Alcoholic Polyneuropathy with Normal Thiamine

Abstract & Commentary

Source: Koike H, et al. Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status. Neurology. 2001;56:1727-1732.

Alcoholism is one of the most common causes of polyneuropathy in the United States. Surprisingly, its etiopathogenesis remains uncertain. Thiamine deficiency, direct ethanol toxicity, or alcohol metabolites may be responsible. What does appear certain, however, is that painful alcoholic polyneuropathy may occur with normal thiamine.

Eighteen patients with painful polyneuropathy and a reported history of daily ethanol consumption > 100 g for at least 10 years prior to symptom onset underwent clinical and electrodiagnostic evaluation, blood, and urine studies, sural nerve biopsy, and cerebrospinal fluid examination, the last in 16. All had normal thiamine blood levels and none manifested Wernicke-Korsakoff syndrome or congestive heart failure. Patients with diabetes, acute or chronic Guillain-Barré syndrome, amyloid, or other neuropathies were excluded.

Painful or burning feet was the initial symptom in all, with slow progression, often (8/18) to the point of inability to walk. Neuropathy was purely sensory in 7, with mild-to-moderate distal motor weakness in 11. Eight each had evidence of dysautonomia or cerebellar ataxia. Nerve conduction studies demonstrated features of axonal neuropathy involving motor and sensory fibers (decreased amplitudes), more so in the legs, with mild prolongation of distal latencies and mild-to-moderate slowing of conduction velocities, but not to the demyelinating range. Sural nerve biopsy revealed relatively selective small fiber axonal degeneration, less prominent large myelinated fiber loss, and only rare segmental demyelination and remyelination. Alcoholic polyneuropathy occurs with normal thiamine blood levels but clinically remains difficult to differentiate from beriberi.

Commentary

Among 76 chronic alcoholic patients studied retrospectively, only 3 demonstrated slightly decreased thiamine levels (Alcohol Alcohol. 2001;36:271-275). Yet, neuropathy was present in 51 (67.1%), 28 (36.8%) of these being subclinical. Nutritional status, evaluated by comparing actual with ideal weight, studying lean body mass, and measuring serum protein, albumin, prealbumin, folate, B1, and B12, was normal in 78% (40/51) of the neuropathic group and 92% (23/25) of the non-neuropathic group. Parental alcoholism was documented in 51% (26/51) and 36% (9/25), respectively. Mean alcohol disease duration and total lifetime dose of ethanol (TLDE) were significantly greater in the neuropathy group. Sural sensory nerve action potential amplitude was significantly lower in neuropathy patients with high TLDE than in those with altered nutritional state or positive family history of alcoholism. Alcohol, rather than a nutritional deficiency, may be the proximate cause of alcoholic polyneuropathy. —Michael Rubin