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Chronic sensorimotor polyradiculopathy with antibodies to P2: An electrophysiological and immunoproteomic analysis
Author(s) -
RojasGarcia Ricard,
Gallardo Eduard,
De La Torre Carolina,
Sanvito Lara,
Illa Isabel
Publication year - 2008
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20999
Subject(s) - pathology , pathogenesis , western blot , gammopathy , medicine , myelin , antibody , lesion , electrophysiology , immunology , biology , monoclonal antibody , monoclonal , central nervous system , biochemistry , gene
In this study we report a patient with chronic progressive sensory ataxia, proximal weakness, immunoglobulin M (IgM) monoclonal gammopathy, and elevated protein levels in the cerebrospinal fluid, who showed a good response to prednisone. Electrophysiological study disclosed abnormalities predominantly of late responses (F waves and H reflexes), with no evidence of demyelination in the peripheral nerves, suggesting motor and preganglionic sensory nerve roots as the site of the lesion. An immune‐mediated pathogenesis was considered and, to identify possible target antigens, we performed bidimensional electrophoresis and a Western blot study. Based on the suspected lesion site, we used human anterior and posterior root extracts. We identified IgM reactivity against peripheral nerve myelin protein P2. Enzyme‐linked immunosorbent assay confirmed IgM reactivity toward one synthetic peptide from P2. To our knowledge, reactivity against P2 has not been reported previously in a paraproteinemic neuropathy. Furthermore, we demonstrated that bidimensional electrophoresis and Western blot of the tissue involved, as determined by clinical and electrophysiological studies, may be useful to establish clinical–immunological correlations in paraproteinemic neuropathies. Muscle Nerve, 2008