Aurora
05-21-2014, 09:23 PM
My mother is an alcoholic (she drinks bottles and bottles of wine every night) She's been an alcoholic for more than 25 years. I'm noticing some serious brain damage. She has a hard time with memory and understanding. I was doing a little research and thought I'd share.
Enjoy!
http://pubs.niaaa.nih.gov/publications/arh27-2/IMAGES/Page127.gif
Areas of the brain that are especially vulnerable to alcoholism–related damage are the cerebral cortex and subcortical areas such as the limbic system (important for feeling and expressing emotions), the thalamus (important for communication within the brain), the hypothalamus (which releases hormones in response to stress and other stimuli and is involved in basic behavioral and physiological functions), and the basal forebrain (the lower area of the front part of the brain, involved in learning and memory) (Oscar–Berman 2000). Another brain structure that has recently been implicated is the cerebellum (Sullivan 2000), situated at the base of the brain, which plays a role in posture and motor coordination and in learning simple tasks.
Alcohol–Related Brain Atrophy. According to one hypothesis, shrinkage (i.e., atrophy) of the cerebral cortex and white matter, as well as possible atrophy of basal forebrain regions, may result from the neurotoxic effects of alcohol (Lishman 1990). Furthermore, thiamine deficiency may result in damage to portions of the hypothalamus (perhaps because blood vessels break in that region). According to this hypothesis, alcoholics who are susceptible to alcohol toxicity2 may develop permanent or transient cognitive deficits associated with brain shrinkage. (2 Some people may have better immunity than others to alcohol’s toxic effects.) Those who are susceptible to thiamine deficiency will develop a mild or transient amnesic disorder, with short–term memory loss as the salient feature. Patients with dual vulnerability, those with a combination of alcohol neurotoxicity and thiamine deficiency, will have widespread damage to large regions of the brain, including structures deep within the brain such as the limbic system. These people will exhibit severe short–term memory loss and collateral cognitive impairments (Oscar–Berman 2000).
Frontal Lobe Vulnerability. Although alcoholics have diffuse damage in the cerebral cortex of both hemispheres of the brain, neuropathological studies performed on the brains of deceased patients as well as findings derived from neuroimaging studies of living brains point to increased susceptibility of frontal brain systems to alcoholism–related damage (Moselhy et al. 2001; Oscar–Berman 2000; Sullivan 2000). The frontal lobes are connected with all other lobes of the brain (i.e., the parietal, temporal, and occipital lobes on both halves of the brain; see figure 1), and they receive and send fibers to numerous subcortical structures. Behavioral neuroscientists have determined that the anterior region of the frontal lobes (i.e., the prefrontal cortex) is important for engaging in ordinary cognitive, emotional, and interpersonal activities. The prefrontal cortex is considered the brain’s executive—that is, it is necessary for planning and regulating behavior, inhibiting the occurrence of unnecessary or unwanted behaviors, and supporting adaptive “executive control” skills such as goal–directed behaviors, good judgment, and problem–solving abilities. Disruptions of the normal inhibitory functions of prefrontal networks often have the interesting effect of releasing previously inhibited behaviors. As a result, a person may behave impulsively and inappropriately, which may contribute to excessive drinking.
There is evidence that the frontal lobes are particularly vulnerable to alcoholism–related damage, and the brain changes in these areas are most prominent as alcoholics age (Oscar–Berman 2000; Pfefferbaum et al. 1997; Sullivan 2000) (see figure 2). Other studies of frontal lobe function in older alcoholics have confirmed reports of a correlation between impaired neuropsychological performance (e.g., executive control skills, as noted above) and decreased blood flow or metabolism (energy use) in the frontal lobes, as seen using neuroimaging techniques (Adams et al. 1998).
http://pubs.niaaa.nih.gov/publications/arh27-2/IMAGES/Page128.gif
Figure 2 Brain MRI scans of age–equivalent men with different histories of alcohol use. The image shows clear evidence of brain shrinkage in the alcoholic compared with the control subject. The graph on the right shows that older alcoholics have less cortical tissue than younger alcoholics, and that the prefrontal cortex is especially vulnerable to alcohol’s effects. The location of the temporal, parietal, and occipital regions of the brain can be seen in figure 1.
*Z–score is a mathematical measure that is useful for showing the difference between the recorded value and a “normal” value.
SOURCE: Pfefferbaum et al. 1997.
To read more... http://pubs.niaaa.nih.gov/publications/arh27-2/125-133.htm
Enjoy!
http://pubs.niaaa.nih.gov/publications/arh27-2/IMAGES/Page127.gif
Areas of the brain that are especially vulnerable to alcoholism–related damage are the cerebral cortex and subcortical areas such as the limbic system (important for feeling and expressing emotions), the thalamus (important for communication within the brain), the hypothalamus (which releases hormones in response to stress and other stimuli and is involved in basic behavioral and physiological functions), and the basal forebrain (the lower area of the front part of the brain, involved in learning and memory) (Oscar–Berman 2000). Another brain structure that has recently been implicated is the cerebellum (Sullivan 2000), situated at the base of the brain, which plays a role in posture and motor coordination and in learning simple tasks.
Alcohol–Related Brain Atrophy. According to one hypothesis, shrinkage (i.e., atrophy) of the cerebral cortex and white matter, as well as possible atrophy of basal forebrain regions, may result from the neurotoxic effects of alcohol (Lishman 1990). Furthermore, thiamine deficiency may result in damage to portions of the hypothalamus (perhaps because blood vessels break in that region). According to this hypothesis, alcoholics who are susceptible to alcohol toxicity2 may develop permanent or transient cognitive deficits associated with brain shrinkage. (2 Some people may have better immunity than others to alcohol’s toxic effects.) Those who are susceptible to thiamine deficiency will develop a mild or transient amnesic disorder, with short–term memory loss as the salient feature. Patients with dual vulnerability, those with a combination of alcohol neurotoxicity and thiamine deficiency, will have widespread damage to large regions of the brain, including structures deep within the brain such as the limbic system. These people will exhibit severe short–term memory loss and collateral cognitive impairments (Oscar–Berman 2000).
Frontal Lobe Vulnerability. Although alcoholics have diffuse damage in the cerebral cortex of both hemispheres of the brain, neuropathological studies performed on the brains of deceased patients as well as findings derived from neuroimaging studies of living brains point to increased susceptibility of frontal brain systems to alcoholism–related damage (Moselhy et al. 2001; Oscar–Berman 2000; Sullivan 2000). The frontal lobes are connected with all other lobes of the brain (i.e., the parietal, temporal, and occipital lobes on both halves of the brain; see figure 1), and they receive and send fibers to numerous subcortical structures. Behavioral neuroscientists have determined that the anterior region of the frontal lobes (i.e., the prefrontal cortex) is important for engaging in ordinary cognitive, emotional, and interpersonal activities. The prefrontal cortex is considered the brain’s executive—that is, it is necessary for planning and regulating behavior, inhibiting the occurrence of unnecessary or unwanted behaviors, and supporting adaptive “executive control” skills such as goal–directed behaviors, good judgment, and problem–solving abilities. Disruptions of the normal inhibitory functions of prefrontal networks often have the interesting effect of releasing previously inhibited behaviors. As a result, a person may behave impulsively and inappropriately, which may contribute to excessive drinking.
There is evidence that the frontal lobes are particularly vulnerable to alcoholism–related damage, and the brain changes in these areas are most prominent as alcoholics age (Oscar–Berman 2000; Pfefferbaum et al. 1997; Sullivan 2000) (see figure 2). Other studies of frontal lobe function in older alcoholics have confirmed reports of a correlation between impaired neuropsychological performance (e.g., executive control skills, as noted above) and decreased blood flow or metabolism (energy use) in the frontal lobes, as seen using neuroimaging techniques (Adams et al. 1998).
http://pubs.niaaa.nih.gov/publications/arh27-2/IMAGES/Page128.gif
Figure 2 Brain MRI scans of age–equivalent men with different histories of alcohol use. The image shows clear evidence of brain shrinkage in the alcoholic compared with the control subject. The graph on the right shows that older alcoholics have less cortical tissue than younger alcoholics, and that the prefrontal cortex is especially vulnerable to alcohol’s effects. The location of the temporal, parietal, and occipital regions of the brain can be seen in figure 1.
*Z–score is a mathematical measure that is useful for showing the difference between the recorded value and a “normal” value.
SOURCE: Pfefferbaum et al. 1997.
To read more... http://pubs.niaaa.nih.gov/publications/arh27-2/125-133.htm