Multifocal Motor Neuropathy (MMN)

Hi Sue, My husband has MADSAM, but was investigated for MMN because he has almost no sensory symptoms. He didn’t have the Anti-GM1 antibodies which are often present in 50-85% of those who have it. I know that steroids make MMN patients worse and IVIG is the treatment of choice.
Laurel

There were several doctors who suggested I might have this condition. Here is what the NIH says about it

“[I]…Is there any treatment? Treatment for multifocal motor neuropathy varies. Some individuals experience only mild, modest symptoms and require no treatment. For others, treatment generally consists of intravenous immunoglobulin (IVIg) or immunosuppressive therapy with cyclophosphamide. …[/I]”

and, more from [url]http://neuromuscular.wustl.edu/antibody/motpn2.htm[/url]

“[I]…B. Electrodiagnostic Classification
Motor neuropathies can be initially subdivided on the basis of electrophysiologic data.

1) Patients with MMN have, by definition, focal block of nerve conduction along the course of motor, but not sensory, axons. Conduction block has been variably defined as a 15% to 50% reduction in the compound muscle action potential at proximal as compared with distal sites of stimulation….[/I]”

The NEUROMUSCULAR DISEASE CENTER Washington University, St. Louis, MO USA article goes on to explain,

“…Immune demyelinating Neuropathies. Although MMN and CIDP are both demyelinating neuropathies, the differences in their clinical, electrophysiological and immunologic features are more prominent than their similarities. MMN commonly presents with distal asymmetric weakness while in CIDP, proximal symmetric weakness is a more common finding. The remitting and relapsing course that may occur in CIDP is uncommon in the motor neuropathies. Patients with MMN rarely have significant sensory symptoms while in CIDP, sensory signs are the rule…”

For those of you not familiar with these two terms, here’s how I look at them:

Distal- means the furthest away from the body

Proximal- nearest the body, connects to the body.

A Pubmed article is quite helpful, to me, in understanding these two diseases.

“[I]Multifocal acquired demyelinating sensory and motor neuropathy: the Lewis-Sumner syndrome.
Saperstein DS, Amato AA, Wolfe GI, Katz JS, Nations SP, Jackson CE, Bryan WW, Burns DK, Barohn RJ.
Source

Department of Neurology, University of Texas Southwestern Medical Center, Dallas, USA.
Abstract

We report 11 patients with multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy, defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and other features of demyelination. The clinical, laboratory, and histological features of these patients were contrasted with those of 16 patients with multifocal motor neuropathy (MMN). Eighty-two percent of MADSAM neuropathy patients had elevated protein concentrations in the cerebrospinal fluid, compared with 9% of the MMN patients (P < 0.001). No MADSAM neuropathy patient had elevated anti-GM1 antibody titers, compared with 56% of MMN patients (P < 0.01). In contrast to the subtle abnormalities described for MMN, MADSAM neuropathy patients had prominent demyelination on sensory nerve biopsies. Response to intravenous immunoglobulin treatment was similar in both groups (P = 1.0). Multifocal motor neuropathy patients typically do not respond to prednisone, but 3 of 6 MADSAM neuropathy patients improved with prednisone. MADSAM neuropathy more closely resembles chronic inflammatory demyelinating polyneuropathy and probably represents an asymmetrical variant. Given their different clinical patterns and responses to treatment, it is important to distinguish between MADSAM neuropathy and MMN.[/I]"