Abstract
Multifocal motor neuropathy (MMN), which was first described in 1986, is a purely motor neuropathy, characterized by progressive distal asymmetric limb weakness that usually starts and predominates in the upper limbs, with minimal or no sensory impairment. Nerve conduction studies show persistent multifocal conduction blocks (CB) on the motor nerves, with normal sensory potentials, which are the hallmark of MMN 1,2. It is a rare disease as its prevalence is estimated to be less than one per 100 000 1, with males more frequently affected than females, at a ratio of 2·7:1, in a recently reported series 3. According to retrospective studies, high titres of serum immunoglobulin (Ig) M antibodies to the ganglioside GM1 have been reported in 43–64% of patients with MMN 3,4. Several methods to increase the detection of autoantibodies in MMN have been published recently in a series of original studies 2.
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