All You Need To Know About Motor Neuropathy

Most motor neuropathy syndromes are immune-mediated and treatable, as opposed to amyotrophic lateral sclerosis. They are often characterized by patterns of weakness, and absence of upper motor neuron signalling. To distinguish it from other disorders such as demyelinating neuropathis, electrodiagnostic studies are conducted as well as serum autoantibodies are measured. Health professionals first used electrodiagnostic testing to diagnose this disease. A blockage of impulses at the focal site along motor axons is detected by using nerve conduction studies, and provides the evidence that the peripheral nerves are the ones affected.

Multifocal motor neuropathy, a type of motor peripheral neuropathy is characterized by a slow, progressive, asymmetric weakness in the arms. It affects more men rather than women, generally between the ages of twenty to seventy five. Findings include atrophy in various degrees and asymmetric weakness. A conduction block is present in medium sized muscles. Symptoms may include cranial nerve signs like external ophthalmoplegia, and paresthesia. Sensory signs are often absent or of no significance in the diagnosis.

The general symptoms seen in patients with a motor neuropathy are due to damage to the motor nerve fibers. Their destruction causes loss of muscle control, weakness, loss of muscle bulk and dexterity. Having cramps can signify motor nerve impairment. Other symptoms of motor neuropathy include difficulty or inability to move a part of the body, or paralysis, muscle shrinking or atrophy, muscle twitching or fasciculation, difficulty in breathing or swallowing, weak knees that causes the legs to buckle and the person to fall, and lack of dexterity -- like being unable to button a shirt. Motor neuropathy in patients is seen as having preserved reflexes in weak muscles but lacking in overt spasticity and bulbar features. Patients with MMN have a prolonged course. Acquired motor neuropathies produce asymmetric weakness which is clearly distinct from the proximal symmetric weakness seen in spinal muscular atrophies.

Motor neuropathies can be first divided into multifocal motor neuropathy and distal lower motor neuron syndrome, based on electrophysiologic data. Characteristics of patients with MMN are the presence of a focal block of nerve conduction along the motor axons with normal sensory studies. With distal lower motor neuron syndrome, there is the absence of the motor axon loss but no conduction block.

Lower motor neuron syndromes are of uncertain etiology and disorders of the motor axon and cell body. They have no evidence of peripheral nerve demyelination or serum antibodies. They have faster progressive weakness typical of other neuropathies. They never develop bulbar dysfunction. So far, no advice has been given on the immunosuppressive treatments with either demyelination or serum autoantibodies.

For treatment, physicians have used Cyclophosphamide or human immune globulin (HIG). These can produce a useful functional improvement in patients with MMN. Cyclophosphamide is probably the only immunosuppressive medication that induces long term benefit in most patients of MMN.

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