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Review
. 2020 Jul 30;10(1):261.
doi: 10.1038/s41398-020-00949-5.

Psychiatric face of COVID-19

Affiliations
Review

Psychiatric face of COVID-19

Luca Steardo Jr et al. Transl Psychiatry. .

Abstract

The Coronavirus Disease 2019 (COVID-19) represents a severe multiorgan pathology which, besides cardio-respiratory manifestations, affects the function of the central nervous system (CNS). The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), similarly to other coronaviruses demonstrate neurotropism; the viral infection of the brain stem may complicate the course of the disease through damaging central cardio-respiratory control. The systemic inflammation as well as neuroinflammatory changes are associated with massive increase of the brain pro-inflammatory molecules, neuroglial reactivity, altered neurochemical landscape and pathological remodelling of neuronal networks. These organic changes, emerging in concert with environmental stress caused by experiences of intensive therapy wards, pandemic fears and social restrictions, promote neuropsychiatric pathologies including major depressive disorder, bipolar disorder (BD), various psychoses, obsessive-compulsive disorder and post-traumatic stress disorder. The neuropsychiatric sequelae of COVID-19 represent serious clinical challenge that has to be considered for future complex therapies.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1. Neuropsychiatric sequelae of COVID-19.
The SARS-COV-2 enters the body through various routes and causes systemic and tissue inflammation. Systemic inflammation compromises the blood-brain barrier (BBB) and floods the brain with pro-inflammatory factors. The virus may also cross the BBB at the level of the circumventricular organs or through retrograde axonal transport via olfactory bulb and infect the brain, thus instigating reactive gliosis, which leads to an increased production and secretion of cytokines and other pro-inflammatory factors. The combination of systemic inflammation, hypoxia resulting from respiratory failure and neuroinflammation may trigger or exacerbate psychiatric diseases.

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