Anti-sulfatide antibodies in neurological disease: binding to rat dorsal root ganglia neurons

Quattrini, Angelo; Corbo, Massimo; Dhaliwal, Sanjit K.; Sadiq, Saud; Lugaresi, Alessandra; Oliveira, Acary; Uncini, Antonino; Abouzahr, Kamil; Miller, James R.; Lewis, Linda M.; Estes, Dorothy; Cardo, Lisa J.; Hays, Arthur P.; Latov, Norman

doi:10.1016/0022-510x(92)90145-b

Cited by 49 publications

(35 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have reported electrodiagnostic findings in patients with anti-sulfatide antibody associated polyneuropathy as including axonal, demyelinating, or normal nerve physiology [1,11,15,21,22]. In our study only two of nine patients with anti-sulfatide antibodies had a predominantly demyelinating neuropathy, and two with clinical signs of neuropathy had no abnormalities in nerve conduction studies.…”

Section: Discussionmentioning

confidence: 62%

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Erb

Ferracin

Fuhr

et al. 2000

Journal of Neurology

View full text Add to dashboard Cite

Thirty-two patients with a peripheral neuropathy and paraproteinemia were tested for IgM antibodies against myelin-associated protein (MAG) and sulfatide by means of enzyme-linked immunosorbent assay. Nine patients (28 %) had increased anti-sulfatide IgM antibodies and showed a chronic, slowly progressive, distally pronounced, and symmetric polyneuropathy with sensory to sensory-motor impairment, ataxia, hyporeflexia, and axonal involvement in electrophysiological studies. Ten patients (31 %) with increased anti-MAG antibodies had a similar, homogeneous polyneuropathy syndrome but presented with demyelinating features. A weak cross-reactivity between anti-MAG and anti-sulfatide antibodies was present in only three patients. In conclusion, although the two neuropathy groups clearly differed in their electrophysiological features, their clinical presentation was rather similar.

show abstract

Section: Discussionmentioning

confidence: 62%

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Erb

Ferracin

Fuhr

et al. 2000

Journal of Neurology

View full text Add to dashboard Cite

show abstract

“…19 Some antisulfatide antibodies crossreact with MAG, P0, or chondroitin sulfate A or C. 19 Passive transfer of antisulfatide antibodies into rabbits or immunization of guinea pigs with sulfatide results in experimental neuropathy. 91 Antisulfatide antibodies have been shown to bind to the surface of the DRG and compact myelin, 94 where they may exert their effects.…”

Section: Differential Diagnosismentioning

confidence: 99%

Clinical features and pathophysiological basis of sensory neuronopathies (ganglionopathies)

Antoine²,

2004

View full text Add to dashboard Cite

Sensory ganglionopathies have a frequent association with neoplastic disorders (paraneoplastic subacute sensory neuronopathy, or SSN) or dysimmune disorders (Sjögren's syndrome, SS; Miller Fisher syndrome; and Bickerstaff's brainstem encephalitis, BBE), with drugs, such as cisplatin or pyridoxine, and with inherited disorders with degeneration of dorsal root ganglion cells. Unsteady gait and pseudoathetoid movements of the hand are the distinctive signs encountered in these disorders. The chronic disorders are characterized by non-length-dependent abnormalities of sensory nerve action potentials (SNAPs) and differ from other sensory neuropathies in showing a global, rather than distal, decrease in SNAP amplitudes. This review focuses on recent advances in defining the mechanisms involved in sensory ganglionopathies. Specific topics include a summary of their clinical features, pathological findings, and immunopathology. In SSN, early diagnosis by the detection of anti-Hu antibodies and early treatment of the cancer gives the best chance of stabilizing the disorder. In SS sensory ganglionitis, response to treatment has been disappointing, but immunomodulating treatments are emerging. The immunological profile common to BBE and Fisher syndrome supports a common pathogenesis. In toxic sensory neuronopathy, no treatment is available. The differential diagnosis involves separating sensory ganglionopathies from other ataxic polyneuropathies, such as infectious neuropathies, sensory neuropathies with various autoantibodies, and the neuropathies seen in celiac disease.

show abstract

“…1- 6 However, previous studies on a few patients have shown the clinical and electrodiagnostic features of polyneuropathies associated with antisulphatide antibody to be variable. Motor findings may be disabling or absent.…”

mentioning

confidence: 99%

Polyneuropathies associated with high titre antisulphatide antibodies: characteristics of patients with and without serum monoclonal proteins.

Lopate

Parks

Goldstein

et al. 1997

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

Anti-sulfatide antibodies in neurological disease: binding to rat dorsal root ganglia neurons

Cited by 49 publications

References 33 publications

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Clinical features and pathophysiological basis of sensory neuronopathies (ganglionopathies)

Polyneuropathies associated with high titre antisulphatide antibodies: characteristics of patients with and without serum monoclonal proteins.

Contact Info

Product

Resources

About