Evoked response studies of the thalamic pain syndrome.

Abstract

Human and animal studies have suggested that the occurrence of thalamic pain (hyperpathia) is not simply a manifestation of a functional deficit in the major lemniscal pathway mediated through the ventral posterior (VP) thalamic nucleus. More effective relief of this pain has occurred following stereotaxic lesions of the centromedianum (CM) than after lesions restricted to VP. Median nerve stimulation has evoked abnormal contralateral somatosensory evoked responses (SER) in patients with lesions of VP. In this study the SERs evoked by contra-lateral stimulation in two patients with thalamic pain secondary to infarction were normal. These results support the hypothesis that thalamic pain can be caused by thalamic lesions sparing VP. The minor change noted in the ipsilateral SER when the abnormal hand was stimulated was consistent with a lesion involving CM or adjacent nonspecific thalamic nuclei.