Abstract

The primary purpose of this study was to test the hypothesis that early and late somatic evoked response (SER) components are mediated, respectively, by activity of the short latency lemniscal pathway and by the extra-lemniscal, bilaterally projecting reticular and non-specific thalamo-cortical pathwats. The scalp-recorded SER was examined in seventeen patients, fourteen of whom had unilateral cerebral lesions that involved parietal cortex and resulted in somatic sensory deficit. In those patients with severe sensory loss, all SER components were markedly reduced or abolished over both hemispheres when the affected side was stimulated. Patients with mild to moderate sensory impairment exhibited either a normal response or a generalized attenuation of all components when the affected side was stimulated. Stimulation of the normal side evoked relatively normal responses over both hemispheres in all patients. These results do not favor a dual projection pathway hypothesis. Our results and others discussed are consistent with the conclusion that the entire contralateral SER is the result of activity in primary somatic cortex mediated solely by the medial lemniscal system. Long latency ipsilateral components are apparently the result of subsequent activation of the ipsilateral hemisphere via an inter-hemispheric pathway, possibly involving the corpus callosum. In agreement with earlier studies, the good correlation betweenm clinical sensory loss and SER alteration provides a basis for future clincial use of this technique.

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