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Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Nerve conduction studies: usually show marked slowing of nerve conduction velocities, and antiganglioside antibodies may be detected in serum; however, in acutely ill patients these tests may not be available in time to influence management
Case 12
Published in Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta, Clinical Cases, 2021
Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta
Although Guillain–Barré syndrome is a clinical diagnosis, there are supportive tests which may be useful.Lumbar puncture shows high protein levels with normal cell counts. This is known as cytoalbuminaemic dissociationRepeated spirometry is required to assess for deterioration in lung functionNerve conduction studies are abnormal in 85% of patientsTesting for antiganglioside antibodies: anti-GM1, anti-GD1b, anti-GT1a, anti-GD1a and anti-GQ1b may all be positive. There is some evidence to suggest that different antibodies are associated with different subtypes of the disease and may reflect prognosis
Inflammatory Demyelination
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
Serological tests for patients with IDN may help in the diagnosis. In patients with GBS, circulating antiganglioside antibodies are found in high concentration more than in non-inflammatory neuropathies. AMAN and AMSAN are associated with serum IgG binding to GM1, GD1a, and GalNAc-GD1a gangliosides. Although antibodies against gangliosides (GM1, GM2, basal lamina components, and several myelin proteins) have been identified in some cases, no characteristic pattern of anti-ganglioside antibodies has been established in AIDN.
Campylobacter jejuni induces autoimmune peripheral neuropathy via Sialoadhesin and Interleukin-4 axes
Published in Gut Microbes, 2022
Ankit Malik, Jean M. Brudvig, Barbie J. Gadsden, Alexander D. Ethridge, Linda S. Mansfield
Campylobacter jejuni infection is primarily linked with the AMAN form of GBS that has been associated with development of autoantibodies targeting gangliosides on peripheral nerves.9,15 Gangliosides are sialic acid containing glycolipid moieties in the myelin sheath and in the outer leaflet of the neuronal plasma membranes. Oligosaccharide motifs on the outer surface of C. jejuni endotoxin (lipooligosaccharide) isolated from AMAN patients have been shown to mimic the peripheral nerve gangliosides, namely GM1, GD1a, GQ1b and others.16,17 Molecular mimicry is thought to play a role in the production of these anti-ganglioside antibodies, which bind to and attack host nerve tissue. Binding of antiganglioside antibodies elicits complement fixation and infiltration of inflammatory cells leading to tissue damage.
Ataxia and ophthalmoplegia: an atypical case of Miller Fisher syndrome (MFS) with anti-GAD antibody
Published in International Journal of Neuroscience, 2022
Ali R. Shoraka, Xiang Fang, Diaa Hamouda, Bhanu Gogia, Xiangping Li
Anti-GQ1b antibody is usually present in 85 to 90 percent of patients with MFS. The first study involving antiganglioside antibodies in the pathogenesis of MFS was published in 1992 by Chiba et al. [3]. They suggested an association between anti-GQ1b antibodies and MFS, and since then several studies have found increased anti-GQ1b antibody titers in MFS [9]. GQ1b antigen is highly expressed at paranodes and the neuromuscular junctions of the oculomotor, trochlear and abducens nerves. Binding at these sites could explain the ophthalmoplegia and ptosis that are seen in MFS. In addition, the group Ia afferents in muscle spindles strongly express GQ1b and so the muscle spindle targets could be responsible for the ataxia experienced in MFS patients. Eventually, infection by microorganisms bearing the GQ1b epitope may induce production of IgG anti-GQ1b antibodies in susceptible patients [10]. In the study that was done by Koga et al., among 207 patients presented with MFS, 12% were found to be GQ1b-seronegative. In addition, there was no obvious clinical differences between seropositive and seronegative patients except extreme male predominance among seronegative cases (11 to 1 ratio in seronegative cases versus 2 to 1 ratio in seropositive cases), higher rate of antecedent GI symptoms and rarer onset of diplopia [11].
Myasthenia gravis and chronic inflammatory demyelinating polyneuropathy in the same patient – a case report
Published in International Journal of Neuroscience, 2018
Weiwei Quan, Junhui Xia, Qiuling Tong, Jie Lin, Xiaolu Zheng, Xuezhi Yang, Dewei Xie, Yiyun Weng, Xu Zhang
About 10 days after admission, we found the symptoms of dysarthria and nasal voice a little fluctuating. Overlap of MG was suspected. Further repetitive nerve stimulation (RNS) testing showed a significant decrement (11%–13%) at 3–5 Hz stimulation in the deltoid muscle and orbicularis oculi muscle. Prostigmine test result was probable positive. The subsequent positive result of acetylcholine receptor (AchR) antibody (>8 nmol/L, normal <0.4 nmol/L) confirmed this diagnosis. Imaging of brain and mediastinum was normal. Antiganglioside antibodies and antibodies related to paraneoplastic neurological syndrome in serum were all negative. He was treated with pyridostigmine bromide, prednisone and mycophenolate mofetil. Good clinical results were observed, followed by consequent improvement of ptosis, dysphagia and dysarthria, and improvement of limb weakness. His muscle strength in four limbs was proximally grade 5/5 at discharge.