Coronavirus disease 2019 (COVID-19), a disease caused by the novel betacoronavirus (SARS-CoV-2), has become a global pandemic threat. The potential involvement of COVID-19 in central nervous system (CNS) has attracted considerable attention due to neurological manifestations presented throughout the disease process. In addition, SARS-CoV-2 is structurally similar to SARS-CoV, and both bind to the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells. Thus, cells expressing ACE2, such as neurons and glial cells may act as targets and are thus vulnerable to SARS-CoV-2 infection. Here, we have reviewed the neurological characteristics of COVID-19 and summarized possible mechanisms of SARS-CoV-2 invasion of the CNS. COVID-19 patients have presented with a number of different neurological symptoms such as headache, dizziness, hyposmia, and hypogeusia during the course of illness. It has also been reported recently that some cases of COVID-19 have presented with concurrent acute cerebrovascular disease (acute ischemic stroke, cerebral venous sinus thrombosis, cerebral hemorrhage, subarachnoid hemorrhage), meningitis/encephalitis, acute necrotizing hemorrhagic encephalopathy, and acute Guillain–Barré syndrome. Furthermore, SARS-CoV-2 RNA detected in a cerebrospinal fluid specimen of a patient with COVID-19 have provided direct evidence to support the theory of neurotropic involvement of SARS-CoV-2. However, the underlying neurotropic mechanisms of SARS-CoV-2 are yet to be established. SARS-CoV-2 may affect CNS through two direct mechanisms (hematogenous dissemination or neuronal retrograde dissemination) or via indirect routes. The underlying mechanisms require further elucidation in the future.

Objectives: To analyze the clinical and imaging characteristics of autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A).Methods: Forty-three patients diagnosed with GFAP-A between March 2017 and July 2023 were retrospectively recruited. The clinical characteristics and magnetic resonance imaging (MRI) features were collected.Results: Twenty-one patients (61.8%) had a fever and 16 (47.1%) had a headache. Five patients (14.7%) had coexisting neural autoantibodies and one patient (2.9%) had a coexisting neoplasm. The most common presentation was meningoencephalomyelitis (13/34, 38.3%), followed by meningoencephalitis (12/34, 35.3%). The other clinical manifestations included blurred visions (5/34, 14.7%) and peripheral nervous system involvement (4/34, 11.8%). Twenty-six patients (76.5%) had elevated nucleated cell count, predominantly lymphocytes (15/15, 100%), and 27 (79.4%) had elevated protein levels of cerebrospinal fluid. One-half (50%) of the patients presented with hyponatremia. A majority of the patients (30/33, 90.9%) exhibited abnormal hyperintense lesions on T2WI, which were often located in juxtacortical white matter (18/33, 54.5%), followed by periventricular white matter (16/33, 48.5%), basal ganglia (15/ 33, 45.5%), brainstem (11/33, 33.3%), and thalamic lesions (9/33, 27.3%). Twenty-four patients (72.7%) had abnormal brain enhancement, with supratentorial leptomeningeal enhancement being the most frequent enhancement pattern (15/33, 45.5%), followed by linear perivascular radial enhancement (14/33, 42.4%). Nineteen patients (70.4%) had hyperintense intramedullary spinal cord lesions, with long segments (15/27, 55.6%) and transverse lesions (14/27, 51.9%) being the most frequent lesions. Most cases were sensitive to immunotherapy, such as glucocorticoids, intravenous immunoglobulin, and tacrolimus, with three patients (8.8%) experiencing relapses. Patients with brainstem lesions had higher onset modified Rankin scale scores and were more prone to intensive care unit admissions. Linear perivascular radial enhancement was positively associated with poor prognosis (p < 0.05).Conclusion: GFAP-A presented with meningoencephalomyelitis and meningoencephalitis. The brain lesions were often located in juxtacortical white matter, periventricular white matter, basal ganglia, brainstem, and thalamus. Long segments and transverse were the most frequent spine lesions. Leptomeningeal enhancement was the most frequent enhancement pattern, followed by linear perivascular radial enhancement, which may provide new insight into the differential diagnosis of GFAP-A.

This study investigates the long-term prognostic significance of non-obstructive coronary artery disease (CAD) in predicting the risk of all-cause death in a multicenter study. Three hospitals in Wuhan participated in this retrospective, observational, multicenter study of 7320 patients with suspected of having CAD and who underwent clinical coronary computed tomography angiography (CTA) from June 2011 to December 2015. According to coronary CTA, the extent of CAD was categorized as non-obstructive, obstructive, and no CAD. The primary outcome was all-cause mortality. A total of 611 patients experienced all-cause mortality with a median duration of 8.0 years (7.2–8.9). The annualized mortality rate was 0.50 (95% CI: 0.43–0.58), 1.31 (95% CI: 1.16–1.47), and 2.18 (95% CI: 1.93–2.46) for the no CAD, non-obstructive CAD, and obstructive CAD, respectively. There was a significant association between the classification and the increased cumulative events, as shown by the Kaplan-Meier survival curve (P < 0.001). The multivariate Cox model showed that the hazard ratios (HR) for predicting all-cause mortality from 1.42 (95% CI: 1.15–1.75, P = 0.001) in non-obstructive CAD to 1.87 (95% CI: 1.50–2.33, P < 0.001) in obstructive CAD compared with no CAD. At 8-year follow-up, patients with non-obstructive CAD detected by coronary CTA had a 1.42-fold increased risk of all-cause mortality compared to patients without evidence of CAD. Thus, these findings suggest that non-obstructive CAD is clinically significant and that further investigation of interventions to improve the prognosis of these patients is warranted.

Background: Simulation-based training is used to improve fiberoptic bronchoscopic skills for novices. We developed a nonanatomical task trainer (named 12-hole clock model) that focused on training manipulation of bronchoscopes. The aim of this study was to evaluate the training effect of this model on bronchoscopic skills and learning interests in simulated normal and difficult airways among anesthesia residents. Methods: Forty-three anesthesia residents without experience in bronchoscopic intubation were randomly divided into control (n = 22) and intervention groups (n = 21). All participants received standard multimedia learning and a baseline test using a normal airway manikin. Then, the control and intervention groups engaged in 60 minutes of training via a traditional airway manikin or the clock model, respectively. After training, the participants completed bronchoscopic performance assessments in simulated normal and difficult airways, as well as an electronic questionnaire related to the course. Results: During training, the total hands-on time of bronchoscopic practice recorded by trainees’ themselves was longer in the intervention group than in the control group (1568 ± 478 seconds vs 497 ± 172 s, P < .0001). Posttraining, the time required to visualize the carina in simulated normal airways was longer in the intervention group than in the control group (22.0 [18.0, 29.0] vs 14.0 [10.8, 18.3], P < .0001), while it was shorter for simulated difficult airways (24.0 [16.0, 32.0] s vs 27.0 [21.0, 35.5] s, P = .0425). The survey results indicated that confidence in bronchoscopic intubation increased in both groups, without significant differences in satisfaction, acceptance, or perceived difficulty between the groups. However, the interest ratings were higher in the intervention group than in the control group. Conclusions: The 12-hole clock model is a simple and feasible method for improving bronchoscopic skills and promoting interest among trainees. Trial registration: NCT05327842 at Clinicaltrials.gov.

Rosia–Dorfman disease (RDD) is a rare benign disease with exceedingly rare neural involvement. In this report, we describe a very rare case of intracranial RDD mimicking a subdural hematoma. The patient presented with headache and a suspected history of head injury. Head computed tomography showed a well-demarcated extra-axial crescentic hyperdense lesion along the right hemisphere convexity, and this lesion was initially mistaken for a subacute subdural hematoma with brain contusion. However, the follow-up examinations during the subsequent month did not show the natural changes characteristic of a subdural hematoma. Thus, a magnetic resonance imaging scan was performed, which showed a crescentic lesion with T1 isointensity, T2 hypointensity, and obvious homogeneous enhancement. Differential diagnoses such as lymphoma and metastases were considered, and surgery was performed. The final histopathologic examination confirmed the diagnosis of RDD. This report describes a rare presentation of RDD. RDD can mimic the appearance of a subdural hematoma and should be considered as a differential diagnosis even in patients with a history of head injury and a “classic” imaging appearance of a subdural hematoma.