These functions are achieved by PKC mediated phosphorylation of other proteins [16]. Apart from above function, over-activation of epsilon form of protein kinase C (PKCε) is known to be involved in mediating neuropathic pain, such as pain induced by cancer chemotherapy (vincristine) [56] and diabetes [57]. PKC and protein kinase A (PKA) are both known to be important in nociceptor function [57–59]. There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy. Dina et al. [16] maintained rats on a diet to simulate chronic alcohol consumption in humans and found mechanical hyperalgesia by the fourth week which was maximal at 10 weeks.
Malnutrition and Micronutrients Deficiency
- Thus, ALN might be induced by the combination of the effects of the direct activity of alcohol metabolites on the nerve fibers along with nutritional deficiencies primarily in a form of thiamine deficiency.
- Recently findings from our laboratory also suggest the benefecial effects of both α-tocopherol and tocotrienol, isoforms of vitamin E, in the prevention of hyperalgesia and allodynia in rats administered ethanol for 10 weeks [55].
- Also, the results of the group of 32 patients with non-alcoholic thiamine deficiency neuropathy were considered.
Alcohol causes neuropathy via multifactorial processes, many of which are still under investigation. Alcohol enters the bloodstream from the digestive system within 5 minutes of consumption, and peak absorption is seen within 30 to 90 minutes. One of the many inhibitory effects of chronic alcohol use is malnutrition. Patients who abuse alcohol tend to consume fewer calories and have poor absorption of nutrients in the gastrointestinal tract. There are also direct toxic effects of alcohol and its metabolites on neurons, affecting cellular cytoskeletons and demyelination of neurons. Spinal cord glial cells are implicated in the exaggerated pain state created by diverse manipulations such as subcutaneous inflammation, neuropathy and spinal immune activation [65, 66].
How soon does alcoholism cause neuropathy?
This study showed that as well as thiamine replacement, corrections of low circulating levels of nicotinic acid, pantothenic acid and vitamin B6 can result in an improvement of alcohol-related peripheral neuropathies. Alcohol-related neuropathy is a condition caused by consuming large amounts of alcohol over a long period. The toxic effects of alcohol may damage your peripheral nerves, which play a role in movement and sensation. Alcohol abuse contributes to peripheral neuropathy development involving both somatic and autonomic nerves [154, 155]. However, impairments of autonomic functions are scarcer and less intensified, and, usually, clinical symptoms are delayed [156].
Enhancing Healthcare Team Outcomes
- 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.
- When speaking with a doctor, a person should be honest about how much alcohol they consume.
- It’s important to share any history of alcohol use with the doctor to receive an accurate diagnosis.
- Once alcohol use has been addressed, a doctor can focus on treating alcohol-related neuropathy itself.
- It is important to stop drinking if you suffer from alcoholic polyneuropathy in order to stop the disease from getting worse and to correct the nutritional imbalance that is damaging the nerves and interfering with the nervous system.
The morphological basis of post-alcoholic damage of neural tissue includes primary axonopathy and secondary demyelination of motor and sensory (especially small) fibers [105]. Demyelination is probably the effect of axoplasmic transmission slowdown; such degeneration so-called dying back bears semblance to Wallerian degeneration [64, 84]. An animal study on axonal transport in vitro using dorsal roots of the sciatic nerve showed decreased axonal transmission after long-term ethanol consumption [106].
Signs and symptoms of alcoholic neuropathy
It is most likely that drinking a lot of alcohol over several years causes direct damage to nerve cells and can also contribute to nutritional deficiencies in the body; these may both be factors in the onset of alcoholic polyneuropathy. Protein kinase C (PKC) is a family of protein kinases consisting of approximately 10 isozymes. PKC is involved in receptor desensitization, modulating membrane structure events, regulating transcription, mediating immune responses, regulating cell growth and in learning and memory.
In total, 585 papers did not meet the inclusion/exclusion criteria and were excluded. By scanning the reference lists of included studies, an additional 4 papers were identified. This study is reported in accordance with the preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines [7]. Statistical calculation of pooled proportions was conducted in R language, using the default settings of the “meta” package and the “metaprop” function with a random effects model [8].
Alcohol-Related Neurologic Disease
If it affects two or more nerves in different areas, it’s called multiple mononeuropathy, and if it affects many nerves, it’s called polyneuropathy. Many deaths were attributed to strokes, since heavy alcohol consumption is a significant risk factor for stroke. Many theories have been raised as to the cause of alcohol-related peripheral neuropathy (ALN). While nutritional deficiencies can contribute to progression of ALN, these are not the primary cause leading to neuropathy.
Further, ECG changes and functions of the digestive tract (dyspeptic symptoms, stomach and gallbladder motility, orocecal transit time) can also be assessed [162, 165]. PCT seems to be valuable due to the correlation between prolongation of pupil oscillation and exacerbations alcohol neuropathy stages of cardiovascular symptoms which presents the colinear involvement of parasympathetic division of ANS. Early alcoholic neuropathy, usually presenting as sensory symptoms in the extremities, is reversible if the patient stops drinking and establishes proper nutrition.
As axons break down, the nerve fibers become less dense and cannot function properly. Based upon these results, vitamin supplementation appears to exert a positive therapeutic effect in alcohol-related neuropathy. The mechanism of this is presently unclear, one possible explanation is that is resolves concomitant vitamin-dependent neuropathy which exacerbates alcohol-related neuropathy.
- Someone who struggles with alcoholism may replace meals with alcohol, take in a lot of empty calories, and not maintain a healthy and balanced diet.
- Regarding the parasympathetic division of ANS, most of the studies are focused on the assessment of nerve conduction mainly in oculomotor and vagus nerves; these include pupil cycle time (PCT) and cardiovascular reflex tests correspondingly [160].
- Another prominent effect of alcoholic neuropathy involves painful and uncomfortable sensations.
- The evidence of positive dynamics at peripheral and segmental nerve system level was supported by neurophysiological data.
- To assess the bias in these we applied the Jadad score which takes into consideration quality of randomisation and blinding as well as reporting of withdrawals to assess bias in RCTs [9].