Nodopathies in the Early Diagnosis of Axonal Forms of Guillain-Barré Syndrome

Urdiales-Sánchez, Sara; González-Montaña, José-Ramiro; Diaz-Pérez, Ricardo; Calvo-Calleja, Pablo; Gutiérrez-Trueba, María-Antonia; Urdiales-Urdiales, Javier

doi:10.3389/fneur.2022.902172

Cited by 4 publications

(2 citation statements)

References 34 publications

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“…Among 23 cases, 19 had ganglioside antibody; 2 cases, neurofascin antibody; and 1, GQ1b (Table 1). [5][6][7][8][9][10][11][12][13][14][15][16][17][18] One had ganglioside and neurofascin. Thus, the most common antibody in acute nodopathy was GM1 antibody in 16 (70%) cases.…”

Section: Findings Acute Nodopathymentioning

confidence: 99%

Nodal Conduction Block and Internodal Conduction Block in Nodopathy

2024

Journal of Clinical Neuromuscular Disease

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Objectives: In 2015, a new term “nodopathy” was introduced to represent a group of neuropathy because of autoantibodies at the node of Ranvier and paranodal area. This review was conducted to highlight the electrophysiologic characteristics of acute and chronic nodopathies by the newly introduced term: “nodal conduction block (CB); CB without temporal dispersion or slow nerve conduction velocity” and by introducing a new term: “internodal CB; CB with temporal dispersion or/and slow nerve conduction velocity”. Methods: Through PubMed searches, 23 cases of acute (<4 weeks of neuropathy) nodopathy and 12 cases of chronic (>4 weeks of neuropathy) nodopathy are identified. Two other required inclusion criteria are positive nodal antibody test and detailed nerve conduction data with or without figure. All existing data were analyzed to see whether these cases had nodal or internodal CB. Results: Among 23 cases of acute nodopathy, 11 had nodal CB, 9 internodal CB, and 3 mixed CB. Thus, nodal CB was observed in 61% of acute nodopathy cases and internodal CB in 52% of acute nodopathy cases. Among 12 cases of chronic nodopathy, all 12 had internodal CB. Conclusions: Nodal CB is the nerve conduction characteristic of acute nodopathy, but internodal CB does not rule out acute nodopathy. Internodal CB is the nerve conduction characteristic of chronic nodopathy.

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Section: Findings Acute Nodopathymentioning

confidence: 99%

Nodal Conduction Block and Internodal Conduction Block in Nodopathy

2024

Journal of Clinical Neuromuscular Disease

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“…These anti-ganglioside antibodies, directed mainly to GM1 and GD1a in the axonal form of GBS and to GQ1b in MFS, cause axonal damage in nodal regions and at nerve terminals, resulting in conduction block, which may be reversible, with subsequent well-being, or alternatively, there may be axonal degeneration and worse clinical condition. The underlying basis for this difference in treatment outcome is unknown [92,93]. In addition to antibody-mediated attack, complement activation contributes to the pathological process by disrupting sodium channel clusters in Ranvier's nodes, and activation of dendritic cells by Campylobacter jejuni lipo-oligosaccharides induces B-cell proliferation through the production of interferon 1 and tumor necrosis factor.…”

Section: Treatmentmentioning

confidence: 99%

Molecular, Electrophysiological, and Ultrasonographic Differences in Selected Immune-Mediated Neuropathies with Therapeutic Implications

Dziadkowiak,

Nowakowska-Kotas,

Rałowska-Gmoch

et al. 2023

IJMS

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The spectrum of immune-mediated neuropathies is broad and the different subtypes are still being researched. With the numerous subtypes of immune-mediated neuropathies, establishing the appropriate diagnosis in normal clinical practice is challenging. The treatment of these disorders is also troublesome. The authors have undertaken a literature review of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), Guillain–Barre syndrome (GBS) and multifocal motor neuropathy (MMN). The molecular, electrophysiological and ultrasound features of these autoimmune polyneuropathies are analyzed, highlighting the differences in diagnosis and ultimately treatment. The immune dysfunction can lead to damage to the peripheral nervous system. In practice, it is suspected that these disorders are caused by autoimmunity to proteins located in the node of Ranvier or myelin components of peripheral nerves, although disease-associated autoantibodies have not been identified for all disorders. The electrophysiological presence of conduction blocks is another important factor characterizing separate subgroups of treatment-naive motor neuropathies, including multifocal CIDP (synonyms: multifocal demyelinating neuropathy with persistent conduction block), which differs from multifocal motor neuropathy with conduction block (MMN) in both responses to treatment modalities and electrophysiological features. Ultrasound is a reliable method for diagnosing immune-mediated neuropathies, particularly when alternative diagnostic examinations yield inconclusive results. In overall terms, the management of these disorders includes immunotherapy such as corticosteroids, intravenous immunoglobulin or plasma exchange. Improvements in clinical criteria and the development of more disease-specific immunotherapies should expand the therapeutic possibilities for these debilitating diseases.

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