They detected comparable MFV increases in both

groups and concluded that cerebral CO2 reactivity is preserved in SAS. Klingelhöfer et al. [66] also observed normal CO2 reactivity (4.4 ± 1.2%) Bcl-2 inhibitor in SAS patients during wakefulness, but the reactivity values increased significantly during sleep stages I and II and reached a maximum during REM sleep with rises of CO2 reactivity up to three times the waking values. The authors interpreted the increase in CO2 reactivity during sleep as hypersensitivity of intracranial CO2 or pH receptors in SAS patients and attributed this to a possible disorder of the central catecholaminergic and cholinergic systems in SAS. They presume that the marked flow velocity fluctuations during apneic episodes and the associated changes in vessel wall tension place a chronic strain on the cerebral blood vessels, thereby promoting the development of micro- and macroangiopathy. This, among other factors, could be a reason

for the increased incidence of cerebral ischemia in patients with SAS. In addition to the apnea-associated increase in CBF velocity, which most authors attribute ZD1839 purchase to apnea-related hypercapnia [64], [65], [66] and [67], it is also notable that a rapid normalization of flow velocity occurs at the end of each apneic episode. Hajak et al. [65] demonstrated in 10 patients (mean age: 37 years) that, in addition to its connection with the restoration of breathing and the associated occurrence of normocapnia, this flow velocity reduction is also regularly associated with the occurrence of EEG arousal or movement arousal. Because arousals represent a type of neuronal activation, the authors concluded that this indicates a direct neuronal influence on flow velocity during apneic episodes. Franklin [68] compared cerebral hemodynamics in

obstructive sleep apneas and central sleep apneas. Cerebral and cardiovascular changes display a different pattern during central and obstructive sleep apneas. By means of their study they revealed that the CBF velocity according to TCD increases during an obstructive apnea and decreases after apnea termination concomitant with changes in arterial pressure. Clomifene Their interpretation of the results was: the changes in cerebral circulation during obstructive apneas could be an immediate effect of rapid changes in blood pressure because cerebral autoregulation is overridden. The opposite pattern was seen during a central apnea, with a decrease in CBF velocity during apnea and an increase after apnea termination (Fig. 9). Changes during obstructive apneas are probably hazardous, with adverse cardiovascular effects including stroke. This may not be the case during central apneas, as Cheyne–Stokes respiration with central apneas is a result of an underlying disorder such as heart failure and stroke and is not a disease entity in itself. Contrary to every study using TCD during obstructive sleep apnea [65], [66], [67], [69] and [70], Netzer et al.