Abstract:AbstractCoronavirus disease (COVID-19) is caused by SARS-CoV-2. Physicians in China reported what is believed to be the first adult case of a SARS-CoV-2 infection associated with acute Guillain-Barré syndrome (GBS), followed by five adult Italian patients and another case in the United States of America. In the current report we present one of the first descriptions of an association of GBS and SARS-CoV-2 infection within a child. In our facility, and eleven ye… Show more
“…In the present study, mean age at onset in patients with GBS largely overlapped that of classic COVID-19 subjects [70,71]. However, pediatric cases with GBS have been increasingly reported in the literature [21,27,35,41], suggesting that, with the spreading of the pandemic, a broader age range might be affected. Moreover, we found a higher prevalence of GBS in males compared to females, as previously reported for Zika virus-GBS [72].…”
Section: Discussionmentioning
confidence: 51%
“…Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18,46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9,27,31,36,37,42,52] and two cases [17,46], respectively ( Table 1).…”
Section: Results Of Electrophysiological Csf Biochemical and Neuromentioning
confidence: 97%
“…1). The mean age at onset was 55 ± 17 years (min 11-max 94), including four pediatric cases [21,27,35,41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643).…”
Section: Epidemiological Distribution and Demographic Characteristicsmentioning
Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain-Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11-max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.
“…In the present study, mean age at onset in patients with GBS largely overlapped that of classic COVID-19 subjects [70,71]. However, pediatric cases with GBS have been increasingly reported in the literature [21,27,35,41], suggesting that, with the spreading of the pandemic, a broader age range might be affected. Moreover, we found a higher prevalence of GBS in males compared to females, as previously reported for Zika virus-GBS [72].…”
Section: Discussionmentioning
confidence: 51%
“…Moreover, brainstem leptomeningeal enhancement was described in two cases with AIDP, both with clinical cranial nerve involvement [18,46]. On the other hand, spinal nerve roots and leptomeningeal enhancement were reported in eight [9,27,31,36,37,42,52] and two cases [17,46], respectively ( Table 1).…”
Section: Results Of Electrophysiological Csf Biochemical and Neuromentioning
confidence: 97%
“…1). The mean age at onset was 55 ± 17 years (min 11-max 94), including four pediatric cases [21,27,35,41]. A significative prevalence of men compared to women was noticed (50 vs. 23 cases: 68.5% vs. 31.5%) with no significant difference in age at onset between men and women (mean: 55 ± 18 vs. 56 ± 16 years, p = 0.643).…”
Section: Epidemiological Distribution and Demographic Characteristicsmentioning
Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain-Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11-max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.
“…For instance, lower limb weakness and paresthesia that may lead to generalized tetraparesis or tetraplegia evolving over a period of several days have been repeatedly observed [ 92 ]. Typically, MRI performed with the administration of gadolinium reveals enhancement of the cauda equina nerve roots on postcontrast findings and asymmetrical thickening and hyperintensity of postganglionic roots of the brachial and lumbar plexuses [ 93 , 94 ]. Moreover, cytoalbuminologic dissociation of the CSF is a characteristic finding in GBS, pointing to nerve root involvement.…”
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus, is responsible for the outbreak of coronavirus disease 19 (COVID-19) and was first identified in Wuhan, China in December 2019. It is evident that the COVID-19 pandemic has become a challenging world issue. Although most COVID-19 patients primarily develop respiratory symptoms, an increasing number of neurological symptoms and manifestations associated with COVID-19 have been observed. In this narrative review, we elaborate on proposed neurotropic mechanisms and various neurological symptoms, manifestations, and complications of COVID-19 reported in the present literature. For this purpose, a review of all current published literature (studies, case reports, case series, reviews, editorials, and other articles) was conducted and neurological sequelae of COVID-19 were summarized. Essential and common neurological symptoms including gustatory and olfactory dysfunctions, myalgia, headache, altered mental status, confusion, delirium, and dizziness are presented separately in sections. Moreover, neurological manifestations and complications that are of great concern such as stroke, cerebral (sinus) venous thrombosis, seizures, meningoencephalitis, Guillain–Barré syndrome, Miller Fisher syndrome, acute myelitis, and posterior reversible encephalopathy syndrome (PRES) are also addressed systematically. Future studies that examine the impact of neurological symptoms and manifestations on the course of the disease are needed to further clarify and assess the link between neurological complications and the clinical outcome of patients with COVID-19. To limit long-term consequences, it is crucial that healthcare professionals can early detect possible neurological symptoms and are well versed in the increasingly common neurological manifestations and complications of COVID-19.
“…Similarly, Demirci Otluoglu et al noted CSF protein was 0.4 mg/L (0.04 mg/dL) and Dharsandiya et al indicated the CSF protein was 39 g/dL (3,900 mg/dL), but both authors described the protein as normal, and Matos et al reported a CSF protein of 0.78 mg/dL, but noted it was mildly elevated; we presumed these were meant to be 0.4g/L (40 mg/dL), 39 mg/dL, and 78 mg/dL, respectively [ 150 , 151 , 200 ]. There were 27/397 (7%) patients who had CSF protein >200 mg/dL (19/27 (70%) with symptoms that localized to the CNS and 8/27 (30%) with symptoms that localized to the PNS) [ 16 , 21 , 31 , 32 , 34 , 44 , 53 , 58 , 78 , 81 , 89 , 104 , 113 , 127 , 128 , 160 , 170 , 173 , 176 , 184 , 199 , [220] , [221] , [222] , 245 ]. Fig.…”
We sought to review the literature on cerebrospinal fluid (CSF) testing in patients with COVID-19 for evidence of viral neuroinvasion by SARS-CoV-2. Methods: We performed a systematic review of Medline and Embase between December 1, 2019 and November 18, 2020 to identify case reports or series of patients who had COVID-19 diagnosed based on positive SARS-CoV-2 polymerase chain reaction (PCR) or serologic testing and had CSF testing due to a neurologic symptom. Results: We identified 242 relevant documents which included 430 patients with COVID-19 who had acute neurological symptoms prompting CSF testing. Of those, 321 (75%) patients had symptoms that localized to the central nervous system (CNS). Of 304 patients whose CSF was tested for SARS-CoV-2 PCR, there were 17 (6%) whose test was positive, all of whom had symptoms that localized to the central nervous system (CNS). The majority (13/17, 76%) of these patients were admitted to the hospital because of neurological symptoms. Of 58 patients whose CSF was tested for SARS-CoV-2 antibody, 7 (12%) had positive antibodies with evidence of intrathecal synthesis, all of whom had symptoms that localized to the CNS. Of 132 patients who had oligoclonal bands evaluated, 3 (2%) had evidence of intrathecal antibody synthesis. Of 77 patients tested for autoimmune antibodies in the CSF, 4 (5%) had positive findings. Conclusion: Detection of SARS-CoV-2 in CSF via PCR or evaluation for intrathecal antibody synthesis appears to be rare. Most neurological complications associated with SARS-CoV-2 are unlikely to be related to direct viral neuroinvasion.
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