Global prevalence of chronic fatigue syndrome among long COVID-19 patients: A systematic review and meta-analysis

Salari, Nader; Khodayari, Yassaman; Hosseinian-Far, Amin; Zarei, Hosna; Rasoulpoor, Shabnam; Akbari, Hakimeh; Mohammadi, Masoud

doi:10.1186/s13030-022-00250-5

Cited by 49 publications

(45 citation statements)

References 88 publications

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“…These symptoms include fatigue, sleep problems, problems thinking, and muscle and joint pain. The high frequency of fatigue has been reported by many researchers (Salari et al, 2022), but the evidence for CFS as a sequela of COVID is limited because many studies do not follow patients long enough to establish a diagnosis of CFS.…”

Section: Discussionmentioning

confidence: 99%

Symptom Clusters in Adults with Post-COVID-19: A Cross-Sectional Survey

et al. 2023

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More than 100 symptoms have been reported for post-coronavirus disease 2019 (COVID-19) and this study aimed to organize self-reported symptoms by identifying symptom clusters. We used a cross-sectional survey with a convenience sample of 491 adults who reported experiencing prolonged symptoms of COVID. A list of 25 symptoms of post-COVID-19 was used to measure the symptoms, and exploratory factor analysis was undertaken to identify symptom clusters for people with symptoms lasting 5 to 8 weeks and 9 weeks or longer. Six symptom clusters were identified for each of the two groups, and five clusters were similar across both groups: respiratory, general viral, smell/taste, cognitive cardiac, and mental health. The >9-week group reported symptoms primarily from two factors: respiratory-muscular and mental health. Post-COVID-19 symptom clusters differ across timeframes. Symptom clusters were useful in establishing coherent patterns of multiple complex symptoms.

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Section: Discussionmentioning

confidence: 99%

Symptom Clusters in Adults with Post-COVID-19: A Cross-Sectional Survey

et al. 2023

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“…However, neuropathy and myopathy are more prevalent than GBS. For example, one study reported a combined rate of 56.3% among 400 hospitalized COVID-19 patients [ 67 ]. The rate of neuropathic pain can be as high as 2.3% in hospitalized patients with COVID-19.…”

Section: Reviewmentioning

confidence: 99%

Review of Neurological Manifestations of SARS-CoV-2

Priyal¹,

Sehgal²,

Kapila³

et al. 2023

Cureus

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect any part of the neuraxis. Many neurological conditions have been attributed to be caused by SARS-CoV-2, namely encephalopathy (acute necrotizing encephalopathy and encephalopathy with reversible splenial lesions), seizures, stroke, cranial nerve palsies, meningoencephalitis, acute disseminated encephalomyelitis (ADEM), transverse myelitis (long and short segment), Guillain-Barré syndrome (GBS) and its variants, polyneuritis cranialis, optic neuritis (ON), plexopathy, myasthenia gravis (MG), and myositis. The pathophysiology differs depending on the time frame of presentation. In patients with concomitant pulmonary disease, for instance, acute neurological illness appears to be caused by endotheliopathy and cytokine storm. Autoimmunity and molecular mimicry are causative for post-coronavirus disease 2019 (COVID-19)-sequelae. It has not yet been shown that the virus can penetrate the central nervous system (CNS) directly. This review aims to describe the disease and root pathogenic cause of the various neurological manifestations of COVID-19. We searched Pubmed/Medline and Google Scholar using the keywords “SARS-CoV-2” and “neurological illness” for articles published between January 2020 and November 2022. Then, we used the SWIFT-Review (Sciome LLC, North Carolina, United States), a text-mining workbench for systematic review, to classify the 1383 articles into MeSH hierarchical tree codes for articles on various parts of the nervous system, such as the CNS, peripheral nervous system, autonomic nervous system, neuromuscular junction, sensory system, and musculoskeletal system. Finally, we reviewed 152 articles in full text. SARS-CoV-2 RNA has been found in multiple brain areas without any histopathological changes. Despite the absence of in vivo virions or virus-infected cells, CNS inflammation has been reported, especially in the olfactory bulb and brain stem. SARS-CoV-2 genomes and proteins have been found in affected individuals’ brain tissues, but corresponding neuropathologic changes are seldom found in these cases. Additionally, viral RNA can rarely be identified in neurological patients’ CSF post hoc SARS-CoV-2 infection. Most patients with neurological symptoms do not have active viral replication in the nervous system and infrequently have typical clinical and laboratory characteristics of viral CNS infections. Endotheliopathy and the systemic inflammatory response to SARS-CoV-2 infection play a crucial role in developing neuro-COVID-19, with proinflammatory cytokine release mediating both pathological pathways. The systemic inflammatory mediators likely activate astrocytes and microglia across the blood-brain barrier, indirectly affecting CNS-specific immune activation and tissue injury. The management differs according to co-morbidities and the neurological disorder.

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“…La fatigue est le symptôme le plus fréquent du syndrome post-COVID-19 [56] . Dans des grandes méta-analyses, elle était rapportée dans 47 [57] et 45 % [58] des cas, respectivement. Elle diminuait significativement à deux ans dans la vaste étude chinoise ayant réévalué une cohorte à ce terme [18] .…”

Section: Symptômes Générauxunclassified