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These data demonstrate partial improvement of some but not all EEG sleep measures in schizophrenic patients through the course of neuroleptic treatment. They suggest that shortened REM latency and disturbed sleep continuity might represent reversible state abnormalities, while reduced slow-wave sleep may represent a more persistent trait abnormality in schizophrenia.

In patients with obstructive sleep apnea and associated rapid-eye-movement (REM) sleep deprivation and disruption, the first night of nasal continuous positive airway pressure (CPAP) is often associated with increases in REM sleep time and REM density (REM rebound). The amount of REM rebound, however, varies considerably. We sought to characterize the magnitude of REM rebound and to determine what factors determine individual differences in REM rebound with initial CPAP treatment. Twenty-six patients with sleep apnea had a baseline nocturnal polysomnogram and a second night with a trial of CPAP. REM sleep time increased by 69% with CPAP, REM density increased by 73%, and REM activity by 169%. REM density was highest in the second REM period. Improvement in respiratory disturbance index with CPAP correlated significantly with increased minutes of REM sleep with CPAP. Of polysomnographic measures on the baseline night, change in minutes of REM sleep with CPAP correlated best with minimum oxygen saturation and to a lesser degree with respiratory disturbance index, and minutes of Stage 1 sleep. One possible explanation for the effect of hypoxemia on subsequent REM rebound is that some physiological functions of REM sleep may fail when oxygen saturation falls below a certain level.

To study the effects of neuroleptic therapy on sleep EEG variables in schizophrenia, as well as the clinical correlates of these variables, we performed polysomnographic (PSG) studies on 14 schizophrenic inpatients before and during neuroleptic therapy. Sleep continuity measures improved after 3 weeks of neuroleptic therapy, showing decreased sleep latency and improved sleep efficiency. REM latency increased with treatment, although half the patients continued to exhibit REM latencies less than 60 min. Other sleep stages and measures of REM sleep (density, activity, number of periods) did not appear to change with neuroleptic treatment. At baseline, REM latency had strong negative correlations with BPRS and SANS scores, but with 3 weeks of such treatment, this association disappeared. Further work is needed to distinguish direct medication effects from the effects of the changing clinical state on PSG measures.