Central post-stroke pain--a study of the mechanisms through analyses of the sensory abnormalities.

The somatosensory abnormalities in 20 men and 7 women (mean age 67 years, range 53-81) with central post-stroke pain (CPSP) have been analysed in detail with traditional neurological tests and quantitative methods. The cerebrovascular lesions were located in the lower brain-stem in 8 patients, involved the thalamus in 9 and in 6 were suprathalamic. In 4 patients the location of the CVL could not be determined. All patients had abnormal temperature and pain sensibility, with a severe deficit in most cases. All except 2 had raised thresholds to thermal pain and all except 1 had abnormal sensibility to pin-prick. Eighty-eight percent exhibited hyperpathia with combined loss and suprathreshold exaggeration of somatic sensibility. In 85% somatic stimuli evoked dysaesthesia and about half of these patients also experienced spontaneous dysaesthesia. Paraesthesias were reported by 41%, radiation of stimuli by 50%, after-sensations by 45% and allodynia by 23%. Vibration sensibility was abnormal in 41%; raised thresholds to the perception of touch were found in 52%, to 2-PD in 35%, to dermolexia in 45% and to joint movements in 37%. The results indicate that all patients with CPSP have lesions that affect the major pathways for temperature and pain sensibility, i.e., the spino-thalamo-cortical pathways. Furthermore it appears that neither the level of the lesion along the neuraxis nor concomitant injury to the medial lemniscal pathways is crucial for the development of CPSP. The results confirm the notion that CPSP is a deafferentation syndrome, but they also provide evidence against the hypothesis that CPSP is a release phenomenon caused by a lesion that removes inhibitory influences of the lemniscal pathways on neurones that evoke pain.