Central pain is common in patients with stroke, multiple sclerosis, syringo
myelia, and spinal cord injury. It frequently develops after a delay of wee
ks or months, is associated with sensory change involving the spinothalamic
pathways, and has a poor prognosis for spontaneous remission. Hypotheses t
o explain the varied clinical manifestations can be divided in two categori
es: those stressing aberrant neural activity in the deafferented circuits a
nd those focusing on the postlesion imbalance between facilitatory and inhi
bitory neural pathways. All models inherently assume a degree of specializa
tion of cerebral structures in pain processing, which has not been proved c
onclusively.