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A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
Published on: November 15, 2024
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Neuroanatomic correlates of poststroke hyperglycemia
Klemens Winder1, Frank Seifert, Tessa Ohnemus
1Departments of Neurology, University Hospital Erlangen, Erlangen, Germany.
Annals of Neurology
|December 3, 2014
Summary
Damage in the right insulo-opercular brain areas is linked to poststroke hyperglycemia (PSH) in non-diabetic patients. This suggests disinhibition of sympathetic outflow may cause elevated blood glucose levels after stroke.
Area of Science:
- Neurology
- Endocrinology
- Medical Imaging
Background:
- Poststroke hyperglycemia (PSH) is a common complication in acute ischemic stroke.
- The precise neuroanatomical correlates of PSH remain incompletely understood.
Purpose of the Study:
- To investigate the association between the specific sites of ischemic stroke lesions and the occurrence of PSH.
- To identify potential mechanisms underlying PSH in non-diabetic patients.
Main Methods:
- Prospective inclusion of non-diabetic patients with first-ever ischemic stroke confirmed by imaging.
- Assessment of blood glucose level (BGL), National Institute of Health Stroke Scale (NIHSS) score, and clinical parameters on admission.
- Voxel-based lesion symptom mapping (VLSM) analysis adjusted for confounding variables to correlate lesion sites with PSH.
Main Results:
- Elevated BGL was associated with older age, higher NIHSS scores, and larger infarct sizes.
- Spearman rank analysis revealed correlations between BGL and age, infarct size, heart rate (HR), and NIHSS scores.
- VLSM analysis identified significant associations between PSH and damaged voxels in the right hemispheric insular and opercular areas.
Conclusions:
- Damage to the right insulo-opercular areas is a significant contributor to PSH.
- An increase in HR associated with BGL suggests that disinhibition of sympathetic outflow may be a key mechanism driving PSH.
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