Psychiatric Manifestations of COVID-19: A Literature Review

Abstract

Background: COVID19 (coronavirus disease of 2019) occurs due to the highly contagious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It uses angiotensin-converting enzyme-2 (ACE-2) as its primary receptor to enter the host cell. Recent reports suggest that this pathogen also has a large impact on the CNS alongside other organs. Various inflammatory mediators such as cytokines, chemokines, and numerous metabolites are poorly regulated during infection as well as in several psychiatric diseases, which leads to conditions of hypoxia and cytokine storm. The persistence of COVID-19 infection may also result in aggravation of the already present neuro-psychiatric symptoms in patients. Methods: We systematically searched various sources of journals and assessed the varied neurological routes of propagation and pathogenesis of SARS-CoV-2 neurotoxicity like ACE2-mediated neuro-invasion induced hypoxia, and the cytokine storm syndrome. Several case studies were also referred to obtain a better idea of the current mental health scenario as a consequence of infection and inflammation due to SARS-CoV-2. Conclusion: Several risk factors for the causation of mental health issues during as well as after the infection include female gender, presence of necrosis, and pain in avascular regions. Most of the psychiatric disorders are directly associated with the socioeconomic and psychosocial changes that occurred as a consequence of the pandemic. These psychiatric manifestations have only started to unravel, which calls for the development of faster means of diagnosis and integrated pharmacological and epidemiological studies to curb the growing rate of neuronal complications as well as mortality.

Susceptibility and severity of COVID-19 and risk of psychiatric disorders in European populations: a Mendelian randomization study

“…This chronic inflammation, especially characterized by imbalances in IL-6 cytokine levels, has been found to be associated with anxiety, depression, and traumatic stress ( 46 ). It is well known that the SARS-CoV-2 virus enters the brain by mediating the angiotensin-converting enzyme-2 (ACE-2) receptor and has a great impact on the central nervous system ( 47 ). Various inflammatory mediators, such as cytokines, chemokines, and various metabolites, are poorly regulated during infection, as well as in several psychiatric disorders, leading to brain tissue hypoxia and cytokine storm syndrome.…”

“…Various inflammatory mediators, such as cytokines, chemokines, and various metabolites, are poorly regulated during infection, as well as in several psychiatric disorders, leading to brain tissue hypoxia and cytokine storm syndrome. Persistence of SARS-CoV-2 infection may also lead to exacerbation of pre-existing neuropsychiatric symptoms in patients ( 47 ). Yet the SARS-CoV-2 infection during the COVID-19 epidemic was not the only factor contributing to the occurrence of psychiatric disorders.…”

Targeting the mammalian target of rapamycin pathway in neurological manifestations of Covid‐19

“…Anosmia, often one of the early neurological symptoms, highlights the virus's neurotropic potential, indicative of its ability to affect the olfactory nerve or central processing centers 12 . This sensory impairment is not only a diagnostic marker but also underscores the complex interaction between SARS‐CoV‐2 and the nervous system 12,13 …”

“…Headache, another frequently reported neurological symptom in Covid‐19 patients, serves as a testament to the multifaceted impact of the SARS‐CoV‐2 12,14 . The mechanisms underlying these headaches are not merely secondary to respiratory distress; they likely involve the direct effects of the virus on neural tissues or the consequences of the immune response within the CNS 14–17 .…”

“…12,13 Headache, another frequently reported neurological symptom in Covid-19 patients, serves as a testament to the multifaceted impact of the SARS-CoV-2. 12,14 The mechanisms underlying these headaches are not merely secondary to respiratory distress; they likely involve the direct effects of the virus on neural tissues or the consequences of the immune response within the CNS. [14][15][16][17] The varied presentations of headaches, ranging from mild discomfort to severe migraines, further emphasise the complex interplay between viral neurotropism and individual host responses.…”