Cerebrovascular diseases (Basel, Switzerland) · 1998
Internal borderzone infarction in patients with ischemic stroke.
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Gandolfo C, Del Sette M, Finocchi C, Calautti C, Loeb C
Аннотация
OBJECTIVE: The mechanism underlying cerebral infarction in the borderzone between the territories of deep and superficial perforating arteries has not yet been clarified. This study was performed to investigate the prevalence, volume, site, and etiology of this type of subcortical infarction in a large unselected group of stroke patients.
METHODS AND PATIENTS: We analyzed a continuous series of 383 patients with recent cerebral infarction observed in our Stroke Unit. Patients underwent a complete clinical and instrumental workup. The subgroup of subjects with internal borderzone infarct alone were compared with the subgroups of patients with other types of cerebral infarcts by uni- and multivariate statistical tests.
RESULTS: There were 90 internal borderzone infarcts of 725 ischemic lesions (12%of the total), with a median volume of 0.32 ml (95% confidence interval 0.24-0.44; range: 0.012- 20.2 ml). Internal borderzone infarcts alone occurred in only 13 of 383 (3.4%) patients. A comparison between patients with 'pure' internal borderzone infarction and patients with other types of cerebral infarcts by multiple logistic regression analysis demonstrated a significant independent causal role of carotid stenosis or occlusion.
CONCLUSION: Our study suggests that 'pure' internal borderzone infarctions are quite rare findings in patients with ischemic stroke, and that the hemodynamic impairment due to atherosclerotic occlusion or stenosis of the carotid system could be the cause in the large majority of cases.
METHODS AND PATIENTS: We analyzed a continuous series of 383 patients with recent cerebral infarction observed in our Stroke Unit. Patients underwent a complete clinical and instrumental workup. The subgroup of subjects with internal borderzone infarct alone were compared with the subgroups of patients with other types of cerebral infarcts by uni- and multivariate statistical tests.
RESULTS: There were 90 internal borderzone infarcts of 725 ischemic lesions (12%of the total), with a median volume of 0.32 ml (95% confidence interval 0.24-0.44; range: 0.012- 20.2 ml). Internal borderzone infarcts alone occurred in only 13 of 383 (3.4%) patients. A comparison between patients with 'pure' internal borderzone infarction and patients with other types of cerebral infarcts by multiple logistic regression analysis demonstrated a significant independent causal role of carotid stenosis or occlusion.
CONCLUSION: Our study suggests that 'pure' internal borderzone infarctions are quite rare findings in patients with ischemic stroke, and that the hemodynamic impairment due to atherosclerotic occlusion or stenosis of the carotid system could be the cause in the large majority of cases.