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Motor NCS are obtained by stimulating a nerve containing motor fibers and recording at the belly of a muscle innervated by that nerve. The compound muscle action potential (CMAP) is the resulting response and depends on the motor axons transmitting the action potential, the status of the neuromuscular junction, and muscle fibers.
[49] [50] This latter condition was later termed multifocal motor neuropathy [51] This distinction is important because multifocal motor neuropathy responds to intravenous immunoglobulin alone, while chronic inflammatory demyelinating polyneuropathy responds to intravenous immunoglobulin, steroids and plasma exchange. [52]
Multifocal motor neuropathy (MMN) is a progressively worsening condition where muscles in the extremities gradually weaken. The disorder, a pure motor neuropathy syndrome, is sometimes mistaken for amyotrophic lateral sclerosis (ALS) because of the similarity in the clinical picture, especially if muscle fasciculations are present.
In the treatment of polyneuropathies one must ascertain and manage the cause, among management activities are: weight decrease, use of a walking aid, and occupational therapist assistance. Additionally, BP control in those with diabetes is helpful, while intravenous immunoglobulin is used for multifocal motor neuropathy.
Electromyographic studies and nerve conduction studies show normal motor conduction velocity and latency with decreased amplitude of compound muscle action potentials. Pathologically, it is a noninflammatory axonopathy without demyelination. [3] Antibodies attack the coating of the motor neurons without causing inflammation or loss of myelin ...
Patients with hereditary motor and sensory neuropathies are diagnosed through a physical evaluation that looks for muscle atrophy, weakness, and sensory responses. [3] In addition to this, electromyography and motor nerve conduction tests can help clinicians decide what type of motor and sensory neuropathy it is and how severe the disease is.
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