Guillain-Barré Syndrome (GBS)- A Review (original) (raw)
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Guillain-Barré Syndrome: What We Know and Where We Can Improve
2018
Guillain-Barre Syndrome (GBS) is a neurological syndrome inwhich the axon andmyelin sheaths of the peripheral nervous system are attacked by the immune system. GBS is characterised by its rapid onset and ascending paralysis. It is classified as post-infectious, as its onset is often preceded by an infection, most commonly Campylobacter jejuni. The mechanism of GBS is not fully understood although it is believed that antigens such as GM1 on the virus capsule mimic those in gangliosides on C. jejuni. Thus leading to T-cell cross-reactivity, and ultimately host nerve cell damage. Currently, plasmapheresis and intravenous immunoglobin (IVIG) administration are the most effective treatments. Advances in this field are needed to better understand the mechanisms behind this condition at the molecular and cellular level, and ultimately improve mortality in the post-treatment period.
Guillain-Barré syndrome: an update
Journal of Clinical Neuroscience, 2009
Guillain-Barré syndrome (GBS) is an acute polyneuropathy consisting of different subtypes. Acute inflammatory demyelinating polyradiculoneuropathy, the classic demyelinating form of GBS, accounts for 90% of all GBS cases in the Western world. Acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN) are axonal forms of GBS that are more prevalent in Asia, South and Central America, often preceded by infection by Campylobacter jejuni. AMAN and AMSAN may be mediated by specific anti-ganglioside antibodies that inhibit transient sodium ion (Na +) channels. The efficacy of plasmapheresis and intravenous immunoglobulin has been established in large international randomised trials, with corticosteroids proven ineffective. Although axonal demyelination is an established pathophysiological process in GBS, the rapid improvement of clinical deficits with treatment is consistent with Na + channel blockade by antibodies or other circulating factors, such as cytokines. This review provides an update on the epidemiology, clinical features, diagnosis, pathogenesis and treatment of GBS.
EPRA International Journal of Multidisciplinary Research (IJMR)
Introduction: Guillain-Barre syndrome is an uncommon, yet potentially fatal, immune-mediated disease affecting peripheral nerves and nerve roots that is commonly generated by infections. Recent studies have shown a strong relationship between Guillain-Barre syndrome and SARS-CoV-2, making SARS-CoV-2 a potential trigger for GBS. Objective: to detail the current information related to Guillain-Barre syndrome, causes, epidemiology, immunopathogenic mechanisms, diagnosis, evaluation, differential and treatment. Methodology: a total of 42 articles were analyzed in this review, including review and original articles, as well as clinical cases, of which 33 bibliographies were used because the other articles were not relevant for this study. The sources of information were PubMed, Google Scholar and Cochrane; the terms used to search for information in Spanish, Portuguese and English were: Guillain-Barre, peripheral nerves, SARS-CoV-2, nerve roots, epidemics, inflammatory disease of the per...
Diagnosis and management of Guillain–Barré syndrome in ten steps
Nature Reviews Neurology
Guillain–Barré syndrome (GBS) is a rare, but potentially fatal, immune-mediated disease of the peripheral nerves and nerve roots that is usually triggered by infections. The incidence of GBS can therefore increase during outbreaks of infectious diseases, as was seen during the Zika virus epidemics in 2013 in French Polynesia and 2015 in Latin America. Diagnosis and management of GBS can be complicated as its clinical presentation and disease course are heterogeneous, and no international clinical guidelines are currently available. To support clinicians, especially in the context of an outbreak, we have developed a globally applicable guideline for the diagnosis and management of GBS. The guideline is based on current literature and expert consensus, and has a ten-step structure to facilitate its use in clinical practice. We first provide an introduction to the diagnostic criteria, clinical variants and differential diagnoses of GBS. The ten steps then cover early recognition and di...
Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome
Guillain-Barré syndrome (GBS) is an important cause of acute neuromuscular paralysis. Molecular mimicry and a cross-reactive immune response play a crucial part in its pathogenesis, at least in those cases with a preceding Campylobacter jejuni infection and with antibodies to gangliosides. The type of preceding infection and patient-related host factors seem to determine the form and severity of the disease. Intravenous immunoglobulin (IVIg) and plasma exchange are eff ective treatments in GBS; mainly for practical reasons, IVIg is the preferred treatment. Whether mildly aff ected patients or patients with Miller Fisher syndrome also benefi t from IVIg is unclear. Despite medical treatment, GBS often remains a severe disease; 3-10% of patients die and 20% are still unable to walk after 6 months. In addition, many patients have pain and fatigue that can persist for months or years. Advances in prognostic modelling have resulted in the development of a new and simple prognostic outcome scale that might also help to guide new treatment options, particularly in patients with GBS who have a poor prognosis.
Guillain-Barre Syndrome: Current Concepts
2020
Although the exact cause of Guillain-Barré syndrome is unknown, recently, some countries have reported an increase in the incidence of GBS after infection with the Zika virus. 5 GBS is currently considered the most commonly acquired demyelinating neuropathy and its diagnosis must be remembered by all doctors.
Guillain-Barré Syndrome: Modern Theories of Etiology
Current Allergy and Asthma Reports, 2011
Guillain-Barré syndrome (GBS) is a classic failure of the immune system with a life-threatening attack upon a critical self-component. The active phase of the disease is short, concordant with the latency of a primary adaptive immune response. Triggers for GBS include infection and (rarely) vaccination; cross-reactivity between infectious and neural epitopes has been well demonstrated, particularly for Campylobacter jejuni and motor axonal forms of GBS in which non-protein gangliosides are antigenic. Most people are probably exposed to a GBS trigger, but only rarely does the disease develop. We propose that GBS illustrates competing determinants of the immune system's decision about whether to mount a response, and that in unlucky affected individuals, copresentation of cross-reactive antigens with danger signals activating pattern-recognition receptors overcomes normal self-recognition such that a primary response is initiated that attacks the nerve. Then, in most cases of GBS, the response rapidly turns off, and second attacks rarely occur. This suggests active restoration of tolerance, and specific privileged site attributes of nerve and declining danger signals as the trigger wanes may contribute to this restoration. Standard immunosuppression has not been effective in GBS. We suggest this is because immune tolerance is already being restored by the time such therapies are initiated. This in turn suggests that improvements in GBS outcomes are likely to come from better protection of the nerve cells under attack while normal resumption of tolerance is permitted to proceed rather than exploring more aggressive immunosuppressive approaches.
The Turkish Journal of Pediatrics, 2019
Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy characterized by frequent rapid progressive, ascending, symmetric weakness and areflexia. We aimed to evaluate the etiology, clinical and electrophysiological findings with treatment and prognosis of the patients with GBS in our clinic. Patients who were diagnosed with GBS in our clinic between 2009 and 2017 were evaluated retrospectively. The study included 20 female and 25 male patients. The most frequent symptom was the absence of walking (95.5%). All of the patients had muscle weakness on examination; in addition to that hyperesthesia (31%), autonomic symptoms (13.3%), sensory loss (11.1%), ataxia (11.1%), bilateral facial nerve palsy (6.6%), oculomotor nerve palsy (2.2%), and multiple cranial nerve involvement (2.2%) were the other detected findings. Ventilation support was required in 6 cases (13.3%). Acute motor axonal neuropathy (AMAN) was found in 20 patients (44.5%), acute inflammatory demyelinating polyradiculoneuropathy (AIDP) was found in 24 patients (53.3%), and acute motor and sensory axonal neuropathy (AMSAN) was only present in 1 patient (2.2%). Intravenous immunoglobulin (IVIG) was administered to 33 of the patients (73.3%). The mean hospital stay was 8.4±3.5 (2-17 days), and the relationship between the duration of hospital stay and the treatment given was statistically significant (p = 0.001). Complete remission was observed in 37 patients (82.3%) and the remaining 5 children (11.1%) experienced incomplete recovery. Three patients (6.7%) died of treatment-resistant hypotension, arrhythmia and severe pulmonary infection. The short duration of neurological deficit following infection, clinical stage of application, need for mechanical ventilation, dysautonomia, cranial nerve involvement, and current subtype were the negative prognostic factors. Although GBS is a self-limiting disease, early diagnosis and treatment are very important to reduce hospital stay with morbidity and mortality. Patients expected to be at high risk should be monitored closely.
Guillain Barre Syndrome: A Retrospective Study of Ten Years
Purpose: Guillain-Barre Sydrome(GBS) is one of the reasons of acute polyneuropathy causing severe morbidity and mortality. Twenty nine patients with GBS were included in our study. Clinical, laboratory, electrophysiological and prognostic features of the patients were evaluated retrospectively. Method: Twenty-nine patients with GBS according to Asburys criteria were retrospectively evaluated for about ten years from 1993 to 2002. The patients were clinically classified according to the criteria of Hughes and Italian GBS study group. Patients were divided in to four groups due to their electrophysiological evaluation: acute inflammatory demyelinating polyneuropathy (AIDP), axonal forms (AMAN, AMSAN), Miller Fishers Syndrome (MFS) and unclassified. All patients were evaluated for age, gender, type of GBS, antecedent events, initial symptoms, CSF features, treatment, scores of GBS and complications. Findings: AIDP were found in 45% of patients, axonal form in 34.5%, MFS in 3.5% and u...