Alcoholic Neuropathy is Not Due to Thiamine Deficiency
Abstract & Commentary
Source: Koike H, et al. Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Ann Neurol. 2003;54:19-29.
Sixty-four patients with alcoholic neuropathy (ALN), comprising 36 without thiamine deficiency and 28 with thiamine deficiency (ALN-TD), were compared to 32 nonalcoholic, thiamine-deficiency neuropathy (TDN) patients to establish whether clinical and pathological features were similar in the 2 groups and to determine how thiamine deficiency related to ALN. ALN and ALN-TD patients all imbibed more than 100 gm of alcohol daily for at least 10 years, whereas TDN patients were teetotalers except for 4 who drank no more than 20 gm on occasion. Thiamine deficiency was due to dietary imbalance or previous surgery for ulcer or gastrointestinal neoplasm. Morbidly obese patients who had undergone gastrectomy for weight control were excluded, as were those with other causes for neuropathy including diabetes, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, or familial amyloid. Thiamine levels were measured using high-performance liquid chromatography, and normal was defined as a blood level of 20-50 ng/mL with normal red blood cell transketolase activity. All patients were evaluated by history, physical examination, and nerve conduction studies. Sural nerve biopsy was performed in 56 patients, 29 ALN, 18 ALN-TD, and 19 TDN. Statistical analysis incorporated the X2 or Mann-Whitney U test as indicated, with significance defined as P < .05.
All patients demonstrated symmetric sensorimotor polyneuropathy, worse in the legs than arms, that began as pain or burning in the toes or ankles. However, compared to TDN, ALN without thiamine deficiency was characterized by (1) slower progression, over a year rather than over a month; (2) sensory rather than motor predominance; (3) less motor involvement of the arms; (4) more subjective pain; (5) small-fiber (pain and temperature) rather than large-fiber (position and vibration) dominance; (6) retained biceps and patellar deep tendon reflexes; and (7) retained ability to walk. Nerve conduction studies were similar between groups save for longer distal motor latencies and lower compound muscle action potential amplitudes in TDN compared to ALN without thiamine deficiency. Sural nerve biopsy revealed more large-fiber axonal loss and subperineurial edema in TDN, with more myelin irregularity and segmental demyelination/remyelination in ALN. Not surprisingly, the ALN-TD group demonstrated characteristics straddling both ALN and TDN. Pure ALN is distinct from pure TDN, and it can evolve in the presence of normal thiamine levels, supporting the notion that ALN may be due to a direct toxic effect of alcohol or its metabolites.
Commentary
Alcohol overuse affects muscles as well, producing either an acute myopathy in 1% of alcoholics following binge drinking or a chronic myopathy, seen in 50% of long-standing alcoholics. Neuropathy and myopathy often coexist in up to 72% of individuals.1 Selective type II fiber atrophy characterizes chronic alcoholic myopathy, and patients can lose up to a third of their musculature. Abnormalities of protein or RNA metabolism or both, rather than nutritional or vitamin deficiencies, are implicated in its pathogenesis, but other factors may be involved, including free radical injury2 and adduct formation.3 Acetaldehyde-protein adducts are formed by their co-valent binding one-to-another, and increased levels of these adducts are found in muscle membrane and subsarcolemmal regions in rats fed nutritionally complete diets including alcohol. Skeletal muscle comprises 40% of body mass and further understanding of this common complication of ethanol abuse will have major consequences on the well-being of a large segment of our population. — Michael Rubin, MD, Professor of Clinical Neurology, New York Presbyterian Hospital-Cornell Campus, Assistant Editor, Neurology Alert.
References
1. Martin F, et al. Q J Med. 1985;55:233-251.
2. Adachi J, et al. Lipids. 2001;36:267-271.
3. Worrall S, et al. Eur J Clin Invest. 2001;31:723-730.
Sixty-four patients with alcoholic neuropathy (ALN), comprising 36 without thiamine deficiency and 28 with thiamine deficiency (ALN-TD), were compared to 32 nonalcoholic, thiamine-deficiency neuropathy patients to establish whether clinical and pathological features were similar in the 2 groups and to determine how thiamine deficiency related to ALN.
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