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AJNR: American Journal of Neuroradiology logoLink to AJNR: American Journal of Neuroradiology
. 1998 Jun-Jul;19(6):1067-74.

Failure to identify cerebral infarct mechanisms from topography of vascular territory lesions.

M Hennerici 1, M Daffertshofer 1, L Jakobs 1
PMCID: PMC8338653  PMID: 9672013

Abstract

PURPOSE

Our purpose was to determine whether topographic patterns of ischemic damage seen on brain imaging studies are useful for evaluating different mechanisms of infarction and for distinguishing embolic from hemodynamic disorders.

METHODS

Early CT scans were reviewed to identify brain infarctions in the middle cerebral artery territory in 800 patients with either significant obstructive lesions of the internal carotid artery (70% stenosis, n = 17; occlusion, n = 85) or nonvalvular atrial fibrillation (n = 186) as the only identified source of stroke. Ninety-nine CT studies were considered suitable for entry into the final analysis. The scans were digitized and superimposed on postmortem brain sections by matching algorithms to display the variability of the cerebrovascular territories.

RESULTS

Cortical borderzone-type infarctions were rare and evenly distributed among patients with cardiac sources of embolism (3.2%) and severe carotid obstructions (3.6%). In contrast, subcortical borderzone infarcts occurred significantly more often in patients with carotid obstructive disease (36% versus 16%). However, on computerized segmentation analysis, the topography of infarction was the same in both groups.

CONCLUSION

The current concept that stroke mechanisms can be inferred from interpretation of stroke patterns on brain scans is heavily confounded by the variability in intracranial arterial territory distributions. Since individual arterial territories cannot be identified in vivo, interpretation of stroke topography is invalidated. In particular, the cortical wedge-type of borderzone infarction, said to result from hemodynamic compromise in low-flow perfusion territories, is an ambiguous observation and may be seen in patients with cerebral embolism and hemodynamic compromise due to severe carotid disease.

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