Publications by authors named "Rahul Wahatule"

Background: Sensory nerve conduction parameters in Guillain Barre Syndrome (GBS) are underemphasized.

Objective: To describe abnormalities on sensory conduction studies in a large cohort of prospectively evaluated patients of GBS and to correlate with clinico-electrophysiological features.

Methods And Materials: Sensory conduction parameters of three nerves (median, ulnar, and sural) were analyzed using standard protocols in 238 patients (M: F 163:75, mean age: 35.

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Article Synopsis
  • Guillain-Barré Syndrome (GBS) is linked to antibodies against gangliosides and can be triggered by prior infections, especially in tropical regions like India.* -
  • The study analyzed serum antibodies in 150 GBS patients and 50 healthy controls, finding significantly higher levels of antibodies against specific gangliosides in patients, particularly linked to previous Japanese encephalitis infection.* -
  • Results reveal a connection between antecedent infections and the development of ganglioside antibodies in GBS, highlighting the role of infections in the disease's immunological processes.*
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Background: The IL-33/ST2 immune axis plays crucial roles in infection and immunity. A dysregulated IL-33/ST2 axis can induce autoimmune reaction and inflammatory responses. Guillain-Barré syndrome (GBS) is an acute peripheral neuropathy, mostly caused by post-infection autoimmunity.

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Guillain-Barré syndrome (GBS) is the commonest post-infectious polyradiculopathy. Although genetic background of the host seems to play an important role in the susceptibility to GBS, genes conferring major risk are not yet known. Dysregulation of Toll-like receptor (TLR) molecules exacerbates immune-inflammatory responses and the genetic variations within TLR pathway-related genes contribute to differential risk to infection.

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Guillain-Barré syndrome (GBS) is the commonest post-infectious inflammatory peripheral neuropathy with undiscerned aetiology. The commonly reported antecedent infections implicated in India include Campylobacter jejuni, chikungunya, dengue, and Japanese encephalitis (JE). In this study from south India, we investigated the role of these four agents in triggering GBS.

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Background: Antibodies against ganglioside complexes (GSCs) are associated with various clinical features and subtypes of Guillain-Barré syndrome (GBS).

Methods: One-hundred patients were evaluated for antibodies to GSCs formed by combination of GM1, GM2, GD1a, GD1b, GT1b, and GQ1b using manual enzyme linked immuno-sorbent assay (ELISA).

Results: Twenty-six patients were GSC antibody-positive, most frequent being against GM1-containing GSC (76.

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Article Synopsis
  • * Researchers found significantly elevated levels of IL-6, IL-17A, and IL-22 cytokines in the CSF of GBS patients compared to controls, with certain cytokines positively or negatively correlated with clinical features.
  • * The findings highlight the Th17 pathway's contribution to GBS pathophysiology and could enhance current knowledge of immune-mediated disorders affecting the nervous system.
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The etiopathogenesis of Guillain Barré Syndrome (GBS) is inadequately understood. The role of immuno-inflammatory Th17 pathway was examined in GBS patients by genetic, gene expression and biochemical studies. Genotyping of G197A single nucleotide polymorphism within IL17 gene was carried out by PCR-RFLP method in 220 GBS patients.

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Guillain Barré Syndrome (GBS) is one of the commonest acquired immune-mediated neuropathies, often preceded by infections. Although cellular immune responses are shown to substantially account for the pathophysiology of GBS, the precise mechanistic basis of risk and disease course remains enigmatic till date. Cytokines are best known for their abilities to drive cellular immunity and inflammation through their co-ordinated actions.

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Introduction: Brain as the seat of behavior is acknowledged from the times of Charaka, however where neurology ends and philosophy begins remains an enigma. It is certainly every neurologist's observation that there is loss of function either region based or domain based in progressive diseases of the nervous system making it the seat of all useful activities. However, there are references to occurrence of new skills seen during various illnesses causing progressive cognitive dysfunction.

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Background: Dementias are fairly slowly progressive degenerative diseases of brain for which treatment options are very less and carry a lot of burden on family and society. A small percentage of them are rapidly progressive and mostly carry a different course outcome. However, there are no definite criteria other than the time line for these patients.

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