Neuropathology of COVID-19 (neuro-COVID): clinicopathological update

Lou, Jerry J.; Movassaghi, Masoud; Gordy, Dominique E; Olson, Madeline G; Zhang, Ting; Khurana, Maya S.; Chen, Zesheng; Perez‐Rosendahl, Mari; Thammachantha, Samasuk; Singer, Elyse J.; Magaki, Shino; Vinters, Harry V.; Yong, William H.

doi:10.17879/freeneuropathology-2021-2993

Cited by 66 publications

(34 citation statements)

References 112 publications

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“…The pathophysiology and management of long COVID is currently an emerging field with little information available [8,54]. Autonomic dysfunction, a chronic inflammatory and autoimmune response, has been proposed as a possible mechanism for long COVID [55], together with means of management [56] and pathological proof of SARS-CoV-2 presence in the vagus nerve structure [57]. Other authors propose that cognitive behavioral therapy may be an effective treatment for post-COVID fatigue syndrome [58].…”

Section: Discussionmentioning

confidence: 99%

Clinical patterns of somatic symptoms in patients suffering from post-acute long COVID: a systematic review

Nguyen

Hoang

Dao

et al. 2022

Eur J Clin Microbiol Infect Dis

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Background Long COVID-19 may affect patients after hospital discharge. Aims This study aims to describe the burden of the long-term persistence of clinical symptoms in COVID-19 patients. Methods We conducted a systematic review by using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guideline. The PubMed and Google Scholar databases were searched for studies that included information on the prevalence of somatic clinical symptoms lasting at least 4 weeks after the onset of a PCR-or serology-confirmed diagnosis of COVID-19. The prevalence of persisting clinical symptoms was assessed and risk factors were described when investigated. Psychological symptoms and cognitive disorders were not evaluated in this study. Results Thirty-seven articles met the inclusion criteria. Eighteen studies involved in-patients only with a duration of followup of either less than 12 weeks, 12 weeks to 6 months, or more. In these studies, fatigue (16-64%), dyspnea (15-61%), cough (2-59%), arthralgia (8-55%), and thoracic pain (5-62%) were the most frequent persisting symptoms. In nineteen studies conducted in a majority of out-patients, the persistence of these symptoms was lower and 3% to 74% of patients reported prolonged smell and taste disorders. The main risk factors for persisting symptoms were being female, older, having comorbidities and severity at the acute phase of the disease. Conclusion COVID-19 patients should have access to dedicated multidisciplinary healthcare allowing a holistic approach. Effective outpatient care for patients with long-COVID-19 requires coordination across multiple sub-specialties, which can be proposed in specialized post-COVID units.

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Section: Discussionmentioning

confidence: 99%

Clinical patterns of somatic symptoms in patients suffering from post-acute long COVID: a systematic review

Nguyen

Hoang

Dao

et al. 2022

Eur J Clin Microbiol Infect Dis

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“…Other comparatively less common symptoms include: nasal and chest congestion, conjunctivitis, headache, muscle or joint pain, skin rashes, nausea or vomiting, diarrhea, or chills. Neurological manifestations of COVID-19 (frequently referred to as neuro-COVID or nCoV [ 12 , 13 ]) are acute encephalitis, encephalopathy, ataxia, tremors, stroke (hemorrhagic or ischemic), hyposmia/anosmia, hypogeusia/dysgeusia/ageusia, Guillain-Barre-like syndrome, peripheral neuropathy and myopathy, delirium, nerve damage, irritability, or dizziness, anxiety, depression, fatigue and sleep disorders ( ; ; accessed on 28 January 2022 [ 14 , 15 , 16 , 17 ]). Occurrence of these symptoms suggests an involvement of the nervous system [ 18 , 19 , 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

A Peek into Pandora’s Box: COVID-19 and Neurodegeneration

Chandra¹,

Johri²

2022

Brain Sciences

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Ever since it was first reported in Wuhan, China, the coronavirus-induced disease of 2019 (COVID-19) has become an enigma of sorts with ever expanding reports of direct and indirect effects of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on almost all the vital organ systems. Along with inciting acute pulmonary complications, the virus attacks the cardiac, renal, hepatic, and gastrointestinal systems as well as the central nervous system (CNS). The person-to-person variability in susceptibility of individuals to disease severity still remains a puzzle, although the comorbidities and the age/gender of a person are believed to play a key role. SARS-CoV-2 needs angiotensin-converting enzyme 2 (ACE2) receptor for its infectivity, and the association between SARS-CoV-2 and ACE2 leads to a decline in ACE2 activity and its neuroprotective effects. Acute respiratory distress may also induce hypoxia, leading to increased oxidative stress and neurodegeneration. Infection of the neurons along with peripheral leukocytes’ activation results in proinflammatory cytokine release, rendering the brain more susceptible to neurodegenerative changes. Due to the advancement in molecular biology techniques and vaccine development programs, the world now has hope to relatively quickly study and combat the deadly virus. On the other side, however, the virus seems to be still evolving with new variants being discovered periodically. In keeping up with the pace of this virus, there has been an avalanche of studies. This review provides an update on the recent progress in adjudicating the CNS-related mechanisms of SARS-CoV-2 infection and its potential to incite or accelerate neurodegeneration in surviving patients. Current as well as emerging therapeutic opportunities and biomarker development are highlighted.

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“…Additionally, diverse cardiac histopathologic findings, including endothelial cell damage and inflammatory cell infiltrates without associated cardiac necrosis ( 10 – 12 ), have been described on autopsy of COVID-19 decedents but at variable prevalence. Subsequently, the detection of microvascular thrombi in the hearts ( 13 , 14 ), lungs ( 15 – 19 ), liver ( 20 ), brain ( 21 ), and skin ( 22 ) of patients with COVID-19 raised the possibility that, in severe cases, COVID-19 may be more akin to a systemic illness. Such reports of multiorgan microthrombi, along with a high incidence of venous thromboembolism in severe and critical COVID-19, have led investigators to hypothesize that severe SARS-CoV-2 infection promotes a hypercoagulable state, referred to as COVID-19–associated coagulopathy ( 23 – 27 ).…”

Section: Introductionmentioning

confidence: 99%