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
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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 visuospatial 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.