In addition, patients with chronic alcoholism tend to consume smaller amounts of essential nutrients and vitamins and/or exhibit impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol. These relationships make chronic alcoholism a risk factor for thiamine deficiency. In addition to thiamine deficiency, recent studies indicate a direct neurotoxic effect of ethanol or its metabolites. Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5]. Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol [6, 13]. The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed.
Alcohol-Related Neurologic Disease
Not only mGluRs but ionotropic glutamate (NMDA) receptors are also involved in alcoholic-induced neuropathic pain. Many different stimuli, including growth factors, cytokines, viral infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. There are many studies alcohol neuropathy stages suggesting the role of MEK/ERK signaling in inflammatory pain in male [60–63] and female rats [64]. The primary axonal damage and secondary demyelination of motor and sensory fibres (especially small diameter fibres) are considered to constitute the morphologic basis of alcoholic damage to nerve tissue at present [20].
Nutritional factors responsible for alcoholic neuropathy (indirect toxicity)
Other findings showed that decreased activity of aldehyde dehydrogenase leads to peripheral neuropathy [76, 91]. Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy. Chronic alcoholism can alter the intake, absorption and utilization of various nutrients (nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate or vitamin E). Thus, these vitamin deficiencies were not considered to be major causal factors of neuropathy [26]. Alcoholic neuropathy is nerve damage that results from the toxic effect of alcohol on nerves. Alcohol-induced peripheral neuropathy is a common complication of alcohol use disorder.Excess alcohol consumption can also result in malnutrition and vitamin deficiencies that have a damaging effect on nerves.
Alcoholism and Alcoholic Neuropathy
Early diagnosis and treatment can help increase your chances of fully recovering. Symptoms of alcohol-related neuropathy are similar to those of peripheral neuropathy. These can affect both your controlled and involuntary movements, as well as sensations. Alcoholism, now called alcohol use disorder (AUD), is a condition in which you have difficulty stopping or managing your alcohol intake despite experiencing negative consequences. Alcoholic neuropathy is a condition in which drinking too much alcohol causes damage to nerve tissue. The use of warm or hot footbaths is a potential hazard in alcoholic neuropathy, because such treatment may cause burns to a patient with an insensate extremity.
Signs and symptoms of alcoholic neuropathy
- Autonomic nerves are concerned with muscular functions which are reflexive, such as breathing, heartbeats and peristalsis (rhythmic movements of the intestines).
- But if you have developed neuropathy as a result of alcohol use, it’s important to stop drinking as soon as possible.
- Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153].
- In a similar study, SSR was used to assess the number of reactive sweat glands (SGN), which turned out to be decreased in alcohol-dependent patients [164].
- A mechanism of cisplatin chemotherapy-induced peripheral neuropathy was elucidated in an in vitro mouse model.
- The available data addressing the role of hepatic dysfunction is presently inconclusive.
Alcohol also alters the function of the stomach, liver, and kidneys in ways that prevent the body from properly detoxifying waste material. This waste then builds up and harms many regions of the body, including the nerves. There’s no exact timeframe for how quickly alcohol-related neuropathy develops. However, stopping consuming alcohol sooner can help stop the progression of nerve damage. It’s important to speak with a healthcare professional if you experience any symptoms of peripheral neuropathy.
Avoiding excessive amounts of alcohol is the primary way to prevent alcoholic neuropathy. If you notice you are developing signs of alcoholic neuropathy (such as numbness after drinking alcohol), in addition to seeing a physician, try to stay away from alcohol altogether. If you are having difficulty avoiding alcohol, there are resources that can help you quit.
Benfotiamine for the treatment of alcohol related peripheral neuropathy
These include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy. The goal of treatment is to impede further damage to the peripheral nerves while also restoring their normal physiology. The journal further reports that alcoholic polyneuropathy is likely caused by nutritional deficiencies and the depletion of thiamine that is caused by heavy and long-term drinking.
How soon does alcoholism cause neuropathy?
It also discusses treatment options, including how to get help for alcohol use disorder. It is likely to get worse if the person continues to use alcohol or if nutritional problems are not corrected. Alcoholic neuropathy is usually not life threatening, but it can severely affect quality of life. Medicines may be needed to treat pain or uncomfortable sensations due to nerve damage.