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Article
December 1993

Anti-Peripheral Nerve Myelin Antibodies and Terminal Activation Products of Complement in Serum of Patients With Acute Brachial Plexus Neuropathy

Author Affiliations

From the Department of Neurology, University of Maryland Hospital and School of Medicine, Baltimore. Dr Vriesendorp is now with the Department of Neurology, University of Texas Health Science Center, Houston.

Arch Neurol. 1993;50(12):1301-1303. doi:10.1001/archneur.1993.00540120016006
Abstract

Objective:  To determine if complement-fixing antibodies to peripheral nerve myelin (anti-PNM antibodies) and terminal complement activation products were increased in serum of patients with brachial plexus neuropathy compared with normal controls.

Design:  Case series.

Setting:  University medical center.

Patients:  Three patients (aged 6, 39, and 51 years) with acute brachial plexus neuropathy were studied during the acute and recovery phase of their disease.

Methods:  Anti-PNM antibodies were measured in serum samples obtained from three patients and 25 normal controls with the Cl fixation and transfer assay. Soluble terminal complement activation products, SC5b-9, were measured by enzyme-linked immunosorbent assay (ELISA) in serum samples of one patient with brachial plexus neuropathy and of five normal controls.

Results:  Both serum anti-PNM antibodies and soluble terminal complement activation products were increased in the acute phase of brachial plexus neuropathy compared with normal control values and decreased several months later during clinical recovery.

Conclusion:  Complement dependent, antibodymediated demyelination may participate in the peripheral nerve damage of brachial plexus neuropathy.

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