Short- and long-latency median nerve somatosensory evoked potentials in stroke patients.

Short- and long-latency somatosensory evoked potentials (SEPs) were elicited by stimulation of the median nerve in 104 stroke patients, 59 men and 45 women. Their ages ranged from 25 to 90 years, with a mean age of 68 years. All of the patients presented with acute unilateral motosensory or sensory deficits. Based on CT findings, the patients were divided into four groups: thalamic hemorrhage (52 cases), thalamic infarct (21 cases), putaminal hemorrhage or infarct (13 cases) and infarction in the corona radiata or subcortical white matter (18 cases). The criteria for abnormal SEP responses were as follows: (1) absence of N18, (2) prolongation of central conduction time, (3) delay in peak latency of N32, (4) delay in peak latency of N60, and (5) decrease in response amplitude. In patients with thalamic stroke, the abnormality rate of SEPs was 93% (68 out of 73 cases). When the lesions were located primarily in the posterolateral thalamus, all SEP components, particularly the N18 (short-latency) component, were affected. Lesions in other thalamic areas caused changes in the N32 (mid-latency) and the N60 (long-latency) components. In putaminal, corona radiata and subcortical lesions, the abnormality rate of SEPs was 84% (26 out of 31 cases). The N18 component was absent in 3 patients with putaminal hemorrhage. Infarct in the corona radiata and subcortex tended to affect the mid- and long-latency components with relative preservation of the short-latency components.