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Alcohol-Related Peripheral Neuropathy: a Systematic Review and Meta- Analysis

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Alcohol-Related Peripheral Neuropathy: a Systematic Review and Meta- Analysis Journal of Neurology https://doi.org/10.1007/s00415-018-9123-1 REVIEW Alcohol-related peripheral neuropathy: a systematic review and meta- analysis Thomas Julian1 · Nicholas Glascow1 · Rubiya Syeed1 · Panagiotis Zis2,3 Received: 30 August 2018 / Revised: 9 November 2018 / Accepted: 12 November 2018 © The Author(s) 2018 Abstract The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropa- thy 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 data- base. 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. Keywords Alcohol · Alcoholic · Neuropathy · Ethanol · Polyneuropathy Introduction which was of greater prominence in the legs than the arms [4]. Presently, peripheral neuropathy amongst chronic alco- Alcohol abuse is known to cause a range of neurological hol abusers remains an entity of disputed character and disorders, including cerebellar ataxia, confusion, cognitive pathogenesis. Its current obscurity is likely attributable to impairment, and peripheral neuropathy [1]. Neuropathy the complex range of physiological derangements that come associated with chronic alcohol abuse may involve large and/ with chronic alcohol abuse—many of which have the capac- or small (including autonomic) fibres and is rather hetero- ity to cause neuropathy. Some of the factors discussed in geneous in its clinicopathological features [2, 3]. The earli- literature which can attribute to the neuropathy presenting est known description of neuropathic symptoms associated in these patients are the direct toxicity of alcohol, nutritional with ingestion of alcohol were noted by Lettsom in 1787, deficiencies (particularly thiamine and B12), hepatic cirrho- describing the presentation of paralysis and hypoesthesia sis, impurities of alcoholic beverages (for instance, lead) and deranged blood glucose [3, 5, 6]. The interaction of these factors has not only complicated discerning the most * Panagiotis Zis important pathological mechanisms of neuropathy in alco- [email protected]; [email protected] hol abuse, but also prevented characterisation of the typical features as the various elements affect the nervous system 1 The Medical School, University of Sheffield, Beech Hill Rd, Sheffield S10 2RX, UK differently. Although alcoholic toxicity is not firmly estab- lished as the only pathogenic factor in neuropathy amongst 2 Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK alcohol abusers, in this review the entity shall be referred to as “alcohol-related neuropathy”. 3 Medical School, University of Cyprus, Nicosia, Cyprus Vol.:(0123456789)1 3 Journal of Neurology The aim of this systematic review is to characterise the 7. Articles which could not be obtained despite Univer- presentation of alcohol-related peripheral neuropathy, to sity inter library request, British Library request and determine the typical ancillary test results, to establish the attempts made to contact the article author. importance of various risk factors and to explore the likely 8. Studies which contained subjects who had consumed pathogenetic mechanisms. Due to the breadth of the litera- any forms of alcohol other than ethanol (e.g., metha- ture surrounding this topic, this review shall focus exclu- nol) or who consumed illegally manufactured or home- sively upon peripheral neuropathy, without discussing auto- made alcohol as this is likely to contain impurities. nomic neuropathy. 9. Articles referring to description of neurophysiological techniques not specific to alcohol-related neuropathy. 10. Articles detailing pilot treatments that have not been Methods replicated or further confirmed with larger studies. Protocol registration All articles were abstract screened by a minimum of three authors in a blinded fashion using Rayyan software to ensure This review was prospectively registered to PROSPERO. The accuracy. Those found to meet any of the exclusion criteria registration number for this review is CRD42018099910. were removed and any conflicts were settled by consensus dur- ing a face-to-face meeting in which the abstracts were reread. Literature search strategy All remaining papers were screened again as a full article by at least two authors and conflicts were settled as before. Where a A systematic search was performed on 10.06.18 using the paper was not available online, University interlibrary request PubMed database. For the search, two medical subject head- was made for the item, British Library request and failing these ing (MeSH) terms were used. Term A was “alcohol OR alco- we attempted to find the authors contact details. holic OR ethanol”. Term B was “neuropathy OR polyneu- ropathy”. Human subject and English language filters were Data collection process applied in our search. The reference lists of included articles were scanned for further articles which may fall within the Data were extracted from each study in a structured cod- scope of this review and were included where appropriate. ing scheme using Google Sheets and included: Population size; demographics; total alcohol consumption and duration Inclusion and exclusion criteria of alcohol consumption; prevalence of alcohol-related neu- ropathy; clinical and neurophysiological data; prognosis; Articles eligible to be included in this review were required biopsy/necropsy results; nutritional status; management; to meet the following criteria: pathogenesis; and risk factors. Where there was uncertainty with respect to how data should be interpreted, at least three 1. The article discussed peripheral neuropathy related to authors discussed the paper to ensure consensus. chronic alcohol consumption. Neuropathy was diag- nosed clinically and/or with nerve conduction studies Synthesis of results (NCS). 2. The study was conducted using human subjects. This study used aggregate data where ever possible. Fre- 3. The article was written in English language. quencies and descriptive characteristics extracted were calculated. This study is reported in accordance with the Articles meeting the following criteria were excluded preferred reporting items for systematic reviews and meta- from our review: analysis (PRISMA) guidelines [7]. Statistical calculation of pooled proportions was conducted in R language, using the 1. Case reports. default settings of the “meta” package and the “metaprop” 2. Non-original articles (i.e., review articles, letters to the function with a random effects model [8]. Editor, expert opinion papers etc.). 3. Animal studies. Assessment of bias 4. Duplicate articles (identical publications). 5. Studies of patient populations with other causes of neu- Randomised control trials were assessed for bias using ropathy or with comorbidities which may cause neu- JADAD scoring [9]. ropathy (e.g., diabetes, vasculitis, mechanical trauma). 6. Studies exclusively detailing other forms of neuropa- thy, such as autonomic or optic neuropathy. 1 3 Journal of Neurology Compliance with ethical guidelines nerve conduction studies (NCS) with or without supplemen- tary electromyogram (EMG) with a focus upon large fibre This article is based upon previously published studies. neuropathy. As seen in Fig. 2, 34 of the studies provided data There are, therefore, no ethical concerns with regard to this regarding the prevalence of peripheral neuropathy diagnosed study. using history and examination, giving a pooled prevalence of 44.2% (CI 35.9–53%, n = 2590) [5, 6, 10–40]. As seen in Fig. 3, 17 of the studies gave prevalence data in popula- Results tions diagnosed peripheral neuropathy using NCS, giving a pooled prevalence of 46.3% (CI 35.7–57.3%; n = 1596) [2, 5, Study characteristics 6, 12, 14, 23, 35, 37–39, 41–47]. Just one study focussed on the prevalence of small fibre neuropathy, in which amongst The literature search heralded 668 results. In total, 585 98 patients, 45 patients had large fibre peripheral neuropathy papers did not meet the inclusion/exclusion criteria and were and 37 patients (37.8%) had small fibre neuropathy [5]. The excluded. By scanning the reference lists of included studies, drawback of this study,
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