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. 2021 Jun 10;20(8):102875. doi: 10.1016/j.autrev.2021.102875

Guillain Barré syndrome associated with COVID-19- lessons learned about its pathogenesis during the first year of the pandemic, a systematic review

Mayka Freire a,⁎, Ariadna Andrade a, Bernardo Sopeña a, Maria Lopez-Rodriguez a, Pablo Varela b, Purificación Cacabelos c, Helena Esteban d, Arturo González-Quintela a
PMCID: PMC8191287  PMID: 34119673

Dear editor,

The disease caused by the coronavirus SARS-CoV-2 (COVID-19), which emerged in China in December 2019 [1], has become a global pandemic in just a few months. The concomitant presentation of COVID-19 and some autoimmune diseases has also been reported, among which is Guillain Barré Syndrome (GBS) [2]. GBS is considered an immune-mediated neuropathy preceded 1 to 6 weeks in 70% of cases by a bacterial or a viral infection. In many cases associated with Campylobacter jejuni (the predominant pathogen) the presence of antiganglioside antibodies is observed. This supports a post-infectious mechanism, with molecular mimicry and antibody cross-response [3]. However, in GBS associated with Zika virus infection, an earlier onset is seen, and associated antiganglioside antibodies are rarely present, suggesting a para-infectious pathogenetic mechanism [4]. There is contradictory information on whether GB associated with COVID-19 has also characteristics that may indicate a para-infectious pathogenetic process [[5], [6], [7]]. To review the accumulated evidence about the pathogenic mechanism of this association, we carried out a review of the literature with a selection of the clinical cases reported until February 1st 2021, adding one own case. We selected studies reporting adult patients with all: Guillain-Barré syndrome, according to diagnostic criteria of the GBS Classification Group [8]; SARS-CoV-2 infection confirmed by nasopharyngeal reverse transcription polymerase chain reaction, antigen-detecting rapid diagnostic tests or serum antibody test; Detailed individual clinical description; A minimum of 6/8 points using the Joanna Briggs Institute Critical Appraisal Checklist for Case Reports and for Case Series studies [,][106], [107]. Finally, we selected 82 full text access articles with information about 104 clinical cases (Table 1 ) to which we added our own case (Patient 32). We searched suggestive features of the three pathogenic pathways proposed to neurologic damage in COVID-19 so far [11,12]: direct damage, dysregulated inflammatory response and antibody-mediated injury (Fig. 1 ). Direct damage: As seen in some viral infections such as poliovirus, enterovirus D68, cytomegalovirus, or other human coronaviruses, SARS-Cov-2 has neuroinvasive capacity [12,13]. The proposed access routes have been through circulation, the blood-brain barrier, or retrograde axonal transport, through the olfactory nerve or the enteric nervous system [12]. Endothelium, glial cells, and neurons express angiotensin-converting enzyme receptor 2 (ACE2) and type II transmembrane serine protease (TMPRSS2), both necessary for the virus to get into the cells [14]. A post mortem study found SARS-CoV-2 RNA in neuroanatomical areas receiving olfactory tract projections [15]. However, PCR in CSF for COVID -19 virus was negative in all reported cases of GBS (Table 1), suggesting no intrathecal viral replication. Furthermore, a recent systematic review and meta-analysis showed that no study detected live SARS-COV-2 in various body fluids beyond day 9 of illness [16] and yet the median days of infection until the debut of GBS in the actual review has been 11 days. Dysregulated inflammatory response: In the ”inflammatory phase” of COVID-19 infection, which characteristically begins throughout the second week of infection, elevated IL-2, IL-2R, IL-6, IL-10, IFN-γ, TNF-α, CCL2, procalcitonin, CRP, erythrocyte sedimentation rate and white blood cell, are characteristic [17]. In 2005, brain autopsy studies demonstrate the infiltration of monocytes, macrophages, and T-lymphocytes into gliocytes and brain mesenchyme of SARS-CoV patients [19]. Pilotto et al. has also described the presence of elevated neuroinflammatory parameters (IL-6, IL-8, β2M and TNF-α) in the CSF of 13 patients with encephalitis and COVID-19 [20]. On the other hand, marked increase of cytokines has previously been reported in GBS and its variants, as well as in experimental autoimmune neuritis, the animal model of GBS [21]. Cell-mediated immunity seems to play a crucial role in immunopathology of all types of GBS, especially the AIDP subtype [22]. Of note, AIDP subtype is the predominant in the current systematic revision (73%, counting with mixed forms) (Table 1). Also, in the present work the medium time between the onset of COVID-19 and the neurological symptoms was 11 days, that is, in the stages of the infection in which inflammatory processes predominate over antibody-mediated. In addition, serum inflammatory parameters were elevated at the beginning of the neurological symptoms in 39/53 patients (73%). Antibody-mediated injury. Anti-GM1 IgG are present in a high proportion of patients with classic GBS, mostly those with AMAN or AMSAN. Also, anti-GQ1b IgG antibodies are present in in 80–95% of patients with Miller-Fisher syndrome (MFS), the most common clinical variant of GBS [23]. Nevertheless, Keddie et al. found no significant similarity between SARS CoV-2 and human genome [24] and only 6/58 cases (10%) in our review had positive antiganglioside antibodies, interestingly only 3 of the 17 patients with Miller-Fisher syndrome (20%) (Table 1). Patient number 92 was seropositive for IgM antibodies against panneurofascin without posterior seroconversion to IgG [25]. However, anti-neurofascin antibodies may also have been triggered by tissue damage related to GBS.

Table 1.

Clinical cases obtained in the systematic review of the literature of patients with Guillen Barre Syndrome and a proven history of SARS-Cov-2 infection. Demographic and clinical characteristics, complementary examinations and evaluation of the quality of the case report.

First author (Ref.) Age Sex Severity COVID19 1 Latency2 GBS Clinical variant3 EMG SARS-COV-2 CSF Antiganglioside antibodies Biomarkers Treatment COVID-19 Treatment GBS Evolution at day 30 Study quality [[106], [107]]
Abbaslou [26] Patient 1 55 F 3 32 paraparetic GBS AMSAN ‐– ‐– ‐– LPV/r Ig iv dead (ARDS) 7/8
Abolmaali [27] Patient 2 88 F 3 ‐−3 classic SGB AMSAN ‐– ‐– ‐– DEXA, LPV/r, HCQ PPH poor 7/8
Patient 3 58 M 4 9 classic SGB AMSAN ‐– ‐– ‐– Remdensivir, Favipiravir, LPV/r, HCQ Ig iv + PPH dead (multi-organ failure) 7/8
Abrams [28] Patient 4 67 F 2 10 classic SGB ‐– PCR Neg Neg elevated DD, CRP, IgM ‐– PPH partial improvement 7/8
Agosti [29] Patient 5 68 M 2 5 classic SGB AIDP ‐– ‐– thrombocythaemia, lymphopenia antiviral Ig iv partial improvement 7/8
Alberti [30] Patient 6 71 M 2 4 classic SGB AIDP PCR Neg ‐– ‐– LPV/r, HCQ Ig iv dead (ARDS) 7/8
Ameer [31] Patient 7 30 M 1 4 classic SGB AMAN PCR Neg Neg lymphopenia ‐– Ig iv complet recovery 8/8
Arnaud [32] Patient 8 64 M 2 21 classic SGB AIDP PCR Neg Neg ‐– CXM, AZM, HCQ Ig iv complet recovery 8/8
Assini [33] Patient 9 55 M 3 ‐– Miller-Fisher AIDP PCR Neg Neg lymphopenia, elevated ferritine, CRP, LDH, oligoclonal bands HCQ, LPV/r Arbidol Ig iv complet recovery 7/8
Patient 10 60 M 3 ‐– classic SGB AMSAN ‐– Neg lymphopenia, elevated LDH y GGT, oligoclonal bands HCQ, LPV/r, TCZ Ig iv partial improvement 6/8
Atakla [34] Patient 11 40 M 3 11 classic SGB AIDP PCR Neg ‐– neutropenia, elevated ESR, CRP AZM Ig iv partial improvement 7/8
Barranchina-Esteve [35] Patient 12 54 F 3 0 classic SGB AMSAN PCR Neg Neg elevated DD, ferritine, LDH CXM, AZM, HCQ, LPV/r, MP, TCZ Ig iv complet recovery 8/8
Bigaut [36] Patient 13 43 M 2 21 classic SGB AIDP PCR Neg Neg ‐– ‐– Ig iv partial improvement 8/8
Patient 14 70 F 3 7 classic SGB AIDP PCR Neg Neg elevated CRP ‐– Ig iv partial improvement 8/8
Boostani [37] Patient 15 37 M 3 15 classic SGB AIDP ‐– ‐– elevated ESR, CRP ‐– Ig iv partial improvement 7/8
Bracaglia [38] Patient 16 66 F 1 ‐– classic SGB AIDP ‐– Neg lymphopenia, elevated CRP, CK, LDH, TGO, TGP, IL-6 LPV/r, HCQ, Ig iv partial improvement 7/8
Bueso [39] Patient 17 60 F 2 22 classic SGB ‐– ‐– ‐– ‐– AZM, HCQ Ig iv partial improvement 7/8
Caamaño [40] Patient 18 61 M 2 10 BWDP ‐– PCR Neg ‐– ‐– HCQ, LPV/r PRED low dose partial improvement 8/8
Camdessanche [41] Patient 19 64 M 2 11 classic SGB AIDP ‐– Neg ‐– LPV/r Ig iv ‐– 6/8
Chan [42] Patient 20 58 M 2 ‐– BWDP AIDP PCR Neg ‐– thrombocythaemia, elevated DD CXM, AZM, Ig iv partial improvement 7/8
Civardi [43] Patient 21 72 F 1 10 classic SGB AIDP PCR Neg anti-GM1, anti-GD1a and anti-GD1b elevated fibrinogen, CRP HCQ, DOX, Ig iv partial improvement 8/8
Coen [44] Patient 22 70 M 1 10 classic SGB AIDP PCR Neg Neg ‐– ‐– Ig iv partial improvement 8/8
Colonna [45] Patient 23 62 M 3 21 classic SGB AIDP ‐– ‐– elevated CRP LPV/r, MP (60 mg/24 h) Ig iv partial improvement 7/8
Defabio [46] Patient 24 70 F 1 90 classic SGB ‐– ‐– ‐– ND ND Ig iv complet recovery 7/8
Diez-Porras [47] Patient 25 54 M 1 5 classic SGB AIDP ‐– IgM for GM2 and GD3 and a weak IgG for GT1b elevated CRP, LDH y CK AZM, HCQ, LPV/r Ig iv partial improvement 7/8
El Otmani [48] Patient 26 70 F 2 3 classic SGB AMSAN PCR Neg ‐– lymphopenia HCQ, AZM Ig iv poor 7/8
Elkhouly [49] Patient 27 75 M ‐– ‐– classic SGB ‐– ‐– ‐– ‐– MP Ig iv partial improvement 6/8
Esteban [50] Patient 28 55 F 2 14 classic SGB AIDP ‐– ‐– elevated CRP HCQ, CXM, AZM Ig iv partial improvement 7/8
Farzi [51] Patient 29 41 M 2 10 classic SGB AIDP ‐– ‐– lymphopenia, elevated CRP LPV/r, HCQ Ig iv partial improvement 7/8
Fernandez-Dominguez [52] Patient 30 74 F 2 15 Miller-Fisher AIDP ‐– Neg ‐– HCQ, LPV/r Ig iv partial improvement 7/8
Ferraris [53] Patient 31 65 F 4 23 classic SGB AIDP ‐– ‐– elevated IL-6 HCQ, HBPM, AZM, TCZ, LPV/r, MP Ig iv partial improvement 7/8
Freire Patient 32 71 M 2 9 classic SGB AIDP ‐– Neg Elevated CRP, DD, LDH, ferritin, IL-6 MP Ig iv partial improvement 7/8
Gale [54] Patient 33 58 M 2 ‐– classic SGB AIDP ‐– ‐– lymphopenia, elevated CRP ‐– Ig iv partial improvement 6/8
Garcia-Manzanedo [55] Patient 34 77 M 2 21 PCBW Mixed ‐– ‐– ‐– LPV/r, HCQ Ig iv partial improvement 7/8
Garnero [56] Patient 35 65 M 2 ‐– classic SGB AIDP ‐– Neg ‐– ‐– Ig iv ‐– 6/8
Patient 36 73 M 2 0 classic SGB ‐– PCR Neg Neg ‐– ‐– Ig iv ‐– 7/8
Patient 37 55 M 2 20 Miller-Fisher-GBS overlap ‐– PCR Neg Neg ‐– ‐– Ig iv ‐– 7/8
Patient 38 46 F 1 3 classic SGB ‐– PCR Neg Neg ‐– ‐– Ig iv ‐– 7/8
Patient 39 60 M 2 20 classic SGB AMSAN PCR Neg Neg ‐– ‐– Ig iv ‐– 7/8
Patient 40 63 F 2 15 classic SGB AMSAN Neg ‐– ‐– Ig iv ‐– 7/8
Ghosh [57] Patient 41 20 M 1 8 classic SGB AMAN ‐– Neg lymphopenia ‐– Ig iv partial improvement 7/8



First author (Ref.) Age Sex Severity COVID191 Latency2 GBS Clinical variant3 EMG SARS-COV-2 CSF Antiganglioside antibodies Biomarkers Treatment COVID-19 Treatment GBS Evolution at day 30 Study quality4
Gigli [58] Patient 42 53 M 2 ‐ – paraparetic SGB AIDP ‐– Neg elevated IL-8, IL-6 ‐– Ig iv partial improvement 7/8
Granjer [59] Patient 43 48 M 1 25 classic SGB AIDP ‐– ‐– ‐– ‐– PPH partial improvement 7/8
Guijarro-Castro [60] Patient 44 70 M 2 21 classic SGB Mixed ‐– Neg lymphopenia thrombocythaemia, HCQ, CXM, AZM, DXM Ig iv partial improvement 7/8
Gutierrez-Ortiz [61] Patient 45 50 M 1 5 Miller-Fisher ‐– PCR Neg anti-GD1b lymphopenia, elevated CRP ‐– Ig iv complet recovery 7/8
Helbok [62] Patient 46 68 M 2 14 classic SGB AIDP PCR Neg Neg elevated CRP, ESR, fibrinogen ‐– Ig iv + PPH partial improvement 8/8
Hirayama [63] Patient 47 54 F 2 20 classic SGB AMAN ‐– Neg normal ‐– partial improvement 8/8
Hutchins [64] Patient 48 21 M 2 16 BWDP Mixed ‐– Neg lymphopenia PPH partial improvement 7/8
Kajani [65] Patient 49 50 M 1 ‐– Miller-Fisher ‐– PCR Neg Neg normal ‐– Ig iv dead (ventricular arrhythmia) 6/8
Khaja [66] Patient 50 44 M 1 0 Bifacial weakness ‐– PCR Neg Neg normal ‐– Ig iv complet recovery 8/8
Kopscick [67] Patient 51 31 M 1 0 Miller-Fisher ‐– ‐– anti-GQ1b ‐– convalescent plasma, TCZ Ig iv partial improvement 7/8
Korem [68] Patient 52 58 F 1 14 classic SGB ‐– ‐– ‐– normal AZM Ig iv partial improvement 7/8
Lampe [69] Patient 53 65 M 1 1 classic SGB AIDP ‐– Neg leucopenia, elevated CRP ‐– Ig iv partial improvement 7/8
Lantos [70] Patient 54 36 M 1 4 Miller-Fisher ‐– ‐– Neg ‐– HCQ Ig iv complet recovery 7/8
Lascano [71] Patient 55 52 F 1 15 classic SGB AIDP PCR Neg Neg normal ‐– Ig iv complet recovery 8/8
Patient 56 63 F 1 7 classic SGB AIDP PCR Neg ‐– lymphopenia, elevated transaminases ‐– Ig iv poor 7/8
Patient 57 61 F 1 22 classic SGB AIDP PCR Neg ‐– lymphopenia ‐– Ig iv partial improvement 7/8
Lowery [72] Patient 58 45 M 2 14 Overlap Miller Fisher + SGB ‐– ‐– anti-GQ1b ‐– HCQ Ig iv partial improvement 8/8
Liberatore [73] Patient 59 49 M 2 12 PCBW AMAN PCR Neg Neg lymphopenia, thrombocythaemia. eElevated CRP HCQ, LPV/r, CXM partial improvement 8/8
MacDonell [74] Patient 60 54 M 2 3 classic SGB ‐– Neg normal HCQ Ig iv complet recovery 8/8
Maideniuc [75] Patient 61 61 F 1 28 classic SGB AMAN PCR Neg normal PPH partial improvement 8/8
Manganotti [76] Patient 62 50 F 2 16 Miller-Fisher ‐– Neg ‐– LPV/r, HCQ Ig iv complet recovery 7/8
Manganotti [77] Patient 63 72 M 2 18 classic SGB AIDP PCR Neg Neg Elevated IL6 HCQ, Oseltamivir, darunavir, MP, TCZ Ig iv partial improvement 8/8
Patient 64 72 M 2 30 classic SGB Mixed PCR Neg Neg Normal HCQ, LPV/r, MP Ig iv partial improvement 8/8
Patient 65 49 F 2 14 Miller-Fisher AIDP PCR Neg Neg Normal HCQ, LPV/r, MP Ig iv partial improvement 8/8
Patient 66 94 M 2 33 classic SGB AIDP ‐– ‐– ‐– MP MP poor 7/8
Patient 67 76 M 2 22 classic SGB AIDP PCR Neg Neg Elevated IL6 HCQ, Oseltamivir, darunavir, MP, TCZ. Ig iv partial improvement 8/8
Marta-Enguita [78] Patient 68 78 F 2 8 classic SGB ‐– ‐– ‐– thrombocythaemia, Elevated DD ‐– – dead 7/8
Naddaf [79] Patient 69 58 F 2 17 classic SGB AIDP PCR Neg Neg Elevated DD, ferritine HCQ, MP PPH partial improvement 8/8
Nanda [80] Patient 70 55 F 1 10 classic SGB AMAN ‐– ‐– elevated CRP, Ferritine, IL6, DD, LDH ‐– Ig iv complet recovery 7/8
Patient 71 72 M 2 6 classic SGB AIDP ‐– ‐– elevated CRP, Ferritine, IL6, DD, LDH ‐– Ig iv dead 7/8
Patient 72 55 M 1 7 classic SGB AMSAN ‐– ‐– Elevated CRP, Ferritine, IL6, DD, LDH ‐– Ig iv complet recovery 7/8
Patient 73 49 M 2 10 classic SGB AMAN ‐– ‐– Elevated ferritin, LDH ‐– Ig iv complet recovery 7/8
Oguz-Akarsu [81] Patient 74 53 F 2 0 classic SGB AIDP PCR Neg ‐– lymphopenia, elevated CRP HCQ, AZM PPH complet recovery 7/8
Ottavani [5] Patient 75 66 F 3 7 classic SGB Mixed PCR Neg Neg lymphopenia, elevated CRP, DD. LPV/r, HCQ, Ig iv ‐– 7/8
Paybast [82] Patient 76 38 M 1 21 classic SGB Mixed ‐– ‐– normal HCQ PPH partial improvement 7/8
Pelea [83] Patient 77 56 F 1 7 classic SGB Mixed PCR Neg Neg normal ‐– PPH + Ig iv partial improvement 8/8
Petrelli [84] Patient 78 57 M 1 17 classic SGB AMAN PCR Neg anti-GM1, anti-GD1a ‐– ‐– Ig iv, DM partial improvement 8/8
Padroni [85] Patient 79 70 F 1 24 classic SGB AIDP ‐– ‐– linfocitosis ‐– Ig iv poor 7/8



First author (Ref.) Age Sex Severity COVID191 Latency2 GBS Clinical variant3 EMG SARS-COV-2 CSF Antiganglioside antibodies Biomarkers Treatment COVID-19 Treatment GBS Evolution at day 30 Study quality4
Raahimi [86] Patient 80 46 M 3 45 classic SGB AIDP ‐– ‐– Normal ‐– Ig iv partial improvement 7/8
Rajdev [87] Patient 81 36 M 3 18 classic SGB AIDP ‐– ‐– ‐– remdesivir Ig iv, PPH partial improvement 7/8
Rana [88] Patient 82 54 M 1 14 overlap Miller Fisher - classic SGB AIDP ‐– ‐– ‐– amoxicilin, short course steroids, HCQ, AZM Ig iv, PPH 7/8
Ray [89] Patient 83 63 M 1 1 Miller Fisher ‐– ‐– ‐– Elevated CRP, lymphopenia, neutropenia ‐– ‐– partial improvement 6/8
Redondo [90] Patient 84 54 F 2 15 classic SGB AIDP PCR Neg ‐– Normales ‐– Ig iv partial improvement 7/8
Reyes-Bueno [91] Patient 85 51 F 1 15 overlap Miller Fisher - classic SGB AIDP Neg ‐– ‐– Ig iv, gabapentina partial improvement 7/8
Riva [92] Patient 86 sixties M 2 20 classic SGB AIDP PCR Neg Neg Elevated IL-6, ferritina, LDH, fibrinógeno ‐– Ig iv ‐– 7/8
Sancho-Saldaña [93] Patient 87 56 F 2 15 classic SGB AIDP Neg ‐– HCQ, AZM Ig iv ‐– 7/8
Scheidl [94] Patient 88 54 F 1 21 classic SGB AIDP ‐– ‐– CRP normal ‐– Ig iv complet recovery 7/8
Sedaghat [95] Patient 89 65 M 2 14 classic SGB AMAN Elevated ESR, CRP HCQ, LPV/r, AZM Ig iv 7/8
Senel [96] Patient 90 61 M 1 20 Miller Fisher AIDP PCRNeg Ac Neg Neg Neurofilament light chain (NfL) protein elevated ‐– Ig iv complet recovery 8/8
Su [97] Patient 91 72 M 1 6 classic SGB AIDP PCR Neg Neg Ig iv poor 7/8
Tard [25] Patient 92 76 M 1 7 overlap Miller Fisher - classic SGB AIDP PCR Neg Neg, Anti-NF155
and anti-NF186 IgM, no IgG seroconversion		 ‐– ‐– Ig iv, PPH, MP partial improvement 7/8
Tiet [98] Patient 93 49 M 1 21 classic SGB AIDP PCR Neg ‐– Elevated CRP, LDH, CK ‐– Ig iv, gabapentina partial improvement 7/8
Toscano [99] Patient 94 77 F 2 7 classic SGB AMAN PCR Neg Neg lymphopenia, Elevated CRP, LDH ‐– Ig iv poor 8/8
Patient 95 23 M 1 10 overlap Miller Fisher - classic SGB AMAN PCR Neg ‐– lymphopenia, Elevated ferritine, CRP, LDH, AST ‐– Ig iv partial improvement 7/8
Patient 96 55 M 2 10 classic SGB AMAN PCR Neg Neg lymphopenia, Elevated CRP, LDH, AST, GGT ‐– Ig iv poor 8/8
Patient 97 76 M 1 5 overlap Miller Fisher - classic SGB AIDP PCR Neg ‐– lymphopenia Raised CRP, ‐– Ig iv partial improvement 7/8
Patient 98 61 M 2 7 classic SGB AIDP PCR Neg Neg Lymphocytopenia Elevated CRP, LDH, AST ‐– Ig iv, PPH poor 8/8
Velayos [100] Patient 99 43 M 2 10 classic SGB AIDP ‐– ‐– ‐– HCQ, LPV/r, corticoids (NE) Ig iv satisfactory 7/8
Virani [101] Patient 100 54 M 2 10 classic SGB ‐– ‐– ‐– ‐– ‐– Ig iv partial improvement 7/8
Webb [102] Patient 101 57 M 2 7 classic SGB AIDP PCR Neg Neg lymphopenia, thrombocythaemia, raised CRP Ig iv partial improvement 8/8
Zhao [103] Patient 102 61 F 2 7 classic SGB AIDP lymphopenia thrombocytopenia arbidol, LPV/r Ig iv complet recovery 8/8
Zito [104] Patient 103 57 M 1 12 classic SGB AMAN Neg elevated CRP Ig iv complet recovery 8/8
Zubair [105] Patient 104 32 M 4 60 classic SGB AMSAN ‐– Neg ‐– TCZ, HCQ, remdesivir Ig iv partial improvement 7/8
Patient 105 61 M 4 60 classic SGB AMSAN ‐– Neg ‐– TCZ Ig iv partial improvement 7/8
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-: information not available; 1 1: uncomplicated disease, 2: mild pneumonia, 3: respiratory distress, 4: septic shock; 2 Days from onset of COVID-19 symptoms to onset of GB symptoms; 3 According to diagnostic criteria for GBS, MFS and their subtypes of the GBS Classification Group [8].; 4 JBI (Joanna Briggs Institute) Critical Appraisal Checklist for Case Reports and for Case Series studies [,]; F: female; M: male; BWDP: bifacial weaknees whit distal parestesias; PCBW: pharyngeal-cervical-brachial weakness; AMSAN: acute motor-sensory axonal neuropathy; AIDP: Acute inflammatory demyelinating polyneuropathy; AMAN: acute motor axonal neuropathy; Neg: negative; Pos: positive; PCR SARS-COV-2 CSF: Polymerase chain reaction detection of SARS-Cov-2 in cerebrospinal fluid; DD: D-dimer; CRP: c-reactive protein; ESR: erythrocyte sedimentation rate; LPV/r: Lopinavir/ritonavir; NE: not specified; HCQ: Hydroxychloroquine; CXM: ceftriaxone; AZM: azithromycin; MP: methylprednisolone; TCZ: tocilizumab; DOX: doxycycline; DXM: dexamethasone; Ig iv: intravenous immunoglobulins; PPH: plasmapheresis; PRED: prednisone; ARDS: acute respiratory distress syndrome.

Fig. 1.

Fig. 1

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Existing hypotheses about pathogenic pathways for neurologic damage associated with COVID-19. A. Direct damage. SARS-COV-2 could reach the central nervous system through circulation or retrograde axonal transport, through the olfactory nerve or the enteric nervous system. B. Dysregulated inflammatory response. IL-2, IL-2R, IL-6, IL-10, IFN-γ and TNF-α, are elevated in the”inflammatory phase” of COVID-19 infection. These molecules can stimulate macrophages, dendritic cells, Schwann cells, and epithelial cells that would damage the nervous system. ACE2: Angiotensin-converting enzyme 2; TMPRSS2: Transmembrane protease, serine 2. C. Autoantibody-mediated injury. The existence of a cross-reactivity between epitopes of the SARS-CoV-2 spike and the glycolipids of the peripheral nerve would be probable. This figure was created using BioRender (https://biorender.com/).

In conclusion, the absence of autoantibodies in most GBS cases associated with SARS-CoV2 infection, would force us to think about pathogenic mechanisms other than molecular mimicry. Both the short of the interval of days between the onset of COVID-19 and the neurological symptoms, and the high proportion of patients with serum elevation of inflammation markers at the beginning of neurological symptoms, support the hypothesis that cell-mediated immunity could play a role, as previously proposed for GBS related to Zika.

Funding

The study had no specific funding.

Declaration of Competing Interest

The authors declare that no conflict of interest exists.

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