Cerebral vasoreactivity decreases overnight in severe obstructive sleep apnea syndrome: a study of cerebral hemodynamics.
BACKGROUND
OSAS has been associated with surrogate markers of atherosclerosis and is a known risk factor for stroke. However, there is limited data on the effects of recurring apneas in severe OSAS on cerebral circulation and their consequences on cerebrovascular reactivity and compliance.


OBJECTIVE
To evaluate cerebral blood flow velocity (CBFV) changes and vascular compliance in patients with severe obstructive sleep apnea syndrome (OSAS) using transcranial Doppler sonography (TCD) and cerebral pulse transit time (PTT).


METHODS
Seven patients (1 woman, 6 men, mean age 57.4 years) with severe OSAS underwent polysomnography at the sleep laboratory of the Neurology Department of Innsbruck Medical University. TCD was performed continuously during the whole night using a pulsed wave probe and was co-registered with routine polysomnography. Cerebrovascular reactivity was assessed by calculation of apnea and hypopnea-related CBFV changes. Arterial compliance was characterized by PTT derived from phase difference analysis between ECG and TCD signals. Sleep time was dichotomized into periods with high density of consecutive respiratory events (CRE) vs. periods with low density of consecutive respiratory events (non-CRE). TCD measurements of CBFV showed a regular, undulating pattern with flow minima immediately before apneas or hypopneas and maxima closely after their termination, reciprocally to peripheral O(2) saturation. CBFV reactivity was significantly diminished in CRE compared to non-CRE periods. PTT phase differences were reduced in non-CRE, and even more so in CRE periods, compared to initial wake phases.


CONCLUSIONS
We found severe disturbances of cerebrovascular reactivity in OSAS patients. Our data demonstrate loss of vasoreactivity and increase of arterial stiffness, indicated by CBF hyporeactivity and PTT reduction, especially during CRE periods. These changes are likely to impair cerebral circulation and may be detrimental to the endothelium.
Furtner
Martin
M
Innsbruck Medical University, Department of Neurology, Anichstrasse 35, Innsbruck, Austria.
Staudacher
Martin
M
Frauscher
Birgit
B
Brandauer
Elisabeth
E
Esnaola y Rojas
Maria M
MM
Gschliesser
Viola
V
Poewe
Werner
W
Schmidauer
Christoph
C
Ritsch-Marte
Monika
M
Högl
Birgit
B
D001783:Blood Flow Velocity / Q000502:physiology; D002536:Cerebral Arteries / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003187:Compliance / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010092:Oximetry; D017286:Polysomnography; D011673:Pulsatile Flow / Q000502:physiology; D012720:Severity of Illness Index; D020181:Sleep Apnea, Obstructive / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D012894:Sleep Stages / Q000502:physiology*; D017585:Ultrasonography, Doppler, Transcranial