Abstract
Nutritional depletion polyneuropathy is a common disorder in our society. Several groups are affected, namely, the poorly nourished, the elderly, the homeless, alcoholics, and recent third-world immigrants. Through several mechanisms, both motor and sensory peripheral nerve tracks are involved. Clinically, most important to the patient are the nociceptive tracks carrying the pain fibers. Thiamine is a necessary coenzyme in the degradation of pyruvic acid to lactic acid. Its deficiency leads to accumulation of pyruvic acid, a known neurotoxin that causes both myelin sheath breakdown and axonal degeneration. 1 Thiamine is also necessary for the production of acetylcholine whose lack further accentuates the breakdown of the neuron. Among affected individuals, pathologic features of the nerve reveal a distal axonopathy, resulting in a dying back of the nerves affected. 2 Once several bundles are involved, erratic impulses are generated and propagated up the spinothalamic tracks and perceived in the thalamus and cortex
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