COVID-19 for neurologists

COVID-19 for neurologists

A myriad of neurologic symptoms, associated with structural brain changes, were reported. Dolatshahi et al. provided evidence to critically discuss the claim that the survived patients could possibly be at increased risk for neurodegenerative diseases via various mechanisms. This virus can directly invade the brain through the olfactory bulb, retrograde axonal transport from peripheral nerve endings, or via hematogenous or lymphatic routes. Infection of the neurons along with peripheral leukocyte activation results in pro-inflammatory cytokine increment, rendering the brain to neurodegenerative changes. Also, occupation of the Angiotensin-converting enzyme 2 (ACE2) with the virus may lead to a decline in ACE-2 activity, which acts as a neuroprotective factor. Furthermore, acute respiratory distress syndrome (ARDS) and septicemia induce hypoxemia and hypoperfusion, which is locally exacerbated due to the hypercoagulable state and micro-thrombosis in brain vessels, leading to oxidative stress and neurodegeneration. Common risk factors for COVID-19 and neurodegenerative diseases, such as metabolic risk factors, genetic predispositions, and even gut microbiota dysbiosis, can contribute to a higher occurrence of neurodegenerative diseases in COVID-19 survivors. However, it should be considered that the severity of the infection, the extent of neurologic symptoms, and the persistence of viral infection consequences are major determinants of this association. Importantly, whether this pandemic will increase the overall incidence of neurodegeneration is not clear, as a high percentage of patients with a severe form of COVID-19 might probably not survive enough to develop neurodegenerative disease1).

see COVID-19 and Guillain-Barré Syndrome.

There is an increased attention to stroke following SARS-CoV-2. The goal of a study was to better depict the short-term risk of stroke and its associated factors among SARS-CoV-2 hospitalized patients.

This multicentre, multinational observational study includes hospitalized SARS-CoV-2 patients from North and South America (United States, Canada, and Brazil), Europe (Greece, Italy, Finland, and Turkey), Asia (Lebanon, Iran, and India), and Oceania (New Zealand). The outcome was the risk of subsequent stroke. Centres were included by non-probability sampling. The counts and clinical characteristics including laboratory findings and imaging of the patients with and without a subsequent stroke were recorded according to a predefined protocol. Quality, risk of bias, and heterogeneity assessments were conducted according to ROBINS-E and Cochrane Q-test. The risk of subsequent stroke was estimated through meta-analyses with random effect models. Bivariate logistic regression was used to determine the parameters with predictive outcome value. The study was reported according to the STROBE, MOOSE, and EQUATOR guidelines.

Shahjouei et al. received data from 26,175 hospitalized SARS-CoV-2 patients from 99 tertiary centres in 65 regions of 11 countries until May 1st, 2020. A total of 17,799 patients were included in meta-analyses. Among them, 156(0.9%) patients had a stroke-123(79%) ischaemic stroke, 27(17%) intracerebral/subarachnoid hemorrhage, and 6(4%) cerebral sinus thrombosis. Subsequent stroke risks calculated with meta-analyses, under low to moderate heterogeneity, were 0.5% among all centres in all countries, and 0.7% among countries with higher health expenditures. The need for mechanical ventilation (OR: 1.9, 95% CI:1.1-3.5, p = 0.03) and the presence of ischaemic heart disease (OR: 2.5, 95% CI:1.4-4.7, p = 0.006) were predictive of stroke.

Interpretation: The results of this multi-national study on hospitalized patients with SARS-CoV-2 infection indicated an overall stroke risk of 0.5%(pooled risk: 0.9%). The need for mechanical ventilation and the history of ischaemic heart disease are the independent predictors of stroke among SARS-CoV-2 patients 2).


International MG/COVID-19 Working Group, Jacob S, Muppidi S, Guidon A, Guptill J, Hehir M, Howard JF Jr, Illa I, Mantegazza R, Murai H, Utsugisawa K, Vissing J, Wiendl H, Nowak RJ. Guidance for the management of myasthenia gravis (MG) and Lambert-Eaton myasthenic syndrome (LEMS) during the COVID-19 pandemic. J Neurol Sci. 2020 Mar 25;412:116803. doi: 10.1016/j.jns.2020.116803. [Epub ahead of print] PubMed PMID: 32247193.


1)

Dolatshahi M, Sabahi M, Aarabi MH. Pathophysiological Clues to How the Emergent SARS-CoV-2 Can Potentially Increase the Susceptibility to Neurodegeneration. Mol Neurobiol. 2021 Jan 8:1–16. doi: 10.1007/s12035-020-02236-2. Epub ahead of print. Erratum in: Mol Neurobiol. 2021 Jan 27;: PMID: 33417221; PMCID: PMC7791539.
2)

Shahjouei S, Naderi S, Li J, et al. Risk of stroke in hospitalized SARS-CoV-2 infected patients: A multinational study [published online ahead of print, 2020 Aug 17]. EBioMedicine. 2020;59:102939. doi:10.1016/j.ebiom.2020.102939

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