Thalamic Stroke and

Disordered Sleep
Kenneth C. Sassower, M.D.
Sleep Disorders Unit
Massachusetts General Hospital

Hypersomnia After Thalamic Stroke:
Traditional Concept
EDS due to insufficient arousal
Interruption of NE and DA activating impulses
ascending from brainstem RF to thalamus
Diurnal sleep behavior composed of NREM
stage I (drowsy) sleep; no deeper sleep
Night sleep mechanisms preserved
Disturbance of wakefulness: De-aroused state
rather than true hypersomnolence

Hypersomnia After Thalamic Stroke:
Revised Concept
Thalamus has a key role in sleep production (as
well as arousal control)
Various thalamic nuclei are targets of projections
coming from certain hypnogenic areas (basal
forebrain, post. hypothalamus, mesencephalic
and pontine RF)
EEG spindles: reticular thalamic nucleus
SWS: thalamo-cortical neurons
FTI: Anterior and DM nuclei of thalamus
Clinical Features
Increased sleep requirements (> 14 hrs/day)
Severe EDS only: vertical gaze palsy; coma
Amnesia; confabulation; psychomotor slowing;
attentional deficits; apathy; blunted affect; lack of
concern; persisting work incapacity (not EDS)
EDS usual; not irresistible; after meals; 2-5 pm;
naps last > 1 hr; difficult to arouse
Day sleep similar to night sleep, but less deep
Save for EDS, narcoleptic symptoms rare
Neuroradiological Findings
Severe EDS: Acute bilateral butterfly-shaped
paramedian thalamic stroke (PTS), or unilateral
PTS involving subthalamic and midbrain areas
Inferior part of DM nucleus typically involved
Medial-anterior part of CM nucleus and VPM
nucleus often involved as well
Anterior and VPL nuclei rarely involved
Sleep Study Findings
Disruption of NREM sleep typical
Increased NREM stage I sleep
Decreased sleep spindle count
Decreased NREM stage II sleep
Severe EDS patients: Significantly more stage I
and less SWS than in mild EDS
REM sleep typically preserved
MSLT results do not parallel severity of EDS
Etiology of PTS Stroke
Distinct stroke syndrome
Affects young and middle-aged subjects
Due to proven or presumed embolic occlusion of
the often unpaired thalamic-subthalamic
perforating arteries arising from top of the
basilar artery
Other Thalamic Strokes
Inferolateral Infarct (VP nuclear group): Sudden or
progressive onset of numbness and tingling on
opposite side of body; hemicorporeal sensory loss
with possible sparing of proprioception ; some
weakness or ataxia; Common
Tuberothalamic Infarct (VL and DM nucleus):
Dysphasia (L); Hemineglect and impaired visuo-
spatial processing (R)
Posterior Choroidal Artery Infarct (LGB): Partial
hemianopia; asymmetric optokinetic response
Hypersomnia not typically associated
Thalamic Hypersomnia After PTS:
Clinical Syndrome
Triad of hypersomnia, neuropsychological
deficits (frontal syndrome, amnesia) and eye
movement disturbances
Vertical gaze palsy: Best clinical predictor of
more severe EDS (amnesia not as predictive)
EDS: Increased sleep requirements; circadian
fluctuations (afternoon); improved with
prolonged naps; stimulant response; disabling
hypersomnia lasting > 1 yr in severe cases, with
resolution; thalamic dementia may persist
Summary
Hypersomnia in PTS may be result of disruption
of BOTH arousal and NREM sleep (REM sleep
preserved)
Insufficient arousal: Difficult to awaken (with
confusion); progressive recovery of
wakefulness; daytime sleep light/not deep;
impaired ability to transition from wake to sleep
NREM sleep disruption: parallels EDS severity;
reduced spindles, NREM stage II sleep, SWS
Summary (Continued)
In patients with PTS, hypersomnia results not only
from an impairment of wakefulness during the day,
but also from chronic NREM sleep deprivation,
which follows insufficient spindling and SWS
production at night.
The most severely affected patients appear to be
suspended in a drowsy state, between
wakefulness and sleep, that is interrupted only by
periods of REM sleep.
De-arousal state normalizes over time; NREM
sleep may remain defective.

Conclusion
Hypersomnia following PTS may be the result of
the disruption of BOTH arousal and NREM
sleep.
This supports the concept of a dual role of the
thalamus in sleep-wake regulation.