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Pediatric stroke is considered an infrequent complication of COVID-19. Focal cerebral arteriopathy (FCA) is one of the most common causes of arterial ischemic stroke in a previously healthy child. The present report describes a toddler with FCA most likely induced by SARS-CoV-2 infection who showed significant clinical improvement that may be related to injection of intra-arterial nimodipine. To our knowledge, this is the first reported use of nimodipine in this setting. • This report describes a toddler with FCA most likely induced by SARS-CoV-2 infection. • We describe significant clinical improvement possibly related to injection of intra-arterial nimodipine. • To our knowledge, this is the first reported use of nimodipine in this setting. • Efficacy and safety of intra-arterial nimodipine administration warrants further investigation. [ABSTRACT FROM AUTHOR]

• Various factors may affect oligoclonal bands detection in the cerebrospinal fluid. • Steroid treatment before lumber puncture did not affect oligoclonal bands detection. • Prior clinical events and pleocytosis were correlated with oligoclonal bands detection. • Oligoclonal bands are a marker of long-standing inflammation in multiple sclerosis. Detection of oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) is important for diagnosis of multiple sclerosis (MS). Previous studies reported that treatment with intravenous methylprednisolone (IVMP) before lumber puncture (LP) could suppress OCBs production. The aim of this study was to assess whether IVMP initiation prior to CSF collection affects OCBs results in patients with an acute demyelinating event. Additionally, we examined which clinical characteristics are associated with the presence of OCBs in the CSF. We retrospectively evaluated patients admitted to the neurology department at rabin medical center (RMC) between 2010 and 2022 who underwent LP with OCBs analysis as part of their demyelinating attack workup. Patients were divided into OCB-positive and OCB-negative groups and demographical and clinical characteristics (including timing and duration of acute steroid treatment and history of prior demyelinating attacks) were analyzed for association with OCBs results. A total of 342 patients were included with a median age of 35 years (IQR, 27–46). Two hundred thirty-eight (69.6 %) were OCB-positive. Initiation of IVMP before LP was not associated with negative OCBs (11.8 % Vs. 13.5 %, P = 0.721), nor was it correlated with OCBs positivity (OR=0.86, P = 0.66). CSF cell count was higher in OCB-positive patients (5 Vs. 3, P = 0.001), and a history of prior demyelinating attacks was associated with- (33.6 % Vs. 20.2 %, P = 0.014) and predictive of OCBs positivity (OR=2, P = 0.013). Timing of steroids was not associated with OCB positivity. However, pleocytosis and a prior attack were associated with OCB positivity in this cohort. Our results suggest that steroid treatment is unlikely to affect OCBs results. Ideally, larger prospective studies would be needed to confirm our observations. [ABSTRACT FROM AUTHOR]

Bilateral thalamic infarction (BTI) typically presents as a sleep-like coma (SLC) without localizing signs, posing a diagnostic challenge that may lead the treating physician to search for toxic or metabolic causes and delay treatment. We review our experience with BTI of different etiologies, and emphasize the critical role of timely imaging, diagnosis, and management in a series of 12 patients with a presentation of SLC and acute BTI who were managed in our Medical Centers from 2006–2015. In 11/12, urgent head CT scans showed normal brain tissue, while diffusion-weighted (DWI) MRI revealed symmetric bilateral thalamic hyperintense lesions with variable degrees of brainstem involvement. In 1/12, CT scans revealed a contralateral subacute stroke from a thalamic infarct 1 month earlier with a unilateral hyperintense lesion on DWI-MRI. From clinical and imaging findings (DWI-MRI, CT angiography and venography), etiology was attributed to embolic causes (cardio-embolism, artery-to-artery mechanism), small vessel disease, or deep sinus vein thrombosis secondary to dural arteriovenous (AV) fistula. Three patients had good outcomes after prompt diagnosis and optimal treatment in <3 hours (intravenous tissue plasminogen activator in two patients cardio-embolic etiology and neuro-endovascular repair in one patient with venous infarction due to a dural AV fistula). The diagnosis was made beyond the therapeutic window in seven patients, who were left with significant neurological sequelae. Higher awareness of BTI presenting as SLC is warranted. Optimal patient management includes urgent DWI-MRI. In cases of BTI, further imaging workup is indicated to provide a comprehensive assessment for etiology. Early diagnosis and prompt, targeted intervention are crucial. [ABSTRACT FROM AUTHOR]

Background: Loss of cortical grey matter is a diagnostic marker of many neurodegenerative diseases, and is a key mediator of cognitive impairment. We postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposits, is associated with cortical tissue loss independent of parenchymal Alzheimer's disease pathology. We tested this hypothesis in patients with hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-D), a monogenetic disease with minimal or no concomitant Alzheimer's disease pathology, as well as in patients with sporadic CAA and healthy and Alzheimer's disease controls.Methods: In this observational case-control study, we included six groups of participants: patients diagnosed with HCHWA-D using genetic testing; healthy controls age-matched to the HCHWA-D group; patients with probable sporadic CAA without dementia; two independent cohorts of healthy controls age-matched to the CAA group; and patients with Alzheimer's disease age-matched to the CAA group. De-identified (but unmasked) demographic, clinical, radiological, and genetic data were collected at Massachusetts General Hospital (Boston, MA, USA), at Leiden University (Leiden, Netherlands), and at sites contributing to Alzheimer's Disease Neuroimaging Initiative (ADNI). The primary outcome measure was cortical thickness. The correlations between cortical thickness and structural lesions, and blood-oxygen-level-dependent time-to-peak (BOLD-TTP; a physiological measure of vascular dysfunction) were analysed to understand the potential mechanistic link between vascular amyloid and cortical thickness. The radiological variables of interest were quantified using previously validated computer-assisted tools, and all results were visually reviewed to ensure their accuracy.Results: Between March 15, 2006, and Dec 1, 2014, we recruited 369 individuals (26 patients with HCHWA-D and 28 age-matched, healthy controls; 63 patients with sporadic CAA without dementia; two healthy control cohorts with 63 and 126 individuals; and 63 patients with Alzheimer's disease). The 26 patients with HCHWA-D had thinner cortices (2·31 mm [SD 0·18]) than the 28 healthy controls (mean difference -0·112 mm, 95% CI -0·190 to -0·034, p=0·006). The 63 patients with sporadic CAA without dementia had thinner cortices (2·17 mm [SD 0·11]) than the two healthy control cohorts (n=63, mean difference -0·14 mm, 95% CI -0·17 to -0·10, p<0·0001; and n=126, -0·10, -0·13 to -0·06, p<0·0001). All differences remained independent in multivariable analyses. The 63 patients with Alzheimer's disease displayed more severe atrophy than the patients with sporadic CAA (2·1 mm [SD 0·14], difference 0·07 mm, 95% CI 0·11 to 0·02, p=0·005). We found strong associations between cortical thickness and vascular dysfunction in the patients with HCHWA-D (ρ=-0·58, p=0·003) or sporadic CAA (r=-0·4, p=0·015), but not in controls. Vascular dysfunction was identified as a mediator of the effect of hereditary CAA on cortical atrophy, accounting for 63% of the total effect.Interpretation: The appearance of cortical thinning in patients with HCHWA-D indicates that vascular amyloid is an independent contributor to cortical atrophy. These results were reproduced in patients with the more common sporadic CAA. Our findings also suggest that CAA-related cortical atrophy is at least partly mediated by vascular dysfunction. Our results also support the view that small vessel diseases such as CAA can cause cortical atrophy even in the absence of Alzheimer's disease, a conclusion that can help radiologists, neurologists, and other clinicians who diagnose these common geriatric conditions.Funding: National Institutes of Health. [ABSTRACT FROM AUTHOR]