Updated June 10, 2006.
Previous studies have demonstrated that the brains of alcoholics are smaller, lighter and "shrunken" when compared to nonalcoholic brains. Symposium speakers at the October 2004 Congress for the International Society for Biomedical Research on Alcoholism in Mannheim, Germany reviewed what is known about the causes, consequences and clinical implications of alcohol-related brain shrinkage. Proceedings were published in the June 2005 issue of Alcoholism: Clinical & Experimental Research.
"The outer layer of brain, also called the cerebral cortex or gray matter, controls most complex mental activities," explained Clive Harper, symposium organizer and professor of neuropathology at the University of Sydney and Royal Prince Alfred Hospital. "The cortex is filled with nerve cells, also called neurons, that connect by single long fibres to different cortical regions and other neurons deep inside the brain and spinal cord. These nerve fibres make up white matter, which comprises the 'hard wiring' of the brain.
"Most of the fibres are insulated by a material called 'myelin' that is similar to the plastic coating around electrical wires. Nerve cells also have shorter and more numerous fibres or processes called dendrites with many fine branching processes ? similar to the root system of a tree ? that allow them to 'talk' with neighbouring neurons, often as many as five to 10,000 at a time."
Alcohol appears to be particularly damaging to the "white matter" or "hard wiring" of the brain, and can also cause shrinkage or retraction of neuronal dendrites; however, the damage appears to be at least partially reversible with abstinence.
"The aim of this symposium was to bring together scientists from different disciplines to compare results from human and animal studies of the effects of alcohol on the brain," said Harper. "Our objective was to better understand the mechanisms underlying alcohol's damage, with the ultimate goal of identifying how to prevent and/or reverse these effects."
Key presentation highlights were:
A number of toxic, metabolic, and nutritional factors interact in a complex way to cause brain damage in those individuals who abuse or are dependent on alcohol.
"The exact ways in which alcohol damages the brain are uncertain," said Harper. "It might be that alcohol, or a metabolic byproduct of alcohol such as acetaldehyde, are toxic. Research on malnutrition, a common consequence of poor dietary habits in some alcoholics, indicates that thiamine deficiency can contribute to impaired cognition. Cirrhosis of the liver, also common in alcoholics, is known to cause clinical and structural changes in the brain. In addition, head injury and sleep apnoea are more common in alcoholics and can contribute to brain damage. All of these factors ? particularly the alcohol, thiamine deficiency and cirrhosis ? are linked and probably contribute in a complex way to cause brain damage."
Both permanent and transient changes may occur in the alcoholic brain.
"The most important permanent structural change is nerve cell loss," said Harper. "Some nerve cells cannot be replaced, those in the frontal cortex, cerebellum and several regions deep in the brain."
However, he added, some changes can be transient, such as the shrinkage of dendrites, those fibers that allow neurons to "talk" with neighbouring neurons. "In experimental animals," he said, "these have been shown to grow and spread again after periods of abstinence ? weeks to months ? and have been accompanied by improved brain function. Structural and functional changes seen in cirrhosis of the liver are also potentially reversible if treated. Furthermore, thiamine deficiency can be treated easily with oral or injected thiamine. Patients with acute deficiency respond very quickly but some permanent damage can occur if patients are not treated and particularly if they suffer repeated episodes of the deficiency."
Previous studies have demonstrated that the brains of alcoholics are smaller, lighter and "shrunken" when compared to nonalcoholic brains. Symposium speakers at the October 2004 Congress for the International Society for Biomedical Research on Alcoholism in Mannheim, Germany reviewed what is known about the causes, consequences and clinical implications of alcohol-related brain shrinkage. Proceedings were published in the June 2005 issue of Alcoholism: Clinical & Experimental Research.
"The outer layer of brain, also called the cerebral cortex or gray matter, controls most complex mental activities," explained Clive Harper, symposium organizer and professor of neuropathology at the University of Sydney and Royal Prince Alfred Hospital. "The cortex is filled with nerve cells, also called neurons, that connect by single long fibres to different cortical regions and other neurons deep inside the brain and spinal cord. These nerve fibres make up white matter, which comprises the 'hard wiring' of the brain.
"Most of the fibres are insulated by a material called 'myelin' that is similar to the plastic coating around electrical wires. Nerve cells also have shorter and more numerous fibres or processes called dendrites with many fine branching processes ? similar to the root system of a tree ? that allow them to 'talk' with neighbouring neurons, often as many as five to 10,000 at a time."
Alcohol appears to be particularly damaging to the "white matter" or "hard wiring" of the brain, and can also cause shrinkage or retraction of neuronal dendrites; however, the damage appears to be at least partially reversible with abstinence.
"The aim of this symposium was to bring together scientists from different disciplines to compare results from human and animal studies of the effects of alcohol on the brain," said Harper. "Our objective was to better understand the mechanisms underlying alcohol's damage, with the ultimate goal of identifying how to prevent and/or reverse these effects."
Key presentation highlights were:
A number of toxic, metabolic, and nutritional factors interact in a complex way to cause brain damage in those individuals who abuse or are dependent on alcohol.
"The exact ways in which alcohol damages the brain are uncertain," said Harper. "It might be that alcohol, or a metabolic byproduct of alcohol such as acetaldehyde, are toxic. Research on malnutrition, a common consequence of poor dietary habits in some alcoholics, indicates that thiamine deficiency can contribute to impaired cognition. Cirrhosis of the liver, also common in alcoholics, is known to cause clinical and structural changes in the brain. In addition, head injury and sleep apnoea are more common in alcoholics and can contribute to brain damage. All of these factors ? particularly the alcohol, thiamine deficiency and cirrhosis ? are linked and probably contribute in a complex way to cause brain damage."
Both permanent and transient changes may occur in the alcoholic brain.
"The most important permanent structural change is nerve cell loss," said Harper. "Some nerve cells cannot be replaced, those in the frontal cortex, cerebellum and several regions deep in the brain."
However, he added, some changes can be transient, such as the shrinkage of dendrites, those fibers that allow neurons to "talk" with neighbouring neurons. "In experimental animals," he said, "these have been shown to grow and spread again after periods of abstinence ? weeks to months ? and have been accompanied by improved brain function. Structural and functional changes seen in cirrhosis of the liver are also potentially reversible if treated. Furthermore, thiamine deficiency can be treated easily with oral or injected thiamine. Patients with acute deficiency respond very quickly but some permanent damage can occur if patients are not treated and particularly if they suffer repeated episodes of the deficiency."