From the Research
Approximately 46.3% of patients with Alcohol Use Disorder (AUD) have evidence of peripheral neuropathy, as confirmed by nerve conduction studies. This estimate is based on a systematic review and meta-analysis published in 2019 1. The wide range of prevalence estimates in the literature reflects variations in diagnostic criteria, assessment methods, and patient populations studied.
Key Findings
- Peripheral neuropathy in AUD patients typically manifests as a symmetrical, predominantly sensory neuropathy affecting the distal lower extremities first, with symptoms including numbness, tingling, burning pain, and weakness.
- The development of neuropathy is related to both the direct toxic effects of alcohol on peripheral nerves and nutritional deficiencies, particularly thiamine (vitamin B1) deficiency, that commonly occur in chronic alcohol users.
- The risk increases with the duration and amount of alcohol consumption, with most cases developing after years of heavy drinking.
Diagnostic Approaches
- Clinical scales, such as the Neuropathy Symptoms Score (NSS) and the Neuropathy Impairment Score (NIS), can be useful in detecting peripheral neuropathy in patients with AUD when neurophysiological testing is not available 2, 3.
- Elevated liver enzymes and fasting glucose levels have been correlated with neuropathy in AUD patients, suggesting that alcohol-related liver dysfunction and hyperglycemia may contribute to the risk of peripheral neuropathy 4.
Treatment and Prevention
- Treatment involves complete alcohol abstinence, nutritional supplementation (particularly B vitamins), pain management if needed, and physical therapy for functional impairment.
- Early recognition and intervention can prevent progression and potentially allow for some recovery of nerve function.
- The use of vitamin supplementation, particularly B-vitamin regimens inclusive of thiamine, is supported by limited data as a management strategy in alcohol-related peripheral neuropathy 1.