Matthias Bischof

TL;DR: Hypocretin ligand deficiency appears not to be the major cause for other hypersomnias, with a possible continuum in the pathophysiology of narcolepsy without cataplexy and idiopathic hypersomnia, however, partial hypocretin lesions without low CSF hypoc retin-1 consequences cannot be definitely excluded in those disorders.

TL;DR: The first case of CWS is reported, in whom neuropsychological functions, extension of the underlying lesion, and sleep architecture changes were assessed, and polysomnography demonstrated an essentially normal sleep architecture with preservation of REM sleep.

TL;DR: Hypocretin dysfunction is not the 'final common pathway' in the pathophysiology of most hypersomnolent syndromes that fall on the borderline for a diagnosis of narcolepsy, but a common hypothalamic, hypocretin-independent dysfunction may be present in some of these syndrome.

TL;DR: Hemispheric strokes can cause insomnia, hypersomnia or changes in sleep needs but only rarely persisting sleep EEG abnormalities, and high sleep EEG continuity in the acute phase of stroke heralds a good clinical outcome.

TL;DR: Acute hemispheric stroke is accompanied by alterations of sleep EEG over the healthy hemisphere that correlate with stroke volume and outcome and may reflect neuronal hypometabolism induced transhemispherically (diaschisis).