Abstract

Sleep is a function of the brain and sleep affects brain function, contributing to cerebral pathology through a diversity of direct and indirect mechanisms. Sleep-disordered breathing (SDB) is a very common disorder and is the major sleep-related risk factor for cerebrovascular disease. Epidemiologic studies have shown a dose-response relationship between the severity of SDB and the odds ratio for development of systemic hypertension. Following stroke, both in the acute and chronic stages, patients have a high prevalence of SDB that reduces the potential for rehabilitation, further increases the risk of secondary stroke, and heightens mortality. There is proof that successful correction of SDB with noninvasive positive airway pressure ventilation lowers mean blood pressure. In patients with advanced SDB, altered cerebral evoked potentials are not corrected with applications of noninvasive ventilation, suggesting permanent cerebral structural damage. This is supported by reports of increased leukoaraiosis in patients with advanced SDB. Circadian changes during sleep may increase the risk of both cardiovascular and cerebrovascular accidents.

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