In anesthetized preparations, GABA and taurine produced rapid, reversible inhibition of the negative component (N20) of the primary somatosensory evoked potential (SEP) without effect on the earlier positivity (P11). This effect was also produced by low doses of 4-aminopyridine. Neither bicuculline or picrotoxin antagonized these drug effects. A predominance of type B GABA receptors in the superficial layers of the somatosensory cortex is proposed.
We studied auditory evoked potentials (AEPs) in an 82-year-old female patient who became suddenly deaf following the second of two strokes. The patient showed markedly elevated pure tone thresholds, was unable to discriminate sounds and could not understand speech. Brain-stem auditory evoked potentials (BAEPs) were normal. CT scans revealed bilateral lesions of the superior temporal plane which included auditory cortex. Two experiments were performed. In the first, tones, complex sounds and speech stimuli were presented at intensities above and below the patient's perceptual threshold. P1, N1 and P2 components were elicited by each of the stimuli--whether or not they were perceived. In particular, stimuli presented below threshold evoked large amplitude, short latency responses comparable to those produced in a control subject. In a second experiment, the refractory properties of the N1-P2 were examined using trains of tones. They were also found to be similar to those of normal subjects. Shifts in the pitch of the tones near the end of the train (when refractory effects were maximal) evoked N1-P2s with enhanced amplitudes, although the change in pitch was not perceived by the patient. In both experiments AEP scalp topographies were normal. The results suggest that bitemporal lesions of auditory cortex can dissociate auditory perception and long-latency auditory evoked potentials. A review of evoked potential studies of cortical deafness suggests that the neural circuits responsible for N1-P2 generation lie in close proximity to those necessary for auditory perception.
Experiments were conducted to study the contribution of prefrontal cortex to the generation and modulation of two varieties of P300 activity. Control subjects generated typical parietal maximal P300 responses to detected target stimuli. Unexpected, novel auditory stimuli presented to controls generated an earlier latency, fronto-centrally distributed P300 response. A similar earlier latency, fronto-central P300 is generated to unexpected, novel visual stimuli. The occurrence of this phenomenon in both the auditory and visual modalities suggests that it may reflect neural activity of a common CNS system involved in the orienting response. Subjects with unilateral prefrontal damage generated P300 complexes to target stimuli that did not differ from the control responses. Prefrontal damage, however, resulted in a specific defect in the P300 response to the unexpected novel stimulus. Prefrontal patients showed neither N200 enhancement nor the fronto-central P300 response to the novel stimulus that was found in control subjects. These findings indicate that prefrontal regions are critical for the organism's response to unexpected novel stimuli. Abnormalities in prefrontal control of sensory-limbic integration may be a critical element in the decreased P300 to novel stimuli found in these unilateral prefrontal lesioned patients. It is suggested that major features of the human frontal lobe syndrome may be explained by a physiological inability to control attention and orientation systems after prefrontal damage.
Acute Wernicke-Korsakoff syndrome is an underdiagnosed cause of reversible coma in the alcoholic patient. Chronic toxic effects of ethanol include nutritional polyneuropathy, cerebellar degeneration, and diffuse cortical damage with resultant alcoholic dementia. The rapid correction of hyponatremia can result in the iatrogenic syndrome of central pontine myelinolysis.
A 60-year-old man had a history of frontal headaches and chewing-related oscillopsia. Examination disclosed a retro-orbital epidermoid cyst that had eroded through the lateral orbital wall and under the temporalis muscle. The illusion of movement was due to mechanical displacement of the tumor mass and eye by contraction of the temporalis muscle. Removal of the cyst produced complete remission of the oscillopsia.