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BACKGROUND: Data on P2Y12 inhibitors responsiveness from the middle east is scarce. We sought to investigate patient responsiveness to P2Y12 inhibitors within a cohort of major races that characterize the UAE population. The secondary objective was to assess risk factors for hyper and hypo-responsiveness in this population. METHODS: We conducted a cross-sectional study on adults who received either clopidogrel or ticagrelor treatments and had platelet responsiveness testing before undergoing neuro-endovascular interventions at our quaternary care hospital between March 2015 and April 2019. RESULTS: During the study period, 249 subjects met the inclusion criteria. Overall, 17.3 % were hyper-responsive and 25.7 % were hypo-responsive to P2Y12 inhibitors. When comparing between the P2Y12 inhibitors, rates of hyper-responsiveness were significantly higher to ticagrelor when compared to clopidogrel (11 versus 6 %, p = 0.02 respectively). Contrarily, hypo-responsiveness rates were significantly higher in clopidogrel treated patients compared to their ticagrelor treated counterparts (23 versus 2 %, p < .001 respectively). Patients of Middle-Eastern origin showed a significantly higher rate of hypo-responsiveness to both clopidogrel and ticagrelor when compared to other races (41.1 % and 26.7 %, P < 0.001 respectively). Asians showed the highest rates of hyper-responsiveness for both agents. Multivariate logistic regression analysis showed that proton pump inhibitors and statin combination, (OR: 6.39, 95 %CI [1.60, 25.392]), and Middle East vs. Indian subcontinent patients (OR: 4.67, 95 %CI [1.79-12.14]) were independent predictors of hypo-responsiveness to both P2Y12 inhibitors. CONCLUSION: This study demonstrated a high rate of hypo-responsiveness to P2Y12 inhibitors in a UAE cohort of patients undergoing neuro-endovascular procedures. In addition, therapeutic responsiveness to P2Y12 inhibitors varied markedly based on the racial background. Future larger studies are needed to evaluate genetic variations that may contribute to this rate of hypo-responsiveness in our population.

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Primary Angiitis of the Central Nervous System (PACNS) is an uncommon disease with kaleidoscopic clinical manifestations. Ischemic strokes are commoner than their hemorrhagic counterpart. Intracranial pseudoaneurysms are rarely reported in PACNS cohorts. We hereby describe the case of a 39-year-old female, who presented for evaluation of acute onset of left middle cerebral artery (MCA) ischemic stroke, with cerebral angiogram showing multifocal stenosis and irregularities in intracranial blood vessels with an aneurysm arising from the lenticulostriate branch of the left MCA M1 segment. A diagnosis of probable PACNS was made and patient initiated on immunomodulatory treatment with corticosteroids. 12 weeks follow up neuroimaging studies revealed resolution of the previously described intracranial aneurysm, thereby postulating the possibility of a pseudoaneurysm related to the underlying angiitis.

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Intracranial non-galenic pial arteriovenous fistula (PAVF) is an extremely rare vascular malformation, where one or more pial arteries feeds directly into a cortical vein without any intervening nidus. Though occasionally they can be asymptomatic, neurological symptoms such as headache, seizure, or focal neurological deficit are more common presenting features. Life threatening or fatal hemorrhage is not uncommon, hence needed to be treated more often than not. Spontaneous occlusion of PAVF is reported only four times before. We report a 49-year-old gentleman, who was diagnosed to have a PAVF, possibly secondary to trauma. He presented 5 months and 22 days from initial digital subtraction angiography (DSA) for treatment, and follow-up angiogram showed complete obliteration. He denied any significant event, medication or alternate treatment during this period. His clinical symptoms were stable as well. We postulate iodinated contrast medium induced vasculopathy as a possible cause, which has been described for other vascular pathologies, but never for PAVF.

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Fibromuscular dysplasia (FMD) is a rare idiopathic, segmental, noninflammatory and nonatherosclerotic arteriopathy of medium-sized arteries. It is classically considered to be a disease of young and middle adulthood, with females more commonly affected than males. FMD is a systemic disease. Although historically considered to be rare, cerebrovascular FMD (C-FMD) has now been recognized to be as common as the renovascular counterpart. Extracranial carotid and vertebral arteries are the most commonly involved vascular territories in C-FMD with the clinical presentation determined by vessels affected. Common symptoms include headaches and pulsatile tinnitus, with transient ischemic attacks, ischemic stroke and subarachnoid or intracerebral hemorrhage constituting the more severe clinical manifestations. Cervical artery dissection involving carotids more often than vertebral arteries and intracranial aneurysms account for the cerebrovascular pathologies detected in C-FMD. Our understanding regarding C-FMD has been augmented in the recent past on account of dedicated C-FMD data from North American, European and other international FMD cohorts. In this review article, we provide an updated and comprehensive overview on epidemiology, clinical presentation, etiology, diagnosis and management of C-FMD.

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Varicella-zoster virus (VZV) infection is notorious for central nervous system involvement, the spectrum of which encompasses vasculopathic manifestations as well. Central nervous system VZV vasculopathy (CVV) most commonly manifests as ischemic strokes or TIA, even though other less common modes of presentation are also well documented in the literature. The pathophysiological mechanism is primarily attributed to active virus infection in the blood vessels secondary to decline in varicella-specific cell-mediated immunity. More than one-third of those with CVV do not have preceding skin lesions of zoster. Hence, a high index of clinical suspicion should be entertained in the appropriate clinical scenario. We hereby describe the case of a 40-year-old lady with systemic lupus erythematosus on long-term oral steroids who presented with acute ischemic stroke involving the right PCA territory, with asymptomatic chronic infarcts in the left MCA. Further evaluation revealed concentric vessel enhancement involving right PCA on high-resolution MR vessel wall imaging with the "Moya-Moya" phenomenon on the left supraclinoid ICA/MCA segment. CSF showed mononuclear pleocytosis with a hemorrhagic component, along with positive VZV DNA PCR. A diagnosis of "CNS VZV Vasculopathy sine herpete" was made and the patient was initiated on appropriate management.

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Primary Sjogren's Syndrome (PSS) is an autoimmune exocrinopathy, with protean manifestations affecting multiple organ systems. Neurological manifestations are documented in about 20% of PSS cohorts in literature, with peripheral manifestations being commoner. Central nervous system manifestations of PSS (CNS-SS) encompass ischemic strokes, demyelinating lesions, aseptic meningitis, encephalitis, cerebellar ataxia, cognitive impairment and movement disorders. Ischemic stroke as presenting manifestation of PSS is extremely rare. We hereby describe a 50-year-old male, who presented for evaluation of 2 episodes of discrete focal neurological deficits over a duration of 6 weeks, with neuro-imaging findings revealing evidence of acute-subacute bihemispheric infarcts. Further evaluation revealed evidence of strongly positive anti phospholipid antibodies (aPL), indirect immunofluorescence antinuclear antibody (IIF-ANA), anti Sjögren's syndrome-A (SS-A/Ro) and anti-Ribonuclear protein (RNP) antibodies, with histopathological evidence of periductal and periacinar lymphocytic infiltration as well as acinar atrophy and interstitial fibrosis of minor salivary glands on lip biopsy, consistent with a diagnosis of Sjögren's syndrome, constituting a diagnosis of Antiphospholipid syndrome (APS) associated with PSS.

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ABSTRACT: Guillain-Barre Syndrome (GBS) is an acute inflammatory polyradiculoneuropathy which can lead to rapid neuromuscular respiratory failure, with an estimated annual incidence of 1-2 per 100,000 person-years. Even though cranial nerve involvement is known to occur in GBS, radiological correlation on neuroimaging studies are less frequently reported in pediatric population. We hereby report the case of a 14-year-old boy with acute motor axonal neuropathy variant of GBS, who had extensive contrast enhancement of multiple cranial nerves on Magnetic Resonance Imaging brain, associated with clinicoradiological dissociation on presentation.

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BACKGROUND: Non-contrast CT (NCCT) brain imaging biomarkers of hematoma expansion in intracerebral hemorrhage (ICH) has gained relevance in recent times. Though intra-hematoma hypodensities (IHH) can predict hematoma expansion and outcome, it is postulated to be time-dependent. AIM: To assess the differential prevalence of IHH in spontaneous ICH over time and assess its predictive valve in early hematoma expansion and functional outcome at 3 months. MATERIAL AND METHODS: Patients with ICH within 48 h of stroke onset were included. Baseline clinical and demographic data were collected. Baseline NCCT brain was analyzed for hematoma volume, characterization of IHH, with 24-hours follow-up NCCT hematoma volume calculated for identification of hematoma expansion. Poor functional outcome was defined as mRS ≥3. RESULTS: Around 92 subjects were included in the study. IHH was found in 40%. Prevalence of IHH was higher in those with baseline NCCT performed within 3 h of symptom onset compared to those beyond 3 h (71% vs 29%, P = 0.002). The hematoma expansion was more common in patients with IHH compared to those without (54% vs 29%; P = 0.02). Multivariate analysis revealed the presence of IHH (rather than pattern or number) to be strongly associated with poor functional outcome at 3 months (OR 3.86; 95% CI: 1.11-13.42, P = 0.03). CONCLUSION: There is a decreasing prevalence of IHH as the time from symptom onset to NCCT increases. Nevertheless, its presence is significantly associated with hematoma expansion and predicted poor short-term functional outcomes in spontaneous ICH.

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BACKGROUND: Cerebral microbleed (CMB) is a novel neuroimaging marker of cerebral small vessel disease. OBJECTIVE: To determine the prevalence of CMB in the subtypes of acute ischemic minor stroke (AIS) and transient ischemic attack (TIA) and to identify the risk factors associated with location and number of CMB. MATERIALS AND METHODS: Patients with AIS (National Institute of Health Stroke Scale of 5 or less) or TIA were included. CMB was characterized using the Microbleed Anatomical Rating Scale (MARS). RESULTS: Of the 488 subjects [mean age (standard deviation): 57.5 years (14.4 years), males (77.7%)] recruited, CMB was noted in 140 (28.7%). About 35% with CMB had a lacunar stroke etiology, whereas LAA and CE subtype constituted 33.6 and 10.7%, respectively (P = 0.000). Lacunar subtype was more likely to harbor multiple CMB (four or more) and CMB in all locations (lobar, deep or infratentorial). On multivariate analysis, systemic hypertension [P = 0.025; odds ratio (OR) 0.33 (95% confidence interval (CI) 0.129-0.874)], serum triglyceride (TG) levels below 150 mg/dL [P = 0.001; OR 3.70 (95% CI 1.698-8.072)], and presence of white matter hyperintensities on magnetic resonance imaging brain [P = 0.026; OR 2.18 (95% CI 1.096-4.337)] were associated with the presence of CMB. Those with serum TG levels of less than 150 mg/dL were more likely to harbor lobar (P = 0.002) or infratentorial CMB (P = 0.022), whereas those with serum creatinine levels of more than1.5 mg/dL have lobar CMB (P = 0.033). CONCLUSION: Our study showed a differential distribution of CMB in ischemic stroke subtypes and association of risk factors with the presence, number and location of CMB.

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OBJECTIVE: To compare ischemic and hemorrhagic stroke patients with COVID-19 to non-COVID-19 controls, and to describe changes in stroke admission patterns during the pandemic. METHODS: This is a single center, retrospective, observational study. All consecutive patients admitted with primary diagnosis of ischemic/ hemorrhagic stroke between March1st -May10th 2020 were included and compared with the same time period in 2019. RESULTS: There was a 41.9% increase in stroke admissions in 2020 (148 vs 210,P = .001). When comparing all ischemic strokes, higher rate of large vessel occlusion (LVO) (18.3% vs 33.8%,P = .008) and significant delay in initiation of mechanical thrombectomy after hospital arrival (67.75 vs 104.30 minutes,P = .001) was observed in 2020. When comparing all hemorrhagic strokes, there were no differences between the two years. Among 591 COVID-19 admissions, 31 (5.24%) patients with stroke including 19 with ischemic (3.21%) and 12 with hemorrhagic stroke (2.03%) were identified. Patients with COVID-19 and ischemic stroke were significantly younger (58.74 vs 48.11 years,P = .002), predominantly male (68.18% vs 94.74%,P = .016), had lesser vascular risk factors, had more severe clinical presentation (NIHSS 7.01 vs 17.05,P < .001), and higher rate of LVO (23.6% vs. 63.1%,P = .006). There was no difference in the rate of endovascular thrombectomy, but time to groin puncture was significantly longer in COVID-19 patients (83.41 vs 129.50 minutes,P = .003). For hemorrhagic stroke, COVID-19 patients did not differ from non-COVID-19 patients. CONCLUSIONS: Stroke continues to occur during this pandemic and stroke pathways have been affected by the pandemic. Stroke occurs in approximately 5% of patients with COVID-19. COVID-19 associated ischemic stroke occurs in predominantly male patients who are younger, with fewer vascular risk factors, can be more severe, and have higher rates of LVO. Despite an increase in LVO during the pandemic, treatment with mechanical thrombectomy has not increased. COVID-19 associated hemorrhagic stroke does not differ from non-COVID-19 hemorrhagic stroke patients.

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The mechanisms and phenotype of ischemic stroke associated with coronavirus disease 2019 (COVID-19) remain uncertain. A retrospective study was conducted in patients with COVID-19 presenting with ischemic stroke from March 1 to May 25, 2020, and cases with large-vessel occlusion were identified. To provide baseline institutional stroke data within and outside the COVID-19 pandemic, all consecutive ischemic stroke and TIA admissions (COVID and non-COVID) to the hospital during a 10-week period from March 1 to May 10, 2020, were collected and compared with data from the same time period in 2019. Among 20 patients with COVID-19 and acute ischemic stroke, 15 (75%) had large-vessel occlusion. These patients were young (mean age, 46.5 years), male (93%), without major burden of traditional cardiovascular risk factors, and had a severe stroke presentation. Large-vessel occlusions were observed in multiple vessels (40%), uncommonly affected vessels, and atypical locations with a large thrombus burden. Systemic thrombosis separate from large-vessel occlusion was not uncommon (26%). At short-term follow-up, stroke etiology remained undetermined in 46% of patients and functional outcome was poor. The above findings raise the possibility of stroke related to mechanisms induced by the COVID-19 infection itself, including a hypercoagulable state and/or endothelial damage. In addition, they document the severe presentation and poor outcomes of large-vessel occlusion in COVID-19 ischemic stroke.

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