The coronavirus disease 2019 (COVID-19) outbreak in Wuhan, China has spread rapidly, with confirmed cases currently appearing in multiple countries. Although many details, such as the source of the virus and its ability to spread between individuals, remain unknown, an increasing number of cases have been confirmed to have been caused by human-to-human transmission. 1,2 The primary symptoms of COVID-19 include fever, dry cough, and fatigue. 2 However, some physicians in affected areas have found that some patients diagnosed with COVID-19 have not shown typical respiratory symptoms, such as fever and coughing, at the time of diagnosis; rather, some infected patients have exhibited only neurological symptoms as the initial symptoms, such as the following: (1) headache, languidness, unstable walking, and malaise, which may be due to non-specific manifestations caused by COVID-19 (the proportion of non-specific manifestations as the first symptoms needs to be further explored); (2) cerebral hemorrhage; (3) cerebral infarction; and (4) other neurological diseases. In a recent study of 214 patients with COVID-19, 78 (36.4%) patients had neurological manifestations, such as headache, dizziness, acute cerebrovascular diseases, and impaired consciousness. 3 Of these 214 patients, 40 (18.7%) patients required intensive care unit (ICU) interventions for their severe neurological involvement. 3 Currently, although there have been many cases of patients with COVID-19 complicated by cerebral hemorrhages, relevant studies on this association are lacking. Hence, the physiological relationship between COVID-19 and the incidence of cerebral hemorrhage remains unclear. Based on several lines of evidence, we hypothesize that COVID-19 may involve cranial hemorrhage. First, recent studies have shown that this novel severe acute respiratory syndrome (SARS) coronavirus, SARS-CoV-2, invades human respiratory

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ObjectiveImpairments in emotion regulation, and more specifically in cognitive reappraisal, are thought to play a key role in the pathogenesis of anxiety disorders. However, the available evidence on such deficits is inconsistent. To further illustrate the neurobiological underpinnings of anxiety disorder, the present meta-analysis summarizes functional magnetic resonance imaging (fMRI) findings for cognitive reappraisal tasks and investigates related brain areas.MethodsWe performed a comprehensive series of meta-analyses of cognitive reappraisal fMRI studies contrasting patients with anxiety disorder with healthy control (HC) subjects, employing an anisotropic effect-size signed differential mapping approach. We also conducted a subgroup analysis of medication status, anxiety disorder subtype, data-processing software, and MRI field strengths. Meta-regression was used to explore the effects of demographics and clinical characteristics. Eight studies, with 11 datasets including 219 patients with anxiety disorder and 227 HC, were identified.ResultsCompared with HC, patients with anxiety disorder showed relatively decreased activation of the bilateral dorsomedial prefrontal cortex (dmPFC), bilateral dorsal anterior cingulate cortex (dACC), bilateral supplementary motor area (SMA), left ventromedial prefrontal cortex (vmPFC), bilateral parietal cortex, and left fusiform gyrus during cognitive reappraisal. The subgroup analysis, jackknife sensitivity analysis, heterogeneity analysis, and Egger’s tests further confirmed these findings.ConclusionsImpaired cognitive reappraisal in anxiety disorder may be the consequence of hypo-activation of the prefrontoparietal network, consistent with insufficient top-down control. Our findings provide robust evidence that functional impairment in prefrontoparietal neuronal circuits may have a significant role in the pathogenesis of anxiety disorder.

Background Anti-N-methyl-D-aspartate (anti-NMDA) receptor encephalitis is a severe autoimmune disease characterized by complicated psychiatric and neurological symptoms and a difficult diagnosis. This disorder is commonly misdiagnosed, and diagnosis is often delayed. The clinical signs can mimic other psychiatric abnormalities, such as neuroleptic malignant syndrome (NMS) that is usually caused by antipsychotic exposure. This fact raises the question of whether the symptoms common to NMS are due to anti-NMDA receptor encephalitis or established NMS. Cases presentation We describe a rare case of a 29-year-old male without psychiatric history who initially presented with a fever, altered consciousness, behavioral changes, rigidity, and elevated creatine kinase. He was initially diagnosed with NMS. NMS-like symptoms did not improve with active treatments and disappeared for a long period after discontinuing antipsychotics. The patient gradually developed a complicated disease progression, including speech impairment, mutism, and movement disorders, and symptom progression led to the final diagnosis of anti-NMDA receptor encephalitis. The related pathophysiological mechanisms, clinical features, and treatment of this disease are reviewed. Conclusion We highlight that the natural progress of anti-NMDA receptor encephalitis can mimic the symptoms of NMS and NMS-like features could be due to anti-NMDA receptor encephalitis upon antipsychotic exposure, and not true NMS. Clinically, the suspicion of NMS may serve as a significant alarm to suspect anti-NMDA receptor encephalitis and lead neurologists or psychiatrists to investigate such a diagnosis.

BackgroundThe General Health Questionnaire-12 (GHQ-12) is a widely used instrument to assess mental health status. However, little is known about its applicability in Chinese healthcare workers. This study aimed to evaluate the reliability and validity of the GHQ-12 in Chinese dental healthcare workers.MethodsDental healthcare workers participated in the first occupational survey in China conducted by the Chongqing Stomatological Association from February 2021 to March 2021 by filling out GHQ-12. The reliability and validity of GHQ-12 were then tested.ResultsA total of 3,020 valid electronic questionnaires were acquired. The positive detection rate of self-reported mental health status was 23.80% (719/3,020). The Cronbach's α coefficient of the GHQ-12 was 0.892, and the Cronbach's α coefficient was 0.877–0.888 after the deletion of individual items, and the split-half reliability was 0.843. The correlation coefficient between the item-total score ranged from 0.465 to 0.762 (P<0.05). The exploratory factor analysis found 2 common factors with a factor load of 0.564–0.818. The confirmatory factor analysis showed that the factor load on the specified items was 0.480–0.790.ConclusionsThe two-factor model of GHQ-12 featured good reliability and validity, which could be used to assess the mental health status of Chinese dental healthcare workers.

Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy has been considered a novel central nervous system autoimmune disease characterized by relapse and responsiveness to corticosteroid with a specific GFAP-Immunoglobulin G (IgG) being noted in cerebrospinal fluid. We report the case of a 21-year-old girl presenting with dysuria and weariness, who subsequently developed blurry vision, slight dysphagia, slurred speech, and sensory abnormality. GFAP-IgG was detected in her cerebrospinal fluid. Magnetic resonance imaging using both T2-weighted and contrast-enhanced T1-weighted images revealed a rare finding of lesions distributed mainly in the entire spinal cord rather than typical brain lesions. After treating with corticosteroids, her clinical symptoms were alleviated, and the spinal cord lesion enhancement was reduced. Our observations extend the clinical spectrum of autoimmune GFAP astrocytopathy. We suggest that rare distributed lesions in the entire spinal cord in patients with autoimmune GFAP astrocytopathy cannot be ignored by neurologists. The identification of potential atypical lesions broadens the understanding of autoimmune GFAP astrocytopathy.

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