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Optimized System for Cerebral Perfusion Monitoring in the Rat Stroke Model of Intraluminal Middle Cerebral Artery Occlusion
Published on: February 17, 2013
Cerebral density and perfusion measured among heart disease patients with and without stroke
K Obara1, J S Meyer, K Muramatsu
1Cerebral Blood Flow Laboratories, Department of Veterans Affairs Medical Center, Houston, TX 77030, USA.
Insights
Cardiogenic emboli reduce cerebral perfusion in non-infarcted brain regions, similar to lacunar strokes. This hypoperfusion is linked to small vessel atherosclerosis and thalamo-cortical disconnections.
Area of Science:
- Neurology
- Cardiology
- Radiology
Background:
- Cardiogenic emboli can cause cerebral infarctions.
- Chronic effects on non-infarcted brain regions require clarification.
Purpose of the Study:
- To investigate chronic effects of cardiogenic emboli on cerebral perfusion and tissue densities.
- To compare these effects in patients with and without heart disease and stroke.
Main Methods:
- Xenon-enhanced CT scanning used to measure local cerebral perfusion and tissue densities.
- Cross-sectional comparison between four groups: normal volunteers (with/without heart disease), patients with lacunar infarctions, and patients with cardiogenic cerebral embolism.
Main Results:
- Patients with cardiogenic cerebral embolism showed reduced perfusion in remaining gray and white matter compared to normal volunteers.
- Perfusion deficits in embolism patients were similar to those with lacunar infarctions.
- Reduced thalamic perfusion ipsilateral to cortical infarctions was observed in embolism patients.
- No significant differences in tissue densities were found between embolism and lacunar infarction groups.
Conclusions:
- Reduced cerebral perfusion in non-infarcted areas in cardiogenic embolism patients is associated with small cerebral vessel atherosclerosis, similar to lacunar infarction patients.
- Thalamo-cortical disconnections also contribute to cerebral hypoperfusion in these patients.
Abstract:
This investigation was designed to clarify the chronic effects of cardiogenic emboli on cerebral perfusion and tissue densities within remaining noninfarcted brain. Local cerebral perfusion and tissue densities were measured by xenon-contrasted CT scanning and compared by cross-sectional designs among normal volunteers without heart disease (Group C, n = 44), normal volunteers with heart disease (Group N, n = 20), patients with heart disease and lacunar infarctions (Group L, n = 31) and patients with heart disease associated with cardiogenic cerebral embolism (Group E, n = 12). In Group E, remaining cortical and subcortical gray and white matter perfusion were reduced compared to Groups C and N (p = 0.01), but did not differ from Group L, who had similar profiles of risk factor for stroke. In Group E, perfusion was reduced within the thalamus ipsilateral to cortical infarctions (p < 0.05). There were no differences in remaining tissue densities between Groups E and L. It is concluded that reduced cerebral perfusion in noninfarcted regions among patients with cardiogenic emboli appears to be related to atherosclerosis of small cerebral vessels in a similar manner to patients with lacunes, but thalamo-cortical disconnections also contribute to cerebral hypoperfusion.
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