Alcohol-related brain damage alters brain structure and function as a result of direct neurotoxic effects of alcohol poisoning or acute alcohol withdrawal. Increased alcohol intake is associated with damage to the brain area including the frontal lobes, the limbic system, and the cerebellum, with broad cerebral atrophy, or brain shrinkage caused by neuron degeneration. This damage can be seen in the neuroimaging scan.
Frontal lobe damage becomes the most prominent because of alcoholic age and can lead to neuropsychological performance disorders in areas such as problem solving, good judgment, and goal-directed behavior. Disturbed emotional processing results from damage to the limbic system. This can cause problems recognizing emotional facial expressions and "interpreting nonverbal emotional cues".
Binge drinking, or heavy episodic drinking, can cause damage to the limbic system that occurs after a relatively short period of time. This brain damage increases the risk of dementia and mood abnormalities and cognitive abilities. Drinkers also have an increased risk of developing chronic alcoholism.
Alcoholism is also associated with many other health problems including memory impairment, high blood pressure, muscle weakness, heart problems, anemia, poor immune function, liver disease, digestive system disorders, and pancreatic problems. It has also been correlated with depression, unemployment, and family problems with an increased risk of domestic violence.
Gender and parental history of alcoholism and/or binge drinking have an influence on susceptibility to alcohol dependence because higher rates are usually seen in males and in those with a family history.
Video Alcohol-related brain damage
Prevalence
Nearly half of American alcoholics show "neuropsychological disability can range from mild to severe" with about two million requiring lifelong care after developing a permanent and debilitating condition. Old alcoholic abstinence can cause an increase in this disability. For those with mild interference, some improvements have been seen within a year, but this can take longer on those with higher damage severity.
Maps Alcohol-related brain damage
Impact
US excessive drinking costs of approximately $ 250 billion in 2010. These costs are broadly including health care, productivity loss, property damage, criminal justice, and motor vehicle accidents. A very large part of this cost is due to a liquor party. This fee falls on taxpayers, including non-drinkers.
Excessive alcohol consumption is responsible for about 1,500,000 deaths and 51,898,400 years of potential life lost globally by 2010.
Population at risk
Teen and genetic factors
Impulsive impulse and sensation seen in adolescence can lead to an increase in alcohol intake and more frequent binge drinking alcohol that causes adolescents particularly at risk of alcohol. The developing teen brain is more susceptible to the neurotoxic and neurodegenerative effects of destructive alcohol. "High impulsivity has also been found in families with alcoholism, which exhibit a genetic relationship, and thus the genetics of impulsivity overlaps with genetic risks for alcohol use disorders and possibly alcohol neurodegeneration."
There is also a genetic risk for proinflammatory cytokines that are mediated by alcohol-related brain damage. There is evidence that this gene variant involved not only contributing to brain damage but also impulsivity and alcohol abuse. These three genetic traits contribute greatly to the disruption of alcohol use.
Neurological deficit
Alcoholics can usually be divided into two categories, not complicated and complicated. Uncomplicated alcoholism has no nutritional status or liver disease, but has a reduction in overall brain volume due to cerebral white matter atrophy. The severity of the atrophy suffered from alcohol consumption is directly proportional to the level and amount of alcohol consumed during one's life. Elaborate alcoholics may have liver damage that affects the structure and function of the brain and/or nutritional deficiencies "that can lead to severe brain damage and dysfunction".
Pathophysiology
The cerebral atrophy that often occurs in alcoholics is due to alcohol-induced neurotoxicity. Neurodegeneration evidence may be supported by increased microglia density and expression of proinflammatory cytokines in the brain. <1> Animal studies find that heavy and regular binge drinking causes neurodegeneration in areas of the corticolimbic brain involved in learning and spatial memory. Affected corticolimbic brain regions include olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and dentate gyrus hippocampal. It was found that a heavy 2-day binge led to extensive neurodegeneration in the entorhinal cortex with a learning deficit outcome in mice.
It is unclear how the frequency and length of this binge drinking session affected human brain damage. Humans who drank at least 100 drinks (men) or 80 drinks (women) per month (concentrated up to 21 times or less per month) over a 3 year period have experienced decision-making skills disorder compared to non-party drinkers. MRI brain scans found that N-acetylaspartate (NAA) levels, metabolite biomarkers for neural integrity, were lower in party drinkers. In addition, an abnormal brain metabolism, loss of white brain matter in the frontal lobe, and higher levels of parietal gray were found. This shows the correlation between binge drinking, poor executive function, and working memory. Decreased levels of frontal lobe NAA are associated with impaired executive function and processing speed in neuro performance tests.
The volume of the corpus callosum, a large white matter channel connecting the two hemispheres, is shown to decrease with alcohol abuse due to loss of myelination. The integration between the two hemispheres and the cognitive function is affected. The limited number of myelin can be recovered by the abstinence of alcohol, leading to a temporary neurological deficit.
Alcohol abuse affects neurons in the frontal cortex that usually have large soma, or body cells. This type of neuron is more susceptible to Alzheimer's Disease and normal aging. Research is still underway to determine whether there is a direct relationship between excessive alcohol consumption and Alzheimer's disease.
The high-order function of the cerebral cortex is governed by the cerebellum. In those with cerebral atrophy, Purkinje cells, or cerebellar output neurons, the vermis is reduced by 43%. The large decrease in purkinje cells leads to a decrease in the organization of the cerebral cortex of high orders. The small brain is also responsible for improving the output of the raw motor of the primary cortex motor. When this improvement is lost, symptoms such as imbalances and ataxia will appear. The potential cause of chronic cerebral dysfunction of alcohol is a change in GABA-A receptors. This dysfunction leads to an increase in GABA neurotransmitters in cerebellum purkinje cells, granular cells, and interneurons leading to interference with normal cell signals.
Kindling and excitotoxicity
Alcoholic and alcoholic drinkers undergoing some detoxification indicate prefrontal cortical dysfunction leading to impairment in executive control tasks. Animal studies have shown that repeated alcoholic withdrawal is associated with an inability to learn new information. The acute effects of alcohol on GABAergic uptake and NMDA suppression cause neurotoxicity and alcohol-induced scratching, or worsening of alcohol withdrawal symptoms with each subsequent withdrawal period. This can cause CNS depression that causes acute tolerance to this withdrawal effect. This tolerance is followed by a destructive rebounding effect during withdrawal. This rebound causes the hypersexitability of the neurotransmission system. If this hyperexcitability occurs several times, kindling and neurotoxicity may occur which leads to an increase in alcohol-related brain damage. Damaging excitotoxicity may also occur as a result of repeated withdrawals. Similar to people who have gone through some detoxification, party drinkers show higher levels of emotional disturbance because of these damaging effects.
Lack of tiamina
Lack of nutrients in thiamine can worsen alcohol-related brain damage. There is a genetic component for thiamine deficiency that causes intestinal malabsorption. More often, thiamine deficiency is caused by excessive alcohol consumption. This causes Wernicke's encephalopathy and Korsakoff's often common syndrome, known as Wernicke-Korsakoff syndrome. Lesions, or brain abnormalities, are usually located in the diencephalon that causes anterograde and retrograde amnesia, or loss of memory.
Neuroimaging
Neuroimaging is used to study the effects of alcohol on the brain. The two main imaging methods are hemo-dynamic and electromagnetic. These techniques have made it possible to study the functional, biochemical, and anatomical changes of the brain due to prolonged alcohol abuse. Neuroimaging provides valuable information in determining a person's risk to develop alcohol dependence and potential treatment efficacy.
Hemo-dynamic method
The hemo-dynamic method records changes in blood volume, blood flow, blood oxygenation, and energy metabolism to produce an image. Positron emission tomography (PET) and single photon emission tomography (SPECT) are common techniques requiring the injection of radioactive labeled molecules, such as glucose, to enable proper visualization. After the injection, the patient is then observed while performing a mental task, such as a memory task. The PET and SPECT studies have confirmed and extended earlier findings suggesting that the prefrontal cortex is particularly susceptible to metabolic reduction in patients who abuse alcohol.
Magnetic resonance imaging (MRI) and functional magnetic resonance imaging (fMRI) are commonly used tenichiques. This method is not invasive, and has no radioactive risks. The fMRI method records the metabolic changes in certain structures or regions of the brain during mental tasks. To detect damage to white matter, standard MRI is not enough. The MRI derivative technique known as Diffusion Tensor Imaging (DTI) is used to determine the orientation and integrity of certain neural pathways, allowing detection of damage. When imaging them with alcoholism, DTI results indicate that heavy drink interferes with the microstructure of nerve fibers. Another MRI derivative technique, magnetic resonance spectroscopy imaging (MRSI), can provide more information about brain neurochemistry and can detect the distribution of certain metabolites, neurotransmitters, and alcohols.
Electromagnetic Method
While hemo-dynamic methods are effective for observing spatial and chemical changes, they can not indicate the timing of this change. The electromagnetic imaging method is capable of capturing real-time changes in the electrical currents of the brain. Electroencephalography imaging (EEG) uses a small electrode attached to the scalp. Recordings are averaged by a technique known as Event-Related Potentials (ERP). This is done to determine the time sequence of activity after exposure to a stimulus, such as a word or image. Magnetoencephalography (MEG) is another imaging method that uses sensors. It measures the magnetic field created as a result of the electrical activity of the brain. These techniques are not invasive, harmless, and provide a great deal of detail about the order and timing of electrical activity. The poor spatial imaging of this method is a big loss.
This neuroimaging method has found that alcohol alters the nervous system at various levels. These include decreased lower brain stem function and high order function, such as problem solving. This method also shows differences in electrical brain activity and is responsive when comparing alcohol-dependent and healthy individuals.
Clinical app
In the Korsakoff patient, MRI shows atrophy of the thalamus and mamillary bodies. PET showed a decrease in metabolism, and therefore decreased activity in the thalamus and other diencephalon structures. Uncomplicated alcoholics, those suffering from Chronic Wernicke Encephalopathy (WE), and Korsakoff's psychosis show significant neuronal loss in the frontal cortex, white matter, hippocampus, and basal forebrain. Uncomplicated alcoholism appears to have shrinkage in raphe neurons, mammary bodies, and thalamus.
Treatment and prevention
Brain damage associated with alcohol can have drastic effects on suffering individuals and their loved ones. Options for treatment are very limited compared to other disorders. Although limited, most patients with alcohol-related cognitive deficits experience a slight increase in their symptoms during the first 2 to 3 months of treatment. Others say to see an increase in brain metabolism as soon as one month after treatment.
Education on prevention of alcoholism is the best supported method to avoid alcohol-related brain damage. By providing information that research has found risk factors and damage mechanisms, efforts to find effective treatments may increase. It can also reduce death by influencing doctors to pay more attention to warning signs.
References
Source of the article : Wikipedia
0 Comments