2.8. Central Nervous System
The forebrain, the midbrain, and the hindbrain can be affected by high chronic alcohol consumption. However, each part of the brain can be affected differently by alcohol abuse. Alcohol abuse has well-recognized neurological and psychological side effects. Neonatal alcohol syndrome, seen in infants born to chronic alcohol abusers, results in impaired neonatal brain development as well as physical and mental disorders.
Alcohol is known to promote brain damage and mental disorders. The neuropsychological consequences of brain damage resulting from chronic alcohol abuse include a change in behavior, memory loss (especially short-term memory), amnesia, and atrophy (shrinkage of the cerebral cortex) [40
]. The areas of the brain most susceptible to alcohol-induced damage are the limbic lobe, the diencephalon, and the basal forebrain.
According to the right hemisphere hypothesis, the right hemisphere of the brain is more susceptible to damage from alcohol abuse, which might explain the disproportionate impact of alcohol on nonverbal, visuospatial, and emotional functions, all of which are thought to be governed by the right hemisphere [40
]. In one study, people with AUD, average drinkers, and non-drinkers were given images to describe and analyze in order to gauge their emotional intelligence and competence. According to the results, the persons with AUD reported emotions that were more intense than the persons without AUD, which suggested that alcohol disrupts emotional competence and emotional intelligence. Additionally, although the persons with AUD were significantly more depressed than the non-drinkers, this did not significantly affect the performance of the two groups.
Estimates of the incidence of Parkinson’s disease range from 7.9 to 19 per 1,000,000 person/year, and a prevalence of 57 to 230 per 100,000 populations [41
]. Although genetics and environmental exposures are recognized as contributors to Parkinson’s disease, researchers have also begun to investigate the relationship between alcohol consumption and the occurrence of Parkinson’s disease [41
]. According to a review article on alcohol consumption and Parkinson’s disease, a prospective study conducted in Finland found that persons who consumed more than 5 g of alcohol per day had an increased risk of developing Parkinson’s disease compared to non-drinkers. Another study from the U.S.A. found an increased risk for the development of Parkinson’s disease in men who consumed 10 to 19.9 g of alcohol per day and in women who consumed 10 to 14.9 g of alcohol per day [42
]. The study also revealed that heavy alcohol consumption, defined as having at least two drinks per day, was associated with an increased risk for Parkinson’s disease, while low to moderate alcohol consumption, i.e., beer drinking, less than one drink a day, was associated with a decreased incidence for the development of Parkinson’s disease.
Drinking more than the recommended limit of alcohol has also been shown to increase a person’s risk of developing Alzheimer’s disease [42
]. Alzheimer’s disease is caused by a concentrated deposition of amyloid-β (Aβ) protein in the brain, memory failure, and dementia [43
]). Preventative measures have encouraged low consumption of alcohol. Studies have reported that moderate consumption of ethanol may protect against the buildup of Aβ protein, though this advice is dangerous because “low to moderate” are poorly defined. The recommended maximum limits of alcohol, as mentioned previously, are reported to be 14 units each week for men and women, spread over three or more days.
Studies have found that a greater intake of alcohol is associated with a higher risk of dementia, which is marked by a decline in cognitive function, severe enough to interfere with daily life [43
]. However, light to moderate consumption of alcohol can reduce one’s chances of developing dementia by 25–28%. The most common form of alcohol-related brain damage in persons with AUD-associated dementia, known as alcohol-related dementia, clinically presents as Korsakoff’s syndrome, called Korsakoff’s psychosis. Korsakoff syndrome is a chronic memory disorder caused by severe deficiency of thiamine (vitamin B1). The most common cause of Korsakoff syndrome is alcohol misuse, but AIDS and poor nutrition can also be associated with it. Since thiamine (vitamin B1) helps brain cells produce energy, when thiamine levels fall too low, the brain cannot generate enough energy to function properly. An overwhelming 80% of persons with AUD are vitamin B1-deficient.
The cerebrum controls mental processes such as memory, movement, and sensory perception. According to the 2nd edition of the Dictionary of Nursing [44
], thiamine deficiency can result in confusion and memory loss. This is associated with Wernicke-Korsakoff syndrome (WKS), which is a disease that includes two separate syndromes: (1) Wernicke’s encephalopathy, which is considered the acute phase with a shorter duration and more serious symptoms, and (2) Korsakoff’s psychosis, a long-lasting and chronic condition that psychologically and socially debilitates the patient.
Korsakoff’s psychosis has been shown to be clearly associated with thiamine deficiency and is defined by severe retrograde and anterograde amnesia, meaning that the patient loses old memories and lacks an ability to form new ones [45
]. In addition to thiamine deficiency, cortical atrophy caused by alcohol intoxication can cause frontal lobe dysfunction which worsens the effects of this condition [45
]. It is important to note that the duration of a history of drinking plays a more significant role in the manifestation of Korsakoff’s psychosis as opposed to the quantity of drinking. People who have been drinking for long periods experience worse effects than those who have consumed significant amounts over a short period.
The pathological lesion associated with Wernicke’s encephalopathy is also located in the cerebrum. The encephalopathy results in extreme mental confusion and forgetfulness. Someone suffering from this component of WKS may have extreme difficulty doing something as common as exiting a room because of the disruption in brain functions, making it virtually impossible to comprehend the idea of a door or of exiting. Treatment is recommended in early stages of WKS and consists of administering vitamin B1. Patients that are unable to reverse their condition during later stages require custodial care and mental support. An article on “Alcoholic Brain Damage about Alcohol Research and Health” states that 25% of cases of WKS develop to a point where custodial care becomes necessary [46
People who consume excessive amounts of alcohol may not walk properly, demonstrate poor coordination, and have impaired balance [47
]. This is due to the effects of alcohol on the cerebellum. Like the cerebrum, the cerebellum is sensitive to excessive alcohol, and its malfunction is also associated with the psychosis characteristic of WKS. About 80% to 90% of persons with AUD who develop Wernicke’s encephalopathy also develop Korsakoff’s psychosis [45
]. Similar to persons with AUD with encephalopathy, patients in this state are confused and have learning and memory problems. The difference, however, is that the psychosis often comes with physical debilitation, as it affects the cerebellum which controls the movements of the body. Although long-term abuse of alcohol is related to the development of the WKS or related dementias, light to moderate alcohol intake has been suggested to reduce the risk of dementia and Alzheimer’s disease [48
]. A population-based prospective study done in Bordeaux, France, found that, for subjects drinking three to four standard glasses of wine per day, categorized as moderate drinkers, the odds ratio was 0.18 for incident dementia and 0.25 for Alzheimer’s disease. After adjusting for age, sex, education, occupation, baseline cognitive performances, and other possible confounders, the odds ratio was, respectively, 0.19 and 0.28. In the 922 mild drinkers (one to two glasses per day) there was a negative association only with Alzheimer’s disease after adjustment. The inverse relationship between moderate wine drinking and the incidence of dementia was explained neither by known predictors of dementia nor by medical, psychological, or socio-familial factors. Light-to-moderate drinking (one to three drinks per day) was significantly associated with a lower risk of dementia.
Alcohol is known to behave as a depressant in the central nervous system [20
], thereby affecting a person’s ability to behave appropriately in response to environmental stimuli. Alcohol can affect the frontal lobe of the brain, which can make an individual act without thinking and makes it difficult to control the emotions. The frontal lobe, thalamus, and middle cerebellar peduncle have been demonstrated to be more vulnerable to the effects of acute alcohol consumption [49
]. The frontal lobe is responsible for decision-making, planning, learning, and self-control. Gamma Aminobutyric Acid (GABA) is the brain’s primary inhibitory neurotransmitter that acts to slow neuronal signals along pathways in the brain, producing a natural calming effect [50
]. When alcohol is present, the activity of the GABA receptors increases. This inhibits neuronal signals longer and allows the GABA receptor to produce its effects more extensively than in the absence of alcohol.
Alcoholism can alter the cognitive process. Some of the effects are memory loss, difficulty with learning, and emotional disturbances. Neuroimaging studies show that acute alcohol administration affects brain structures implicated in motivation and behavior control, and chronic intoxication is correlated with structural and functional abnormalities [51
]. The cerebral cortex, which is responsible for thinking, senses, and the ability to make good judgments or to think clearly, is often impaired by alcohol.
When affected by alcohol, the hippocampus, which controls memory, can experience blackouts, possibly followed by memory loss. The hypothalamus coordinates important activities in the pituitary gland and autonomic nervous system and controls body temperature, hunger, thirst, and other homeostatic systems. After drinking too much alcohol, hunger, thirst, blood pressure, and the urge to urinate increase, while body temperature decreases.
The medulla oblongata is also affected by AUD [40
]. The medulla is responsible for involuntary functions, such as body temperature regulation and breathing. When the medulla is affected, the body temperature drops, and respiration can be depressed.