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Background: Up to 20% of lacunar infarcts are clinically misdiagnosed as cortical infarcts and vice versa. The reasons for this discrepancy are unclear. We assessed clinical and imaging features which might explain this ‘clinical-imaging dissociation’ (C-ID). Methods: Patients with an acute stroke syndrome (cortical or lacunar) underwent magnetic resonance imaging including diffusion-weighted imaging (DWI). We recorded DWI-positive infarcts and proximity to cortex for small subcortical infarcts. We examined factors associated with C-ID. Results: 137 patients with a mild cortical or lacunar syndrome had an acute ischemic lesion on DWI. Of these, 21/93 (23%) with a cortical syndrome had an acute lacunar infarct and 7/44 (16%) with a lacunar syndrome had an acute cortical infarct. From 72 patients with an acute lacunar infarct on DWI, lesion proximity to cortex (odds ratio (OR) 14.5, 95% confidence interval (CI) 1.61–130.1), left hemisphere location (OR 8.95, 95% CI 1.23–64.99) and diabetes (OR 17.1, 95% CI 1.49–196.16) predicted C-ID. On multivariate analysis of all 137 patients, C-ID was associated with diabetes (OR 7.12, 95% CI 1.86–27.2). Conclusions: C-ID occurs in a fifth of patients with mild stroke. Lacunar infarcts lying close to cortex are more likely to cause cortical symptoms. Diabetes is associated with any clinical-imaging mismatch. Stroke misclassification which can arise with clinical classification alone should be minimized in research by verification with high-sensitivity imaging.

We recently generated a high-resolution supratentorial vascular topographic atlas using diffusion-weighed MRI in a population of large artery infarcts. These MRI-based topographic maps are not easily applicable to CT scans, because the standard-reference-lines for axial image orientation (i.e., anterior-posterior commissure line versus orbito-meatal line, respectively) are ‘not parallel’ to each other. Moreover, current, widely-used CT-based vascular topographic diagrams omit demarcation of the inter-territorial border-zones. Thus, we aimed to generate a CT-specific high-resolution atlas, showing the supratentorial cerebrovascular territories and the inter-territorial border-zones in a statistically rigorous way. The diffusion-weighted MRI lesion atlas is based on 1160 patients (67.0 ± 13.3 years old, 53.7% men) with acute (<1-week) cerebral infarction due to significant (>50%) stenosis or occlusion of a single large cerebral artery: anterior, middle, or posterior cerebral artery. We developed a software package enabling the transformation of our MR-based atlas into a re-oriented CT space corresponding to the axial slice orientations used in clinical practice. Infarct volumes are individually mapped to the three vascular territories on the CT template-set, generating brain maps showing the voxelwise frequency of infarct by the affected parent vessel. We then mapped the three vascular territories collectively, generating a dataset of Certainty-Index (CI) maps to reflect the likelihood of a voxel being a member of a specific vascular territory. Border-zones could be defined by using either relative infarct frequencies or CI differences. The topographic vascular territory atlas, revised for CT, will allow for easier and more accurate delineation of arterial territories and borders on CT images.

BackgroundA common-stem origin of lenticulostriate arteries (CS-LSAs) is an anatomical variation that supplies a moderate to large section of the basal ganglia. We hypothesized that CS-LSAs with a patent orifice are located at distal positions of the acute-occluded middle cerebral artery (MCA) and that the blood flow of CS-LSAs is supplied by pail arterial anastomoses and results in hypoperfusion of CS-LSAs, similar to a deep watershed (DWS) infarction.ObjectiveOur study evaluated the possibility of CS-LSAs in patients with DWS infarction and MCA occlusion and also assessed the safety of endovascular therapy (ET) in these patients.MethodsA cohort of consecutive patients with DWS infarction and MCA occlusion and in whom full recanalization via ET was achieved were identified. Patients were divided into two groups based on the presence of CS-LSAs observed during ET. In addition, radiological and clinical data were retrospectively analyzed.ResultsThirty-three patients were included, and CS-LSAs were observed in 48.5% (16/33) of patients. The possibility (72.2%, 13/18) of CS-LSAs was high in patients with DWS infarction companied with basal ganglia infarction. A good clinical outcome was similar in patients with CS-LSAs and basal ganglia infarction and in patients without CS-LSAs and basal ganglia infarction (69.2% vs. 81.8%, P = 0.649).ConclusionsThe possibility of CS-LSAs was 48.5% in patients with DWS infarction and MCA occlusion, and the revascularization procedure was safe and feasible in these patients despite the moderate-to-large basal ganglia infarction.

Among patients with occlusion of a large intracerebral vessel who had a clinical deficit that was disproportionately severe relative to the infarct volume, 90-day outcomes for disability were better with late thrombectomy plus standard care than with standard care alone.

White matter hyperintensities (WMH) are prevalent. Although arteriolar disease has been implicated in their pathogenesis, venous pathology warrants consideration. We investigated relationships of WMH with histologic venous, arteriolar and white matter abnormalities and correlated findings with premortem neuroimaging. Three regions of periventricular white matter were sampled from archived autopsy brains of 24 pathologically confirmed Alzheimer disease (AD) and 18 age-matched nonAD patients. Using trichrome staining, venous collagenosis (VC) of periventricular veins (<150 µm in diameter) was scored for severity of wall thickening and occlusion; percent stenosis by collagenosis of large caliber (>200 µm) veins (laVS) was measured. Correlations were made between WMH in premortem neuroimaging and vascular and white matter pathology. We found greater VC (U(114) = 2092.5, p = 0.005 and U(114) = 2121.5, p = 0.002 for small and medium caliber veins, respectively) and greater laVS (t(110) = 3.46, p = 0.001) in patients with higher WMH scores; WMH scores correlated with VC (rs(114) = 0.27, p = 0.004) and laVS (rs(110) = 0.38, p < 0.001). By multiple linear regression analysis, the strongest predictor of WMH score was laVS (β = 0.338, p < 0.0001). VC was frequent in patients with periventricular infarcts identified on imaging. We conclude that periventricular VC is associated with WMH in both AD and nonAD patients and the potential roles of VC in WMH pathogenesis merit further study.

Objective: To evaluate the diagnostic accuracy of cranial ultrasound (CUS) for detection of neonatal arterial territory cerebral infarction in term infants. Methods: CUS scans from term infants with neonatal magnetic resonance imaging (MRI) evidence of neonatal infarction were reviewed. The scans were grouped by acquisition time after birth: 1–3 days (early) or 4–14 days (late). Results: Brain MRI showed infarction in the territory of the middle cerebral artery in 43 of 47 infants, anterior cerebral artery in one, and posterior cerebral artery in three. Twelve of the 47 had minor changes on MRI in the white matter in the contralateral hemisphere, and four infants had bilateral infarctions. The early CUS scans were abnormal in 68% of the infants; the late CUS scans were abnormal in 87%. The late CUS scans were correct for laterality and site of lesion in 25/47 (53%) infants. In six infants with smaller lesions of the cortical middle cerebral artery branch or lesions in the posterior cerebral artery territory, the CUS scans were persistently normal. Conclusion: Normal early CUS scans do not exclude a diagnosis of neonatal stroke, although most scans are abnormal. CUS scans performed after day 3 were abnormal in 87% of infants. CUS scan findings were accurate for lesion laterality and site in 53%, and, in 34%, the scans showed abnormality strongly suggestive of infarction but not always site specific. For optimal prognostic information, infants with clinical histories or CUS scan findings suggestive of infarction should have a neonatal brain MRI scan.

BackgroundEmbolectomy is the standard of care for emergent large vessel occlusion (ELVO), and needs to be done as quickly as possible for the best possible outcomes. Optimization of workflow and process is certainly paramount. One aspect of this is process improvement to standardize as much as possible the procedure in order to decrease variability among operators, which breeds familiarity for the entire team.ObjectiveTo evaluate the impact of a standardized approach to ELVO cases in decreasing times from groin puncture to first deployment of a stent-retriever and final recanalization.MethodsA retrospective review of 83 consecutive patients consisting of a pre-standardization phase (group 1) and those after standardization (group 2). The standardization process involved all three neurointerventional radiologists agreeing on a standard approach to the cases and to the equipment to be used. Times from groin puncture to first deployment of the stent-retriever and from puncture to final reperfusion were evaluated. Angiographic outcomes were scored using the Modified Thrombolysis in Cerebral Ischemia (mTICI) score. Complications from intracranial catheter manipulation (such as wire perforation) were also recorded. Clinical outcomes were assessed based on admission and discharge National Institute of Health Stroke Scale score.ResultsThere were 22 patients in group 1 and 61 patients in group 2. Mean times from groin puncture to first deployment were 39.8 min in group 1 and 20 min in group 2, a difference which was statistically significant (p<0.0001). Overall times from puncture to final recanalization were reduced from 68.2 to 37 min, also a statistically significant difference (p<0.001). There were no cases of intraprocedural complications such as wire perforation or subarachnoid hemorrhage.ConclusionsA standardized approach to the equipment used and process for ELVO cases at a single institution can dramatically reduce procedure times.

In patients with acute stroke and a large infarct of unrestricted size, use of thrombectomy and medical care within 7 hours after symptom onset led to better functional outcomes and lower mortality than medical care alone.

Preclinical models of stroke have shown that intravenous glyburide reduces brain swelling and improves survival. We assessed whether intravenous glyburide (RP-1127; glibenclamide) would safely reduce brain swelling, decrease the need for decompressive craniectomy, and improve clinical outcomes in patients presenting with a large hemispheric infarction. For this double-blind, randomised, placebo-controlled phase 2 trial, we enrolled patients (aged 18–80 years) with a clinical diagnosis of large anterior circulation hemispheric infarction for less than 10 h and baseline diffusion-weighted MRI image lesion volume of 82–300 cm3 on MRI at 18 hospitals in the USA. We used web-based randomisation (1:1) to allocate patients to the placebo or intravenous glyburide group. Intravenous glyburide was given as a 0·13 mg bolus intravenous injection for the first 2 min, followed by an infusion of 0·16 mg/h for the first 6 h and then 0·11 mg/h for the remaining 66 h. The primary efficacy outcome was the proportion of patients who achieved a modified Rankin Scale (mRS) score of 0–4 at 90 days without undergoing decompressive craniectomy. Analysis was by per protocol. Safety analysis included all randomly assigned patients who received the study drug. This trial is registered with ClinicalTrials.gov, number NCT01794182. Between May 3, 2013, and April 30, 2015, 86 patients were randomly assigned but enrolment was stopped because of funding reasons. The funder, principal investigators, site investigators, patients, imaging core, and outcomes personnel were masked to treatment. The per-protocol study population was 41 participants who received intravenous glyburide and 36 participants who received placebo. 17 (41%) patients in the intravenous glyburide group and 14 (39%) in the placebo group had an mRS score of 0–4 at 90 days without decompressive craniectomy (adjusted odds ratio 0·87, 95% CI 0·32–2·32; p=0·77). Ten (23%) of 44 participants in the intravenous glyburide group and ten (26%) of 39 participants in the placebo group had cardiac events (p=0·76), and four of 20 had serious adverse events (two in the intravenous glyburide group and two in the placebo group, p=1·00). One cardiac death occurred in each group (p=1·00). Intravenous glyburide was well tolerated in patients with large hemispheric stroke at risk for cerebral oedema. There was no difference in the composite primary outcome. Further study is warranted to assess the potential clinical benefit of a reduction in swelling by intravenous glyburide. Remedy Pharmaceuticals.

Background and Purpose: Hemodynamic patterns after borderzone (BZ) infarction are variable and dynamic. However, stroke mechanisms in different types of BZ infarctions have not been systematically studied by magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD). Methods: Forty-nine patients who experienced a stroke limited to the territory of either the superficial or internal borderzone proved on MRI included in our registry, corresponding to 4% of 1,200 patients with ischemic stroke, were studied. All these patients underwent MRA, extracranial Doppler ultrasonography, TCD and other investigations from the standard protocol of our registry. Twenty of them (41%) had a posterior BZ infarct, 14 (29%) an anterior BZ infarct, 10 (20%) a subcortical BZ infarct and 5 (10%) bilateral BZ infarcts. Results: Unilateral internal carotid artery (ICA) tight stenosis or occlusion ipsilateral to the lesion was present in 14 patients (70%) with a posterior BZ infarct, in 72% of those with an anterior BZ infarct, in 80% of those with a subcortical BZ infarct and in 80% of those with bilateral BZ infarcts. TCD showed cross-filling of the middle cerebral artery via the anterior communicating artery in 5 patients (25%) with a posterior BZ infarct and 10% had an increased mean flow velocity (MFV) in the ipsilateral P1 posterior cerebral artery (PCA). In patients with an anterior BZ infarct, 3 (23%) had an MFV increase in the contralateral A1 anterior cerebral artery (ACA), and 2 (15%) had a higher MFV in the ipsilateral PCA. An elevated velocity at midline depths with reversed A1 ACA flow direction was seen in 2 patients (20%) with a subcortical infarct, and 1 patient (10%) had an MFV increase in the ipsilateral P1 PCA. Left ventricular systolic dysfunction (ejection fraction <40%) was present in 50% of patients with a posterior BZ infarct, in 36% of those with an anterior BZ infarct, in 20% of those with a subcortical BZ infarct and bilateral BZ infarcts each. Conclusion: The association of severe ICA stenosis or occlusion with cardiopathies and left ventricular dysfunction may play a critical role in those with BZ infarcts having inadequate collateral supply, while a cardioembolism or acute ICA dissection may also cause BZ infarction due to the rapidity of the occlusive process and the inability of the cerebral vasculature to recruit collateral pathways quickly enough.