Guillain-Barre Syndrome Publications (7591)

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Guillain-Barre Syndrome Publications

Posterior reversible encephalopathy syndrome (PRES) is a rare occurrence in patients with Guillain-Barré syndrome (GBS). Two patients with neuroradiological evidence of PRES without central nervous system (CNS) symptoms were recently reported. We present the case of a GBS patient with minimal CNS symptoms and magnetic resonance imaging findings consistent with PRES. Read More

PRES in GBS might be an underestimated condition. It should be suspected in GBS patients in the presence of even mild CNS symptoms. A timely PRES diagnosis along with early correction of autonomic system dysfunction in GBS patients is recommended to prevent possible dangerous CNS complications.

2015Apr
World Neurosurg
World Neurosurg 2015 Apr 27. Epub 2015 Apr 27.
Department of Neurology, the Second Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, China. Electronic address: lixiangey@sina.cn.
2015Apr
J. Neurosci.
J Neurosci 2015 Apr;35(17):6770-85
Department of Neurology, University of Texas Medical School at Houston, Houston, Texas 77030 kazim.sheikh@uth.tmc.edu.
2015Apr
Pract Neurol
Pract Neurol 2015 Apr 27. Epub 2015 Apr 27.
Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
2015Apr
Int. J. Infect. Dis.
Int J Infect Dis 2015 Apr 16;35:34-36. Epub 2015 Apr 16.
Angelo Bianchi Bonomi Haemophilia and Thrombosis Center, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università degli Studi di Milano, Luigi Villa Foundation, Milan, Italy. Electronic address: flora.peyvandi@unimi.it.
2015Apr
Neurol. Neurochir. Pol.
Neurol Neurochir Pol 2015 12;49(2):137-8. Epub 2015 Mar 12.
Department of Neurology, Wrocław Medical University, Wrocław, Poland.

Miller-Fisher Syndrome (MFS) is a rare acute polyneuropathy composed of the clinical triad of ataxia, areflexia and ophthalmoplegia, with a monophasic, self-limited course and spontaneous improvement.
The authors present a 65-year-old man with Miller-Fisher syndrome consisting of bilateral ophthalmoplegia, trigeminal and facial nerve palsy, mild ataxia and peripheral neuropathy. The disease had a progressive, subacute course within 3 months. Read More

A high titer of anti-GQ1b antibodies was detected. As a result of plasmapheresis, complete recovery was achieved.
The presented case was atypical in its clinical course and treatment. It could support the theory of the continuity between MFS, Bickerstaff brainstem encephalitis (BBE), and Guillain-Barré syndrome (GBS).

2015Apr
Public Health
Public Health 2015 Apr 15. Epub 2015 Apr 15.
French Army Centre for Epidemiology and Public Health, Marseille, France; École du Val-de-Grâce, Paris, France.

French military personnel are subject to a compulsory vaccination schedule. The aim of this study was to present the results of surveillance of vaccine adverse events (VAEs) reported from 2011 to 2012 in the French armed forces.
VAEs were surveyed among all French armed forces from 2011 to 2012 by the epidemiological departments of the military health service. Read More

For each case, a notification form providing patient and clinical information was provided.
Case definitions were derived from the French drug safety guidelines. Three types of VAE were considered: non-serious, serious and unexpected. Incidence rates were calculated by relating VAEs to the number of vaccine doses delivered.
In total, 161 VAE cases were reported. The overall VAE reporting rate was 24.6 VAEs per 100,000 doses, and the serious VAE rate was 1.3 per 100,000 doses (nine cases). The serious VAEs included two cases of Guillain-Barré syndrome, one case of optic neuritis, one case of a meningeal-like syndrome, one case of rheumatoid purpura, one case of acute asthma and three cases of fainting. The highest rates of VAE were observed with the Bacille Calmette-Guérin vaccine (BCG) (482.3 per 100,000 doses), inactivated diphtheria-tetanus-poliovirus with acellular pertussis vaccine (dTap-IPV) (106.1 per 100,000 doses) and meningococcal quadrivalent glycoconjugate vaccine (MenACWY-CRM) (39.3 per 100,000 doses).
The global rates of VAE observed in 2011 and 2012 confirm the increase that has been observed since 2009 in the French armed forces, which could reflect improved practitioner awareness about VAEs and the use of certain vaccines added to the vaccination schedule recently (dTap-IPV in 2008 and MenACWY-CRM in 2010). VAEs appear to be relatively rare, particularly serious VAEs, which indicates acceptable tolerance of vaccines.

2015May
J. Neurol. Sci.
J Neurol Sci 2015 May 10;352(1-2):135-6. Epub 2015 Apr 10.
Department of Neurology, Warren Alpert Medical School of Brown University, 110 Lockwood Street, Suite 324, Providence, RI 02903, USA. Electronic address: muhib_khan@brown.edu.
2015Apr
J Pediatr Neurosci
J Pediatr Neurosci 2015 Jan-Mar;10(1):67-9
Department of Pediatrics, Pediatric Intensive Care Unit, Max Superspecialty Hospital, Saket, New Delhi, India.
2015Apr
J Pediatr Neurosci
J Pediatr Neurosci 2015 Jan-Mar;10(1):61-3
Department of Pediatrics, MGIMS, Sevagram, Wardha, Maharashtra, India.

Acute disseminated encephalomyelitis (ADEM) and Guillain-Barré syndrome (GBS) are distinct demyelinating disorders that share an autoimmune pathogenesis and prior history of viral infection or vaccination. Our patient is a 10 years with acute flaccid paralysis, quadriparesis (lower limbs affected more than upper limbs), generalized areflexia and urinary retention. He had difficulty in speech and drooling of saliva. Read More

He also presented with raised intracranial pressure with papilledema; then bilateral optic neuritis developed during the later course of illness. Based on the temporal association and exclusion of alternative etiologies, diagnosis of the association between ADEM and GBS was made. Electro-diagnosis (electromyography-nerve conduction velocity) and magnetic resonance imaging study supported our diagnosis. He improved remarkably after treatment with intravenous immunoglobulin and intravenous methylprednisolone.

2015Apr
Neuroradiology
Neuroradiology 2015 Apr 16. Epub 2015 Apr 16.
Department of Radiology, Baskent University Faculty of Medicine, 44. Sokak No:11/8, Bahcelievler, Ankara, Turkey, fuldemyildirim@yahoo.com.
2015Apr
Berl. Munch. Tierarztl. Wochenschr.
Berl Munch Tierarztl Wochenschr 2015 Mar-Apr;128(3-4):90-7

Campylobacter (C.) jejuni is the most important reported cause for bacterial diarrhoea. The infection can be accompanied by fever and abdominal cramps and in rare cases the Guillain-Barré syndrome or reactive arthritis can develop as a post-infection complication. Read More

Several biological properties of Cjejuni, e. g. motility and chemotaxis, contribute to the biological fitness of the pathogen. For this, deficiencies in the function of these features clearly reduce the pathogenicity of C. jejuni without being a virulence factor per se. Opposing to this, there are two essential requirements to determine the virulence of C. jejuni which represent the adherence to, and the invasion of host cells. Thereby, adherence, as a virulence factor, is mediated by many different bacterial-derived components like proteins but also by several oligo- and polysaccharide structures that are linked to surface proteins but also to the flagella. In addition, several invasion-relevant features of C. jejuni have been detected so far. Whereas some of them are described functionally to modulate cytoskeleton arrangement of the host cell, others are only described as invasion relevant. Indeed, investigations with respect to the pathogenic potential of some adherence- and invasion-relevant components did not give identical results indicating that their relevance might depend on the interplay of the respective C. jejuni strains used in these studies with the corresponding host cells. This review summarizes the C. jejuni components for adherence to and invasion of host cells together with their particular mode of action if known.

 Life-threatening Streptococcus pneumoniae infections often occur after hematopoietic stem cell transplant (HSCT); vaccination is important for prevention.
 In an open-label study, patients (n = 251) 3-6 months after allogeneic HSCT received 3 doses of 13-valent pneumococcal conjugate vaccine (PCV13) at 1-month intervals, a fourth dose 6 months later, and 1 dose of 23-valent pneumococcal polysaccharide vaccine (PPSV23) 1 month later. Immunogenicity at prespecified time points and vaccine safety were assessed. Read More


 In the evaluable immunogenicity population (N = 216; mean age, 37.8 years), geometric mean fold rises (GMFRs) of immunoglobulin G geometric mean concentrations from baseline to postdose 3 showed significant increases in antibody levels across all PCV13 serotypes (GMFR range, 2.99-23.85; 95% confidence interval lower limit, >1); there were significant declines over the next 6 months, significant increases from predose 4 to postdose 4 (GMFR range, 3.00-6.97), and little change after PPSV23 (GMFR range, 0.86-1.12). Local and systemic reactions were more frequent after dose 4. Six patients experienced serious adverse events possibly related to PCV13 (facial diplegia, injection-site erythema and pyrexia, autoimmune hemolytic anemia, and suspected lack of vaccine efficacy after dose 3 leading to pneumococcal infection), PCV13 and PPSV23 (Guillain-Barré syndrome), or PPSV23 (cellulitis). There were 14 deaths, none related to study vaccines.
 A 3-dose PCV13 regimen followed by a booster dose may be required to protect against pneumococcal disease in HSCT recipients. Dose 4 was associated with increased local and systemic reactions, but the overall safety profile of a 4-dose regimen was considered acceptable.
 NCT00980655.

2015Apr
PLoS ONE
PLoS One 2015 13;10(4):e0124004. Epub 2015 Apr 13.
Department of Neurology, Dokkyo Medical University, Tochigi, Japan; Departments of Medicine and Physiology, National University of Singapore, Singapore, Singapore.

Molecular mimicry between Campylobacter jejuni lipo-oligosaccharides (LOSs) and human gangliosides GM1 and GD1a induces the production of anti-GM1 and anti-GD1a antibodies, and the development of Guillain-Barré syndrome. Complexes of two different gangliosides form new molecular shapes capable of enhancing recognition by anti-ganglioside antibodies. To test the hypothesis that the complex of GM1-like and GD1a-like LOSs of C. Read More

jejuni induces the development of anti-GM1b antibodies in Guillain-Barré syndrome patients.
Mass spectrometry analysis determined the LOS outer core structures, with which mice were immunized. IgG antibodies to single gangliosides and complex of gangliosides were tested in sera from Guillain-Barré syndrome patients from whom C. jejuni LOS had been isolated.
Two isolates from GBS patients who had anti-GM1b antibodies, but neither anti-GM1 nor -GD1a antibodies, expressed both GM1-like and GD1a-like LOSs, but not GM1b-like LOS. Anti-GM1b antibodies were induced in one of the mice immunized with the C. jejuni bearing GM1-like and GD1a-like LOS. Sera from 20 patients had antibodies to the complex of GM1 and GD1a, all of which carried anti-GM1b reactivity. Five of these sera harbored neither anti-GM1 nor anti-GD1a antibodies. IgG antibodies to the complex were absorbed by GM1b, but by neither GM1 nor GD1a.
GM1-like and GD1a-like LOSs form a GM1b epitope, inducing the development of anti-GM1b antibodies in patients with Guillain-Barré syndrome subsequent to C. jejuni enteritis. Here, we present a new paradigm that the complex of two different structures forms a new molecular mimicry, inducing the production of autoantibodies.

2014Aug
J Assoc Physicians India
J Assoc Physicians India 2014 Aug;62(8):734-6

The clinical manifestations of Guillain Barre syndrome are usually confined to the nervous system, however in 20% cases there can be cardiovascular involvement in patients with dysautonomia contributing to the mortality. The cardiovascular manifestations of Guillain Barre syndrome are electrocardiographic changes, cardiac enzyme abnormalities and reversible left ventricular dysfunction. The term neurogenic stunned myocardium has been used to summarise these cardiovascular abnormalities in the setting of severe central nervous system injury, in the absence of coronary artery disease. Read More

Our case report of reversible cardiomyopathy in Guillain Barre syndrome documents the occurrence of cardiovascular changes in a case of Guillain Barre syndrome with dysautonomia which were reversible with appropriate treatment.

2015May
Cochrane Database Syst Rev
Cochrane Database Syst Rev 2015 9;4:CD009950. Epub 2015 Apr 9.
Department of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, China, 100053.

Pain in Guillain-Barré syndrome (GBS) is common, yet it is often under recognised and poorly managed. In recent years, a variety of pharmacological treatment options have been investigated in clinical trials for people with GBS-associated pain. This is an updated version of the original Cochrane review published in Issue 10, 2013. Read More


To assess the efficacy and safety of pharmacological treatments for various pain symptoms associated with GBS, during both the acute and convalescent (three months or more after onset) phases of GBS.
On 3 November 2014, we searched the Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL, MEDLINE and EMBASE. In addition, we searched ClinicalTrials.gov and the World Health Organization (WHO) International Clinical Trials Registry Platform.
We included randomised controlled trials (RCTs) and quasi-RCTs in participants with confirmed GBS, with pain assessment as either the primary or secondary outcome. For cross-over trials, an adequate washout period between phases was required for inclusion.
Two review authors independently screened the titles and abstracts of identified records, selected studies for inclusion, extracted eligible data, cross-checked the data for accuracy and assessed the risk of bias of each study.
Three short-term RCTs, which enrolled 277 randomised participants with acute phase GBS, were included. Risk of bias in the included studies was generally unclear due to insufficient information. None of the included studies reported the primary outcome selected for this review, which was number of patients with self reported pain relief of 50% or greater. One small study investigated seven-day regimens of gabapentin versus placebo. Pain was rated on a scale from 0 (no pain) to 10 (maximum pain). Amongst the 18 participants, significantly lower mean pain scores were found at the endpoint (day 7) in the gabapentin phase compared to the endpoint of the placebo phase (mean difference -3.61, 95% CI -4.12 to -3.10) (very low quality evidence). For adverse events, no significant differences were found in the incidence of nausea (risk ratio (RR) 0.50, 95% CI 0.05 to 5.04) or constipation (RR 0.14, 95% CI 0.01 to 2.54). A second study enrolling 36 participants compared gabapentin, carbamazepine and placebo, all administered over seven days. Participants in the gabapentin group had significantly lower median pain scores on all treatment days in comparison to the placebo and carbamazepine groups (P < 0.05). There were no statistically significant differences in the median pain scores between the carbamazepine and placebo groups from day 1 to day 3, but from day 4 until the end of the study significantly lower median pain scores were noted in the carbamazepine group (P < 0.05) (very low quality evidence). There were no adverse effects of gabapentin or carbamazepine reported, other than sedation. One large RCT (223 participants, all also treated with intravenous immunoglobulin), compared a five-day course of methylprednisolone with placebo and found no statistically significant differences in number of participants developing pain (RR 0.89, 95% CI 0.68 to 1.16), number of participants with decreased pain (RR 0.95, 95% CI 0.63 to 1.42) or number of participants with increased pain (RR 0.85, 95% CI 0.52 to 1.41) (low quality evidence). The study did not report whether there were any adverse events.
Since the last version of this review we found no new studies. While management of pain in GBS is essential and pharmacotherapy is widely accepted as being an important component of treatment, this review does not provide sufficient evidence to support the use of any pharmacological intervention in people with pain in GBS. Although reductions in pain severity were found when comparing gabapentin and carbamazepine with placebo, the evidence was limited and its quality very low. Larger, well-designed RCTs are required to further investigate the efficacy and safety of potential interventions for patients with pain in GBS. Additionally, interventions for pain in the convalescent phase of GBS should be investigated.

Ipilimumab is an approved treatment for patients with advanced melanoma. We aimed to assess ipilimumab as adjuvant therapy for patients with completely resected stage III melanoma at high risk of recurrence.
We did a double-blind, phase 3 trial in patients with stage III cutaneous melanoma (excluding lymph node metastasis ≤1 mm or in-transit metastasis) with adequate resection of lymph nodes (ie, the primary cutaneous melanoma must have been completely excised with adequate surgical margins) who had not received previous systemic therapy for melanoma from 91 hospitals located in 19 countries. Read More

Patients were randomly assigned (1:1), centrally by an interactive voice response system, to receive intravenous infusions of 10 mg/kg ipilimumab or placebo every 3 weeks for four doses, then every 3 months for up to 3 years. Using a minimisation technique, randomisation was stratified by disease stage and geographical region. The primary endpoint was recurrence-free survival, assessed by an independent review committee, and analysed by intention to treat. Enrollment is complete but the study is ongoing for follow-up for analysis of secondary endpoints. This trial is registered with EudraCT, number 2007-001974-10, and ClinicalTrials.gov, number NCT00636168.
Between July 10, 2008, and Aug 1, 2011, 951 patients were randomly assigned to ipilimumab (n=475) or placebo (n=476), all of whom were included in the intention-to-treat analyses. At a median follow-up of 2·74 years (IQR 2·28-3·22), there were 528 recurrence-free survival events (234 in the ipilimumab group vs 294 in the placebo group). Median recurrence-free survival was 26·1 months (95% CI 19·3-39·3) in the ipilimumab group versus 17·1 months (95% CI 13·4-21·6) in the placebo group (hazard ratio 0·75; 95% CI 0·64-0·90; p=0·0013); 3-year recurrence-free survival was 46·5% (95% CI 41·5-51·3) in the ipilimumab group versus 34·8% (30·1-39·5) in the placebo group. The most common grade 3-4 immune-related adverse events in the ipilimumab group were gastrointestinal (75 [16%] vs four [<1%] in the placebo group), hepatic (50 [11%] vs one [<1%]), and endocrine (40 [8%] vs none). Adverse events led to discontinuation of treatment in 245 (52%) of 471 patients who started ipilimumab (182 [39%] during the initial treatment period of four doses). Five patients (1%) died due to drug-related adverse events. Five (1%) participants died because of drug-related adverse events in the ipilimumab group; three patients died because of colitis (two with gastrointestinal perforation), one patient because of myocarditis, and one patient because of multiorgan failure with Guillain-Barré syndrome.
Adjuvant ipilimumab significantly improved recurrence-free survival for patients with completely resected high-risk stage III melanoma. The adverse event profile was consistent with that observed in advanced melanoma, but at higher incidences in particular for endocrinopathies. The risk-benefit ratio of adjuvant ipilimumab at this dose and schedule requires additional assessment based on distant metastasis-free survival and overall survival endpoints to define its definitive value.
Bristol-Myers Squibb.

2015Mar
World Neurosurg
World Neurosurg 2015 Mar 30. Epub 2015 Mar 30.
Department of Neurosurgery, Houston Methodist Hospital Neurological Institute, Houston, Texas. Electronic address: rgrossman@houstonmethodist.org.
2015Mar
Mol. Immunol.
Mol Immunol 2015 Mar 25. Epub 2015 Mar 25.
Rheumatology Research Center, Department of Medicine, Hadassah-Hebrew University, Jerusalem, Israel.

CD59 encodes a 77 amino acid glycosylphosphatidylinositol (GPI)-anchored cell surface glycoprotein that inhibits the final step of membrane attack complex (MAC) formation. CD59 deficiency is a common finding in adult patients with paroxysmal nocturnal hemoglobinuria (PNH). In this condition, there is a clonal expansion of hematopoietic stem cells that have acquired a mutation in the PIGA gene (phosphatidylinositol glycan anchor biosynthesis, class A). Read More

PIGA encodes a GPI biosynthesis protein, phosphatidylinositol N-acetylglucosaminyltransferase subunit A, and erythrocytes deficient in GPI-anchored membrane proteins, including CD59, undergo complement-mediated hemolysis. We have recently described a primary homozygous Cys89Tyr CD59 deficiency in humans that resulted in the amino acid substitution p.Cys89Tyr with resulting failure of proper localization of the CD59 protein to the cell surface. The Cys89Tyr mutation in CD59 was clinically manifested in infancy, and associated with chronic hemolysis and relapsing peripheral demyelinating disease resembling recurrent Guillain-Barré syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP). In this review we describe differences and similarities in the pathogenesis and clinical manifestations of PNH and primary CD59 Cys89Tyr mutation with the aim of tracking the contribution of CD59 deficiency to the pathophysiology and perhaps deepening our understanding of both diseases.

2015Mar
Infection
Infection 2015 Mar 27. Epub 2015 Mar 27.
Service des Maladies Infectieuses et Tropicales, Centre Hospitalo-Universitaire Nord, 42055, Saint-Etienne Cedex 2, France, delphine.vergnon@hotmail.fr.
2015Mar
J Family Med Prim Care
J Family Med Prim Care 2015 Jan-Mar;4(1):137-8
Department of Neurology, Lakeshore Hospital and Research Centre, Kochi, Kerala, India.

A 30 year old male presented with numbness of palms and soles followed by weakness of upper limbs and lower limbs of 5 days duration, which was ascending and progressive. Three months back he was treated for oral and genital ulcers with oral steroids. His ulcers improved and shifted to indigenous medication. Read More

His clinical examination showed polyneuropathy. CSF study did not show albuminocytological dissociation. Nerve conduction study showed demyelinating polyneuropathy. His blood samples and the ayurvedic drug samples were sent for toxicological analysis.
Acute toxic neuropathy - Arsenic.

2015Mar
Int J Crit Illn Inj Sci
Int J Crit Illn Inj Sci 2015 Jan-Mar;5(1):62-3
Department of Medicine, Dr. Rajendra Prasad Government Medical College Kangra, Tanda, Kangra, Himachal Pradesh, India.
2015Mar
Muscle Nerve
Muscle Nerve 2015 Mar 25. Epub 2015 Mar 25.
University Hospitals Case Medical Center and Case Western Reserve University School of Medicine, Cleveland, Ohio.