Polyneuropathy

Common polyneuropathies results from axonal damage which leads to degeneration in the distal portion of the longest nerves and symptoms that begin in the toes, ascend the legs, and only later appear in the fingers in proximal parts of the body.

Acute disease progresses over days to a few weeks and is most often related to an immune mediated process and probably a variant of Guillain-Barre syndrome.

Classified as axonal or demyelinating, and also by the diameter of affected nerve fibers.

Most cases, such as diabetic type, are axonal.

Larger fibers are heavily myelinated and are subject to processes that damage myelin.

Tingling is characteristic of acquired demyelinating neuropathy and is related to the spontaneous firing of sensory nerves from exposed sodium channels in denuded segments.

Perception of vibration and sense of joint position are conducted by large fibers.

Romberg sign suggests large fiber demyelinating neuropathy.

Distal weakness with preservation of muscle bulk suggests demyelinization, because preserved trophic motor nerve terminals on the muscle membrane maintains muscle size.

Axonal neuropathy can cause early muscle atrophy.

The most common cause for demyelinating polyneuropathy is chronic inflammatory demyelinating polyneuropathy (CIDP).

Causes of demyelinating polyneuropathy: Charcot-Marie-Tooth disease, type I, Diptheria toxin, Amiodarone, taxol, chronic inflammatory demyelinating polyneuropathy, monoclonal gammopathy of unknown significance, multiple myeloma, Waldenstrom’s macroglobulinemia, amyloidosis, POEMS syndrome, antobodies against sulfatides, and myelin associated glycoprotein, lymphoma, HIC, sarcoid and Lyme disease.

Genetically determined demyelinating polyneuropathy as seen in Charcot-Marie-Tooth disease is a chronic process.

Immune demyelinating polyneuropathy is associated with monoclonal gammopathy, a paraprotein neuropathy.