Isolated motor conduction block associated with infliximab

TNF-alpha antagonists have been associated with various types of peripheral neuropathies, including multifocal motor neuropathy with conduction block and mononeuropathies [1]. We present two patients treated with infliximab who developed unifocal motor neuropathy with conduction block. A 34-year-old female with Crohn’s disease developed painless weakness of right-hand pincer grip of insidious onset. She had previously received five courses of infliximab infusions (5 mg/kg) and a further dose 3 days after symptom onset. Infliximab partially controlled gastrointestinal symptoms and she was otherwise well. Regular medication included the oral contraceptive pill, levothyroxine, folate, omeprazole, B12 injections, and iron infusions. Examination revealed MRC grade 4 power of the right abductor pollicis brevis, flexor pollicis longus, flexor digitorum profundus (median), and opponens pollicis. Flexor carpi radialis was mildly weak (4?) but forearm pronation remained strong. There were no sensory signs and systemic examination was unremarkable. A detailed four-limb neurophysiological examination 6 weeks after symptom onset revealed isolated severe right median motor conduction block 2.5–6.5 cm proximal to the antecubital fossa skin crease (Fig. 1). Median and other sensory conduction responses were normal. EMG of median innervated forearm muscles including abductor pollicis brevis and flexor pollicis longus was consistent with conduction block, with reduced recruitment of motor units but no spontaneous activity or other evidence of motor axon loss. Right median sympathetic skin response, somatosensory evoked potentials, and thenar thermal threshold testing were all normal. There was evidence for systemic active inflammation with mild leukocytosis, thrombocytosis, and normocytic anemia; ESR 102 mm/h and CRP 51 mg/l. Anti-DNA antibodies, ANCA, ANA, RA latex, glycolipid and antiGAD antibodies, anti-GM1, and anti-GQ1b antibodies were either normal or negative. An MRI with gadolinium showed hyperintensity of the right median nerve in the lower third of the right arm on TIRM and T2-weighted images, with subtle enhancement but no enlargement. This corresponded to the site of conduction block. No specific treatment was given, but there was significant improvement of power in weak muscles within 4 weeks of presentation, and complete recovery at 1 year. Patient 2, a 41-year-old female with ankylosing spondylitis, had been treated with regular infliximab infusions since 2003. In April 2009, she awoke with painless weakness of left finger and wrist extension 3 days after an infliximab infusion (270 mg). Examination revealed MRC grade 0 finger extension and 4wrist extension with radial deviation and no sensory loss. Initial neurophysiological examination 1 week after symptom onset showed profound A. W. Michell (&) Department of Clinical Neurophysiology, Box 124 Addenbrooke’s Hospital, Cambridge CB2 0QQ, UK e-mail: andrew.michell@addenbrookes.nhs.uk