Search

Background and purposeAlberta Stroke Program Early Computed Tomographic Score (ASPECTS) has been used to estimate diffusion-weighted imaging (DWI) lesion volume in acute stroke. We aimed to assess correlations of DWI-ASPECTS with lesion volume in different middle cerebral artery (MCA) subregions and reproduce existing ASPECTS thresholds of a malignant profile defined by lesion volume ≥100 mL.MethodsWe analyzed data of patients with MCA stroke from a prospective observational study of DWI and fluid-attenuated inversion recovery in acute stroke. DWI-ASPECTS and lesion volume were calculated. The population was divided into subgroups based on lesion localization (superficial MCA territory, deep MCA territory, or both). Correlation of ASPECTS and infarct volume was calculated, and receiver-operating characteristics curve analysis was performed to identify the optimal ASPECTS threshold for ≥100-mL lesion volume.ResultsA total of 496 patients were included. There was a significant negative correlation between ASPECTS and DWI lesion volume (r=-0.78; P

Early neurological deterioration (END) in lenticulostriate artery (LSA) infarction is associated with perforating artery hypoperfusion. As middle cerebral artery (MCA) tortuosity may alter hemodynamics, we investigated the association between MCA tortuosity and END in LSA infarction. We reviewed patients with acute LSA infarction without significant MCA stenosis. END was defined as an increase of ≥ 2 or ≥ 1 in the National Institutes of Health Stroke Scale (NIHSS) total or motor score, respectively, within first 72 h. The MCA tortuosity index (actual /straight length) was measured. Stroke mechanisms were categorized as branch atheromatous disease (BAD; lesions > 10 mm and 4 axial slices) and lipohyalinotic degeneration (LD; lesion smaller than BAD). Factors associated with END in LD and BAD were investigated. END occurred in 104/390 (26.7%) patients. A high MCA tortuosity index (adjusted odds ratio, aOR 10.63, 95% confidence interval [2.57–44.08], p = 0.001) was independently associated with END. In patients with BAD, high initial NIHSS score (aOR 1.40 [1.03–1.89], p = 0.031) and presence of parental artery disease (stenosis < 50%; aOR 10.38 [1.85–58.08], p = 0.008) were associated with END. In patients with LD, high MCA tortuosity (aOR 41.78 [7.37–237.04], p < 0.001) was associated with END. The mechanism causing END in patients with LD and BAD may differ. [ABSTRACT FROM AUTHOR]

Two different stroke mechanisms are involved in small vessel disease: branch atheromatous disease (BAD) and lipohyalinotic degeneration (LD). We compared mechanisms of stroke in lenticulostriate arteries (LSA) vs. anterior pontine arteries (APA) and verified factors associated with stroke mechanisms, including shape of middle cerebral artery (MCA) and basilar artery (BA). We retrospectively reviewed patients with acute ischemic stroke with penetrating artery territory confirmed by MRI. The mechanisms of stroke were categorized based on diffusion-weighted imaging; BAD was defined as lesion larger than 10 mm in LSA and lesions involving basal pontine in APA. Other lesions were classified as LD. The shapes of MCA and BA were classified as straight, with one angle, or with two angles (U, C or S shape, respectively) using anterior–posterior view. The study included 221 patients. LD was more common in LSA infarcts, but BAD was more common in APA infarcts (p < 0.001). Low initial National Institutes of Health Stroke Scale [Adjusted Odds ratio (aOR) = 0.78; p < 0.001], absence of hyperlipidemia [aOR = 0.31; p = 0.002], previous statin use [aOR = 4.35; p = 0.028] LSA infarcts [reference = APA territory; aOR = 11.07; p < 0.001], and S-shaped vessels (reference = straight shaped vessels; aOR = 3.51; p = 0.004) were independently associated with LD. Angulations in the mother vessels may be more associated with true small vessel disease more with LD than BAD. [ABSTRACT FROM AUTHOR]

Background: Clinical syndromes secondary to infarcts in the distal basilar artery (BA) area have been described as "top of the basilar" (TOB) syndrome. However, in the era of advanced imaging technology, it has been realized that the clinical and imaging features are quite diverse in patients with distal BA occlusion. The aim of the present study was to investigate the patterns and clinical outcomes of TOB assessed with modern images and categorize TOBs accordingly. Additionally, we examined the possible influence of the posterior communicating artery (PcoA) on the patterns of TOB. Methods: Patients with distal BA occlusion on magnetic resonance angiography were categorized as TOB-A, and those with multiple lesions in the distal BA territory on diffusion-weighted magnetic resonance imaging as TOB-L. Patients with angiographically and lesion distribution-defined TOB were classified as having TOB-A&L; those with angiographically defined TOB as having TOB-A without TOB-L; and those with lesion distribution-defined TOB as having TOB-L without TOB-A. The PcoA was categorized as "textbook-type" (good P1) and "fetal-type" (absent P1). Factors associated with unfavorable short-term outcomes (modified Rankin Scale 5–6 at discharge), and 1-year and long-term mortalities, were assessed. Results: Of 1,466 patients with ischemic stroke in the posterior circulation who were admitted to Asan Medical Center within 24 h of symptom onset, 124 (8.5%) had TOB, including 45 with TOB-A&L, 44 with TOB-A, and 35 with TOB-L. NIHSS scores (21 [9.5–26] vs. 6 [3–11.5] vs. 6 [3–9]; p < 0.01) and rates of motor deficit (75.6 vs. 54.5 vs. 34.4%; p < 0.01), concomitant pontine lesions (17.8 vs. 25.0 vs. 2.9%; p < 0.01), PcoA presence (44.4 vs. 68.2 vs. 25.7%; p < 0.01), and unfavorable short-term outcomes (62.2 vs. 25.0 vs. 14.3%; p < 0.01) differed significantly in the 3 patient groups. Multivariate analysis showed that textbook-type PcoA was independently associated with a lower frequency of unfavorable short-term outcomes (OR 0.15, 95% CI 0.03–0.70). Reperfusion therapy (hazard ratio [HR] 0.25, 95% CI 0.07–0.89) and the presence of textbook-type PcoA (HR 0.20, 95% CI 0.05–0.90) were associated with a lower 1-year mortality rate after stroke. Conclusion: Patterns and clinical outcomes of TOB vary and are affected by the hemodynamic status of the arterial system, such as BA recanalization and the presence of textbook-type PcoA. [ABSTRACT FROM AUTHOR]

Background: Lateral medullary infarction (LMI) is not an uncommon disease. Although lesions are usually restricted to the lateral medullary area, some patients have additional infarcts in other parts of the brain. The clinical features and prognosis of isolated LMI (pure LMI, LMIpr) have been investigated. However, it remains unclear whether clinical characteristics, prognosis and factors associated with prognosis differ between patients with LMIpr and those with additional lesions (LMI plus, LMIpl). Methods: Patients with LMI identified by MRI were enrolled. The demographic and clinical characteristics, in-hospital outcome (intensive care unit [ICU] admission, pneumonia and modified Rankin scale [mRS] at discharge), and long-term residual symptoms (vertigo/dizziness, sensory disturbances, dysphagia) and outcomes (occurrence of stroke, acute coronary syndrome [ACS], death, and mRS at follow-up) were compared between LMIpr and LMIpl patients. Factors associated with poor functional outcome (mRS 2–6) at the follow-up were analyzed. Results: Among 248 LMI patients, 161 (64.9%) had LMIpr and 87 (35.1%) had LMIpl. During admission, patients with LMIpl more frequently experienced ICU care, pneumonia and had a higher discharge mRS (3 vs. 2; p < 0.001) than LMIpr patients. The occurrence of stroke, ACS, frequency of death and functional outcome was not different during follow-up. However, residual neurologic symptoms such as dizziness (p = 0.002), dysphagia (p = 0.04) and sensory symptoms (p < 0.001) were more frequent in LMIpr than in LMIpl patients. In LMIpr patients, the rostral location of LMI was associated with poor functional outcome (p = 0.041), whereas in LMIpl patients, the presence of medial posterior-inferior cerebellar artery lesion was associated with good functional outcome (p = 0.030). Conclusion: Although the short-term outcome is poorer in LMIpl than LMIpr patients, long-term residual symptoms are more common in LMIpr patients. The location of the LMI and extra-medullary lesion affects the long-term functional outcome of LMIpr and LMIpl patients respectively. [ABSTRACT FROM AUTHOR]

Background: Decompressive hemicraniectomy reduces secondary brain injury related to brain edema and increased intracranial pressure (ICP) in patients with malignant middle cerebral artery infarction (MMI). However, a substantial proportion of patients still die despite hemicraniectomy due to refractory brain swelling. Objective: We aim to investigate whether ICP measured immediately after hemicraniectomy may indicate decompression effects and predict survival in patients with MMI. Methods: We included 25 patients with MMI who underwent ICP monitoring and brain computed tomography within the first hour of hemicraniectomy. Midline shifts were measured as radiological surrogates of decompression. The Glasgow Coma Scale and pupillary enlargements during the first day after hemicraniectomy were assessed as clinical surrogates of decompression. Long-term survival status at 6 months was used as the final outcome. We analyzed the relationships between early ICP and findings of midline shift, Glasgow Coma Scale, pupillary enlargement, and survival. Results: Initial ICP was correlated with mean ICP (P < .001) and maximal ICP (P < .001) during the first postoperative day. Intracranial pressure was associated with midline shifts (P = .009), lower Glasgow Coma Scale scores (P = .025), and the pupillary enlargement (P = .015). Sixteen (64.0%) patients survived at 6 months. In a Cox proportional hazard model, elevated ICP was associated with mortality at 6 months (hazard ratio: 1.13; 95% confidence interval: 1.03-1.24; P = .008). Conclusion: Increase in ICP soon after hemicraniectomy was associated with midline shift, poor neurological status, and mortality in patients with MMI. Measurements of ICP soon after hemicraniectomy may permit earlier interventions as well as more refined clinical assessments. [ABSTRACT FROM AUTHOR]

Background: The stroke mechanism for anterolateral pontine infarction (ALPI) is poorly understood. We aimed to investigate the perforator arteries relevant to ALPI using highresolution MRI (HR-MRI). Methods: Of 62 patients with ALPI who were admitted to the Asan Medical Center, 13 patients agreed to participate in this study. We used HR-MRI with a 3-Tesla scanner and assessed the perforating branches directly connected with the infarcted area. Results: Perforating arteries penetrating ALPI were identified in all 13 patients. Perforators arising from the basilar artery (BA) were involved in the stroke mechanism in 9 patients, the superior cerebellar artery (SCA) perforator in 1 patient, and the anterior inferior cerebellar artery perforator in 1 patient. In 2 patients, both BA and SCA perforators were involved. Conclusions: Using 3-Tesla HR-MRI may allow visualization of the perforating branches presumably related to ALPI. Identification of the relevant cerebral perforating arteries may help us to understand the stroke mechanism in patients with posterior circulation territory infarction. [ABSTRACT FROM AUTHOR]

Abstract: It remains unknown whether subacute lesion volume increase is related to neurologic progression (NP) and clinical outcome (CO) in patients with single subcortical infarct (SSI) in the middle cerebral artery (MCA) territory. We studied 77 patients who underwent diffusion-weighted MRI (DWI) within 48 h after stroke onset, which revealed unilateral SSI in the MCA territory, and follow-up DWI and MR angiography within 7 days of onset. Neurologic progression was defined as the increase of the National Institutes of Health Stroke Scale (NIHSS) score by ≥2 during the first week. Clinical outcome was dichotomized as good (≤2) and poor (≥3) according to the modified Rankin Scale at 1 month after the onset. Lesion volume increase was defined when the infarct volume in the follow-up MRI exceeds the initial one by either ≥30% or 50%. Fourteen patients (18.2%) had NP, and 17 (22.1%) had poor CO. Increase in lesion volume, found in 42 patients (54.5%) when defined by 50% increase and in 51 (66.2%) by 30%, was significantly associated with NP (50%, p =0.010; 30%, p =0.027) and poor CO (50%, p =0.040; 30%, 0.111). Multivariate logistic analyses revealed that lesion volume increase was independently related to NP (odd ratio, 8.48; 95% CI, 1.55–46.46) and that NP was the important predictor for poor CO (odd ratio, 39.69; 95% CI, 3.44–458.68). We conclude that subacute lesion volume growth is closely related to the NP and that the NP predicts subsequent poor CO. [Copyright &y& Elsevier]

Background Ischemic lesions dynamically evolve during the acute phase of stroke. Although the ischemic lesion volume has been considered as a predictor of clinical outcome, it is still controversial whether early changes in ischemic lesion have prognostic information in addition to clinical variables. We hypothesized that early infarct growth on diffusion-weighted imaging (DWI) might be independently associated with long-term outcome in acute ischemic stroke patients. Methods This was a prospective study for acute ischemic stroke patients admitted to the Stroke Unit of Asan Medical Center. The patients underwent DWI at baseline (within 24 h) and subsequently at 5 days after stroke onset. Early infarct growth was defined as the absolute difference between follow-up and baseline infarct volumes. Poor outcome was a modified Rankin Scale (mRS) at 3 months of 2–6 or 3–6. The association between infarct growth on DWI and clinical outcome was explored using multivariate analysis adjusting for demographics, risk factors for stroke, and other clinical variables. The cut-off values of early infarct growth predicting long-term outcomes were estimated using receiver operating characteristic analysis. Results Of 409 patients enrolled, 345 (84.4%) showed any infarct growth (median, 0.63 cm 3 ; interquartile range [IQR], 0.11–6.33 cm 3 ; mean ± standard deviation, 9.55 ± 25.54 cm 3 ). At the 3-month follow-up, the good outcomes were observed in 217 patients (53.1%) for mRS 0–1 and 303 patients (74.1%) for mRS 0–2. The larger infarct growth was associated with poor clinical outcome (for mRS 2–6, 0.29 cm 3 [IQR 0.04–2.19] vs. 2.16 cm 3 [IQR 0.26–17.68], p < 0.001; and for mRS 3–6, 0.39 cm 3 [IQR 0.05–3.25] vs. 7.36 cm 3 [IQR 0.57–26.48], p < 0.001). After adjusting age, diabetes, baseline National Institutes of Health Stroke Scale, and baseline infarct volume by multivariate logistic regression analysis, infarct growth was an independent predictor of poor clinical outcomes (for mRS 2–6, odds ratio [OR], 1.03, 95% confidence interval [CI], 1.004–1.06, p = 0.03; and for mRS 3–6, OR, 1.03, 95% CI, 1.01–1.05, p = 0.01). The cut-off values of infarct growth discriminating between good and poor outcomes were 0.99 cm 3 for mRS 0–1 vs. 2–6 (area under curve, 0.685; P < 0.001) and 8.86 cm 3 for mRS 0–2 vs. 3–6 (area under curve, 0.736; P < 0.001). Conclusions Our present study findings show that infarct growth within a week of onset independently predicts 3-month clinical outcomes. This suggests that short-term changes in infarct volume may serve as a surrogate marker of long-term clinical outcomes after ischemic stroke. [ABSTRACT FROM AUTHOR]

Abstract: Ibudilast, a non-selective phosphodiesterase inhibitor, is clinically used in patients with stroke or dizziness. However, whether the compound exerts a beneficial effect on acute ischemic stroke remains to be established. We used a rat model of transient focal cerebral ischemia using middle cerebral artery occlusion (MCAO) and reperfusion, and explored the effects of ibudilast on infarction size, brain edema, atrophy, and nerve cell death. Neurological outcomes (behavior and mortality) of rats were also assessed. An intravenous administration of ibudilast attenuated the size of cerebral infarction in a dose-dependent manner, with the most significant reduction achieved at the dose of 10mg/kg. Ibudilast induced a significant reduction in infarct size when administered 30min before MCAO or 0–2h after reperfusion, with the largest reduction observed at 30min before MCAO and 1h after reperfusion. Ibudilast significantly attenuated brain edema formation, cerebral atrophy and apoptosis of nerve cells preferentially in the cortical penumbra area, and also significantly reduced mortality and improved neurological outcomes. Expression of various inflammatory mediator molecules in both hemispheres was markedly suppressed by ibudilast. We conclude that ibudilast exerts beneficial effects against acute brain ischemia in an animal model. [Copyright &y& Elsevier]

Abstract: Background: An acute perfusion–diffusion mismatch is known to be the strongest predictor of infarct growth. However, the differential patterns of clinical and radiological evolution according to stroke mechanism are unknown. Methods: The study retrospectively reviewed consecutive patients who had 1) acute middle cerebral artery (MCA) territory infarction, 2) diffusion- and perfusion-weighted imaging (DWI and PWI) and MR angiography within 24 h of onset, and follow-up DWI 5 days later, 3) stenosis (≥50%) or occlusion of MCA on baseline imaging, 4) a baseline PWI–DWI mismatch >20%, and 5) either atherosclerotic MCA disease (MCAD) or cardioembolism (CE). National Institutes of Health Stroke Scale (NIHSS) scores and infarct volume at baseline and 5 days were obtained. Results: Of 90 patients, 52 had MCAD and 38 had CE. At baseline, CE group had more severe stroke (median NIHSS, 9 vs. 5; p =0.001) and larger infarct volume (median 8.32 cc vs. 3.0 cc; p =0.034) than MCAD group. During the 1-week period, CE group had larger infarct volume growth (median 12.85 cc vs. 3.02 cc; p =0.004) than MCAD group, although clinical improvement based on NIHSS (baseline minus 5-day) tended to be higher for CE than MCAD group (median 3 vs. 1; p =0.08). The correlation between infarct volume and NIHSS score was stronger in CE (r =0.841) compared to MCAD (r =0.582) group at 5-day. Conclusions: Substantial differences in the clinico-radiological evolution of acute ischemic stroke exist according to stroke mechanism. These data emphasize the importance of the stroke mechanism in the design of MRI-based acute stroke trials. [Copyright &y& Elsevier]