Presentation on theme: "Thalamic Stroke and Disordered Sleep Kenneth C. Sassower, M.D. Sleep Disorders Unit Massachusetts General Hospital."— Presentation transcript:
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.