Evaluation of Cerebral Vasomotor Reactivity by Various Vasodilating Stimuli: Comparison of CO2 to Acetazolamide

To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMR TOT ), during hypercapnia alone, and after injection of 1 g acetazolamide (VMR ACE ). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO 2 -induced with acetazolamide-induced VMR ( r = 0.69 in VMR TOT versus VMR ACE and 0.79 in versus VMR ACE ; p < 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO 2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO 2 -induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease. Acetazolamide has the advantage of being independent of the patient's cooperation. However, it has the disadvantage of increasing the intracranial pressure and not permitting evaluation of the vasoconstrictor capabilities of the cerebral vasculature.