Alcoholic Paralysis Health Article

Diseases and brain damage related to alcoholism

Wernicke-Korsakoff syndrome is caused by deficiency of the B-vitamin thiamine, and can also be seen in people who don't drink but have some other cause of thiamine deficiency, such as chronic vomiting, that prevents the absorption of this vitamin. Patients with this condition have the sudden onset of Wernicke encephalopathy; the symptoms include marked confusion, delirium, disorientation, inattention, memory loss, and drowsiness. Examination reveals abnormalities of eye movement, including jerking of the eyes (nystagmus) and double vision. Problems with balance make walking difficult. People may have trouble coordinating their leg movements, but usually not their arms. If thiamine is not given promptly, Wernicke encephalopathy may progress to stupor, coma, and death.

If thiamine is given and death averted, Korsakoff's syndrome may develop in some patients, who suffer from memory impairment that leaves them unable to remember events for a period of a few years before the onset of illness (retrograde amnesia) and unable to learn new information (anterograde amnesia). Most patients have very limited insight into their memory dysfunction and have a tendency to make up explanations for events they have forgotten (confabulation).

Severe alcoholism can cause cerebellar degeneration, a slowly progressive condition affecting portions of the brain called the anterior and superior cerebellar vermis causing a wide-based gait, leg incoordination, and an inability to walk heel-to-toe in tightrope fashion. The gait disturbance usually develops over several weeks, but may be relatively mild for some time, and then suddenly worsen after binge drinking or an unrelated illness.

Fetal alcohol syndrome

Fetal alcohol syndrome (FAS) occurs in infants born to alcoholic mothers when prenatal exposure to ethanol retards fetal growth and development. Alcohol is a known teratogen (an agent capable of causing physical abnormalities in developing fetuses) that affects both the infant's body and brain. It can cause this damage across the entire pregnancy, not just the first trimester. Affected infants often have a distinctive appearance with a thin upper lip, flat nose and mid-face, short stature and small head size. Almost half are mentally retarded, and most others are mildly impaired intellectually or have problems with speech, learning, and behavior.

Up to three births of every thousand in the industrialized countries of the world will produce a child born with FAS. This condition is considered more apt to occur following continuous, heavy alcohol intake by the mother, but has also been seen following intermittent or binge drinking. A study by Dr. John W. Olney, of Washington University School of Medicine, found that because brain cells building the connections necessary for memory, learning and thought begin to develop in the sixth month in-utero, one brief (four-hour) drinking binge during that period of time can damage millions of developing cells.

Causes and symptoms

Acute excess intake of alcohol can cause drunkenness (intoxication) or even death, and chronic or long-term abuse leads to potentially irreversible damage to virtually any level of the nervous system. Any given patient with long-term alcohol abuse may have no neurologic complications, a single alcohol-related disease, or multiple conditions, depending upon the genes they have inherited, how well nourished they are, and other environmental factors, such as exposure to other drugs or toxins.

Neurologic complications of alcohol abuse may also result from nutritional deficiency, because alcoholics tend to eat poorly and may become depleted of thiamine or other vitamins important for nervous system function. Persons who are intoxicated are also at higher risk for head injury or for compression injuries of the peripheral nerves. Sudden changes in blood chemistry, especially sodium, related to alcohol abuse may cause central pontine myelinolysis, a condition of the brainstem in which nerves lose their myelin coating. Liver disease complicating alcoholic cirrhosis may cause dementia, delirium, and movement disorder.

Alcoholic myopathy, or weakness secondary to breakdown of muscle tissue, is also known as alcoholic rhabdomyolysis or alcoholic myoglobinuria. Males are affected by acute (sudden onset) alcoholic myopathy four times as often as females. Breakdown of muscle tissue (myonecrosis) can come on suddenly during binge drinking or in the first days of alcohol withdrawal. In its mildest form, this breakdown may cause no noticeable symptoms, but may be detected by a temporary elevation in blood levels of an enzyme found predominantly in muscle, called the MM fraction of creatine kinase.

The severe form of acute alcoholic myopathy is associated with the sudden onset of muscle pain, swelling, and weakness; a reddish tinge in the urine caused by myoglobin, a breakdown product of muscle excreted in the urine; and a rapid rise in muscle enzymes in the blood. Symptoms usually worsen over hours to a few days, and then improve over the next week to 10 days as the patient is withdrawn from alcohol. Muscle symptoms are usually generalized, but pain and swelling may selectively involve the calves or other muscle groups. The muscle breakdown of acute alcoholic myopathy may be worsened by crush injuries, which may occur when people drink so much that they compress a muscle group with their body weight for a long time without moving, or by withdrawal seizures with generalized muscle activity.

In patients who abuse alcohol over many years, chronic alcoholic myopathy may develop. Males and females are equally affected. Symptoms include painless weakness of the limb muscles closest to the trunk and the girdle muscles, including the thighs, hips, shoulders, and upper arms. This weakness develops gradually, over weeks or months, without symptoms of acute muscle injury. Muscle atrophy, or decreased bulk, may be striking. The nerves of the extremities may also begin to break down, a condition known as alcoholic peripheral neuropathy, which can add to the person's difficulty in moving. Symptoms of peripheral neuropathy, too, typically develop slowly, over a period of months.

The way in which alcohol destroys muscle tissue is still not well understood. Proposed mechanisms include muscle membrane changes affecting the transport of calcium, potassium, or other minerals; impaired muscle energy metabolism; and impaired protein synthesis. Alcohol is metabolized (broken down) primarily by the liver, with a series of chemical reactions in which ethanol is converted to acetate. Acetate is metabolized by skeletal muscle, and alcohol-related changes in liver function may affect skeletal muscle metabolism, decreasing the amount of blood sugar available to muscles during prolonged activity. Because not enough sugar is available to supply needed energy, muscle protein may be broken down as an alternate energy source. However, toxic effects on muscle may be a direct result of alcohol itself rather than of its breakdown products.

Although alcoholic peripheral neuropathy may contribute to muscle weakness and atrophy by injuring the motor nerves controlling muscle movement, alcoholic neuropathy more commonly affects sensory fibers. Injury to these fibers can cause tingling or burning pain in the feet, which may be severe enough to interfere with walking. As the condition worsens, pain decreases but numbness increases.