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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.

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A strong association between HLA-DR2, DQ1 and narcolepsy-cataplexy has been known since 1986. In 1990 a subdivision (HLA-DR15, DQ6) was shown to be equally associated. Narcolepsy symptoms include rapid eye movement (REM)-sleep intrusion hallucinations during the day. Some narcoleptics may be so hallucinated that they become delusional and receive a diagnosis of schizophrenia. Fifty-six inpatient schizophrenics and 56 normal controls were compared to see if there was an excess of the narcolepsy-associated antigens (NAA) among schizophrenics. Patients had frequency of the NAA 3.89 times higher than controls. After a subset was studied by night (n = 9) and day (n = 7) polysomnography, two patients were found to be true narcoleptics. Their psychosis improved with treatment for narcolepsy. When NAA(+) and NAA(-) schizophrenics were compared, the NAA(+) subgroup had significantly higher Brief Psychiatric Rating Scale (BPRS) scores and more hospitalizations. There were no effects attributable only to gender or race. We conclude that narcolepsy can simulate schizophrenia in some cases, and that even in nonnarcoleptic patients, the HLA-DR15,DQ6 antigens mark a group of severe schizophrenics that merits further study.

Because patients with Cushing' syndrome (CS) and Major depressive disorder (MDD) share features of hypercortisolism and the depressive syndrome, we compared electro-encephalographic (EEG) sleep in patients with pituitary-ACTH-dependent Cushing's syndrome (Cushing's disease, CD), patients with ACTH-independent Cushing's syndrome (AICS), patients with major depressive disorder (MDD), and normal subjects. There were substantial similarities in the abnormal polysomnography profiles of patients with CD, AICS, and MDD. All three patient groups demonstrated poorer sleep continuity, shortened rapid eye movement (REM) latency, and increased first REM period density compared with normal subjects. In addition, AICS patients and MDD patients had elevated REM activity and density. These findings are discussed in terms of models of pathophysiology that relate abnormalities in sleep, mood, and hypothalamic-pituitary-adrenal function.