Alcoholic polyneuropathy (A.K.A feet of alcohol ) is a neurological disorder in which the entire peripheral nerves are simultaneously damaged. It is defined by axonal degeneration in sensory and motor system neurons and initially occurs at the distal end of the longest axon in the body. This nerve damage causes an individual to experience motor pain and weakness, first in the legs and hands and then develop centrally. Alcoholic polyneuropathy is primarily caused by chronic alcoholism; however, vitamin deficiency is also known to contribute to its development. This disease usually occurs in chronic alcoholics who have some kind of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and non-alcohol use.
Video Alcoholic polyneuropathy
Signs and symptoms
Alcoholic polyneuropathy usually has a gradual onset for months or even years although axonal degeneration often begins before a person develops any symptoms. Early warning signs (prodrome) from the possibility of developing alcoholic polyneuropathy, especially in chronic alcoholics, is weight loss because this usually indicates a nutritional deficiency that can lead to disease progression.
This disease usually involves sensory and motor loss, as well as painful physical perception (paresthesia), although all sensory modalities may be involved. Symptoms affecting the sensory and motor systems appear to be growing symmetrically. For example, if the right foot is affected, the left leg will be affected simultaneously or immediately affected. In most cases, the legs are affected first, followed by the arm. The hands usually become involved when the symptoms reach above the ankle. This is called the sensory-and-glove distortion pattern.
Polyuropathy covers varying degrees of severity. Some cases appear to be asymptomatic and can only be recognized on careful examination. The most severe cases can cause deep physical defects.
Sensoric
Common manifestations of sensory problems include numbness or painful sensations in the arms and legs, abnormal sensations such as "pins and needles", and heat intolerance. The pain experienced by an individual depends on the severity of the polyneuropathy. It may be tedious and constant in some individuals while sharp and lancinating in others. In many subjects, tenderness is seen in muscle palpitations in the legs and feet. Certain people may also feel the sensation of cramps in the affected muscles and others say there is a burning sensation in their legs and calves.
Motor
Sensory symptoms are gradually followed by motor symptoms. Motor symptoms may include muscle cramps and weakness, erectile dysfunction in men, urinary problems, constipation, and diarrhea. Individuals may also experience muscle wasting and decreased or loss of deep tendon reflexes. Some people may experience frequent falls and run unstable due to ataxia. This ataxia can be caused by cerebellar degeneration, sensory ataxia, or distal muscle weakness. Over time, alcoholic polyneuropathy can also cause difficulty swallowing (dysphagia), speech disorders (dysarthria), muscle spasms, and muscle atrophy.
In addition to alcoholic polyneuropathy, individuals may also exhibit other related disorders such as Wernicke-Korsakoff syndrome and cerebellar degeneration resulting from an alcohol-related nutritional disorder.
Maps Alcoholic polyneuropathy
Cause
The common cause of this disease is prolonged and heavy alcohol consumption accompanied by nutritional deficiencies. There is some debate as to whether the main cause is the direct toxic effect of the alcohol itself or whether the disease is the result of alcohol-related malnutrition.
Often alcoholics have disrupted social relationships in their lives and have an irregular lifestyle. This can cause alcohol to change their eating habits including more missed food and poor food balance. Alcoholism can also cause loss of appetite, alcohol gastritis, and vomiting, which reduces food intake. Alcohol abuse damages the lining of the gastrointestinal system and reduces nutrient absorption. The combination of these can lead to nutritional deficiencies associated with the development of alcoholic polyneuropathy.
There is evidence that providing individuals with adequate vitamins improves symptoms despite continued alcohol intake, suggesting that vitamin deficiency may be a major factor in the development and development of alcoholic polyneuropathy. In the experimental model of alcoholic polyneuropathy using rats and apes did not yield convincing evidence that proper nutrient intake along with alcohol resulted in polyneuropathy.
In addition, alcohol consumption can lead to accumulation 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 it is possible that ethanol (or its metabolites) may cause alcoholic polyneuropathy. There is evidence that polyneuropathy is also prevalent in good nutritious alcoholics, supporting the idea that there is a direct toxic effect of alcohol.
Many studies conducted observing polyneuropathy alcohol in patients are often criticized because their criteria are used to assess malnutrition in the subject because they may not completely rule out the possibility of nutritional deficiencies in the origins of polyneuropathy. Many researchers like the nutritional origin of the disease, but the possibility of alcohol having a toxic effect on peripheral nerves has not been completely ruled out.
Pathophysiology
The pathophysiology of alcoholic polyneuropathy is the current field of research. Damage to the nervous system occurs before symptoms appear in individuals, beginning with segmental depletion and loss of myelin at the peripheral end of the longest nerve. Segmental thinning is the demyelination of axons in small parts at a time. This incident increases the leakage of potential action flowing into the axon, so this is very weak at the peripheral end. The current decrease in causes of myelin depletion.
In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency. Alcohol, carbohydrates, increases metabolic demand for thiamine (vitamin B1) because of its role in glucose metabolism. Tiamina levels are usually low in alcoholics because they reduce nutritional intake. In addition, alcohol interferes with the absorption of thiamine intestinal, thereby further lowering thiamine levels in the body. Thiamin is important in three reactions in glucose metabolism: decarboxylation of pyruvic acid, d-ketoglutarate acid, and transketolase. The lack of thiamine in the cells therefore can prevent neurons from maintaining the level of adenosine triphosphate (ATP) required as a result of glycolosis disorders. Thiamine deficiency alone may explain the impaired neural conduction in those with alcoholic polyneuropathy, but other factors may play a role.
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 alcoholic. This deficiency will also disrupt glycolosis and alter the metabolism, transport, storage, and activation of important nutrients.
Malnutrition of many alcoholics robs them of the cofactors essential for the oxidative metabolism of glucose. Neural networks rely on this process for energy, and cycle disruption will damage cell growth and function. Schwann cells produce myelin that wraps the sensory and motor nervous axons to increase the conduction potential action at the periphery. Lack of energy in Schwann cells will explain the loss of myelin in peripheral nerves, which can result in axon damage or loss of nerve function altogether. In peripheral nerves, the activity of oxidative enzymes is most concentrated around the Ranvier node, making this location most vulnerable to cofactor deprivation. The lack of important cofactors reduces myelin impedance, increases leakage current, and slows down signal transmission. Interference in the first conductance affects the peripheral end of the longest and largest peripheral nerve fibers as they suffer most from the decreased potential of action propagation. Thus, nerve damage occurs in an accelerating cycle: myelin damage reduces the conductance, and reduces the conductance contributing to myelin degradation. The slowing conduction of the action potential in the axon causes segmental demyelination to proximal lengthwise; this is also known as retrograde degeneration.
Acetaldehyde is toxic to peripheral nerves. There is an increase in the levels of acetaldehyde produced during ethanol metabolism. If acetaldehyde is not metabolized rapidly, nerves may be affected by the accumulation of acetaldehyde to toxic levels.
Diagnosis
Alcoholic polyneuropathy is very similar to other axonal degenerative polyneuropathies and is therefore difficult to diagnose. When alcoholics have sensorimotor polyneuropathy as well as nutritional deficiencies, the diagnosis of alcoholic polyneuropathy is often achieved.
To confirm the diagnosis, doctors should rule out other causes of similar clinical syndromes. Other neuropathies can be distinguished on the basis of typical clinical or laboratory features. The differential diagnosis for alcoholic polyneuropathy includes amyotrophic lateral sclerosis, beriberi, Charcot-Marie-Tooth disease, diabetic lumbosacral plexopathy, Guillain Barre Syndrome, diabetic neuropathy, multiplex mononeuritis and post-polio syndrome.
To clarify the diagnosis, medical examinations most often involve laboratory tests, although, in some cases, imaging, neural conduction research, electromyography, and vibrometer testing may also be used.
A number of tests can be used to rule out other causes of peripheral neuropathy. One of the first symptoms of diabetes mellitus may be peripheral neuropathy, and hemoglobin A1C can be used to estimate average blood glucose levels. Increased blood creatinine levels may indicate renal insufficiency and may also be the cause of peripheral neuropathy. Screen toxicity of heavy metals should also be used to rule out lead toxicity as a cause of neuropathy.
Alcoholism is usually associated with nutritional deficiencies, which may contribute to the development of alcoholic polyneuropathy. Thiamine, vitamin B-12, and folic acid are vitamins that play an important role in the peripheral and central nervous system and must be among the first to be analyzed in laboratory tests. It has been difficult to assess thiamine status in individuals because of difficulties in developing methods to directly assess thiamine in blood and urine. Liver function tests may also be ordered, as alcohol consumption may lead to elevated liver enzyme levels.
Management
Although there is no known cure for alcoholic polyneuropathy, there are a number of treatments that can control symptoms and increase independence. Physical therapy is useful for weakened muscle strength training, as well as for walking and balance exercises.
Nutrition
To manage symptoms well, not consuming alcohol is very important. Abstinence from alcohol encourages proper diet and helps prevent the development or recurrence of neuropathy. Once a person stops consuming alcohol, it is important to ensure that they understand that substantial recovery is usually not seen for several months. Some subjective improvements may appear immediately, but this is usually due to the overall benefit of alcohol detoxification. If alcohol consumption continues, vitamin supplementation alone is not sufficient to improve the symptoms of most individuals.
Nutritional therapy with parenteral multivitamins is useful for application until the person can maintain adequate nutritional intake. Treatment also includes vitamin supplements (especially thiamine). In more severe cases of nutritional deficiency 320 mg/day benfotiamine for 4 weeks followed by 120 mg/day for 4 weeks may be prescribed in an attempt to restore thiamine levels to normal.
Pain
The painful dis- sessions caused by alcoholic polyneuropathy can be treated using gabapentin or amitriptyline in combination with over-the-counter pain medications, such as aspirin, ibuprofen, or acetaminophen. Tricyclic antidepressants such as amitriptyline, or carbamazepine can help relieve pain and have anticholinergic effects and central and peripheral sedatives. These agents have a central effect on the transmission of pain and block the active reuptake of norepinephrine and serotonin.
Anticonvulsant drugs such as gabapentin block the active reuptake of norepinephrine and serotonin and have properties that alleviate neuropathic pain. However, these drugs take several weeks to become effective and rarely used in the treatment of acute pain.
Topical analgesics such as capsaicin also can relieve mild pain and muscle and joint pain.
Prognosis
It is difficult to assess the patient's prognosis as it is difficult to convince a chronic alcoholic to not drink alcohol completely. It has been shown that a good prognosis can be given for mild neuropathy if alcoholics do not drink for 3-5 years. During the early stages of the disease, the damage appears reversible when people take adequate amounts of vitamins, such as thiamine. If polineuropathy is mild, individuals usually experience improvement and significant symptoms can be completely eliminated within weeks until months after proper nutrition is established. When people who are diagnosed with alcoholic polyneuropathy undergo recovery, it is considered the result of regeneration and increased collateral axon is damaged.
As disease develops, damage can become permanent. In the case of severe thiamine deficiency, some positive symptoms (including neuropathic pain) can persist indefinitely. Even after restoring a balanced nutritional intake, patients with severe or chronic polyneuropathy may experience lifelong sequelae. Alcoholic polyneuropathy is not life-threatening but can significantly affect a person's quality of life. The effects of the disease range from mild discomfort to severe disability.
Epidemiology
The incidence rate of alcoholic polyneuropathy involving sensory and motoric polyneuropathy varies from 10% to 50% alcoholic depending on subject selection and diagnostic criteria. If electrodiagnostic criteria are used, alcoholic polyneuropathy can be found in up to 90% of the individuals assessed. The distribution and severity of the disease depends on regional eating habits, individual drinking habits, and individual genetics. Major studies have been conducted and show that the severity and incidence of polyneuropathy alcohol correlates best with total lifetime alcohol consumption. Factors such as nutritional intake, age, or other medical conditions are correlated in a lower degree. For unknown reasons, alcoholic polyneuropathy has a high incidence in women.
Certain alcoholic beverages may also contain congeners that may also be bioactive; Therefore, the consumption of various alcoholic beverages can result in different health consequences. Individual nutritional intake also plays a role in the progression of this disease. Depending on certain dietary habits, they may have a deficiency of one or more of the following: thiamine (vitamin B1), pyridoxine (vitamin B6), pantothenic acid and biotin, vitamin B12, folic acid, niacin (vitamin B3), and vitamin A.
Acetaldehyde
It is also estimated that there is a genetic tendency for some alcoholics that result in increased frequency of alcoholic polyneuropathy in certain ethnic groups. During the body process of alcohol, ethanol is oxidized to acetaldehyde primarily by alcohol dehydrogenase; acetaldehyde is then oxidized to acetate primarily by aldehyde dehydrogenase (ALDH). ALDH2 is an isozyme ALDH and ALDH2 has polymorphism (ALDH2 * 2, Glu487Lys) which makes ADLH2 inactive; This allele is more common between Southeast and East Asia and results in a failure to metabolize acetaldehyde rapidly. The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of alcoholic polyneuropathy.
History
The first description of symptoms associated with alcoholic polyneuropathy was recorded by John C. Lettsome in 1787 when he recorded hyperesthesia and paralysis in the legs over the patient's arm. Jackson has also been credited with describing polyneuropathy in chronic alcoholics in 1822. The clinical title of alcoholic polyneuropathy was widely recognized by the late nineteenth century. It is thought that polyneuropathy is a direct result of the toxic effects of alcohol on peripheral nerves when used overload. In 1928, George C. Shattuck argued that polyneuropathy is caused by vitamin B deficiency that is usually found in alcoholics and he claims that alcoholic polyneuropathy should be related to beriberi. This debate continues today about what exactly causes this disease, some argue that it is just alcohol poisoning, others claim the vitamin deficiency is to blame and others say it is a combination of the two.
Direction of research
The axonal degeneration mechanism has not been clarified and is an area of ​​continuous research on alcoholic polyneuropathy.
Further research is looking at the effects of alcohol consumption and the choice of alcoholic beverages on the development of their alcoholic polyneuropathy. Some drinks may include more nutrients than others (such as thiamine), but the effect of this is related to helping with undernourishment in alcoholics is unknown.
There is still controversy about the reasons for the development of alcoholic polyneuropathy. Some argue it is a direct result of the toxic effects of alcohol on the nerves, but others say factors such as malnutrition or chronic liver disease can play a role in development as well. This debate is ongoing and research continues in an effort to find the real cause of alcoholic polyneuropathy.
References
Source of the article : Wikipedia
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