Authors : Anusha B.; Ariharasivakumar G.

Volume/Issue : Volume 10 - 2025, Issue 8 - August

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DOI : https://doi.org/10.38124/ijisrt/25aug1134

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Abstract : Guillain-Barré Syndrome (GBS) is an acute, immune-mediated polyneuropathy that represents one of the leading causes of rapid-onset neuromuscular paralysis worldwide. It is commonly triggered by preceding infections such as Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, Zika virus, and SARS-CoV-2, which induce an aberrant immune response through molecular mimicry, resulting in demyelination, axonal injury, or both. GBS encompasses several clinical subtypes, including acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy (AMSAN), Miller Fisher syndrome (MFS), and chronic inflammatory demyelinating polyneuropathy (CIDP), each exhibiting unique pathophysiological mechanisms and clinical patterns. Early diagnosis and prompt intervention remain crucial for preventing severe complications, including respiratory failure and autonomic dysfunction. Therapeutic strategies such as intravenous immunoglobulin (IVIG) and plasma exchange (PLEX) are the mainstay treatments and significantly improve functional recovery. Despite advancements, challenges persist in predicting disease progression and individual patient outcomes due to its heterogeneous nature. This review consolidates current insights into the epidemiology, pathogenesis, clinical variants, diagnostic approaches, and management of GBS. Furthermore, it highlights recent findings on immune dysregulation and potential therapeutic targets, emphasizing the need for ongoing research to develop precision-based treatment strategies and improve long-term outcomes for affected individuals.

Keywords : Guillain-Barré Syndrome, Immune-Mediated Neuropathy, Molecular Mimicry, Demyelination, Intravenous Immunoglobulin, Plasma Exchange.

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