Stroke is not only a leading cause of death, but also significantly contributes to long-term disability in both industrialized and developing countries. Central post-stroke pain (CPSP) is a sequelae of stroke that is characterized by neuropathic pain in areas of the body that have lost part of their sensory innervation by the stroke and has been considered by patients more distressing than other stroke sequelae. The IASP defines CPSP as pain following an unequivocal stroke episode, where a psychogenic, nociceptive, or peripheral neurogenic cause is considered highly unlikely. Although CPSP was originally termed "thalamic syndrome," it is now recognized that CPSP may also result from extrathalamic lesions and it is now known that this type of pain can occur following lesions located anywhere from the medulla to the cerebral cortex.
Only one prospective epidemiologic study of CPSP has been reported which found the 1-year prevalence of CPSP among stroke survivors was 8%. Patients may report the onset of pain as late as 2-3 years after a stroke, and while some patients reported pain immediately after a stroke.
Attempts to understand the mechanism of central pain have been largely based on clinical features, imaging studies, and neurophysiologic studies. Current hypothesis suggests that the most likely pain-driving mechanisms result after a disconnection or disinhibition of soma-totopically organized somatosensory pathways resulting in hyperactivity in brainstem nuclei that mediate the polysynaptic portion of the pain pathway.
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