👉🏻 Introduction :-
- Amavata is a painful condition which has been explained in Ayurvedic texts. The disease initially manifests as a gut disorder with symptoms of indigestion and anorexia.
- Later the disease is seen to encroach all the tissues, mainly bones, muscles and joints and multiple organs to cause a symptom complex.
- This condition is often compared to Rheumatoid arthritis of modern day. Some authors have also compared it to stages of gouty arthritis.
👉🏻 *Causes*
- Viruddha ahara – mutually incompatible foods.
-Viruddha chesta – unwholesome lifestyle practices
- Mandagni – having low metabolism and sluggish digestion for a longer period.
-Nischala – sedentary life activities.
-Snigdha bhojana, vyayama – consuming unctuous, oily and high caloric food and immediately getting indulged in exercises.
👉🏻 *Pathogenesis*
- The impairment of Agni will produce the condition of Ama. Mainly agnimandya initially affects digestion followed by metabolism.
- Hence in this state of Agni, the Rasadhatu is not formed up to the standard level & it is considered as Ama.
- This ‘Ama’ along with Vyana Vayu and also by virtue of its Vishakari guna it quickly moves to all kapha sthanas, through Hridaya and Dhamanes.
- This Vidhagada Ama, in kapha sthana is further contaminated by doshas and assumes different colours, because of the Atipichhilata.
- If Ama gets obstructed in to channels and promotes further vitiation of vata dosha, this morbid Ama circulates ubiquitously in the body propelled by vitiated vata with predilection for sleshma sthana.
- On the dhamanies with the other doshas it facilitates sroto abhisyanda and srotorodha causing sthanasmsraya manifested stabdhata (stiffness), sandhisula (joint-pain), sandhishotha (swelling), Anga-marda(bodyache), Apaka(indigestion), Jwara (fever), Anga gourava (heaviness of body), Alasya(laoghess) etc symptoms of Amavata.
👉🏻 Formation of Amavata(Rheumatoid arthritis):-
- The disease is formed due to vicious amalgamation of morbid Vata and ama.
• Ama – is the immature nutritional essence formed in the stomach due to sluggish digestion (agnimandhya and ajeerna).
- This essence goes into circulation in immature and unprocessed form. It is made available to all the tissues and organs of the body.
- Since it is immature, the tissues can take it but cannot metabolize it due to lack of identification.
- They are therefore stored in the cells and are neither digested nor flushed out.
- Owing to their sticky nature ama blocks and clogs all the channels of nutrition in the body.
- This depletes the nutrition and essential materials to the tissues and organs. As a result there is multiple tissue damage and wide array of diseases are manifested.
👉🏻 *Pathology of Rheumatoid arthritis:-*
- RA primarily starts as a state of persistent cellular activation leading to autoimmunity and immune complexes in joints and other organs where it manifests.
- The clinical manifestations of disease are primarily inflammation of the synovial membrane and joint damage, and the fibroblast-like synoviocytes play a key role in these pathogenic processes.
• Three phases of progression of RA are:-
1. Initiation phase (due to non-specific inflammation)
2. Amplification phase (due to T cell activation),
3. Chronic inflammatory phase
1) Non-specific inflammation:-
- Factors allowing an abnormal immune response, once initiated, become permanent and chronic.
- These factors are genetic disorders which change regulation of the adaptive immune response.
- Genetic factors interact with environmental risk factors for RA, with cigarette smoking as the most clearly defined risk factor.
- Other environmental and hormonal factors may explain higher risks for women, including onset after childbirth and hormonal medications.
- A possibility for increased susceptibility is that negative feedback mechanisms – which normally maintain tolerance – are overtaken by positive feedback mechanisms for certain antigens, such as IgG Fc bound by rheumatoid factor and citrullinated fibrinogen bound by antibodies to citrullinated peptides (ACPA - Anti–citrullinated protein antibody).
- A debate on the relative roles of B-cell produced immune complexes and T cell products in inflammation in RA has continued for 30 years, but neither cell is necessary at the site of inflammation, only autoantibodies to IgGFc, known as rheumatoid factors and ACPA, with ACPA having an 80% specificity for diagnosing RA.
- As with other autoimmune diseases, people with RA have abnormally glycosylated antibodies, which are believed to promote joint inflammation.
2) Amplification Phase:-
- Once the generalized abnormal immune response has become established – which may take several years before any symptoms occur – plasma cells derived from B lymphocytes produce rheumatoid factors and ACPA of the IgG and IgM classes in large quantities.
- These activate macrophages through Fc receptor and complement binding, which is part of the intense inflammation in RA.
- Binding of an autoreactive antibody to the Fc receptors is mediated through the antibody's N-glycans, which are altered to promote inflammation in people with RA.
- This contributes to local inflammation in a joint, specifically the synovium with edema, vasodilation and entry of activated T-cells, mainly CD4 in microscopically nodular aggregates and CD8 in microscopically diffuse infiltrates.
- Synovial macrophages and dendritic cells function as antigen-presenting cells by expressing MHC class II molecules, which establishes the immune reaction in the tissue.
3) Chronic inflammation:-
- The disease progresses by forming granulation tissue at the edges of the synovial lining, pannus with extensive angiogenesis and enzymes causing tissue damage.
- The fibroblast-like synoviocytes have a prominent role in these pathogenic processes.
- The synovium thickens, cartilage and underlying bone disintegrate, and the joint deteriorates, with raised calprotectin levels serving as a biomarker of these events.
- Cytokines and chemokines attract and accumulate immune cells, i.e. activated T- and B cells, monocytes and macrophages from activated fibroblast-like synoviocytes, in the joint space.
- By signalling through RANKL and RANK, they eventually trigger osteoclast production, which degrades bone tissue.
- The fibroblast-like synoviocytes that are present in the synovium during rheumatoid arthritis display altered phenotype compared to the cells present in normal tissues.
- The aggressive phenotype of fibroblast-like synoviocytes in rheumatoid arthritis and the effect these cells have on the microenvironment of the joint can be summarized into hallmarks that distinguish them from healthy fibroblast-like synoviocytes.
- These hallmark features of fibroblast-like synoviocytes in rheumatoid arthritis are divided into 7 cell-intrinsic hallmarks and 4 cell-extrinsic hallmarks.
- The cell-intrinsic hallmarks are: reduced apoptosis, impaired contact inhibition, increased migratory invasive potential, changed epigenetic landscape, temporal and spatial heterogeneity, genomic instability and mutations, and reprogrammed cellular metabolism.
- The cell-extrinsic hallmarks of FLS in RA are: promotes osteoclastogenesis and bone erosion, contributes to cartilage degradation, induces synovial angiogenesis, and recruits and stimulates immune cells.
👉🏻 *Symptoms*
- Initially the symptoms appear like those of indigestion.
- In this condition, the disease process has just begun and the morbidity has not reached the joints.
• These symptoms are:
- Angamarda – pain in body parts, general body ache.
-Aruchi – anorexia, tastelessness.
- Trishna – thirst
- Alasya – lethargy, weakness.
- Gaurava – heaviness of the body.
- Jwara – fever.
- Apaka – indigestion.
- Shunata – swelling of body parts.
- In the later stages when the disease spreads to the joints, tissues and organs the symptoms of multiple tissue and organ damage occur.
• They are:(Ref:- Ma.Ni.)
- Saruja shopha – painful swelling in the joints of hasta (hand), pada (foot), shira (head and neck), gulpha (ankle), trika (sacrum and coccygeal), janu (knee), uru (thigh, i.e. hip).
- Vrishika damshavat peeda – pain mimicking that of a scorpion sting.
- Agni dourbalya – sluggish digestion.
- Praseka – excessive salivation, nausea.
-Aruchi – tastelessness, anorexia.
- Gouravam – heaviness of the body.
- Utsaha hani – lack of enthusiasm.
- Vairasyam – feeling of perverted and abnormal tastes in the mouth.
-Daaha – burning sensation.
- Bahumutrata – excessive urination.
- Grahani dosha – contamination of intestines.
- Apakwa mala – stools comprise of indigested food.
- Kukshi kathinata – hardness of abdomen.
- Shulam – colic.
- Nidra viparyaya – sleep disturbances.
- Trishna – thirst.
-Chardi – vomiting
-Bhrama – giddiness
-Murcha – fainting
-Hrid graham – feeling of tightness of chest.
-Antra kujana – gurgling sounds in the abdomen.
-Anaha – flatulence.
👉🏻 *Treatment*
• Basic principles of treatment of Amavata
लङ्घनं स्वेदनं तिक्तं दीपनानि कटुनि च।
विरेचनं स्नेहपानम् बस्तयश्च आममारुते।।
सैन्धवाध्येनानुवास्य क्षारबस्तिः प्रशस्यते।।
(भै.र.)
- Langhana – fasting
- Swedana – fomentation, sweating treatment, steaming, sudation.
- Tikta, katu deepana – digestion promoting medicines having bitter and pungent tastes.
- Virechana – purgation.
-Vasti – enemas.
👉🏻 *External treatments*
- Swedana – steaming treatments.
- Pinda sweda – bolus fomentation especially churna pinda sweda (medicated powder bolus), Patra pinda sweda (leaf bolus) and Valuka sweda (sand bolus).(Ref:- Yogaratnakara)
- Dhara – stream pouring of medicated liquids, mainly dhanyamla dhara (fermented herbal liquids).(Ref.:- Dhara kalpa Sushruta)
- Upanaha – poultices.
👉🏻 *Classical formulations*
- Shuntyadi Kwatha – decoction of shunti (ginger) and gokshura (Tribulus terrestris).
- Shatyadi kwatha – decoction of shati (Hedychium spicatium), shunti (ginger), haritaki (Terminalia chebula), vacha (Acorus calamus), devadaru (Cedrus deodara), Ativisha (Aconitum heterophyllum), Guduchi (Tinospora cordifolia).
- Pippalyadi Kwatha – decoction of Pippali (long pepper), pippalimula (root of long pepper), chavya (Piper retrofractum), chitraka (Plumbago zeylanica) and Shunti (ginger).
- Dashamula Kashayam decoction of 10 roots mixed with eranda taila (castor oil)
- Shunti-guduchi kwatha – decoction of shunti (ginger) and guduchi (Tinospora cordifolia).
- Shunti-guda – Powder of shunti (ginger) taken with powder of guda (jaggery).
- Bhallatakadi churna – powder of bhallataka (Semecarpus anacardium), tila (sesame) and haritaki (Terminalia chebula) with guda (jaggery).
- Panchasama churna – powder of shunti (ginger), haritaki (Terminalia chebula), Pippali (long pepper), trivrit (Operculina turpethum) and Saindhava lavana (rock salt).
- Phalatrikadi churna – powder of amalaki (Emblica officinalis), Haritaki (Terminalia chebula), bibhitaki (Terminalia bellirica) and shunti (ginger).
- Hingwadi churna – powder of hingu (asafoetida), chavya (Piper retrofractum), vida lavana (bida salt), shunti (ginger), pippali (long pepper), jeeraka (cumin) and pushkara mula (Inula racemosa).
- Nagara churna – powder of nagara or ginger taken with kanji (fermented herbal drink).
- Panchakola churna – powder of Pippali (long pepper), pippalimula (root of long pepper), chavya (Piper retrofractum), chitraka (Plumbago zeylanica) and Shunti (ginger) taken with hot water.
- Eranda Beeja – the payasa (sweetened milk recipe) prepared from purified eranda beeja (seeds of castor plant).
- Erandabeejadi yoga – the pulp of seeds of eranda beeja (castor seeds) mixed with shunti churna (powder of dry ginger) and sharkara (sugar) mixed together should be taken early in the morning.
👉🏻 *External applications:*
• Shatapushpadi lepa:-(Ref:- Bhaishajya Ratnavali, Amavata chapter)
- paste of shatapushpa (dill seeds), vacha (Acorus calamus), shunti (ginger), gokshura (Tribulus terrestris), varuna (Crataeva nurvula), devadaru (Cedrus deodara), punarnava (Boerhavia diffusa), kachura (Curcuma zedoaria), mundi (Sphaeranthus indicus), prasarini (Paederia foetida) and madana phala (Randia dumetorum).
• Himsradhi lepa(Ref:- Bhaishajya Ratnavali)
👉🏻 *Diet*
• Pathya – wholesome foods in Amavata
-Barley – Hordeum vulgare
-Horse gram – Dolichos biflorus.
-Red Rice – Oryza sativa
-Shyamaka – Setaria italica / Echinochloa esculenta – Barnyard millet
-Kodrava – Paspalum scrobiculatum – Kodo millet / ditch millet / rice grass / cow grass / Indian paspalum.
- Drumstick – Moringa oliefera.
- Pointed gourd – Trichosanthes dioica.
- Bitter gourd – Momordica charantia.
- Ginger – Zingiber officinale.
- Punarnava – Boerhavia diffusa.
-Hot water and
Garlic processed in buttermilk.
-Meat of animals living in desert like regions.
👉🏻 *Apathya – unwholesome foods in Amavata*
- Curds
- Fish
- jaggery
- Milk
- Upodika – Basella alba – Malabar spinach.
- Flour prepared from black gram.
- Contaminated water
Wind blowing from the East.
- Wrong food combination.
- Unconducive foods
Forcibly controlling the natural body urges.
- Habit of keeping awake throughout the night.
- Irregular eating habits & foods which are heavy to digest.
- Foods which cause blockage in the tissues and channels of the body.
👉🏻 *Clinical features of Amavata in comparison with Rheumatoid arthritis*
1. Hasta sandhi shotha & shoola - Inflammation & severe pain in metacarpo-phalangeal joints & proximal inter
phalangeal joints are affected most severely in Rheumatoid Arthritis.
2. Paad sandhi shotha and shoola - The feet are often involved especially the metatarso phalangeal joints &
subtalar joints are affected.
3. Jaanu gulpha sandhi shotha - R.A. involves first smaller
joints of hands & feet and then symmetrically affects the
joints of wrist, elbow, ankle & knee.
4. Angagourav - Feeling of heaviness in the body.
5. Stabdhata - In R.A. stiffness of joints, particularly
observed in morning hours.
6. Jaadhya - Due to deformity limited movements in the
joints, weakness in grip or triggering of fingers occurs in R.A.
7. Angavaikalya - Deformity in joints.
8.Vikunchana-This mpared to volar subluxation,
ulnar deviation which occurs at metatarsophalangeal
joints .
observed in R.A.
9. Angamarda - Body ache in R.A.
