Attenuation of dipoles modelled from SEP due to a lacunar infarct or altered stimulus rate.

In normal subjects and patients with sensory, sensorimotor or motor deficit, due to a unilateral infarct affecting the thalamocortical radiation, SEPs to median nerve stimulation were analyzed by a spatiotemporal dipole model which describes an evoked potential by a limited number of stationary dipoles with time varying amplitudes. In the normal subjects the SEPs were explained by one dipole in the brainstem and two dipoles in the cortical hand area contralateral to stimulation, all with different time courses. Increasing the stimulus rate to 6.2 Hz yielded a reduction of the moment of both cortical dipoles but hardly affected brainstem dipole moment. In the five patients with sensory or sensorimotor deficit the strength of one or both cortical dipoles was reduced on the side of the lesion. In the patients with pure motor deficit cortical dipole activity was normal. The brainstem dipole was preserved in all patients.