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Insular cortex hypoperfusion and acute phase blood glucose after stroke: a CT perfusion study
Fiona C Moreton1, Michael McCormick, Keith W Muir
1Division of Clinical Neurosciences, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, Scotland, UK.
Stroke
|December 30, 2006
Summary
This study found no link between reduced blood flow in the insular cortex and hyperglycemia after stroke. These findings suggest the insular cortex may not be the primary driver of acute hyperglycemia post-stroke.
Area of Science:
- Neurology
- Neuroscience
- Radiology
Background:
- The insular cortex plays a role in sympathetic nervous system regulation.
- Ischemia in the insular cortex is hypothesized to trigger hyperglycemia following a stroke.
Purpose of the Study:
- To investigate the association between insular cortex hypoperfusion and acute hyperglycemia after stroke.
- To determine if insular cortex ischemia mediates sympathetic stimulation leading to hyperglycemia.
Main Methods:
- Retrospective analysis of 35 patients who underwent perfusion CT.
- Assessment of insular perfusion (relative cerebral blood flow) at a median of 180 minutes post-stroke onset.
Main Results:
- No significant association was found between insular hypoperfusion and early (<6 hours) or delayed (<72 hours) hyperglycemia.
- Hemispheric lateralization of hypoperfusion did not correlate with hyperglycemia.
Conclusions:
- Insular cortex hypoperfusion within 6 hours of stroke onset is not associated with hyperglycemia.
- The proposed mechanism of insular cortex ischemia mediating hyperglycemia requires further investigation.
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