0.001), hydrocortisone acetate (p < 0.005), ibuprofen (p < 0.01), and

acetylsalicylic acid (p < 0.001).23

11.12.2.3 Vitex negundo Linn. (Verbenaceae) and Withania somnifera Linn.

(Solanaceae)

The aqueous extract of Vitex negundo Linn. at the dose of 1 g/kg i.p. produced antiinflammatory

activity by 45, 60, and 44% at 2, 3, and 4 h of treatment in the carrageenininduced

rat’s paw edema model. W. somnifera also exhibited anti-inflammatory activity in

carrageenin induced rat’s paw edema. The inflammation was recorded as 61, 56, and 27%

at the first, second, and third hour of treatment, respectively. The study further revealed

that W. somnifera acts by blocking histamine h1 and h2 receptors in early phase followed

by inhibition of prostaglandin in delayed phase of acute inflammatory reaction. However,

anti-inflammatory activity of V. negundo is mediated through histamine and 5-HT, which

is further maintained during delayed phase.24

11.12.2.4 Ricinus communis Linn. (Euphorbiaceae)

Petroleum ether extract of R. communis exhibited significant anti-inflammatory activity

against formaldehyde and adjuvant-induced rat’s paw arthritis.25

11.12.2.5 Pluchea lanceolata (DC) Clarke (Compositae) and Allium sativum Linn.

(Liliaceae)

The water-soluble portion of the 90% alcoholic extract of P. lanceolata administered orally

in the dose of 2000 mg/kg/day produced significant anti-inflammatory activity in formalin

induced albino rat’s hind paw arthritis and granuloma pouch in comparison with

betamethasone. The pharmaceutical preparation allisatin, a concentrated formulation of

fresh Allium sativum, was suspended in water and administered in the dose of 2000 mg/

kg/day. The results showed slight anti-inflammatory activity against formalin-induced

arthritis but not against granuloma pouch.26

11.12.2.6 Sida cordifolia Linn. (Malvaceae)

An aqueous extract of S. cordifolia was administered orally at a dose of 400 mg/kg body

weight. The results showed a significant inhibition of carrageenin induced rat’s paw

edema but did not block the edema induced by arachiodonic acid.27

11.12.2.7 Tinospora cordifolia (willd.) Miers. (Ex Hook. f.) and Thoms.

(Menispermaceae)

Water extract of stem of T. cordifolia (neem giloe) at the dose of 500 mg/kg given orally

and i.p. inhibited acute inflammatory response evoked by carrageenin, significantly

(p < 0.05). Analgesic and antipyretic actions have also been observed in the study.28

11.13 Discussion

Although sciatica is not a terminal disease, lack of proper treatment may lead to difficulty

in walking and other movements. The most often prescribed drugs in the treatment of

sciatica are nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, muscle relaxants,

and opioids. Several randomized double-blind studies demonstrate that NSAIDs are

superior to placebo, but they provide short-term relief to patients.1 Allergic reactions have

also been reported by the use of drugs. The use of opioids, benzdiazepines, and tricyclics

may be helpful, but in many cases drug dependence, tolerance, and drowsiness have been

observed. Muscle relaxants provide short-term relief, but drowsiness often limits their daytime

use.7 Using chymopapain to dissolve herniated disc material proved most effective in

relieving sciatica, but severe neurologic complications restrict its use. Traction, acupuncture,

and exercise programs have failed to show benefits of these therapies in sciatica.

In spite of the fact that the spinal diseases are difficult to cure, the Ayurvedic concept of

treatment for sciatica is more effective and suitable as compared with the modern mode of

treatment. The therapies can be used for prolonged periods of time without any toxic side

effects. Oleation is considered the most effective remedy in the treatment of vata diseases.

Medicated oils either given orally or applied externally, or both, help in the restoration of

muscle strength. Massage increases circulation, prevents nerve degeneration, and promotes

tissue building. It renders the body soft and helps in the elimination of accumulated waste

materials that obstruct the channels causing vitiation of vata. Oleation followed by fomentation

liquefies dosas adhered in the channels and brings them to the gastrointestinal tract

(kostha) where they are expelled by the downflow action of purgation. Hemoglobin levels

increased in one study in both albino rats and humans after oleation.29 Heat applied by

steam, poultice, hot sandbags, or other means reduces the stiffness and muscle spasms by

decreasing efferent activity, improving tissue flexibility, and hastening tissue healing by

increasing the blood flow and nutrients to the injured area. Heat application has a vasodilatory

effect that can lead to edema; therefore, it should be used cautiously.30 The role of

bloodletting in the management of sciatica has also proved to be significant.

11.14 Monoplegia and Paraplegia

11.14.1 Definition

When vitiated vata situated in the low back region hurts the tendons of single lower limb

(sakthi), the person is considered affected by monoplegia. When both the limbs are paralyzed,

the disease is called paraplegia.

11.14.2 Etiology

Monoplegia and paraplegia both are vata-predominant diseases. Degeneration of essential

constituents, trauma (especially on the oscoccygis bone [kukunder marma]), and obstructions

caused in normal passage are the basic factors causing vitiating vata. According to

conventional medicine, monoplegia is usually caused by lower motor neuron diseases. A

small thoracic cord lesion, tumor, or demyelinative plaque may result in upper motor

neuron diseases. Paraplegia results from injuries at T1 vertebra and below. Compression

in the low thoracic and lumbar region causes a conus medularis or cauda equina syndrome.

Upper motor neuron and occasionally lower motor neuron diseases, epidural metastases,

and spinal cord ischemia may be associated with monoplegia. Acute onset of paraplegia

results from diseases of cerebral hemisphere (i.e., anterior cerebral artery ischemia, superior

sagital sinus thrombosis, and cortical venous thrombosis). Gradual onset over weeks

or months is almost always due to multiple sclerosis, intraparenchymal tumor, and chronic

spinal cord compression from degenerative diseases of the spine.

11.14.3 Clinical Course and Prognosis (Sadhyasadhyata)

The overall prognosis of monoplegia and paraplegia can be improved by the use of

panchakarma therapy. In acute onset these therapeutic modalities produced a remission

in the number of patients. Prognosis is poorer in epidural metastases, intraparenchymal

tumor, lumbar intraspinal metastases, and in patients ages 60 and over with acute onset.

Over time, the disease fails to respond to Ayurvedic therapy. Disease usually requires

prolonged course of treatment if the condition is more chronic and the prognosis is not

good.

11.14.4 Diagnosis

Monoplegia with acute onset presenting sensory loss or pain is usually caused by lower

motor neuron diseases. A localized lower motor neuron disease presents progressive

weakness with atrophy in one limb that develops over weeks or months. Distribution of

weakness is commonly localized to a single nerve root or peripheral nerve within one

limb. EMG and nerve conduction studies confirm the diagnosis in such cases. Monoparesis

of distal and nonantigravity muscle without sensory loss or pain indicate an upper motor

neuron lesion. Weakness of one limb with numbness is generally due to an involved

peripheral nerve, spinal nerve root, or lumbosacral plexus. If numbness is absent, segmental

anterior horn cell disease is likely. Paraplegia with numbness, frequent micturition,

and fecal incontinence results from acute spinal cord disease. Drowsiness, confusion, and

seizures present the disease with cerebral origin. Gradual onset over weeks or months

indicates spinal cord compression due to degenerative diseases of the spine, intraparenchymal

tumor, or multiple sclerosis. MRI of the spinal cord or brain may be helpful in

diagnosis.

11.14.5 Therapy (Chikitsa)

Treatment plan advised in Ayurveda for the management of monoplegia and paraplegia

involves oleation, fomentation, purgation, and enema along with guggul orally. Khanjanikari

ras, Ekangvir ras, and Gorochanadi gutika are the some Ayurvdic formulas that have

shown better results in studies.21

These formulas are listed in Table 11.1. Recent controlled

trials have documented the efficacy of Sirovasti and nasya (refer panchakarma) in monoplegia

and paraplegia with cerebral or motor neuron disease origin.

References

1. Haffernan, J.J., Textbook Of Primary Care Medicine, 3rd ed., Noble, J. et al., Eds., C.V. Mosby, St.

Louis, 2001, chap. 127.

2. Susruta, Susruta Samhita, Part 1, 8th ed., commentary by Shastri, K., Ambikadatta, Chowkhamba

Sanskrit Sansthan, Chowkhamba, Varanasi, India, Samavat 2038, 1981, nidan sthanam 234,

1993, chap. 1.

3. Vagbhatta, Ashtang Hridayam, 4th ed., commentary by Gupta, K., Atrideva, Chowkhamba

Sanskrit Series Office, Varanasi, India nidan sthanam 279, 1970, chap. 15.

4. Charaka, Charak Samhita, Part 2, 3rd ed., commentary by Shastri, K. and Chaturvedi, G.N.,

Chowkhamba Vidya Bhavan, Varanasi, India, chikitsa sthanam 787, 1970, chap. 28.

5. Madhavkar, Madhav Nidanam, Purvardham, 4th ed., madhukosh commentary by Shastri, S.S.,

Chowkhamba Sanskrit Series Office,Varanasi, India, 1970, 437, chap. 22.

6. Olmarkar, K., Radicular pain: recent pathophysiologic concepts and therapeutic implications,

Schmerz, Dec. 15(6), 425–429, 2001.

7. Engstrom, J.W., Harrison’s Principles of Internal Medicine, 15th ed.,Vol. 1, Braunwald, E. et al.,

Eds., McGraw-Hill, Medical Publishing Division, New Delhi, 1999, chap. 16.

8. Brisby, H. et al., Glyco sphingolipid antibodies in serum in patients with sciatica, Spine, 27,

380, 2002.

9. Hao, J.X. et al., Development of a mouse model of neuropathic pain following photochemically

induced ischemia in the sciatic nerve, Exp. Neurol., 163, 231, 2000.

10. Hao, J.X., Xu, X.J., and Wiesenfeld-Hallin, Z., Effects of intrathecal morphine, clonidine and

baclofen on allodynia after partial sciatic nerve injury in the rat, Acta Anaesthesiol. Scand., 43,

1027, 1999.

11. Tao, L. et al., Depletion of macrophages, reduces axonal degeneration and hyperalgesia following

nerve injury, Pain, 86, 25, 2000.

12. Sawaya, R.A., Idiopathic sciatic mononeuropathy, Clin. Neurol. Neurosurg., 101, 256, 1999.

13. Yogratnakar, Yogratnakarah purvardham, 3rd ed., commentary by Shastri, V.L., Chowkhamba

Sanskrit Sansthan, Varanasi, India, 1983, pp. 502 and 515.

14. Olmarkar, K. and Rydevik, B.J., Pathophysiology of spinal nerve roots as related to sciatica

and disc herniated, The Spine, 4th ed., Vol. 1, Herkowitz, H.N. et al., Eds., W.B. Saunders,

Philadelphia, 1999, p. 159.

15. Susruta, Susrut Samhita, Part I, 8th ed., sira vyadh vidhi shariram, commentary by Shastri, K.

Ambikadatta, Chowkhamba Sanskrit Sansthan Varanasi, samvat 2038, 1981, Sharir sthanam,

65, 1993, chap. 8.

16. Datta, C., Chakradatta, 3rd ed., commentary by Tripathi, S.J.P., Chowkhamba Sanskrit Series

Office, Varanasi, India, Vata vyadhi chikitsa, 1961.

17. Nanda, G.C. et al., Effect of trayodashang guggul and vistinduk vati along with abhyanga

and svedan in the management of gridhrasi, J. Res. Ayurveda Siddha, 19, 116, 1998.

18. Singh, S. et al., Effect of siravedha in gridhrasi, J. Res. Ayurveda Siddha, 22, 173, 1999.

19. Nair, P.R. et al., The effect of nirgundi panchang and guggul in shodhan cum shaman treatment,

JRIMYH, 13, 14, 1978.

20. Nair, P.R. et al., Clinical evaluation of prabhanjan vimardanam taila and shodhan therapy in

the treatment of gridhrasi, J. Res. Ayurveda Siddha, 12, 41, 1991.

21. Madhavi, K.P. et al., Shaman therapy versus panchkarma therapy in the management of

pangu, J. Res. Ayurveda Siddha, 19, 112, 2000.

22. Maurya, Singh, D.P. and Acharya, M.V., Anti inflammatory activity of yograj guggul and rasna

saptak decoction in albino rat’s hind paw induced arthritis, under publication.

23. Arora, R.B. et al., Isolation of a crystalline steroidal compound from Commiphora mukul and

its anti inflammatory activity, Ind. J. Exp. Biol., 9, 403, 1971.

24. Srivastava, D.N., Sahni, Y.P., and Gaidhani, S.N., Anti inflammatory activity of some indigenous

medicinal plants in albino rats, J. Med. Aromatic Plant Sci., 22–23, 73, 2000–2001.

25. Banarjee, S. et al., Further studies on the anti inflammatory activities of Ricinus communis in

albino rats, Indian J. Pharmacol., 23, 149, 1991.

26. Prasad, D.N., Bhattacharya, S.K., and Das, P.K., A study of anti inflammatory activity of some

indigenous drugs in albino rats, Indian J. Med. Res., 54, 582, 1966.

27. Franzotti, E.M. et al. Anti inflammatory, analgesic activity and acute toxicity of Sida cordifolia

L.(Malva-branca), J. Ethnopharmacol., 72, 273, 2000.

28. Pendse, V.K. et al., Anti inflammatory, immuno suppressive and some related pharmacological

actions of the water extract of neem giloe (tinospora cordifolia), a preliminary study, Indian J.

Pharmacol., 9, 221, 1977.

29. Nair, P.R. et al., Effect of snehapan on haemoglobin: a serendipitous find, J. Res. Ayurveda

Siddha, 10, 125, 1989.

30. Ekbot, S.V. and Kher, S.S., Recent Advances in Orthopedics, Kulkarni, G.S., Ed., Jaypee Brothers,

Medical Publishers (O.) Ltd., Daryaganj, New Delhi, 1997, chap. 19.

31. Anon., Ayurvedic Formulary of India, Part II, (1st English ed.), Ministry of Health and Family

Welfare, Government of India, 5(2), 94; 6(3), 102; 8(3), 138, 2000.

32. Mishra, Bhava, Bhav Prakash Uttarardham, commentary by Pt., Shri Brahmashankar Mishra,

Chowkhamba Sanskrit Sansthan, Varanasi, India, 1980, chap. 24.

33. Das, S.G., Bhaisajya Ratnavali, 3rd ed., commentary by Shastri, Ambikadatta, Chowkhamba

Sanskrit Series Office Varanasi, India, 1969, chap. 26.

34. Anon., Ayurvedic Formulary of India, Part 1, 1st ed., Ministry of Health and Family Planning,

Deptartment of Health, Government of India, 5(2), 60; 5(10), 59; 8(32), 111, 1976.

35. Sharngdharacharya, Sharngdhar Samhita, commentary by Sharma, Shri Prayagdatta,

Chowkhamba Amar Bharati Prakashan, Varanasi, India, 1981, pp. 152, 188, 235, 239, 430.

36. Prem Kishore and Padhi, M.M., The role of hingu triguna taila in the treatment of gridhrasi,

J. Res. Ayurveda Siddha, 6, 36, 1985.

37. Nair, P.R. et al., A comparative study on ekang vir rasa and mahamash taila with shodhan

therapy in khanj and pangu, J. Res. Ayurveda Siddha, 15, 98, 1994.

Allergic Reaction

Lakshmi Chandra Mishra

12.1 Introduction

Allergic reaction illnesses (ARIs), drug allergies, or hypersensitivities are considered

kaphadominated

diseases in Ayurveda. Examples are asthma and eczema. In Allopathic medicine,

the treatment of these diseases clusters around the use of steroids, antihistamines,

and bronchodilators (beta-adrenergic blockers). Ayurveda has approaches worth investigating

for the management of ARI. These approaches and available studies on herbs are

discussed.

12.2 Definition and Clinical Description

There is no specific definition of ARI given in Ayurveda, but these disorders fall under

the broad category of

kaphaja

diseases. In the conventional system of medicine, ARIs are

characterized as disorders of the immune system. Clinical signs and symptoms of ARI

differ according to organs involved. For example, an allergic reaction occurring in the

upper respiratory tract would show an inflammation of the tract and congestion (allergic

rhinitis). An allergic reaction occurring in the lungs would show the symptoms of an

asthma attack. If it occurs in the skin, it may show the signs and symptoms of urticaria,

eczema, psoriasis, or contact dermatitis. One common ARI is allergic rhinitis, which

accounts for at least 2.5% of all physician’s office visits and costs about $2.4 billion on

prescriptions and on counter medication and $1.1 billion physician billings per year in

the U.S.

1

Other common ARI are allergic asthma and skin reactions.

12.3 Etiology

No specific etiology of ARI is available in ancient Ayurvedic texts. ARI in Ayurveda is

described as intolerance developed in the body due to a variety of unwanted toxic materials

generated inside the body; this intolerance is either caused by poor digestion of food

materials, inadequate metabolism of nutrients (

ama-visa

), or exposure to environmental

pollutants (

dushi-visa

).

Ayurvedic etiology of ARI is related to a decrease in immunity or

vyadhiksamatva

(resistance

to diseases) that protects a person from diseases. Immunity is recognized as natural

as well as acquired. This resistance is associated with or due to a biological material present

in humans called

ojas

. Ayurveda has a number of herbs and herbal formulas called

rasayanas

or dietary supplements that are used to strengthen immunity and improve

resistance to diseases.

ARIs are currently known in conventional medicine to be mediated by the immune

system. Allergic reactions are described as adverse reactions caused by a second exposure

of a subject to the same chemical or a structurally similar chemical or an organic material

after the subject has been sensitized earlier with the chemical or the organic material. The

reactions are invoked not only by exposure to exogenous antigens but also by endogenous

(intrinsic to the body) antigens. This etiology of ARI is similar to that stated in classic

Ayurvedic texts. Intrinsic antigens are known to be responsible for many of the important

immune diseases, such as autoimmune diseases (immune reaction against the individual’s

own tissue, e.g., rheumatoid arthritis, systemic lupus erythematosus), immunologic deficiency

syndrome, and amyloidosis.

12.4 Pathogenesis

Ayurveda includes all body tissues as possible targets of ARI. The pathogenesis of ARI

involves invasion of various organs by vitiated

kapha

. The pathology in general consists

of inflammation and excessive secretion of fluid.

In conventional medicine, the pathology of allergic reactions in general is also similar

to that described in Ayurveda with respect to inflammation of the tissue and excessive

secretion of fluid. On the basis of the immunologic mechanisms mediating the disease,

ARI has been categorized in four types.

2

Type I reactions, also called anaphylactic shock,

are mediated by immunoglubulin E (IgE) antibodies. The examples are food allergies, skin

allergies (urticaria and atopic dermatitis), allergic rhinitis, asthma, and anaphylactic shock.

Type II or cytolytic reactions are mediated by immunoglobulins G and M (IgG and IgM),

and the common examples of this reaction are penicillin-induced hemolytic anemia, quinidine-

induced thrombocytopenic purpura, sulfonamide-induced granulocytopenia, and

procainamide-induced systemic lupus erythematosus. Type III reactions, or serum sickness,

are primarily mediated by IgG. It involves antigen-antibody complex formation that

deposits in the vascular epithelium, causing inflammation of the tissue, urticarial skin

eruptions, arthritis, lymphadenopathy and fever. Type IV reactions (delayed sensitivity)

are mediated by previously sensitized T-lymphocytes and macrophages. An example of

this type of reaction is contact dermatitis caused by poison ivy.

12.5 Diagnosis and Prognosis

Diagnosis is made based on the history of occurrence of the reaction and possible association

with certain chemicals or organic materials. Skin tests are used to determine specific

allergens. An ARI may be discomforting and may take weeks to subside. The acute phase

involving lungs may be fatal, although rare, if not treated appropriately.

12.6 Therapy

allergens, avoiding the exposure to them, using drugs to relieve acute symptoms, improving

digestion, and cleaning the intestine of toxic materials in the gut (

ama

). Emesis is

recommended to treat allergy and asthma because ARI are considered

kaphaja

disease.

Sitopaldi churn

is useful in upper respiratory tract ARI. The following single herbs are

commonly used in ARI and scientific studies in support of the use are listed below:

1.

Clerodendrum seratum

3

2.

Benincasa hispida

4

4.

Aquilaria agallocha

5

4.

Albezia lebbeck

6

5.

Curcuma longa

7

6.

Inula racemosa

7.

Galphimia glauca

8.

Picrorhiza kurora

9.

Adhatoda vasica

12.7 Scientific Basis

The herbs listed in the previous section have been investigated primarily in type I hypersensitivity

models. The studies summarized here appear to support the use of these herbs

in Ayurvedic therapies of ARI.

Dietary recommendations include diet that suppresses kapha as discussed in Chapter 3.

The treatment of allergic reactions in Ayurveda essentially consists of identifying the

Treatment specific to skin diseases and asthma are discussed in Chapters 17 and 18.

Prolonged administration of a saponin from the

Clerodendron serratum

plant has been

reported to exhibit antihistaminic and antiallergic activity.

3

Alcoholic extract of the root

of

Inula racemosa

, prepared by continuous heat extraction, was studied for its antiallergic

effect in experimental models of type I hypersensitivity (egg-albumin–induced passive

cutaneous anaphylaxis [PCA] and mast cell degranulation) in albino rats.

8

LD

50

of this

extract was found to be 2100 ± 60 mg/kg intraperitoneally (i.p.). The extract was given

orally for 7 days or once only. As a positive control for mast cell degranulation, compound

48/80 was given with the same dosage schedule. Remarkable protection against eggalbumin–

induced PCA was observed on the extract treated group after a single dose. The

extract also protected against compound 48/80-induced mast cell degranulation, and the

protection was similar to that of an antiallergic drug disodium cromoglycate. The 7-day

drug treatment schedule showed greater protection than did disodium cromoglycate

intraperitoneally. The results suggest that

I. racemosa

possesses potent antiallergic properties

in rats.

The methanol extract of wax gourd, the fruits of

Benincasa hispida

(

Kooshamanda

),

4

was

found to show inhibitory activity on the histamine release from rat exudate cells induced

by an antigen-antibody reaction. Four known triterpenes and two known sterols were

isolated as active components based on the bioassay. The other constituents isolated were

flavonoid C-glycoside, an acylated glucose, and a benzyl glycoside. Two triterpenes,

alnusenol and multiflorenol, were found to be potent inhibitors of histamine release.

An aqueous extract of stems of

Aquilaria agallocha

(

agaru

) has been investigated on the

immediate hypersensitivity reactions.

5

The aqueous extract of stems showed inhibitory

effects on passive cutaneous anaphylaxis, anaphylaxis induced by compound 48/80, and

histamine release from rat peritoneal mast cells (RPMC). The extract also prevented the

degranulation of RPMC in rats. The authors concluded that the aqueous extract inhibits

the immediate hypersensitivity reaction by the inhibition of histamine release from mast

cells.

Decoction of

Albizzia lebbeck

bark has been investigated to determine its possible antiallergic

activity.

6

The effect of the decoction on the degranulation rate of sensitized peritoneal

mast cells of albino rats challenged with antigen (horse serum) was studied. Triple

vaccine was used as an adjuvant and disodium cromoglycate (DCG) and prednisolone

were used for comparison. Drugs were given during the first or second week of sensitization

and the mast cells were studied at the end of the second or third week. Serum from

these rats was used to passively sensitize recipient rats whose peritoneal mast cells were

then studied. The effects of

A. lebbeck

and DCG on the degranulation rate of the sensitized

mast cells were also studied

in

vitro

. The results show that

A. lebbeck

had a significant

cromoglycate-like action on the mast cells. In addition, it appears that it inhibited the early

processes of sensitization, and synthesis of reaginic-type antibodies. If the decoction were

given during the first week of sensitization, it markedly inhibited the early sensitizing

processes; if given during the second week, it suppressed antibody production during the

period of drug administration. The active ingredients of the bark appear to be heat stable

and water soluble.

Several plants used in traditional medicine for the treatment of bronchial asthma have

been investigated.

9

Thiosulfinates and cepaenes have been identified as active antiallergic

compounds in onion extracts. They exert a wide spectrum of pharmacologic activities,

both

in vitro

and

in vivo

. Tetragalloyl quinic acid from

Galphimia glauca,

suppressed

allergen- and platelet-activating factor (PAF)-induced bronchial obstruction, PAF-induced

bronchial hyperreactivity (5 mg/kg orally)

in vivo

,

and thromboxane biosynthesis

in vitro

.

Adhatoda vasica

alkaloids (not identified) showed pronounced protection against allergeninduced

bronchial obstruction in guinea pigs (10 mg/ml aerosol). Androsin from

Picrorhiza kurroa

prevented allergen- and PAF-induced bronchial obstruction (10 mg/kg

orally; 0.5 mg inhalative). Histamine release

in vitro

was inhibited by other unidentified

chemical constituents of the plant extract.

Compound 73/602 (AA) is a structural analogue of vasicinone, an alkaloid, present in

the leaves and roots of

Adhatoda vasica

(acanthaceae); this compound was found to possess

potent anti-allergic activity in mice, rats, and guinea pigs.

10

The immunologic effect of

curcumin, a natural product of plants obtained from

Curcuma longa

(turmeric), has been

reported in animal models.

7,11

12.8 Summary

Ayurvedic management of ARI is basically similar to conventional medicine — identify

the allergen and avoid the exposure to it. In addition, the Ayurvedic approach includes

dietary

kapha

-suppressing foods, herbs, and herbal formulas for treatment.

References

1. deShazo, R.D., Allergic rhinitis, in

Cecil Text Book of Medicine,

Goldman, L. and Bennett, J.C.,

Eds., W.B. Saunders, Philadelphia, 2000, chap. 274.

2. Coombs, R.R.A. and Gell, P.G.H., Classification of allergic reactions responsible for clinical

hypersensitivity and disease, in

Clinical Aspects of Immunology,

Gell, P.G.H., Coombs, R.R.A.,

and Lachman, P.J., Eds., Blackwell Scientific, Oxford, 1975, p. 761.

3. Gupta, S.S., Development of antihistamine and anti-allergic activity after prolonged administration

of a plant saponin from

Clerodendron serratum

, J. Pharm. Pharmacol.,

10, 801, 1968.

4. Yoshizumi, S., Murakami, T., Kadoya, M., Matsuda, H., Yamahara, J., and Yoshikawa, M.,

Medicinal foodstuff. XI. Histamine release inhibitors from wax gourd, the fruit of Benincas

hispida,

Yakugaku Zasshi,

118, 188, 1998.

5. Kim, Y.C., Lee, E.H., Lee, Y.M., Kim, H.K., Song, B.K., Lee, E.J., and Kim, H.M., Effect of the

aqueous extract of Aquilaria agallocha stems on the immediate hypersensitivity reactions,

J.

Ethnopharmacol.,

58, 31, 1997.

6. Tripathi, R.M., Sen, P.C., and Das, P.K., Studies on the mechanism of action of Albizzia lebbeck,

an Indian indigenous drug used in the treatment of atopic allergy,

J. Ethnopharmacol.

, 1, 385,

1979

7. Madan, B., Gade, W.N., and Ghosh, B., Curcuma longa activates NF-kappaB and promotes

adhesion of neutrophils to human umbilical vein endothelial cells,

J. Ethnopharmacol

., 75, 25,

2001.

8. Srivastava, S., Gupta, P.P., Prasad, R., Dixit, K.S., Palit, G., Ali, B., Misra, G., and Saxena, R.C.,

Evaluation of antiallergic activity (type I hypersensitivity) in rats,

Indian J. Physiol. Pharmacol.,

43, 235, 1999.

9. Dorsch, W. and Wagner, H., New antiasthmatic drugs from traditional medicine?,

Int. Arch.

Allergy Appl. Immunol.

, 94, 262, 1991.

10. Paliwa, J.K., Dwivedi, A.K., Singh, S., and Gutpa, R.C., Pharmacokinetics and in-situ absorption

studies of a new anti-allergic compound 73/602 in rats,

Int. J. Pharm.,

197, 213, 2000.

11. Kang, B.Y., Song, Y.J., Kim, K.M., Choe, Y.K., Hwang, S.Y., and Kim, T.S., Curcumin inhibits

Th1 cytokine profile in CD4+ T cells by suppressing interleukin-12 production in macrophages,

Br. J. Pharmacol.,

Bronchial Asthma

Rakesh Lodha and Sushil K. Kabra

13.1 Introduction

Bronchial asthma is a common global health problem. Individuals of all ages are affected

by this chronic airway disorder that can be severe and occasionally fatal. The prevalence

of asthma is increasing worldwide, especially in children.

1

Over the past few decades, there have been significant scientific advances leading to

improved understanding of the disease and better management. However, the current

modes of therapy in conventional medicine do not cure the disorder but control the

symptomatology. There is a need to explore safe alternative therapies, such as Ayurvedic

medicine, so that they can be successfully integrated with conventional therapy to provide

maximal benefits to patients.

13.2 Definition

Ayurveda:

Svasa

(increased or difficult breathing, dyspnea) refers to the disorders of the

respiratory system. There are five kinds:

ksudraka

,

tamaka

,

chchinna

,

mahan

, and

urdhava

.

Of these,

tamaka svasa

refers to asthma.

2–5

Modern medicine:

Asthma is a chronic inflammatory disorder of the airway in which

many types of cells and cellular elements play a role. The chronic inflammation causes an

associated increase in airway hyperresponsiveness that leads to recurrent episodes of

wheezing, breathlessness, chest tightness, and coughing, especially at night or in the early

morning. These episodes are usually associated with widespread but variable airflow

obstruction that is often reversible either spontaneously or with treatment.

13.3 Epidemiology

Asthma is currently a worldwide problem, and there is evidence that the prevalence has

been increasing in many countries.

1

There are no clear-cut data from the Ayurvedic texts

about the extent of the problem in ancient times. It is likely that the prevalence of the

disorder was much less in ancient India because of factors discussed later in the chapter.

13.3.1 Children

The prevalence of asthma symptoms in children may be as high as 30%. The differences

among various populations may be consequences of responses to environment, industrialization,

or different allergen loads.

1

Asthma may develop less frequently in children who

are exposed to infections and parasitic infestations early in life.

6,7

13.3.2 Adults

The prevalence of asthma symptoms in adults varies from 1 to 25%.

8–11

Similar symptoms

from cardiac failure and chronic obstructive pulmonary disease make accurate estimates

of asthma in older individuals difficult.

8–11

Mortality data from developed countries show that the rates vary from 0.1 to 0.8 per

100,000 persons aged 5 to 34.

12–14

13.4 Etiology

According to Ayurveda, the general etiology of

svasa roga

is that all things, materials, and

conditions that could help increase

vata

dosa

and

kapha

dosa

are causally responsible for

tamaka svasa

. This develops from an increase in cough

(

kasa

), undigested materials (

ama

),

diarrhea, vomiting (

vamathu

), poison (

visa

), anemia (

pandu

), and fever (

jvara

); coming into

contact with air containing dust, irritant gases, pollens, or smoke; injuring vital spots;

using very cold water; and residing in cold and damp places.

2–5

Excessive use of dry food

and astringent food and irregular dietary habits may also trigger an attack. In addition,

constipation, excessive fasting, excessive use of cold water, excessive sexual indulgence

in adults, exposure to extremes of temperature, anxieties, grief, disturbance of peace of

mind, and debility may all precipitate an attack. Cough and coryza have also been implicated

as etiologic agents. The habitual use of lablab-bean, black gram,

til

preparations,

irritant spicy food, and

kapha

-producing diet may also be involved in development of the

disease.

2–5

In modern medicine the risk factors for asthma are classified under two categories: host

factors and environmental factors.

The host factors include genetic predisposition, atopy, airway hyperresponsiveness,

gender, and ethnicity. Asthma can be considered to be a heritable disorder.

15,16

More boys

than girls develop asthma during childhood; this difference disappears by age 10.

17,18

Subsequently, females are at greater risk for developing asthma. Environmental factors

influence the susceptibility to developing asthma in predisposed individuals, precipitate

asthma exacerbations, and cause persistence of asthma. The important allergens that play

a role in asthma are domestic mites, cockroach allergens, animal allergens, various fungi,

and pollen.

19–22

Exposure to tobacco smoke and various pollutants may play a role in

enhancing symptoms in susceptible individuals.

23

Infections do cause exacerbations in

asthmatic individuals.

24,25

Severe viral respiratory infections in early childhood have been

shown to be associated with the development of asthma.

26,27

According to the hygiene hypothesis, improvement in hygiene and reduced incidence

of common infections is associated with increased prevalence of asthma and atopy in

developed countries.

28

This may explain the apparent low prevalence of the disorder in

the ancient era.

Risk factors for acute exacerbations trigger inflammation or cause bronchoconstriction

or both. There is a wide interindividual variation in triggers. The triggers include exposure

to various allergens and irritant gases, exercise, cold air, various drugs, and emotional

changes. Various indoor and outdoor allergens and air pollutants are implicated in precipitating

acute exacerbations. There is strong evidence linking acute viral respiratory

infections to acute exacerbations of asthma; the most common are rhinovirus and respiratory

synticial virus infections. They are particularly important in children. Emotional

stress can trigger an asthma exacerbation. These possibly act via hyperventilation, which

can cause airway narrowing.

29

Other conditions, like sinusitis, can be associated with

exacerbations. In children, gastroesophageal reflux may lead to the exacerbation of asthma.

From the above it is clear that even in the ancient era there was an excellent understanding

of the etiologic factors of bronchial asthma.

13.5 Pathology and Pathogenesis

The pathogenesis of asthma, according to Ayurvedic texts, appears to arise from an

abnormal interaction between

vata

and

kapha

. The initial step is the increase in

vata

. Because

of the obstruction to normal movements of

vata

by

kapha

,

vata

begins to move in all

directions. This disturbs the channels of respiration (

prana

), food (

anna

), and water (

udaka

)

located in the chest, and produces dyspnea (

svasa

) originating from the stomach (

amasaya

).

This suggests that the root cause of asthma is related to the digestive tract.

2–4

Modern medicine recognizes the inflammatory processes in the airway as the key pathogenetic

mechanism for asthma. Current evidence shows that the T-lymphocytes have an

important role in regulating the inflammatory response through the release of various

cytokines. Eosinophils and mast cells are the key effector cells; these cells secrete a wide

range of chemicals that act on airways both directly and indirectly through neural mechanisms.

30,31

There is a continuum of disease: acute inflammation, persistent disease, and

remodeling.

32

Asthma is frequently found in association with atopy (the production of abnormally

high amounts of immunoglobin E [IgE] directed against common environmental allergens

such as animal proteins, dust mites, pollen and fungi).

33

Because of this, mast cells are

sensitized and upon activation lead to inflammation. Atopy is one of the strongest risk

factors for asthma. The process of sensitization may begin

in utero

. The potential for allergic

sensitization and risk for wheezing appears to be influenced by many factors in early life,

including viral respiratory infections, exposure to endotoxin, exposure to tobacco smoke,

use of antibiotics, house dust-mite sensitization, and diet.

34

Airway hyperresponsiveness and acute airflow limitation are the two major manifestations

of abnormalities of lung function in asthma. Hyperresponsiveness is the presence of

an exaggerated bronchoconstrictor response to a wide variety of endogenous and exogenous

stimuli. Airway inflammation is the key factor for hyperresponsiveness.

Airflow limitation is produced by acute bronchoconstriction, swelling of the airway

wall, chronic mucus plug formation, and airway remodeling. Allergen-induced bronchoconstriction

results from the IgE-dependent release of histamine, prostaglandins, and

leukotrienes by the mast cells.

35

The lungs of individuals who died of asthma were hyperinflated; the small and large

airways were filled with plugs formed by mucus, serum proteins, inflammatory cells, and

debris. The microscopy (both autopsy material and now on endobronchial biopsies)

reveals extensive infiltration by eosinophils and lymphocytes in the airway wall and

lumen.

36,37

In addition, there are features of microvascular leakage, epithelial disruption,

and airway remodeling.

13.6 Clinical Features

The prodromal symptoms described in the Ayurvedic texts include pain in the region of

the chest and flanks, movement of

prana

(

vata

) in an upward direction, distension of

abdomen, and cutting pain in temples. Other premonitory symptoms are pain in the

temporal region, restlessness, anorexia, abnormality in taste, flatulence, and pain.

There are several symptoms of

tamaka svasa

.

Vata

, undergoing an increase, travels in an

upward direction in the passages, causes increase of

kapha

, and seizes the head and neck.

There is pain in the chest and flanks, a noisy cough (from the throat and the chest), an

increase in breathing effort, and wheezing (

ghur ghur

sounds).

Om Tat Sat

                                                        

(Continued...) 

(My humble salutations to H H Maharshi ji,  Brahmasri Sreeman Lakshmi Chandra Mishra ji and other eminent medical scholars and doctors   for the collection)