Poster 114 Multifocal Acquired Demyelinating Sensory and Motor (MADSAM) Neuropathy Secondary to Infliximab Infusion: A Case Report

Abstract

Disclosures: A. Sinha, No Disclosures. Case Description: A 69-year-old man with a history of ulcerative colitis, status post C4-C7 fusion (secondary to myelopathy over 10 years ago), presented with a 1-year history of right upper extremity pain and paresthesia. Recent MRI of the cervical spine showed evidence of a well-healed fusion from C4-C7 with findings of degenerative changes at C3-4 and C7-T1. The patient did have an MRI of the brachial plexus, which was unremarkable. The patient denied any lower extremity symptoms; however, he did have some paresthesias in the sole of his feet. The patient noted that most of his symptoms began after infliximab infusion therapy for ulcerative colitis. His last infliximab infusion was 8 weeks prior to this appointment. He denied any bowel or bladder dysfunction. On physical examination, the patient was neurologically intact, except for except for 4/5 strength in the right hand intrinsics. There were no upper motor neuron signs. Setting: Outpatient spine practice. Results or Clinical Course: Electrodiagnostic studies of the upper and lower extremities showed prolonged latencies, diminished amplitudes and conduction velocities, in multiple nerves in a non-focal distribution. Diminished recruitment and polyphasic potentials were found in the majority of muscles in the upper and lower extremities. The patient was diagnosed with multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy. He was referred to neurology where he was advised to begin intravenous immunoglobulin (IVIg) therapy. Discussion: Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and features of demyelination. Also known as Lewis-Sumner syndrome, this neuropathy is a rarely reported complication in patients undergoing treatment with the antitumor necrosis factor (TNF) monoclonal antibody infliximab. Symptoms may resolve after cessation of the antibody treatment; however IV Ig infusion therapy is the treatment of choice if symptoms persist. Conclusions: We present a rarely reported case of MADSAM, or Lewis-Sumner syndrome, following infliximab treatment. Clinicians should be aware that electrodiagnostic studies are essential in the diagnosis of this complex neuropathy.