Alcoholic polyneuropathy

Alcoholic polyneuropathy
Other names	Alcohol leg
An illustration of a neuron's structure. In alcoholic polyneuropathy myelin loss and axonal degeneration occurs.
Specialty	Neurology

Alcoholic polyneuropathy is a

An early warning sign (prodrome) of the possibility of developing alcoholic polyneuropathy, especially in a chronic alcoholic, would be weight loss because this usually signifies a nutritional deficiency that can lead to the development of the disease.^[1]

Alcoholic polyneuropathy usually has a gradual onset over months or even years, although axonal degeneration often begins before an individual experiences any

Sensory

Common manifestations of sensory issues include numbness or painful sensations in the arms and legs, abnormal sensations like "pins and needles," and heat intolerance.^[5] Pain experienced by individuals depends on the severity of the polyneuropathy. It may be dull and constant in some individuals while being sharp and lancinating in others.^[4] In many subjects, tenderness is seen upon the palpitation of muscles in the feet and legs.^[1] Certain people may also feel cramping sensations in the muscles affected and others say there is a burning sensation in their feet and calves.^[4]

Motor

Sensory symptoms are gradually followed by motor symptoms.

In addition to alcoholic polyneuropathy, the individual may also show other related disorders such as Wernicke–Korsakoff syndrome and cerebellar degeneration that result from alcoholism-related nutritional disorders.^[1]

Severity

Polyneuropathy spans a large range of severity. Some cases are seemingly asymptomatic and may only be recognized on careful examination. The most severe cases may cause profound physical disability.^[1]

Causes

The general cause of this disease appears to be prolonged and heavy consumption of alcohol accompanied by a nutritional deficiency. However, there is ongoing debate over the active mechanisms,^[6][7] including whether the main cause is the direct toxic effect of alcohol itself or whether the disease is a result of alcoholism-related malnutrition.^[1] A 2019 metastudy found that the relationship between ethanol toxicity and neuropathy remained unproven.^[8]

Effects due to nutritional deficiency

Frequently alcoholics have disrupted social links in their lives and have an irregular lifestyle. This may cause an alcoholic to change their eating habits including more missed meals and a poor dietary balance.

There is evidence that providing individuals with adequate vitamins improves symptoms despite continued alcohol intake, indicating that vitamin deficiency may be a major factor in the development and progression of alcoholic polyneuropathy.[2] In experimental models of alcoholic polyneuropathy utilizing rats and monkeys no convincing evidence was found that proper nutritional intake along with alcohol results in polyneuropathy.^[1]

In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency. Alcohol, a

Many of the studies conducted that observe alcoholic polyneuropathy in patients are often criticized for their criteria used to assess nutritional deficiency in the subjects because they may not have completely ruled out the possibility of a nutritional deficiency in the genesis of the polyneuropathy.[1] Many researchers favor the nutritional origin of this disease, but the possibility of alcohol having a toxic effect on the peripheral nerves has not been completely ruled out.^[1]

Effects due to alcohol ingestion

The consumption of alcohol may lead to the buildup of certain toxins in the body. For example, in the process of breaking down alcohol, the body produces acetaldehyde, which can accumulate to toxic levels in alcoholics. This suggests that there is a possibility ethanol (or its metabolites) may cause alcoholic polyneuropathy.^[4] There is evidence that polyneuropathy is also prevalent in well nourished alcoholics, supporting the idea that there is a direct toxic effect of alcohol.^{[citation needed]}

The metabolic effects of liver damage associated with alcoholism may also contribute to the development of alcoholic polyneuropathy. Normal products of the liver, such as lipoic acid, may be deficient in alcoholics. This deficiency would also disrupt glycolysis and alter metabolism, transport, storage, and activation of essential nutrients.^[2]

Acetaldehyde is toxic to peripheral nerves. There are increased levels of acetaldehyde produced during ethanol metabolism. If the acetaldehyde is not metabolized quickly the nerves may be affected by the accumulation of acetaldehyde to toxic levels.^[4][12]

Pathophysiology

The pathophysiology of alcoholic polyneuropathy is unclear.^[12]

Diagnosis

Alcoholic polyneuropathy is very similar to other

To clarify the diagnosis, medical workup most commonly involves laboratory tests, though, in some cases, imaging, nerve conduction studies, electromyography, and vibrometer testing may also be used.^[3]

A number of tests may be used to rule out other causes of peripheral neuropathy. One of the first presenting symptoms of

Although there is no known cure for alcoholic polyneuropathy, there are a number of treatments that can control symptoms and promote independence. Physical therapy is beneficial for strength training of weakened muscles, as well as for gait and balance training.^[3]

Nutrition

To best manage symptoms, refraining from consuming alcohol is essential. Abstinence from alcohol encourages proper diet and helps prevent progression or recurrence of the neuropathy.^[13] Once an individual stops consuming alcohol it is important to make sure they understand that substantial recovery usually isn't seen for a few months. Some subjective improvement may appear right away, but this is usually due to the overall benefits of alcohol detoxification.^[11] If alcohol consumption continues, vitamin supplementation alone is not enough to improve the symptoms of most individuals.^[4]

Nutritional therapy with

Anticonvulsant drugs like gabapentin or pregabalin block the active reuptake of norepinephrine and serotonin and have properties that relieve neuropathic pain. However, these medications take a few weeks to become effective and are rarely used in the treatment of acute pain.^[3]

Alcoholic polyneuropathy is not life-threatening but may significantly affect one's quality of life. Effects of the disease range from mild discomfort to severe disability.[5]

It is difficult to assess the prognosis of a patient because alcohol dependence results in difficulty maintaining abstinence from drinking alcohol. It has been shown that a good prognosis may be given for mild neuropathy if the person has abstained from drinking for 3–5 years.^[12]

Early stage

During the early stages of the disease the damage appears reversible when people take adequate amounts of vitamins, such as thiamine.^[2] If the polyneuropathy is mild, the individual normally experiences a significant improvement and symptoms may be eliminated within weeks to months after proper nutrition is established.^[1] When those people diagnosed with alcohol polyneuropathy experience a recovery, it is presumed to result from regeneration and collateral sprouting of the damaged axons.^[4]

Progressed disease

As the disease progresses, the damage may become permanent. In severe cases of thiamine deficiency, a few of the positive symptoms (including neuropathic pain) may persist indefinitely.^[12] Even after the restoration of a balanced nutritional intake, those patients with severe or chronic polyneuropathy may experience lifelong residual symptoms.^[1]

Epidemiology

In 2020 the NIH quoted an estimate that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy.^[7] The rate of incidence of alcoholic polyneuropathy involving sensory and motor polyneuropathy has been stated as from 10% to 50% of alcoholics depending on the subject selection and diagnostic criteria. If electrodiagnostic criteria are used, alcoholic polyneuropathy may be found in up to 90% of individuals being assessed.^[4]

The distribution and severity of the disease depends on regional dietary habits, individual drinking habits, as well as an individual's genetics.^[12] Large studies have been conducted and show that alcoholic polyneuropathy severity and incidence correlates best with the total lifetime consumption of alcohol. Factors such as nutritional intake, age, or other medical conditions are correlate in lesser degrees.^[11] For unknown reasons, alcoholic polyneuropathy has a high incidence in women.^[4]

Certain alcoholic beverages can also contain

It is also thought there is perhaps a genetic predisposition for some alcoholics that results in increased frequency of alcoholic polyneuropathy in certain ethnic groups. During the body's processing of alcohol, ethanol is oxidized to acetaldehyde mainly by alcohol dehydrogenase; acetaldehyde is then oxidized to acetate mainly by aldehyde dehydrogenase (ALDH). ALDH2 is an isozyme of ALDH and ALDH2 has a polymorphism (ALDH2*2, Glu487Lys) that makes ADLH2 inactive; this allele is more prevalent among Southeast and East Asians and results in a failure to quickly metabolize acetaldehyde. The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of alcoholic polyneuropathy.^[4][12]

History

In 2001 research directions included the effect that an alcoholics' consumption and choice of alcoholic beverage might have on their development of alcoholic polyneuropathy. Some beverages may include more nutrients than others (such as thiamine), but the effects of this with regards to helping with a nutritional deficiency in alcoholics is yet unknown.[10]

Research also continued on reasons for the development of alcoholic polyneuropathy. Some argue it is a direct result of alcohol's toxic effect on the nerves, but others say factors such as a nutritional deficiency or chronic liver disease may play a role in the development as well. Multiple mechanisms may be present.^[11]

References