Dissociation of parietal and frontal somatosensory evoked potentials in central nervous system diseases.

The mean latency and waveform of early and late SEPs recorded on 50 and 200 ms were studied in 20 normal subjects, for the parietal (P), prerolandic (F) and prefrontal (pF) regions, ipsiand contralateral to the stimulated median nerve, using either the midfrontal or ear lobe electrode as reference. N17 (thalamic) potential occurred in the ipsilateral P and both F and pF regions (when using an ear lobe reference). The study was also performed in 145 patients with central nervous system diseases. Abnormal, especially early components were observed in 32 of 50 patients with multiple sclerosis. Abnormally delayed SEPs were found in 5 of 13 patients with brainstem lesions presenting sensory disorders. The patients with severe cortical parietal lesions (19 cases) or severe thalamic lesions (4 cases) had also severe abnormalities of all components of the SEPs in both P and F regions. A "dissociated" aspect of the SEPs, with absence of early components on the F side and normal components on the P side, occurred in patients with slight thalamic lesions, ataxic hemiparesis or pure motor deficits (prerosublandic lesions). Another dissociated aspect was noted between the normal early SEPs and the abnormal late components in patients with partial parietal lesions, aphasia or in children with acute sclerosing panencephalitis. These "dissociated" aspects of the SEP suggest different, independent afferent pathways, which may be selectively altered. The late components of the SEP may originate from the primary somatosensory cortex and depend on its integrity. Patients with only a pain sensory loss had abnormal late SEP components.