Mood and Anxiety Program, Department of Psychiatry, University of Maryland School of Medicine, 685 W. Baltimore Street, Suite# 930, Baltimore, MD, USA.
VA Rocky Mountain Mental Illness Research Education and Clinical Center (MIRECC), Rocky Mountain Regional Veterans Affairs (VA) Medical Center (RMRVAMC), Aurora, CO, USA.
Curr Psychiatry Rep. 2021 Oct 1;23(10):68. doi: 10.1007/s11920-021-01275-3.
We present biological and psychological factors implicated in psychiatric manifestations of SARS-CoV-2, as well as its neuroinvasive capability and immune pathophysiology.
Preexisting mental illness leads to worse clinical outcomes in COVID-19. The presence of the virus was reported in the cerebrospinal fluid (CSF) and brain tissue post-mortem. Most common psychiatric manifestations include delirium, mood disorders, anxiety disorders, and posttraumatic stress disorder. "Long-COVID" non-syndromal presentations include "brain-fogginess," autonomic instability, fatigue, and insomnia. SARS-CoV-2 infection can trigger prior vulnerabilities based on the priming of microglia and other cells, induced or perpetuated by aging and mental and physical illnesses. COVID-19 could further induce priming of neuroimmunological substrates leading to exacerbated immune response and autoimmunity targeting structures in the central nervous system (CNS), in response to minor immune activating environmental exposures, including stress, minor infections, allergens, pollutants, and traumatic brain injury.
本文介绍了与 SARS-CoV-2 相关的精神科表现有关的生物学和心理学因素，以及其神经侵袭能力和免疫病理生理学。
先前存在的精神疾病会导致 COVID-19 的临床结局更差。有报道称病毒存在于脑脊液（CSF）和死后脑组织中。最常见的精神科表现包括谵妄、情绪障碍、焦虑障碍和创伤后应激障碍。“长新冠”非综合征表现包括“脑雾”、自主神经不稳定、疲劳和失眠。SARS-CoV-2 感染可根据小胶质细胞和其他细胞的启动，基于年龄和精神及躯体疾病的诱导或持续存在，引发先前的脆弱性。COVID-19 可进一步引发神经免疫底物的启动，导致针对中枢神经系统（CNS）结构的免疫反应和自身免疫加重，从而对轻微的免疫激活环境暴露（包括应激、轻微感染、过敏原、污染物和创伤性脑损伤）产生反应。
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