Obstructive sleep apnoea (OSA) is significantly associated with the risk of stroke, and this association is independent of other risk factors, including hypertension, atrial fibrillation and diabetes mellitus. Therefore, additional pathogenic mechanisms may exist, which contribute to the increased risk of stroke. OSA is characterized by prolonged sympathetic overactivity; however the role of the sympathetic nervous system in regulating cerebral circulation remains a matter of controversy. Converging data indicate that brain perfusion is significantly distorted in OSA, with reported decreases in cerebral blood flow as well as intermittent surges in blood pressure and cerebral blood flow velocity. Based on recent research, there is accumulating evidence that sympathetic nerve activity is an important element in brain protection against excessive increases in perfusion pressure during blood pressure surges and flow during rapid eye movement sleep. The aim of this article was to review: (i) the current physiological knowledge related to the role of the sympathetic system in the regulation of cerebral blood flow, (ii) how the influence of the sympathetic system on cerebral vessels is affected by apnoea (increased PaCO(2)) and (iii) the potential significance of the pathological sympathetic system/PaCO(2) interplay in OSA. Sympathetic system seems to be at least partially involved in pathogenesis of distorted haemodynamics and stroke in OSA patients. However, there are still several open questions that need to be addressed before the effective therapeutic strategies can be implemented.