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We studied the amplitude maps of median SEP parameters in patients with Huntington's disease (HDP) and their relatives at risk (HDF). Corresponding to the small amplitude of SEP in HDP, the power (microV2) was significantly smaller at all electrodes, and the maximum power was shifted anteriorly as a result of greater reduction of the power in the parietal than in the frontal region. In HDF, significant power reduction at the parietal region resulted in a similar anterior shift of the power to that noted in HDP. In addition to the overall reduction of SEP amplitude, the field distributions of parietal N20, frontal N29 and central N60 were significantly different in HDP, as compared to the normals. The typical relationship of the frontal positive and parietal negative fields normally present at N20 latency was lost in HDP due to the loss of the frontal P20. Frontal N29 was absent. Also N60 field shifted anteriorly. In HDF, the degree of deviation was in between those of HDP and normals. These alterations of SEP amplitude, wave form and field distribution in HDP and in some of HDF may be viewed as a result of aberrant modulatory effect exerted by the non-sensory system upon the somatosensory input.

In normal subjects, cerebral potentials were evoked by brief, passive extension of the wrist joint at various interstimulus intervals (ISIs). The resulting somatosensory evoked potentials (SEPs) were found to decrease during repetitive stimulation. The greatest decrement occurred between the first and second responses of each series. After cessation of stimuli, the SEP amplitude returned to control values over a prolonged, exponential time course. The authors postulate that the observed response decrement may be a form of habituation, which provides a model for studying the neuronal substrates of behavior.

We studied the field distribution of referentially recorded negative potentials after stimulation of the median nerve at the wrist in 15 normal subjects. When recorded from multiple sites along the lateral aspect of the arm with the reference electrode at the knee, 3 negative peaks, N3, N6 and N9, appeared at fixed latencies. Of these N3 and N6 were highest in amplitude at the distal insertion of the brachioradialis and the distal end of the deltoid, respectively, and N9, at the acromion. With stimulation of the finger, the negative peaks shifted in latency by about 3 msec, indicating an anatomically fixed generator source for each component. When compared to far-field potentials, N9 was of the same latency as scalp recorded P9, that extended to the arm contralateral to the side of stimulation and to the upper half of the trunk. In contrast, N6 extended to the scalp with P6 spreading to the lower half of the body. When two subjects were connected by the arm, stationary negative or positive peaks were transmissible from the stimulated to the non-stimulated subject. When the stimulated arm of the first subject was in contact with the second subject, N3, N6 and N9 were recorded in the latter. Only P9 was registered when the unstimulated arm was in contact with the second subject. We conclude that N3, N6 and N9 are stationary negative potentials generated at certain points along the nerve pathway, probably representing a negative counterfield for positive far-field peaks, P3, P6 and P9. These stationary potentials can spread widely in a volume conductor and can even be detected in a non-stimulated subject making a close contact to the generator source.