PN is damage to one or more peripheral nerves, leading to sensory, motor, and autonomic dysfunction. The prevalence of PN ranges from 2.4% to 8% per 100,000 individuals worldwide. The Foundation for Peripheral Neuropathy and the US Food and Drug Administration estimate that 20 million people in the US experience PN. Alcohol-induced peripheral neuropathy (PN) is a chronic and painful condition in which the neurotoxic effects of alcohol and nutritional deficiencies cause a pathologic response in nerve function.
- Vigilant foot care and the use of shoes with an enlarged toe box are useful in preventing foot ulcers.
- Chronic abuse of alcohol depletes the pool of liver proteins which are consumed for energy production and insufficient intake of proteins only worsens this imbalance.
- It may also be that comorbid hepatic dysfunction is a risk factor for alcohol-related peripheral neuropathy.
This can be achieved by complete alcohol abstinence and a balanced diet primarily supplemented by B6, B12, and E vitamins, as well as folate, thiamine, and niacin. Benzodiazepines are commonly used to reduce the symptoms of alcohol withdrawal syndrome; acamprosate and naltrexone are effective to treat alcohol dependence; however, the latter usually induces withdrawal symptoms . Further, serotonin-norepinephrine reuptake inhibitors are prescribed to treat alcohol-induced neuropathic pain via exerting antinociceptive properties by increasing serotonergic and noradrenergic neurotransmissions . In an animal model, Kaur et al. (2017) showed that curcumin and sildenafil administrated alone or in combination represent a therapeutic advantage in alcohol-induced neuropathic pain . The median and ulnar nerves are evaluated for motor function and the median, ulnar, and sural nerves are evaluated for sensory function.
Providing the Best Available Care for Patients with Neuropathy
Early diagnosis and treatment give you the best chance for controlling your symptoms and preventing further damage to your peripheral nerves. Early alcoholic neuropathy, usually presenting as sensory symptoms in the extremities, is reversible if the patient stops drinking and establishes proper nutrition. However, more severe cases may be intractable, even with abstinence, and lead to lifelong impairment. 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.
The following sections provide a brief overview of several neurologic conditions related to alcohol consumption. Thus, treatment with TCAs may provide symptomatic relief in patients with alcoholic neuropathy. Therefore, topical application with capsaicin may provide symptomatic relief from neuropathic pain in patients suffering from alcoholic neuropathy. The combined actions of catecholamines and glucocorticoids, via their receptors on sensory neurones, demonstrate a novel mechanism by which painful alcoholic neuropathy is induced and maintained. Autonomic nerve damage may cause a fluctuation in heart rate and BP, leading to orthostatic hypotension. Patients are likely to experience heat intolerance, excessive sweating, difficulty while swallowing, nausea, diarrhea, and constipation.
Alcoholic Neuropathy Treatment
However, if caught early enough, you can minimize the damage from alcoholic neuropathy. Avoiding alcohol and improving your diet can sometimes lead to a moderate to full recovery. Four studies addressed the management of patients with alcohol-related peripheral neuropathy.
Long-term heavy alcohol use, particularly when accompanied by nutritional deficiencies, can damage the body’s nerves, leading to a host of painful and debilitating symptoms. Alcoholic neuropathy can affect both sensory and motor nerves, causing pain, hypersensitivity, numbness, muscle weakness, and lack of coordination and fine motor controls, largely in the extremities. Thirteen studies provided data from the biopsy of the sural nerve or the skin in patients with alcohol-related peripheral neuropathy. Alcohol-related peripheral neuropathy alcoholic neuropathy recovery time appears to be characterised by severe loss of myelinated fibres; and although profound small fibre loss can also be present, this appears to occur more variably [3, 51, 53, 59, 85]. The data indicates that there is both small and large fibre loss in alcohol-related neuropathy, but that small fibre loss is generally predominant [3, 51, 53, 56, 59, 63, 86]. 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].
However, compared to males, the symptoms of excessive alcohol consumption manifest earlier in females [129, 130]. Alcohol-related liver cirrhosis may occur even a few years earlier in females compared to males . The prevalence of alcoholic cardiomyopathy appears to be similar among males and females; however, males present a higher disease burden [132, 133]. Furthermore, females tend to be more vulnerable to the brain damage and neurotoxic effects of alcohol . Computed tomography (CT) scans showed that among alcohol-dependent patients, the brain volumes were reduced to increase the volume of cerebrospinal fluid; these changes were induced in females in less time [135, 136]. The mouse model of the injection of β-estradiol in males resulted in higher activity of cytosolic alcohol dehydrogenase (ADH), microsomal aniline hydroxylase (ANH), and aldehyde dehydrogenase (ALDH) which are crucial in ethanol metabolism .
Thus, alpha-lipoic acid may have a potential in the treatment of patients with alcoholic neuropathy. Patients with neuropathic pain may be less mobile, predisposing them to conditions such as pneumonia, deep vein thrombosis, skin breakdown, muscle atrophy and weakness, and depression. Physical therapy should be included in the treatment plan to improve flexibility, strength, and balance.
Sexual drive and performance are diminished in both men and women, including erectile dysfunction in men. Patients may also have a deficiency in vitamin B12 (cobalamin), affecting the axon and causing muscle weakness, sensory disturbances, and anemia. Vitamin B9 (folic acid) levels tend to be decreased, reducing the density of small and large nerve fibers.
- Consult your doctor for more information about the symptoms of diabetic neuropathy and the treatment options available.
- As a result, new blood vessels begin to grow (a process called angiogenesis) as well as new nerve tissue (called neurogenesis) so that actual, physical restoration will follow.
- Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy.
- The National Institute on Alcohol Abuse and Alcoholism reports that 16 million people in the US have been diagnosed with alcohol use disorder (AUD).
Further research has confirmed the role of thiamine in the pathogenesis of ALN—the well-balanced diet and vitamin B1 supplementation significantly decreased the severity of ALN symptoms [147, 148]. However, the limitations of those studies include the lack of the possibility to measure the amount of vitamin B1 in the serum; further, patients who were involved in the study have received an unrefined form of the supplement. Later, the results have been supported by Victor and Adams (1961)—among 12 patients with ALN, neuropathic symptoms were alleviated just after thiamine supplementation, even though the alcohol consumption was previously completely reduced . Koike et al. (2003) compared clinical and histological differences between ALN with and without thiamine deficiency . Also, the results of the group of 32 patients with non-alcoholic thiamine deficiency neuropathy were considered. Thiamine deficiency resulted in the progression of sensory dysfunctions; further, histological examination of the sural nerves revealed the loss of small nerve fibers and segmental demyelination.
Red blood cells (RBCs) tend to be larger than normal (macrocytosis) and reduced in number from a deficiency in vitamin B9 or B12 or GI bleeding. There may be an increase in erythrocyte macrocytic volume because alcohol interferes with the development of normal RBCs. Glucose fluctuation, hyponatremia, hypokalemia, and hypomagnesemia are common features.
Abstinence can prevent the progression and reoccurrence of neuropathy and, after a few months, improve symptoms in some people. However, vulnerability to neuropathy and its severity and speed of progression varies. Women, continuous as opposed to episodic drinkers, and people with a family history of the disorder appear to be more vulnerable to alcoholic neuropathy and more severe presentations. Impotence, diarrhea, constipation, or other symptoms are treated when necessary.