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Neurology 1999;52:516
© 1999 American Academy of Neurology


Articles

Physiologic events initiating REM sleep in patients with the postpolio syndrome

H. Siegel, MD, C. McCutchen, MD, M. C. Dalakas, MD, A. Freeman, BS, B. Graham, REEGT, RPsgT, D. Alling, MD, PhD and S. Sato, MD

From the EEG Section, Office of the Clinical Director (Drs. Siegel, McCutchen, and Sato, and A. Freeman and B. Graham), and the Neuromuscular Disease Section (Dr. Dalakas), Medical Neurology Branch, National Institute of Neurological Disorders and Stroke (NINDS); and Office of the Director (Dr. Alling), National Institutes of Health, Bethesda, MD.

Address correspondence and reprint requests to Dr. Susumo Sato, Chief, EEG Section, Office of the Clinical Director, National Institutes of Health, Building 10, Room 5C-101, 9000 Rockville Pike, Bethesda, MD 20892; e-mail: sato{at}helix.nih.gov

BACKGROUND: We previously studied the occurrence of muscle tone reduction (MTR), sawtooth waves (STW), and REM in sleep, and found a stereotypical sequence of these events in normal subjects. Patients with the postpolio syndrome may have involvement of the reticular formation in the brainstem, an area known to mediate initiation of REM sleep. We hypothesized that such brainstem pathology might affect the stereotyped sequence of events initiating REM sleep.

METHODS: We measured the latencies to the onsets of the first MTR, the first STW, and the first REM in 13 patients with postpolio syndrome, 7 of whom had bulbar involvement. All latencies were calculated from the last body movement before the onset of REM sleep.

RESULTS: Using analysis of variance, we found highly significant differences among the overall mean latencies of the three types of onset (MTR, STW, REM) and also between the mean latencies of the two subgroups of patients (bulbar, nonbulbar). Although the latencies for the entire group were longer than those of the normal volunteers, the differences were not significant. However, when the bulbar and nonbulbar groups were compared, analysis of variance showed significantly longer latencies for the bulbar group than for the nonbulbar group (p < 0.0001). The values for the nonbulbar patients closely resembled those for the normal controls. Although the latencies differed, the slopes of the regressions of REM on STW, STW on MTR, and REM on MTR resembled each other closely (p = 0.924).

CONCLUSION: Prolongation of these latencies may be due to prolonged recruitment time for neurons in the pontine tegmentum, following damage from polio. This may be a sensitive marker of a brainstem lesion, and may also represent a type of sleep pathology not previously explored.







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