Alcoholic neuropathy is clinicopathologically distinct from thiamine‐deficiency neuropathy

Koike, Haruki; Iijima, Masahiro; Sugiura, Makoto; Mori, Keiko; Hattori, Naoki; Itô, Haruo; Hirayama, Masaaki; Sobue, Gen

doi:10.1002/ana.10550

Cited by 220 publications

(223 citation statements)

References 44 publications

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“…Neurological evaluation frequently reveals loss of tendon reflexes, alterations in tactile perception and vibration perception, weakness and decreased muscle coordination (Kemppainin et al, 1982;Sosenko et al, 1991). The pathophysiology of alcoholic polyneuropathy is thought to be twofold, combining the toxic effect of alcohol with nutritional deficiency caused by longterm heavy alcohol consumption (Koike et al, 2003;Koike & Sobue, 2006;Koike et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Nunes¹,

Jr²,

Goldberg³

et al. 2013

RNIJ

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Section: Introductionmentioning

confidence: 99%

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Nunes¹,

Jr²,

Goldberg³

et al. 2013

RNIJ

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“…It is often illuminating to probe into an alcohol consumption history in a thorough, nonjudgmental, and nonthreatening way. 8 Past medical and medication history are also important considerations for elaborating the patient's unique clinical setting. Diabetes, renal disease, malnutrition, HIV, and paraproteinemia are some of the disorders that are risk factors.…”

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confidence: 99%

The Evaluation of Polyneuropathies

Burns

Mauermann²

2011

Neurology

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olyneuropathy has an estimated prevalence of 2%-3% in the general population and a prevalence as high as 8% in people over the age of 55 years.1 Roughly one-third of polyneuropathies will have a genetic cause, one-third an acquired etiology, and onethird will be idiopathic, despite appropriate diagnostic evaluation.2 There are over 100 known acquired and inherited disorders that may cause polyneuropathy, a fact that presents challenges and can contribute to uncertainty about the scope, direction, and level of aggressiveness of any evaluation.3 This sometimes leads to a one-size-fits-all diagnostic strategy, a strategy that is unfocused, inefficient, and costly, and sometimes places the patient at unnecessary risk of a procedure-related complication (e.g., nerve biopsy).In this article, we present a simple and easy-toremember algorithm for diagnosing polyneuropathy, based on first answering 4 clinical questions: what, where, when, and what setting (figure 1).3 The 4-step clinical characterization should almost always be followed by electrodiagnostic (EDX) characterization with appropriate nerve conduction and needle EMG. The clinical and EDX characterization can then be combined, as necessary, with a consultation of appropriate tables and lists of differentials or the figure we provide in this article, allowing for the generation of a focused differential diagnosis and appropriate and efficient evaluation. CLINICAL APPROACH TO NEUROPATHY What?The question "what?" refers to which nerve fiber modalities (sensory, motor, autonomic, or a combination) are involved. Identification of sensory nerve involvement allows the clinician to exclude from consideration

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“…Although regeneration of nerve fibers is known to occur in the peripheral nervous system, little information supports such a mechanism in the central nervous system (Kim et al, 2006). In the peripheral neuropathy caused by thiamine deficiency (both alcoholic and nonalcoholic), large myelinated fibers are affected more than small myelinated fibers (Koike et al, 2003). By contrast, these authors noted that in pure alcoholic neuropathy, small myelinated fibers seem to be more affected.…”

Section: White Matter Constituents and Morphologymentioning

confidence: 99%

Interaction of Thiamine Deficiency and Voluntary Alcohol Consumption Disrupts Rat Corpus Callosum Ultrastructure

Sullivan

Stankovic

et al. 2007

Neuropsychopharmacol

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The relative roles of alcohol and thiamine deficiency in causing brain damage remain controversial in alcoholics without the WernickeKorsakoff syndrome. Experimental control over alcohol consumption and diet are impossible in humans but can be accomplished in animal models. This experiment was designed to differentiate the separate and combined effects on the macro-and ultrastructure of the corpus callosum of thiamine deficiency and voluntary alcohol consumption. Adult male alcohol-preferring (P) rats (9 chronically alcoholexposed and 9 water controls) received a thiamine-deficient diet for 2 weeks. There were four groups: five rats previously exposed to alcohol were treated with pyrithiamine (a thiamine phosphorylation inhibitor); five rats never exposed to alcohol were treated with pyrithiamine; four alcohol-exposed rats were treated with thiamine; and four rats never exposed to alcohol were treated with thiamine. On day 14, thiamine was restored in all 18 rats; 2 weeks later the 10 pyrithiamine-treated rats received intraperitoneal thiamine. The rats were perfused 61 days post-pyrithiamine treatment at age 598 days. Brains were dissected and weight and volumes were calculated. Sagittal sections were stained to measure white matter structures. The corpus callosum was examined using transmission electron microscopy to determine density of myelinated fibers, fiber diameter, and myelin thickness. The corpus callosum in the alcohol/ pyrithiamine group was significantly thinner, had greater fiber density, higher percentage of small fibers, and myelin thinning than in the alcohol/thiamine and water/thiamine groups. Several measures showed a graded effect, where the alcohol/pyrithiamine group had greater pathology than the water/pyrithiamine group, which had greater pathology than the two thiamine-replete groups. Across all 16 rats, thinner myelin sheaths correlated with higher percentage of small fibers. Myelin thickness and axon diameter together accounted for 71% of the variance associated with percentage of small fibers. Significant abnormalities in the alcohol/pyrithiamine group and lack of abnormality in the alcohol-exposed/thiamine-replete group indicate that thiamine deficiency caused white matter damage. The graded abnormalities across the dually to singly treated animals support a compounding effect of alcohol exposure and thiamine depletion, and indicate the potential for interaction between alcohol and thiamine deficiency in human alcohol-related brain damage.

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Alcoholic neuropathy is clinicopathologically distinct from thiamine‐deficiency neuropathy

Cited by 220 publications

References 44 publications

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

Alcoholic Polyneuropathy: Clinical Assessment of Treatment Outcomes Following Therapy with Nucleotides and Vitamin B12

The Evaluation of Polyneuropathies

Interaction of Thiamine Deficiency and Voluntary Alcohol Consumption Disrupts Rat Corpus Callosum Ultrastructure

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