From the Guidelines
Individuals with Alcohol Use Disorder (AUD) develop length-dependent, axonal, sensorimotor peripheral neuropathy primarily due to the toxic effects of alcohol combined with nutritional deficiencies, as supported by the most recent and highest quality studies 1. The pathogenesis of this condition involves the direct damage of nerve fibers by alcohol's toxic metabolites, particularly acetaldehyde, which interferes with normal nerve function and transport mechanisms. Additionally, alcoholism frequently leads to thiamine (vitamin B1) deficiency, as alcohol impairs its absorption and utilization, and thiamine is essential for nerve cell metabolism and myelin sheath maintenance. Other B vitamin deficiencies, including B6 and B12, further contribute to nerve damage, and poor nutritional status among heavy drinkers exacerbates these deficiencies.
Key characteristics of this neuropathy include:
- Length-dependent distribution, with symptoms typically beginning in the feet and progressing upward
- Axonal damage, with reduced amplitude of the sensory nerve action potentials (SNAPs) on nerve conduction studies
- Sensorimotor symptoms, including numbness, tingling, burning sensations, and weakness
- Dose-dependent relationship between alcohol consumption and neuropathy severity
The most effective treatment involves:
- Complete alcohol cessation
- Nutritional supplementation, particularly with B vitamins
- Pain management, if needed
- The condition may partially improve with abstinence and proper nutrition, though complete recovery is not always possible if significant axonal damage has occurred 1.
It is essential to note that the evidence from studies on chemotherapy-induced peripheral neuropathy 1 and peripheral neuropathy in multiple myeloma patients 1 also supports the understanding of the pathogenesis and treatment of length-dependent, axonal, sensorimotor peripheral neuropathy in individuals with AUD. However, the most recent and highest quality study 1 provides the strongest evidence for the development and treatment of this condition.
From the Research
Pathogenesis of Alcohol Use Disorder (AUD) related Peripheral Neuropathy
The development of length-dependent, axonal, sensorimotor peripheral neuropathy in individuals with Alcohol Use Disorder (AUD) is a complex process, involving multiple mechanisms. Some of the possible explanations include:
- Activation of spinal cord microglia after chronic alcohol consumption, oxidative stress leading to free radical damage to nerves, activation of mGlu5 receptors in the spinal cord and activation of the sympathoadrenal and hypothalamo-pituitary-adrenal (HPA) axis 2
- Nutritional deficiency, especially thiamine deficiency, and/or the direct toxic effect of alcohol or both 2, 3
- Direct neurotoxic effects of ethanol on peripheral nerves, as suggested by an experimental model of alcohol-related peripheral neuropathy 4
Characteristics of Alcohol-related Peripheral Neuropathy
Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy 3. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% when confirmed via nerve conduction studies 3. 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 3.
Diagnosis and Assessment of Alcohol-related Peripheral Neuropathy
Peripheral neuropathy involving large and small nerve fibers, with a symmetrical length-dependent pattern, is common among patients with AUD and related to the duration of the disorder 5. The Neuropathy Symptoms Score (NSS) and the Neuropathy Impairment Score (NIS) scales could be used for the assessment of neuropathy in clinical practice, when the essential neurophysiological testing is not available 5. Skin biopsy is a useful, minimally invasive biomarker that could extend studies to understand the effect of alcohol on the peripheral nerves and to evaluate potential therapeutic agents in larger clinical trials 6.