Alcohol-related brain damage
Alcohol-related brain damage
Frontal lobe damage becomes the most prominent as alcoholics age and can lead to impaired neuropsychological performance in areas such as problem solving, good judgment, and goal-directed behaviors.[2] Impaired emotional processing results from damage to the limbic system. This may lead to troubles recognizing emotional facial expressions and "interpreting nonverbal emotional cues".[2]
Gender and parental history of alcoholism and binge drinking has an influence on susceptibility to alcohol dependence as higher levels are typically seen in males and in those with a family history.[5]
Prevalence
Nearly half of American alcoholics exhibit "neuropsychological disabilities [that] can range from mild to severe"[2] with approximately two million requiring lifelong care after developing permanent and debilitating conditions. Prolonged alcohol abstinence can lead to an improvement in these disabilities. For those with mild impairments, some improvement has been seen within a year, but this can take much longer in those with higher severity damage.[2]
Populations at risk
Adolescents and genetic factors
The impulsivity and sensation seeking seen in adolescence may lead to increased alcohol intake and more frequent binge drinking episodes leaving adolescents particularly at risk for alcoholism. The still developing brain of adolescents is more vulnerable to the damaging neurotoxic and neurodegenerative effects of alcohol.[6] "High impulsivity has [also] been found in families with alcoholism, suggestive of a genetic link. Thus, the genetics of impulsivity overlaps with genetic risks for alcohol use disorder and possibly alcohol neurodegeneration".[6]
There is also a genetic risk for
Neurological deficits
Alcoholics can typically be divided into two categories, uncomplicated and complicated.[3] Uncomplicated alcoholics do not have nutritional deficiency states or liver disease, but have a reduction in overall brain volume due to white matter cerebral atrophy. The severity of atrophy sustained from alcohol consumption is proportional to the rate and amount of alcohol consumed during a person's life.[7] Complicated alcoholics may have liver damage that impacts brain structure and function and nutritional deficiencies "that can cause severe brain damage and dysfunction".[3][7]
Pathophysiology
Adolescents are much more vulnerable to alcohol-related brain damage in the form of persistent changes in neuroimmune signalling from binge drinking.[8] The endocrine system includes the hypothalamic–pituitary–adrenal axis, the hypothalamic–pituitary–gonadal axis, the hypothalamic–pituitary–thyroid axis, the hypothalamic–pituitary–growth hormone/insulin-like growth factor-1 axis, and the hypothalamic–posterior pituitary axis, as well as other sources of hormones, such as the endocrine pancreas and endocrine adipose tissue. Alcohol abuse disrupts all of these systems and causes hormonal disturbances that may result in various disorders, such as stress intolerance, reproductive dysfunction, thyroid problems, immune abnormalities, and psychological and behavioral disorders.[9]
The cerebral atrophy that alcoholics often present with is due to alcohol induced neurotoxicity.[6][10] Evidence of neurodegeneration can be supported by an increased microglia density and expression of proinflammatory cytokines in the brain. Animal studies find that heavy and regular binge drinking causes neurodegeneration in corticolimbic brain regions areas which are involved in learning and spatial memory. The corticolimbic brain regions affected include the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and the hippocampal dentate gyrus. It was found that a heavy two-day drinking binge caused extensive neurodegeneration in the entorhinal cortex with resultant learning deficits in rats.[5]
It is unclear how the frequency and length of these binge drinking sessions impacts brain damage in humans. Humans who drank at least 100 drinks (male) or 80 drinks (female) per month (concentrated to 21 occasions or less per month) throughout a three-year period had impaired decision-making skills compared to non-binge drinkers.
The volume of the corpus callosum, a large white matter tract that connects the two cerebral hemispheres, is shown to decrease with alcohol abuse due to a loss of myelination. This integration between the two cerebral hemispheres and cognitive function is affected. A limited amount of myelin can be restored with alcohol abstinence, leading to transient neurological deficits.[7]
Alcohol abuse affects neurons in the frontal cortex that typically have a large soma, or cell body. This type of neuron is more susceptible to Alzheimer's disease and normal aging. Research is still being conducted to determine whether there is a direct link between excessive alcohol consumption and Alzheimer's disease.[7]
Higher order functioning of the cerebral cortex is organized by the cerebellum. In those with cerebral atrophy,
Kindling and excitotoxicity
Binge drinkers and alcoholics who go through multiple detoxifications show
Thiamine deficiency
Neuroimaging
Neuroimaging is used to study the effect that alcohol has on the brain. The two main imaging methods are hemodynamic and electromagnetic. These techniques have allowed for the study of the functional, biochemical, and anatomical changes of the brain due to prolonged alcohol abuse.[2] Neuroimaging provides valuable information in determining the risk an individual has for developing alcohol dependence and the efficacy of potential treatment.[2][16]
Hemodynamic methods
Magnetic resonance imaging (MRI) and functional magnetic resonance imaging (fMRI) are other commonly used tenichiques. These methods are noninvasive, and have no radioactive risk involved. The fMRI method records the metabolic changes in a particular brain structure or region during a mental task. To detect damage to white matter, the standard MRI is not sufficient. An MRI derivative technique known as diffusion tensor imaging (DTI) is used to determine the orientation and integrity of specific nerve pathways, allowing the detection of damage.[2] When imaging those with alcoholism, the DTI results show that heavy drinking disrupts the microstructure of nerve fibers.[2] Another MRI derivative technique, magnetic resonance spectroscopy imaging (MRSI), can provide further information about the brain's neurochemistry and can detect the distribution of certain metabolites, neurotransmitters, and alcohol.[citation needed]
Electromagnetic methods
While the hemo-dynamic methods are effective for observing spatial and chemical changes, they cannot show the time course of these changes. Electromagnetic imaging methods are capable of capturing real-time changes in the brain's electrical currents.[17]Electroencephalography (EEG) imaging utilizes small electrodes that are attached to the scalp. The recordings are averaged by a technique known as event-related potentials (ERP). This is done to determine the time sequence of activity after being exposed to a stimulus, such as a word or image.[2] Magnetoencephalography (MEG) is another imaging method that utilizes sensors. This measures the magnetic field created as a result of the brain's electrical activity. These techniques are noninvasive, harmless, and provide a large amount of detail regarding the order and timing of electrical activity. The poor spatial imaging of these methods are a large downside.[citation needed]
These neuroimaging methods have found that alcohol alters the nervous system on multiple levels.[2] This includes impairment of lower order brainstem functions and higher order functioning, such as problem solving. These methods have also shown differences in electrical brain activity and responsiveness when comparing alcohol-dependent and healthy individuals.[2]
Clinical applications
In Korsakoff patients, MRI shows atrophy of the thalamus and mamillary bodies. PET showed decreased metabolism, and therefore decreased activity in the thalamus and other diencephalon structures.[13] Uncomplicated alcoholics, those with chronic Wernicke's encephalopathy (WE), and Korsakoff psychosis showed significant neuronal loss in the frontal cortex, white matter, hippocampus, and basal forebrain.[13] Uncomplicated alcoholics were seen to have a shrinkage in raphe neurons, the mamillary bodies, and the thalamus.[13]
Treatment and prevention
Alcohol-related brain damage can have drastic effects on the individuals affected and their loved ones. The options for treatment are very limited compared to other disorders. Although limited, most patients with alcohol-related cognitive deficits experienced slight improvement of their symptoms over the first two to three months of treatment.[7] Others have said to see increase in cerebral metabolism as soon as one month after treatment.[2]
Education on the prevention of alcoholism is the best supported method of avoiding alcohol-related brain damage.[7] By providing information that studies have found on risk factors and the mechanisms of damage, the efforts to find an effective treatment may increase. This may also reduce mortality by influencing doctors to pay closer attention to the warning signs.[7]
References
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