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The present study examined the nature of the negative shift of event-related potential (ERP) recorded during the fully awake state, wakefulness with minor awareness deficit (light drowsiness) and stage 1 of NREM sleep. The cortical responses evoked by two types of auditory stimuli were recorded in nine subjects at the different levels of consciousness described above. A negative component with peak latency of 250-350 msec, N300, was identified in ERP during light drowsiness but not in the fully awake state. In stage 1a (stage 1 without vertex sharp waves), the amplitude of N300 was higher than that in light drowsiness, and it was higher in stage 1b than in stage 1a. The scalp distribution of N300 was predominantly on the vertex. It also confirmed that the vertex sharp wave evoked during stage 1 is maximal on the vertex and its peak latency is approximately 300 msec. Considering the similarity in scalp distribution and peak latency between N300 and vertex sharp wave, it is possible that these electroencephalogram phenomena are generated by an identical synchronizing mechanism in the brain. We assumed that N300 observed during light drowsiness may be an incomplete product of vertex sharp wave.

Bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) usually appear transiently in patients with severe disturbances of consciousness and are indicative of a poor prognosis. Recurrent BIPLEDs have not previously been reported in the literature. We report a 64-year-old patient with bilateral hippocampal lesions (cerebral infarction) who exhibited persistent periodic lateralized epileptiform discharges (PLEDs) (chronic PLEDs) associated with recurrent BIPLEDs. Electroencephalography was recorded for more than 6 months. Left hemispheric PLEDs appeared first. Next, PLEDs shifted to the right hemisphere and BIPLEDs occasionally developed. Brain magnetic resonance imaging and single-photon emission computed tomography with technetium-99-hexamethyl-propyleneamine oxime was performed before and after the appearance of BIPLEDs. The patient had no remarkable clinical symptoms aside from mild memory impairment for this period of time. This is the first case of recurrent 'benign' BIPLEDs, that is, BIPLEDs with a positive prognosis.

In spite of the accumulation of knowledge regarding the neuropharmacological action of benzodiazepines (Bz), the physiological process by which their sedative/hypnotic effects are induced remains poorly understood. We conducted a single-blind, crossover trial to evaluate the role of the thermoregulatory process in sleepiness and impaired psychomotor performance induced by a standard Bz, diazepam (DZP). Each of the eight healthy young male volunteers (mean age, 19.75 years; range, 18-23 years) was given a single oral dose of either 5 or 10 mg of DZP or placebo 12 h after his average sleep onset time. Changes in plasma DZP concentration, proximal body temperature (p-BT), distal body temperature (d-BT), subjective sleepiness measured by the Visual Analog Scale and Stanford Sleepiness Scale, and psychomotor performance measured by Choice Reaction Time were monitored under a modified constant routine condition in which various factors affecting thermoregulation, alertness, and psychomotor performances were strictly controlled. Orally administered DZP induced a significant transient decrease in p-BT and psychomotor performance as well as an increase in d-BT and subjective sleepiness. DistalÀp-BT gradient (DPG; difference between d-BT and p-BT), which is an indicator of blood flow in distal skin regions, showed a strong positive correlation with the plasma DZP concentration, indicating that DZP in clinical doses promotes heat loss in a dose-dependent manner. The DPG also correlated positively with the magnitude of subjective sleepiness and impaired psychomotor performance. These findings indicate that the sedative/hypnotic effects of Bz could be due, at least in part, to changes in thermoregulation, especially in the process of heat loss, in humans.

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