Neurological manifestations of COVID-19, SARS and MERS

Verstrepen, Kato; Baisier, Laure; Cauwer, Harald De

doi:10.1007/s13760-020-01412-4

Cited by 58 publications

(52 citation statements)

References 56 publications

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“…When he was seen six months later he was continuing to make slow improvement [ 4 ]. SARS, another subspecies in the coronavirus family, also has documented cases of polyneuropathy [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Peripheral Neuropathy as a Complication of SARS-Cov-2

Bureau¹,

Obeidat²,

Dhariwal³

et al. 2020

Cureus

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Previous reports have shown various neurological manifestations in about 36.4% of patients infected with SARS-Cov-2. However, peripheral neuropathy was only reported once before. A 40-year-old healthy woman presented with two weeks of cough, nasal congestion, sore throat, intermittent fevers, fatigue, and myalgia but no weakness. She tested positive for the SARS-Cov-2. Physical exam showed no neurologic deficit. Two weeks later, respiratory symptoms were improving but she developed sudden leg pain, numbness, and weakness. She described it as a “pain crisis”. Neurological exam showed bilateral symmetrical, non-ascending lower extremity weakness and normal, symmetric reflexes. She had normal magnetic resonance imaging of the brain and spine, spinal fluid analysis, serum studies including creatinine kinase and C-reactive protein. She had elevated lactate dehydrogenase, low serum copper (72.9 (ref: 80.0-155.0 ug/dL)) and low vitamin B6 (14.6 (ref: 20.0-125.0 nmol/L)). A diagnosis of SARS-Cov-2-associated peripheral neuropathy was considered. We pursued empiric treatment with intravenous steroids (1000 mg methylprednisolone for three days), followed by a total of 2 g/kg of intravenous immunoglobulins (IVIG) given over five days. Pain management was done with gabapentin and ketorolac. We replaced copper and vitamin B6. Six weeks later, she reported improvement and was closer to baseline, but she endorsed residual, exertional, mild bilateral lower extremity pain, numbness, and weakness. Previous reports of treatment of SARS-Cov-2-associated neuropathy included corticosteroids and IVIG. Our patient saw the most symptomatic improvement with gabapentin. In our case, the preserved reflexes, lack of ascending pattern, sudden onset of symptoms, and normal cerebrospinal fluid (CSF) argued against Guillain-Barre syndrome. Copper deficiency can result in myelopathy but not peripheral neuropathy, so is unlikely the sole explanation. Awareness and early treatment of peripheral neuropathy in SARS-Cov-2 can result in improved clinical outcomes for patients.

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“…When he was seen six months later he was continuing to make slow improvement [ 4 ]. SARS, another subspecies in the coronavirus family, also has documented cases of polyneuropathy [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Peripheral Neuropathy as a Complication of SARS-Cov-2

Bureau¹,

Obeidat²,

Dhariwal³

et al. 2020

Cureus

View full text Add to dashboard Cite

show abstract

“…It is assumed that human coronaviruses' neurovirulence might contribute to short- and long-term neurological diseases such as encephalomyelitis and multiple sclerosis. As they longer persist in the CNS, the more long-term sequelae could develop [ 10 ]. There is mounting evidence that focused on similarities between coronaviruses and their neurotropism features, which could be applicable for SARS-CoV-2 [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Demyelinating Changes Alike to Multiple Sclerosis: A Case Report of Rare Manifestations of COVID-19

Yavari

Raji

Moradi

et al. 2020

Case Reports in Neurological Medicine

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COVID-19, as a global concern and pivotal issue in the healthcare system, could have various presentations, leading to difficulty in diagnosis and management. Neuroinvasive potency, as claimed by preliminary studies, is a considerable pathogenesis. Serious neurological disorders like multiple sclerosis (MS) were out of the blue to be the first demonstration of COVID-19. This report highlights the representation of MS in a young woman, which resulted in a COVID-19 diagnosis.

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“…SARS-CoV-2 infection also induces long-term neurological sequelae in at least one-third of human cases. Infection with other coronaviruses, such as mouse hepatitis virus (MHV) in mice and SARS-CoV-1 and Middle East Respiratory Syndrome (MERS) virus in humans, has been shown to cause neurological disease [ 11 , 12 ]. However, little is known about the pathophysiology of SARS-CoV-2-associated neurological disease in humans.…”

Section: Introductionmentioning

confidence: 99%

Neuroinvasion and Encephalitis Following Intranasal Inoculation of SARS-CoV-2 in K18-hACE2 Mice

Kumari

Rothan

Natekar

et al. 2021

Viruses

238

222

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Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can cause neurological disease in humans, but little is known about the pathogenesis of SARS-CoV-2 infection in the central nervous system (CNS). Herein, using K18-hACE2 mice, we demonstrate that SARS-CoV-2 neuroinvasion and encephalitis is associated with mortality in these mice. Intranasal infection of K18-hACE2 mice with 105 plaque-forming units of SARS-CoV-2 resulted in 100% mortality by day 6 after infection. The highest virus titers in the lungs were observed on day 3 and declined on days 5 and 6 after infection. By contrast, very high levels of infectious virus were uniformly detected in the brains of all the animals on days 5 and 6. Onset of severe disease in infected mice correlated with peak viral levels in the brain. SARS-CoV-2-infected mice exhibited encephalitis hallmarks characterized by production of cytokines and chemokines, leukocyte infiltration, hemorrhage and neuronal cell death. SARS-CoV-2 was also found to productively infect cells within the nasal turbinate, eye and olfactory bulb, suggesting SARS-CoV-2 entry into the brain by this route after intranasal infection. Our data indicate that direct infection of CNS cells together with the induced inflammatory response in the brain resulted in the severe disease observed in SARS-CoV-2-infected K18-hACE2 mice.

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Neurological manifestations of COVID-19, SARS and MERS

Cited by 58 publications

References 56 publications

Peripheral Neuropathy as a Complication of SARS-Cov-2

Peripheral Neuropathy as a Complication of SARS-Cov-2

Demyelinating Changes Alike to Multiple Sclerosis: A Case Report of Rare Manifestations of COVID-19

Neuroinvasion and Encephalitis Following Intranasal Inoculation of SARS-CoV-2 in K18-hACE2 Mice

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