A 75-year-old man suffered a cardiac arrest and severe anoxic encephalopathy. A serial study of electroencephalograms during 4 days showed sequential changes from periodic approximately 2 Hz spike activity to absence-like status (ALS) and then into a suppression-burst pattern. Intravenous administration of phenytoin had no effect on ALS. A small dose of intravenous diazepam reduced a suppression-burst pattern. We speculate that the ALS originates in the midline structures, spreading bilaterally and synchronously to the "dysfunctional" cortex; the sustained discharges were a manifestation of associated reticular lesions, and we believe that intravenous diazepam suppressed the spread of ALS to the "dysfunctional cortex," leading to the appearance of the suppression-burst pattern. The only limitation for definitive conclusions may be a lack of postmortem verification. Autopsy findings, however, could not have confirmed the dynamic changes that occurred during the 5 days before the patients death.

A 50-year-old woman developed intractable excessive sleepiness after undergoing the surgical removal of a brainstem cholesteatoma. The 24-hour ambulatory monitoring revealed a normal architecture of sleep contents, with 62.7% of the time spent in sleep. Auditory and somatosensory evoked responses showed abnormal patterns. The MRI scan of her brain showed an extensive nonprogressive lesion in the brainstem. We speculate that the problem underlying the patient's hypersomnia is a defect in the ascending reticular activating system (ARAS) rather than in the REM and NREM sleep mechanisms.

An usual combination of diffuse theta activity with intermittent bursts of spindle-like activity, followed by 2-3 Hz rhythmic discharges and lasting about 7 seconds, was noted in a coma patient after cardiac arrest. We speculate that the theta pattern coma and spindle-like bursts originated in the pontine region, and that those bursts in turn triggered or recruited rhythmic slow-wave complexes similar to absence discharges.