Coronavirus disease 2019 (COVID-19) is a viral illness, caused by the novel severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). It is currently affecting millions of people worldwide and is associated with coagulopathy, both in the venous and arterial systems. The proposed mechanism being excessive inflammation, platelet activation, endothelial dysfunction, and stasis. As an ongoing pandemic declared by WHO in March 2020, health systems worldwide are experiencing significant challenges with COVID-19-related complications. It has been noticed that patients with COVID-19 are at greater risk of thrombosis.

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2. COVID-19-associated thrombotic events are recognized. A wide variety of neurological presentations have been recently documented. We report the first case of COVID-19 presenting with generalized seizure secondary to cerebral venous sinus thrombosis.

Background The association of cardiac wall motion abnormalities (CWMAs) in patients with stroke who have major adverse cardiovascular events (MACE) remains unclear. The purpose of this study was to estimate the 50‐month risk of MACE, including stroke recurrence, acute coronary events, and vascular death in patients with stroke who have CWMAs. Methods and Results We performed a retrospective analysis of prospectively collected acute stroke data (acute stroke and transient ischemic attack) over 50 months by electronic medical records. Data included demographic and clinical information, vascular imaging, and echocardiography data including CWMAs and MACE. Of a total of 2653 patients with acute stroke/transient ischemic attack, CWMA was observed in 355 (13.4%). In patients with CWMAs, the embolic stroke of undetermined source (50.7%) was the most frequent index stroke subtype and stroke recurrences ( P =0.001). In multivariate Cox regression after adjustment for demographics, traditional risk, and confounding factors, CWMA was independently associated with a higher risk of MACE (adjusted hazard ratio [HR], 1.74; 95% CI, 1.37–2.21 [ P =0.001]). Similarly, CWMA independently conferred an increased risk for ischemic stroke recurrence (adjusted HR, 1.50; 95% CI, 1.01–2.17 [ P =0.04]), risk of acute coronary events (aHR, 2.50; 95% CI, 1.83–3.40 [ P =0.001]) and vascular death (adjusted HR, 1.57; 95% CI, 1.04–2.40 [ P =0.03]), in comparison to the patients with stroke without CWMA. Conclusions In a multiethnic cohort of ischemic stroke with CWMA, CWMA was associated with 1.7‐fold higher risks of MACE independent of established risk factors. Embolic stroke of undetermined source was the most common stroke association with CWMA. Patients with stroke should be screened for CWMA to identify those at higher risk of MACE.

Malignant middle cerebral artery [MMCA] infarction has a different topographic distribution that might confound the relationship between lesion volume and outcome. Retrospective study to determine the multivariable relationship between computerized tomographic [CT] infarct location, volume and outcomes in decompressive hemicraniectomy [DHC] for MMCA infarction. The MCA infarctions were classified into four subgroups by CT, subtotal, complete MCA [co-MCA], Subtotal MCA with additional infarction [Subtotal MCAAI] and co-MCA with additional infarction [Co-MCAAI]. Maximum infarct volume [MIV] was measured on the pre-operative CT. Functional outcome was measured by the modified Rankin Scale [mRS] dichotomized as favourable 0–3 and unfavourable ≥4, at three months. In 137 patients, from least favourable to favourable outcome were co-MCAAI, subtotal MCAAI, co-MCA and subtotal MCA infarction. Co-MCAAI had the worst outcome, 56/57 patients with additional infarction had mRS ≥ 4. Multiple comparisons Scheffe test showed no significant difference in MIV of subtotal infarction, co-MCA, Subtotal MCAAI but the outcome was significantly different. Multivariate analysis confirmed MCAAI [7.027 (2.56–19.28), p = 0.000] as the most significant predictor of poor outcomes whereas MIV was not significant [OR, 0.99 (0.99–01.00), p = 0.594]. Other significant independent predictors were age ≥ 55 years 12.14 (2.60–56.02), p = 0.001 and uncal herniation 4.98(1.53–16.19), p = 0.007]. Our data shows the contribution of CT infarction location in determining the functional outcome after DHC. Subgroups of patients undergoing DHC had different outcomes despite comparable infarction volumes.

Since the arrival of the global COVID-19 pandemic scientists around the world have been working to understand the pathological mechanisms resulting from infection. There has gradually been an understanding that COVID-19 triggers a widespread endotheliopathy and that this can result in a widespread thrombosis and in particular a microthrombosis. The mechanisms involved in the microthrombosis are not confined to infection and there is evidence that patients with aneurysmal sub-arachnoid haemorrhage (SAH) also suffer from an endotheliopathy and microthrombosis. In this article we attempt to shed light on similarities in the underlying processes involved in both diseases and suggest potential treatment options.

In patients with acute ischemic stroke, pial collaterals play a key role in limiting neurological disability by maintaining blood flow to ischemic penumbra. We hypothesized that patient with poor pial collaterals will have greater corneal nerve and endothelial cell abnormalities. In a cross-sectional study, 35 patients with acute ischemic stroke secondary to middle cerebral artery (MCA) occlusion with poor (n = 12) and moderate-good (n = 23) pial collaterals and 35 healthy controls underwent corneal confocal microscopy and quantification of corneal nerve and endothelial cell morphology. In patients with MCA stroke, corneal nerve fibre length (CNFL) (P < 0.001), corneal nerve fibre density (CNFD) (P = 0.025) and corneal nerve branch density (CNBD) (P = 0.002) were lower compared to controls. Age, BMI, cholesterol, triglycerides, HDL, LDL, systolic blood pressure, NIHSS and endothelial cell parameters did not differ but mRS was higher (p = 0.023) and CNFL (p = 0.026) and CNBD (p = 0.044) were lower in patients with poor compared to moderate-good collaterals. CNFL and CNBD distinguished subjects with poor from moderate-good pial collaterals with an AUC of 72% (95% CI 53–92%) and 71% (95% CI 53–90%), respectively. Corneal nerve loss is greater in patients with poor compared to moderate-good pial collaterals and may act as a surrogate marker for pial collateral status in patients with ischemic stroke.

The anterior choroidal artery (AChA) is a small artery commonly arising from the supraclinoid segment of the internal carotid artery (ICA). The significance of the AChA is related to its strategic supply to various important structures of the brain, such as the optic tract, the posterior limb of the internal capsule, the cerebral peduncle, the lateral geniculate body, medial temporal lobe, medial area of pallidum, and the choroid plexus [<i>J Neurol</i>. 1988;235:387–91]. The AChA syndrome in its complete form consists of the triad of hemiplegia, hemisensory loss, and hemianopia. However, incomplete forms are more frequent in clinical practice [<i>Stroke</i>. 1994;25:837–42]. Isolated infarction in the AChA territory is relatively rare. The presumed pathogenic mechanisms of AChA infarction are cardiac emboli, large-vessel atherosclerosis, dissection of the ICA, small-vessel occlusion, or other determined or undetermined causes [<i>Stroke</i>. 1994;25:837–42 and <i>J Neurol Sci</i>. 2009;281:80–4].

Coronavirus disease 2019 (COVID-19) is a viral illness caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). There is worldwide emerging evidence of multisystem involvement including different neurological manifestations in COVID-19 patients. As a result, healthcare systems worldwide are not only experiencing diagnostic but also therapeutic and prognostic challenges with COVID-19-related complications. Cerebral microbleeds and leukoencephalopathy have been described in COVID-19 patients; although the mechanism remains unknown, possibilities include endotheliitis with thrombotic microangiopathy, excessive inflammation, prolonged respiratory failure, and hypoxemia. We describe here the clinical, radiological, and laboratory findings as well as the 90-day outcome of a 72-year-old gentleman who presented with severe SARS-CoV-2 infection, leading to diffuse cerebral microhemorrhages and ischemic infarct causing severe morbidity. He was tested positive for COVID-19 confirmed by reverse transcriptase polymerase chain reaction.