An excellent example of the variable severity and pervasive nature of cognitive impairment associated with chronic WKS is provided by Pitel and colleagues (Pitel et al., 2011. When the diagnosis is based on severe, selective amnesia (Butters and Cermak, 1980), it appears that is chronic WKS rare Subtle changes in signal intensity are visible in the abducens nuclei (arrows) D) Midbrain tectum and periaqueductal gray show changes in signal intensity (arrow).
ALCOHOL-RELATED DEMENTIA AND BRAIN DAMAGE
A comparison of AUD rates in the US between 1992 and 2002 also found an increase in 12-month alcohol abuse in both sexes during this time (3.0 to 4.7 percent) despite a decrease in rates of alcohol dependence (Grant et al., 2004. A A prospective study conducted over three years in the USA also showed a higher likelihood of dementia in those who consumed more alcohol (Mukamal et al., 2003.
CULTURAL CONSIDERATIONS IN ALCOHOL USE AND MISUSE
European contact and colonization brought about changes in the social, political and economic context of alcohol use in Indigenous societies (Dietler, 2006; Westermeyer, 1996. In Australia, it is estimated that the prevalence of harmful alcohol use among Indigenous Australians is approximately twice that of the Not clear , the extent to which the high prevalence of harmful alcohol use in Indigenous populations translates into alcohol-related brain damage (ARBD).
Research into the effect of SES on alcohol use and alcohol-related consequences is complex. There are fairly consistent findings between lower SES and increased hazardous alcohol use and its consequences. The impact of other health behaviors is likely to exacerbate the negative impact of alcohol use among people who are socioeconomically disadvantaged.
Findings regarding the socioeconomic gradient on alcohol use outcomes often indicate a different pattern for men and women (Batty et al., 2012; Bloomfield et al., 2006. Characteristics of the workplace environment are also important, as workplace Harassment is associated with alcohol use and abuse (Marchand, 2008.
COMORBIDITY AND COMPLEXITY IN CHRONIC ALCOHOL MISUSE
The three drugs used to treat alcohol abuse, namely disulfiram, naltrexone and acamprosate, have rarely been evaluated in the treatment of patients with co-occurring mental health problems. Among all antidepressants, the selective serotonin reuptake inhibitors (SSRIs) and the tricyclic antidepressants (TCAs) have been evaluated in patients with comorbid depression and alcohol use. There is a lack of evidence to suggest the superiority of any type of antipsychotic for the treatment of patients with comorbid psychotic illness and alcohol abuse.
Strong sedative medications or medications that reduce the seizure threshold in a patient with alcohol abuse can be problematic (Haber et al., 2009. Psychosocial and psychological treatments for co-existing problems Psychosocial and psychological interventions have a strong evidence base in the treatment of both alcohol use disorders and psychological Disorders Twelve-step programs have been the focus of controversy in addiction medicine, particularly for treating people with comorbid alcohol use and mental health problems.
Conversely, in patients with severe mental health problems such as acute psychosis or major depression, the priority should be to stabilize the mental health problems and not focus solely on alcohol use. Alcohol use disorders in Australia: Findings from the National Survey of Mental Health and Wellbeing.
ALCOHOL AND COGNITIVE IMPAIRMENT
The Alcohol-Use Disorders Identification Test (AUDIT) was developed by the World Health Organization as a brief screening tool mainly for use in primary care settings (Babor et al., 2001. Unlike the other scales, the ARPS is able to identify a cohort of people at risk for alcohol-related impairment due to their comorbid medical illnesses or concomitant medications (Fink et al., 2002b. The MoCA has been shown to have criterion-related validity and good accuracy in correctly distinguishing cases of alcohol-related cognitive impairment (Copersino et al., 2009.
There also appears to be a general reluctance to engage in such a conversation with an older client (Duru et al., 2010. The Australian Hospital Dementia Services Project provided additional support for this relatively high number of cases (Draper et al ., 2011).Conversely, it has even been suggested that a non-binge, light to moderate pattern of alcohol consumption plays a neuroprotective role (Collins et al., 2009.
Older people are also susceptible to withdrawal at lower levels of alcohol intake than younger people, and they have a greater number of withdrawal symptoms that persist for a longer period of time (Brower et al., 1994. A more recent approach to managing alcohol withdrawal in older people is a symptom-triggered dosing regimen (Taheri et al., 2014.
ALCOHOL-RELATED BRAIN DAMAGE AND NEUROPATHOLOGY
One suggestion is that hippocampal volume loss may be caused by a reduction in white matter, rather than gray matter (Harding et al., 1997). Decreased volume of the corpus callosum and degeneration of white matter in the cerebellum, particularly the vermis, have been reported (Sullivan et al., 2000a;Sullivan et al., 2000b). In addition, mice drinking large amounts of ethanol had a small loss (approximately 9 to 15 percent) of neurons in the AT and MD thalamus (Berecochea et al., 1987.
Graded effects of volume deficits (total volume: CON>ALC>WKS) were found in the medial part of the thoracic bodies and the left insula. White matter volume loss was also observed in patients with alcoholism and WKS patients in the corpus callosum, fornix, cingulum and cerebellar peduncles. Long periods of fasting have been associated with reduced third ventricle volume (Pfefferbaum et al., 1995).
With alcohol relapse, however, there is an expansion of the third ventricle and shrinkage of white matter (Pfefferbaum et al., 1995. Projections from the anterodorsal and anteroventral nuclei of the thalamus to the limbic cortex in the rat.
THE RELATION OF ALCOHOL- INDUCED BRAIN CHANGES
MRI studies have specified that individuals with alcoholism have regional cortical volume deficits (Jernigan et al., 1991; Pfefferbaum et al., 1992. This highly connected region supports the processing of motivational or affective meaning of stimuli (Amaral et al. , 2003. A significant reduction in gray matter volume in the amygdala has been reported in those with uncomplicated alcoholism (Cardenas et al., 2011; Fein, McGillivray, & Finn, 2006.
Included in the brainstem, the medulla oblongata, the pons and midbrain have been described to be altered in MRI studies performed in those with alcoholism (Chanraud et al., 2007; Sullivan, 2003. Shrinkage of the corpus callosum has been consistently found in structural MRI studies of people with alcoholism, with the genu predominantly affected (Hommer et al., 1996; Pfefferbaum et al., 1996. White matter volume deficits in alcoholism may be explained by fewer white matter fibers in this group than controls (Chanraud et al. ., 2009.
More recent research has shown that changes in the fronto-cerebellar circuitry (Figure 8.3) may be better predictors of executive dysfunction than damage to the prefrontal lobes (Sullivan, 2003; Zahr et al., 2010). shrinkage of the gray matter of the frontal lobes, pons, thalamus and cerebellum (Chanraud et al., 2007; Sullivan, 2003.
ALCOHOL, AGEING AND COGNITIVE FUNCTION
Genetic factors also contribute to some differences in alcohol metabolism in the population. A longitudinal study by Schafer found that, in addition to the chronic neurotoxic effect of alcohol, a number of different medical and psychiatric factors, as well as the cellular effects of alcohol, contribute to patients' cognitive scores at various points in the clinical course. (Schafer et al., 1991. Melatonin and related metabolites, crucial in the regulation of the sleep-wake cycle, are synthesized from 5-HT in the dark phase.
High concentrations of the kynurenines are excreted in the urine of patients with rheumatoid arthritis, tuberculosis, leukemia, Hodgkin's disease and bladder tumors. Excitotoxicity results in overstimulation of NMDA receptors in the hippocampus, which affects long-term potentiation and the cellular basis of learning. As protection becomes less efficient, reductive oxygen species (ROS) can damage critical biological molecules in the brain, such as proteins, cell membrane lipids (Joseph et al., 1999), and nucleic acids (Tokumaru, Iguchi, & Kojo, 1996).
From a public health perspective, alcohol-related harm is linked to the availability and consumption of alcohol in the community. Effect of orally administered L-tryptophan on serotonin, melatonin and the innate immune response in rats.
NEUROPSYCHOLOGICAL ASSESSMENT OF ALCOHOL-RELATED COGNITIVE
The initial assessment should take into account biological, psychological and social factors that may affect the person's cognitive functioning. A comprehensive neuropsychological assessment can be lengthy and tiring and may have been requested to assess difficulties of which the person is not fully aware. It is important to interview a relative or relatives who know the person well, because of the possibility of impaired memory and insight, especially with alcohol-related cognitive impairment.
Gather information about the person's context and history: are there friends or family members who might have a special interest. Gather information about the person's current functional abilities, including reports from other staff, caregivers, and family members. Assess at different times of the day on a variety of occasions in order to get a reliable and consistent picture of the person's cognitive abilities.
A comprehensive assessment can also provide a profile of strengths and weaknesses that can be used to support the person to exercise any remaining capacity and overcome barriers to decision-making. Vignettes or scenarios tailored to the decision to be made can be used as a way of providing structure and support for the person to consider possible scenarios.
ETHICAL ISSUES ASSOCIATED WITH ALCOHOL-RELATED COGNITIVE
The doctor must try to understand the individual's belief system and his own, so as not to impose a point of view that the patient does not have. A person must be properly informed and aware of their situation, have a choice and know that they have a choice. Informed consent requires a person to receive appropriate person-centered information, including the diagnosis, proposed treatment, and risks and benefits.
Symptoms of frontal lobe dysfunction, such as amotivation, poor judgment, and personality changes, may be difficult to distinguish from the effects of alcohol use if the person is still drinking. It is not always clear whether a person's disability is a temporary or permanent feature. If the ability to drive is impaired and the person does not stop voluntarily (or forgets), then it may be necessary to discuss the risk with the family and/or notify the appropriate authority.
In each of these cases, the breach of confidentiality must be weighed against the seriousness of the risk the person poses by his actions. Of course, one should not override the wishes of a person with capacity, but it may be in the person's best interest to do this if they lack capacity.
