Predictors and Prognostic Factors of Gullian Barrie Syndrome Outcome

Overview

This study aims to identify clinical and biological determinants and factors that predict outcome including primary outcome (percentage of changes in clinical scales pre- and after 3 months ) and secondary outcome depending on neurophysiologiacal studies and prognostic factors in individual patients with Guillain-Barre syndrome i individuals managed by plasmapheresis and IVIG immunoglobulin . This information will be used to understand the diversity in clinical presentation and response to treatment of GBS.

Guillain-Barré syndrome (GBS) is an acute onset, monophasic, immune-mediated peripheral nerve and root disorder (termed polyradiculoneuropathy), GBS has become the most common cause of acute flaccid paralysis worldwide and is a neurological emergency .Guillain-Barré syndrome (GBS) encompasses group of acute immune-mediated disordes restricted to peripheral nerves and roots. Good circumstantial evidence exists for a pathogenic role for molecular mimicry in GBS pathogenesis,especially with its axonal forms, providing insights that could guide future immunotherapy :Intravenous immunoglobulin (IVIg) and plasma exchange (PE) . Clinical presentation is a sudden onset of rapidly progressive and symmetrical weakness of the limbs, with or without peripheral sensory disturbance, reduction in or loss of tendon reflexes , and cerebrospinal fluid (CSF) analysis showing elevated protein concentrations with a normal white cell count, termed albuminocytologic dissociation, to distinguish it from infections that typically demonstrate elevated protein and white cell counts. The symptoms typically reach maximal severity within four weeks from symptom onset. Most patients generally require hospitalization for treatment, with close cardiopulmonary monitoring performed. Many patients also develop symptoms or signs of autonomic nervous system dysfunction, termed dysautonomia. These commonly consist of sinus tachycardia, arrhythmias,, orthostatic hypotension, increased sweating and bladder and gastrointestinal dysfunction. Antecedent infections, typically within 4 weeks of neurological symptom onset, commonly occur in GBS patients, resulting in the commonly cited molecular mimicry hypothesis, in which the immune system becomes activated in response to infectious antigen with structural similarity to peripheral nerve myelin or axonal components, with resultant tissue-specific peripheral nerve and nerve root injury in susceptible individuals. Epidemiological data implies that about two-thirds of GBS adult patients had a prior respiratory or gastrointestinal infection.Pathophysiology and immunopathology of the preceding infections are pathogenically associated with GBS, and may play an essential role in triggering the initial peripheral nerve/ nerve root-specific systemic immune system activation that causes cross-reactive humoral and cellular immune responses with resultant demyelination, axonal injury or both involving peripheral nerves and roots. Optimal treatment of individual patients may depend on the pathogenesis and clinical severity. Patients with severe forms of GBS may possibly need more intensive treatment to recover. Patients with a milder course that fully recover after standard therapy could suffer from possibly more side effects of more aggressive forms of treatment. This could only be possible if there are prognostic models that accurately predict the clinical course in individual patients. Ideally such models should be based on clinical and biological predictors that are strongly associated with disease course and known as early as possible in the acute phase of illness, when treatment with immunomodulatory therapy is most effective. Prognostic models could help to guide selective trials in specific GBS subtypes. Because of this it will be possible to treat GBS with more effective and more individual therapy

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Eligibility

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Outcomes