Alcohol-Related Neurological Disease
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Alcohol-related neurological disease Definition Alcohol-related neurological disease represents a broad spectrum of conditions caused by acute or chronic alcohol intake. Description Alcohol, or ethanol, is a poisonous chemical that has direct and toxic effects on nerve and muscle cells. The effects can be profound, and symptoms can include incoordination, weakness, seizures , memory loss, and sensory deficits. Alcohol has a profoundly negative effect on both the central nervous system (i.e., the brain and spinal cord) and the peripheral nervous system (i.e., nerves that send impulses to peripheral structures such as muscles and organs). Alcohol can have negative effects on neurological centers that regulate body temperature, sleep, and coordination. Alcohol can significantly lower body temperature. It disrupts normal sleep patterns because it decreases rapid eye movement (REM) during the dreaming stage of sleep. It also adversely affects muscle coordination, causing imbalance and staggering—alcohol is a toxic insult to the cerebellum , which is responsible for balance. Additionally, the chronic use of alcohol can cause a broad spectrum of abnormalities in mental functioning. Generally, persons exhibit poor attention, difficulty with abstraction and problem solving, difficulty learning new materials, reduced visuospatial abilities (capacity to discriminate between two- dimensional or three-dimensional space), and often require extra time to integrate visual information. Other related problems include thiamine deficiency (vitamin B-1) and liver disease (liver cirrhosis and possibly liver cancer). Acute effects of alcohol When alcohol is ingested, it moves from the bloodstream into every part of the body that contains water, including the brain, lungs, kidneys, and heart. Alcohol distributes itself equally both inside and outside cells. Ninety-five percent of alcohol is eliminated from the body by breakdown in the liver, and 5% is eliminated through urine, sweat, and breath. Alcohol is broken down (metabolized) in the liver by a complex process called zero-order kinetics (broken down at a certain amount at a time). This means that alcohol is metabolized at a rate of 0.3 oz (8.8 ml) of pure ethanol per hour. Within moments after ingestion, alcohol reaches the brain and produces acute effects such as euphoria, sedation (calmness), anesthesia, and a sleepy hypnotic state. Further effects include release of inhibitions and judgment, blunting of sexual desire, aggressiveness, and mood changes. Physical effects of intoxication (with continued consumption) include impairment of motor ability, muscle function, eyesight, reaction time, night vision, and depth perception. Continued consumption can be lethal because alcohol can depress heart and lung function, which can slow breathing and circulation. Lethality occurs when levels are high enough to paralyze breathing. However, death due to alcohol consumption is rare because body defenses tend to eliminate the chemical by vomiting or the person becomes comatose. Alcohol "hangovers" usually cause persons to have headache (due to dilation of blood vessels in the head), dehydration (alcohol acts as a diuretic increasing urine output), and upset stomach (due to irritation of stomach lining). Specific neurological damage The effects of alcohol can include damage or impairment to brain systems and to specific regions in the brain. The limbic system, located deep inside the brain, has several functions, including memory. Long- term users of alcohol often exhibit memory loss due to damage of the limbic system structures called the amygdala and hippocampus, located in the temporal lobes. Damage to other parts of the limbic system can produce symptoms such as abnormalities in emotional functioning and in the ability to use one of the senses (e.g., eyesight or the sense of smell) or in the ability to learn using the senses (e.g., learning through the sense of touch). Damage to the diencephalon (major relay station for nerve signals moving within the brain, associated with memory functioning) occurs and is associated with chronic usage and malnutrition (a late-onset condition). The cerebral cortex (folded outer layer of the brain) is composed of nerve cells called gray matter, which functions as the center of intelligent behavior and higher consciousness. Neuroimaging studies reveal that there are definitive signs of morphological change such as cortical atrophy (a decrease in size of the cerebral cortex). Cortical atrophy induced by alcoholism is associated with deficits in spatial memory and visual associations, learning related to or caused by touch, and problem solving. Alcoholic subjects also exhibit a decrease in blood nourishing the frontal lobe (portion of the brain behind the forehead), whose functions include planning, carrying out, and monitoring goal-directed and socially acceptable behaviors. Neurotransmitter deficits and the progression of alcoholism Neurotransmitters are brain chemicals that allow nerve cells to communicate. These chemicals are released and picked up by specialized structures (receptors) in a space between nerve cells called a synapse. Alcohol can cause "up"-regulation or "down"-regulation effects on neurotransmitters. Over prolonged periods of alcohol abuse, the levels of receptors change. Genes that produce molecular copies of receptors may by turned off (decreasing activity) or on (increasing activity). Levels of glutamate (an amino acid that is an excitatory neurotransmitter in the brain) are abnormally altered. Glutamate is correlated with long-term potentiation (mechanism vital for learning and memory) in the brain. Even minute amounts of alcohol have profound effects on brain glutamate action. Interference with glutamate chemistry in the brain can cause memory impairment and may account for the short- lived condition called "blackouts." Because alcohol suppresses the excitatory effect of glutamate on nerve cells, this can result in strokes and seizures. Another neurochemical that is altered due to chronic intake of alcohol is gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain. Initially, alcohol increases the effects of GABA, which produces a state of mild sedation. Over time with continued abuse, the GABA system is down regulated and, when alcohol is not present in the system, the inhibitory effects are lost and overexcitation of the brain results. Alcoholism is a chronic disease, with a natural history that progresses to death if the intake does not completely stop. The progress consists of three stages. During the beginning stage, the alcoholic becomes dependent on the mood-altering effects of alcohol. In the middle stage, drinking starts earlier and there is tolerance (when more alcohol is needed to produce effects); during this stage, alcohol consumption is out of control and alcoholics frequently exhibit denial. Heavy consumption causes symptoms of anxiety, depression , fatigue , anger, rage, lack of self-esteem, and self-loathing. Symptoms worsen as the disease progresses, and alcoholics develop hand tremors and shaking (delirium tremens) and morning hangover. The final stages of alcoholism progress to round-the-clock consumption despite extremely negative personal and social consequences. The disease progresses with symptoms of intense guilt and remorse (suppressed by more drinking), fear of crowds and public places, financial debt, legal problems, and ill health (including malnutrition). Late-stage disease typically involves liver degeneration (cirrhosis) and severe, even life-threatening, clinical signs (shakes and convulsions) during withdrawal without treatment. Insanity due to brain damage or death may occur during this stage. Alcohol can cause thiamine deficiency (vitamin B-1). The Wernicke-Korsakoff syndrome is a late complication due to vitamin B deficiency, resulting from malnutrition. These alcoholics have a condition called hepatic encephalopathy , caused by diminished capacity of the liver to metabolize and detoxify chemicals in the body. Symptoms of Wernicke-Korsakoff syndrome include agitation, confusion, and altered personality. There is peripheral neuropathy (damage to peripheral nerves), which is symmetrical and affects the lower extremities. If untreated, this syndrome can further cause brain (cerebellum) degeneration, abnormal gait (walking), memory deficits (retrograde amnesia), and difficulty with abstract thinking and the acquisition of new learning (anterograde amnesia). Even if successfully treated with vitamin therapy, patients may still have amnesia (a condition called Korsakoff Syndrome). Fetal alcohol syndrome is a condition that occurs in infants born to alcoholic mothers. Prenatal exposure to alcohol can impair and retard fetal development and growth. Affected infants have a characteristic appearance that consists of a flat nose, flat mid face, small head size, short stature, and a thin upper lip. Approximately 50% are mentally deficient and most others exhibit intellectual deficits. Affected babies typically suffer from poor coordination, decreased adipose (fat) tissue, cleft palate, attention deficit hyperactivity disorder (ADHD), decreased muscle tone, heart defects, eye/ear defects, and smaller jaw. Alcoholic myopathy (disorder affecting muscle tissue) can be either acute (rapid onset of symptoms) or chronic (slower onset to develop symptoms). Acute alcoholic myopathy can involve symptoms such as muscular cramps, weakness, swelling, and tenderness in affected areas of muscle. Chronic