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 C1 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, antibody-mediated demyelination may participate in the peripheral nerve damage of brachial plexus neuropathy.
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 C1 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, antibody-mediated demyelination may participate in the peripheral nerve damage of brachial plexus neuropathy.
Authors: Jeroen J J van Eijk; Richie G Madden; Annemiek A van der Eijk; Jeremy G Hunter; Johan H J Reimerink; Richard P Bendall; Suzan D Pas; Vic Ellis; Nens van Alfen; Laura Beynon; Lucy Southwell; Brendan McLean; Bart C Jacobs; Baziel G M van Engelen; Harry R Dalton Journal: Neurology Date: 2014-01-08 Impact factor: 9.910