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Hypersomnia following paramedian thalamic stroke: A report of 12 patients
Author(s) -
Bassetti Claudio,
Marhis Johannes,
Gugger Matthias,
Lovblad Karl O.,
Hess Christian W.
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410390409
Subject(s) - non rapid eye movement sleep , k complex , wakefulness , sleep spindle , thalamus , slow wave sleep , psychology , sleep (system call) , delta wave , anesthesia , sleep stages , neuroscience of sleep , sleep disorder , polysomnography , medicine , insomnia , audiology , electroencephalography , neuroscience , psychiatry , computer science , operating system
Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, which in the absence of systematic sleep‐wake studies has been attributed to disruption of ascending activating impulses and considered a “earoused” state. However, an increasing amount of data suggests a role of the thalamus in sleep regulation and raises the possibility that a sleep disturbance contributes to hypersomnia in PTS. We evaluated 12 patients with magnetic resonance imaging‐proven isolated PTS and hypersomnia with 10 to >20 hours of sleep behavior per day. Nocturnal polysomnographic findings paralleled the severity of hypersomnia. All subjects had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and reduced numbers of sleep spindles. In patients with severe hypersomnia, slow‐wave (stages 3‐4) NREM sleep was often reduced, but there were no major REM sleep alterations. Daytime sleep behavior was associated mostly with stage 1 sleep by electroencephalogram; there was no correlation between hypersomnia and results of nap tests. We conclude that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow‐wave sleep production at night. These observations support the hypothesis of a dual role of the paramedian thalamus as “final common pathway” for both maintenance of wakefulness and promotion of NREM sleep.