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To the Editor: I read with interest the article by Dr. Garcia et al. on the frontal wave of somatosensory evoked potentials (SEPs) (named N30) in patients with Parkinson's disease (PD). [1] We first studied extensively the topography of the wave in normal subjects [2] and reported that it is selectively depressed in amplitude in a consistent percentage of PD patients. [3] Since then, other studies as well as ours have shown that in normal subjects the amplitude of the N30 wave is inversely correlated with the appearance of ``late'' (possibly long-loop, cortically mediated) muscular responses, [4] is linked with the modulation of motor cortex excitability induced by an afferent stimulus during magnetic brain stimulation, [5,6] is strongly depressed during programming and execution of hand movements, and is partially depressed during mental execution of movements without motor performance. [7,8] On clinical grounds the frontal N30 is altered (depressed or absent) in isolation or together with the parietal components in several types of brain lesions-besides Parkinson's disease-that induces motor abnormalities (stroke, [9] Huntington's disease, [10] dystonia, myoclonus).
The N30 depression can be transiently ameliorated by apomorphine administration in early stages of PD and-at a lesser level-in other types of …
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