ThalamicStrokeandDisorderedSleep：丘脑卒中和睡眠紊乱.pptVIP

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 an