key: cord-1044323-7gbgtqhh
authors: Sriwastava, Shitiz; Kataria, Saurabh; Tandon, Medha; Patel, Jenil; Patel, Riddhi; Jowkar, Abbas; Daimee, Maha; Bernitsas, Evanthia; Jaiswal, Preeti; Lisak, Robert P.
title: Guillain Barré Syndrome and its variants as a manifestation of COVID-19: A systemic review of case report and case series
date: 2020-12-09
journal: J Neurol Sci
DOI: 10.1016/j.jns.2020.117263
sha: 71bb44525cb9cf3569b1091655950696a5188a08
doc_id: 1044323
cord_uid: 7gbgtqhh

BACKGROUND: The COVID-19 pandemic caused by SARS-COV-2 began in Wuhan, China in December 2019. Reports of COVID-19 with central (CNS) and peripheral nervous (PNS) system manifestations are emerging. In this systematic review, we compared and summarized the demographics, clinical features, Brighton criteria, immunological and laboratory findings with a focus on modified Erasmus GBS Outcome Score (mEGOS) in SARS-CoV-2 patients with GBS and its variants. METHODS: Based on PRISMA guidelines, we searched three databases (PubMed, Scopus, and Google Scholar) for studies on COVID-19 and GBS between December 1, 2019 to July 15, 2020. For descriptive analysis, we studied two groups with: 1) acute inflammatory demyelinating polyradiculoneuropathy (AIDP) variant, and 2) Non-AIDP/Other variants. We compared mEGOS scores for patients in both groups along with other key clinical features. RESULTS: Of the 50 GBS cases identified from 37 studies, 33 (66%) had acute inflammatory demyelinating polyradiculopolyneuropathy (AIDP) while 17 (34%) were of other (non-AIDP) variants. There mEGOS scores did not differ between AIDP patients and AMAN/AMSAN patients. Majority of the AIDP (66.7%) and AMAN/AMSAN (57.2%) patients belonged to Brighton level 1 indicating maximum diagnostic certainty. CONCLUSION: To our knowledge, this is among the first reviews that includes GBS variants and the clinical prediction tool mEGOS for prognostication in COVID-19 patients. Further research is needed to assess whether IVIG is preferable over plasmapheresis in this population of GBS patients. It would also be crucial to follow these patients over time to identify the long-term disability as well as treatment outcomes.

The novel coronavirus disease-2019 (COVID-19), a disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), was officially declared a pandemic on March 11 , 2020 by the World Health Organization (WHO) due to its rapid spread worldwide [1] .

Previous outbreaks of coronaviruses have included the severe acute respiratory syndrome (SARS) in 2002 and the Middle East respiratory syndrome (MERS) in 2012 [1] [2] [3] [4] . SARS-COV-2 novel coronavirus shares several common viral characteristics with SARS-CoV. Importantly, it has an even stronger affinity towards Angiotensin Converting Enzyme 2 (ACE2) receptor found in the human glial cells, neurons, respiratory epithelial and vascular endothelial cells [5] [6] [7] .

Studies have found that the most frequent neurological manifestations among COVID-19 infected individuals are ischemic stroke, Guillain-Barré syndrome (GBS) and encephalopathy due to ICU syndrome, cytokine storm with high fevers and ventilator use [8, 9] . Similar neurological outcomes have been reported in previous coronavirus epidemics caused by SARS-

The critical appraisal checklist for case reports provided by the Joanna Briggs Institute (JBI) was used to perform assessment of overall quality of case series and case reports.

From the selected studies, we extracted the following variables for our analysis: study type, date of publication, country of case origin, age, gender, clinical presentation of GBS and its variants (including paraparesis/quadriparesis, cranial nerve deficits and diarrhea ), diagnostic tests for SARS-CoV-2 infection in including RT-PCR nasopharyngeal and serum antibodies, latency between COVID-19 symptom onset and initial symptoms of GBS, severity of COVID-19 (based on IDSA/ATS criteria which includes either vasopressor use due to septic shock or requirement of mechanical ventilation [61] , mEGOS scoring scale that we calculated based on clinical data reported in paper, treatments including standard commercially available IVIG, PLEX, chloroquine, hydroxychloroquine (HCQ), azithromycin, IL-6 blockers (tocilizumab), corticosteroids, cerebrospinal fluid (CSF) total protein levels, anti-ganglioside antibodies, imaging findings, EMG/NCS findings, Brighton electrophysiological criteria and mortality outcomes.

Pooled descriptive analyses were conducted to assess differences among two main types of GBS variants for all patients across the 37 case reports and case studies: 1) AIDP and 2)

Others GBS variants (comprising of AMSAN, AMAN, BFP, MFS, Polyneuritis cranialis). We assessed the differences in two groups for the above-mentioned variables using chi-square test for categorical covariates and t-test for continuous covariates. Further, sub-analysis of the differences in frequencies and percentages was performed among three groups consisting of J o u r n a l P r e -p r o o f AIDP vs. AMSAN/AMAN vs. Others, using chi-square test. Stata v15 (Statacorp, College Station, TX) was used to conduct the analysis.

A total of 50 patients with COVID-19 diagnosed with GBS were used for analyses from the 37 case reports and case series published in 13 different countries. with RT-PCR, one patient tested negative and SARS-CoV2 antibody was positive. Ganglioside antibody tests were reported for 28 patients, 17 patients in the AIDP group and 11 in Non-AIDP group. One patient in AIDP and one patient in non-AIDP group were positive for antiganglioside antibodies. Further, we also explored the mean mEGOS scores for AIDP patients and compared them with AMAN/AMSAN patients for the probability of walking independently after 6 months of admission. Mean mEGOS score for patients with AIDP variant (6.8 ± 3.8) was lower compared to AMSAN/AMAN (8 ± 5.2), p=0.57 (Table 2) . (Table 3) . A total of 8(24%) patients presented with diarrhea in the AIDP sub-group, whereas 4 cases with diarrhea (40%) were reported in other variants; no diarrhea was reported in AMSAN/AMAN variants sub-group (Table 3) . The mean latency for the AIDP group was 12.5 + 7.7, for AMSAN/AMAN was 11.1 + 4.9 and for others was 9.2 + 6.0 (0.34).

CSF protein levels were highest in the AMAN/AMSAN (103.1 + 52.9), and AIDP groups (100.5 + 61.5) and then other variants (65.7 + 23.7) but the differences were not significant.

Further details of clinical characteristics are described in Table 3 . Albuminocytological J o u r n a l P r e -p r o o f dissociation was present in 26 out of 31 AIDP patients (84%), 5 out of 6 patients in AMSAN/AMAN (83%) and 5 out of 7 patients with other variants (71%) (refer Table 3 ).

In our entire cohort, we found a total of 17 cases in which MRI imaging of brain and cranial nerves was reported. Amongst them, 6 (35%) had abnormal findings that included cranial nerve CN III, CN VI and CN VII enhancement. Apart from these, one case of leptomeningeal enhancement of brainstem and cervical spine was noted (24) . MRI of the lumbosacral spine was also performed in 36% of the cases (18/50), of which 5 (27%) were found to have abnormal spine nerve root enhancement and the remaining 73% (13/18) had normal spine imaging Table 3 ).

We also compared differences in treatments of GBS variant groups administered for both COVID-19 and GBS (refer Table 4 Finally, Table 5 shows a detailed breakdown of the studies with respect to Brighton criteria, mEGOS scores and mEGOS score percentage probability of being unable to walk independently after 6 months of admission, EMG findings, to summarize our reported findings.

In current analysis, we identified and reviewed a total of 50 cases of GBS with COVID-19 from 39 studies identified worldwide through different case series and reports [5, 8, 15, 16, 18, . The cases were categorized into two groups for further statistical analysis, "AIDP" versus "Non-AIDP/Other variants" which included MFS, AMSAN, BFP, AMAN and Polyneuritis cranialis; and further into "AMAN/AMSAN" and "other variants" within the non-AIDP group for subanalysis of specific variables where indicated. The novel addition to our review was use of Brighton criteria for strength of diagnosis and employment of mEGOS score for prognosis on the appropriate GBS variants. GBS is a relatively rare disease of the peripheral nervous system (PNS) having an incidence of 1.6 /100,000 person-years [17] . Studies in COVID-19 patients have suggested a link between GBS and SARS-CoV-2. A large Italian study of 1200 patients admitted with SARS-CoV-2 reported an incidence of 0.42% for GBS, much J o u r n a l P r e -p r o o f higher than that for the general population [8] . Recent studies interestingly found GBS as one of the most frequent neurological manifestations of peripheral nervous system in COVID-19 patients [5, 8, 15, 16, 18, .

The most frequent GBS variant in association with COVID-19 in our analysis was AIDP, which is consistent with the literature in general [17] nearly 66% of GBS cases had AIDP. We found significant differences between AIDP vs. Non-AIDP/Other variants in age at onset; the mean age for AIDP was 62 + 9.9, 58 + 17. [21, 52] . This has been well demonstrated in several GBS variants as well as J o u r n a l P r e -p r o o f GM1 gangliosides IgG Ab with C. jejuni infection [62] and has been postulated with other infectious agents including Mycoplasma pneumoniae, H pylori and several viruses [10, 11, 13, [21] [22] [23] [24] [25] .

For GBS triggered by SARS-COV-2, it is hypothesized that the attachment of SARS-CoV-2 to cell surfaces is mediated by the viral spike (S) protein, which binds to angiotensinconverting enzyme 2 Receptor and also to gangliosides containing sialic acid residues, including the GalNAc residue of GM1 [7, 14, 20] . It has been suggested that cross-reactivity between the viral protein-associated gangliosides and peripheral nerve gangliosides as the result of molecular mimicry. In our review, we identified 28 patients in the entire cohort (56%) for whom ganglioside antibody tests were performed. Serum ganglioside antibodies were found to be positive in 2 cases (7%), one in each group (i.e., AIDP and Non-AIDP/Other variants). GD1b

IgG antibodies were positive in the MFS subtype of GBS case whereas GM2 IgM, IgG was positive in AIDP variant [32, 57] . Interestingly, a case reported by Lantos and colleagues had equivocal lab values of GM1 antibody [34] .

Alternatively, the mechanism of nerve damage may be primarily facilitated by T-cell activation and release of inflammatory mediators by macrophages. A systematic evaluation of associations of ganglioside antibodies in GBS with COVID-19 will be needed before the mechanisms are clarified. A novel parainfectious mechanism for GBS mediated by the generalized, hyperinflammatory response that occurs with COVID-19 was suggested by some authors because the acute symptoms overlap with the onset of GBS and autoantibodies were not detected in their cases [8, 43] . However, when all of the cases are considered, the clinical, antiganglioside testing and electrodiagnostic patterns are similar to those of typical GBS cases [14, 29, 50] .

J o u r n a l P r e -p r o o f RT-PCR nasopharyngeal swab and serological antibody tests are currently standard and recommended for diagnosing SARS-CoV-2 infection [63] . In our review, out of a total cohort of 50 patients, 49 patients (98%) underwent nasopharyngeal RT-PCR test. A positive test was obtained in 45 patients (91%) and the rest 4 (9%) had a negative test result. The remaining 5 cases (10%) were diagnosed with COVID-19 with a confirmatory serum SARS-CoV-2 IgG antibody test [5, 8, 33, 37, 53] (Table 2) . Interestingly, none of the reported patients had positive PCR for SARS-CoV-2 in the CSF. The absence of evidence of active infection when the patients have clinical GBS infection supports an immune-mediated mechanism is the most likely pathophysiology behind GBS associated with SARS-CoV-2 .Whether this immune-mediated process results from molecular mimicry triggered in the peripheral immune system or results from release of PNS antigens by earlier asymptomatic damage by the virus leading to release of PNS into the peripheral immune system which responds by initiating an autoimmune process is not clear [15, 16, 37] . Indeed, different scenarios in different patients are possible.

In addition to the clinical evaluation, CSF protein elevation is a known critical biomarker which can be a useful tool to identify the disease severity and extent [64] .Additionally, mean CSF total protein levels were highest among patients with AMAN/AMSAN (103.1 ± 52.9) and AIDP-GBS (101 ± 61.6 mg/dl) variants. For our analysis, we considered CSF total protein of >45 mg/dl as elevated . Albumino-cytological dissociation was found in 36 patients (72%), of which 26 had AIDP (72%) and 10 had other variants (28%) ( Table 2) .

Modified Erasmus GBS Outcome score (mEGOS) is a key prognostic indicator that helps predict the long-term outcomes of patients based on their clinical presentation at day 7 of admission. Therefore, the higher the score, the greater probability of inability to walk independently at 6 months after admission. This score has been shown to be of significant J o u r n a l P r e -p r o o f predictive value in multiple cohort studies in GBS patients [65, 66] . On further analysis, the mean mEGOS score for both groups of patients (AIDP vs AMSAN/AMAN) were compared, and did not show a significant difference. Mean mEGOS score for patients with AIDP (6.8 ± 3.8) was considerably lower compared to AMAN/AMSAN variants (8 ± 5.2) ( Table 5) . We also used the Brighton criteria to differentiate the certainty of classification of the reported variants of GBS [59] . The Brighton criteria is an important tool to evaluate patients using different features for confirmation of diagnosis of GBS and classification of its variants, including MFS. It assesses the patient's clinical presentation, exam findings, and diagnostic testing to help scoring levels 1-4 of diagnostic certainty (level 1 being the highest certainty). The criteria are key is assisting with diagnosis in low to high risk patients, as well as prompt diagnosis early on in the course of disease. It also helps in guiding different treatment options according to the patient's diagnosis.

All of the cases included in our analysis fulfilled the Brighton Criteria. Majority of the AIDP cases (66.6%) and the AMAN/AMSAN cases (57.1%) belonged to Level 1, marking the highest diagnostic certainty. While the majority of the patients belonging to the other variants (80%) were in Level 4 indicating the least diagnostic certainty (Table 3 ).

In our entire cohort, we found a total of 17 cases in which MRI imaging of brain and cranial nerves was reported. Amongst them, 6 (35%) had abnormal findings that included cranial nerve CN III, CN VI and CN VII enhancement [8, 27, 29, 34, 44, 47] . Apart from these, one case of leptomeningeal enhancement of brainstem and cervical spine was noted [27] . MRI of the lumbosacral spine was also performed in 36% of the cases (18/50), of which 5 (27%) were found to have abnormal spine nerve root enhancement and the remaining 73% (13/18) had normal spine imaging [8, 27, 45, 46] .

There is still no specific treatment for COVID-19. However, at the time of reporting of some of the cases in this study there was a proposed approval by WHO for the use of HCQ which was later withdrawn, and antivirals like Ritonavir, Lopinavir, some of which were also proven to be ineffective against COVID-19 and IL-6 receptor (R) blockers such as Tocilizumab as needed [67, 68] . Dexamethasone has proved useful in severely affected patients likely by inhibiting the destructive excess inflammatory response in these patients [69] . Our analysis also Furthermore, 11 patients who received antivirals also received IVIG, 13 patients who got HCQ, and 1 patient who received IL-6 blocker, also received IVIG therapy in combination (Table 4 ).

Standard management for GBS includes IVIG and PLEX [70, 71] . In our review, we found 44 patients receiving IVIG 30 patients (68%) were in the AIDP group while 14 (32%) were in Non-AIDP/Other variants (Table 4) . We further reviewed the number of patients receiving 0.4 g/kg/day x 5 days versus 2 g/kg IVIG administered over 5 days. Information about different IVIG regimens was not available in 14 cases (10 in the AIDP group and 4 in the Non-AIDP group). 14 patients (70%) in the AIDP group received 0.4 g/kg/day divided over 5 days, the other 6 patients (30%) received 2 g/kg IVIG regimen divided over 5 days. On the other hand, in the Non-AIDP /Other variants group, total patients on 0.4 g/kg and 2 g/kg IVIG regimen were 8 (80%) and 2 (20%) respectively. In total, out of 30 patients on IVIG in the entire cohort, 22 patients (73%) were on 0.4 g/kg dosage and 8 (27%) were on 2 g/kg dosage divided over 5 days.

In addition, 7 patients (14%) out of 50 underwent PLEX. Six cases (85%) were in the AIDP group while 1 case (15%) on PLEX was diagnosed with BFP included in the other variants group. Four patients (4/44, 9%) who were on IVIG also received PLEX.

Although IVIG has known association with thromboembolic adverse event, and SARS-COV-2 is associated with a pro-thrombotic state [72] , none of the SARS-COV-2 GBS patients who received IVIG treatment developed thrombotic complications. Based on our review, we propose further studies to identify the consideration of IVIG and plasma-exchange as potential standardized treatment options for GBS in COVID-19 patients. While PLEX and IVIG have been shown to be equally effective for treatment of GBS, it would be interesting to compare the issue of side effects in this particular population of GBS patients. There is the potential for thrombotic events with IVIG which is prothrombotic and the potential for cardiovascular events with rapid fluid shifts in moderate and severe cases of COVID-19 [72] . The clinical manifestations of GBS are variable, with most cases having a mild clinical course and recovery with a good response to standard treatment with IVIG or PLEX. However, some cases have also had poor or fatal outcomes in GBS as per literature [17] . It is vital to understand the severity and mortality outcomes of COVID-19 associated peripheral nervous systems disorders; especially GBS, as respiratory failure can be a coinciding symptom of GBS and SARS-CoV-2 individually.

Approximately 30% of the GBS patients have had poor outcomes secondary to the respiratory insufficiency [17] . In our review, 30 patients out of total 50 cases reviewed had severe COVID-19 (severity is based on the IDSA/ATS guidelines), classified as patients requiring mechanical intubation [73] [61] . Out of the 30 severe cases, 20 (67%) were in the AIDP group while 10 (33%) were in the other groups. Information on intubation and mechanical ventilation were available in 48 cases. Information on outcomes were not available for 5 of the cases. (Table 2 ).

Three AIDP and 2 of the other variants were fatal with a overall fatality rate of 11%. Of the patients who died, 3 (60%) were on combination therapy of 0.4 g/kg/day x 5 days IVIG, HCQ and antivirals; 1 (20%) was managed on antibiotics and IVIG (data not available) and the remaining 1 (20%) was treated with 0.4 g/kg/day x 5 days IVIG. al. has a greater number of cases in their review as pediatric GBS cases have also been included, while our study did not include pediatric population. Our study also differs from other studies, in terms of analyzing mEGOS scale, the use of the Brighton classification and also comparing these scale and classification between different variants of GBS [58, 59] . Additionally, our study also includes a brief review of pathophysiology of COVID-19 and GBS, as well as the pathophysiology of the treatments for GBS and their correlation. Since both these studies are comparatively new and refer to a rapidly emerging pandemic, we did not discuss a comparison as our study is inclusive of the cases used in the prior studies and also focused on comparison of the different GBS variant cohorts.

The diagnosis of GBS in SARS-CoV-2 is especially challenging as symptoms such as shortness of breath and fatigue could be misinterpreted as being secondary to SARS-CoV-2 delaying the evaluation for GBS. Thus, it is highly advisable that physicians should promptly think about neuromuscular cause such as GBS in their differential when encountering SARS-CoV-2 patients even with minor initial clinical findings such as paresthesia, facial numbness or diplopia and ptosis. During this pandemic it is also useful to test for CoV-2 in patients with GBS who do not manifest clinical symptoms and signs of COVID-19 as there were such cases in our review [28, 32, 44] .

Given the higher rates of requiring mechanical ventilation in SARS CoV-2 associated GBS patients, it is suggested by some that COVID-19 is a trigger for a rapidly progressing neuropathy [42] although some of the need for ventilator support may relate to lung damage (required for mEGOS calculation were unavailable for majority of cases before day 7). It is also important to note that this score was calculated based on the clinical details reported in the cases included in our study and the score would be inaccurate if some pertinent clinical detail was not reported.

In this systematic review, we compared and summarized the clinical presentations, outcomes, and neurological complications in SARS-CoV-2 patients with GBS and its variants. It is to our knowledge, the only study which also includes GBS variants and the clinical prediction tool mEGOS for prognostication. Mean age in both the comparison group was greater than fifty and there were also greater proportion of males as compared to females. Lower range of mEGOS scores were the highlight of the GBS-AIDP cohort when comparing it with the AMAN/AMSAN, however, the values were not statistically significant. As a standardized management approach to GBS, nearly all the patients were treated with IVIG. Most of the patients had either full recovery or partial recovery, whereas five patients died. In our opinion, further studies are warranted to J o u r n a l P r e -p r o o f explore and compare the efficacy of various treatment modalities, especially IVIG and plasmapheresis, as the latter imposes significant stressors on an already fragile hemodynamic milieu of critically ill SARS-CoV-2 infected patients and increases the risk of exposure to health care workers caring for these patients, whereas IVIG, at least in theory, has prothrombotic potential in a disease that has frequent thrombotic complications including stroke and pulmonary infarction. It would also be important to follow these patients over time to learn more about longterm prognosis. 

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Table 1: Study Origin, Types, Demographics and GBS Variants S

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