Borderzone Infarct Subtypes: Preliminary Study of the Presumed Mechanism

Mounier‐Véhier, F.; Leys, D.; Godefroy, Olivier; Rondepierre, Ph.; Marchau, M.; Pruvo, JP

doi:10.1159/000117001

Cited by 22 publications

(20 citation statements)

References 15 publications

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“…5 Previous reports have described IBI as the effect of hemodynamic impairment, due to severe carotid stenosis or occlusion, or to severe heart disease. 3,4,26,27 The "hemodynamic theory" of IBI etiology is indirectly supported by some PET studies, which report a functional reduction of rCBF in the cortical watershed areas of patients with severe carotid disease. 28,29 A recent study performed with SPECT showed a significantly lower perfusion reserve in patients with deep watershed infarction.…”

Section: Discussionmentioning

confidence: 94%

Internal Borderzone Infarction

Sette

Eliasziw²,

Streifler³

et al. 2000

Stroke

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Background and Purpose-Among subcortical infarctions, internal borderzone infarcts (IBI) are considered to be separate entities from perforating artery infarcts (PAI). The purpose of the present study is to examine the relationship between the presence of IBI and the degree of angiographically defined internal carotid artery (ICA) stenosis in symptomatic patients. Methods-A review of 1253 brain CTs from patients recruited by the North American Symptomatic Carotid Endarterectomy Trial was performed, using templates for the identification of subcortical and cortical vascular territories. Results-A total of 413 patients had visible ischemic lesions on the side ipsilateral to their symptomatic ICA. Of these, 138 had PAI, 108 had IBI, 122 had cortical infarcts, and 45 had a combination of different lesions. Mean (ϮSD) lesion diameter was larger for IBI (11.0Ϯ5.9 mm) than for PAI (7.1Ϯ4.7 mm) (PϽ0.001 for comparing 2 means). IBI was associated with higher degrees of ICA stenosis (PϽ0.001). Sixty-three percent of the patients with IBI had severe (70% to 99%) ICA stenosis compared with 42% of patients with PAI; 18% of the IBI patients had stenosis of 90% or more compared with 8% of the patients with PAI. Multiple logistic regression did not identify any patient characteristics as confounders. Conclusions-Among

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Section: Discussionmentioning

confidence: 94%

Internal Borderzone Infarction

Sette

Eliasziw²,

Streifler³

et al. 2000

Stroke

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“…To the best of our knowledge, only 4 studies have explicitly examined differences in the pathophysiology of IBZ and CBZ infarctions [21][22][23][24] (see the supplemental Table I, available online at http://stroke.ahajournals.org). None of these studies used DWI, and 3 of them were carried out under the context of carotid stenosis or occlusion.…”

Section: Discussionmentioning

confidence: 99%

“…As a result, it is not clear whether the mechanisms of stroke differ between IBZ and CBZ infarcts. Few studies [21][22][23][24] have focused on differences in the characteristics of each type of border-zone, and the results of these studies are inconsistent.…”

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confidence: 99%

Internal and Cortical Border-Zone Infarction

Yong

Bang

Lee

et al. 2006

Stroke

125

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Background and Purpose-The pathogenesis of internal border-zone (IBZ) and cortical border-zone (CBZ) infarcts is unclear. Both types of infarct have been combined into a single group in most previous reports, which has produced conflicting results. We hypothesized that different pathogenic mechanisms underlie IBZ and CBZ infarcts. Methods-We reviewed 946 consecutive patients with ischemic stroke within the middle cerebral artery territory. IBZ and CBZ infarcts were selected based on diffusion-weighted imaging templates to identify vascular territories. Baseline patient characteristics, clinical courses, and neuroradiological features were compared between patients with IBZ and CBZ infarcts. Results-We identified 45 IBZ and 75 CBZ infarct patients. Compared with the CBZ infarct patients, IBZ infarct patients had a higher degree of stenosis or occlusion in either the middle cerebral or internal carotid artery (Pϭ0.008) and exhibited a rosary-like pattern of infarction more frequently (PϽ0.001). In contrast, concomitant small cortical infarcts were observed more frequently in CBZ infarct patients (PϽ0.001). Clinical deterioration during the first 7 days of admission and poor outcome after 3 months after stroke was more prevalent in IBZ infarct patients than in CBZ infarct patients (Pϭ0.002 and Pϭ0.003, respectively). Conclusions-IBZ

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“…Some studies have observed that IBIs might be associated with severe carotid stenosis or occlusion [3, 4, 5]and have suggested a hemodynamic etiology. Moreover, other studies have shown a higher prevalence of diabetes mellitus [4]or heart disease [6]and suggest small vessel disease and cardioembolism as possible causes. Clear identification of the pathophysiological mechanism inducing ischemic stroke is very important for treatment and secondary prevention.…”

Section: Introductionmentioning

confidence: 99%

Internal Borderzone Infarction in Patients with Ischemic Stroke

Sette¹,

Finocchi²,

Calautti³

et al. 1998

Cerebrovasc Dis

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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.

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Borderzone Infarct Subtypes: Preliminary Study of the Presumed Mechanism

Cited by 22 publications

References 15 publications

Internal Borderzone Infarction

Internal Borderzone Infarction

Internal and Cortical Border-Zone Infarction

Internal Borderzone Infarction in Patients with Ischemic Stroke

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