Abstract

Background Multifocal motor neuropathy (MMN) almost purely involves motor nerve. About 20% MMN patients develop minor sensory symptoms in the course of disease. Material and method We reported a 62-year-old male who developed a slowly progressive asymmetrical limb weakness for five years. Motor nerve conduction studies showed definite CB in left median and ulnar nerves, and probable CB in right tibial nerve. Although the patient complained of no sensory symptom, sensory never conduction studies showed absent sensory nerve action potential (SNAP) for bilateral medial plantar and fibular nerves, left sural nerve and reduced amplitude for left median, ulnar and radial nerves. Conduction velocities were otherwise normal. One month after receiving intravenous immunoglobulin (IVIg), his weakness alleviated apparently. A substantial increase in motor amplitude recorded with stimulation at the PF indicated a partial reversal of CB. The SNAP amplitude of left median, ulnar and radial nerves increased more than 50% and the return of bilateral fibular nerve potentials provided evidence of reversible conduction failure in sensory nerves. We reviewed related literature for this performance. Result Three previously published studies reported such a decrease of SNAP amplitude in MMN patients. Such features suggest a more prominent axonal damage more than demyelination. The hyperpolarization of axolemma, resulting from axonal Na+/K+ pump inhibition at the lesion site and overactivity at the adjacent site may constitutes the prominent mechanism of CB. Conclusion Amplitude reduction of SNAP combined with motor CB, which recovered rapidly after IVIg, may suggest axonal damage rather than demyelination.

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