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From the Centre d'étude du sommeil (Drs. Montplaisir, Petit, and Décary), Hôpial du Sacré-Coeur/Université de Montréal; the Department of Neurology (Dr. Masson), Hôpital Notre-Dame; the Department of Psychology (Dr. Bédard), Université du Québec à Montréal; the McGill Center for Studies in Aging/McGill University (Drs. Panisset and Gauthier); and the Department of Neurology (Dr. Rémillard), Hôpital du Sacré-Coeur, Montreal, Canada.
Address correspondence and reprint requests to Dr. Jacques Montplaisir, Centre d'étude du sommeil, Hôpital du Sacré-Coeur, 5400 Boul. Gouin Ouest, Montréal, Québec, Canada H4J 1C5.
Sleep architecture and quantitative EEG from wakefulness and REM sleep were studied in six patients (mean age, 70.5 years) with progressive supranuclear palsy (PSP) and compared with that of six control subjects (mean age, 69.8 years). Particular attention was given to quantifying REM sleep variables because of the known PSP-associated degeneration of the pedunculopontine tegmentum (PPT)-a critical structure in REM sleep generation. Patients with PSP had a shorter total sleep time, a lower sleep efficiency, a drastic reduction in sleep spindles, an atonic slow-wave sleep, and a lower percentage of REM sleep. The lower percentage of REM sleep was the result of both a reduction in the number of REM periods and a reduction in mean period of duration. REM density was also reduced while REM efficiency, atonia, and phasic EMG were similar to control values. REM sleep findings are consistent with the known role of the PPT in REM sleep induction. A slowing of the awake EEG was found for the six frontal leads and for C4, P4, and T4 in PSP patients. The frontal EEG slowing found in wakefulness is in accord with imaging and neuropsychological studies showing impairment of the frontal lobes in these patients. REM sleep EEG was not significantly slower in any regions. Because all previous studies on PSP have relied on visual inspection of the EEG tracings, the present finding of EEG slowing in the frontal lobes (rather than in the temporal regions or diffusely) suggests that our quantitative EEG approach may be more useful in determining specific regions of impaired cortical activity.
Supported by a partnership grant from the Fonds de la Recherche en Santé du Québec/Hydro Québec, Canada.
Received December 26, 1996. Accepted in final form March 12, 1997.
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