Thalamic Stroke and Disordered Sleep

Kenneth C. Sassower, M.D.Sleep Disorders UnitMassachusetts 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.