A case of possible atypical demyelinating event of the central nervous system following COVID-19

Abstract

After the novel coronavirus disease outbreak first began in Wuhan, China, in December 2019, the viral epidemic has quickly spread across the world, and it is now a major public health concern. Here we present a 21-year-old male with encephalomyelitis following intermittent vomiting and malaise for 4 days. He reported upper respiratory signs and symptoms 2 weeks before this presentation. Two cerebrospinal fluid (CSF) analyses were notable for mononuclear pleocytosis, elevated protein (more than 100 mg/dl), and hypoglycorrhachia. Brain Magnetic Resonance Imaging (MRI) showed bilateral posterior internal capsule lesions extending to the ventral portion of the pons and a marbled splenium hyperintensity pattern. Cervical and thoracic MRI showed longitudinally extensive transverse myelitis (LETM), none of which were enhanced with gadolinium. Both the AQP4 and MOG antibodies were negative. Spiral chest computed tomography (CT) scan confirmed to COVID-19 as did the high IgG level against coronavirus, but the oropharyngeal swabs were negative. Neurological manifestations of COVID-19 have not been adequately studied. Some COVID-19 patients, especially those suffering from a severe disease, are highly likely to have central nervous system (CNS) manifestations. Our case is a post-COVID-19 demyelinating event in the CNS.

Brain abnormalities in COVID-19 acute/subacute phase: A rapid systematic review

“…However, the analyzed data further suggest that the prevalence of LA is higher in this patient population than expected for age. Other possible interpretations may include encephalitis as suggested in several reports (Anzalone et al, 2020;Asfar et al, 2020;Espinosa et al, 2020;Hayashi et al, 2020;Kremer et al, 2020), acute necrotizing encephalitis (Virhammar et al, 2020), encephalomyelitis (Abdi et al, 2020;Zoghi et al, 2020), demyelination (Zanin et al, 2020;Parsons et al, 2020;Zoghi et al, 2020), or microangiopathy (Fischer et al, 2020). Therefore, we encourage future studies to report more detailed description of the WM changes in order to establish differential characteristics of COVID-19-related vs. age-related changes in WM.…”

“…The midline structures of the brain were affected in 12/124 (10%) affected cases and mainly included abnormalities in the corpus callosum, i.e., hyperintensities [L (Hayashi et al, 2020); β (Zoghi et al, 2020)], hemorrhage [I] (Franceschi et al, 2020) Additionally, one of those patients [F] (Dixon et al, 2020) showed signs of swelling and hemorrhage in brain stem and hemorrhage in pons. Hyperintensities were noted in midbrain [A (Abdi et al, 2020); Z (Virhammar et al, 2020)] and pons [D (Asfar et al, 2020); β (Zoghi et al, 2020)].…”

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

“…Further investigation through brain imaging revealed hemorrhagic rim enhancing lesions within the bilateral thalami, medial temporal lobes and subinsular regions, coherent with the diagnosis of this rare type of encephalopathy. Furthermore, Zoghi and colleagues [63] described the case of a 21-year-old man who developed encephalomyelitis with atypical demyelination pattern revealed by MRI. The patient had negative medical history.…”

Detection of SARS-CoV-2 nucleic acid in CSF by ultrahigh depth sequencing in a patient with COVID-19 and neurological dysfunction: a case report

“…However, among these recognized human respiratory pathogens, at least HCoV-OC43, HCoV-229E, and SARS-CoV could be associated with the triggering or the exacerbation of neurological diseases as viral RNA or infectious virus can be detected in human brains [9][10][11]. Preliminary reports showed some COVID-19 patients showed CNS manifestations, such as dizziness, headache, nausea, vomiting, impaired consciousness, acute cerebrovascular disease, ataxia, and seizure, which warned that SARS-CoV-2 could have neuroinvasive potential [4][5][6][7][8][9][10][11][12][13]. Similar to SARS-CoV, SARS-CoV-2 also bind to the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells [14].…”

“…Recently, a study reported that SARS-CoV-2 can productively infect human neural progenitor cells and brain organoids, highlighting the potential of direct viral involvement in neurological symptoms in COVID-19 patients [5]. However, proof of a direct involvement of SARS-CoV-2 is missing in the most cases of COVID-19 with central nervous system (CNS) symptoms have been reported until now, because the virus or nucleic acid was not detected in cerebrospinal uid (CSF) [6][7][8]. Here, we report a case of involvement of the CNS by the SARS-CoV-2, which was con rmed by ultrahigh depth metagenomic next generation sequencing (mNGS).…”