Abstract
Short-latency somatosensory evoked potentials (SSEPs) were recorded from 10 parkinsonian patients in ‘off’ and ‘on’ states induced by apomorphine and levodopa. The effects of apomorphine and long-term levodopa treatment on the frontal N30 component were assessed and compared with healthy controls. Nine of 10 patients tested with apomorphine showed a significant improvement (p
Highlights
Short-latency somatosensory evoked potentials (SSEPs) to median nerve stimulation at the wrist are characterized in the frontal region by a wave called N30 (Desmedt and Cheron, 1980)
Recent observations showed that abnormalities of the frontal N30 component correlate with dysfunction of neuronal circuits involved in movement disorders (Parkinson's disease, Huntington's disease, dystonia, progressive supranuclear palsy and MPTP-treated monkeys (Rossini et at., 1989; Onofrj et at., 1990; Abbruzzese et at., 1991; Reily et at., 1992; Topper et at., 1993)
Our results are at variance with the findings of Maugiere et ai. (1993), who described no changes in SSEPs after chronic apomorphine therapy in parkinsonian patients and with the study by Onofrj et at. (1995) who found no changes after acute challenge with levodopa and chronic dopaminergic therapy
Summary
Short-latency somatosensory evoked potentials (SSEPs) to median nerve stimulation at the wrist are characterized in the frontal region by a wave called N30 (Desmedt and Cheron, 1980). The clinical response to apomorphine and levodopa is identical in individual parkinsonian patients (Kempster et at., 1990; Rodriguez et at., 1994), as is the improvement in regional cerebral blood flow in the supplementary motor area (Jenkins et at., 1992; Rascol et at., 1994). We have studied changes in the N30 potential induced by both apomorphine and levodopa in a group of parkinsonian patients and its characteristics in a healthy control group.
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