Wednesday, March 18, 2020

Reducing Out-Group Bias in Huntingtons Disease Patients

Reducing Out-Group Bias in Huntingtons Disease Patients Free Online Research Papers Huntington’s disease (HD) is a genetic condition, which results in a variety of physical and psychological symptoms. The disease leads to loss of neurons in the striatum, with more severe neuronal loss as the disease progresses. The present study aims to investigate how such degeneration may affect social stereotyping. Perspective taking has been used by numerous authors to try and reduce stereotypes, and bias against groups outside of one’s own. It was hypothesised that due to degeneration of brain areas thought to be key to the process of perspective taking and reducing bias, that HD patients would be unable to use a perspective taking task to reduce their in-group bias. The participants for this study were nine HD patients attending the Queen Elizabeth Psychiatric Hospital HD clinic, and fourteen control participants, matched for educational background. A number of measures were used, including a relative positivity scale andtrait overlap to measure in-group bias, and tests of prefrontal cortex function. Analysis showed no support for the hypothesis, with no significant differences found on the measures of relative positivity and trait overlap. However, a number of methodological problems are discussed, along with directions for future research. Introduction Huntington’s disease (HD) is an inherited, degenerative illness, thought to affect between four to ten individuals of Caucasian origin in every 100 000 (Reddy, Williams and Tagle, 1999). The disease results in a variety of motor and psychiatric symptoms. These symptoms usually begin around the age of 40 to 50 years. In the early stages of the disease, these symptoms include fidgeting, clumsiness, dance like movements referred to as chorea, absentmindedness, depression, apathy, irritability and psychosis. As the disease progresses, these symptoms worsen, with speech deterioration, facial grimacing and the development of an inability to swallow. There is also a decline in cognitive functions, especially spatial deficits, and executive function (Brandt, Leroi, O’Hearn, Rosenblatt and Margolis, 2004). In its juvenile form, the age of onset is much earlier, and the symptoms more severe. The disease eventually leads to death. Snowden, Gibbons, Blackshaw, Doubleday, Thompson, Crauford, Foster, Happe and Neary (2003) also reported some social cognition deficits in patients with HD. In their study, HD patients were found to have deficit compared to controls in the comprehension and understanding of humourous cartoons and story vignettes, although these deficits were more pronounced in patients with frontotemporal dementia, another disorder affecting the frontostriatal systems. HD is an autosomal dominant genetic condition. The disease has been linked to a mutation of the IT15 gene on chromosome 4 (the Huntington’s Disease Collaborative Research Group, 1993). The mutation of this gene causes the polymorphic trinucleotide repeat of the sequence CAG, which codes for the huntingtin preotein, to expand to over 36 repeats. This in turn causes the protein Huntingtin to fold abnormally (Li and Li, 2004), initiating a protective cellular response meant to prevent the build up of the Huntingtin protein. However, this response puts the endoplasmic reticulum of the mitochondria under stress (Rao and Bredesen, 2004), affecting mitochondrial homeostasis (Bezprozvanny and Hayden, 2004). This eventually leads to cell death. The number of CAG repeats is inversely proportional to the age on onset that the symptoms of the disease begin to manifest themselves (Andrew and Hayden, 1995). It has been suggested that the number of CAG repeats also correlates to psych iatric symptoms experienced by HD sufferers, however studies have failed to find any such correlation (Berrios, Wagle, Markova, Wagle, Ho, Rubinsztein, Whittaker, Ffench-Constant, Kershaw, Rosser, Bak and Hodges, 2001). Although the IT15 gene is found in many body tissues, the primary site of degeneration is the brain (Reddy at al, 1999), in particular the striatum. In the early stages of the disease, the dorsomedial striatum is affected, then as the disease progresses, there is more pronounced degeneration of striatal neurons, with damage spreading to the cerebral cortex. The localised pathological changes found in HD patients account for the symptoms it produces. The degeneration of the basal ganglia, in particular the striatum, affects all five of the frontal subcortical neural circuits, which have been summarised by Cummings (1993). These circuits begin in the frontal cortex, which then project to regions of the striatum, the globus pallidus and the thalamus (Tekin and Cummings, 2002). The disruption caused to the motor circuit accounts for the movement disorders seen in HD, the dorsolateral prefrontal circuit the executive function problems, the orbitofrontal circuit the depression, and the anterior cingulate circuit the apathy (Tekin and Cimmings, 2002). Cummings (1993) also reported HD patients with antisocial personality disorder, and suggested a link between HD and obsessive compulsive disorder, thought to be due to the degeneration of one of the frontal subcortical neural circuits. Previous work has highlighted the role of the prefrontal cortex in the capacity to attribute thoughts and feelings to others, therefor it is plausible that HD patients may have a problem in doing this. Ruby and Decety (2004) used a perspective taking task in their neuroimaging study to highlight the importance of the frontalpolar, the somatosensory cortex and inferior parietal lobe in distinguishing the self and the other. Furthermore, Ehlers and Bratt (1996) showed that patients with serious injury to the frontal lobes had a general lack of empathy and inability to see situations from a perspective other than their own. The ability to see the perspective of others and the reduction of stereotypes has long been discussed in social psychology. Dasgupta and Asgari (2004) cite the early writings of Allport in 1935 and his opinion that attitudes are ‘rigid’, and unlikely to be changed or modified unless ‘under the provocation of serious affective disorganisation’. However, recent theories have taken the view that attitudes are more fluid and subject to change (Dasgupta and Asgari, 2004). Being able to take the perspective of another (perspective taking) is essential for avoiding the over use of social stereotypes. Galinsky and Moskowitz (2000) investigated perspective taking in normal subjects. They found that perspective taking was an effective strategy for reducing bias against members of a social group outside of the participants’ own. Research using caregivers of cancer patients has also shown that perspective taking ‘helped to prompt adjustments down from a self orientated viewpoint’ (Lobchuk and Voruer, 2003). Davis, Conklin, Smith and Luce (1996) have also looked at perspective taking in normal participants. In their study, it was found that the use of perspective taking resulted in the participants attributing traits to novel targets that they had previously used to describe themselves. In the second part of their study, the participants were given a memory task as a distracter while completing the original perspective taking task. In this condition, it was found that there was a reduced overlap between traits assigned to self and the novel group. This would imply that persepctive taking is only effective if the perspective taking task is remembered clearly. Memory is an executive function. Using the assumption of executive function being controlled by the dorsolateral prefrontal circuit as proposed by Cummings and Tekin (2002), is it possible that damage to the dorsolateral prefrontal circuit, such as that caused by HD, could cause some patients to also have a reduced overlap in t raits assigned to a novel group and the self? Galinsky (2002) suggests that bias between out-groups and the self may be due to internal psychological processes, in particular categorisation and egocentrism. Work conducted by Filoteo, Maddox and Dais (2001) has shown that patients with HD perform poorly on categorisation tasks, such as simple line stimuli categorisation into one of two groups, leading them to conclude that HD causes deficits in learning categorisation rules. Furthermore, a neuropsychological theory of categorisation published by Ashby, Alfonso-Reese, Turken and Waldron in 1998 highlights the role of caudate nucleus, anterior cingulate and prefrontal cortices in category learning. . A similar category learning deficit has also been found in patients with Parkinson’s disease (Ashby, Noble, Filoteo, Waldron and Ell, 2003), which has similar pathology to HD, affecting the brain areas involved in frontal subcortical circuits. The above evidence has illustrated a number of deficits and potential deficits in HD patients, linked to the degeneration of the striatum and frontal subcortical circuits. Given this evidence, the present study aims to investigate the potential deficits in ingroup bias and the effect of perspective taking to reduce in group bias in patients with HD. It is hypothesised that due to the degeneration of the striatum and associated prefrontal dysfunction caused by HD, and the loss of psychological functions associated with the damaged frontal subcortical circuits, HD sufferers will be unable to use a perspective taking exercise, similar to that used by Galinsky and Moskowitz (2000), to reduce their ingroup bias. This hypothesis will be tested using asylum seekers as an out group, as it is unlikely any of the participants will have had any direct contact with members of this group. Trait lists containing positive and negative items will be used to measure any bias. Method Participants Information packs about the study were sent to all patients attending the Huntington’s Disease clinic at the Queen Elizabeth Psychiatric Hospital, whom the Clinic Consultant deemed able to participate in the study (a copy of this pack can be found in Appendix A). All of these patients had a confirmed diagnosis of Huntington’s disease, via genetic testing. Of these, eleven patients volunteered to participate in the study. Two patients’ data was excluded from the data analysis due to failure to complete the experimental protocol. The remaining nine participants were four males and five females, with a mean age of 52.4. These participants were at various stages of the disease, however, due to time constraints, no formal measure of the severity of the disease could be taken. Control participants were recruited by opportunity sampling. A total of fifteen control participants were tested, of which one participants’ data was discarded due to a large number of outliers in their performance across all tasks in the experimental protocol. These participants had no diagnosis of Huntington’s disease, nor any family history of the disease. The fourteen control participants whose data was used were seven males and seven females, with a mean age of 59.4. Procedure Patients were tested either in their homes or at the Huntington’s Disease Clinic at the Queen Elizabeth Psychiatric Hospital, in accordance with their preference. Patients were permitted to bring one friend or relative into the testing room if they desired. The control patients were tested in their homes. At the beginning of each testing session, all participants were asked to sign a consent form, and complete a short questionnaire regarding demographic information, including age, gender and educational background (a copy of this questionnaire can be found in Appendix B). Participants were then asked to complete each task from the experimental protocol (a copy of the protocol can be found in Appendix B). The testing session was recorded using a Dictaphone recording device in all sessions. After analysis, these recordings were destroyed. If any participant was unable to complete the pen and paper elements of the protocol due to reading difficulties or difficulties associated to their movement disorder, these sections were read to the participant and recorded by the experimenter. At the end of the testing session, each participant was debriefed, and given a debriefing letter to take away with him or her (a copy of this debriefing letter can be found in Appendix A). Measures FAS The FAS Word Fluency Test was used as a general measure of prefrontal cortex functioning. In this test, participants were asked to generate as many words as they could in one minute which began with the letter F, then repeat the task with the letters A and S. This test was used to assess if there was any significant difference in prefrontal cortex functioning between the patient and control groups. Emotional Stroop The Emotional Stroop tests were used to evaluate prefrontal functioning, and to measure reduction of in-group bias. This task was repeated before and after the perspective taking task. Three conditions were used; an XXXX condition, in which rows of XXXX were presented to serve as a control for the word conditions, neutral words, and words seeded with words salient to the out-group (asylum seekers). The words salient with the out group were gained via a pilot study. Initially, an opportunity sample of students from the University of Birmingham were interviewed and asked to generate words they felt were most frequently associated with asylum seekers. The words collected from this pilot study were then compiled into a questionnaire used in a second pilot study. Again, an opportunity sample of students from the University of Birmingham were used, and asked to tick the ten words from the list they felt were most frequently associated with asylum seekers. The ten highest scoring wo rds from this pilot study were then used in the stroop test. Words for the neutral and seeded conditions were matched for word frequency and word length. Perspective Taking Task A perspective taking task was used in order to try and reduce in-group bias. The participant was given a picture of a mythical asylum seeker, with a number of prompting words printed under the picture, and asked to ‘Adopt the perspective of an asylum seeker and imagine the day in their life as if you were that person, looking at the world through his/her eyes and walking in their shoes’, and describe a typical day in that persons’ life. The prompting words can be found in the experimental protocol, in Appendix B. Trait Lists Trait questionnaires were used to assess in-group bias before and after the perspective taking task. The trait list contained ten positive and ten negative traits, and the order of the words on the trait lists was randomised as such that the traits listed were not in the same order for the second presentation. Analysis Relative Positivity A measure of relative positivity was obtained. This was achieved by first subtracting the number of negative traits from the number of positive ones for each pair of trait lists (self on first presentation, out-group at first presentation, self at second presentation, outgroup at second presentation). This created a measure of positivity. The numbers generated from this exercise were then used in a second calculation. The positivity of the out-group before perspective taking was subtracted from the positivity of self before perspective taking. This was repeated for the after perspective taking results. Trait Overlap In order to gain the data for the trait overlap analysis, traits assigned to both the self and the out-group for each repetition of the task (before / after perspective taking) was measured. Where a trait was shared, a score of 1 was recorded, and where a trait was not shared, a score of 0 was allocated. Results FAS Word Fluency Test Table 1.1 Mean number of words generated in the FAS test. Group Mean number of words generated Standard deviation Patients 25.00 17.62 Controls 53.50 17.99 Participants in the patient condition generated fewer words (mean score = 25, SD = 17.62) than the control condition (mean score = 53, SD = 17.99). The 95% confidence interval for the estimated general population is between –12.64 and –44.36. An independent t-test showed that if there was no significant difference between the scores of patients and controls, this result would be highly unlikely (t = -3.737, DF =21, p

No comments:

Post a Comment

Note: Only a member of this blog may post a comment.