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Backround Guillain-Barré syndrome (GBS) is an immune-mediated disease that affects the peripheral nervous system and may occur after some bacterial-viral infections. Aim The aim of this study is to determine and compare the epidemiological, clinical and laboratory characteristics of the patients followed up in our clinic with the diagnosis of GBS in the 15 month periods before and after March 2020. At the same time, we aimed to examine the importance of these markers as prognostic indicators by investigating the relationship of D-dimer, CRP, albumin and transferrin levels with Hughes functional grading scale score (HFGSS). Material and Methods The medical files of the patients who were followed up with the diagnosis of GBS between December 2018 and May 2021 were retrospectively analyzed. The patients were divided into groups as pandemic, pre-pandemic, post-COVID-19 and non-COVID-19. Epidemiological and clinical characteristics of GBS patients and plasma D-dimer, serum albumin, CRP and transferrin levels were recorded. Results No significant difference was found between the pandemic and pre-pandemic periods in terms of age, gender, GBS subtype, seasonal distribution and treatment characteristics of GBS patients. PostCOVID-19 GBS patients had significantly higher HFGSS both at admission and at discharge (p

Highlights • A whole new group of unprecedented acute and late neurological complications related with SARS-CoV-2 are being reported around the world. • Unexpected neurological syndromes, initially poorly understood, can be better understood by gathering several “rare” cases and establishing causality. • Facial Diplegia is a rare Guillain-Barré Syndrome variant, compatible with our case report and a previously reported one, suggesting it might not be so weird for COVID-19 infection related neurological disease, but more cases are needed for conclusions., We present a case of facial diplegia after 10 days of SARS-CoV-2 confirmed infection symptoms in a 61 year old patient without prior clinically relevant background. There are few known cases of Guillain-Barré Syndrome (GBS) related to SARS-CoV-2 infection; we propose this case as a rare variant of GBS in COVID-19 infection context, due to Its chronology, clinical manifestations and cerebrospinal fluid (CSF) findings.

• A novel coronavirus (COVID-19) was detected in Wuhan City, Hubei Province of China. • The most symptoms of disease have reported fever, cough, dyspnea, myalgia, headache, and diarrhea. • We followed up GBS symptoms in one infected patient with COVID-19. • The limbs weakness of patient completely improved after treatment with IVIG.

Guillain-Barré syndrome (GBS) is an immune-mediated acute disorder of the peripheral nervous system. Despite treatment, there is an associated mortality and severe disability in 9 to 17% of the cases. Decitabine (DAC) is a hypomethylating drug used in myelodisplastic syndrome, that has been shown to exert immunomodulatory effects. We have evaluated the effects of DAC in two rodent models of GBS, the Experimental Allergic Neuritis (EAN). Both prophylactic and therapeutic treatment with DAC ameliorated the clinical course of EAN, increasing the numbers of thymic regulatory T cells and reducing the production of proinflammmatory cytokines. Our data suggest the possible use of decitabine for the treatment of GBS.

Lyme disease is the most common tick-borne disease in the United States. Left untreated, it can lead to neuroborreliosis. Here we describe a case of early disseminated Lyme disease-associated Guillain Barre Syndrome in a previously healthy adult that early clinical suspicion and accurate testing led to proper diagnosis and case management. It is important to be aware of Guillain Barre Syndrome as an early consequence of Lyme disease especially during tick activity season. This case report is meant to raise awareness among clinicians and calls for protective measures especially where there is significant outdoor activity.

The events triggering and/or sustaining the auto-immune response underlying chronic inflammatory demyelinating polyneuropathy (CIDP) are unknown. Similar to Guillain-Barre syndrome (GBS), a viral infection might play a role in CIDP. In this study, an virus detection method (VIDISCA-next generation sequencing) capable of detecting known and unknown viruses, was used to analyze the virome in serum of 47 CIDP patients at different time points of the disease and, when available, in cerebrospinal fluid (CSF) samples (N: 17). Serum samples of GBS patients (N:24) and healthy controls (N:114) were used for comparisons. In 5/47 (10.6%; 95% CI: 4–23) CIDP samples, 10/24 (42%; 95% CI: 22–63) GBS samples and 32/114 (28.1%; 95% CI: 20–37) healthy controls samples, anelloviruses were detected, generally regarded as a non-pathogenic species. Parvovirus B19 and GB virus C were found in two CIDP samples (4%). Parvovirus B19, HIV-1 and GB virus C were found in three GBS samples (13%). In 2/17 CIDP CSF samples, an anellovirus and polyomavirus were detected, probably due to contamination during lumbar puncture. No sequences of other viruses were detected in serum or CSF. A (persistent) viral infection sustaining the auto-immune response in CIDP seems therefore unlikely.

Background Guillain Barre Syndrome (GBS) and Miller Fisher Syndrome (MFS) are emerging as known consequences of COVID-19 infection. However, there have been no reported cases with positive GM1 or GQ1b antibodies in the literature to date. Although clinically similar, the pathophysiology of COVID-19 related GBS and MFS may be significantly different from cases in the pre-pandemic era. Case presentation We present a patient with ascending areflexic weakness consistent with GBS with positive GM1 antibody. The patient had recovered from COVID-19 infection two weeks prior with mild viral illness and symptoms. Her weakness was isolated to the lower extremities and improved after intravenous immunoglobulin treatment. Patient recovered eventually. Conclusions – The general lack of reported ganglioside antibodies supports a novel target(s) for molecular mimicry as the underlying etiology, which raises the concern for possible vaccine induced complication. Whether the current GM1 positive case is a sequalae of COVID-19 or a mere coincidence is inconclusive. Further understanding of the disease mechanism of pandemic era GBS and MFS, including antigen target(s) of COVID-19, may be of utmost importance to the development of a safe COVID-19 vaccine.

Several reports have linked the presence of high titers of anti-Gg Abs with delayed recovery/poor prognosis in GBS. In most cases, failure to recover is associated with halted/deficient axon regeneration. Previous work identified that monoclonal and patient-derived anti-Gg Abs can act as inhibitory factors in an animal model of axon regeneration. Further studies using primary dorsal root ganglion neuron (DRGn) cultures demonstrated that anti-Gg Abs can inhibit neurite outgrowth by targeting gangliosides via activation of the small GTPase RhoA and its associated kinase (ROCK), a signaling pathway common to other established inhibitors of axon regeneration. We aimed to study the molecular basis of the inhibitory effect of anti-Gg abs on neurite outgrowth by dissecting the molecular dynamics of growth cones (GC) cytoskeleton in relation to the spatial-temporal analysis of RhoA activity. We now report that axon growth inhibition in DRGn induced by a well characterized mAb targeting gangliosides GD1a/GT1b involves: i) an early RhoA/ROCK-independent collapse of lamellipodia; ii) a RhoA/ROCK-dependent shrinking of filopodia; and iii) alteration of GC microtubule organization/and presumably dynamics via RhoA/ROCK-dependent phosphorylation of CRMP-2 at threonine 555. Our results also show that mAb 1B7 inhibits peripheral axon regeneration in an animal model via phosphorylation/inactivation of CRMP-2 at threonine 555. Overall, our data may help to explain the molecular mechanisms underlying impaired nerve repair in GBS. Future work should define RhoA-independent pathway/s and effectors regulating actin cytoskeleton, thus providing an opportunity for the design of a successful therapy to guarantee an efficient target reinnervation. Fil: Rozés Salvador, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Heredia, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Berardo, Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Palandri, Anabela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Wojnacki Fonseca, José Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Vivinetto, Ana Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Sheikh, Kazim A.. University Of Texas Medical School At Houston; Fil: Caceres, Alfredo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina Fil: Lopez, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina. Universidad Nacional de Córdoba; Argentina

We review post-infectious and post-vaccination neurological syndromes involving peripheral and central nervous system (CNS) and report an illustrative case of simultaneous occurrence of Guillain-Barré syndrome (GBS), confirmed by nerve conduction velocities, plus MRI-demonstrated transverse myelitis (TM) and acute encephalitis [acute disseminated encephalomyelitis] (ADEM+GBS) affecting a 24-year-old woman from Cúcuta, Colombia, who developed acute Zika virus (ZIKV) infection confirmed by serum reverse transcriptase-polymerase chain reaction (RT-PCR) and convalescent ZIKV IgG antibodies. With intensive care treatment, respiratory support, steroids, and intravenous immunoglobulin (IVIg), patient survived with residual flaccid paraparesis. She had preexisting immunity against Chikungunya virus (CHIKV) and Dengue virus (DENV) acquired before the arrival of ZIKV in Colombia. From reports in the Caribbean, Central and South America we review 19 cases of ZIKV-associated TM, encephalitis and ADEM occurring after a mean latent period of 10.5 days (range 1–96) post-infection. Although GBS and ADEM are usually considered post-infectious and associated with development of antibodies against peripheral nerve and CNS epitopes, we postulate that our case of ADEM+GBS is para-infectious, induced by acute ZIKV neurotropism boosted by active immunity against other arboviruses. Animal models of ZIKV demonstrated strong viral neurotropism enhanced by passive immunity with antibodies against arboviruses such as West Nile virus, CHIKV, or DENV. These considerations are relevant to prevent potential ZIKV vaccine-induced reactions involving central and peripheral nervous system. © 2018 The Authors

Therapeutic plasma exchange (TPE), is a procedure, changing pathologic substances in the plasma of patients with replacement fluid. TPE has an increasing list of indications in recent years such as neurological, connective tissue, hematological, nephrological, endocrinological and metabolic disorders. We report our multicenter data about therapeutic plasma exchange in patients with neurological diseases. Six University Hospitals' aphaeresis units medical records about neurologic diseases were reviewed retrospectively. Hundred and fifteen patients and 771 TPE sessions from six aphaeresis units' were included to this study. Of the 115 patients, 53 (46%) were men and 62 (54%) were women. The median age was 50 (range: 5-85) years. Of these patients 58.3% were Guillain-Barre syndrome (GBS), 17.4% were acute disseminated encephalomyelitis (ADEM), 10.4% were chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), 7% were multiple sclerosis, 6.1% were myasthenia gravis (MG) and 0.9% were Wilson disease (WD). The median number of TPE sessions per patient was 5 (range 1-72). Human albumin was used as a replacement fluid in 66% and fresh frozen plasma was used in 34% of cases. TPE was done through central venous catheters in 66%, and peripheral venous access in 34% of patients. Some complications were seen in patients (18.3%) during TPE sessions. These complications were, complications related to catheter placement procedure (8.7%), hypotension (3.5%), hypocalcaemia (3.5%) and allergic reactions (1.7%). The complication ratios were 2.7% in total 771 TPE procedures. TPE procedure was terminated in 6% of sessions depending on these complications. Overall responses to TPE were noted in 89.5% of patients.In conclusion; Therapeutic plasma exchange is an effective treatment option in several neurologic diseases. © 2013 Elsevier Ltd.