All kinds of lesions in the central nervous system can induce central neuropathic pain (e.g., stroke, multiple sclerosis, spinal cord injury, syringobulbia, syringomyelia). The location is the most important feature of the lesion. In stroke, the onset of pain is often delayed. It is mostly constant, but it may be intermittent or paroxysmal. In stroke patients the pain is frequently a hemipain (75%), whereas in the 28% of all multiple sclerosis patients who develop central pain it dominates in the legs (87%) and 5% have trigeminal neuralgia caused by lesions in the brainstem. There is a large variation in the quality of central pain. Central pain is associated with abnormalities in sensitivity to temperature and pain. It is hypothesized that central pain is caused by lesions of the spinothalamic pathways, including their thalamocortical projections, but some other (unknown) factors appear to be crucial for the development of the pain because many patients with such lesions do not develop central pain. Central pain usually responds poorly to analgesics. The first-line treatments are tricyclic antidepressants and antiepileptic drugs.
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http://dx.doi.org/10.1016/S0072-9752(10)97058-9 | DOI Listing |
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