The significance of somatosensory evoked potentials for localization of unilateral lesions within the cerebral hemispheres.

Thirty patients with unilateral lesions of the cerebral hemisphere and clinical signs of an affected somatosensory system (mainly disturbances of kinesthesia and stereoesthesia) were investigated. SEP recordings were abnormal in 27. The degree of sensory loss (especially kinesthesia) correlated well with the SEP abnormalities in 26. These SEP abnormalities could be segregated into 4 groups (types 1-4). A type 1 SEP with pathological evoked potentials from P15 on (but a normal P13/14 complex with ear- or extracephalic reference recordings) correlated with lesions of the thalamus, the internal capsule, and the centrum semiovale. A type 2 SEP characterized by loss or severe attenuation of N20 and the following components was found in patients with lesions of the postcentral gyrus. A variant (type 2a) showed isolated loss of N20, but preserved subsequent components and may be due to lesions restricted to area 3b. A third pattern of SEP abnormality is characterized by a preserved primary cortical response and loss of all the subsequent potentials. It is assumed to correlate with lesions of the parietal association cortex. In only 1 case was a type 4 SEP found, with pathological features from N3 (N55) on, caused by an ischemic stroke in area 39. Loss of all evoked responses after P13/14, including P15, suggests a lesion between thalamus and centrum semiovale. Lesions located close to the postcentral cortex lead to a loss of N20 and a variable cut off of the rising negativity following P15. Preservation of the primary cortical complex and distortion or loss of the later components point to a parietal lesion. Severe disturbances of kinesthesia and stereognosia in patients with a normal primary cortical complex and isolated abnormality of the following potentials suggests that the adjacent association cortex may be important for the perception of this complex somatosensory information. Thus the neuronal activity underlying the primary cortical response does not suffice for perception of motion and for stereoesthesia.