Transverse myelitis pathophysiology: Difference between revisions
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Revision as of 14:45, 14 December 2012
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Transverse myelitis Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Axonal demyelination arises idiopathically following infections or vaccination, or due to multiple sclerosis. One major theory of the cause is that an immune-mediated inflammation is present as the result of exposure to a viral antigen. The lesions are inflammatory, and involve the spinal cord on both sides.
Pathophysiology
Researchers are uncertain of the exact mechanisms of transverse myelitis. The inflammation that causes such extensive damage to nerve fibers of the spinal cord may result from viral infections or abnormal immune reactions.
In post-infectious cases of transverse myelitis, immune system mechanisms, rather than active viral or bacterial infections, appear to play an important role in causing damage to spinal nerves. Although researchers have not yet identified the precise mechanisms of spinal cord injury in these cases, stimulation of the immune system in response to infection indicates that an autoimmune reaction may be responsible. In autoimmune diseases, the immune system, which normally protects the body from foreign organisms, mistakenly attacks the body’s own tissue, causing inflammation and, in some cases, damage to myelin within the spinal cord.
Because some affected individuals also have autoimmune diseases such as systemic lupus erythematosus, Sjogren’s syndrome, and sarcoidosis, some scientists suggest that transverse myelitis may also be an autoimmune disorder. In addition, some cancers may trigger an abnormal immune response that may lead to transverse myelitis.