HYPERSOMNIA FOLLOWING PARAMEDIAN THALAMIC STROKE - A REPORT OF 12 PATIENTS

Citation
C. Bassetti et al., HYPERSOMNIA FOLLOWING PARAMEDIAN THALAMIC STROKE - A REPORT OF 12 PATIENTS, Annals of neurology, 39(4), 1996, pp. 471-480
Citations number
38
Categorie Soggetti
Clinical Neurology",Neurosciences
Journal title
ISSN journal
03645134
Volume
39
Issue
4
Year of publication
1996
Pages
471 - 480
Database
ISI
SICI code
0364-5134(1996)39:4<471:HFPTS->2.0.ZU;2-3
Abstract
Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, wh ich in the absence of systematic deep-wake studies has been attributed to disruption of ascending activating impulses and considered a ''dea roused'' 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 p atients with magnetic resonance imaging-proven isolated PTS and hypers omnia with 10 to >20 hours of sleep behavior per day. Nocturnal polyso mnographic findings paralleled the severity of hypersomnia. All subjec ts had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and r educed numbers of sleep spindles. In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were n o major REM sleep alterations. Daytime sleep behavior was associated m ostly with stage I sleep try electroencephalogram; there was no correl ation between hypersomnia and results of nap tests. We conclude that h ypersomnia following PTS is accompanied by deficient arousal during th e day and insufficient spindling and slow-wave sleep production at nig ht. These observations support the hypothesis of a dual role of the pa ramedian thalamus as ''final common pathway'' for both maintenance of wakefulness and promotion of NREM sleep.