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Alcohol-Related Peripheral Neuropathy: Nutritional, Toxic, Or Both? Michelle Mellion, Md,1 James M

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Alcohol-Related Peripheral Neuropathy: Nutritional, Toxic, Or Both? Michelle Mellion, Md,1 James M INVITED REVIEW ALCOHOL-RELATED PERIPHERAL NEUROPATHY: NUTRITIONAL, TOXIC, OR BOTH? MICHELLE MELLION, MD,1 JAMES M. GILCHRIST, MD,1 and SUZANNE DE LA MONTE, MD2 1 Department of Neurology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Medical Office Center, 2 Dudley Street, Suite 555, Providence, Rhode Island 02905, USA 2 Department of Neuropathology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA Accepted 15 October 2010 ABSTRACT: Alcohol-related peripheral neuropathy (ALN) is a neurological diseases such as Wernicke encephal- potentially debilitating complication of alcoholism that results in opathy and beriberi, both the result of thiamine sensory, motor, and autonomic dysfunction. Unfortunately, ALN is rarely discussed as a specific disease entity in textbooks deficiency, led to declining enthusiasm about the because it is widely assumed to primarily reflect consequences potential role of alcohol as a neurotoxin. The simi- of nutritional deficiency. This hypothesis is largely based on lar clinical, electrophysiological, and histopatholog- observations first made over eight decades ago when it was demonstrated that thiamine deficiency (beriberi) neuropathy was ical features of ALN compared with beriberi led to clinically similar to ALN. In recent studies, failure of thiamine the hypothesis that ALN and beriberi were the treatment to reverse ALN, together with new information demon- same disease and that both were caused by thia- strating clinical and electrophysiological distinctions between 3 ALN and nutritional deficiency neuropathies, suggests that alco- mine deficiency. Despite these similarities, deca- hol itself may significantly predispose and enhance development des of clinical research have failed to definitively of neuropathy in the appropriate clinical setting. We reviewed the demonstrate that thiamine deficiency is the pri- evidence on both sides and conclude that ALN should be regarded as a toxic rather than nutritional neuropathy. mary etiologic factor that causes ALN, or that its 4 Muscle Nerve 43: 309–316, 2011 repletion serves as an effective treatment for ALN. Extensive animal and human research of etha- Alcohol-related peripheral neuropathy (ALN) is a nol neurotoxicity in alcoholic brain and liver dis- potential complication of chronic alcoholism that ease provides a possible mechanism by which etha- results in sensory, motor, and autonomic dysfunc- nol may effect the peripheral nervous system tion, which can lead to significant disability. (PNS). The direct toxic effect of ethanol in the Patients with ALN sustain repeated injury, infec- central nervous system and liver has been well tion, and falls that lead to major head trauma and documented, particularly its effect on insulin and permanent disablement. The disabilities caused by insulin-like growth factor (IGF) resistance and oxi- ALN compound the already significant health, dative stress.5–7 Recently, similar results have been social, and economic consequences of chronic obtained in experimental animal models of alcoholism. The prevalence of ALN is difficult to ALN.8,9 Improved understanding of the role etha- ascertain because obtaining accurate regular levels nol plays in the pathogenesis of ALN and the of alcohol intake and assessing nutritional status of mechanism by which it exerts its neurotoxic effects subjects is problematic. Criteria used to classify are crucial for developing effective treatments. and detect neuropathy may also underestimate This information would lead to a more accurate prevalence. ALN may affect up to half of patients classification of ALN based on its etiology. The pri- who suffer from alcoholism, but in studies that mary goal of this article is to review the evidence employ clinical and electrophysiological criteria, of proposed mechanisms in the development of 25–66% of chronic alcoholics may be affected.1,2 ALN, specifically those related to thiamine defi- The etiology of ALN has been debated for ciency and ethanol. nearly a century. ALN was originally considered a toxic neuropathy caused by the effects of ethanol and its metabolites on peripheral nerves. The dis- THE THIAMINE STORY covery that nutritional deficiencies caused other Background. Thiamine deficiency plays a contro- versial role in the development of ALN. Although there is a relatively clear association between thia- Abbreviations: ALN, alcohol-related peripheral neuropathy; CMAP, com- pound muscle action potential; CNS, central nervous system; IGF, insulin- mine deficiency and the onset of some central like growth factor; PNS, peripheral nervous system; SNAP, sensory nerve nervous system manifestations of chronic alcohol- action potential Key words: alcohol; beriberi; neuropathy; nutrition; polyneuropathy; ism, such as Wernicke encephalopathy, the role it thiamine; toxic plays in ALN continues to be debated.10 When first Correspondence to: M. Mellion; e-mail: [email protected] described by Lettsom in 1787, the etiology of ALN VC 2011 Wiley Periodicals, Inc. Published online 15 February 2011 in Wiley Online Library was ascribed to the direct neurotoxic effect of alco- 11 (wileyonlinelibrary.com). DOI 10.1002/mus.21946 hol. For over a century, ethanol was believed to Alcoholic Polyneuropathy MUSCLE & NERVE March 2011 309 be a neurotoxin that caused what James Jackson, improved when thiamine was added to their diet, MD, in 1822 referred to as a ‘‘peculiar disease the investigators concluded ALN must be the resulting from the use of ardent spirits.’’ He and result of nutritional deficiency.19 The majority of others observed that this particular disease, which patients were observed for only 2 weeks and, in he named arthrodynia a potu, started insidiously, first nearly all cases, the improvement was purely symp- involving the lower limbs and extending upward to tomatic.19 Most of the aforementioned clinical tri- affect the hands and arms. Pain was a predominant als were also flawed by relatively short observation symptom that could wax and wane, and at times periods (usually too short to allow recovery from be excruciating.12 He also described autonomic what was presumed to be an axonal neuropathy), disturbances of the gastrointestinal tract and cardio- subjective reports of improvement, and unreliable vascular system. His treatments for ALN included dietary histories. They also failed to account for abstinence from alcohol, the use of opium for pain, malnourishment and the improvement that could warm baths, and relief of constipation to improve be seen from enhanced nutritional status. None some of the debilitating symptoms.12 had reliable methods to objectively assess for thia- The hypothesis that alcohol was a direct neuro- mine deficiency. toxin prevailed until the early twentieth century. Animal Studies. Despite the shortcomings of these Physicians at that time were perplexed by the fact early clinical trials, animal studies helped to that not all patients exposed to alcohol developed strengthen the argument of a nutritional versus ALN. They believed there had to be another mod- toxic etiology causing ALN. Windebank et al. eval- ulating factor. Shattuck suggested ALN was caused uated 16 adequately nourished rats, half control by nutritional deficiency of B vitamins, specifically and the other half exposed to 16.8 g of alcohol thiamine, based on his observations of the similar per kilogram of body weight per day. No weight clinical presentations of beriberi to ALN.3 His loss occurred in either group over the 9 months of observation was followed by clinical investigations the study. Nerve tissue analyzed at 3 and 9 months by Strauss, Minot, and Cobb, who concluded that failed to show any evidence of neuropathy on 1-lm dietary deficiency, specifically of vitamin B , played 1 thin sections or on teased-fiber analysis.20 an important role in the development and perpetu- Primate models provided similar findings. ation of ALN. Their investigations allowed patients Hallett et al. evaluated the effect of alcohol on 5 to continue their usual intake of alcohol in the set- male rhesus monkeys as compared with 4 controls ting of a well-balanced diet and supplementation over a 5-year period. Four of the monkeys were fed with a non-purified form of B vitamins.13,14 They a nutritious diet supplemented with lipotropics, observed that symptoms improved in all instances amino acids, and 50% of calories provided by alco- and concluded that improvement must be related hol in place of other carbohydrates. One monkey to thiamine supplementation, although at the time had a diet deficient in choline and amino acids, pure vitamin B was not available and there were no 1 also with 50% of calories provided by alcohol. assays to assess vitamin B levels. Other investigators, There was no histological or electrophysiological including Blankenhorn and Spies, Jolliffe and evidence of peripheral neuropathy.21 The same Colbert, and Wechler, also concluded that vitamin group evaluated 10 female Macaca fascicularis mon- B deficiency and not alcohol was the cause of poly- keys fed a nutritionally complete diet and 9 age- neuropathy in the alcohol addict and thus, dubbed and gender-matched monkeys fed a diet with 30% thiamine the anti-neuritic vitamin.15–17 of calories provided by alcohol in place of carbohy- Given the results of the aforementioned stud- drate calories over a 3-year span. They, too, did ies, the main treatment for ALN included a high- not show any electrophysiological or histological vitamin, high-calorie diet supplemented
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