Cerebral haemodynamics in obstructive sleep apnoea and Cheyne-Stokes respiration.

Abstract

Obstructive sleep apnoeas are common among stroke patients and, as different from central apnoeas, they do not decline during stroke rehabilitation. Cerebral and cardiovascular changes display a different pattern during central and obstructive sleep apnoeas. The cerebral blood flow velocity according to transcranial Doppler increases during an obstructive apnoea and decreases after apnoea termination concomitant with changes in arterial pressure. The changes in cerebral circulation during obstructive apnoeas could be an immediate effect of rapid changes in blood pressure because cerebral autoregulation is overridden. Low cerebral blood flow, low arterial pressure and hypoxemia after apnoea termination may predispose to nocturnal cerebral ischaemia. The opposite pattern is seen during a central apnoea, with a decrease in cerebral blood flow velocity during apnoea and an increase after apnoea termination. Changes during obstructive apnoeas are probably hazardous, with adverse cardiovascular effects including stroke. This may not be the case during central apnoeas, as Cheyne-Stokes respiration with central apnoeas is a result of an underlying disorder such as heart failure and stroke and is not a disease entity in itself. It is suggested that obstructive sleep apnoea is a risk factor for stroke as it is common among stroke victims and cerebral hypoperfusion occurs after an obstructive apnoea. The treatment of sleep apnoea should also be taken into account among stroke patients. Large cohort studies, treatment studies and further studies of possible mechanisms for apnoea-induced stroke are, however, essential in order to evaluate whether obstructive sleep apnoea is an independent risk factor for stroke.