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
Skelton WP, Skelton NR. Nutritional Depletion Polyneuropathy and Valproic Acid. Arch Intern Med. 1993;153(7):902-905. doi:10.1001/archinte.1993.00410070080017