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Background: We studied the evolution over time of diffusion weighted imaging (DWI) lesion volume and the factors involved on early and late infarct growth (EIG and LIG) in stroke patients undergoing endovascular treatment (EVT) according to the final revascularization grade. Methods: This is a prospective cohort of patients with anterior large artery occlusion undergoing EVT arriving at 1 comprehensive stroke center. Magnetic resonance imaging was performed on arrival (pre-EVT), Results: We included 98 patients (mean age 70, median National Institutes of Health Stroke Scale score 17, final mTICI≥2b 86%). Median EIG and LIG were 48 and 63.3 mL in patients with final mTICIρ =0.667; P ρ =0.614; P Conclusions: Infarct grows during and after EVT, especially in nonrecanalizers but also to a lesser extent in recanalizers. In recanalizers, number of passes and DWI volume influence EIG, while number of passes, DWI, and hypoperfused volume after the procedure determine LIG.

Introduction: We aimed to evaluate venous delay before and after treatment as a marker of radiological and clinical outcome in stroke patients receiving endovascular treatment (EVT). Methods: Prospective cohort of patients with anterior intracranial occlusion undergoing EVT. Brain MRI was performed on arrival (pre-EVT), Results: From 98 included patients (median NIHSS 17, final mTICI≥2b 86%), 89 pre-EVT dMRIs and 88 post-EVT dMRIs were evaluable. The median venous delay pre-EVT and post-EVT were -31.9[-58.1;-16.7]% and -13.5[-34.5;-7.5]%, respectively. Venous delay pre-EVT was not related to infarct volume or clinical outcome. When final mTICI≥2B, venous asymmetry decreased but still persisted. For each 10% of increment in venous delay post-EVT, there was an adjusted increase of 0.12[0.05-0.19]ml in the final infarct volume. Venous delay post-EVT was independently associated with mRS at 90 days (cOR 1.013 [95%CI 1.001-1.0256]). Conclusion: Cortical vein delay assessed after but not before EVT, is associated with a larger final infarct volume and with a worse clinical outcome.

A risk for developing progressive multifocal leukoencephalopathy is a major barrier to natalizumab use. Extended dosing intervals have been proposed as a way to maintain therapeutic efficacy and reduce progressive multifocal leukoencephalopathy incidence. This is the first reported case of progressive multifocal leukoencephalopathy in a patient using an extended dosing regimen (300 mg/6 weeks). A close clinical and imaging monitoring allowed early detection, which is a major prognostic factor. A favorable outcome was seen with a therapy comprising plasma exchange therapy, mirtazapine, mefloquine and cidofovir. Further studies will be needed to assess the potential role of extended dosing intervals to improve prognosis in patients receiving natalizumab and also to measure its impact clinically and/or radiologically.

a b s t r a c t Background and purpose: The ongoing population-based Barcelona-Asymptomatic Intracranial Atherosclerosis (Barcelona-AsIA) study is a prospective study that plans to investigate the natural his- tory of asymptomatic intracranial atherosclerosis (AsIA) in a Caucasian-Mediterranean population, which remains unknown until now. The present study aims to determine the prevalence of AsIA and associated risk factors in the final study cohort. Methods: Crossover, population-based study of a representative sample (randomly selected from our ref- erence population) older than 50 with a moderate-high vascular risk assessed by the vascular equation REGICOR and prior history of neither stroke nor ischemic heart disease. Anthropometric, demographic, clinical data and blood samples were collected at baseline. All individuals underwent a complete extracra- nial and transcranial color-coded duplex (TCCD) examination. TCCD criteria were used to identify and classify the degree of intracranial stenoses. Results: A total of 933 subjects (64% men, mean age 66.3 years) were included in the study. One or more intracranial stenoses were detected at baseline in 80 subjects (8.6%) of whom 31 (3.3%) had moderate- severe lesions. The higher the REGICOR scores the greater the prevalence of AsIA (6.6%, 10.2% and 25% for REGICOR scores 5-9, 10-14 and ≥15, p < 0.001). Diabetes (OR 2.95; 95% CI (1.68-5.18); p < 0.001), age (OR 1.05; 95% CI (1.02-1.08); p = 0.001) and hypertension (OR 1.78; 95% CI (1.02-3.13); p = 0.04) were independently associated with any degree of AsIA, while diabetes (OR 2.85; 95% CI (1.16-6.96); p = 0.02) and age kept independently associated with moderate-severe AsIA. Conclusion: The prevalence of AsIA and moderate-severe AsIA in stroke-free Caucasians with a moderate- high vascular risk were 8.6% and 3.3% respectively. Diabetes and age were independently associated with moderate-severe AsIA.

Background: Hyperintensity of distal vessels on FLAIR-MRI has been associated with a higher grade of arterial collaterals and a smaller infarct volume in acute stroke patients. No studies analyze the influence of the hyperintense vessel (HV) sign on the speed of the ischemia progression during the first hours. Our aim was to study the association of the HV sign with progression of infarction in acute stroke patients. Methods: From a prospectively derived stroke database, we retrospectively selected acute stroke patients with a large artery occlusion of the anterior circulation admitted to our comprehensive stroke center with available baseline CT scan and a multimodal MRI carried out thereafter to make a decision about endovascular treatment. Progression of the ischemic area was calculated as the difference in the Alberta Stroke Program Early CT Scan (ASPECTS) score between CT scan and diffusion-weighted imaging (DWI). Slow progression was considered as no change or 1 point decrease on the ASPECTS score between both exams. The presence of HV on FLAIR sequence was graded as absent, subtle or prominent by two readers. Results: A total of 70 patients were included in the study. Mean time between baseline CT and MRI was 124 ± 82 min. ASPECTS score on baseline CT was 10 in 34% of patients, 9 in 49% and 8 or less in 17%. ASPECTS score was 2 (1–3) points lower in the DWI and this decrease did not correlate with the time elapsed between the two exams. Distal HV sign was observed in 57/70 (81%) patients (subtle in 33 and prominent in 24). HV was more frequently observed in patients with proximal artery occlusion. There were no differences regarding stroke severity, stroke subtype and ASPECTS score on baseline CT between groups. Patients with prominent HV showed a lower progression of the ischemic area [median ASPECTS score decrease, 1 (1–0)] compared with patients with subtle HV [median ASPECTS score decrease, 2 (2–1)] and patients with absence of HV [median ASPECTS score decrease, 3 (4–3)] (p < 0.001). Prominent HV was independently associated with slow progression of ischemia in a multivariate logistic regression analysis adjusted by systolic blood pressure on admission, site of occlusion and time elapsed between both neuroimaging exams compared to the absence of HV (OR, 16.2; 95% CI, 2.1–123.1) and to subtle HV sign (OR, 6.1; 95% CI, 1.5–23.9). Conclusion: HV sign on FLAIR, especially if prominent, is associated with a slow progression of the ischemic area in acute stroke patients with cerebral artery occlusion of the anterior circulation. This radiological sign may predict the speed of the ischemia progression, opening an opportunity for reperfusion therapies in longer time windows.

e14039Background: GBM is associated with a uniformly poor prognosis. The evaluation of response to treatment by MRI is imperfect some results may difficulties to deciding changing treatment. We ana...

OBJECTIVE. Spontaneous rectus sheath hematoma can become clinically relevant and necessitate hemostatic intervention. The aim of this study was to describe the efficacy of percutaneous arterial embolization in the management of this condition.CONCLUSION. Selective transcatheter embolization is effective hemostatic treatment of patients with large, clinically relevant rectus sheath hematoma.

The proven efficacy and safety of medical ozone therapy remains controversial [1–6]. In rats, ozone inhalation was shown to promote neuronal activation in stress-responsive regions of the central nervous system (CNS) [7], electrical activity alterations and changes in brain major neurotransmitter systems [8, 9]. We here describe two patients who developed cortical blindness and seizures shortly after intraarticular ozone infiltrations. There is only a prior report of top of the basilar stroke and Anton syndrome following ozone therapy [10]. A 75-year-old man complained of dizziness, slurred speech, tingling in the left extremities and visual loss, which developed 10 min after receiving a paravertebral ozone therapy session and autohemotherapy for spondylarthrosis. On admission he was fully aware with left neglect, cortical blindness, left central facial paralysis, and numbness and mild weakness of the left extremities. A brain magnetic resonance imaging (MRI) scan showed subcortical/juxtacortical white matter chronic ischemic lesions in the right cerebral hemisphere without evidence of acute lesions (Fig. 1a). Stenosis of the distal branch of the left cerebral posterior artery and a severe stenosis of the right carotid artery on MR angiograms were found. An EEG showed an alpha rhythm (8 Hz) predominantly in the left posterior region and a slow attenuated delta rhythm in the right hemisphere. A Tc-ECD brain SPECT showed bilateral hypoperfusion areas particularly in the left occipitotemporal region (Fig. 2). Twenty-four hours later, the patient presented visual hallucinations, various episodes of forced oculocephalic deviation to the left, clonus on left extremities and a tonic–clonic seizure. He was successfully treated with valproic acid and levetiracetam. A brain MRI performed 7 days later showed one small juxtacortical subacute ischemic lesion in the right occipital lobe (Fig. 1b). A 60-year-old woman presented with posterior cortical blindness and history of a tonic–clonic seizure, which developed shortly after intraarticular infiltration of ozone and procaine for the treatment of a left shoulder joint disease. On admission she was disoriented with repetitive speech, anterograde memory impairment and cortical blindness. The brain MRI showed a right acute ischemic cerebellar lesion (Fig. 1c). The EEG showed slowed brain D. V. Rolan (&) J. L. B. Cunat J. V. Hervas D. Escudero Neuroscience Department, Hospital Universitari Germans Trias i Pujol, Universitat Autonoma de Barcelona, Carretera de Canyet s/n, 080916 Badalona, Barcelona, Spain e-mail: doloviro@hotmail.com

Background: Laterality of the posterior cerebral artery (LPCA) in acute stroke has been related with a better leptomeningeal collateral circulation and with improved functional outcome at 6 months in patients treated with IV tPA. We aim to study the association between LPCA and the amount of brain tissue at risk of infarction in patients with anterior circulation arterial occlusion. Methods: From our prospective database of ischemic stroke we selected patients with anterior circulation arterial occlusion who underwent multimodal MRI < 12h of symptom onset. We considered LPCA when the following criteria were accomplished: a) ipsilateral PCA to the occlusion site was extended in 1 or more segments compared to the contralateral PCA and b) ipsilateral P4 segment was visible on axial TOF images. Two independent readers blinded to clinical data retrospectively assessed the presence of LPCA (k=0.65). We analyzed the association between LPCA and the volume of ischemic penumbra at baseline (Tmax>6s) and the final infarct volume (CT 24h). Good outcome was defined as mRS ≤ 2 at 90 days. Results: Seventy-two patients were included in the study (mean age 67y, 45% male). LPCA was present in 39 (54.1%). There were no differences between groups with or without LPCA, except a lower baseline NIHSS in the LPCA group (15 vs 19; p=0.003). Proportion of patients treated with reperfusion therapies was similar between groups. Patients with LPCA had a smaller lesion in Tmax>6s (54 vs 79cc; p=0.02), smaller final infarct volume (47 vs 111cc; p=0.013), and higher proportion of good outcome (52.8% vs 27.3%; p=0.03). In a multivariate analysis, LPCA was independently associated with smaller lesion volume on Tmax>6s (B -18, IC95% [-36,-0.3]), smaller final infarct volume (B -64.8, IC95% [-100,-29]) and better clinical outcome (OR 4.66, IC95% [1.04,20.8]). Conclusion: LPCA sign in patients with anterior circulation arterial occlusion is associated with smaller volume of brain tissue at risk resulting in smaller infarct volume and better clinical outcome. These findings suggest favorable leptomeningeal collaterals.

Background and Purpose— Intracranial atherosclerotic disease (ICAD) remains a challenge for stroke primary and secondary prevention. Molecular pathways involved in the development of ICAD from its asymptomatic stages are largely unknown. In our population-based study, we aimed to compare the risk factor and biomarker profiles associated with intracranial and extracranial asymptomatic cerebral atherosclerosis. Methods— The Asymptomatic Intracranial Atherosclerosis (AsIA) study cohort includes a random sample population of 933 white subjects >50 years with a moderate to high vascular risk (based on REGICOR score) and without a history of stroke (64% males; mean age, 66 years). Carotid and intracranial atherosclerosis were screened by cervical and transcranial color-coded Duplex ultrasound, being moderate to severe stenoses confirmed by MR angiography. We registered clinical and anthropometric data and created a biobank with blood samples at baseline. A panel of biomarkers involved in atherothrombogenesis was determined: C-reactive protein, asymmetric-dimethylarginine, resistin, and plasminogen activator inhibitor-1. Insulin resistance was quantified by Homeostasis Model Assessment index. Results— After multinomial regression analyses, male sex, hypertension, smoking, and alcoholic habits were independent risk factors of isolated extracranial atherosclerotic disease. Diabetes and metabolic syndrome conferred a higher risk for ICAD than for extracranial atherosclerotic disease. Moreover, metabolic syndrome and insulin resistance were independent risk factors of moderate to severe ICAD but were not risk factors of moderate to severe extracranial atherosclerotic disease. Regarding biomarkers, asymmetric-dimethylarginine was independently associated with isolated ICAD and resistin with combined ICAD–extracranial atherosclerotic disease. Conclusions— Our findings show distinct clinical and biological profiles in subclinical ICAD and extracranial atherosclerotic disease. Insulin resistance emerged as an important molecular pathway involved in the development of ICAD from its asymptomatic stage.