Pain Management through Ayurveda

Pain is a more terrible lord of mankind than himself even death.

Albert schweitzh.

What is Pain

v Pain is an uncomfortable feeling that tells you something may be wrong. It can be steady, throbbing, stabbing, aching, pinching, or described in many other ways. Sometimes, it’s just a nuisance, like a mild headache. Other times it can be debilitating.

v Pain can bring about other physical symptoms, like nausea, dizziness, weakness or drowsiness. It can cause emotional effects like anger, depression, mood swings or irritability. Perhaps most significantly, it can change your lifestyle and impact your job, relationships and independence.

v Pain is classified as either acute or chronic. Acute pain is usually severe and short-lived, and is often a signal that your body has been injured. Chronic pain can range from mild to severe, is present for long periods of time, and is often the result of a disease that may require ongoing treatment.

v Currently, the best way to treat the pain is to manage the symptoms. If the source of your pain can’t be treated, or isn’t known, our pain medicine specialists can offer options for pain control.

v Examples of pain conditions which can be treated by Ayurveda

              1-Sciatica                     

              2-Sprains

              3-Accute fissure

              4-Perianal abscess

              5-Cellulitis

              6-Gout (vata Rakta)

              7-Amavata (R.A.)

              8-Planter fasciitis or calcanial spur

              9-fracture

              10-Osteoarthritis

              11-Vrana sopha

              12-Cevical spondilitis

              13 -Strain

              14-External piles

              15-Varicose vein

              16-Appendicitis

              17-Renal stone & uretric stone

              18-Soph18-frozen shoulder

             19-corn

             20-prolaps of intervertibral disc

             21-Back pain

            22- Dislocation of joint

            23-Migrane

            24-Glucoma

            25-Burn

           26-sinusitis

           27-fistula

           28-epididymitis

           29-bursitis

           30-DVT

           31-conjunctivitis

           32-Inflammed externointernal piles

Other pain full conditions.

v Low back pain

v Spinal stenosis

v Vertebral Compression Fractures

v Cervical and lumbar facet joint disease

v Sciatica/Radiculopathy

v Sacroiliac joint disease

v Neuropathic (Nerve) pain

v Head pain / Occipital neuralgia (Scalp/head pain)

v Intercostals neuralgia (Rib pain)

v Peripheral neuropathy (Diabetic nerve pain)

v Complex regional pain syndrome (Reflex Sympathetic Dystrophy - RSD)

v Neck pain

v Shoulder and knee arthritic pain (osteoarthritis)

v Myofascial (Muscular) pain

v Post surgical pain

v Cancer pain (pancreatic, colorectal, lung, breast, bone)

v Pain from peripheral vascular disease

v Anginal pain (chest pains)

v Post-herpetic neuralgia (shingles pain)

v Nerve entrapment syndromes

v Spastisticy related syndromes/ pain

v Spinal Cord Injury (central pain)

v Pelvic pain

v There are different types of pain. Acute pain is a type of pain that typically lasts less than 3 to 6 months, or pain that is directly related to soft tissue damage such as a sprained ankle or a paper cut.

v Acute pain is of short duration but it gradually resolves as the injured tissues heal. Acute pain is distinct from chronic pain and is relatively more sharp and severe

v Chronic pain is any pain that lasts for more than three months. The pain can become progressively worse and reoccur intermittently, outlasting the usual healing process.

v After injured tissue heals, pain is expected to stop once the underlying cause is treated, according to conventional ideas of pain. However, chronic pain can persist after injuries heal for no apparent biological cause.

v The most common sources of chronic pain include low back pain, headache and arthritic pain. Chronic pain can cause significant psychological and emotional trauma and often limits an individual’s ability to fully function.

Ayurveda’s Approach to Pain Relief-

Ayurveda suggests a different approach to pain relief. It begins by viewing pain as a mind-body experience that's highly subjective. Pain is approached through a phenomenon called "self-efficacy." The brain contains many pain-relieving chemicals, and these can be triggered mentally, which is why taking a placebo leads to pain relief in a significant proportion of people.

Subjects unknowingly self-regulate their pain. This isn’t just the mind fooling us. Brain scans show that a placebo, when effective, changes the brain in the same way as do active pills, and these changes can be found in the spinal cord, not just the brain. The implications are strong for chronic pain over an extended period, too. Studies in arthritis patients have shown that the placebo effect can last more than two years. In fact, self-efficacy is more powerful and more long-lasting than is generally realized, even among physicians. Ayurveda recognizes this power of the mind to relieve pain, and strengthens.

v Lifestyle’s Role in Pain Management

The lifestyle components of Ayurveda—such as positive relationships, nurturing emotions, massage balanced activity, rest, and diet—are some of the means to rebalance, strengthen, and purify the mind/body variables that lower our pain sensitivity. Love and human touch are other potent pain relievers. Studies have shown that a 20-second hug can relieve pain and stress by acting on nerve cells to release pain-relieving brain chemicals such as oxytocin and reduce the release of the stress hormone cortisol.  

1.      Local analgesics:

 Local analgesics are topically applied to a particular part of the body, and often include paste preparations (known as Belladonna);

2.    Central analgesics: 

Central analgesics (known as Dhatura) are more powerful than local analgesics, and are sometimes combined with strict dietetic restrictions;

3.      body-ache medications:

 Body-ache medicines are used to fight stress and fatigue (which we have generally known as Balam and Patala).There are more than 100 plants in ayurveda that are recognized to have pain-relieving properties, but some are really excellent.

v The application of this plant and herbs are equivalent as used in muscle pain and other pain, relaxants in ayurveda is alike as that of the modern symptomatic treatment like use of drugs that act as sedative, tranquilizers and anti spasmodic.

v There are specific terms in ayurveda Vednasthapak (which refer as painkiller) Shulaghan (high degree painkiller) adyavatahara (medications for anti convulsion and related complications), and the oil preparation used for massage are the categories of muscle relaxants and other pain used in ayurveda.

v Apart from this, all the remedies that are used for treatment the stroke, tetanus and different disturbance due to physiological and pathological factors are also having the effects of muscle relaxants and other pain.

1. Garlic for Earache Cure

2. Clove for Toothache Pain Relief

3. Honey for Mouth Ulcers

4. Ginger Root for Muscle Pain

5. Vinegar for Heartburn and Acid Reflux

6. Epsom Salt Bath for Leg Pain.

 

7. Cherries for Pain Relief.

8. Diabetic Pain Treatment with Turmeric

9. Fish Oil for Stomach Problems.

10. Buttermilk for Pre-Menopause.

v Ayurveda advises buttermilk for pre and post menopausal syndromes and menstrual pains. You can possess natural buttermilk two to three times; it’s truly efficient in curing vaginal infections and itching. Buttermilk is also highly effective in curing yeast infection.

v Try to have a plain glass of buttermilk together with cumin seeds; this may truly help in your condition. Researchers conducted have shown the favourable results of buttermilk in treating gynaecological problems. The calcium in buttermilk dispassionate the physical and psychological irritability led to during PMS.

v Pain management by Ayurveda

1-siravedha

2-leech therapy

3-shnehana

4-swedna

5-pradeha

6-lepa

7-Agnikarma

8-Acupressor

9-Aqupuncture

10-Awgaha sweda

12-Basti Chikitsha

13-Tarpan

14-Sarvang sweda

15-virechna

16-Deep yantra

17-Sirovirechna

v Ayurvedic Medicines for pain

1-Guggulu

2-Tail

3-Upanaha

4-Dashmool kwatha

5-Rashnadi kwatha

6-Yastimadhu tail

7-Yashtimadhu Ghrita

8-Colchicine

9-Nashya

10-Triphla Guggulu

11-Sirovasti

12-bednasthapak mahakashaya

13-sool prashmana mahakshaya

14-Ahiphena 

15-sura (alcohol)

16-yoga

17-swarn yogaraj guggulu

18-pidan chikitsha

19-Aswashan 

ANALGESIC AND ANTI-INFLAMMATORY EFFECT OF LEECH THERAPY (JALAUKAVCHARAN) IN THE PATIENTS OF OSTEOARTHRITIS (SANDHIGATA VATA)

Osteoarthritis (degenerative joint disease) is the most common joint disorder. It mostly affects cartilage. The top layer of cartilage breaks down and wears away. Osteoarthritis is of two types, primary (idiopathic) and secondary. In idiopathic osteoarthritis, the most common form of the disease, no predisposing factor is apparent. Secondary OA is pathologically indistinguishable from idiopathic OA but is attributable to an underlying cause. In Ayurveda the disease Sandhivata resembles with osteoarthritis which is described under Vatavyadhi. The NSAID’s are the main drugs of choice in modern medicine which have lots of side effects and therefore are not safe for long-term therapy. Raktamokshan, i.e., blood letting is one of the ancient and important parasurgical procedures described in Ayurveda for treatment of various diseases. Of them, Jalaukavacharana or leech therapy has gained greater attention globally, because of its medicinal values. The saliva of leech contains numerous biologically active substances, which have anti-inflammatory, analgesic as well as anesthetic properties. Encouraging results were seen with application of the leech therapy.

OTHER SUPPORTIVE AYURVEDIC TREATMENT FOR OSTEOARTHRITIS

1-MATRA  BASTI

2-PANCHTIKT GRITA KSHEER BASTI

3-JANU BASTI FOR JANU SANDHI

4-PANCHTIKT GHRITA GUGGULU

5-AABHA GUGGULU

6-MAHAYOGRAJ GUGGULU

7-RASHNADI KWATHA

8-RASHAYNA 

9-MAHANARYAN AND MAHAMASH TAIL

10-LEECH THERAPY 

11-DASANG LEPA

12-GUDUCHYADI KWTHA 

13- SHNEHANA AND SWEDNA 

14-LAKCHADI GUGGULU 

SCRUB TYPHUS FEVER- CAUSES, DIAGNOSIS AND TREATMENT

Introduction 

1.  Scrub typhus or bush typhus is a form of typhus caused by the intracellular parasite Orientia tsutsugamushi, a Gram-negative α-proteobacterium of family Rickettsiaceae first isolated and identified in 1930 in Japan.
2. Scrub typhus is transmitted by some species of trombiculid mites ("chiggers", particularly Leptotrombidium deliense), which are found in areas of heavy scrub vegetation. The bite of this mite leaves a characteristic black eschar that is useful to the doctor for making the diagnosis.
3. Scrub typhus is endemic to a part of the world known as the tsutsugamushi triangle (after O. tsutsugamushi) This extends from northern Japan and far-eastern Russia in the north, to the territories around the Solomon Sea into northern Australia in the south, and to Pakistan and Afghanistan in the west. It may also be endemic in parts of South America, too.
4. It affects females more than males in Korea, but not in Japan, and which may be because sex-differentiated cultural roles have women tending garden plots more often, thus being exposed to vegetation inhabited by chiggers. The incidence is increasing in the southern part of the Indian subcontinent and in northern areas around Darjeeling.

Symptoms and Signs

1. Incubation period of 6 to 21 days (mean 10 to 12 days).
2. fever, chills, headache, and generalized lymphadenopathy start suddenely.
3. Muscle pain, cough, and gastrointestinal symptoms.   
4.  Morbilliform rash, eschar, splenomegaly, and lymphadenopathies are typical signs.                      
5.  At onset of fever, an Escher often develops at the site of the chigger bite. 
6. The typical lesion of scrub typhus, common in whites but rare in Asians, begins as a red, indurated lesion about 1 cm in diameter; it eventually vesiculates, ruptures, and becomes covered with a black scab.
7. Regional lymph nodes enlarge
8. Fever rises during the 1st wk, often to 40 to 40.5° C. Headache is severe and common, as is conjunctival  injection. A macular rash develops on the trunk during the 5th to 8th day of fever, often extending to the arms and legs. 
9. It may disappear rapidly or become maculopapular and intensely collared. Cough is present     during the 1st wk of fever, and pneumonitis may develop during the 2nd wk.
10. In severe cases, pulse rate increases; BP drops; and delirium, stupor, and muscular twitching develop. Splenomegaly may be present, and interstitial myocarditis is more common than in other rickettsial diseases. In untreated patients, high fever may persist ≥ 2 wk, then falls gradually over several days. With therapy, defervescence usually begins within 36 h. Recovery is prompt and uneventful.
    

Diagnosis

The cheapest and most easily available serological test is the Weil-Felix test, but this is notoriously unreliable.

• Clinical features

• Biopsy of rash with fluorescent antibody staining to detect organisms

• Acute and convalescent serologic testing (serologic testing not useful acutely)

• PCR

Treatment

1. Doxycycline
2. Primary treatment is doxycycline 200 mg po once followed by 100 mg bid until the patient improves, has been afebrile for 48 h, and has received treatment for at least 7 days.
3. Chloramphenicol 500 mg po or IV qid for 7 days is 2nd-line treatment.
4. Clearing brush and spraying infested areas with residual insecticides eliminate or decrease mite populations. Insect repellents (eg, diethyltoluamide [DEET]) should be used when exposure is likely.

Vaccine

No licensed vaccines are available.

Bone healing, or fracture healing.

 Bone healing is a proliferative physiological process in which the body facilitates the repair of a bone fracture.

1-Generally bone fracture treatment consists of a doctor reducing (pushing) displaced bones back into place via relocation with or without anaesthetic, stabilizing their position to aid union, and then waiting for the bone's natural healing process to occur.

2-Adequate nutrient intake has been found to significantly affect the integrity of the fracture repair. Age, Bone type, drug therapy and pre existing bone pathology are factors which affect healing. The role of bone healing is to produce new bone without a scar as seen in other tissues which would be a structural weakness or deformity.

3-The process of the entire regeneration of the bone can depend on the angle of dislocation or fracture. While the bone formation usually spans the entire duration of the healing process, in some instances, bone marrow within the fracture has healed two or fewer weeks before the final remodeling phase.

4-While immobilization and surgery may facilitate healing, a fracture ultimately heals through physiological processes. The healing process is mainly determined by the periosteum (the connective tissue membrane covering the bone). The periosteum is one source of precursor cells which develop into chondroblasts and osteoblasts that are essential to the healing of bone. The bone marrow (when present), endosteum, small blood vessels, and fibroblasts are other sources of precursor cells.

There are three major phases of fracture healing

1. Reactive phase

       Fracture and inflammatory phase

  Granulation tissue formation

2. Reparative phase

       Cartilage callus formation

      Lamellar bone deposition

3. Remodeling phase

    . Remodeling to original bone contour

Reactive

After fracture, the first change seen by light and electron microscopy is the presence of blood cells within the tissues adjacent to the injury site. Soon after fracture, the blood vessels constrict, stopping any further bleeding. Within a few hours after fracture, the extra vascular blood cells form a blood clot, known as a hematoma. These cells release cytokines and increase blood capillary permeability. All of the cells within the blood clot degenerate and die. Some of the cells outside of the blood clot, but adjacent to the injury site, also degenerate and die. Within this same area, the fibroblasts survive and replicate. They form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue. This tissue reduces strain across the fracture site. Osteoclasts move in to reabsorb dead bone ends and other necrotic tissue are removed.

Reparative

Days after fracture, the cells of the periosteum replicate and transform. The periosteal cells proximal (closest) to the fracture gap develop into chondroblasts which form hyaline cartilage. The periosteal cells distal to (further from) the fracture gap develop into osteoblasts which form woven bone. The fibroblasts within the granulation tissue develop into chondroblasts which also form hyaline cartilage. These two new tissues grow in size until they unite with their counterparts from other parts of the fracture. These processes culminate in a new mass of heterogeneous tissue which is known as the fracture callus. Eventually, the fracture gap is bridged by the hyaline cartilage and woven bone, restoring some of its original strength.

The next phase is the replacement of the hyaline cartilage and woven bone with lamellar bone. The replacement process is known as endochondral ossification with respect to the hyaline cartilage and bony substitution with respect to the woven bone. Substitution of the woven bone with lamellar bone precedes the substitution of the hyaline cartilage with lamellar bone. The lamellar bone begins forming soon after the collagen matrix of either tissue becomes mineralized. At this point, the mineralized matrix is penetrated by channels, each containing a microvessel and numerous osteoblasts. The osteoblasts form new lamellar bone upon the recently exposed surface of the mineralized matrix. This new lamellar bone is in the form of trabecular bone.^[12] Eventually, all of the woven bone and cartilage of the original fracture callus is replaced by trabecular bone, restoring most of the bone's original strength.

Remodelling

The remodeling process substitutes the trabecular bone with compact bone. The trabecular bone is first resorbed by osteoclasts, creating a shallow resorption pit known as a "Howship's lacuna". Then osteoblasts deposit compact bone within the resorption pit. Eventually, the fracture callus is remodelled into a new shape which closely duplicates the bone's original shape and strength. The remodeling phase takes 3 to 5 years depending on factors such as age or general condition. This process can be enhanced by certain synthetic injectable biomaterials, such as cerament, which are osteoconductive and actively promote bone healing.

Obstructions to Bone Healing

1.   Poor blood supply which leads to the death of the osteocytes. Bone cell death is also dependent on degree of fracture and disruption to the Haversian system.

2.   Condition of the soft tissues. Soft tissue in between bone ends restrict healing.

3.   Nutrition and drug therapy. Poor general health reduces healing rate. Drugs that impair the inflammatory response impede healing also.

4.   Infection. Diverts the inflammatory response away from healing towards fighting of the infection.

5.   Age. Young bone unites more rapidly than adult bone.

6.   Pre existing Bone malignancy.

7. Fracture healing is determined by mechanical factors and obstructions to healing include the bone not aligned and too much or little movement. Excess mobility can disrupt the bridging callus interfering with union. Slight biomechanical motion is also seen to improve callus formation

The Stages of Wound Healing

1-    Haemostasis,

2-    Inflammation,

3-    Proliferation and

4-    Maturation.

Although the stages of wound healing are linear, wounds can progress backward or forward depending on internal and external patient conditions. The four stages of wound healing are:

Hemostasis Phase

Haemostasis is the process of the wound being closed by clotting.

Haemostasis starts when blood leaks out of the body. The first step of haemostasis is when blood vessels constrict to restrict the blood flow. Next, platelets stick together in order to seal the break in the wall of the blood vessel. Finally, coagulation occurs and reinforces the platelet plug with threads of fibrin which are like a molecular binding agent. The haemostasis stage of wound healing happens very quickly. The platelets adhere to the sub-endothelium surface within seconds of the rupture of a blood vessel's epithelial wall. After that, the first fibrin strands begin to adhere in about sixty seconds. As the fibrin mesh begins, the blood is transformed from liquid to gel through pro-coagulants and the release of prothrombin. The formation of a thrombus or clot keeps the platelets and blood cells trapped in the wound area. The thrombus is generally important in the stages of wound healing but becomes a problem if it detaches from the vessel wall and goes through the circulatory system, possibly causing a stroke, pulmonary embolism or heart attack.

Inflammatory Phase

Inflammation is the second stage of wound healing and begins right after the injury when the injured blood vessels leak transudate (made of water, salt, and protein) causing localized swelling. Inflammation both controls bleeding and prevents infection. The fluid engorgement allows healing and repair cells to move to the site of the wound. During the inflammatory phase, damaged cells, pathogens, and bacteria are removed from the wound area. These white blood cells, growth factors, nutrients and enzymes create the swelling, heat, pain and redness commonly seen during this stage of wound healing. Inflammation is a natural part of the wound healing process and only problematic if prolonged or excessive.

Proliferative Phase

The proliferative phase of wound healing is when the wound is rebuilt with new tissue made up of collagen and extracellular matrix. In the proliferative phase, the wound contracts as new tissues are built. In addition, a new network of blood vessels must be constructed so that the granulation tissue can be healthy and receive sufficient oxygen and nutrients. Myofibroblasts cause the wound to contract by gripping the wound edges and pulling them together using a mechanism similar to that of smooth muscle cells. In healthy stages of wound healing, granulation tissue is pink or red and uneven in texture. Moreover, healthy granulation tissue does not bleed easily. Dark granulation tissue can be a sign of infection, ischemia, or poor perfusion. In the final phase of the proliferative stage of wound healing, epithelial cells resurface the injury. It is important to remember that epithelialisation happens faster when wounds are kept moist and hydrated. Generally, when occlusive or semi occlusive dressings are applied within 48 hours after injury, they will maintain correct tissue humidity to optimize epithelialisation

Maturation Phase

Also called the remodelling stage of wound healing, the maturation phase is when collagen is remodelled from type III to type I and the wound fully closes. The cells that had been used to repair the wound but which are no longer needed are removed by apoptosis, or programmed cell death. When collagen is laid down during the proliferative phase, it is disorganized and the wound is thick. During the maturation phase, collagen is aligned along tension lines and water is reabsorbed so the collagen fibres can lie closer together and cross-link. Cross-linking of collagen reduces scar thickness and also makes the skin area of the wound stronger. Generally, remodeling begins about 21 days after an injury and can continue for a year or more. Even with cross-linking, healed wound areas continue to be weaker than uninjured skin, generally only having 80% of the tensile strength of unwounded skin.

The stages of wound healing are a complex and fragile process. Failure to progress in the stages of wound healing can lead to chronic wounds. Factors that lead up to chronic wounds are venous disease, infection, diabetes and metabolic deficiencies of the elderly. Careful wound care can speed up the stages of wound healing by keeping wounds moist, clean and protected from reinjury