Alcohol–induced brain damage
Alcohol can damage the brain in many ways. The brain is vulnerable to the toxic effects of alcohol itself and can be affected by alcohol-related damage to other organs, including the liver, pancreas, and heart.
The risk of alcohol– induced brain damage and related neurobehavioral deficits varies from person to person and is influenced by factors such as age, gender, drinking history, and nutrition. In the U.S., up to 2 million individuals with alcoholism have permanent and debilitating conditions that require lifetime custodial care. Examples of such conditions include alcohol–induced persisting amnesic disorder (also called Wernicke–Korsakoff syndrome) and dementia, which seriously affects many mental functions in addition to memory (e.g., language, reasoning, and problem–solving abilities).
In 1881, Carl Wernicke, a German neurologist and psychiatrist, first described an illness that consisted of paralysis of eye movements, ataxia, and mental confusion. Sergey S. Korsakoff, a Russian psychiatrist, described the disturbance of memory in the course of long-term alcoholism in a series of articles from 1887-1891. He termed this syndrome psychosis polyneuritica. The term Wernicke encephalopathy is used to describe the symptom complex of ophthalmoplegia, ataxia, and an acute confusional state. If persistent learning and memory deficits are present, the symptom complex is termed Wernicke-Korsakoff syndrome. Alcohol interferes with people’s ability to form new long–term memories, and the magnitude of memory impairment increases with increasing alcohol use.
A deficiency of thiamine (vitamin B-1) is responsible for the symptom complex manifested in Wernicke-Korsakoff syndrome. The vitamin thiamine plays a key role in the breakdown of carbohydrates in brain cells. Without thiamine, cells cannot form vital brain chemicals such as neurotransmitters as well as other molecules that are essential for building proteins and DNA. The result may be the development of serious brain disorders, including Wernicke–Korsakoff syndrome. This condition, found primarily in persons with alcoholism, occurs when a person does not take enough thiamine in his or her diet, when thiamine absorption from the gastrointestinal tract is compromised, or when thiamine is not used sufficiently by the cells.
Brain damage in idividuals with alcoholism can be a direct effect of alcohol’s action on the brain as well as a side effect of alcoholic liver disease. Persistent alcohol–related liver dysfunction leads to the accumulation of toxic ammonia and manganese in the blood and brain, leading to hepatic encephalopathy—a serious and potentially fatal brain disorder. Patients with hepatic encephalopathy suffer from sleep disturbances, changes of mood and personality, severe cognitive effects (e.g., a shortened attention span), psychiatric conditions such as anxiety and depression, as well as motor disturbances, including motor incoordination and a type of flapping tremor of the hands called asterixis. In the most serious cases, the patients no longer respond to external stimuli and may fall into a coma (i.e., hepatic coma), which can be fatal.
The brain shrinkage
Research using brain imaging techniques has revealed that certain brain areas are often smaller in volume in people with a history of alcoholism than they are in nonalcoholic subjects. This brain shrinkage as well as the disruption of fibers that carry information between brain cells (i.e., white matter) and impairment of associated cognitive and motor functions are examples of the brain damage that may occur as a result of excessive alcohol consumption.
Disruption in neurogenesis
For years it was believed that each person was born with a finite number of brain cells, which could not be re–created. Recent research demonstrates, however, that stem cells in some brain regions are capable of giving rise to new cells (a process known as neurogenesis) throughout life. Heavy alcohol use can disrupt neurogenesis in adults, leading to long–term effects on brain structure and function. More moderate but chronic drinking appears to affect neurogenesis, possibly through a process similar to the neurodegeneration associated with chronic alcoholism.
Brain damage may result from head trauma caused by falls or other accidents occurring under the influence of alcohol. Binge drinking is a major risk factor for head trauma among trauma patients. The relative risk for head injury markedly increases with increasing blood alcohol levels.
Women who drink while pregnant are at high risk for giving birth to children with birth defects. Prenatal exposure to alcohol may lead to changes in brain anatomy (i.e., neuroanatomy) as well as to impaired cognitive and behavioral function. These changes include significantly smaller brain sizes as well as alterations in cellular activity. A wide range of neuropsychological deficits have been found in children prenatally exposed to alcohol, including deficits in visuospatial functioning, verbal and nonverbal learning, attention, and executive functioning. These children also exhibit a variety of behavioral problems that can further affect their daily functioning. No single mechanism is responsible for the array of alcohol- derived fetal injuries. However, some putative mechanisms are particularly significant in early pregnancy, such as excessive cell death in a special population of embryonic cells that give rise to facial structures and certain peripheral nerves. To prevent birth defects women should stop drinking alcohol during all phases of pregnancy.