Excessive alcohol intake has a great impact on the cognitive function of a person. It leads to a person to have a poor cognitive function. Which can be affected the persons perception, attention, memory, motor skills, language, visual and spatial processing. To some extent, study indicates that high level of impulsivity in alcohol consumptions of a person has an effect on the frontal lobe related to their behavioral problem (Lyvers et. al. ). Furthermore, alcohol intoxication causes disruption of prefrontal cortical functioning and thereby impairs executive cognitive performance.
As executive cognitive ability is concerned this is the prefrontal cortex, which is responsible for problem solving, cognitive flexibility, planning, organization, abstract reasoning and social conduct. A person who is in inebriated situation is more likely to do risky, impulsive behavior such as unprotected sex, violence and drunk driving. In some situation, severe alcoholics’ gets complication, serious organic cerebral impairment; it is the common complication occurring in about 10 percent of patient (Horvath 1975).
Lishman 1981; American Psychiatric Association 1987, the diverse signs of severe brain dysfunction that persist after cessation of alcohol consumption have been conceptualize in terms of two organic mental disorders: alcohol amnestic disorder (memory disorder) and dementia associated with alcoholism. Alcohol amnestic disorder, commonly called Korsakoff’s psychosis or Wernicke- Korsakoff syndrome, it is characterized by short term memory, impairments and behavioral changes that occur without clouding of consciousness or general loss of intellectual abilities.
Dementia associated with alcoholism consist of global loss of intellectual abilities with an impairment in memory function together disturbance(s) of abstract thinking, judgment, other higher cortical function or personality change without a clouding of consciousness. These two mental disorders are also cause by a severe deficiency of Thiamine (vitamin B1) and are often precipitated by a sudden influx of glucose. A number of things have been shown to lead to a severe enough thiamine deficiency to trigger wet brain.
Wet brain or Wernicke-Korsakoff Syndrome has a sudden onset--it is not something which happens gradually over time. The first stage of wet brain is called Wernicke's encephalopathy. When there is a sudden influx of glucose in a brain which is deprived of thiamine the brain cells begin to die. This is because the chemical reactions which supply these brain cells with energy for life use thiamine to turn glucose into energy in a chemical process called the Krebs cycle.
When there is an influx of glucose and no thiamine to help metabolize it, these brain cells burn out like a car engine running on high octane gasoline at high speed with no oil. The brain cells which die first are the ones which require the most thiamine to function. These brain cells are located around the middle of the brain and are the brain cells which are associated with memory and muscular movement. The brain cells of the cerebellum, which controls balance, are also affected.
Korsakoff's syndrome includes loss of past memories, inability to learn new things, confabulation (remembering things which never happened), lack of coordination and unsteady gait, and in severe cases dementia. These are the possible reaction to a person who takes excessive alcohol consumptions. More evident in explaining the effect of excessive intake of alcohol in a person’s cognitive function is that he/she will experienced less adept at certain learning tests and visual- spatial integration. Likewise it cause premature aging (Tarter and Edwards, 1986) and it is still under active investigation.
In addition, it has long been an established fact that actively drinking, alcohol dependent subjects have smaller brain volumes than normal control subjects who do not drink alcohol. Thus, early researchers assumed that this was because alcohol killed the brain cells of alcohol dependent subjects, but other research disapproves this hypothesis but it could be partially true unless there has been brain damage as a result of liver failure or thiamine deficiency, the majority of brain cells of heavy drinkers are intact even though the brain has shrunk.
Meanwhile, in some study stated that alcohol consumption in a moderate mode has an effect to help a person to decrease the incidence of having diabetes. Likewise, it can help to preserve brain vasculature prevents sub-clinical strokes and could result in better cognition function. But drinking too much of alcohol leads to have poor cognitive function that causes to a person to have brain damage. Some research shows that alcohol adversely affects the brain.
When health professionals encounter patients who are having cognitive difficulties, such as impaired memory or reasoning ability, alcohol use may be the cause of the problem. The human brain consists of white cells and gray cells. The gray cells are responsible for thinking and feeling and decisions--they correspond to the Central Processing Unit (CPU) of the computer. The white cells are like the cables of the computer which connect the keyboard and the monitor to the CPU.
Jensen and Pakkenberg (1993) did brain cell counts which compared the number of cells in the brains of heavy drinkers with those of non-drinkers. They found out that the number of gray cells was the same in both the heavy drinkers and the non-drinkers. However, there were fewer white brain cells in the brains of the drinkers which imply that alcohol kills a white brain cell that is responsible to the connection to pass the message or transaction of the brain to connect with the feeling and decision making of a person.
Hence, excessive alcohol intake disrupts the connection or breaks the normal function of the brain to react and to have a better cognitive function. Moreover, George Fein (2009) discovered that there was one part of the brain in the parietal lobe--which is associated with spatial processing--where alcohol kills gray cells. Fein claims that this explains why even after alcohol dependent subjects regain use of all their other cognitive functions they still seem to have difficulties with spatial processing.
Parker et al. (1983) stated that there is significant decrease in test performance have been found for people whose self-reported alcohol consumption was in the range of what was considered social drinking. They found it out when they conducted a certain neuropsychological tests, the results of one general population study (Bergman et al. 1983). Those people were not clinically impaired; they only exhibited certain performance deficits that correlated with alcohol consumption.
Parsons (1986) concluded that data on the relationship of cognitive impairment to amount of alcohol consumed by social drinkers are inconclusive but has the chance to have similar correlation. There is some evidence that both the amount of brain shrinkage and the amount of cognitive deficit are dependent on the quantity of alcohol consumed and the number of years of heavy drinking. Thus, it only proves that there is an adversely effect on the cognitive function of a person in drinking too much of it. Hence, there is no good effect on the brain or body function of a person. (copyright of ISLA BONITAS 2012) |
