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#85

"EDS: Psych vs Sleep"

Differences in nocturnal and daytime sleep
between primary and psychiatric hypersomnia:
diagnostic and treatment implications

Alexander N. Vgontzas, MD, Edward O. Bixler, PhD, Anthony Kales, MD, Carrie Criley, BA, and Antonio Vila-Bueno, MD

Sleep Research and Treatment Center and Department of Psychiatry, Pennsylvania State University College of Medicine, Hershey, Pennsylvania; and Sleep Disorders Center and Autonomous University, Madrid, Spain

Published in Psychosomatic Medicine, 62:220-226, 2000

SUMMARY

    The authors note that excessive daytime sleepiness (EDS), the commonest complaint among people presenting themselves to sleep clinics, in 10-15% of patients ends up diagnosed as either primary or idiopathic hypersomnia (that is, of unkown cause) or insomnia related to a mental disorder. At present, the only official criterion that differentiates the two is that in psychiatric hypersomnia, EDS is judged to be related to a mental disorder, a confusing situation when you consider that mental disorders often exist as complications of hypersomnia, whatever the cause or lack thereof.

    This study examined the nocturnal sleep and daytime naps of 59 patients diagnosed with primary (idiopathic) hypersomnia, 23 with psychiatric insomnia, and 50 control subjects without either sleep or mental disorders. In selecting patients for the study, they eliminated those with known sleep apnea, narcolepsy, hypersomnia due to a medical condition, or insomnia complaints. One exception to the exclusion of patients with OSA was that, in 5 cases, they included in the primary hypersomnia group patients with OSA being treated with CPAP without resolution of hypersomnia despite elimination of sleep-disordered breathing.

    They performed standard all-night polysomnography on all subjects, followed by a modification of the Multiple Sleep Latency Test in which subjects were allowed two opportunities of one hour each to nap during the morning and afternoon.

    Ages of subjects in all three groups were similar, averaging 38-43 with a range of 16 to 74 years. Patients with primary hypersomnia were significantly heavier than controls, as measured by Body Mass Indices (27 vs. 24).

    Among the 23 patients with psychiatric hypersomnia, the largest number (12) had a mood disorder. Of those 59 patients with primary hypersomnia, 36% also had a psychiatric diagnosis, again most often (15) a mood disorder. In these cases, the psychiatric disorder was considered secondary to the sleep disorder.

    There were several features of nocturnal sleep that differentiated these groups. In general, patients with psychiatric hypersomnia showed more disturbance of sleep than those with primary hypersomnia, or controls. They took longer to fall asleep than the other two groups (54 minutes vs. 16 and 28). They spent more of the night awake after first falling asleep (79 minutes vs. 57 and 51). They spent more of the night awake (134 minutes vs. 72 and 79. They had less Rapid Eye Movement Sleep (56 minutes vs. 79 and 80).

    During the daytime naps, patients with psychiatric hypersomnia also took longer to fall asleep (34 minutes vs. 17 and 24) and slept less. They showed more stage 1 sleep than the other two groups (28% vs. 15% and 17%); they also had less stage 2 sleep.

    In contrast, patients with primary hypersomnia fell asleep more rapidly than controls, spent less time awake after first falling asleep than either of the other two groups.

    Statistical analyses taking into account the factors of age and body mass did not alter these findings.

    The authors considered their results to show that sleep studies had substantial value in making differential diagnoses between primary hypersomnia and psychiatric hypersomnia. They even suggested that these findings being incorporated into the official diagnostic criteria.

    The authors observed that, even though patients with psychiatric hypersomnia complained of excessive sleepiness, they showed less of an objective tendency to sleep than either patients with primary hypersomnia or normal controls. In contrast, patients with primary hypersomnia tended to sleep "better" (i.e., more) than controls. They conceptualized these different pictures as indicating that patients with psychiatric hypersomnia suffered from excessive arousal, whereas those with primary hypersomnia suffered from insufficient arousal. Thus, they suggested, stimulant drugs might be contraindicated in cases of psychiatric hypersomnia, in whom sedative sleeping medications might prove useful, whereas the opposite would apply to cases of primary hypersomnia.

    

 

MY COMMENTS

    I was both fascinated and pleased to come across this study and its findings. For a long time, I had thought that the differentiation of "primary hyprsomnia" (or, for that matter, hypersomnia due to known causes like OSA) from hypersomnia associated with depressed presented complex issues, but also potential resolutions to those issues. Some of my conjectures were supported by the results of this study.

    One point I had made repeatedly, that met with little enthusiasm among other physician, was that depressed people may feel very tired, fatigued, exhausted, etc, and spend a lot of time in bed, doing little or nothing, but rarely do they really sleep excessively. In other words, I consider "psychiatric hypersomnia" a bit of a contradiction in terms, and accordingly this study found virtually no indication that these patients had any increased tendency to sleep--to the contrary, they took longer to fall asleep, awoke more often, and had lighter sleep, than patients with primary hypersomnia or controls.

    As you can see, I am in enthusiastic agreement with the authors. However, there is one area in which I take exception to their conclusions and suggestions.

    When the authors jump from their one study, done with a relatively small number of subjects (especially in the psychiatric hypersomnia group) to suggesting that their findings be incorporated in official diagnostic criteria for the disorders, I consider them too easily convinced. Even less supportable is their contention that these findings should direct treatment choices--something their study never addressed--such as "contraindicating" stimulants in psychiatric hypersomnia.

 nbsp;nbsp;nbsp;What we have here is another early-phase research project, which will need repeated confirmation by larger and better-designed studies before we can take its findings as proven fact, suitable for application in clinical settings. However, I feel grateful that the authors have advanced the process of research in a relatively obscure area, where we seem to have hit "pay dirt" in finding something new and, in my opinion, quite likely real, about the difference between psychiatric and sleep disorders.

 

"Preserve me from unseasonable and immoderate sleep."

Dr. Samuel Johnson, 1709-1784

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This page was updated on July 14, 2000

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