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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Primary blepharospasm (BPS) is a focal dystonia characterized by involuntary blinking and eyelid spasms. The pathophysiology of BPS remains unclear. Several neuroimaging studies have suggested dysfunction of sensory processing and sensorimotor integration, but the results have been inconsistent. This study aimed to determine whether patients with BPS exhibit altered functional brain connectivity and to explore possible correlations between these networks and clinical variables. Twenty-five patients with BPS and 25 healthy controls were enrolled. We found that the patient group exhibited decreased connectivity within the sensory-motor network (SMN), which involved regions of the bilateral primary sensorimotor cortex, supplementary motor area (SMA), right premotor cortex, bilateral precuneus and left superior parietal cortex. Within the right fronto-parietal network, decreased connections were observed in the middle frontal gyrus, dorsal lateral prefrontal cortex and inferior frontal gyrus. Regarding the salience network (SN), increased connectivity was observed in the left superior frontal gyrus and middle frontal gyrus. These findings suggest the involvement of multiple neural networks in primary BPS.

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.

According to the cognitive model of panic disorder (PD), panic attacks are triggered and maintained by catastrophic misappraisals of bodily sensations. Clinically, PD is associated with impaired cognitive emotion regulation strategies involving cognitive reappraisal. To investigate the neural correlates and time course of cognitive reappraisal in patients with PD, event-related potentials were recorded from patients with PD and demographically matched control group during passive viewing of affective images under three conditions: (a) neutral pictures preceded by neutral descriptions, (b) unpleasant pictures preceded by negative descriptions, and (c) unpleasant pictures preceded by neutral descriptions. The late positive potential (LPP), an event-related potential component sensitive to cognitive change strategies, was examined as an index of cognitive reappraisal. Consistent with previous results, the unpleasant pictures preceded by negative descriptions had decreased valence ratings, increased arousal ratings, and increased LPP amplitudes compared with the unpleasant pictures preceded by neutral descriptions in the control group. In contrast, no reliable effect of description condition was observed for valence ratings in the PD group. The patients demonstrated differing response patterns from the control participants, with higher arousal ratings and larger LPPs during the 1000-2000 ms window when unpleasant pictures were preceded by a neutral description than when unpleasant pictures were preceded by a negative description. The present study suggests that emotion regulation is impaired in patients with PD. These findings describe the first electrophysiological correlates of abnormal cognitive reappraisal in patients with PD.

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Elderly depressed patients manifest pronounced executive dysfunction compared with younger subjects with depressive disorder. Aging-related brain changes may result in executive dysfunction in geriatric depression. We investigated the neural correlates of inhibitory control processing in depressed subjects at different ages using event-related potentials (ERPs). A equiprobable visual Go/Nogo task was used in 19 young (27.4 ± 5.0 years) and 18 elderly (70.8 ± 6.9 years) depressed subjects and their age-matched healthy controls (20 young subjects, 26.2 ± 3.7 years, and 18 elderly subjects, 68.1 ± 4.8 years). The responses were based on two types of equilateral triangular figures of upright (Go) and inverted triangle (Nogo). The elderly subjects exhibited later N2 and P3 latencies, and larger Go-N2 and P3 amplitudes, compared with the younger subjects. Further, the elderly controls displayed smaller P3 in the central and parietal regions, and yielded larger Nogo-P3 amplitude in the frontal region compared with younger controls. While the young depressed patients yielded smaller P3 amplitude than the controls across frontal, central and parietal regions, elderly depressed patients yielded smaller P3 than the elderly controls only in the frontal region. Our results suggest that the inhibitory control subprocesses are differentially affected by depression and aging. The stimulus response speed and the effort intensity of inhibition control are specifically impaired in the elderly depressed patients. And the diminished amplitudes of frontal P3 in the elderly depression imply a frontal dysfunction mechanism.