Manifestations and mechanisms of central nervous system damage caused by SARS-CoV-2.

The global pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its threat to humans have drawn worldwide attention. The acute and long-term effects of SARS-CoV-2 on the nervous system pose major public health challenges. Patients with SARS-CoV-2 present diverse symptoms of the central nervous system. Exploring the mechanism of coronavirus damage to the nervous system is essential for reducing the long-term neurological complications of COVID-19. Despite rapid progress in characterizing SARS-CoV-2, the long-term effects of COVID-19 on the brain remain unclear. The possible mechanisms of SARS-CoV-2 injury to the central nervous system include: 1) direct injury of nerve cells, 2) activation of the immune system and inflammatory cytokines caused by systemic infection, 3) a high affinity of the SARS-CoV-2 spike glycoprotein for the angiotensin-converting enzyme ACE2, 4) cerebrovascular disease caused by hypoxia and coagulation dysfunction, and 5) a systemic inflammatory response that promotes cognitive impairment and neurodegenerative diseases. Although we do not fully understand the mechanism by which SARS-CoV-2 causes nerve injury, we hope to provide a framework by reviewing the clinical manifestations, complications, and possible mechanisms of neurological damage caused by SARS-CoV-2. With hope, this will facilitate the early identification, diagnosis, and treatment of possible neurological sequelae, which could contribute toward improving patient prognosis and preventing transmission.

[Investigation of anxiety and depression in patients from the emergency department during COVID-19 epidemic].

OBJECTIVE: To investigate the status of anxiety and depression in patients requiring emergency treatment during the epidemic of COVID-19 to identify the patients with acute psychological stress disorder. METHODS: During the COVID-19 epidemic, the medical staff divided the patients visiting the emergency department into suspected group, fever group and control group through interview of the patients at triage. Self-rating anxiety scale (SAS) and self-rating depression scale (SDS) were distributed to each patient, and a trained medical staff was responsible for assisting the patient to complete the scales. RESULTS: A total of 557 sets of scales were distributed, including 211 in suspected COVID-19 case group, 167 in fever group and 179 in the control group. A total of 516 scales were retrieved, including 197 in suspected case group, 151 in fever group and 168 in control group. In the 3 groups, the incidence rates of anxiety and depression were 57.87% and 58.88%, 48.34% and 43.71%, and 18.31% and 18.99%, respectively, and the rates were significantly higher in suspected group and fever group than in the control group (P < 0.01), and significantly higher in suspected group than in fever group (P < 0.05). The standardized anxiety and depression scale scores in suspected case group, fever group and control group were 57.38±16.25 and 42.58±14.27, 51.23±15.29 and 38.32±15.39, and 32.58±17.8 and 12.25±12.94, respectively. Compared with the control group, both suspected case group and fever group had significantly higher standard scores for anxiety and depression (P < 0.01), and suspected case group had significantly higher standardized scores than fever group (P < 0.01). CONCLUSIONS: Among the patients visiting the emergency treatment, the patients with suspected COVID-19 and common fever are more likely to develop anxiety and depressive symptoms.