Background Progressive multifocal leukoencephalopathy (PML) is a severe demyelinating disease caused by JC polyomavirus (JCV), affecting immunocompromised individuals. We describe PML demographic, clinical, radiological, and laboratory characteristics and survival over time and according to underlying condition in a large retrospective patient cohort. Methods This is a retrospective cohort including Italian PML patients observed between 1987 and 2024, with known year of diagnosis and underlying disease. Results We included 456 cases with either a definite (n = 376, 82.4%) or clinico-radiological (n = 80, 17.6%) PML diagnosis. The relative frequency of human immunodeficiency virus (HIV)-associated cases decreased through four time periods (1987-1996; 1997-2004; 2005-2012; 2013-2024) from 99% to 43%, in parallel with increasing age (P < .0001), proportion of women (P < .001) and CD4(+) counts (P < .001) but not cerebrospinal fluid (CSF) or plasma JCV-DNA levels at diagnosis. One-year survival probability increased from 23.8% in 1987-1996 to 59.2% in 2013-2024, with highest values in natalizumab-treated multiple sclerosis (93.8%), followed by combination antiretroviral treatment (cART)-treated HIV infection (55%), hematological malignancies (50.8%), primary immunodeficiencies (41.3%), and cART-untreated HIV infection (11.9%). At multivariate analysis excluding cART-untreated people with HIV, JCV-DNA levels in both CSF and plasma were independently associated with an increased mortality risk of 2.9% and 7.2%, respectively, for each Log increase in JCV-DNA. Conclusions This observational study showed a changing epidemiological context over 37 years. Although survival improved over time, it remained poor even in the last decade, with a one-year survival probability of 59.2%

BACKGROUND:COVID-19 primarily affects the respiratory system, with pulmonary function tests (PFTs) evaluating respiratory impairments and chest CT imaging revealing structural lung abnormalities. However, the disease's multisystem impact - including vascular dysfunction and neurological complications associated with MRI neuroimaging alterations - raises the possibility of shared mechanisms underlying both pulmonary and cerebral involvement, potentially mediated by vascular damage. MATERIALS AND METHODS:The study included 27 consecutive COVID-19 patients (median age 59.0 [IQR 50.5 - 70.0] years, 37% female) presenting with concurrent respiratory and neurological symptoms. All patients underwent PFTs, chest CT, and brain MRI. CT images were processed to quantify lung parenchyma, airways, and vasculature, including small-vessel volume (SVV) and air-to-perfusion ratio (APR). Brain MRI analysis assessed gray matter (GM) integrity (volume and cortical thickness), white matter (WM) diffusion metrics (Apparent Diffusion Coefficient, ADC), and GM perfusion (cerebral blood volume, CBV; cerebral blood flow, CBF). Relationships between pulmonary and cerebral metrics were explored using Spearman correlations and multivariable linear regression. RESULTS:GM volume was positively associated with diffusing capacity for carbon monoxide (DLCO), and cortical thickness was positively associated with alveolar volume (VA). No associations were observed for WM ADC. In contrast, lower pulmonary function (DLCO, VA, forced expiratory volume in 1 s (FEV1), and forced vital capacity (FVC)) were associated with higher GM perfusion. CONCLUSIONS:COVID-19-related pulmonary impairment is associated with reduced GM structural integrity and altered cerebral perfusion, suggesting a lung-brain interplay potentially driven by systemic vascular dysfunction and adaptive cerebrovascular mechanisms. These findings underscore the importance of integrated pulmonary and neurological assessment in post-COVID-19 patients and highlight the need for longitudinal studies to clarify the evolution and clinical consequences of these alterations.

Background and Objectives JC virus (JCV) reactivation causing progressive multifocal leukoencephalopathy (PML) is a complication in patients with multiple sclerosis (MS) treated with disease-modifying therapies (DMTs). Although natalizumab (NTZ) is most frequently involved, PML also occurs less commonly with sphingosine-1-phosphate receptor modulators (S1P-RM), dimethyl fumarate (DMF), and ocrelizumab. This study aimed to identify factors predicting worse outcomes, focusing on the influence of PML-immune reconstitution inflammatory syndrome (PML-IRIS), plasma exchange (PlEx), corticosteroids, and DMT reintroduction. Methods This retrospective multicenter cohort study analyzed patients with MS who had JCV-associated pathology (PML or granule cell neuronopathy) from 42 centers (2009-2022). The primary outcome was disability at 12 months, measured by the modified Rankin Scale (mRS). Multivariable analyses identified predictors of poor outcomes, PML-IRIS development, and recurrent MS activity. Results Of 96 identified patients, 94 were analyzed. Most cases occurred under NTZ (77%), followed by S1P-RM (22%) and DMF (1%). Twelve-month survival was 91.5%, with a median mRS of 3 [IQR: 2-4]. Multivariable analysis showed that higher pre-PML disability (OR: 1.95 [95% CI 1.46-2.60], p < 0.001), elevated CSF JCV viral load (OR: 2.45 [95% CI 1.55-3.87], p < 0.001), and symptomatic presentation at onset (OR: 3.93 [95% CI 1.23-12.55], p = 0.021) were associated with worse outcomes. Conversely, PML-IRIS was associated with better outcomes (OR: 0.28 [95% CI 0.09-0.86], p = 0.025). PlEx and corticosteroid use had no negative effect. Discussion This study provides valuable insights into the management of iatrogenic PML in patients with MS. The findings may guide clinicians in making informed decisions, particularly regarding the use of PlEx, corticosteroids, and the management of PML-IRIS.

BACKGROUND:The metabolic component of cerebral autoregulation is crucial in traumatic brain injury (TBI), yet continuously monitored indices are limited. This study introduces the ICP-EtCO2 Slope (IESlope), quantifying the dynamic relationship between end-tidal CO2 (EtCO2) and intracranial pressure (ICP), and evaluates its association with 12-month mortality and unfavorable outcome (Glasgow Outcome Scale-Extended, GOSE≤4). Second, IESlope visualization and its ability to predict short-term ICP changes during EtCO2 variations are assessed. METHODS:Intensive care unit records of 218 adult and pediatric TBI patients were retrospectively analyzed (median age 44, IQR: 24-66; 76% male). IESlope was calculated as the angle of the linear regression between EtCO2 and ICP over 60-minute moving windows and visualized using streamline mapping (ICP-EtCO2 space). IESlope values were averaged to obtain a single patient-level metric used in univariate and multivariable analyses (area under the curve, AUC). Predictive capability was assessed by comparing predicted versus observed ICP changes at 5, 10, and 20 minutes during significant EtCO2 variations. RESULTS:Lower IESlope values were associated with mortality and GOSE≤4 (median: 7.76 vs. 14.8 and 10.5 vs. 18.6, respectively, P<0.001), independent of age or decompressive craniectomy. Streamline maps showed expected CO2 reactivity patterns, with peak values at moderate ICP and EtCO2 levels and reductions at extremes and after decompressive craniectomy. IESlope maintained significant associations with outcomes (AUC ∼0.900) and accurately predicted short-term ICP responses to EtCO2 changes (mean absolute error, MAE=0.600-1.686 mm Hg). CONCLUSIONS:IESlope provides a continuous, quantitative measure of CO2-related ICP reactivity and may support individualized ventilatory management in TBI, pending prospective validation.

PURPOSE:Neuroradiological findings associated with neurological presentations in acute SARS-CoV-2 infection are very heterogeneous. We aimed to develop a standardized framework for describing MR neuroimaging patterns in Covid-19, to test this in an international multicentre study and to determine the prevalence of observed MRI patterns and their association with clinical presentation and outcome. METHODS:An international expert consortium developed a framework for assessment of brain MRI patterns in Covid-19 based on published literature and professional experience. We performed a retrospective analysis of the proposed framework, involving brain MRI scans from 458 Covid-19 patients with neurological symptoms, including data from 1 February to 31 May 2020. Two readers at 25 centres across five countries assessed the local MRI studies regarding the presence of one or more predefined MRI patterns. Imaging and clinical data were analysed using Bayesian statistics. RESULTS:Of 458 patients, 58.5% had an abnormal MRI. Overall, 94% of all imaging pathologies seen were captured by our proposed classification. Ischemic strokes were the most frequent pattern overall (25.6%), followed by microhaemorrhages (15.9%). Ischemic infarct patterns were more frequent in non-ICU patients, while the haemorrhagic patterns were more frequent in ICU patients. White matter lesions (10.9%) were more frequent than grey matter lesions (8.1%), and leptomeningeal contrast enhancement was present in 8.3% of patients. Patient outcome was not associated with any MRI patterns. CONCLUSION:Our proposed classification of specific MRI patterns in Covid-19, covered 94% of observed abnormalities, while patient outcome, death or home discharge, was not associated with any MRI patterns.

BACKGROUND:Traumatic brain injury (TBI) often leads to neurobehavioral disorders (NBDs) that hinder functional recovery. Although demographic (gender, age, years of education) and clinical factors (post-traumatic amnesia duration [PTA], Glasgow Coma Scale severity) have been studied as potential predictors of NBDs, the impact of the levels of cognitive functioning (LCF) and traumatic axonal injury (TAI) has received less attention. AIM:This study investigates the relationship between the variables and the onset of NBDs following TBI. It also examines the correlation between NBDs and patients' functional outcome and community participation, as measured by the Glasgow Outcome Scale Extended (GOSE) and the Community Integration Questionnaire (CIQ). DESIGN:Observational, longitudinal study. SETTING:Inpatient rehabilitation setting. POPULATION:The study cohort comprised 54 TBI patients (12 females, 42 males; mean age 46.1 years). METHODS:Patients underwent comprehensive neuropsychological, neurobehavioral, and psychological assessments at 12 months. Clinical variables were collected during the acute/subacute phase, and functional outcomes were measured in the chronic phase (GOSE and CIQ). RESULTS:The most frequent NBDs observed by caregivers included anger, difficulty controlling temper, impulsivity, and irritability. The findings highlight years of education, PTA duration, LCF score at rehabilitation admission (LCFa) and TAI as the key drivers of long-lasting NBDs (R2≈0.4-0.5). There was a significant moderate negative correlation between NBDs and GOSE (r=-0.67, P<0.001) as well as CIQ (r=-0.71, P<0.001). CONCLUSIONS:The study highlights that lower education levels, prolonged PTA duration, lower LCFa, and presence of TAI are linked to a higher likelihood of developing persistent NBDs, which negatively impact functional outcomes and community participation. CLINICAL REHABILITATION IMPACT:Regular monitoring and early intervention for patients with these risk factors - lower education, prolonged PTA, lower LCFa and TAI - could help mitigate the long-term effects of NBDs, improving rehabilitation outcomes through timely and targeted therapeutic approaches.

Neurological manifestations are frequent in patients with SARS-CoV-2 infection and can be correlated with different pathogenic mechanisms which can be divided into two categories: direct invasion of the central nervous system by the virus and indirect effects deriving from the severity of the systemic infection and by the inflammatory response correlated with cytokine storm. Among the neurological manifestations, acute encephalopathy is very frequent and its nomenclature has recently been updated. The occurrence of a condition of altered mental status, reduced consciousness, delirium up to coma represents an element associated with a greater severity of the infection and mortality both in an Intensive Care Unit setting and in an Emergency Department setting. The tissue damage mechanisms found in COVID-19 patients' encephalopathy and neuroimaging patterns, as well as histopathology, are similar to those described in sepsis-associated encephalopathy, further confirming the role of indirect mechanisms, with no CNS invasion by the virus. The available data have some limitations, notably the underuse of diagnostic neuroimaging techniques in severely affected patients, particularly in the first wave of the pandemic.

Background The ultra-low-frequency pressure reactivity index (UL-PRx) has been established as a surrogate method for bedside estimation of cerebral autoregulation (CA). Although this index has been shown to be a predictor of outcome in adult and pediatric patients with traumatic brain injury (TBI), a comprehensive evaluation of low sampling rate data collection (0.0033 Hz averaged over 5 min) on cerebrovascular reactivity has never been performed. Objective To evaluate the performance and predictive power of the UL-PRx for 12-month outcome measures, alongside all International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) models and in different age groups. To investigate the potential for optimal cerebral perfusion pressure (CPPopt). Methods Demographic data, IMPACT variables, in-hospital mortality, and Glasgow Outcome Scale Extended (GOSE) at 12 months were extracted. Filtering and processing of the time series and creation of the indices (cerebral intracranial pressure (ICP), cerebral perfusion pressure (CPP), UL-PRx, and deltaCPPopt (ΔCPPopt and CPPopt-CPP)) were performed using an in-house algorithm. Physiological parameters were assessed as follows: mean index value, % time above threshold, and mean hourly dose above threshold. Results A total of 263 TBI patients were included: pediatric (17.5% aged ≤ 16 y) and adult (60.5% aged > 16 and < 70 y and 22.0% ≥ 70 y, respectively) patients. In-hospital and 12-month mortality were 25.9% and 32.7%, respectively, and 60.0% of patients had an unfavorable outcome at 12 months (GOSE). On univariate analysis, ICP, CPP, UL-PRx, and ΔCPPopt were associated with 12-month outcomes. The cutoff of ~ 20–22 for mean ICP and of ~ 0.30 for mean UL-PRx were confirmed in all age groups, except in patients older than 70 years. Mean UL-PRx remained significantly associated with 12-month outcomes even after adjustment for IMPACT models. This association was confirmed in all age groups. UL-PRx resulted associate with CPPopt. Conclusions The study highlights UL-PRx as a tool for assessing CA and valuable outcome predictor for TBI patients. The results emphasize the potential clinical utility of the UL-PRx and its adaptability across different age groups, even after adjustment for IMPACT models. Furthermore, the correlation between UL-PRx and CPPopt suggests the potential for more targeted treatment strategies. Trial registration : ClinicalTrials.gov identifier: NCT05043545, principal investigator Paolo Gritti, date of registration 2021.08.21.

Anderson–Fabry disease (AFD) is a genetic sphingolipidosis involving virtually the entire body. Among its manifestation, the involvement of the central and peripheral nervous system is frequent. In recent decades, it has become evident that, besides cerebrovascular damage, a pure neuronal phenotype of AFD exists in the central nervous system, which is supported by clinical, pathological, and neuroimaging data. This neurodegenerative phenotype is often clinically characterized by an extrapyramidal component similar to the one seen in prodromal Parkinson’s disease (PD). We analyzed the biological, clinical pathological, and neuroimaging data supporting this phenotype recently proposed in the literature. Moreover, we compared the neurodegenerative PD phenotype of AFD with a classical monogenic vascular disease responsible for vascular parkinsonism and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). A substantial difference in the clinical and neuroimaging features of neurodegenerative and vascular parkinsonism phenotypes emerged, with AFD being potentially responsible for both forms of the extrapyramidal involvement, and CADASIL mainly associated with the vascular subtype. The available studies share some limitations regarding both patients’ information and neurological and genetic investigations. Further studies are needed to clarify the potential association between AFD and extrapyramidal manifestations.

INTRODUCTION:The COVID-19 pandemic has affected millions worldwide, causing mortality and multi-organ morbidity. Neurological complications have been recognized. This study aimed to assess brain structural, microstructural, and connectivity alterations in patients with COVID-19-related olfactory or cognitive impairment using post-acute (time from onset: 264[208-313] days) multi-directional diffusion-weighted MRI (DW-MRI). METHODS:The study included 16 COVID-19 patients with cognitive impairment (COVID-CM), 35 COVID-19 patients with olfactory disorder (COVID-OD), and 14 controls. A state-of-the-art processing pipeline was developed for DW-MRI pre-processing, mean diffusivity and fractional anisotropy computation, fiber density and cross-section analysis, and tractography of white-matter bundles. Brain parcellation required for probing network connectivity, region-specific microstructure and volume, and cortical thickness was based on T1-weighted scans and anatomical atlases. RESULTS:Compared to controls, COVID-CM patients showed overall gray matter atrophy (age and sex corrected p = 0.004), and both COVID-19 patient groups showed regional atrophy and cortical thinning. Both groups presented an increase in gray matter mean diffusivity (corrected p = 0.001), decrease in white matter fiber density and cross-section (corrected p < 0.05), , and COVID-CM patients also displayed an overall increased diffusivity (p = 0.022) and decreased anisotropy (corrected p = 0.038) in white matter. Graph-based analysis revealed reduced network modularity, with an extensive pattern of connectivity increase, in conjunction with a localized reduction in a few connections, mainly located in the left hemisphere. The left cingulate, anterior cingulate, and insula were primarily involved. CONCLUSION:Expanding upon previous findings, this study further investigated significant alterations in brain morphology, microstructure, and connectivity in COVID-19 patients with olfactory or cognitive disfunction. These findings suggest underlying neurodegeneration, neuroinflammation, and concomitant compensatory mechanisms. Future longitudinal studies are required to monitor the alterations over time and assess their transient or permanent nature.

BACKGROUND AND OBJECTIVES:Progressive multifocal leukoencephalopathy (PML) is a severe neurologic disease resulting from JC virus reactivation in immunocompromised patients. Certain multiple sclerosis (MS) disease-modifying therapies (DMTs) are associated with PML risk, such as natalizumab and, more rarely, sphingosine-1-phosphate receptor modulators (S1P-RMs). Although natalizumab-associated PML is well documented, information on S1P-RM-associated PML is limited. The aim of this study is to compare clinical presentations and outcomes between the 2 groups. METHODS:A retrospective multicenter cohort study included patients with PML from 2009 to 2022 treated with S1P-RMs or natalizumab. Data on clinical and radiologic presentation, outcomes, immune reconstitution inflammatory syndrome (IRIS), survival, disability (using the modified Ranking scale-mRS), and MS relapses post-PML were analyzed. RESULTS:Of 88 patients, 84 were analyzed (20 S1P-RM, 64 natalizumab). S1P-RM-associated PML was diagnosed in older patients (median age 52 vs 44 years, p < 0.001) and after longer treatment duration (median 63.9 vs 40 months, p < 0.001). Similarly, S1P-RM patients were more prone to show symptoms at diagnosis (100 vs 80.6%, p = 0.035), had more disseminated lesions (80% vs 34.9%, p = 0.002), and had higher gadolinium enhancement (65% vs 39.1%, p = 0.042). Natalizumab patients had a higher IRIS development rate (OR: 8.3 [1.92-33.3]). Overall, the outcome (mRS) at 12 months was similar in the 2 groups (OR: 0.81 [0.32-2.0]). Yet, post-treatment MS activity was higher in S1P-RM cases (OR: 5.7 [1.4-22.2]). DISCUSSION:S1P-RM-associated PML shows reduced IRIS risk but higher post-treatment MS activity. Clinicians should tailor post-PML treatment based on pre-PML medication.

OBJECTIVES:Neurogenic muscle hypertrophy (NMH) is a rare condition characterized by focal muscle hypertrophy caused by chronic partial nervous injury. Given its infrequency, underlying mechanisms remain poorly understood. Inspired by two clinical cases, we conducted a systematic review to gain insights into the different aspects of NMH. METHODS:We systematically searched online databases up until May 30, 2023, for reports of muscle hypertrophy attributed to acquired neurogenic factors. We conducted an exploratory analysis to identify commonly associated features. We also report two representative clinical cases. RESULTS:Our search identified 63 reports, describing 93 NMH cases, to which we added our two cases. NMH predominantly affects patients with compressive radiculopathy (68.4%), negligible muscular weakness (93.3%), and a chronic increase in muscle bulk. A striking finding in most neurophysiological studies (60.0%) is profuse spontaneous discharges, often hindering the analysis of voluntary traces. Some patients exhibited features consistent with more significant muscle damage, including higher creatine phosphokinase levels, muscle pain, and inflammatory muscle infiltration. These patients are sometimes referred to in literature as "focal myositis." Treatment encompassed corticosteroid, Botulinum Toxin A, decompressive surgery, antiepileptic medications, and nerve blocks, demonstrating varying degrees of efficacy. Botulinum Toxin A yielded the most favorable response in terms of reducing spontaneous discharges. INTERPRETATION:This systematic review aims to provide a clear description and categorization of this uncommon presentation of an often-overlooked neurological disorder. Though questions remain about the underlying mechanism, evidence suggests that aberrant fiber overstimulation along with increased workload that promotes focal damage may result in muscle hypertrophy. This may serve as a guide for therapeutic interventions.

PURPOSE:Creating an effective MRI protocol for examining the brachial plexus poses significant challenges, and despite the abundance of protocols in the literature, there is a lack of reference standards for basic sequences and essential parameters needed for replication. The aim of this study is to establish a reproducible 1.5 T brachial plexus imaging protocol, including patient positioning, coil selection, imaging planes, and essential sequence parameters. METHODS:We systematically investigated MRI sequences, testing each parameter through in vivo experiments, examining their effects on signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), visual quality scores, and acquisition time. Sequences were refined based on optimal quality and timing scores. The final protocol was tested on scanners from two other vendors for reliability. RESULTS:The final protocol included a combination of 2D turbo-spin-echo and 3D SPACE T1, SPACE STIR, and VIBE DIXON sequences. Recommendations for imaging planes, phase encoding, field of view, TR, TE, resolution, number of slices, slice thickness, fat and blood suppression, and acceleration strategies are provided. The protocol was successfully translated to other vendor's scanners with comparable quality. CONCLUSION:We present an optimized protocol detailing the essential parameters for reproducibility. Our comprehensive list of experiments describes the impact of each parameter on image quality and scan time, addressing common artifacts and potential solutions. This protocol can benefit both young radiologists new to the field and experienced professionals seeking to refine their existing protocols.

Purpose: This multicentric study aims to characterize and assess the occurrence of neuroradiological findings among patients with SARS-CoV-2 infection during the first Italian wave of the pandemic outbreak. Materials and Methods: Patients' data were collected between May 2020 and June 2020. Clinical and laboratory data, chest imaging, brain CT, and MRI imaging were included. Acquired data were centralized and analyzed in two hospitals: ASST Spedali Civili, Brescia, and IRRCS San Raffaele Research Hospital, Milan, Italy. COVID-19 patients were classified into two different subgroups, vascular and nonvascular. The vascular pattern was further divided into ischemic and hemorrhagic stroke groups. Results: Four hundred and fifteen patients from 20 different Italian Centers were enrolled in the study. The most frequent symptom was focal neurological deficit, found in 143 patients (34.5%). The most frequent neuroradiological finding was ischemic stroke in 122 (29.4%) patients. Forty-four (10.6%) patients presented a cerebral hemorrhage. Forty-seven patients had non-stroke neuroimaging lesions (11.3%). The most common was PRES-like syndrome (28%), SWI hypointensities (22%), and encephalitis (19%). The stroke group had higher CAD risk (37.5% vs 20%, p = .016) and higher D-dimer levels (1875 ng/mL vs 451 ng/mL, p < .001) compared to the negative group. Conclusion: Our study describes the biggest cohort study in Italy on brain imaging of COVID-19 patients and confirms that COVID-19 patients are at risk of strokes, possibly due to a pro-thrombotic microenvironment. Moreover, apart from stroke, the other neuroradiological patterns described align with the ones reported worldwide.

AbstractObjectiveThe aim of this study was to assess COVID‐19‐related gray matter (GM) structural alterations in two distinct groups of patients presenting with the prevailing and distinctive COVID‐19‐related neurological symptoms – isolated olfactory disorders as sole neurological manifestation (COVID‐OD) and cognitive disorders (COVID‐CD) – as compared to a control group of unaffected individuals.MethodsThe study included 61 COVID‐CD patients (57 [60–63] years, 62% females), 84 COVID‐OD patients (49 [35–57] years, 60% females), and 17 controls (51 [41–52] years, 41% females). Region‐based morphometry (RBM) and voxel‐based morphometry (VBM) were performed on T1‐weighted MRI scans to assess GM regional volume and voxel‐wise density differences between COVID‐19 patients and controls. Surface‐based morphometry (SBM) was applied to investigate cortical thickness alterations. The statistical models built to assess GM structural differences among groups included total intracranial volume and age as nuisance variables.ResultsThe multi‐morphometric analysis revealed statistically significant (p < 0.05 corrected for multiple comparisons) reduction in GM regional volumes, in voxel‐wise GM density and in cortical thickness in both COVID‐CD and COVID‐OD patient groups as compared to controls. Across all three analyses, COVID‐CD patients showed more distributed and severe GM loss than COVID‐OD patients. The most prominently affected GM regions in the COVID‐CD group included the hippocampus, putamen, cingulate gyrus, precuneus, precentral and postcentral gyri, amygdala, lingual gyrus, and caudate nucleus.InterpretationOur MRI findings show that COVID‐19‐related olfactory and cognitive disorders both induce GM atrophy, although at different degrees of severity, likely indicative of neurodegeneration and neuroinflammation.

To determine the incidence of acute neuroimaging (NI) findings and comorbidities in the coronavirus disease of 2019 (COVID‐19)‐infected subjects in seven U.S. and four European hospitals.