Pathophysiology Of Guillain-Barré Syndrome Research Articles

Guillain-barré syndrome after purified vero cell rabies vaccination: An unusual case report

Guillain-Barré syndrome (GBS) can be described as a collection of clinical syndromes that manifests as an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes. Regarding pathophysiology of GBS, it is believed that autoimmunity- molecular mimicry plays a role in its pathogenesis. As the vaccines have an effect on the immune system it is reasonable that immunizations may be associated with subsequent GBS. Although rabies vaccines containing neural elements are very well known cause for GBS, no such positive correlation has been proven after newer formulations of rabies vaccine, derived from chick embryo cells. Here we report a case of GBS which developed after 5 weeks of anti-rabies vaccination (Purified Vero cell rabies vaccine) which was given after dog bite.

Association between Helicobacter pylori infection and Guillain-Barré Syndrome: A meta-analysis.

Helicobacter pylori (Hpylori) is a Gram-negative bacterium, considered to trigger autoimmune gastrointestinal disorders. This pathogen has also been linked to the autoimmune sequelae in extra-gastrointestinal diseases and peripheral neuropathies. Guillain-Barré syndrome (GBS) is a serious autoimmune demyelinating disorder of peripheral nerves, usually with a post-infectious onset. About 30% of cases of GBS attributed to by Campylobacter jejuni, so, Hpylori, could be also involved. Growing evidence suggests the likely involvement of Hpylori infection in the development of GBS. The aim of the current study was to therefore estimate the prevalence of Hpylori antibodies in GBS. A search of the literature was performed, using the PUBMED database, until December 2018. Data were extracted from six case-control studies, and a stratification analysis was conducted according to cerebrospinal fluid (CSF) or serum detection material. Among 29 records found, 6 studies met in the inclusion criteria for the meta-analysis. In the CSF subgroup, 105 participants were involved (40 GBS patients and 65 controls), while the serum subgroup included 325 participants (152 GBS and 173 controls). Data were combined using a fixed-effects model. Anti-Hpylori IgG were significantly more prevalent in GBS patients compared to controls, in both CSF (95% CI: 9.66-186.56, OR: 42.45, Pz<.00001) and serum (95% CI: 1.30-4.11, OR: 2.31, Pz: .004) subgroups. The present meta-analysis showed a strong association between GBS and the presence of Hpylori antibodies, especially in CSF, thereby suggesting a role of Hpylori infection in the pathophysiology of GBS.

Vaccines and Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is the leading cause of acute flaccid paralysis in developed countries and is characterized by various degrees of weakness, sensory abnormalities and autonomic dysfunction. Although the underlying aetiology and pathophysiology of GBS are not completely understood, it is broadly believed that immune stimulation plays a role in its pathogenesis. Thus, since vaccines have an effect on the immune system it is biologically plausible that immunizations may be associated with subsequent GBS. The objective of this article is to review the current body of evidence that either supports or does not support a causal, rather than just temporal, association between various vaccines and GBS, and to provide an evidence-based review of this issue. The scope of the article includes published reports that, regardless of method of case ascertainment, appeared in peer-reviewed literature between 1950 and 2008. Our review indicates that, with rare exceptions, associations between vaccines and GBS have been only temporal. There is little evidence to support a causal association with most vaccines. The evidence for a causal association is strongest for the swine influenza vaccine that was used in 1976-77. Studies of influenza vaccines used in subsequent years, however, have found small or no increased risk of GBS. Older formulations of rabies vaccine cultured in mammalian brain tissues have been found to have an increased risk of GBS, but newer formulations of rabies vaccine, derived from chick embryo cells, do not appear to be associated with GBS at a greater than expected rate. In an earlier review, the Institute of Medicine concluded that the evidence favoured a causal association between oral polio vaccine and tetanus toxoid-containing vaccines and GBS. However, recent evidence from large epidemiological studies and mass immunization campaigns in different countries found no correlation between oral polio vaccine or tetanus toxoid-containing vaccines and GBS. Spontaneous reports to the US Vaccine Adverse Events Reporting System shortly after the introduction of quadrivalent conjugated meningococcal vaccine (MCV4) raised concerns of a possible association with GBS. Comparisons with expected rates of GBS, however, were inconclusive for an increased risk, and lack of controlled epidemiological studies makes it difficult to draw conclusions about a causal association. For other vaccines, available data are based on isolated case reports or very small clusters temporally related to immunizations, and no conclusion about causality can be drawn. There are certain circumstances in which immunizing individuals, particularly those with a prior history of GBS, may require caution. However, the benefit of vaccines in preventing disease and decreasing morbidity and mortality, particularly for influenza, needs to be weighed against the potential risk of GBS.

Prevalence of anti-heat shock protein antibodies in cerebrospinal fluids of patients with Guillain–Barré syndrome

We examined antibodies against 10 heat shock proteins (HSPs) in cerebrospinal fluids (CSF) and sera from patients with Guillain–Barré syndrome (GBS). Significantly higher IgG antibody titers against HSP27, HSP60, HSP70 and HSP90 family, including mycobacterial HSP65 and Escherichia coli GroEL, were found in CSF from GBS patients as compared with motor neuron disease. Serum IgG antibodies against each HSP showed no difference between GBS patients and normal controls. GBS seems to be induced by reactive autoimmune responses frequently triggered by infections. The CSF antibodies against HSPs may modify the immune responses and/or cell-protective functions of HSPs in the pathophysiology of GBS.

Dysfunction at the motor end-plate and axon membrane in Guillain-Barré syndrome: a single-fiber EMG study.

In nine patients with Guillain-Barré syndrome (GBS), stimulation single-fiber electromyography (SFEMG) and serological studies were performed in the acute stage of the illness. Increased jitter and intermittent blocking of muscle fiber action potentials occurred to a varying degree in all patients. Five patients had elevated titers of antiganglioside antibodies. The most remarkable EMG phenomenon was the occurrence in all patients of impulse blocking at normal or slightly increased jitter. The assumption that this phenomenon was due to an axolemmal dysfunction was confirmed by the occurrence in two patients of concomitant blocking of two muscle fiber action potentials at strictly normal jitter values. In one patient this sign of axonal dysfunction was demonstrated with SFEMG at voluntary activation. In another patient, concomitant blocking was associated with greatly increased but completely independent jitter of both components. The results of this study show that both a disorder of neuromuscular transmission and an axolemmal dysfunction play a role in the pathophysiology of GBS.

Clinical correlation with anti-peripheral-nerve myelin antibodies in Guillain-Barré syndrome.

Anti-peripheral-nerve myelin antibodies (anti-PNM Ab) can be detected in the serum of all patients with acute-phase Guillain-Barré syndrome (GBS) thus far tested. Correlation of the titer of this antibody with the clinical course would help to establish a role for the humoral immune system in the pathophysiology of GBS. In this study, anti-PNM Ab levels were measured in serial serum samples of 7 patients with GBS with an assay that detects antibodies bound to peripheral nerve myelin antigens by fixation of the first component of complement. Although the titers of anti-PNM Ab detected in these patients varied between 0 and 256 U/ml, the antibody titer was always highest on admission (35 to 256 U/ml) and rapidly declined during a one-to-three-week period. Disappearance of antibodies or very low levels of them correlated with cessation of progression and considerable clinical improvement as documented by increased pulmonary vital capacity and muscular strength. Low but measurable antibody titers (5 to 12 U/ml) were frequently found up to four months following the acute neurological deficit. The close temporal relationship between anti-PNM Ab titer and the clinical course in GBS suggests that antibody most likely participates through complement activation in peripheral nerve demyelination.