Reappraisal of alcoholic myopathy: Clinical and biopsy study on chronic alcoholics without muscle weakness or wasting

Faris, Amin A.; Reyes, Marc G.

doi:10.1136/jnnp.34.1.86

Cited by 41 publications

(8 citation statements)

References 12 publications

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“…Nine studies reported EMG findings in alcohol-related peripheral neuropathy patients. Reduced recruitment pattern of motor units was a frequently reported outcome [16, 28, 67, 70]. Active denervation (presence of positive waves and fibrillations) was also present in the majority of patients.…”

Section: Resultsmentioning

confidence: 99%

Alcohol-related peripheral neuropathy: a systematic review and meta-analysis

et al. 2018

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The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case–control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7– 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy. The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor. There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine.

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Section: Resultsmentioning

confidence: 99%

Alcohol-related peripheral neuropathy: a systematic review and meta-analysis

et al. 2018

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“…Weakness observed in chronic alcoholics has been debated to be the result of either a combination of these neuromuscular mechanisms or isolated to a single factor. For example, some have suggested that alcohol‐induced weakness is initiated by denervation‐associated peripheral neuropathy (Agelink et al, 1998 ; Faris & Reyes, 1971 ; Julian et al, 2019 ; Rossouw et al, 1976 ), while others have argued pathology originates within the muscle itself (Martin et al, 1985 ; Slavin et al, 1983 ; Trounce et al, 1987 ). These seemingly conflicting results may be related to difficulties quantifying and controlling for potential confounding factors such as the amount, type, and duration of alcohol intake as well as nutrition, genetics, activity levels, various socioeconomic and environmental factors (Kimball & Lang, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Neuromuscular mechanisms of weakness in a mouse model of chronic alcoholic myopathy

Moser

Brown

Clark

et al. 2022

Alcoholism Clin & Exp Res

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Background Weakness is a common clinical symptom reported in individuals with chronic alcohol use disorder. However, it remains unclear whether low strength in these individuals is directly related to excessive ethanol intake, other deleterious factors (lifestyle, environment, genetics, etc.), or a combination of both. Therefore, we examined whether (and how) ethanol reduces the muscle’s force‐producing capacity using a controlled in vivo preclinical mouse model of excessive ethanol intake. Methods To establish whether chronic ethanol consumption causes weakness, C57BL/6 female mice consumed 20% ethanol for 40 weeks (following a 2‐week ethanol ramping period), and various measures of muscular force were quantified. Functional measures included all‐limb grip strength and in vivo contractility of the left ankle dorsiflexors and plantarflexors. Once confirmed that mice consuming ethanol were weaker than age‐matched controls, we sought to determine the potential neuromuscular mechanisms of muscle dysfunction by assessing neuromuscular excitation, muscle quantity, and muscle quality. Results Mice consuming chronic ethanol were 13 to 16% weaker (p ≤ 0.016) than controls (i.e., mice consuming 100% water) with the negative impact of ethanol on voluntary grip strength (ƞ2 = 0.603) being slightly larger than that of electrically stimulated muscle contractility (ƞ2 = 0.482). Relative to controls, lean mass and muscle wet masses were 9 to 16% lower in ethanol‐consuming mice (p ≤ 0.048, ƞ2 ≥ 0.268). No significant changes were observed between groups for indices of neuromuscular excitation at the level of the motor unit, neuromuscular junction, or plasmalemma (p ≥ 0.259, ƞ2 ≤ 0.097), nor was muscle quality altered after 40 weeks of 20% ethanol consumption (p ≥ 0.695, ƞ2 ≤ 0.012). Conclusions Together, these findings establish that chronic ethanol consumption in mice induces a substantial weakness in vivo that we interpret to be primarily due to muscle atrophy (i.e., reduced muscle quantity) and possibly, to a lesser degree, loss of central neural drive.

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“…The patterns of weakness can be alcohol dose-dependent, and abate or resolve with abstinence [ 11 ]. A diagnosis of primary myopathy in alcoholics can be confirmed by electromyography [ 12 ]. In addition, the main histopathological features include, selective atrophy of glycolytic, fast-twitch (Type 2) myofibers, compensatory hypertrophy of Type 1 (aerobic) myofibers [ 6 , 13 ], and scattered myofibers with moth-eaten appearances in sections stained for oxidative enzyme activity.…”

Section: Introductionmentioning

confidence: 99%

Impaired Insulin/IGF Signaling in Experimental Alcohol-Related Myopathy

Nguyen

Tong

et al. 2012

Nutrients

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Alcohol-related myopathy (Alc-M) is highly prevalent among heavy drinkers, although its pathogenesis is not well understood. We hypothesize that Alc-M is mediated by combined effects of insulin/IGF resistance and oxidative stress, similar to the effects of ethanol on liver and brain. We tested this hypothesis using an established model in which adult rats were pair-fed for 8 weeks with isocaloric diets containing 0% (N = 8) or 35.5% (N = 13) ethanol by caloric content. Gastrocnemius muscles were examined by histology, morphometrics, qRT-PCR analysis, and ELISAs. Chronic ethanol feeding reduced myofiber size and mRNA expression of IGF-1 polypeptide, insulin, IGF-1, and IGF-2 receptors, IRS-1, and IRS-2. Multiplex ELISAs demonstrated ethanol-associated inhibition of insulin, IRS-1, Akt, and p70S6K signaling, and increased activation of GSK-3β. In addition, ethanol-exposed muscles had increased 4-hydroxy-2-nonenal immunoreactivity, reflecting lipid peroxidation, and reduced levels of mitochondrial Complex IV, Complex V, and acetylcholinesterase. These results demonstrate that experimental Alc-M is associated with inhibition of insulin/IGF/IRS and downstream signaling that mediates metabolism and cell survival, similar to findings in alcoholic liver and brain degeneration. Moreover, the increased oxidative stress, which could be mediated by mitochondrial dysfunction, may have led to inhibition of acetylcholinesterase, which itself is sufficient to cause myofiber atrophy and degeneration.

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Reappraisal of alcoholic myopathy: Clinical and biopsy study on chronic alcoholics without muscle weakness or wasting

Cited by 41 publications

References 12 publications

Alcohol-related peripheral neuropathy: a systematic review and meta-analysis

Alcohol-related peripheral neuropathy: a systematic review and meta-analysis

Neuromuscular mechanisms of weakness in a mouse model of chronic alcoholic myopathy

Impaired Insulin/IGF Signaling in Experimental Alcohol-Related Myopathy

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