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Open Access Journal of Pulmonary & Respiratory Sciences Editorial 5 min read

Post-Acute-COVID-19-Illness Neuropsychiatric Sequelae

Cheepsattayakorn A*
* Corresponding author
ISSN: 2642-1143  10.23880/oajprs-16000143  Received: June 18, 2021  Published: June 25, 2021
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Keywords
Acute-COVID-19 Neuropsychiatric Sequelae
Abstract

Direct viral invasion, neurodegeneration, microvascular thrombosis, neuroinflammation, and severe systemic inflammation can be the causes of post-acute-COVID-19- illness neuropathology [1-4], supported by brain parenchyma and vessel changes of possibly driven inflammation in neurons, supportive cells, and brain vasculature in COVID-19 autopsy series [5,6]

Introduction

Direct viral invasion, neurodegeneration, microvascular thrombosis, neuroinflammation, and severe systemic inflammation can be the causes of post-acute-COVID-19- illness neuropathology [1, 2, 3, 4], supported by brain parenchyma and vessel changes of possibly driven inflammation in neurons, supportive cells, and brain vasculature in COVID-19 autopsy series [5, 6]. A role in persistent brain effects of SARS- CoV-2 (COVID-19) may be played by an accumulation of memory T cells, a biomarker of immunosenescence in tissue injury and aging, accompanying with the decreased ability to respond to new antigens that are demonstrated in chronic low-level brain inflammation [7]. Cognitive-behavioral changes directly associated with the levels of immune activation [8]. Passive diffusion and axonal transport via the olfactory complex, viral invasion in the extracellular spaces of olfactory epithelium and dysfunctional lymphatic drainage from circumventricular organs [9, 10]. Elevated peripheral blood levels of neurofilament light chain, a biomarker of brain injury with a more sustained increase in severe infections has been identified in post-acute-COVID-19-illness phase. Post-traumatic-stress disorder (PTSD) or deconditioning may be mechanisms that are hypothesized in critically ill COVID-19 patients with post-acute-COVID-19-illness brain fog whereas dysautonomia may be the cause of post-acute- COVID-19-illness brain fog in previously mild-COVID-19 patients [11, 12, 13, 14, 15]. Approximately, 20 %-40 % of patients with previously critical-COVID-19 illness demonstrated long-term cognitive impairment [16]. Non-restorative sleep, depressive symptoms, diffuse myalgia, post-viral syndrome of chronic malaise late-onset headaches ascribed to high cytokine levels, and migraine-like headaches (frequently refractory to traditional analgesics have been reported in post-COVID-19 survivors. Around 38 % of post-acute-COVID-19-illness patients had ongoing headaches after 6 weeks [17, 18, 19, 20, 21, 22]. At up to 6 months follow-up, approximately, 10 % of post- acute-COVID-19-illness survivors may persist loss of smell and taste [23, 24, 25, 26]. Ischemic or hemorrhagic stroke hypoxic- anoxic brain damage, posterior reversible encephalopathy syndrome and acute disseminated myelitis [27, 28, 29, 30], may contribute to required-extensive-rehabilitation permanent or lingering neurological deficits.

Conclusion

In conclusion, further studies are urgently needed to identify the exact mechanisms and biomarkers of the neurological post-acute-COVID-19-illness sequelae.

References

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Cite this article

BibTeX
APA
RIS
@article{cheepsattayakorn2021,
  title   = {Post-Acute-COVID-19-Illness Neuropsychiatric Sequelae},
  author  = {Cheepsattayakorn A},
  journal = {Open Access Journal of Pulmonary & Respiratory Sciences},
  year    = {2021},
  volume  = {6},
  number  = {1},
  doi     = {10.23880/oajprs-16000143}
}
Cheepsattayakorn A (2021). Post-Acute-COVID-19-Illness Neuropsychiatric Sequelae. Open Access Journal of Pulmonary & Respiratory Sciences, 6(1). https://doi.org/10.23880/oajprs-16000143
TY  - JOUR
TI  - Post-Acute-COVID-19-Illness Neuropsychiatric Sequelae
AU  - Cheepsattayakorn A
JO  - Open Access Journal of Pulmonary & Respiratory Sciences
PY  - 2021
VL  - 6
IS  - 1
DO  - 10.23880/oajprs-16000143
ER  -
BETA

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