We describe a patient with chronic asymmetric motor neuropathy, which began in the upper extremity. The paretic muscles showed abundant fasciculations and myokymia but only little amyotrophy. Electrophysiologic examination revealed (1) proximal multifocal persistent conduction block (CB) not located at the usual entrapment sites, and (2) arrhythmic isolated or grouped fasciculation potentials originating distally on blocked axons. Over the years, new CBs developed, which led to tetraplegia, and amyotrophy slowly increased with progressive denervation. This patient differs from the cases of chronic acquired demyelinating polyneuropathy described in the literature by the absence of sensory deficit and the proximal location of CB.

When a target grating is flashed into a larger, surrounding grating, its contrast is perceived to be lower when both gratings are oriented collinearly rather than orthogonally. This effect can be used to dissociate the perceived contrast from the physical contrast of a target grating. We recorded the transient electric potentials and magnetic fields evoked by flashed target gratings and compared them with psychophysical judgments of perceived contrast. Both early (100 ms) and late (150 ms) transients were reduced in amplitude when targets were flashed into a collinear rather than orthogonal surround, thus paralleling the reduction in perceived contrast. Although targets in orthogonal backgrounds required 40% lower physical contrast to match the perceived contrast of collinear targets, the amplitudes of electrophysiological transients of matching stimuli were almost identical. Thus the responses correlated better with perceived than with physical target contrast. This holds especially for the late transient response. Source localization indicated that the transients in question may originate in primary visual cortex. Our results therefore identify the activity of primary visual cortex as one possible neural correlate of perceived contrast.

A collision method in a single axon was used to determine the origin of 100 fasciculations in various lower motor neuron lesions. For 80% of the fasciculations, it was situated on the distal extremity of the axon regardless of the type of lesion, its duration, or the severity of the denervation. For several reasons, this proportion is underestimated. The fasciculations of distal origin were sometimes, associated with double discharges, the mechanism of production and clinical significance of which probably differ.

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