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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-6-11
pubmed:abstractText
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 "dearoused" state. However, an increasing mount 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
471-80
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Hypersomnia following paramedian thalamic stroke: a report of 12 patients.
pubmed:affiliation
Department of Neurology, Inselspital-University Hospital, Bern Switzerland.
pubmed:publicationType
Journal Article