Introduction
Methods
Protocol registration
Literature search strategy
Inclusion and exclusion criteria
Data collection process
Synthesis of results
Assessment of bias
Compliance with ethical guidelines
Results
Study characteristics
Prevalence
Prevalence of peripheral neuropathy amongst chronic alcohol abusers
Prevalence of alcohol-related peripheral neuropathy amongst those with polyneuropathy
Natural history
Clinical presentation
Nerve conduction studies and electromyography
Risk factors
Alcohol intake
Sex
Genetics
Alcohol type consumed
The role of malnutrition
The role of hepatic dysfunction
Biopsy results
The role of inflammation
The role of oxidative stress
Management
Abstinence
Vitamins
Assessment of bias
Conclusions
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Alcohol-related peripheral neuropathy is common, with signs and symptoms in 44% of chronic alcohol abusers and representing 10% of polyneuropathies. When utilising NCS to identify subclinical neuropathy amongst alcohol abusers, the rate is higher.
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The pooled prevalence of pain amongst alcoholic neuropathy sufferers is 42%. Although this figure should be interpreted with caution as it is based on a small number of studies, it suggests that alcohol-related neuropathy is one of the least painful neuropathies [89‐93]. There is a need for more careful mapping and description of the symptoms of neuropathy in research and clinical practice.
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Alcohol-related peripheral neuropathy is primarily an axonal, length-dependent, sensorimotor neuropathy with dominant sensory features.
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TLDE is currently the best validated risk factor for development of alcohol-related peripheral neuropathy. Other risk factors include pattern of alcohol consumption, parental history of alcohol abuse, male gender, and mutation of ALDH2.
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Some authors identify hepatic dysfunction and malnutrition, particularly of thiamine, to be central to the pathological process in alcohol-related neuropathy. The evidence presented in this review may suggest that this is not that case, but that these might represent additional risk factors or perhaps cause neuropathy independently which is superimposed upon that caused by the neurotoxic effects of alcohol. However, the relationship between ethanol toxicity and neuropathy is as of yet unproven and there are other possible risk factors not yet addressed by the literature. To give one such example, there is a well-documented association between smoking tobacco and alcoholism, and smoking has been associated with increased risk of peripheral neuropathy in other populations such as in those with diabetes [94, 95]. Further studies are required to investigate the relationships between these factors and to translationally explore the relationship between ethanol consumption and neuropathy.
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There is presently little literature regarding the optimal management strategy for those with alcohol-related neuropathy. Vitamin supplementation appears to currently have the best evidence.
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Although NCS are better in determining the presence of peripheral neuropathy and its severity, they were not used consistently in all studies. Additionally, the neurophysiological parameters used were inconsistent. Routine use of NCS of lower and upper limbs in the diagnosis of PN in patients is advised.
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There is currently very little data focussed upon the prevalence of small fibre neuropathy in the context of alcoholic neuropathy. This should be a focus of future research.
Limitations
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There was a great deal of heterogeneity between studies with respect to the definitions of alcohol abuse and the means used to diagnose peripheral neuropathy. Alcohol misuse/addiction was defined in a number of ways, sometimes using validated criteria such as diagnostic and statistical manual of mental disorders (DSM), and sometimes arbitrarily. With regards to neuropathy, the present study aimed to be clear whether patients were diagnosed based upon clinical features, nerve conduction studies or both when discussing prevalence. The variation in definitions of alcohol abuse, however, was not resolvable, though this review removed patients who were not chronic abusers and aimed to draw distinctions between duration of alcohol consumption and duration of abuse between studies where possible.
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There were no restrictions in date of publication applied in this review. This was a deliberate decision made to review the full range of literature pertinent to the topic in question. However, as the included literature dates as far back as 1964 it is feasible that modern investigations may have identified causes of neuropathy other than alcoholism amongst some included patients. Another consequence of inclusion of older literature is heterogeneity in the means used to measure thiamine deficiency, with some studies having used the less accurate, indirect approach of erythrocyte transketolase activity assay to discern thiamine status.
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Nutrition and liver function were not addressed in all studies. Therefore, in some studies it cannot be certain to what degree the neurological dysfunction is a consequence of alcohol toxicity.