SUBMITTED 19 JAN 22 1 REVISION REQ. 9 MAR 22; REVISION RECD. 24 APR 22 2 ACCEPTED 17 MAY 22 3 ONLINE-FIRST: MAY 2022 4 DOI: https://doi.org/10.18295/squmj.5.2022.040 5 6 Guillain-Barre Syndrome Associated with SARS-CoV-2 in Two Pediatric 7 Patients 8 Fatema Al Amrani,1 Raghad Al-Abdwani,2 Fatma Al Rashdi,3 Eiman Al 9 Ajmi,4 *Amna Al Futaisi5 10 11 1Pediatric Neurology Unit and 2Pediatric Intensive Care Unit, Department of Child Health 12 and 3Pediatric Emergency Unit, Emergency Medicine Department, Sultan Qaboos 13 University Hospital, Mucat, Oman; 4Department of Radiology, Sultan Qaboos University 14 Hospital, Mucat, Oman; 5Pediatric Neurology Unit, Department of Child Health, College 15 of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman. 16 *Corresponding Author’s e-mail: amnaf@squ.edu.om. 17 18 Abstract 19 Guillain-Barre syndrome (GBS) is a recognized complication of severe acute respiratory 20 syndrome coronavirus 2 (SARS-CoV-2). We report two children with GBS associated with 21 SARS-CoV-2 presented to a tertiary center in Muscat, Oman in 2021: The first patient was 22 a 3-month-old female infant who presented with bradypnea, encephalopathy, and 23 generalized weakness that required mechanical ventilation. Polymerase chain reaction 24 (PCR) testing of the nasopharyngeal swabs (NPS) was positive for SARS-CoV-2. She had 25 axonal variant GBS based on a nerve conduction study, cerebrospinal fluid analysis, and 26 neuroimaging findings. The second patient was a 6-year-old girl with fever, vomiting, and 27 diarrhea followed by ascending weakness who presented with quadriplegia and facial 28 weakness. Subsequently, she developed respiratory muscle weakness and required 29 mechanical ventilation. PCR testing of NPS was negative for SARS-Cov-2, however IgG 30 serology analysis was positive. The clinical course of these two patients was rapidly 31 progressive and both of them required mechanical ventilation. The patient with axonal 32 variant GBS made an incomplete recovery. 33 Keywords: Acute Inflammatory Demyelinating Polyradiculoneuropathy, SARS-CoV-2, 34 Oman. 35 36 Introduction 37 A wide array of neurological manifestations is linked to SARS-CoV-2 involving both the 38 central and peripheral nervous systems.1 These manifestations appear to be a combination 39 of non-specific complications of systemic disease, the effects of direct viral infection, or 40 inflammation of the nervous system and vasculature, which can be para-infectious or post-41 infectious.2 Peripheral nervous system is less frequently involved and disorders that are 42 described to be associated with COVID-19 include Guillain-Barre syndrome (GBS), 43 Polyneuritis cranialis, myopathy and rhabdomyolysis.1 44 45 GBS is an immune-mediated disorder that can present in either a demyelinating or axonal 46 form.3 The demyelinating variant is characterized by autoantibodies that bind to the myelin 47 sheath of Schwann cells and initiate complement activation, leading to a cascade of events 48 resulting in focal destruction of the myelin sheath. In the axonal variant autoantibodies 49 attack the nodal axolemma leading to the formation of membrane attack complex (MAC), 50 which subsequently leads to axonal degeneration.3 51 52 Similar to adults, GBS is one of the most commonly reported neurological manifestations 53 associated with COVID-19 in pediatric populations.4 Most children developed GBS after 54 COVID-19 but asymptomatic patients were also described. The clinical presentations and 55 electrophysiologic findings are similar to the classic GBS with slight prevalence of acute 56 inflammatory demyelinating polyneuropathy (AIDP) over acute motor axonal neuropathy 57 (AMAN).5 The prognosis is favorable with 70% of patients showing good response to 58 intravenous immunoglobulins. The prognosis is worse in the older age groups which is also 59 similar to the classic GBS. 60 61 We describe two pediatric patients with different variants of Guillain-Barre syndrome 62 (GBS) associated with SARS-CoV-2 infection and their clinical course and outcome. 63 64 Case Reports 65 Patient One 66 A 3-month-old female infant born at 34 weeks gestation (corrected 8 weeks) had an 67 uneventful antenatal and postnatal history and adequate growth and development. She 68 presented to the emergency department (ED) with a two-day history of poor feeding, 69 lethargy, shallow slow breathing, and decreased urine output. Ten days prior, she had one 70 day of fever, vomiting, and diarrhea. Physical examination revealed an encephalopathic 71 infant with a weak cry and Glasgow Coma Scale of E1V2M3. The patient was pale, 72 tachycardic, hypertensive, poorly perfused; in compensated shock, bradypneic with 73 intermittent episodes of apnea requiring intubation and mechanical ventilation. Further 74 examination showed hypotonia with lower extremity weakness and absent deep tendon 75 reflexes (DTR). She was resuscitated with fluid and covered with broad-spectrum 76 antimicrobials (ceftriaxone, vancomycin and acyclovir) for the possibility of septic shock 77 and meningoencephalitis. Initial testing showed that the nasopharyngeal aspirate (NPA) 78 was positive for SARS-Cov-2, respiratory viral screen was positive for adenovirus and 79 negative for the rest of viruses including parechoviruses, human bocavirus, influenza A & 80 B, parainfluenza 1, 2, 3, 4, rhinovirus, respiratory syncytial virus (RSV), human 81 metapneumovirus, enterovirus and H1N1. NPA for mycoplasma pneumoniae polymerase 82 chain reaction (PCR) was negative. PCR for cytomegalovirus (CMV), and Epstein Barr 83 virus (EBV) from the serum was negative. Computed tomography (CT) of the brain was 84 normal; cerebrospinal fluid (CSF) analysis showed high protein 0.64 g/L (normal range: 85 0.15–0.45) and glucose 4.1 mmol/L(normal range: 3.3–4.4) with no leucocytes. CSF 86 culture showed no growth, and viral PCR for herpes simplex virus (HSV), parechovirus, 87 enterovirus, varicella zoster virus and mumps viruses.was negative. 88 89 The patient remained persistently tachycardic and hypertensive despite hydration and 90 sedation but was controlled with propranolol. Renal ultrasound and magnetic resonance 91 angiography of the aorta and renal arteries were normal. Echocardiography revealed left 92 ventricular hypertrophy with moderate outflow obstruction. In view of this clinical 93 presentation, magnetic resonance imaging (MRI) of the brain was performed which showed 94 leptomeningeal enhancement on the surface of the brainstem and within the internal 95 auditory canals. MRI of the spine showed diffuse enhancement of the spinal nerve roots, 96 which was more conspicuous along the cauda equina nerve roots, with surface 97 enhancement of the cord at the conus (Figure 1). Nerve conduction studies (NCS) showed 98 sensorimotor axonal polyneuropathy. Moreover metabolic screen including lactate, 99 ammonia, lactase dehydrogenase, thyroid function test, neonatal metabolic screen and 100 createnine kinase (CK) were normal. Furthermore patient had whole exome sequencing 101 (WES) that came negative with no pathogenic variants or variants of unknown significance. 102 103 The patient was diagnosed with GBS based on the results of CSF analysis, NCS, and 104 neuroimaging. She was treated with intravenous immunoglobulin (IVIG; 2g/kg) followed 105 by plasma exchange (PLEX; five cycles) and a second dose of IVIG. The patient was 106 successfully extubated to bilevel positive airway pressure (BiPAP) but could not be weaned 107 off due to generalized muscle weakness and bradypnea so we planned for a tracheostomy 108 and home ventilation. However, because of her difficult socioeconomic status, the parents 109 refused tracheostomy, and the patient was eventually discharged home and palliated on 110 continuous BiPAP and exclusive nasogastric tube feeding. 111 112 Patient Two 113 A 6-year-old previously healthy girl presented to a community hospital with one week 114 history of fever, vomiting, constipation, and abdominal pain followed by lower extremity 115 weakness on day 7 of illness. The weakness progressed to involve the upper extremities 116 and respiratory muscles requiring intubation and mechanical ventilation. CSF analysis 117 revealed cytoalbuminologic dissociation with protein of 0.94 g/L (normal range: 0.15–118 0.45), glucose of 3.93 mmol/L (normal range: 3.3–4.4), WBC of 0 and RBCs of 512. The 119 patient was treated with IVIG but showed no major improvement so was transferred to our 120 institution for further management. Here, she was found to have bilateral facial weakness as 121 well as axial and appendicular hypotonia with a strength of 1/5 on the right and 0/5 on the 122 left side. DTR were absent, and the plantar flexors showed no clonus. No signs of 123 autonomic involvement were observed. The NPA was negative for SARS-Cov-2, however 124 IgG serology testing was positive. Poliovirus PCR in the stool was negative. 125 126 The NCS showed a sensorimotor demyelinating polyneuropathy with conduction blocks. 127 The patient underwent PLEX followed by IVIG, and was eventually extubated and 128 discharged home with follow up at four weeks showing normalization to her baseline 129 functional status. 130 131 Consents were taken from patients’ parents for these case reports publication. 132 133 Discussion 134 GBS is classified as either acute inflammatory demyelinating polyradiculoneuropathy 135 (AIDP) or acute axonal neuropathy which is further classified as acute motor axonal 136 neuropathy (AMAN) or acute motor sensory axonal neuropathy (AMSAN).3 Other GBS 137 variants include Miller-Fisher syndrome, Bickerstaff encephalitis, pharyngeal-cervical-138 brachial variant, and pandysautonomia variant.3 This autoimmune-mediated disorder can be 139 triggered by viruses such as cytomegalovirus, Epstein-Barr virus (EBV), influenza, 140 hepatitis E, and Zika, or by bacteria such as Campylobacter jejuni or Mycoplasma 141 pneumoniae.5,65 SARS-Cov-2 has been reported to be a potential trigger that could be 142 associated with GBS. The first case of GBS associated with SARS-Cov-2 was reported in 143 early 2020 in an adult.2 Since this initial report, there have been multiple case reports, case 144 series, and systemic reviews demonstrating this association including in the pediatric 145 population.5,7-12 Table 1 summarizes GBS cases associated with SARS-Cov-2 in pediatric 146 population. 147 148 Here, we report two pediatric patients who were diagnosed with GBS and tested positive 149 for SARS-Cov-2. The first patient is of particular interest because of the age at presentation 150 of 8 weeks. GBS usually occurs after the age of 3 years; onset in infancy is extremely rare. 151 There are reported cases of congenital GBS but the youngest patient reported was 11 152 months old.13, 14 Our patient had symptoms of infection such as fever, vomiting, and 153 diarrhea 10 days prior to her presentation to the ED. PCR testing of the nasopharyngeal and 154 throat swabs were positive for SARS-Cov-2 and adenovirus. PCR testing of the CSF for 155 SARS-Cov-2 was not performed. GBS in our patient was likely triggered by SARS-Cov-2 156 infection, as this association has been previously reported and adenovirus infection is not 157 among the reported potential infectious triggers of GBS. 5, 7 However, there is a question 158 regarding the possible association between the adenovirus vaccine and GBS as a possible 159 complication.15 SARS-Cov-2 is likely the potential trigger for GBS, due to either surface 160 epitope mimicry of SARS-Cov-2 to the antigens on Schwann cell myelin sheaths in the 161 demyelinating variant or to the nodal axolemma in the axonal variant.3 This molecular 162 mimicry has been reported with other viruses, such as varicella zoster virus (VZV), EBV 163 and CMV in patients infected with human immunodeficiency virus.16 Both patients had 164 cytoalbuminologic dissociation, which has been well documented in previous reports.5, 7 165 The neurophysiological evaluation of our first patient showed a picture suggestive of 166 AMSAN. The AMSAN variant has been reported in association with SARS-Cov-2. In a 167 recent systematic review of different GBS variants, there were seven cases of AMSAN 168 reported, with an age range of 23–77 years and no cases in the pediatric age group.17 169 Recently, Akçay et al. reported the first pediatric patient with axonal variant GBS 170 associated with SARS-Cov-2.10 Our patient is the youngest reported pediatric patient with 171 AMSAN associated with SARS-Cov-2. The AMSAN variant of GBS has been reported in 172 children but is mainly associated with C. jejuni gastroenteritis.18 Our patient’s diagnosis 173 was based on the presence of sensorimotor axonal polyneuropathy, cytoalbuminologic 174 dissociation in the CSF, and cauda equina root enhancement on neuroimaging. 175 Furthermore, she had features of dysautonomia, including persistent hypertension that was 176 initially refractory to medical treatment and pupillary abnormalities. The persistent 177 hypertension likely led to a hypertrophic left ventricle. Autonomic disturbances are among 178 the clinical features of GBS, especially during the acute clinical presentation. These clinical 179 features may include blood pressure and heart rate instability, sweating disturbances, bowel 180 and bladder retention, incontinence, and vasomotor instability.19 In addition, the presence 181 of dysautonomia correlates with illness severity, and this is particularly true for 182 hypertension and tachycardia.20 Moreover, this patient had rapid progression of the disease 183 requiring intubation and mechanical ventilation at the time of presentation, indicating a 184 rapidly progressive course of her illness and a short peak to disability. She required a 185 prolonged period of mechanical ventilation in the PICU before weaning to non-invasive 186 ventilation was possible. This course is similar to that of a previously reported pediatric 187 patient with axonal GBS associated with SARS-Cov-2.10 This patient had multiple poor 188 prognostic factors, including the rapid deterioration of her clinical status requiring 189 mechanical ventilation on presentation, the axonal variant of GBS and the presence of 190 dysautonomia.22, 23 Peak disability has been reported as an independent risk factor for 191 outcomes.22 Although the combination of GBS and encephalopathy in this patient seems 192 unusal, the early resolution of encephalopathy and longer-persisting neuropathy may permit 193 the consideration of GBS as a possible diagnosis. 194 195 In the second patient, PCR testing of the NPS and throat swab were negative for SARS-196 Cov-2, but IgG serology was positive. Hence, GBS was likely part of a parainfectious 197 process associated with SARS-Cov-2. Her clinical course was similar to a previously 198 reported case of the demyelinating variant of GBS associated with SARS-Cov-2.24 Her 199 outcome was more favorable than that of the first patient, although her initial presentation 200 was rapidly progressive, and she had a short peak to disability. Prognosis was more 201 favorable in the demyelinating variant than in the axonal variant, which is well documented 202 in the literature.25 In addition, this patient did not have dysautonomia, and her period of 203 mechanical ventilation was shorter. Given that SARS-Cov-2 diagnosis in this patient was 204 based on IgG serology and that other antimicrobial causes were not excluded, GBS may not 205 be related to SARS-Cov-2. 206 207 In both cases, the clinical course was severe with rapid progression, which is likely related 208 to the severe autoimmune response that is mounted by the body in response to SARS-Cov-209 2 infection.26 210 211 Conclusion 212 GBS should be considered in the differential diagnosis of any child presenting with acute 213 flaccid paralysis even in patients less than one year of age. There is growing evidence that 214 there is association between SARS-Cov-2 infection and GBS. 215 216 Authors’ Contribution 217 AAF conceptualized the idea. FAA and AAF drafted the manuscript. FAR and RA-A drafted 218 the case history. EAA prepared the images, annotation and description. FAA, RA-A and 219 AAF revised the manuscript. All authors approved the final version of the manuscript. 220 221 References 222 1. Guerrero JI, Barragán LA, Martínez JD, Montoya JP, Peña A, Sobrino FE, et al. 223 Central and peripheral nervous system involvement by COVID-19: a systematic 224 review of the pathophysiology, clinical manifestations, neuropathology, 225 neuroimaging, electrophysiology, and cerebrospinal fluid findings. BMC Infect Dis 226 2021; 21:515. https://doi.org/10.1186/s12879-021-06185-6. 227 2. Zhao H, Shen D, Zhou H, Liu J, Chen S. Guillain-Barrarryndrome associated with 228 SARS-CoV-2 infection: causality or coincidence? The Lancet Neurology. 2020 May 229 1;19(5):383–4. https://doi.org/10.1016/S1474-4422(20)30109-5. 230 3. Yuki N, Hartung H-P. Guillain-Barré syndrome. N Engl J Med. 2012 Jun 231 14;366(24):2294–304. https://doi.org/10.1056/NEJMra1114525. 232 4. Sánchez-Morales AE, Urrutia-Osorio M, Camacho-Mendoza E, Rosales-Pedraza G, 233 Dávila-Maldonado L, González-Duarte A et al. Neurological manifestations 234 temporally associated with SARS-CoV-2 infection in pediatric patients in 235 Mexico. Childs Nerv Syst. 2021;37(7):2305-2312. https://doi: 10.1007/s00381-021-236 05104-z5 237 5. Abu-Rumeileh S, Abdelhak A, Foschi M, Tumani H, Otto M. Guillain-Barré syndrome 238 spectrum associated with COVID-19: an up-to-date systematic review of 73 cases. J 239 Neurol. 2021 Apr;268(4):1133–70. https://doi.org/10.1007/s00415-020-10124-x. 240 6. Grygorczuk S, Zajkowska J, Kondrusik M, Pancewicz S, Hermanowska-Szpakowicz T. 241 [Guillain-Barré Syndrome and its association with infectious factors]. Neurol 242 Neurochir Pol. 2005 Jun;39(3):230–6. 243 7. Sansone P, Giaccari LG, Aurilio C, Coppolino F, Esposito V, Fiore M, et al. Post-244 Infectious Guillain-Barrrr its association to SARS-CoV-2 Infection: A Systematic 245 Review. Life (Basel). 2021 Feb 21;11(2). https://doi.org/10.3390/life11020167. 246 8. Al-Zadjali MM, Shibli EA, Maskari MA, Gujjar AR, Asmi AA. Post COVID-19 247 Guillain-Barré-Syndrome (GBS): A case report from Oman. Sultan Qaboos Univ Med 248 J [Internet]. 2021 Jun 27 [cited 2021 Dec 29]; Available from: 249 https://journals.squ.edu.om/index.php/squmj/article/view/4390. 250 https://doi.org/10.18295/squmj.6.2021.090 251 9. Curtis M, Bhumbra S, Felker MV, Jordan BL, Kim J, Weber M, et al. Guillain-252 BarrrrBarré-Syndrome (GBS): A case report from Oman. Siatrics. 2021;147(4). 253 https://doi.org/10.1542/peds.2020-015115. 254 10. AkAk42/peds.2020-015115.ker MV, Jordan BL, Kim J, Weber M, et al. Guillain-255 BarrrrBarré-Syndrome (GBS): A case report from Oman. Siatrics. 2021;147(4). J 256 [Internet]. 2021 Jun 27 https://doi.org/10.1002/jmv.27018. 257 11. Khalifa M, Zakaria F, Ragab Y, Saad A, Bamaga A, Emad Y, et al. Guillain-258 BarrrrrrBarré-Syndrome (GBS): Severe Acute Respiratory Syndrome Coronavirus 2 259 Detection and Coronavirus Disease 2019 in a Child. J Pediatric Infect Dis Soc. 2020 260 Sep 17;9(4):510–3. https://doi.org/10.1093/jpids/piaa086. 261 12. Frank CHM, Almeida TVR, Marques EA, de Sousa Monteiro Q, Feitoza PVS, Borba 262 MGS, et al. Guillain-Barré Syndrome Associated with SARS-CoV-2 Infection in a 263 Pediatric Patient. J Trop Pediatr. 2021 Jul 2;67(3):fmaa044. 264 https://doi.org/10.1093/tropej/fmaa044. 265 13. Luijckx GJ, Vles J, Baets M de, Buchwald B, Tmost J. Guillain-Barré syndrome in 266 mother and newborn child. The Lancet. 1997 Jan 4;349(9044):27. 267 https://doi.org/10.1016/s0140-6736(97)24001-8. 268 14. Kannan MA, Ch RK, Jabeen SA, Mridula KR, Rao P, Borgohain R. Clinical, 269 electrophysiological subtypes and antiganglioside antibodies in childhood Guillain-270 Barré syndrome. Neurology India. 2011 Sep 1;59(5):727. 271 https://doi.org/10.4103/0028-3886.86549. 272 15. McNeil MM, Paradowska-Stankiewicz I, Miller ER, Marquez PL, Seshadri S, Collins 273 LC, et al. Adverse events following adenovirus type 4 and type 7 vaccine, live, oral in 274 the Vaccine Adverse Event Reporting System (VAERS), United States, October 275 2011-July 2018. Vaccine. 2019 16;37(44):6760–7. 276 https://doi.org/10.1016/j.vaccine.2019.08.087. 277 https://doi.org/10.18295/squmj.6.2021.090 16. Gnann JW. Varicella-zoster virus: atypical presentations and unusual complications. J 278 Infect Dis. 2002 Oct 15;186 Suppl 1:S91-98. https://doi.org/10.1086/342963. 279 17. Robinson-Papp J, Simpson DM. Neuromuscular diseases associated with HIV-1 280 infection. Muscle Nerve. 2009 Dec;40(6):1043–53. 281 https://doi.org/10.1002/mus.21465. 282 118. Sriwastava S, Kataria S, Tandon M, Patel J, Patel R, Jowkar A, et al. Guillain 283 BarrrrMuscle Nerve. 2009 Dec;40(6):1043–53.S91-98.pe 4 and type 7 vaccine, live, 284 oral in the Vaccineand case series. J Neurol Sci. 2021 15;420:117263. https://doi.org/ 285 10.1016/j.jns.2020.117263. 286 19. Heikema AP, Islam Z, Horst-Kreft D, Huizinga R, Jacobs BC, Wagenaar JA, et al. 287 Campylobacter jejuni capsular genotypes are related to Guillainin vaccine, lme. 288 Clinical Microbiology and Infection. 2015 Sep 1;21(9):852.e1-852.e9. https://doi.org/ 289 10.1016/j.cmi.2015.05.031. 290 20. Zaeem Z, Siddiqi ZA, Zochodne DW. Autonomic involvement in Guillain-Barrrr al. 291 Campylobacter jejuni capsular genotypes are relatedhttps://doi.org/10.1007/s10286-292 018-0542-y. 293 21. Dimario FJ, Edwards C. Autonomic dysfunction in childhood Guillain-Barrrrr al. 294 Campylobacter jejuni capsular genotypes 295 arhttps://doi.org/10.1177/0883073811420872. 296 22. Kalita J, Kumar M, Misra UK. Prospective comparison of acute motor axonal 297 neuropathy and acute inflammatory demyelinating polyradiculoneuropathy in 140 298 children with Guillain-Barré syndrome in India. Muscle Nerve. 2018;57(5):761–5. 299 https://doi.org/10.1002/mus.25992. 300 23. Chakraborty T, Kramer CL, Wijdicks EFM, Rabinstein AA. Dysautonomia in Guillain-301 Barré Syndrome: Prevalence, Clinical Spectrum, and Outcomes. Neurocrit Care. 302 2020;32(1):113–20. https://doi.org/10.1007/s12028-019-00781-w. 303 24. Hasan I, Saif-Ur-Rahman KM, Hayat S, Papri N, Jahan I, Azam R, et al. Guillain-Barré 304 syndrome associated with SARS-CoV-2 infection: A systematic review and individual 305 participant data meta-analysis. J Peripher Nerv Syst. 2020;25(4):335–43. 306 https://doi.org/ 10.1111/jns.12419. 307 25. Estrade S, Guiomard C, Fabry V, Baudou E, Cances C, Chaix Y, et al. Prognostic 308 factors for the sequelae and severity of Guillain-Barré syndrome in children. Muscle 309 Nerve. 2019;60(6):716–23. https://doi.org/10.1002/mus.26706. 310 26. Garcrc/mus.26706.rd C, Fae, Inflammation, and the Clinical Spectrum of COVID-19. 311 Front Immunol. 2020;11:1441. https://doi.org/ 10.3389/fimmu.2020.01441. 312 313 Table 1: Clinical Characteristics of reported pediatric patients with Guillian-Barre syndrome –associated with SARS-Cov-2 314 315 Abbreviations: yr: age in years, IV: invasive ventilation, D: days, CN: cranial nerves, Dx from symp onset: diagnosis from symptom onset, CSF: cerebrospinal 316 fluid, IVIG: intravenous immunoglobulin, PLEX: Plasma Exchange, PCR: polymerase chain reaction, Abs: Antibodies, AIDP: acute inflammatory demyelinating 317 polyradiculopathy, AMAN: acute motor axonal neuropathy, NA: not available 318 Author Sex Age at onset (yr) Time to loss functional ability IV Dx from symp onset (D) Clinical Features CN involve ment Dysaut onomia CSF cytoalb umin dissocia tion IVI G regi men PLE X Invasi ve ventil ation period (D) Nasoph aryngea l SARS- Cov-2 PCR CSF SARS- Cov-2 PCR Serum SARS- Cov-2 serolog y Anti- gangliosides Abs GBS-variant 1 Curtis et al 9 M 8 Few days + 12 Flaccid weakness - - + 2 g/ kg over 2D - 4 + - NA NA AIDP 2 Khalifa et al 11 M 11 Few days - 2 Distal weakness of the U & LE - - + 2 g/ kg over 2D - - + NA NA NA AIDP 3 Frank CHM et al 12 M 15 Few days - NA Progressi ve U and LE weakness - - + 0.4 g/kg x 5D - - + - + - AMAN 4 Akçay et al 10 M 6 4D + 14 Flaccid weakness - - + 2 g/ kg over 2D + 30 + NA NA - AMAN 319 320 321 Figure 1. (A) A gadolinium-enhanced axial T1-weighted image through the posterior fossa shows bilateral enhancement in the internal auditory canals (arrows). (B) An axial T2-weighted image of the lumbar spine doesn’t show abnormal thickening of the cauda equina nerve roots. There is however uniform enhancement of the spinal nerve roots on gadolinium-enhanced axial T1-weighted image (C). (D) The enhancement on the surface of the disatal cord and cauda equina nerve roots is also shown on sagittal post-contrast T1 weighted image (arrows). A B C D