Rationale: Obstructive sleep apnea (OSA) increases the risk of stroke independent of known vascular and metabolic risk factors. Although patients with OSA have higher prevalence of hypertension and evidence of hypercoagulability the mechanism of this increased risk is unknown. Obstructive apnea events are associated with surges in blood pressure, hypercapnia and fluctuations in cerebral blood flow. These perturbations can adversely affect the cerebral circulation. We hypothesized that patients with OSA have impaired cerebral autoregulation making them more susceptible to cerebral ischemia and stroke. Methods: We examined the cerebral autoregulation in patients with and without OSA by employing transcranial Doppler method. We followed the middle cerebral artery blood flow velocity (CBFV) and arterial blood pressure using Finapres during orthostatic hypotension and recovery as well as during 5% CO₂ inhalation. Cerebral vascular conductance and reactivity were determined. Results: Forty-eight subjects, 26 controls (age 41.0±2.3) and 22 OSA (age 46.8±2.3) free of cerebrovascular and active coronary artery disease participated in this study. OSA patients had a mean apnea-hypopnea index of 78.4±7.1 vs. 1.8±0.3 events/hr in controls. The oxygen saturation during sleep was significantly lower in the OSA group 78±2% vs. 91±1% in controls. The dynamic vascular analysis showed mean CBFV was significantly lower in OSA patients compared to controls, 48±3 vs. 57 cm.s^-1, P <0.05, respectively. The OSA group had a lower rate of recovery of cerebrovascular conductance for a given drop in blood pressure compared to controls (0.06±0.20 vs. 0.20±0.06 cm.s^-2. mmHg.s^-1, P < 0.05). There was no difference in cerebrovascular vasodilatation in response to CO₂. Conclusion: Patients with OSA have decreased CBFV at baseline and blunted cerebrovascular compensatory response to changes in blood pressure but not to CO₂. These perturbations may increase the risk of cerebral ischemia during obstructive apnea.