Guillain-Barre Syndrome Publications (8528)


Guillain-Barre Syndrome Publications

Biochem. Biophys. Res. Commun.
Biochem Biophys Res Commun 2017 Jan 17. Epub 2017 Jan 17.
University of São Paulo, Department of Surgery, Stem Cell Laboratory, São Paulo, São Paulo, 05508-270, Brazil; School of Arts Sciences and Humanities, Department of Obstetrics, São Paulo, SP, 03828-000, Brazil. Electronic address:

The recent outbreak of ZIKV in Brazil called the attention of the world because the effects of viral infection in the brain under development in fetuses. Consequences of vertical infection comprise brain malformation, especially microcephaly, eye and musculoskeletal abnormalities, among others. In adults, outcomes of infection include meningoencephalitis and Guillain-Barré syndrome. Read More

Recent data specific suggest that neural progenitor cells are the main targets of ZIKV infection, causing massive cellular death, which in turns, causes impairment in the neurogenesis process. Here we review the fetal and adult brain damage after ZIKV exposure, exploring models to study the mechanisms underlying the pathways related to microcephaly and cell death.


Experimental autoimmune neuritis (EAN) is a CD4(+) T cell-mediated autoimmune inflammatory demyelinating disease of the peripheral nervous system. It has been replicated in an animal model of human inflammatory demyelinating polyradiculoneuropathy, Guillain-Barré syndrome. In this study, we evaluated the therapeutic efficacy of a selective inhibitor of the immunoproteasome subunit, low-MW polypeptide 7 (PR-957) in rats with EAN. Read More

Our results showed that PR-957 significantly delayed onset day, reduced severity and shortened duration of EAN, and alleviated demyelination and inflammatory infiltration in sciatic nerves. In addition to significantly regulating expression of the cytokine profile, PR-957 treatment down-regulated the proportion of proinflammatory T helper (Th)17 cells in sciatic nerves and spleens of rats with EAN. Data presented show the role of PR-957 in the signal transducer and activator of transcription 3 (STAT3) pathway. PR-957 not only decreased expression of IL-6 and IL-23 but also led to down-regulation of STAT3 phosphorylation in CD4(+) T cells. Regulation of the STAT3 pathway led to a reduction in retinoid-related orphan nuclear receptor γ t and IL-17 production. Furthermore, reduction of STAT3 phosphorylation may have directly suppressed Th17 cell differentiation. Therefore, our study demonstrates that PR-957 could potently alleviate inflammation in rats with EAN and that it may be a likely candidate for treating Guillain-Barré syndrome.-Liu, H., Wan, C., Ding, Y., Han, R., He, Y., Xiao, J., Hao, J. PR-957, a selective inhibitor of immunoproteasome subunit low-MW polypeptide 7, attenuates experimental autoimmune neuritis by suppressing Th17 cell differentiation and regulating cytokine production.

Infect. Genet. Evol.
Infect Genet Evol 2017 Jan 14;49:134-137. Epub 2017 Jan 14.
Laboratoire MIVEGEC, UMR 224 IRD/CNRS/UM, Montpellier, France. Electronic address:

ZIKA virus (ZIKV) is a newly emerging arbovirus. Since its discovery 60years ago in Uganda, it has spread throughout the Pacific, Latin America and the Caribbean, emphasizing the capacity of ZIKV to spread to non-endemic regions worldwide. Although infection with ZIKV often leads to mild disease, its recent emergence in the Americas has coincided with an increase in adults developing Guillain-Barré syndrome and neurological complications in new-borns, such as congenital microcephaly. Read More

Many questions remain unanswered regarding the complications caused by different primary isolates of ZIKV. Here, we report the permissiveness of primary human astrocytes for two clinically relevant, Asian and African ZIKV strains and show that both isolates strongly induce antiviral immune responses in these cells albeit with markedly different kinetics. This study describes for the first time the specific antiviral gene expression in infected primary human astrocytes, the major glial cells within the central nervous system.

Muscle Nerve
Muscle Nerve 2017 Jan 17. Epub 2017 Jan 17.
Departments of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

We proposed electrodiagnostic criteria for early reversible conduction failure (ERCF) in axonal Guillain-Barré syndrome (GBS) and applied them to a cohort of GBS patients.
Serial nerve conduction studies (NCS) were retrospectively analyzed in 82 GBS patients from 3 centers. The criteria for the presence of ERCF in a nerve were i) 50% increase in amplitude of distal compound muscle action potentials or sensory nerve action potentials, or ii) resolution of proximal motor conduction block with accompanying decrease in distal latencies or compound muscle action potential duration or increase in conduction velocities. Read More

Of 82 patients from 3 centers, 37(45%) had ERCF, 21(26%) had a contrasting evolution pattern, and 8 (10%) had both. Sixteen patients did not show amplitude increase of at least 50%.
Our proposed criteria identified a group of patients with a characteristic evolution of NCS abnormality that is consistent with ERCF. This article is protected by copyright. All rights reserved.

Expert Rev Neurother
Expert Rev Neurother 2017 Jan 17. Epub 2017 Jan 17.
d Consultant neurologist , Gloucestershire Hospitals NHS Foundation Trust Ringgold standard institution , Great Western Road, Gloucester , United Kingdom of Great Britain and Northern Ireland.

Autoimmunity is an important cause of disease both in the central and peripheral nervous systems. Aetiologies and clinical manifestations are complex and heterogeneous. Inappropriate control of complement activation at inappropriate sites has been recognized as a major determinant in several neurological conditions, including Guillain-Barré syndrome and neuromyelitis optica. Read More

In each case pathogenesis is thought to be associated with generation of autoantibodies which upon binding guide activation of the complement system to self-tissue. Areas covered: Modulation of the complement system activation at such sites may represent a novel therapeutic approach for treatment of immune-mediated inflammatory conditions. In this review we focus on the therapeutic effects of complement inhibitors in Guillain-Barré syndrome and neuromyelitis optica and highlight recent developments within the field. Expert Commentary: Conventional first line treatment strategies in GBS and NMO have the potential disadvantage of causing widespread immunosuppressive effects. A more targeted approach may therefore be more effective and less disruptive to the immune system, especially in the case of NMO, which requires long term immunosuppression. Modulation of the complement system may hold the key and has already been shown to be of clinical benefit in other non-neurological conditions, including paroxysmal nocturnal hemoglobinuria and hereditary angioedema.

J. Neurol.
J Neurol 2017 Jan 16. Epub 2017 Jan 16.
Batten/Harris Neuromedical Intensive Care Unit, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK.

We report a retrospective review of 110 patients with acute Guillain-Barré syndrome (GBS) admitted to a specialised intensive care unit (ICU) in a tertiary referral centre over a 25 year period, the start of which coincided with the widespread introduction of plasma exchange (PE) and intravenous immunoglobulin (IVIG). The results were analysed by comparing 52 patients admitted in the first decade (1991-2000; Group 1) with 58 patients admitted between 2001-2014 (Group 2). Patients in both groups were comparable with respect to age and sex, and had a similar incidence and range of ICU complications. Read More

They received a comparable range of immunomodulatory treatments including IVIG and PE. However, the delay from presentation to referral to the tertiary ICU was longer in patients in Group 2. They also required mechanical ventilation for a longer duration, and had longer ICU and hospital stays. In Group 2, there was a higher incidence of axonal neuropathy (51%, compared to 24% in Group 1). Despite the longer delay to referral, the prevalence of axonal neuropathy and the duration of ventilation, overall mortality showed a downward trend (Group 1: 13.5%; Group 2: 5.2%). There was no late mortality in either group after step-down to neuro-rehabilitation or following discharge home or to the referring hospital. The rehabilitation outcomes were similar. This data show a shift in the pattern of referral to a tertiary referral ICU between the first and second decades following the wider availability of IVIG and PE for the treatment of GBS. The possible causes and implications of these findings are discussed.

Am J Case Rep
Am J Case Rep 2017 Jan 16;18:52-59. Epub 2017 Jan 16.
Department of Medicine, Riverside University Health System, Moreno Valley, CA, USA.
MBio 2017 Jan 10;8(1). Epub 2017 Jan 10.
Institute for Human Infections and Immunity and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA

The mechanisms responsible for the dramatic emergence of Zika virus (ZIKV), accompanied by congenital Zika syndrome and Guillain-Barré syndrome (GBS), remain unclear. However, two hypotheses are prominent: (i) evolution for enhanced urban transmission via adaptation to mosquito vectors, or for enhanced human infection to increase amplification, or (ii) the stochastic introduction of ZIKV into large, naive human populations in regions with abundant Aedes aegypti populations, leading to enough rare, severe infection outcomes for their first recognition. Advances in animal models for human infection combined with improvements in serodiagnostics, better surveillance, and reverse genetic approaches should provide more conclusive evidence of whether mosquito transmission or human pathogenesis changed coincidentally with emergence in the South Pacific and the Americas. Read More

Ultimately, understanding the mechanisms of epidemic ZIKV emergence, and its associated syndromes, is critical to predict future risks as well as to target surveillance and control measures in key locations.