Severity Of Guillain-Barre Syndrome Research Articles

Correlation of Cerebrospinal Fluid Total Protein and Serum Neutrophil-to-Lymphocyte Ratio with Clinical Outcomes of Guillain-Barre Syndrome Variants.

To evaluate the correlation of cerebrospinal fluid total protein and serum neutrophil-to-lymphocyte ratio with the clinical outcomes and the various clinical and electrophysiological variants of Guillain-Barre syndrome. Cross-sectional study. Place and Duration of the Study: Department of Neurology, Mayo Hospital and King Edward Medical University, Lahore, Pakistan, from November 2022 to April 2023. Fourty-six Guillain-Barre syndrome patients, aged 12-70 years, were included in the study diagnosed by using the Brighton's criteria. Functional disability and respiratory insufficiency were assessed by using the modified Hughes disability score and the Erasmus Guillain-Barre syndrome respiratory insufficiency score, respectively.Serum neutrophil-to-lymphocyte ratio and cerebrospinal fluid total protein were calculated for each patient at the time of admission. Axonal variants had a higher mean neutrophil-to-lymphocyte ratio (5.29 ± 4.38) than demyelinating variants (4.71 ± 3.4) and Miller-Fischer syndrome (3 ± 2.828). This ratio was positively correlated with the modified Hughes's disability score (r = 0.790, p = 0.001) and the Erasmus Guillain-Barre syndrome respiratory insufficiency score (r = 0.936, p = 0.002). Mean cerebrospinal fluid total protein was higher for demyelinating (218 ± 136 mg/dl) than axonal variants (86 ± 56 mg/dl) and Miller-Fischer syndrome (34 ± 21 mg/dl). However, higher modified Hughes disability score (4-6) (r = 0.020, p = 0.117) and a high Erasmus Guillain-Barre syndrome respiratory insufficiency score (5-7) (r = 0.115, p = 0.302) did not significantly affect mean cerebrospinal fluid total proteins. Serum neutrophil-to-lymphocyte ratio can be regarded as a reliable biomarker to assess disease severity and clinical outcome in Guillain-Barre syndrome. Cerebrospinal fluid total protein is a poor predictor of the prognosis and severity of Guillain-Barre syndrome. Guillain-Barre syndrome (GBS), Clinical outcome, Cerebrospinal fluid total protein (CSF-TP), Neutrophil-to-lymphocytic ratio (NLR), Prognostic biomarker.

Specificity of recovery in acute motor axonal neuropathy with conduction blocks on the example of two clinical cases

Introduction. The heterogeneity of the forms and severity of Guillain-Barre syndrome explains the variability of recovery: from rapid and complete (in most cases) to slow with the development of persistent residual deficiency (rarely). It is unclear how effective the Erasmus Guillain–Barre syndrome Outcome Scores and its modified version are for different forms of the disease.The aim of the study – to demonstrate the features of recovery in acute motor axonal neuropathy with conduction blocks on the example of 2 clinical cases; to show the possibilities of Erasmus Guillain–Barre syndrome Outcome Scores and its modified version in predicting recovery in this form of the disease.Materials and methods. Data from 2 patients with acute motor axonal neuropathy with motor conduction blocks were retrospectively analyzed. Calculation of the score and assessment of the prognosis of walking recovery by 6 months from the onset of the disease were performed using the online calculator International Guillain-Barre syndrome Outcome Study Prognosis tool in the acute period.Results. In both patients, the forecast of recovery of walking by half a year from the onset of the disease on the Erasmus Guillain–Barre syndrome Outcome Scores and modified Erasmus Guillain–Barre syndrome Outcome Scores scales in the acute period was erroneous. In the first case, the total score on the Erasmus Guillain–Barre syndrome Outcome Scores and its modification in the acute period was 5 and 10 points respectively (poor prognosis), which foreshadowed a long rehabilitation process and incomplete recovery. However, the regression of disorders was dramatic and complete, and by the second month of the disease, only minimal motor disorders remained. In the second patient, on the contrary, the total Erasmus Guillain–Barre syndrome Outcome Scores and its modification during the period of increasing symptoms was 3 and 7 points respectively (good prognosis), while recovery was delayed – only by 5 months from the onset of the disease, the ability to move with support was restored.Conclusion. The Guillain–Barre syndrome is a disease with a favorable prognosis for recovery. However, the prediction of regression of motor disorders should be approached carefully, because in some cases, generally accepted criteria and prognostic scales may not work. Acute motor axonal neuropathy with conduction blocks is a unique form of the disease that has pathophysiological and clinical-neurophysiological features, which should be taken into account when managing this category of patients.

Fc-gamma IIIa-V158F receptor polymorphism contributes to the severity of Guillain-Barré syndrome.

ObjectiveGuillain‐Barré syndrome (GBS) is a rare, life‐threatening disorder of the peripheral nervous system. Immunoglobulin G Fc‐gamma receptors (FcγRs) mediate and regulate diverse effector functions and are involved in the pathogenesis of GBS. We investigated whether the FcγR polymorphisms FcγRIIa H/R131 (rs1801274), FcγRIIIa V/F158 (rs396991), and FcγRIIIb NA1/NA2, and their haplotype patterns affect the affinity of IgG‐FcγR interactivity and influence GBS susceptibility and severity.MethodsWe determined FcγR polymorphisms in 303 patients with GBS and 302 ethnically matched healthy individuals from Bangladesh by allele‐specific polymerase chain reaction. Pairwise linkage disequilibrium and haplotype patterns were analyzed based on D ´statistics and the genotype package of R statistics, respectively. Logistic regression analysis and Fisher’s exact test with corrected P (Pc) values were employed for statistical comparisons.ResultsFcγRIIIa‐V158F was associated with the severe form of GBS compared to the mild form (P = 0.005, OR = 2.24, 95% CI = 1.28–3.91; Pc = 0.015); however, FcγR genotypes and haplotype patterns did not show any association with GBS susceptibility compared to healthy controls. FcγRIIIa‐V/V158 and FcγRIIIb‐NA2/2 were associated with recent Campylobacter jejuni infection (P ≤ 0.001, OR = 0.36, 95% CI = 0.23–0.56; Pc ≤ 0.003 and P = 0.004, OR = 1.70, 95% CI = 1.18–2.44; Pc ≤ 0.012, respectively). Haplotype 1 (FcγRIIa‐H131R‐ FcγRIIIa‐V158F‐ FcγRIIIb‐NA1/2) and the FcγRIIIb‐NA2/2 genotype were more prevalent among anti‐GM1 antibody‐positive patients (P = 0.031, OR = 9.61, 95% CI = 1.24–74.77, Pc = 0.279; P = 0.027, OR = 1.62, 95% CI = 1.06–2.5, Pc = 0.081, respectively).InterpretationFcγR polymorphisms and haplotypes are not associated with susceptibility to GBS, though the FcγRIIIa‐V158F genotype is associated with the severity of GBS.

Venous thromboembolism in patients with Guillain-Barre syndrome

To perform an in-depth prospective analysis of the prevalence, risk factors, specific characteristics of venous thromboembolism (VTE) and the dynamics of venous thrombosis during the treatment with low-molecular-weight heparin (LMWH) in patients with different forms and severity of Guillain-Barre syndrome (GBS) admitted to an intensive care unit (ICU). Prevalence, risk factors and course of VTE were analyzed for the first time in 65 ICU inpatients with various forms and severity of GBS. Neurological status was evaluated at baseline and in dynamics, duplex scanning of veins of the legsin the system of inferior vena cava was performed. Despite the preventive using of LMWH, a half of patients with GBS, regardless of the form of the disease during the progression of neurological symptoms, have VTE (deep vein thrombosis--52%, pulmonary embolism--15%). Significant risk factors include: severe disease course requiring artificial ventilation, bed rest for more than 3 days, infectious complications, the presence of the catheter in the central vein, age over 40 years. Venous thrombosis in the system of inferior vena cava in patients with GBS does not differ from that in other critical illnesses suggesting that this pathological process is universal. Preventive measures for this category of patients is insufficient and requires a search for other prevention strategies.

Clinical Usefulness of Serum Alpha2-Globulin in Guillain-Barre Syndrome To Predict Its Clinical Course (P06.143)

Objective: Serum alpha2-globulin on admission may be high in severe Guillain-Barre syndrome (GBS) cases. Background We can easily (and cheaply, quickly) obtain serum alpha2-globulin on admission. Serum alpha2-globulin reflects immunoreactive response. GBS has immunoreactive response to the ganglioside (for example,antiganglioside antibodies). Serum alpha2-globulin on admission may predict severity of GBS and its clinical course. Design/Methods: From January 2006 to September 2011, 36 GBS patients were admitted to our hospital. On admission we evaluated serum alpha2-globulin before the treatment. We also evaluated their final outcome by using modified Rankin Scale(mRS). Results: We can obtain serum alpha2-globulin on admission in 21 cases. Serum alpha2-globulin is significantly higher in high mRS (>3) group (n=6) than in low mRS( Conclusions: By using serum alpha2-globulin on admission, we can evaluate severity of GBS, and predict its final outcome. Disclosure: Dr. Mori has received personal compensation for activities with Kurashiki Central Hospital as an employee.

A way out of the maze

In the last decade, experimental and clinical studies have laid a solid foundation under the molecular mimicry hypothesis to explain the pathogenesis of the Guillain-Barre syndrome (GBS). Bacterial or viral infections and genetic host factors are important. In brief, in the weeks following infection with known and unknown micro-organisms, previously healthy persons develop a devastating acute inflammatory disease of the peripheral nervous system. The immune system of the patient is apparently deceived by bacterial ganglioside-like epitopes that mimic peripheral nerve components, thereby triggering a cascade of inflammatory responses against peripheral nerves. Cross-reactive anti-ganglioside antibodies may be directed against myelin, Schwann cell components, and axonal membranes.1,2 Mechanisms by which damage is induced include activation of inflammatory cells by interaction of antibodies with Fcγ receptors (FcγRs) on macrophages and γ/δ T cells. Efficient FcγR-IgG interactions increase efficacy of leukocyte effector functions such as phagocytosis, cellular cytotoxicity, and cytokine production. FcγRIII genotypes are host factors that could modify severity of GBS.3 Also, an association has been found between polymorphisms in genes that are involved in immune homeostasis and the presence of …