Abnormalities of short-latency somatosensory evoked potentials in parkinsonian patients

Twenty-two patients (16 affected by parkinsonian syndromes, 6 by other neurological diseases) and 12 age-matched controls were examined. Short-latency somatosensory evoked potentials were recorded from 30 scalp electrodes in the 45–52 msec following separate left and right median nerve stimulation a...

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Published inElectroencephalography and clinical neurophysiology Vol. 74; no. 4; pp. 277 - 289
Main Authors Rossini, P.M., Babiloni, F., Bernardi, G., Cecchi, L., Johnson, P.B., Malentacca, A., Stanzione, P., Urbano, A.
Format Journal Article
LanguageEnglish
Published Shannon Elsevier Ireland Ltd 01.07.1989
Amsterdam Elsevier
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Summary:Twenty-two patients (16 affected by parkinsonian syndromes, 6 by other neurological diseases) and 12 age-matched controls were examined. Short-latency somatosensory evoked potentials were recorded from 30 scalp electrodes in the 45–52 msec following separate left and right median nerve stimulation at the wrist. Bit-colour maps were generated on a 4096 pixel matrix via quadratic interpolation. Peak latencies and amplitudes of the parietal, central and frontal components were evaluated. Moreover, the amplitude ratios between parietal and frontal components on the same hemiscalp and between peaks on homologous right and left scalp districts were taken into account. The unique significant difference between parkinsonians and controls was represented by a depressed frontal N 30 wave. This peak was absent in 3 and reduced in 7 out of 16 parkinsonians, with an overall abnormality rate of 47% of the examined arms. Average maps pooling data of parkinsonians and controls confirmed the presence of reduced evoked activity for the whole duration of wave N 30 on those mid- and parasgittal frontal districts where this peak is maximally represented in normals. A similar abnormality was found in 1 of the 6 non-parkinsonian neurological patients suffering from a meningioma of the falx compressing the left supplementary motor area. Possible pathophysiology of such wave N 30 abnormalities in parkinsonians is discussed.
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ISSN:0168-5597
0013-4694
1872-6380
DOI:10.1016/0168-5597(89)90058-0