Effect of Extracranial-Intracranial Bypass on Cerebral Blood Flow and Vasomotor Reactivity in patients with Compromised Cerebral Hemodynamics.
- Author:
Hak Seung LEE
1
;
Yo Sik KIM
;
Sung Don KANG
Author Information
1. Department of Neurology, School of Medicine Wonkwang University, Korea. yosik@wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Vasomotor reactivity;
Cerebral blood flow;
Hemodynamic impairment;
EIAB
- MeSH:
Acetazolamide;
Arteries;
Brain;
Carotid Artery, Internal;
Cerebral Infarction;
Female;
Follow-Up Studies;
Hemodynamics*;
Humans;
Ischemic Attack, Transient;
Male;
Middle Cerebral Artery;
Stroke;
Tomography, Emission-Computed, Single-Photon
- From:Journal of the Korean Neurological Association
2002;20(5):453-458
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The obstruction of intracranial arteries causes cerebral hemodynamic impairment. It is now evident that patients with cerebral hemodynamic compromise have a higher risk of stroke than those with normal cerebral blood flow. The purpose of this study is to investigate the changes of cerebral blood flow and vascular reactivity after extra-intracranial arterial bypass (EIAB) surgery in patients with cerebral hemodynamic compromise. METHODS: We enrolled 16 consecutive patients (8 female and 8 male patients) with transient ischemic attack or cerebral infarction resulted from the occlusion of distal internal carotid artery (ICA) or middle cerebral artery (MCA). We measured the relative regional cerebral blood flow (rrCBF) at rest and after Diamox infusion, and vasomotor reactivity by using single photon emission computed tomography (SPECT). We performed extra-intracranial arterial bypass (EIAB) surgery in patients with impaired vasomotor reactivity. Follow-up brain SPECT was done at 3months after EIAB. We compared the rrCBF and vasomotor reactivity before and after EIAB, and evaluated the effect of collateral vessels on the cerebral hemodynamic after surgery. RESULTS: EIAB increases the vasomotor reactivity significantly (-19.6+/-10 before EIAB, 11.2+/-27 after EIAB, p=0.003) but does not increase the cerebral blood flow at rest (70.5% before EIAB, 70.9% after EIAB). The degree of collateral vessel development did not influence on the restoration of vasomotor reactivity. CONCLUSIONS: These results demonstrate that EIAB increases the vasomotor reactivity of the distal part on the occluded ICA or MCA, but does not increase the cerebral blood flow at rest.
