Description, Causes and Risk Factors:
Algoneurodystrophy is a poorly understood phenomenon embracing several overlapping syndromes including Sudeck's atrophy and 'shoulder hand syndrome'." In the latter, the patient initially presents with a red, painful, edematous hand and forearm with a stiff painful shoulder. Gradually, pain diminishes and edema may subside. The skin becomes cold, pale and shiny and the muscles atrophy. Radiographs show increasing osteoporosis and, if untreated, the patient is eventually left with a cyanotic, functionally useless hand with severe osteoporosis.
Algoneurodystrophy involves a malfunction of the nervous system that causes pain (often diffuse, intense and unrelenting) and related sensory abnormalities. There may also be abnormal blood flow and sweating in the affected area, problems with movement of the muscles and changes in the structure of the tissues ('trophic' changes).
Injuries are the origin of 50% of algoneurodystrophy. There is no relationship with the severity of the injury, minimal initial trauma may go unnoticed. The time between the trauma and the algoneurodystrophy is variable: some days a few weeks. Circumstances such as surgery, fracture, sprain or dislocation of the shoulder, a painful reeducation active can cause or worsen dystrophy. The causes of non-traumatic shoulder algoneurodystrophy may include neurological hemiplegia, meningeal hemorrhage, head trauma, cerebral tumor, rarely reaching the peripheral nervous system: sciatica, neuralgia, shingles.
Algoneurodystrophy can occur at any age and there is an equal sex incidence. Between 15 and 50% of cases are idiopathic; the remainder are precipitated by events such as trauma, neurological damage (especially root or peripheral nerve lesions) and ischemic heart disease (ISH).
The initial acute stage, which may last up to a few months, causes pain, often described as burning, and excess sweating in the affected part of the limb, which also becomes warm and red. During this stage, someone with algoneurodystrophymay notice their hair and nails grow faster than usual. The joints of the affected limb may also become painful.
Stage two can last up to a year and is known as the dystrophic stage. The affected limb may be constantly swollen, causing wrinkles in the skin to disappear. Fingernails become brittle, and the pain and stiffness spread up the limb and along the same side of the body, or may spread to the opposite limb.
After a year, algoneurodystrophyenters stage three - the atrophic stage. The muscles may waste away and the skin usually becomes stretched, shiny and pale. The pain may lessen but is constant, and the part of the body affected is stiff. The skin may also be hypersensitive to touch. Once this stage has been reached, the chance of recovering movement diminishes.
The diagnosis can often be made on clinical grounds alone. However, a range of diagnostic tools is available. Plain radiographs may show evidence of osteopenia in the affected area, indicating bone loss of at least 30%. The pattern of bone loss depends on the stage of the syndrome, with patchy loss occurring early and diffuse loss seen in the later stages. Another diagnostic and validated method is thermography. An infrared camera semi-quantifies heat emission from the skin, and vasomotor instability may be monitored. Threephase bone scintigraphy typically demonstrates increased local blood flow and increased soft tissue uptake immediately following administration of the radioactive isotope. Delayed images, at 3-4h, indicate increased uptake within the bone, and if these strict criteria are met, the sensitivity and specificity of this technique are high. The changes seen in stage 3 disease are difficult to interpret and are often indistinguishable from a disuse syndrome. More recently, magnetic resonance imaging (MRI) has been used with success and has the advantage of excluding other pathologies, for example stress fracture.
Currently, the mainstay of treatment is mobilization and physiotherapy. Although the pathogenesis of algoneurodystrophy is unclear, decreased mobility of the affected limb per se may be important. Finsterbush and Friedman demonstrated synovial changes and vascular proliferation in the immobilized knees of rabbits similar to that demonstrated in humans with algoneurodystrophy.
If identified early, algoneurodystrophy is treatable.
Treatment is aimed at controlling pain, enabling the person to regain or improve the function of the affected limb, and providing emotional support.
In early stages, a course of steroid tablets have been shown to be effective, reducing inflammation and bringing pain relief. Nerve blocks are also effective - these are injections of local anesthetic into the affected nerve (if one can be identified). A number of other medicines may also be used to relieve symptoms, including painkillers and drugs such as amitriptyline, which is most commonly used to treat depression but can treat nerve pain too. Other drugs that may be prescribed include gabapentin.
Most patients benefit from being treated, if possible, in a Specialised Pain Clinic where they can be given a wide variety of treatments and psychological support.
Physiotherapy is important to help regain function and relieve symptoms. Occupational therapy can help someone learn how to overcome the difficulties they're facing with everyday activities.
If algoneurodystrophy has progressed significantly, surgery may be recommended.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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