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.