Hemodynamic effects of middle cerebral artery stenosis and occlusion.

Journal Article (Journal Article)

BACKGROUND AND PURPOSE: Middle cerebral artery (MCA) stenosis and occlusion may cause ischemic symptoms through both hemodynamic and embolic mechanisms. The purpose of this investigation was to determine the hemodynamic effects of these lesions. METHODS: Ten patients with angiographically confirmed symptomatic occlusion (n = 5) or stenosis (n = 5) of the M1 segment of the MCA were studied by clinical examination, arteriography, and positron emission tomography (PET). Arterial supply to the distal MCA territory was classified from a review of the angiogram as being through the stenosis or from pial collaterals from anterior or posterior cerebral arteries. Regional measurements of cerebral blood flow, cerebral blood volume, cerebral rate of oxygen metabolism, oxygen extraction fraction, and ratio of cerebral blood volume/cerebral blood flow (mean vascular transit time, MTT) were obtained using PET. Hemodynamic status was categorized from PET scans as stage 0, normal hemodynamics; stage 1, autoregulatory vasodilatation (increased MTT); or stage 2, increased oxygen extraction fraction. RESULTS: Of five patients with MCA occlusion, three had autoregulatory vasodilatation (stage 1) and two had increased oxygen extraction fraction distal to the lesion (stage 2). The MCA territory was supplied solely by pial collaterals in all five patients. Four of the five patients with focal MCA stenosis had normal hemodynamics (stage 0). One patient had stage 1 hemodynamic status. Blood flow to the MCA territory was through the stenosis in all patients; no pial collaterals were identified. CONCLUSION: The frequency of hemodynamic compromise in patients with MCA occlusion is high. Pial collateralization is not a specific sign of increased oxygen extraction fraction in patients with MCA occlusion.

Full Text

Duke Authors

Cited Authors

  • Derdeyn, CP; Powers, WJ; Grubb, RL

Published Date

  • September 1998

Published In

Volume / Issue

  • 19 / 8

Start / End Page

  • 1463 - 1469

PubMed ID

  • 9763379

Pubmed Central ID

  • PMC8338700

International Standard Serial Number (ISSN)

  • 0195-6108


  • eng

Conference Location

  • United States