Cited by 964Long-Term Effects of COVID-19COVID-19 and Mental HealthInfectious Encephalopathies and Encephalitis

Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms

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Troyer, Emily A., Kohn, Jordan N., Hong, Suzi·2020·Brain, Behavior, and Immunity

Abstract

The coronavirus disease 19 (COVID-19) pandemic is a significant psychological stressor in addition to its tremendous impact on every facet of individuals' lives and organizations in virtually all social and economic sectors worldwide. Fear of illness and uncertainty about the future precipitate anxiety- and stress-related disorders, and several groups have rightfully called for the creation and dissemination of robust mental health screening and treatment programs for the general public and front-line healthcare workers. However, in addition to pandemic-associated psychological distress, the direct effects of the virus itself (several acute respiratory syndrome coronavirus; SARS-CoV-2), and the subsequent host immunologic response, on the human central nervous system (CNS) and related outcomes are unknown. We discuss currently available evidence of COVID-19 related neuropsychiatric sequelae while drawing parallels to past viral pandemic-related outcomes. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes, may accompany acute viral infection, or may follow infection by weeks, months, or longer in recovered patients. The potential mechanisms are also discussed, including viral and immunological underpinnings. Therefore, prospective neuropsychiatric monitoring of individuals exposed to SARS-CoV-2 at various points in the life course, as well as their neuroimmune status, are needed to fully understand the long-term impact of COVID-19, and to establish a framework for integrating psychoneuroimmunology into epidemiologic studies of pandemics.

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Crossref · 10.1016/j.bbi.2020.04.027

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  • SARS-CoV-2 might act as a neurotrophic agent that enters via the olfactory bulb, raising neuropsychiatric symptoms in survivors.

    “Taken together this indicates that SARS-CoV-2 could be neurotrophic entering the brain through the olfactory bulb, leading to an increase in neuropsychiatric symptoms among the patients surviving COVID-19.”

    From COVID-19 pandemic and mental health consequences: Systematic review of the current evidence (2020) · cites this paper as Troyer et al., 2020

    The “Viral infiltration into the central nervous system” section describes possible coronavirus entry via the olfactory nerve and discusses SARS-CoV-2 neuroinvasion. The “Sub-acute to chronic neuropsychiatric sequelae” section says long-term outcomes in COVID-19 survivors were still unknown. The paper does not specifically identify the olfactory bulb as the entry route or establish that this route would increase neuropsychiatric symptoms in survivors. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • The higher depression risk in COVID-19 patients could be due to the coronavirus affecting the brain directly or indirectly via a massive cytokine response.

    “This higher risk could be due to the corona-virus affecting the brain directly or indirectly by inducing a massive cytokine response affecting the brain (Troyer et al., 2020).”
  • Multimorbidity in people with dementia is associated with faster functional decline and worse quality of life for people with dementia and their family carers.

    “Multimorbidity in people with dementia is associated with faster functional decline248 and worse quality of life for people with dementia and their family carers.249”

    From Dementia prevention, intervention, and care: 2020 report of the Lancet Commission (2020) · cites this paper as [249]

    Citation 249 is attached to the claim about worse quality of life for people with dementia and their family carers; citation 248 covers faster functional decline. The cited paper’s Encephalopathies and Neurodegenerative disorders sections (page numbers unavailable) discuss COVID-19-related neurological outcomes, but the passages found when searching for dementia, multimorbidity, carers and quality of life do not address that association. (LLM, conf=0.75)

    Experimental — accuracy not yet measured
  • The host immune response to SARS-CoV-2, persistent psychological stress, and possible direct viral infection of the central nervous system are possible mechanisms for neuropsychiatric sequelae.

    “The host immune response to SARS-CoV-2 infection, the persistent psychological stress before and during infection (Korman et al., 2020, Vai et al., 2020), and a possible direct viral infections of the central nervous system represent possible mechanisms to induce neuropsychiatric sequelae (Troyer et al., 2020).”
  • SARS-CoV-2 may cause neuropsychiatric symptoms through indirect mechanisms including a hypercoagulable state, neuro-inflammation, immunological and epigenetic changes.

    “SARS-CoV-2 may cause neuropsychiatric symptoms by various indirect mechanisms, such as a hypercoagulable state, neuro-inflammation, immunological and epigenetic changes [132].”

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Authors
Troyer, E. A., Kohn, J. N., & Hong, S.
Affiliations
University of California San Diego (US)
Corresponding author
Hong, Suzi
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2020-07
Volume
87
Pages
34-39
ISSN
0889-1591 (ISSN-L)
OpenAlex
W3015706105
Cited by
964
References
81
Citations by year
2026: 8 · 2025: 27 · 2024: 65 · 2023: 153 · 2022: 200 · 2021: 299 · 2020: 208 · 2019: 2
FWCI
24.12
Type
journal article
Language
en
Open access
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Aging (R03AG063328)
  • National Heart, Lung, and Blood Institute (R01HL126056)
  • National Center for Advancing Translational Sciences (TL1TR001443)
  • National Institute of Mental Health (T32MH018399)
Topics
  • Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
  • Social Sciences › Psychology › Clinical Psychology › COVID-19 and Mental Health
  • Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
Keywords
COVID-19 pandemic, SARS-CoV-2, neuropsychiatric sequelae, long COVID, psychoneuroimmunology, neuroimmune mechanisms, encephalopathy, mood disorders, psychosis, neuromuscular dysfunction, demyelination, mental health during pandemic
MeSH terms
Betacoronavirus, Cytokine Release Syndrome, COVID-19, SARS-CoV-2, Acute Disease, Anxiety, Mental Disorders, Chronic Disease, Demyelinating Diseases, Depression, Humans, Immunologic Factors, Mental Health, Nervous System Diseases, Pneumonia, Viral, Psychoneuroimmunology, Psychotic Disorders, Public Health, Stress Disorders, Post-Traumatic, Coronavirus Infections, Bacterial Translocation, Neurodegenerative Diseases, Pandemics

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