Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome

doi:10.1016/S1474-4422(08)70215-1

The Lancet Neurology

Volume 7, Issue 10, October 2008, Pages 939-950

https://doi.org/10.1016/S1474-4422(08)70215-1 Get rights and content

Summary

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 effective treatments in GBS; mainly for practical reasons, IVIg is the preferred treatment. Whether mildly affected patients or patients with Miller Fisher syndrome also benefit 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.

Introduction

Almost a century ago, the French neurologists Guillain, Barré, and Strohl described two soldiers who developed acute paralysis with areflexia that spontaneously recovered.¹ They reported the combination of increased protein concentration with a normal cell count in the CSF, or albuminocytological dissociation, which differentiated the condition from poliomyelitis.¹ Despite the fact that Landry had already reported similar cases in 1859,² the combination of these clinical and laboratory features became known as Guillain-Barré syndrome (GBS). Until now, GBS has remained a descriptive diagnosis of a disorder for which there are no specific diagnostic tests. The combination of rapidly progressive symmetrical weakness in the arms and legs with or without sensory disturbances, hypoflexia or areflexia, in the absence of a CSF cellular reaction, remains the hallmark for the clinical diagnosis of GBS. Over the past 20 years, randomised controlled trials (RCTs) have shown the efficacy of plasma exchange (PE) and intravenous immunoglobulin (IVIg), and some factors—in particular, Campylobacter jejuni, but also other preceding infections that induce antiganglioside antibodies—have been found to be important in the pathogenesis of GBS. We focus on the diagnosis and the expanding clinical spectrum of GBS, the frequent occurrence of pain and autonomic dysfunction, and recent insights into the pathogenesis of the syndrome. In addition, we discuss prognostic modelling and the current treatment options available during the course of GBS. The Review aims to integrate the latest laboratory and clinical developments that could lead to better therapeutic options for patients with GBS.

Section snippets

Epidemiology

GBS is a common cause of neuromuscular paralysis, and has been reported worldwide. The annual incidence of GBS is reported to be 1·2–2·3 per 100 000.3, 4, 5, 6, 7, 8, 9 Most studies have found that the incidence increases linearly with age and that men are about 1·5 times more likely to be affected than women.4, 5, 7 A recent epidemiological report from the USA indicated that the incidence of GBS among patients aged 18 years or older did not change over the period from 2000 to 2004.⁶ Reports on

Diagnosis

GBS is most commonly a post-infectious disorder that usually occurs in otherwise healthy people, and is not typically associated with an autoimmune or other systemic disorder. In typical cases, among the first symptoms are pain, numbness, paraesthesia, or weakness in the limbs. The main features of GBS are rapidly progressive bilateral and relatively symmetric weakness of the limbs with or without involvement of respiratory muscles or cranial-nerve-innervated muscles.12, 13 Diagnostic criteria

Antecedent infections

About two-thirds of patients have symptoms of an infection in the 3 weeks before the onset of weakness. One Japanese study found that the most frequent antecedent symptoms in GBS and related disorders were fever (52%), cough (48%), sore throat (39%), nasal discharge (30%), and diarrhoea (27%).¹⁹ In most GBS studies, symptoms of a preceding infection in the upper respiratory tract or gastrointestinal tract predominate, although many other types of infections have been reported. Furthermore, an

Immunobiology

Studies in patients and animals have provided convincing evidence that GBS, at least in some cases, is caused by an infection-induced aberrant immune response that damages peripheral nerves.31, 32, 33, 34, 35, 36, 37, 38 Four key factors have been identified that control this process (figure 2).

Clinical spectrum

The extent and distribution of weakness, sensory involvement, and the neurophysiological characteristics vary tremendously between individuals with GBS. The most common subtype of GBS in Europe and North America is the sensory-motor form, AIDP.⁴ In Europe and North America, fewer than 5–10% of patients have one of the axonal subtypes—AMAN or acute motor and sensory axonal neuropathy.4, 17, 85, 86 Facial nerve palsy is the most common form of cranial nerve involvement in GBS, occurring in at

Natural history

Rapidly progressive weakness is the core clinical feature of GBS. By definition, maximum weakness is reached within 4 weeks, but most patients have already reached their maximum weakness within 2 weeks.12, 13 Patients then have a plateau phase of varying duration, which ranges from days to several weeks or months. This phase is followed by a usually much slower recovery phase of varying duration. In Europe, about a third of patients with GBS remain able to walk (mildly affected patients).5, 89,

General care

Patients with GBS are in particular need of excellent multidisciplinary care to prevent and manage potentially fatal complications (panel 3).⁹⁸ Thus, patients need careful and regular monitoring of pulmonary function (at least vital capacity and respiration frequency) and possible autonomic dysfunction (heart beat frequency, blood pressure), and infections need to be prevented.⁹⁹ Among other issues that need attention early in the course of disease are prophylaxis for deep-vein thrombosis,

Beneficial effects of immunotherapy

The first large trial to show a positive effect of immunotherapy on GBS was the North American PE study.¹⁰⁰ This positive effect was confirmed by a large French PE trial.101, 102 PE was beneficial when applied within the first 4 weeks of onset, but the largest effect was seen when started early (within the first 2 weeks).100, 103 The usual regimen is PE five times during 2 weeks, with a total exchange of about five plasma volumes. The first RCT on the use of IVIg was published in 1992, and

Pain in the acute and chronic phases

Pain is a common and severe symptom in patients with GBS. Recognition of pain is important, especially in patients who are unable to communicate due to intubation. Pain as a presenting symptom before the onset of weakness might be confusing and can cause a delay in making a diagnosis of GBS. Pain has been described in up to 89% of patients with GBS.134, 135, 136 Different symptoms of pain associated with GBS have been distinguished during different phases of disease: paraesthesia or

Prognosis

The prognosis of GBS is difficult to predict in individual patients because of the substantial variation in outcome. Advanced age, however, is generally reported to be indicative of a worse prognosis. The severity of GBS seems to be determined in the early phase of the disease.¹²² RCTs that have investigated the effect of IVIg or PE in patients who were unable to walk have concluded that about 20% of patients remained unable to walk unaided after 6 months.⁹¹ Neurophysiological testing is

Future directions

New treatment options in GBS are necessary because the prognosis in a large proportion of patients with GBS is still far from good. One option in the acute phase could be a second course of IVIg treatment in patients with a bad prognosis. Recent studies indicate that agents that interfere with complement activation are potentially attractive candidates to be tested in the very early phase of GBS.74, 75 When it is possible to predict outcome in individual patients more accurately, new drugs or

Search strategy and selection criteria

References for this Review were identified by searches of PubMed, Embase, and the Cochrane Library from January, 1985, to June, 2008, by use of the terms “Guillain-Barré syndrome”, “acute inflammatory demyelinating polyneuropathy”, “AMAN”, “Miller Fisher syndrome”, and “Fisher syndrome”. Articles resulting from that search and relevant references cited in those articles were considered. The articles were chosen if they focused on the latest advances in the field. Articles were also

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The pathophysiological role of endoneurial inflammatory edema in early classical Guillain-Barré syndrome
2024, Clinical Neurology and Neurosurgery
The objective of this review was to analyze the pathophysiological role of endoneurial inflammatory edema in initial stages of classic Guillain-Barré syndrome (GBS), arbitrarily divided into very early GBS (≤ 4 days after symptom onset) and early GBS (≤ 10 days). Classic GBS, with variable degree of flaccid and areflexic tetraparesis, encompasses demyelinating and axonal forms. Initial autopsy studies in early GBS have demonstrated that endoneurial inflammatory edema of proximal nerve trunks, particularly spinal nerves, is the outstanding lesion. Variable permeability of the blood-nerve barrier dictates such lesion topography. In proximal nerve trunks possessing epi-perineurium, edema may increase the endoneurial fluid pressure causing ischemic changes. Critical analysis the first pathological description of the axonal form GBS shows a combination of axonal degeneration and demyelination in spinal roots, and pure Wallerian-like degeneration in peripheral nerve trunks. This case might be reclassified as demyelinating GBS with secondary axonal degeneration. Both in acute motor axonal neuropathy and acute motor-sensory axonal neuropathy, Wallerian-like degeneration of motor fibers predominates in the distal part of ventral spinal roots abutting the dura mater, another feature re-emphasizing the pathogenic relevance of this area. Electrophysiological and imaging studies also point to a predominant alteration at the spinal nerve level, which is a hotspot in any early GBS subtype. Serum biomarkers of axonal damage, including neurofilament light chain and peripherin, are increased in the great majority of patients with any early GBS subtype; endoneurial ischemia of proximal nerve trunks could contribute to such axonal damage. It is concluded that inflammatory edema of proximal nerve trunks is an essential pathogenic event in early GBS, which has a tangible impact for accurate approach to the disease.
High risk and low prevalence diseases: Guillain-Barré syndrome
2024, American Journal of Emergency Medicine
Guillain-Barré syndrome (GBS) is a rare but serious condition that carries with it a high rate of morbidity and mortality.
This review highlights the pearls and pitfalls of GBS, including presentation, diagnosis, and management in the emergency department (ED) based on current evidence.
GBS is a rare immune-mediated neurologic disorder with peripheral nerve injury. It most commonly presents weeks after a bacterial or viral infection, though there are a variety of associated inciting events. The diagnosis is challenging and often subtle, as only 25–30% of patients are diagnosed on their initial healthcare visit. Clinicians should consider GBS in patients with progressive ascending weakness involving the lower extremities associated with hyporeflexia, but the cranial nerves, respiratory system, and autonomic system may be involved. While the ED diagnosis should be based on clinical assessment, further evaluation includes laboratory testing, cerebrospinal fluid (CSF) analysis, and potentially neuroimaging. Not all patients demonstrate albumino-cytological dissociation on CSF testing. Several criteria exist to assist with diagnosis, including the National Institute of Neurological Disorders and Stroke criteria and the Brighton criteria. Management focuses first on assessment of the patient's hemodynamic and respiratory status, which may require emergent intervention. Significant fluctuations in heart rate and blood pressure may occur, and respiratory muscle weakness may result in the need for airway protection. Neurology consultation is recommended, and definitive treatment includes PLEX or IVIG.
An understanding of GBS can assist emergency clinicians in diagnosing and managing this potentially deadly disease.
Use of functional magnetic resonance imaging to assess cognition and consciousness in severe Guillain-Barré syndrome
2023, International Journal of Clinical and Health Psychology
Functional neuroimaging may provide a viable means of assessment and communication in patients with Guillain-Barré Syndrome (GBS) mimicking the complete locked-in state. Functional neuroimaging has been used to assess residual cognitive function and has allowed for binary communication with other behaviourally non-responsive patients, such as those diagnosed with unresponsive wakefulness syndrome. We evaluated the potential application of functional neuroimaging using a clinical-grade scanner to determine if individuals with severe GBS retained auditory function, command following, and communication.
Fourteen healthy participants and two GBS patients were asked to perform motor imagery and spatial navigation imagery tasks while being scanned using functional magnetic resonance imaging. The GBS patients were also asked to perform additional functional neuroimaging scans to attempt communication.
The motor imagery and spatial navigation task elicited significant activation in appropriate regions of interest for both GBS patients, indicating intact command following. Both patients were able to use the imagery technique to communicate in some instances. Patient 1 was able to use one of four communication tasks to answer a question correctly. Patient 2 was able to use three of seven communication tasks. However, two questions were incorrectly answered while a third was non-verifiable.
GBS patients can respond using mental imagery and these responses can be detected using functional neuroimaging. Furthermore, these patients may also be able to use mental imagery to provide answers to ‘yes’ or ‘no’ questions in some instances. We argue that the most appropriate use of neuroimaging-based communication in these patients is to allow them to communicate wishes or preferences and assent to previously expressed decisions, rather than to facilitate decision-making.
Long-Term Neurological, Behavioral, Functional, Quality of Life, and School Performance Outcomes in Children With Guillain-Barré Syndrome Admitted to PICU
2023, Pediatric Neurology
Most children with Guillain-Barré syndrome (GBS) recover but may suffer from long-term sequelae, interfering with development and quality of life. Owing to the lack of published data, we aimed to assess the long-term neurological, behavioral, functional, quality of life, and school performance outcomes them.
Design: Cross-sectional observational. Setting: Pediatric intensive care unit. Patients: Children, aged one to 12 years, with GBS admitted over five years (July 2012 to June 2017) were enrolled during one year (July 2017 to June 2018). These children were assessed for the following outcomes: neurological (Hughes disability score, Pediatric Cerebral Performance Category [PCPC], Pediatric Overall Performance Category [POPC], and Glasgow Outcome Scale-Extended Pediatric version [GOS-E Peds] scales), behavioral (Childhood Psychopathology Measurement Schedule [CPMS]), functional (Vineland Social Maturity Scale [VSMS]-Indian Adaptation), quality of life (Pediatric Quality of Life [PedsQL]), and school performance (Parent-Directed Questionnaire).
Eighty children were enrolled after a median of 3.0 (1.3-4.2) years from discharge. The majority (95%) had favorable neurological recovery (Hughes disability score 0 to 1). Favorable outcome was noted in 95% of children on PCPC, 87.5% on POPC, 60% on GOS-E Peds, 86.2% on CPMS, 92.5% on VSMS, and 98% on PedsQL. The majority (97.5%) of childre were attending schools, and 57.7% had satisfactory school performance. The presence of quadriparesis at admission, mechanical ventilation, tracheostomy requirement, poor ambulatory status at discharge, and longer pediatric intensive care unit and hospital stay predicted unfavorable neurological outcome on different tools. Absence of quadriparesis at admission and no requirement of mechanical ventilation predicted a favorable result on all outcome measures.
On long-term follow-up, most children with severe GBS showed favorable neurological, behavioral, functional, and quality of life outcomes. Severe clinical presentation and prolonged intensive care unit stay predict poor long-term outcome.
Guillain-barré syndrome (GBS) with antecedent chikungunya infection: a case report and literature review
2024, Neurological Research and Practice
Guillain–Barre syndrome of acute motor axonal neuropathy (AMAN) type associated with herpes zoster: a case report
2024, BMC Neurology

View all citing articles on Scopus

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ReviewClinical features, pathogenesis, and treatment of Guillain-Barré syndrome

Summary

Introduction

Section snippets

Epidemiology

Diagnosis

Antecedent infections

Immunobiology

Clinical spectrum

Natural history

General care

Beneficial effects of immunotherapy

Pain in the acute and chronic phases

Prognosis

Future directions

Search strategy and selection criteria

Lancet

Lancet

J Neuroimmunol

Vaccine

Vaccine

J Neuroimmunol

J Neurol Sci

J Neuroimmunol

J Neuroimmunol

Trends Neurosci

Lancet Infect Dis

J Neurol Sci

J Biol Chem

J Neuroimmunol

J Neuroimmunol

J Neuroimmunol

J Neuroimmunol

J Neuroimmunol

J Neuroimmunol

J Neuroimmunol

J Neurol Sci

Lancet

Sur un syndrome de radiculo-nevrite avec hyperalbuminose du liquide cephalorachidien sans reaction cellulaire. Remarques sur les caracteres cliniques et graphiques des reflexes tendineux

Bull Soc Med Hop Paris

Note sur la paralysie ascendante aigue

Gazette Hebdomadaire Méd Chir

Mild forms of Guillain-Barré syndrome in an epidemiologic survey in The Netherlands

Neurology

Guillain-Barré syndrome: incidence and mortality rates in US hospitals

Neurology

Incidence and clinical features of acute inflammatory polyradiculoneuropathy in Lombardy, Italy, 1996

Acta Neurol Scand

Incidence of Guillain-Barré syndrome in Alberta, Canada: an administrative data study

J Neurol Neurosurg Psychiatry

Incidence of Guillain-Barré syndrome in Germany

J Peripher Nerv Syst

Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies

Brain

Gastroenteritis-associated Guillain-Barré syndrome on the Caribbean island Curacao

Neurology

Assessment of current diagnostic criteria for Guillain-Barré syndrome

Ann Neurol

Diagnostic and classification criteria for the Guillain-Barré syndrome

Eur Neurol

Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy: immune mechanisms and update on current therapies

Ann Neurol

Comparative proteomics analysis of cerebrospinal fluid of patients with Guillain-Barré syndrome

Cell Mol Neurobiol

Patterns of recovery in the Guillain-Barré syndromes

Neurology

Paralytic ileus as a presenting symptom of Guillain-Barré syndrome

J Neurol

Antecedent symptoms in Guillain-Barré syndrome: an important indicator for clinical and serological subgroups

Acta Neurol Scand

Preceding infections, immune factors, and outcome in Guillain-Barré syndrome

Neurology

The spectrum of antecedent infections in Guillain-Barré syndrome: a case-control study

Neurology

Guillain-Barré syndrome: an Italian multicentre case-control study

Neurol Sci

Guillain-Barré syndrome following influenza vaccination

JAMA

Vaccines and Guillain-Barré syndrome

BMJ

Review
Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome