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Background: The Guillain Barre' syndrome (GBS) is a heterogeneous disease with various subtypes, the prevalence of which would depend on the geographic region. Recognition of these subtypes is of clinical importance since each subtype has an independent pathogenesis and different type of pathology and prognosis. Objectives: To study the various subtypes of GBS using the various published electrophysiological criteria. Design: Retrospective descriptive study. Materials and Methods: In a tertiary care hospital setting, the study compared the various published criteria for demyelination in GBS. The charts of 115 consecutive patients referred for electrodiagnostic evaluation to the Electromyography laboratory between July 2000 and June 2006 were reviewed. Results: Of the 115 patients, 51 (44.4%) patients had axonal forms of GBS and 44 (38.2%) patients had acute inflammatory demyelinating polyradiculoneuropathy (AIDP). Applying the various published criteria, the number of patients categorized under the AIDP subtype ranged between 23.4% and 67.2%. Conclusion: In this study 44% patients had axonal forms of the disease, 38.2% patients had AIDP subtype and 17% remained unclassified. The most sensitive criteria to identify AIDP were the criteria proposed by Albers and colleagues and the Dutch group.

To guide the decision-making for the case definition and guidelines, a literature search was performed by a Cochrane Collaboration professional search person for Guillain-Barré syndrome and other peripheral neuropathies in the context of immunization (MEDLINE 1976-2006; search terms included among others \"Guillain-Barré syndrome\", \"acute inflammatory demyelinating polyradiculoneuropathy\", \"peripheral neuropathy\", \"peripheral demyelination\", \"vaccine\", and \"immunization\"). First described by French neurologists Guillain, Barré, and Stohl in 1916, understanding of the disorder has increased tremendously in the past 2 decades [5]. 0 Healthy 1 Minor symptoms or signs of neuropathy but capable of manual work/capable of running 2 Able to walk without support of a stick (5m across an open space) but incapable of manual work/running 3 Able to walk with a stick, appliance, or support (5m across an open space) 4 Confined to bed or chair bound 5 Requiring assisted ventilation (for any part of the day or night) 6 Death

Background Guillain–Barré syndrome (GBS), when severe, involves the autonomic nervous system; our objective was to assess the spectrum and predictors of dysautonomia, and how it may impact functional outcomes. Methods A retrospective review of patients admitted to the Mayo Clinic in Rochester, MN between January 1, 2000, and December 31, 2017, with GBS and dysautonomia was performed. Demographics, comorbidities, parameters of dysautonomia, clinical course, GBS disability score, and Erasmus GBS Outcome Score (EGOS) at discharge were recorded. Results One hundred eighty seven patients were included with 71 (38%) noted to have at least one manifestation of dysautonomia. There are 72% of patients with a demyelinating form of GBS and 36% of patients with demyelination had dysautonomia. Ileus (42%), hypertension (39%), hypotension (37%), fever (29%), tachycardia or bradycardia (27%), and urinary retention (24%) were the most common features. Quadriparesis, bulbar and neck flexor weakness, and mechanical ventilation were associated with autonomic dysfunction. Patients with dysautonomia more commonly had cardiogenic complications, syndrome of inappropriate antidiuretic hormone, posterior reversible encephalopathy syndrome, and higher GBS disability score and EGOS. Mortality was 6% in patients with dysautonomia versus 2% in the entire cohort ( P  = 0.02). Conclusions Dysautonomia in GBS is a manifestation of more severe involvement of the peripheral nervous system. Accordingly, mortality and functional outcomes are worse. There is a need to investigate if more aggressive treatment is warranted in this category of GBS.

Background Guillain–Barre syndrome (GBS) is an inflammatory polyradiculoneuropathy characterized by rapidly evolving weakness and areflexia, reaching nadir within 4 weeks. Data on the characteristic of GBS in Saudi Arabia are limited. This study aimed to describe the clinical, electrophysiological, and laboratory characteristics and outcome of a multicenter cohort of patients with GBS. Methods This is a retrospective multicenter nationwide study. Patients who had GBS, identified through Brighton Criteria, between January 2015 and December 2019 were included. Data collected included demographics, clinical features, cerebrospinal fluid profile, reported electrophysiological patterns, treatment, and outcome. Reported GBS subtypes were compared using chi-square, Fisher's exact, or Mann–Whitney U tests, as appropriate. Results A total of 156 patients with GBS were included (men, 61.5%), with a median age of 38 (interquartile range, 26.25–53.5) years. The most commonly reported antecedent illnesses were upper respiratory tract infection (39.1%) and diarrhea (27.8%). All but two patients (98.7%) had weakness, 64.1% had sensory symptoms, 43.1% had facial diplegia, 33.8% had oropharyngeal weakness, 12.4% had ophthalmoplegia, and 26.3% needed mechanical ventilation. Cytoalbuminological dissociation was observed in 69.1% of the patients. GBS-specific therapy was administered in 96.8% of the patients, of whom 88.1% had intravenous immunoglobulin, and 11.9% had plasmapheresis. Approximately half of the patients were able to walk independently within 9 months after discharge, and a third regained the ability to walk independently thereafter. Death of one patient was caused by septicemia. Acute inflammatory demyelinating polyradiculoneuropathy was the most commonly reported GBS subtype (37.7%), followed by acute motor axonal neuropathy (29.5%), and acute motor-sensory axonal neuropathy (19.2%). Conclusion The clinical and laboratory characteristics and outcome of GBS in the Arab population of Saudi Arabia are similar to the international cohorts. The overall prognosis is favorable.

Background: Guillain-Barré syndrome (GBS) has been the most common cause of flaccid paralysis in children after the decline in the incidence of poliomyelitis. There are not any published data from the Indian subcontinent documenting electrophysiological patterns and antiganglioside antibodies in pediatric GBS. Materials and Methods: The study population included children with GBS referred for electrodiagnostic evaluation and also children with GBS admitted to our institute between August 2006 and July 2007. Nerve conduction studies were done to determine GBS subtypes and serum antiganglioside antibodies were measured using enzyme-linked immunosorbent assay (ELISA). Clinical and electrophysiological features were correlated with antiganglioside antibody results. Results: Of the 43 (male to female ratio = 2.1:1) children studied, 97.6% had motor weakness, 76.7% had cranial nerve palsies, 13.9% had autonomic disturbances and respiratory paralysis was found in 9.3% children. Antecedent illness was recorded in 69.8% children. The GBS subtype distribution was as follows: acute inflammatory demyelinating polyradiculoneuropathy (AIDP) in 21 (48.8%), acute motor axonal neuropathy (AMAN) in 19 (44.2%), and 3 (6.9%) children were unclassified. The severity of illness was similar in both AMAN and AIDP subtypes and the recovery in both the subtypes was complete without any significant difference in the duration of recovery. Preceding diarrheal illness was more common in AMAN subtype as compared to AIDP subtype (57.9% vs. 4.7%, P = 0.007). Sensory symptoms were more common in AIDP subtype than in AMAN subtype (66.6% vs. 21%, P = 0.03}. The commonest ganglioside antibody was IgM GM2. Anti GM3 antibodies were exclusively seen in children with AMAN and IgG GD1b was significantly associated with (36.7 vs. 4%; P = 0.007) AMAN subtype. IgG GT1b was identified in 50% of patients with AIDP as compared to 22.7% in patients with AMAN. Conclusion: In this study, AMAN subtype accounted for a significant proportion of pediatric GBS. AMAN was associated with diarrhea and specific antiganglioside antibodies. Recovery in children with GBS was complete, irrespective of the subtype.

Objective: The diagnosis of acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is based mainly on motor nerve conduction studies (NCSs), which may lead to inconclusive results, especially early in the course of the disease. The present study aimed to evaluate sensory NCSs as an additional tool to aid the identification of this illness.Materials and Methods: We retrospectively evaluated the sensory and motor nerve conduction findings of patients with AIDP and compared them with laboratory controls. The sensitivity and specificity of the NCS parameters and sural sparing pattern (SSP) were also assessed. The NCS patterns were categorized as normal, abnormal, and no response. The association of sensory nerve action potential (SNAP) amplitude patterns and effect of the timing of the electrodiagnostic examination on sensory and motor NCS patterns were analyzed.Results: The most sensitive sensory nerve conduction findings were reduced ulnar (79.3%) and median (75.9%) SNAP amplitudes, which were more sensitive than the compound muscle action potential amplitudes and forearm motor nerve conduction velocities of these nerves. Employing ulnar SNAP for SSP identification was more useful than using the median SNAP. The timing of the electrodiagnostic studies did not affect the patterns of the sensory nerve conduction parameters.Conclusion: The reduction in the median and ulnar SNAP amplitudes along with SSP, with the ulnar SNAP amplitude used for comparison, is beneficial for diagnosing AIDP regardless of the timing of the electrodiagnostic examination.

The molecular determinants and mechanisms involved in leukocyte trafficking across the blood–nerve barrier (BNB) in the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) variant of Guillain–Barré syndrome are incompletely understood. Prior work using a flow-dependent in vitro human BNB model demonstrated a crucial role for α M -integrin (CD11b)-intercellular adhesion molecule-1 interactions in AIDP patient leukocyte trafficking. The aim of this study is to directly investigate the biological relevance of CD11b in AIDP pathogenesis. Immunohistochemistry was performed on three AIDP patient sural nerve biopsies to evaluate endoneurial leukocyte CD11b expression. A severe murine experimental autoimmune neuritis (sm-EAN) model was utilized to determine the functional role of CD11b in leukocyte trafficking in vivo and determine its effect on neurobehavioral measures of disease severity, electrophysiological assessments of axonal integrity and myelination and histopathological measures of peripheral nerve inflammatory demyelination. Time-lapse video microscopy and electron microscopy were employed to observe structural alterations at the BNB during AIDP patient leukocyte trafficking in vitro and in situ, respectively. Large clusters of endoneurial CD11b+ leukocytes associated with demyelinating axons were observed in AIDP patient sural nerves. Leukocyte CD11b expression was upregulated during sm-EAN. 5 mg/kg of a function-neutralizing monoclonal rat anti-mouse CD11b antibody administered after sm-EAN disease onset significantly ameliorated disease severity, as well as electrophysiological and histopathological parameters of inflammatory demyelination compared to vehicle- and isotype antibody-treated mice. Consistent with in vitro observations of leukocyte trafficking at the BNB, electron micrographs of AIDP patient sural nerves demonstrated intact electron-dense endoneurial microvascular intercellular junctions during paracellular mononuclear leukocyte transmigration. Our data support a crucial pathogenic role of CD11b in AIDP leukocyte trafficking, providing a potential therapeutic target for demyelinating variants of Guillain–Barré syndrome.

To our knowledge this is the first reported case of AIDP that developed as a complication of DBS surgery.2 Case Our patient is a 66-year-old Caucasian woman with medically refractory essential tremor, hypertension, diabetes mellitus type 2, obstructive sleep apnea and chronic pain who presented to the emergency department 14 days after initial DBS lead placement for evaluation of progressive dysphagia and generalized weakness. After a course in inpatient rehab she was able to return home and at her most recent clinic evaluation was largely back to previous baseline.3 Discussion We present case of AIDP following DBS lead implantation. AIDP should be considered in patients with unexplained progressive weakness following DBS lead placement.Declaration of Competing Interest None.Appendix A Supplementary data Supplementary material related to this article can be found, in the online version, at doi:https://doi.org/10.1016/j.clineuro.2020.106124.Appendix A Supplementary data The following is Supplementary data to this article:

Here, we present a case of late-onset Guillain-Barré syndrome (GBS) associated with COVID-19. A 70-year-old woman presented with ascending paralysis and right lower motor neuron facial weakness 2 months after COVID-19 infection. Test results for SARS-CoV-2 immunoglobulin were positive at the time of presentation. Lumbar puncture showed albuminocytological dissociation, and electrophysiology showed features of demyelination with secondary axon loss. In the published literature on GBS associated with COVID-19, almost all patients presented with neurological symptoms 1–4 weeks after the infection. GBS can be an early or late manifestation after COVID-19. Patients with signs of paraparesis and facial weakness after COVID-19 should be carefully evaluated for immune-mediated central and peripheral nervous system disorders.

Objectives: It has been suggested that autoimmunity to peripheral myelin proteins is involved in the pathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We aimed to compare reactivity of peripheral blood mononuclear cells (PBMC) to antigens of peripheral myelin proteins in patients with GBS and patients with CIDP with that of healthy controls and patients with other non-immune mediated neuropathies (ON). Methods: We prepared PBMC from blood from 83 healthy controls and from 64 patients with GBS, 54 with CIDP, and 62 with ON. PBMC were tested in antigen specific proliferation assays against peptides from myelin proteins P0, P2, PMP22, and myelin basic protein (MBP), which is identical to myelin P1, and against whole human MBP. Interferon-gamma (IFN-γ) and interleukin (IL)-5 enzyme linked immunospot (ELISPOT) assays were also performed in some subjects to assess spontaneous and peripheral myelin antigen specific PBMC cytokine secretion. Results: Antigen specific PBMC proliferation assays showed no significant elevation of peptide specific T cell responsiveness in patients with GBS or CIDP compared with healthy controls or patients with ON. Levels of spontaneous ELISPOT IFN-γ secretion were increased in patients with GBS and significantly increased in those with CIDP compared with healthy controls and patients with ON. No convincing differences in antigen specific ELISPOT IFN-γ secretion levels to individual peptides were detectable in patients with GBS. The proportion of patients with CIDP with an increased number of PBMC producing IFN-γ in response to peptide PMP-2251–64 was significantly increased compared with healthy controls and patients with ON. No significant differences in antigen specific ELISPOT IL-5 secretion levels were detectable in patients with GBS or CIDP compared with controls, but levels of spontaneous IL-5 secretion were significantly higher in patients with CIDP than in healthy controls or patients with ON. Conclusions: Although the lack of significantly increased antigen specific PBMC proliferation in GBS and CIDP does not support a role for T cells, the more sensitive ELISPOT technique detected increased numbers of PBMC secreting IFN-γ spontaneously in 25% of patients with GBS, providing further evidence for a role of T cells in the immunopathology of GBS. Increased numbers of spontaneous IFN-γ and IL-5 secreting cells, and increased IFN-γ secretion in response to PMP-2251–64, in patients with CIDP provide further evidence for a role of myelin specific T cells in CIDP.