Cortical Border-zone Infarcts Research Articles

Characteristics of Atherosclerotic Plaques and Stroke Mechanism in Patients with Border-Zone Infarcts: A High-resolution Magnetic Resonance Imaging Study

BackgroundRelatively little is known about the plaque characteristics of border-zone infarcts and how they differ between cortical border-zone (CBZ) and internal border-zone (IBZ) infarcts. MethodsWe conducted a prospective observational cohort study of patients of intracranial atherosclerotic disease who underwent high-resolution magnetic resonance imaging (HR-MRI) examination. Individuals with border-zone infarcts in the middle cerebral artery (MCA) territory, detected by diffusion-weighted imaging, were enrolled. Plaque morphological and compositional parameters of both IBZ and CBZ groups were compared. Independent predictors were identified using a binary logistic regression model, and the sensitivity and specificity of the model were assessed using a receiver operating characteristic curve. Kaplan-Meier survival analysis further explored differences in stroke recurrence between BZ patients with mono or dual antiplatelet therapy. ResultsWe reviewed 101 symptomatic patients with border-zone infarcts (BZ) within the MCA territory in the study. Out of the patients meeting the imaging eligibility criteria, we detected 34 cases with isolated IBZ, 23 cases with isolated CBZ, and 6 cases with both IBZ and CBZ infarcts. Those with IBZ infarcts had a higher plaque burden than those without (p<0.001), and those with CBZ infarcts exhibited a complicated plaque less frequently than those without (37.9% vs 67.6%, p=0.018). In those with isolated IBZ or CBZ infarcts, plaque burden was independently associated with isolated IBZ infarcts (odd ratio=1.08; 95% CI, 1.02-1.15; p=0.023). During the median follow-up period of 37 (27, 50) months, 13.8% of patients receiving early dual antiplatelet treatment and 30.4% of those on single antiplatelet therapy experienced stroke recurrence (p=0.182). ConclusionsIntracranial atherosclerotic plaque morphology and composition differ between patients with IBZ and those with CBZ infarcts. Higher plaque burden is more associated with IBZ infarcts.

Cerebral hemodynamics and stroke risks in symptomatic intracranial atherosclerotic stenosis with internal versus cortical borderzone infarcts: A computational fluid dynamics study

There may be different mechanisms underlying internal (IBZ) and cortical (CBZ) borderzone infarcts in intracranial atherosclerotic stenosis. In 84 patients with symptomatic, 50-99% atherosclerotic stenosis of M1 middle cerebral artery (MCA-M1) with acute borderzone infarcts in diffusion-weighted imaging, we classified the infarct patterns as isolated IBZ (n = 37), isolated CBZ (n = 31), and IBZ+CBZ (n = 16) infarcts. CT angiography-based computational fluid dynamics models were constructed to quantify translesional, post-stenotic to pre-stenotic pressure ratio (PR) in the MCA-M1 lesion. Those with IBZ infarcts were more likely to have a low PR (indicating impaired antegrade flow across the lesion) than those without (p = 0.012), and those with CBZ infarcts were more likely to have coexisting small cortical infarcts (indicating possible embolism) than those without (p = 0.004). In those with isolated IBZ or CBZ infarcts, low PR was independently associated with isolated IBZ infarcts (adjusted odds ratio = 4.223; p = 0.026). These two groups may also have different trajectories in the stroke risks under current medical treatment regimen, with a higher risk of same-territory ischemic stroke recurrence within 3 months in patients with isolated IBZ infarcts than isolated CBZ infarcts (17.9% versus 0.0%; log-rank p = 0.023), but similar risks later in 1 year.

Venous and arterial cerebral thrombosis: a COVID-19 dual pathology and single possible etiology\u2014a case report

BackgroundCorona virus disease of the year 2019 (COVID-19) is still devastating the world for more than 19 months since its declaration as a pandemic by world health organization. Its manifestations does not stand at respiratory system but involves other body systems including central nervous system and its vasculature. In the following case report, cerebral venous and arterial thrombosis is detected in a case just in convalescence from COVID-19 with still detected positive IgM.Case presentationA 68-year-old female presenting with disturbed conscious level, bilateral convergent squint, single attack of generalized seizures, left sided dense weakness within a short time from catching COVID-19 and while still in quarantine hospital in recovery phase from infection. Magnetic resonance studies revealed bilateral cortical border zone infarcts as well as left lateral dural sinus and deep venous thrombosis.ConclusionAlong the forth wave, COVID-19 is still hitting hardly the central nervous system vasculature.

Abstract WP183: Borderzone Infarcts Predict Early Recurrence in Patients With Large Artery Atherosclerotic Subtype Despite Medical Treatment

Introduction: Large artery atherosclerosis subtype carries a high risk of early recurrent stroke despite medical management. Predictors of recurrence remain poorly understood. We hypothesized that borderzone infarcts are associated with a higher risk of recurrence. Objectives: We aim to investigate infarct patterns and 90-day recurrence in patients with symptomatic intracranial and/or extracranial atherosclerotic disease. Methods: We included consecutive patients admitted to NYU Langone Health (Manhattan and Brooklyn campuses) over 32-months with a diagnosis of acute ischemic stroke secondary to symptomatic intracranial or extracranial atherosclerosis. The primary predictor was infarct pattern (borderzone vs. non-borderzone infarction), defined in accordance to previous studies. Borderzone infarcts were divided into internal borderzone and cortical borderzone. We used univariate and multivariable cox-regression models to determine associations between infarct pattern and recurrent cerebrovascular events (RCVE) at 90-days. Results: Fifty-five patients met the inclusion criteria; 38 were intracranial, 3 tandem, 14 extracranial. Nearly 71% of patients were treated with dual antiplatelet therapy and 96% were treated with high intensity statin. The RCVE rate was 23.6%. In multivariable models, borderzone infarcts were associated with increased risk of RCVE (adjusted HR 9.8 95% CI 2.1-44.8, p=0.003). The risk of RCVE was highest among internal borderzone infarcts (47.3%) as opposed to cortical borderzone infarcts (33.3%) or non borderzone infarcts (18.8%). Conclusions: Borderzone (and particularly internal borderzone) infarcts are a surrogate marker of impaired distal blood flow and are associated with RCVE despite medical treatment. This highlights the need to develop alternate treatment strategies for this high-risk cohort.

Clinical Significance of Fluid-Attenuated Inversion Recovery Vascular Hyperintensities in Borderzone Infarcts.

Fluid-attenuated inversion recovery vascular hyperintensities (FVHs) are seen in some cases with cerebral hemodynamic impairment and collateral flow. Because the worst outcomes of patients with borderzone infarcts were mainly correlated with impaired hemodynamics, the presence of FVH might provide another clue for predicting the prognosis of patients with borderzone infarcts. We reviewed 1377 consecutive patients with ischemic stroke. Cortical borderzone (CBZ) and internal borderzone infarcts were selected based on diffusion-weighted imaging. FVHs were defined as tubular- or serpentine-shaped hyperintensities in the subarachnoid space. We investigated the clinical significance of FVHs in borderzone-infarcted patients. Among 87 patients with borderzone infarcts, the presence of FVH was observed in 30 (34.5%). We identified 62 patients with CBZ infarcts and 25 patients with internal borderzone infarcts. In the cases with CBZ infarcts, the initial National Institutes of Health Stroke Scale scores and the portions of nonfavorable outcome at 3 months in the FVH(+) group were significantly higher than in the FVH(-) group (P<0.05 and P<0.001, respectively). Unlike the cases with CBZ infarcts, there were no significant differences of these clinical features between the FVH(+) group and the FVH(-) group in the patients with internal borderzone infarcts. The findings of FVH are associated with relatively severe clinical presentation and nonfavorable prognosis in patients with CBZ infarcts, but not in patients with internal borderzone infarcts. The presence of FVH may help to identify CBZ-infarcted patients who require close observation and hemodynamic control.

Early Magnetic Resonance Imaging Predicts Early Neurological Deterioration in Acute Middle Cerebral Artery Minor Stroke

Early neurological deterioration (END) is an important factor associated with worse clinical outcome in minor strokes. Early magnetic resonance imaging (MRI) findings can provide better sensitivity to delineate stroke pathophysiology and have diagnostic value associated with causative mechanisms. The aim of this study was to investigate the relationship between early MRI finding and the presence of END in minor stroke patients with lesions in the middle cerebral artery (MCA) territory. Consecutive MCA minor stroke patients who were admitted to our center within 24 hours of symptom onset were included in this study. All patients underwent MRI within 24 hours of admission. We analyzed baseline characteristics, infarction patterns, and treatment algorithms. The correlation between early MRI findings and END, defined as National Institutes of Health Stroke Scale score increasing more than 2 points during 72 hours after admission, was also determined. Across 211 patients meeting entry criteria between January 2010 and December 2013, internal border-zone (IBZ) infarcts on early MRI scan were observed in 23 of 65 patients with END (35.4%) and in 18 of 146 patients without END (12.3%, P < .001). Patients with IBZ infarcts were found to have more hyperlipidemia, less perforating artery infarcts, more pial artery infarcts, more cortical border-zone infarcts and more ipsilateral large arterial stenosis. Logistic regression analysis revealed that IBZ infarct was independently associated with END after adjustment for other factors (odds ratio, 2.50; 95% confidence interval, 1.09-5.74; P = .031). Early MRI patterns of IBZ infarction are associated with END in minor stroke patients with acute infarcts of the MCA territory.

The Relationship between Neurological Worsening and Lesion Patterns in Patients with Acute Middle Cerebral Artery Stenosis

Background: Intracranial atherosclerotic disease is one of the most common causes of ischemic stroke especially in Asians, Hispanics and blacks. Although middle cerebral artery (MCA) stenosis is increasingly being recognized with the advent of magnetic resonance angiography (MRA) or transcranial Doppler ultrasonography, few studies have focused on acute neurological worsening (NW) in patients with MCA stenosis. We investigated the relationship between NW and lesion patterns detected by diffusion-weighted imaging (DWI). Methods: We studied 44 consecutive patients out of a total of 2,863 consecutive patients who had symptomatic lesions in the territory of the MCA and in whom MRA and/or conventional angiography showed isolated MCA stenosis ≥50% in the MCA trunk. Acute DWI lesion patterns were classified as follows: (1) pial artery territory infarcts (PAI); (2) small cortical and/or subcortical infarcts (SCS); (3) deep penetrating artery territory infarcts (DPI); (4) cortical border zone infarcts (CBZ), and (5) internal border zone infarcts (IBZ). NW was defined as worsening by ≥2 points on the National Institutes of Health Stroke Scale (NIHSS) during the first 7 days. Functional outcome was assessed by the modified Rankin Scale (mRS) at 3 months after stroke onset. Poor outcome was defined as ≥3 on the mRS. The severity of MCA stenosis on MRA was further categorized as 50-75% (moderate) and >75% or focal signal loss with the presence of distal MCA signal (severe). Results: There were 14 patients (31.8%) who showed NW and 16 patients (36.3%) who showed poor outcomes. Nine of the 14 patients with NW showed poor outcomes (64.2%). The most frequent lesions in the present study were SCS (n = 16, 36.3%), followed by IBZ (n = 12, 27.2%) and DPI (n = 11, 25.0%). Prevalence of IBZ was significantly higher in the group with NW compared to that without NW (p = 0.0081), while the prevalence of SCS, DPI, PAI and CBZ did not differ between the two groups. Logistic regression analysis showed significantly high age- and sex-adjusted odds ratios (ORs) for NW only for IBZ (OR 10.9, p = 0.0051). The degree of stenosis did not correlate with NW and lesion patterns. Conclusions: Only IBZ among various lesion patterns correlated strongly with NW. IBZ are considered to be more associated with hemodynamic compromise, while embolic pathogeneses contribute more to CBZ or SCS. Early interventional medical treatments such as thrombolytic or anti-platelet therapy or stenting should be considered in cases of IBZ in MCA stenosis.

Cortical border-zone infarcts: clinical features, causes and outcome

ObjectiveTo report the clinical features, causes and outcome of cerebral cortical border-zone infarcts BZI (C-BZI).MethodsThe authors prospectively included patients with MRI-confirmed C-BZI among individuals consecutively admitted in Stroke Unit.ResultsForty-five patients...

Response to Letter by Phan et al

HomeStrokeVol. 37, No. 11Response to Letter by Phan et al Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Letter by Phan et al Seok Woo Yong Oh Young Bang Seok Woo YongSeok Woo Yong Department of Neurology, Ajou University School of Medicine, Suwon, South Korea Search for more papers by this author Oh Young BangOh Young Bang Department of Neurology, Stroke and Cerebrovascular Center, Samsung Medical Center, Sungkyunkwan University School of Medicine,, Seoul, South Korea Search for more papers by this author Originally published21 Sep 2006https://doi.org/10.1161/01.STR.0000244813.13221.ccStroke. 2006;37:2659Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 21, 2006: Previous Version 1 Response:We thank Dr Phan and his colleagues for their comments. They pointed out that the relationship between internal border-zone (IBZ) infarcts and severe carotid artery stenosis/occlusion has not been demonstrated in some studies. As we mentioned in our article, this inconsistency is likely to have resulted from (a) not using diffusion-weighted imaging (DWI) and (b) not considering the stenosis of the middle carotid artery.1 The articles that Dr Phan et al mentioned are no exception.We agree that stroke topography does not equate with stroke mechanism, ie, hemodynamic versus nonhemodynamic. In addition, it may be difficult to separate these 2 mechanisms of stroke because a synergic association of these 2 mechanisms has been postulated.2 As Phan et al commented, the use of hemodynamic and nonhemodynamic mechanisms rather than the topographic terms for border-zone infarcts may be more ideal. However, the pathological and imaging characteristics of border-zone infarcts are well described and easily recognizable in clinical practice, while it is impossible to perform comprehensive workups in all patients with border-zone infarcts. More importantly, different types of border-zone infarcts may require different therapeutic approaches. In a previous analysis of DWI lesion patterns, an unstable hospital course (often with enlargement of the infarct) and poor long-term outcome were frequently observed in patients with IBZ infarcts, whereas recurrent strokes after the index stroke were more common in those who had small superficial infarcts, including cortical border-zone (CBZ) infarcts. These findings suggest that the DWI lesion pattern is helpful in recognizing the likely differences in the early prognostic end points after ischemic stroke, and the topographic approach may guide targeted interventions to prevent negative outcomes.3Concerning the topographic approach, it is well known that the vascular territories can vary greatly across individuals, which might cause a territorial infarct to be misinterpreted as a border-zone infarct. However, almost every article on border-zone infarcts has used the topographic site as the definition. (How else could one define a border-zone infarction?) This is perhaps an inherent limitation of all studies of border-zone infarction.The significant difference in the degree of stenosis (Figure 2 in the article1) was not the sole evidence that led us to propose different mechanisms in the 2 stroke groups. We also found that patients with IBZ infarcts had fewer small cortical infarcts outside the border-zone territory, and more often assumed a rosary pattern, both of which indicate that IBZ infarction is closely related to hemodynamic compromise. Recently, a comprehensive review of cerebral perfusion studies examined the mechanisms of border-zone infarcts in carotid disease.4 It showed that although severe hemodynamic compromise appears to underlie combined CBZ and IBZ infarction, artery-to-artery embolism might play an important role in isolated CBZ infarcts. Although Phan et al worry about there being insufficient evidence to rule out embolic sources, we believe that the differences we have put forward for the 2 groups strongly indicate that these 2 stroke syndromes have different pathogeneses. Increasing applications of diffusion- and perfusion-weighted imaging and microemboli detection using transcranial Doppler ultrasonography may allow a better understanding of the mechanisms of border-zone infarcts.DisclosuresNone.1 Yong SW, Bang OY, Lee PH, Li WY. Internal and cortical border-zone infarction: clinical and diffusion-weighted imaging features. Stroke. 2006; 37: 841–846.LinkGoogle Scholar2 Caplan LR, Hennerici M. Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Arch Neurol. 1998; 55: 1475–1482.CrossrefMedlineGoogle Scholar3 Bang OY, Lee PH, Heo KG, Joo US, Yoon SR, Kim SY. Specific DWI lesion patterns predict prognosis after acute ischaemic stroke within the MCA territory. J Neurol Neurosurg Psychiatry. 2005; 76: 1222–1228.CrossrefMedlineGoogle Scholar4 Momjian-Mayor I, Baron JC. The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke. 2005; 36: 567–577.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails November 2006Vol 37, Issue 11 Advertisement Article InformationMetrics https://doi.org/10.1161/01.STR.0000244813.13221.cc Originally publishedSeptember 21, 2006 PDF download Advertisement

Internal and Cortical Border-Zone Infarction

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. 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. 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 (P=0.008) and exhibited a rosary-like pattern of infarction more frequently (P<0.001). In contrast, concomitant small cortical infarcts were observed more frequently in CBZ infarct patients (P<0.001). 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 (P=0.002 and P=0.003, respectively). IBZ infarcts are caused mainly by hemodynamic compromise, whereas embolic pathogenesis appears to contribute greatly to the genesis of CBZ infarcts. Patients with IBZ infarcts showed poor early and late clinical courses. Our findings suggest that different therapeutic approaches may be required to prevent early clinical deterioration in patients with different types of border-zone infarcts.

Cobalt-55 positron emission tomography in symptomatic atherosclerotic carotid artery disease: borderzone versus territorial infarcts

Background: Borderzone as well as territorial infarcts can occur in severe atherosclerotic carotid artery disease. It remains controversial whether the borderzone distribution of infarcts is due to hypoperfusion or due to artery-to-artery embolism. Purpose: The present study investigates whether cobalt-55 ( 55Co) positron emission tomography (PET) shows a different pattern of ischaemia according to the topography of the infarct in severe atherosclerotic carotid artery disease. Patients and methods: Five patients with a cortical borderzone and seven with a territorial infarct, due to symptomatic carotid artery disease, were investigated with 55Co PET 3–6 months after stroke. Average 55Co counts in the infarct area, the adjacent cortical zone, the deep white matter and, contralateral cerebral cortex and white matter, were compared to the values in the cerebellum used as reference. Results: No differences in 55Co ratio were observed in the different regions of interest (ROIs) between patients with cortical borderzone and those with territorial infarcts. The 55Co uptake was similar or lower than the reference value for all ROIs in all individual patients. Conclusion: In patients with borderzone as well as with territorial infarcts no evidence was found for subclinical ischaemic injury in or around the infarcts. These data do support the conclusion that cortical borderzone infarcts may not be due to ongoing chronic haemodynamic impairment, but by no means is this conclusive evidence.

Cerebral hypoperfusion induces cortical watershed microinfarcts which may further aggravate cognitive decline in Alzheimer's disease

Increasing number of data, including the existence of common risk factors, indicate an association between cerebrovascular disease and Alzheimer's disease (AD). AD is known to be often associated with cerebral hypoperfusion. Recent histopathological evidence showed a significant association between watershed cortical microinfarcts and AD indicating that cerebral hypoperfusion induces not only white matter damage, known as leuko-araiosis, but cortical border zone infarcts as well, further aggravating the degenerative process and worsening dementia. In late stages of Alzheimer's disease - in cases with neuropathologically confirmed definite AD - the occurrence of watershed cortical microinfarcts was ten times higher than in aged matched control cases. Congophilic angiopathy and perturbed hemodynamic factors were found to be important factors in the genesis of watershed microinfarcts. To consider the vulnerability of the cerebral blood flow and the perturbed cortical vascular network in AD is important. Neuroleptic and sedative treatments frequently employed in AD may further accentuate cerebral hypoperfusion by decreasing blood pressure. Therefore, to treat and prevent arterial hypotension and maintain cerebral perfusion at an appropriate level in AD is essential.

Atherothrombotic middle cerebral artery territory infarction: topographic diversity with common occurrence of concomitant small cortical and subcortical infarcts.

MRI has superior capabilities for the detection of cerebral infarcts compared with CT. CT was used to locate infarcts in most previous studies of atherothrombotic middle cerebral artery (MCA) territory infarcts. Thus, there was a possibility of missing concomitant small infarcts. More accurate identification of topographic lesions in MCA territory with MRI may help to establish the pathogenesis of stroke. The present study determines topographic patterns, distribution of vascular lesions, and probable mechanisms. Forty-two patients with MCA territory infarcts on routine MRI and no major cause of cardioembolism were studied with conventional angiography or MR angiography. The topographic patterns seen on MRI were subdivided into 4 groups: cortical border-zone infarcts (n=6), pial territory infarcts without insular infarct (n=3), pial territory infarcts with insular infarct (n=14), and large subcortical infarcts (n=19). Of 6 patients with cortical border-zone infarcts, 4 had concomitant small cortical or subcortical multiple lesions. Angiography showed intrinsic MCA disease in 4 patients. Of 3 patients with pial territory infarcts without insular infarct, 2 also had small multiple centrum ovale lesions. All had intrinsic MCA disease. Pial territory infarcts with partial or whole insular lesions were present in 10 and 4 patients, respectively. Five patients had additional multiple cortical or subcortical lesions. Ten patients had intrinsic MCA disease. Of the 19 patients with large subcortical infarcts, 12 had centrum ovale infarcts, and 4 had both basal ganglia and centrum ovale lesions. Ten had concomitant small cortical or subcortical lesions. Six patients had intrinsic MCA disease. Similar vascular lesions induce different topographic patterns in MCA territory infarction, which are related to individual vascular variability, degree of primary and secondary collateralization, and pathogenesis of infarcts. Our study indicates that concomitant small cortical or subcortical lesions are also commonly associated findings in diverse patterns of MCA territory infarction, which can mostly be explained by probable embolic mechanism.

Comparison of CT in patients with cerebral ischaemia with or without non-rheumatic atrial fibrillation. European Atrial Fibrillation Trial and Dutch T I A Trial Study Groups.

In an attempt to distinguish between the CT characteristics of strokes of presumed cardioembolic origin and strokes caused by arterial disease, a comparison was made between the baseline CT of two prospective cohorts of patients with transient ischaemic attack or minor ischaemic stroke, with (n = 985) or without (n = 2987) non-rheumatic atrial fibrillation (NRAF). Of the patients with NRAF 54% had evidence of cerebral infarction v 41% of the controls (patients with sinus rhythm (SR); odds ratio (OR) 1.7; 95% confidence interval (95% CI) 1.4-1.9). Patients with NRAF more often had multiple infarcts (OR 1.4; 95% CI 1.1-1.8), and more often infarcts that were not related to current neurological symptoms (OR 1.5; 95% CI 1.2-1.8). For symptomatic infarcts, patients with NRAF more often had cortical end zone infarcts (OR 3.1; 95% CI 2.6-3.8) and cortical border zone infarcts (OR 1.9; 95% CI 1.3-2.9) than patients with SR. Conversely, symptomatic small deep infarcts (lacunae) were more often seen in patients with SR (OR 3.9; 95% CI 2.8-5.4). Multivariate analyses showed that all these findings were independent of differences in baseline characteristics between the two study groups. The CT characteristics overlapped and did not allow a reliable distinction between cardioembolic and atherosclerotic causes of stroke in patients with NRAF.