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Several distinct autoimmune neuropathies can be referred to collectively as Guillain–Barré syndrome (GBS). Wakerley and colleagues argue that confusing terminology hinders diagnosis, and they present a revised classification of 'classic' GBS, Miller Fisher syndrome and related conditions. This new approach to diagnosis might facilitate work-up, thereby helping to identify the correct treatment as quickly as possible. Guillain–Barré syndrome (GBS) and its variant, Miller Fisher syndrome (MFS), exist as several clinical subtypes with different neurological features and presentations. Although the typical clinical features of GBS and MFS are well recognized, current classification systems do not comprehensively describe the full spectrum of either syndrome. In this Perspectives article, GBS and MFS are classified on the basis of current understanding of the common pathophysiological profiles of each disease phenotype. GBS is subclassified into classic and localized forms (for example, pharyngeal–cervical–brachial weakness and bifacial weakness with paraesthesias), and MFS is divided into incomplete (for example, acute ophthalmoparesis, acute ataxic neuropathy) and CNS subtypes (Bickerstaff brainstem encephalitis). Diagnostic criteria based on clinical characteristics are suggested for each condition. We believe this approach to be more inclusive than existing systems, and argue that it could facilitate early clinical diagnosis and initiation of appropriate immunotherapy.

No American playwright is more revered on the international stage than Arthur Miller. In Arthur Miller's Global Theater—a fascinating collection of new essays by leading international critics and scholars—readers learn how and why audiences around the world have responded to the work of the late theatrical icon. With perspectives from diverse corners of the globe, from Israel to Japan to South Africa, this groundbreaking volume explores the challenges of translating one of the most American of American playwrights and details how disparate nations have adapted meaning in Miller's most celebrated dramas. An original and engaging collection that will appeal to theater aficionados, scholars, students, and all those interested in Miller and his remarkable oeuvre, Arthur Miller's Global Theater illustrates how dramas such as Death of a Salesman, The Crucible, and A View from the Bridge developed a vigorous dialogue with new audiences when they crossed linguistic and national borders. In these times when problems of censorship, repressive regimes, and international discord are increasingly in the news, Arthur Miller's voice has never been more necessary as it continues to be heard and celebrated around the world.

Background and purpose Antiganglioside antibodies (AGAs) might be involved in the etiopathogenesis of many neurological diseases, such as Miller–Fisher syndrome (MFS) and Guillain–Barré syndrome (GBS). Available comprehensive reference data regarding AGA positivity rates and cross‐responsiveness among AGAs (where one line immunoblot is positive for ≥1 AGA) during routine clinical care are scant. Methods In this 10‐year monocentric retrospective study, 3560 immunoglobulin (Ig) G and IgM line blots (GA Generic Assays' Anti‐Ganglioside Dot kit) obtained using cerebrospinal fluid (CSF) and serum samples from 1342 patients were analyzed for AGA positivity in terms of 14 diagnosis categories and AGA cross‐responsiveness. Results Of all 3560 line blots 158 (4.4%) and of all CSF samples 0.4% (4/924) CSF line blots were AGA positive. For serum IgG, blots with positivity rates higher than the standard deviation of 15.6% were associated with MFS (GD3, GD1a, GT1a and GQ1b) and acute motor axonal neuropathy (AMAN) (GM1, GD1a and GT1a). For serum IgM, blots with positivity rates higher than the standard deviation of 8.1% were associated with AMAN (GM2, GT1a and GQ1b), MFS (GM1, GT1a and GQ1b), multifocal motor neuropathy (MMN) (GM1, GM2 and GQ1b) and chronic inflammatory demyelinating polyneuropathy (CIDP) (GM1). Cross‐responsiveness was observed in 39.6% of all positive serum AGA. Conclusions Testing for AGAs during routine clinical care rarely led to positive findings, both in serum and even less in CSF, except for the diagnoses AMAN, MFS, MMN and CIDP. Nonspecific findings found as cross‐responsiveness between different AGA samples occur frequently, impacting the positivity of most AGA subtypes.

We present a rare case of a 56-year-old female presenting with overlapping features of Miller Fisher syndrome (MFS), Bickerstaff’s brainstem encephalitis (BBE) and Guillain-Barré syndrome (GBS), despite seronegativity for anti-GQ1b, GM1, GD1b, GT1a, and GT1b IgG antibodies. The patient developed sequential neurological deficits (ophthalmoplegia, ataxia, tetraparesis, and altered consciousness) following an upper respiratory infection. Electrophysiological studies confirmed acute motor-sensory axonal neuropathy, while cerebrospinal fluid analysis showed albuminocytological dissociation. Dual intravenous immunoglobulin (IVIG) courses and methylprednisolone therapy led to partial recovery, with independent ambulation achieved by day 76. This case underscores the complexity of overlapping anti-GQ1b antibody syndromes and highlights the need for alternative diagnostic biomarkers in seronegative patients. •Rare Triple Overlap Syndrome: A case presented with concurrent features of MFS, BBE, and GBS, despite seronegativity for antibodies.•Unique Diagnostic Challenges: The case underscores the complexity of diagnosing overlap syndromes in seronegative patients, emphasizing the need for clinical vigilance beyond antibody testing.•Implications for Research: Highlights the potential role of non-ganglioside targets in seronegative cases, urging exploration of novel biomarkers.•Literature Context: Among only 8 reported triple overlap cases, this adds to evidence supporting a broader clinical spectrum of anti-GQ1b antibody syndromes.

Former Capitals forward Kelly Miller remembers the 1998 Stanley Cup Finals against Detroit – and the moment the series got away from Washington.

IntroductionSince the initial identification of Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE),significant milestones have been achieved in understanding these diseases.Discoveries of common serum antibodies (IgG anti-GQ1b), antecedent infections, neurophysiological data, andneuroimaging suggested a shared autoimmune pathogenetic mechanism rather than distinct pathogenesis, leadingto the hypothesis that both diseases are part of a unified syndrome, termed “Fisher-Bickerstaff syndrome”. The subsequent identification of atypical anti-GQ1b-positive forms expanded the classification to a broader condition known as “Anti-GQ1b-Antibody syndrome”.MethodsAn exhaustive literature review was conducted, analyzing a substantial body of research spanning from the initialdescriptions of the syndrome’s components to recent developments in diagnostic classification and researchperspectives.ResultsAnti-GQ1b syndrome encompasses a continuous spectrum of conditions defined by a common serological profilewith varying degrees of peripheral (PNS) and central nervous system (CNS) involvement. MFS and BBE represent theopposite ends of this spectrum, with MFS primarily affecting the PNS and BBE predominantly involving the CNS.Recently identified atypical forms, such as acute ophthalmoparesis, acute ataxic neuropathy withoutophthalmoparesis, Guillain-Barré syndrome (GBS) with ophthalmoparesis, MFS-GBS and BBE-GBS overlap syndromes,have broadened this spectrum.ConclusionThis work aims to provide an extensive, detailed, and updated overview of all aspects of the anti-GQ1b syndromewith the intention of serving as a stepping stone for further shaping thereof. Special attention was given to therecently identified atypical forms, underscoring their significance in redefining the boundaries of the syndrome.

[This corrects the article DOI: 10.1371/journal.pone.0235441.].[This corrects the article DOI: 10.1371/journal.pone.0235441.].

The clinical features of Guillain–Barré syndrome (GBS) are highly variable, according to the type of antecedent infection. Although a major GBS phenotype, Fisher syndrome (FS), has been shown to be preceded by infections similar to those preceding GBS, whether or not the clinical features in FS also vary according to antecedent infection remains unclarified. Frequent antecedent infections among this study of 70 FS patients included Haemophilus influenzae [n = 15 (21%)], Campylobacter jejuni [n = 10 (14%)], and cytomegalovirus (CMV) [n = 6 (8.6%)]. Compared with other FS patients, H. influenzae-seropositive FS patients more frequently had a history of prior upper respiratory tract infection; double vision as the initial symptom; and, except for oculomotor disturbance, more rarely showed cranial nerve involvement. C. jejuni-related FS occurred predominantly in younger male patients and characteristically presented with blurred vision. According to GBS disability scale, CMV-related FS tended to be more severe, although every patient received immunotherapy. Serum anti-GQ1b IgG antibodies were detected in most cases, regardless of antecedent infection type. At the nadir of illness, the most frequent diagnosis in H. influenzae-related cases was “pure FS” without limb weakness or central nervous system involvement (71%), in C. jejuni-related cases “incomplete FS” such as acute ophthalmoparesis with or without ataxia (60%), and in CMV-related cases (50%) advanced conditions such as GBS overlap and Bickerstaff brainstem encephalitis. These findings indicate that the type of preceding infection determined the neurological features of FS. CMV-related FS appeared to be similar to H. influenzae- and C. jejuni-related FS regarding anti-GQ1b antibody-mediated pathogenesis, as opposed to CMV-related GBS.

Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain–Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11–max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.