Neurological Effects of Alcohol Abuse
This paper looks into the neurological effects of alcohol abuse. Of importance to this work are the theoretical foundations of these effects with a focus on repressed traumatic memories and neuronal pathways change as a result of prolonged depression. A review of the theoretical understandings of depression in relation to alcohol abuse is also provided. The claims on the neurological effects of alcohol abuse in this paper are based on empirical research findings. Finally, the implications of these findings for clinical application are discussed.
Neurological effects of alcohol abuse
There are a number of neurological defects that are known to result from chronic alcoholism. All parts of the nervous system (central and peripheral) are affected by alcohol with effects differing depending on factors such as amount of alcohol intake and the specific part of the nervous system. Berman et al (1997) that alcohol lead to a decrease in body temperature which can be detrimental if the individual is already exposed to cold environments. Another common effect of heavy alcohol consumption is abnormal sleeping patterns. Rapid eye movement (REM) sleep seems to be affected by even small quantities of alcohol. It is also a common experience of alcohol intake to have increased agitation. The neurological effects of alcohol are also felt a few days after alcohol intake and these appear as withdrawal symptoms. The most common alcohol withdrawal symptom is that the individual experiences hallucinations which may take up to six days to cease.
NIAAA (2004) notes that there is a neuronal excitation that follows in up to 48 hours after withdrawing from alcohol and some individuals experience seizures. At this stage, the person is also likely to have status epilepsy before moving to another stage of alcohol withdrawal syndrome known as delirium tremens. This experience is quite severe with the main characteristics being disorientation, impaired thought, and increase in autonomic hyperactivity as well as visual and auditory hallucinations. All these effects are as a result of disturbed nervous system. The brain seems to be the most affected part of the nervous system by chronic alcoholism. Impaired muscular coordination as characterized by staggering in individuals who have taken alcohol indicates a disturbance of the cerebellum which controls balance (Berman et al, 1997). The effect of alcohol abuse on the peripheral nervous system is also witnessed where the peripheral organs such as the hands experience numbness although malnutrition in alcoholics is a significant determinant.
The chronic intake of alcohol is not only related to the above neurological consequences but there are other abnormalities more so in line with the neuropsychological functions. The neuropsychological effects of alcohol abuse may be clinically evaluated with their end effects being serious syndromes such as Korsakoffs syndrome, polyneuropathy, alcoholic dementia and Wernickes syndrome among others (Cairney et al, 2007). Cairney asserts that these severe neuropsychological dysfunctions follow after progressive decline in cognitive ability and they are mainly irreversible. Images of the brain have shown several abnormalities in the brains of alcoholism with reduction of neurons and shrinkage of the brain being amongst the paramount features. In addition, there are tests administered by neurophysiologists such as the CogState test battery that help in evaluating neuropsychological dysfunctions caused by alcohol abuse. The CogState battery test has been used by Cairney et al (2007) to study cognitive impairments among Aborigines with heavy alcohol dependence.
Looking into some of the neuropsychopathologies of alcohol abuse is important in exploring the extent of damage that alcohol abuse can cause to the brain. Known as among the severest effects of alcohol abuse for a long period, Karsakoffs syndrome renders the memory of the individual deeply impaired and unable to remember even the most recent activities. Berman et al (1997) indicates that the loss of short-term memory in Karsakoffs syndrome patients live in the past. Although there are genetic and nutritional deficiency explanations to this, the dominant factor is that alcohol abuse has a direct effect. Notable is that the long-term memory of these individuals is usually intact with standard intelligence quotient tests mainly showing stable IQ.
In Wernicke syndrome appears as a mild form of Karsokoffs syndrome but it is an encephalopathy characterized mainly by confusion and oculomotor disturbances since the nerves that serve the eyes are paralyzed. Nerve paralysis also leads to impaired muscular coordination (NIAAA, 2004). Thiamine deficiency is mentioned to be related with development of this disorder but the contribution of alcohol is never ruled out. The occurrence of the Karsokoffs syndrome in relation to Wernicke syndrome makes the syndrome to be termed as Wernicke-Karsokoffs syndrome.
Several studies have been carried out to demonstrate the damage caused by alcohol abuse in the brain thus explaining the behavior characterized in the alcohol related syndromes. By imaging the brain as well as doing autopsy examinations, evidence shows that brain damage such as brain shrinkage as well as neuronal degeneration occurs in significant parts of the brain such as cerebellum, cerebral cortex and the limbic system. Relatedness of the whole brain in coordinating various functions implies that an effect on one part of the brain may be felt in another. Since the limbic system specifically the amygdala and the hippocampus are known to be responsible for memory maintenance, the loss of memory experienced with alcohol abuse is thought be out of damage on these parts of the brain. Alcoholics have deficits in the limbic system as expressed by such symptoms as impaired vision and sense of touch (Berman et al, 1997).
The cerebral cortex contains the gray and white mater with the gray mater containing the cell bodies of the neurons. Since this part of the brain coordinates intelligence and high conscience, its impairment has far reaching effects. The neural connections found in this region are also significant as virtually all body parts get coordinated in this region. Alcohol abuse leads to the impairment of this important brain part by causing the fissures to widen with the ventricles also enlarging. In general, the cerebral cortex seems to reduce in size leading to impaired functioning. The characteristics seen in a patient suffering from Karsokoffs syndrome are the best indicator of how the cerebral cortex is affected by chronic alcoholism.
Alcoholism is associated with alteration in the brain neurotransmitters. In that case, alcohol can lead to either up regulation or down regulation of the various neurotransmitters leading to neurological problems. Alcohol for instance interferes with glutamate action by inhibiting its effects with chronic alcohol intake leading to epileptic seizures and impaired memory. Alcohol also increases the effects of gamma-aminobutyric acid leading to brain sedation and epileptic seizures upon chronic use of alcohol. Alcohol intake also results to increased serotonin release thus increasing aggressiveness among other effects. Other effects of alcohol on the brain include inhibition of nerve growth proteins, changes in membrane lipids (Berman et al, 1997).
To ascertain that alcohol abuse leads to neuropsychological problems, several studies have been carried out. Lange, Iverson and Franzen (2007) studied how individuals developed short-term neuropsychological problems in individuals who got mild traumatic brain injury while intoxicated with alcohol against those who got traumatic brain injury prior to intoxication. This research was based on the argument that cognitive outcomes in individuals who get brain injury on the day of alcohol intoxication are worse compared to individuals who get injured while sober. In the study that involved 169 patients, Lange and colleagues identified that contrary to the common believe, pre-injury alcohol abuse had a higher effect on the short-term neuropsychological effects. Nevertheless, this study acknowledged that day-of-injury intoxication has a significant effect on cognitive outcomes. The study may have brought about conflicting results due to its focus on short-term and not long-term effects. After all, it is already established that traumatic brain injury is largely contributed to by alcohol abuse. If a person gets traumatic brain injury while on alcohol, it has been observed that their levels of consciousness are usually low which eventually leads to neurological impairment.
In an other study carried out by Dikmen et al (1993) trying to asses how use of alcohol affected neuropsychological outcomes following head injury, these researchers noted that the outcome highly depended on how severe the head injury was as well as the amount and frequency of alcohol use. This study was also influenced by the findings that head injuries are mainly related with alcohol abuse as individuals are likely to fall or get involved in traffic accidents. Although this study identified that heavy alcohol users experienced more severe neuropsychological outcomes if the heady injury was severe compared to low alcohol users, there are other factors that are determinant factors. It was also noted that high alcohol dependence was related to impairment of several cognitive functions such as intelligence, and psychomotor functions. Verbal intelligence was in particular highlighted to be highly affected by the severity of alcohol use. Other factors related to the neuropsychological outcomes following alcohol abuse included the history of alcohol abuse, the individuals lifestyle and level of education although these were not further investigated.
Having identified that alcohol abuse leads to a number of neuropsychological dysfunctions, some studies have been carried out to test how well individuals recover after abstinence. Goldman, Williams and Klisz (1983) sought to understand the recoverability of visual spatial dysfunction. In this study, age was put to consideration whereby they studied alcoholics aged 20-29, 30-39 and those aged above 40 years separately. The recovery was determined through a test battery for a period of three months post alcohol use abstinence. From this study, it was identified that it only took two to three weeks for individuals aged below forty years to recover from alcohol related functional impairments. However, alcoholics aged forty years and above did not recover completely from some visual-spatial functions after the period of three months. Also notable in this study was that the drinking history of an individual was not a determinant of the continued neuropsychological deficits. This research was based on the arguments that it is possible to recover from effects of alcohol following cessation. This study was able to related age with likelihood of recovery with age advancement resulting to poor recovery from functional impairments. The most likely reasons were cited as either an increase in the vulnerability of the neurological functioning with age or reduction in the potential to recover from neuropsychological loss.
The subject of how age determines neurological functioning of individuals with abuse of alcohol is very important. This is particularly when focusing on effect of alcohol abuse during adolescence. Brown et al (2009) have focused on the abuse of alcohol during late adolescence (16-20 years) by first looking into the developmental processes that occur during this stage. From these, the effects of alcohol abuse at this age are then easily predicted. The high rate of brain development during late adolescence is associated with significant changes in cognitive functioning thus affecting social and emotional well being of the adolescents. Among the prevalent behavior during late adolescent is alcohol abuse including binge drinking hence the need to understand its likely effects. Brown et al (2009), mentions that alcohol use disorders are most prevalent during 18-20 years of age compared to any other age period.
During late adolescents, it is identified that synapses in the neurons of the brain get refined whereby the volume of the gray matter reduces while the white matter increase due to increase in myelin. The outcome is that neural signals get transmitted faster and efficiently thus enabling high consciousness functions. This implies that abuse of alcohol at this age is likely to interfere with these developmental processes hence impairment of the functions thereof. The cognitive development of the adolescent is particularly severely affected by alcohol abuse with executive functions suffering most. Working memory which is also in the process of development in late adolescence also suffers from the effects of alcohol abuse. Working memory is mainly a function of the frontal brain region which is usually impaired by alcohol use. Even with the many developments in the late adolescence stage, it is unfortunate that this is when most of them initiate alcohol abuse with binge drinking and heavy drunkenness being prevalent.
Since maturation of the frontal cortex occur during late adolescent to young adulthood, anatomical and physiological changes are affected if these individuals become alcohol abusers. Brown et al (2009) states that alcohol abuse at this stage leads to impaired memory as well as visual-spatial abilities. Animal studies on the neuropsychological effects of alcohol during adolescence show that neurogenesis in the hippocampus reduces and reduce serotonin signaling. Although adolescents are not at a very high risk of dysfunction of motor functions, heavy drinking at this stage leads to future alcoholism tendency which has its negative neurological effects.
It has also been identified that alcohol abuse during pregnancy has adverse effects on the developing fetus. These are usually after the birth of the child. Fetal alcohol syndrome is a major adverse effect of alcohol abuse during pregnancy. The neurological effects on the infant are characterized by microencephaly, and few neuron numbers that are functional. Resultantly, the child develops learning and behavioral problems. Physical malformations include short stature, thin upper lip, small eye opening, and small mid face among other abnormal facial characteristics (NIAAA, 2004).
The neurological effects of alcohol abuse are directly related to the quality of life especially as far as levels of depression and anxiety is concerned. Describing quality of life as being determined by psychological, psychosocial and physiological well being, Saatcioglu Yapici and Cakmak (2008) explore the effects of alcohol abuse on quality of life. This study identifies that alcohol addiction leads to depression and anxiety which in effect increases the problems thereof eventually lowering the overall quality of life. Persons addicted to alcohol experience anxiety disorders mood disorders and antisocial disorders which are related to increased anxiety and depression following alcohol abuse. By studying alcohol dependent individuals who had anxiety and depression against those who did not have, these researchers noted that there was an increase in anxiety and depression in persons who depended on alcohol. Alcohol dependent individuals suffering from anxiety and depression performed poorly in physical, social and psychological health. Withdrawal symptoms as discussed earlier were a common observation in depressed alcoholics. An overall observation is that depression and anxiety are part and parcel of alcoholism.
An overall understanding of the neurological effects of alcohol abuse is very pertinent for evidence-based clinical practice. For instance, knowledge of the various parts and functions of the brain that are affected by alcohol can help physicians make decisions on reversing these situations. An understanding of the effects alcohol on various neurotransmitters may also be important in development of drugs that improve brain functioning once alcohol alters the balance. Regarding the neuropsychological outcomes following alcohol abuse, nurses are better position to handle alcohol related cases if they have this information. For instance, understanding the recoverability of visual-spatial abilities depending on the age of the patient helps in devising management options that best fits a particular age group. Accurate diagnosis is also facilitated by the understanding of the likely effects of alcohol on the development of the brain. Finally, an informed nurse can be equality informative to the community (more so adolescents and pregnant mothers) on the adverse effects of alcohol abuse and the need to abstain from the same.
Conclusion
Although alcohol abuse has a variety of effects on the body, its effects on the nervous system (more so the brain) are quite adverse. The neurological effects thereof include impaired brain function, impaired brain development and consequently impaired cognitive abilities. The quality of life is also severely affected as characterized by high depression and anxiety levels in alcoholics. Studies on neurological effects of alcohol abuse have proved this and hence the need for clinicians to use this knowledge for evidence-based practice. With this information, it is also possible to equip individuals on the risks of alcohol abuse which would eventually translate to improved quality of life.
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