Hintergrund: Mangelnde Krankheitseinsicht bei Schizophrenie ist ein verbreitetes Phänomen, dessen Zusammenhänge mit Outcome-Maßen wie Krankheitsverlauf, Funktionsniveau und Lebensqualität vielfach belegt sind. Trotz vieler unterschiedlicher Ansätze zur Erklärung der Entstehung von Krankheitseinsicht ist sie bisher nur unzureichend verstanden. Obwohl angenommen wird, dass verschiedene Faktoren wie kognitive und motivationale Voraussetzungen Einsicht limitieren können, stehen die Identifikation von spezifischen Einflussgrößen sowie die empirische Überprüfung distinkter Prozesse und deren Wirkgefüges aus. Die Integration unterschiedlicher Ansätze in mehrfaktorielle Modelle, wie Startup (1996) nahe legt, gilt als vielversprechend. Diese sollten insbesondere vermutete motivationale Einflussgrößen enthalten, die bisher nur unzulänglich berücksichtigt wurden. Methoden: Es wurden drei empirische Studien zur Überprüfung und Erweiterung des multifaktoriellen Ansatzes von Startup (1996) zur Erklärung mangelnder Krankheitseinsicht (G12 aus der Positive and Negative Syndrome Scale [PANSS]: Kay, Fiszbein & Opler, 1987) durchgeführt. An großen heterogenen Stichproben (N = 248; N = 111; N = 95) wurden zunächst das Regressionsmodell nach Startup (1996) sowie die dort implizierten Einsichts-subtypen überprüft. Zweitens wurden zur Vorhersage von Einsicht (Scale to Assess Unawareness of Mental Disorder [SUMD]: Amador & Strauss, 1990) schrittweise soziodemographische, klinische (PANSS) und kognitive Maße (Wisconsin Card Sorting Test [WCST]: Heaton, Chelune, Talley, Kay & Curtiss, 1993) sowie Stigmatisierung (Self-Stigma of Mental Illness Scale [SSMIS]: Corrigan, Watson & Barr, 2006) als ein Maß motivational relevanter Einflüsse in ein multiples Regressionsmodell eingefügt. Zur Charakterisierung unterschiedlicher Einsichts-Subgruppen wurden diese drittens anhand von soziodemographischen, klinischen und kognitiven Variablen sowie zusätzlich durch subjektive Krankheitskonzepte (Illness Perception Questionnaire for Schizophrenia [IPQS]: Lobban, Barrowclough & Jones, 2005) vorhergesagt. Ergebnisse: Der von Startup (1996) berichtete kurvilineare Zusammenhang zwischen Einsicht und Neurokognition wurde regressionsanalytisch bestätigt. Die Varianzaufklärung der Einsicht durch neurokognitive Maße fiel jedoch eher gering (R2 = .052) aus. Durch das Hinzufügen einer Stigmatisierungsvariable (Zustimmung der Patienten zu negativen schizophreniespezifischen Stereotypen) in das Regressionsmodell wurde die Varianzaufklärung signifikant, aber schwach verbessert (ΔR2 = .049). Je mehr die Patienten den negativen Stereotypen zustimmten, desto uneinsichtiger waren sie. Es konnten außerdem drei Einsichtssubgruppen identifiziert werden: eine Gruppe ohne Einsichts- und Kognitionseinschränkungen, eine mit Defiziten in beiden Bereichen und eine Gruppe, die trotz intakten kognitiven Vermögens mangelnde Einsicht vorwies (17 - 30 %). Zur multinomialen Vorher-sage der letztgenannten Subgruppe trugen insbesondere die subjektiven Bewertungen zur Kontrollierbarkeit und zur eigenen emotionalen Reaktion signifikant bei (R²N = .56). Patienten, die die eigene Erkrankung für weniger kontrollierbar und stärker emotional relevant hielten, hatten niedrigere Einsichts-Scores. Diskussion: Die vorliegende Arbeit gilt als Beleg für die Existenz unterschiedlicher einsichtslimitierender Prozesse und ergänzt damit bisherige, überwiegend monokausale Ansätze zur Erklärung der Genese mangelnder Krankheitseinsicht. Die Bedeutung kognitiver Defizite scheint für einen Teil der Patienten evident. Darüber hinaus wurde für einen substantiellen Anteil an Patienten auch die Annahme motivierter Uneinsichtigkeit gestützt. Erstmalig wurden spezifisch mit motivational reduzierter Einsicht assoziierte Faktoren aufgedeckt: die stärkere Zustimmung zu negativen Stereotypen als Hinweis auf Stigmatisierungsprozesse, geringere wahrgenommene Kontrollierbarkeit der eigenen Erkrankung und eine stärkere emotionale Reaktion auf die Erkrankung. Es wird angenommen, dass verringerte Einsicht die Bedeutung dieser negativen Kognitionen (z. B. zur Kontrollierbarkeit, zur emotionalen Bedeutung oder zu Stereotypen wie Gewalttätigkeit) reduzieren kann, da diese wegen der Uneinsichtigkeit nicht auf die eigene Person übertragen werden. Der Mangel an Einsicht könnte daher auch einen Selbstschutz darstellen. In Bezug auf therapeutische Interventionen erscheinen kognitive Trainings folglich nur für einige Patienten sinnvoll, während für andere eher motivierende und an den subjektiven Einstellungen und Bewertungen ansetzende Behandlungsmaßnahmen zu berücksichtigen sind. Dafür bieten sich insbesondere moderne kognitiv-verhaltenstherapeutische Behandlungsansätze wie Motivational Interviewing oder Methoden der kognitiven Umstrukturierung an. Die Entwicklung und Integration einsichtsspezifischer Interventionen, für die aus der vorliegenden Arbeit Ansatzpunkte ableitbar sind, wird darüber hinaus empfohlen.

Thesis (Ph.D. (Psychology)) -- University of Limpopo, 2016 / After the World Health Organization (WHO) declared 2010 a decade of indigenous knowledge systems, there has been an increase in the studies on the role of African traditional healers in describing mental illness and its treatment. Studies have pointed to the relevance of traditional healing in primary health care in many developing countries. The aim of the present study was to explore the conceptualisation and treatment of mental illness by Zezuru Shona traditional healers in Goromonzi District in Zimbabwe. A qualitative research design, and in particular, the phenomenological method was used in the present study. Ten Shona traditional healers were selected through purposive and snowball sampling and requested to participate in the study. Data was collected through in-depth interviews and analysed using Hycner’s phenomenological explicitation process. Five major themes related to the traiditonal healers’ conceptualisation on mental illness were identified. These are: a). Types/characteristics of mental illness; b). Causes of mental illness; c). Diagnosis and treatment of mental illness; d). Challenges faced by traditional healers; and, e). Facilitating factors in the work of traditional healers. The study further revealed that there are a number of illnesses that are are not mental illness but could be closely associated with mental illness. These are epilepsy (pfari), locking (kusungwa) and sexual dysfunctions. Culture was found to play a central role in the traditional healers’ conceptualisation and treatment of mental illness. In this regard, spirituality was found to be a critical factor in the work of traditional healers in diagnosing, interpreting, treating and preventing mental illness and the associated conditions of ill health. These results were discussed in the context of indigenous knowledge systems and mental illness. The study is concluded by recommending the need to have a holistic understanding of mental illness and associated conditions.

Asthma management in school-aged children, particularly controller medication use, is best conceptualized as parent-child shared management. Controller medication nonadherence is common, and leads to higher disease morbidity such as cough, sleep disruption, poor activity tolerance, and asthma exacerbation. The purpose of this study was to describe asthma illness representations of both school-aged children (6-11 years) with persistent asthma and their parents, and to examine their interdependence. The Common Sense Model of Self-regulation, modified to include Parent-Child Shared Regulation, provided the framework for this descriptive, cross-sectional study. Thirty-four parent-child dyads independently reported on asthma control, controller medication adherence, and asthma illness representations by completing the Childhood Asthma Control Test, Medication Adherence Report Scale for Asthma, Brief Illness Perception Questionnaire, and Beliefs about Medicines Questionnaire. Using intraclass correlations, moderate agreement was evident between the parent and child timeline (perceived duration) illness representation domain (ICC= .41), and there was a weak association between the parent and child symptoms domain (ICC = .13). The remaining controllability and consequences domains showed no agreement. Hierarchical regression analyses were used to test parent and child illness representation domain variables as predictors of parent or child estimates of medication adherence. With parent-reported medication adherence as the dependent variable, regression models used parent illness representation variables followed by the corresponding child variable. Parent beliefs about medication necessity versus concerns was a significant predictor of parent-reported treatment adherence (β = .55, p < .01). Child-reported treatment control was also predictive of parent-reported treatment adherence (β -.50, p < .01). When child-reported medication adherence was the dependent variable, the child illness representation variable was entered first followed by the parent variable. Child beliefs about medication necessity versus concerns was the only significant predictor of child-reported adherence (child β .50, p < .01), none of the parent variables reached significance. Findings from this study indicate that although there are similarities between parent and child asthma illness representations, parental illness representations do not predict children's estimation of controller medication adherence. These findings indicate that school-aged children develop illness representations somewhat independent from their parents and, therefore, are critical participants in both asthma care as well as research.

This study is based on eight interviews with six people. What these people have in common is that their illnesses are not verifiable from a normal medical perspective. The overall purpose of this study is to generally investigate the importance of music in everyday medical contexts, and specifically study how people with illness relate to their bodies, both in the encounter with standard medical care and with the use of music. The primary philosophical inspiration comes from Maurice Merleau-Ponty, while the theory owes much to phenomenology. The descriptions of subjects’ interaction with the healthcare system is also analysed from the perspective of discourse theory. The study shows that music ought to be understood holistically; a complex interplay between subject, object and context. When patients are treated in the established healthcare, they must consciously adjust their body with makeup, clothing, tone of voice, and gesture in order to be trusted. This leads to the embodiment of the idea of disease, which makes them feel even worse. The study also shows how music, when it’s chosen and enjoyed can actualize our healthy aspects. The use of music as self-treatment cultivates health-promoting habits which expand our worlds, and can thereby mitigate the illness we experience / <p>Daniel Gabrielsson</p><p>daniel@varia.nu</p><p>0702884547</p>

Current treatment practice guidelines in a number of countries mandate the assessment of violence risk in all patients diagnosed with schizophrenia. Although more than 100 different instruments have been developed to facilitate the assessment of violence risk, few have been specifically validated for use in those with schizophrenia. Recent work instead suggests that these instruments are typically associated with lower predictive validity in samples with schizophrenia when compared to that achieved in diagnostically heterogeneous samples, leading to concerns that these instruments omit risk factors that may be specific to the prediction of violence risk in this population. The present thesis therefore aimed to investigate the predictive validity of a number of risk factors for violence in those with schizophrenia. Firstly, to identify key risk factors for violence, a meta-analysis was undertaken, finding that although a number of criminal history risk factors are strongly associated with violence risk, nonetheless a number of risk factors rarely assessed by existing violence risk assessment instruments were significantly associated with violence in those with schizophrenia; most notably a history of attempted suicide. Results of this review also suggested that although the criminal history domain is most strongly associated with violence risk, nonetheless, there is considerable variability in the magnitude of association for the individual risk factors. Study two therefore aimed to investigate this variability and found that a history of violence was most strongly associated with subsequent violence. Study three aimed to identify whether suicidal behaviour, which has rarely been considered risk factors for violence in previous work, incrementally contributes to the prediction of violence. A simple risk model composed of young age, comorbid substance use disorder, previous violence, and a history of suicidal threats, explained as much predictive validity, as measured by the area under the receiver operating characteristic curve, as established risk assessment instruments such as the HCR–20, LSI–R, PCL–R, and VRAG. Current risk assessment approaches may therefore need revision in light of these findings.

G-protein coupled receptor 50 (GPR50) is a genetic risk factor for psychiatric illness. It is a member of the melatonin receptor family, which includes the well characterised melatonin receptors 1 and 2 (MT1 and MT2). However, the ligand for GPR50 remains elusive and little is known about GPR50 signalling pathways. Despite this, GPR50 is known to enhance neurite outgrowth and inhibit the actions of the neurite outgrowth inhibitor NOGO-A. Existing evidence also indicates a role in lipid metabolism; GPR50 knockout mice displayed abnormalities in energy homeostasis and weight control, whilst sequence variants are associated with altered lipid levels in humans. Further, a yeast-2-hybrid screen identified SREBF2 and ABCA2, regulators of lipid homeostasis, as GPR50 interactors. This thesis explores the role of GPR50 in neuronal development and lipid metabolism. The work presented in this thesis shows that GPR50 promotes neuronal differentiation. Overexpression significantly increased the number of neurites per cell in SH-SY5Y cells. Further, dendritic branching was enhanced by GPR50 transfection in hippocampal and cortical neurons (DIV 14). In hippocampal neurons, GPR50 transfection also lead to a shift towards spine maturity although it had no effect on spine morphology, suggesting GPR50 enhances spine development but may not alter synaptic strength. The effect of GPR50 on neuronal morphology may be driven by actin remodelling. Immunocytochemistry showed an enrichment of GPR50 in highly dynamic regions of the membrane, i.e. the lamellipodia and dendritic spines. Overexpression in SH-SY5Y cells also resulted in an increase in WAVE-2 and phosphorylated RAC1/CDC42, key modulators of actin dynamics. Additionally, GPR50 transfection altered the protein level and localisation of α- catenin, another regulator of actin organisation, in HEK293 and SH-SY5Y cells respectively. An involvement of GPR50 in lipid metabolism has also been demonstrated in this thesis. Verification of the Y2H study suggested GPR50 does not physically interact with SREBF2 or ABCA2. However, ABCA2 appears to induce the intracellular localisation of GPR50 in several cell lines. In SH-SY5Y cells, this was mimicked by the inhibition of cholesterol trafficking, suggesting the translocation of GPR50 to the plasma membrane is dependent on cholesterol transport. Further, the depletion of lipoproteins resulted in the downregulation of GPR50, indicating a responsiveness to lipid levels. Finally, GPR50 increased lipid metabolism, as seen by a decrease in intracellular lipid droplets upon GPR50 overexpression. The data presented here extends previous work indicating a role of GPR50 in neurodevelopment. It also highlights a potential mechanism by which GPR50 regulates neuronal morphology, i.e. via actin remodelling. Reports that GPR50 is involved in energy homeostasis is also supported in this thesis, further, results presented here suggest GPR50 is specifically involved in lipid metabolism. These processes are often disrupted in mental illness, thus this work may provide a functional link between GPR50 and psychiatric disorders.

The genetic contribution to the aetiology of psychiatric illness is well-established; however, few variants that alter the encoded protein have been irrefutably identified as causative, leading to the hypothesis that variants affecting gene regulation may play a pathogenic role. This thesis focuses on two genes, Neuregulin 1 (NRG1) and Disrupted in Schizophrenia 1 (DISC1), for which there is strong genetic evidence for involvement in psychiatric illness, as well as evidence for altered expression in patients. Association analysis was carried out to assess the involvement of six intronic NRG1 single nucleotide polymorphisms (SNPs) in schizophrenia and bipolar disorder in two independent samples from the Scottish (Scottish 2; n = 307 control subjects, 303 schizophrenic patients, and 239 bipolar disorder patients and German populations (n = 397 control subjects, 396 schizophrenic patients, and 400 bipolar disorder patients). These SNPs form two haplotypes, one encompassing the 5’ and promoter region of the gene and the other located at the 3’ end of the gene, that were previously associated with schizophrenia and bipolar disorder in a Scottish sample (Scottish 1). The location of these haplotypes, together with the prior evidence for altered NRG1 expression in schizophrenia, suggested the potential involvement of regulatory variants. On combining the Scottish 1 and Scottish 2 samples (combined n = 765 control subjects, 682 schizophrenic patients and 601 bipolar disorder patients), a two- SNP haplotype spanning both coding and non-coding regions in the 3’ region was associated with schizophrenia (p = 0.0037, OR=1.3, 95% CI: 1.1-1.6) and the combined schizophrenia and bipolar disorder case group (p = 0.0080, OR=1.2, 95% CI: 1.1-1.5), with both these associations remaining significant after permutation analysis (p = 0.022 and p = 0.044, respectively). To further understanding of how DISC1, a leading candidate gene for schizophrenia that has also been implicated in other psychiatric disorders, is regulated the previously uncharacterised promoter region was assessed both bioinformatically and in vitro using the dual luciferase reporter assay. The region was found to lack canonical promoter motifs but to contain a CpG island, consistent with DISC1’s ubiquitous pattern of expression. A region located 300bp to -177bp relative to the transcription start site (TSS) was identified as contributing positively to DISC1 promoter activity, whilst a region -982bp to -301bp relative to the TSS was found to confer a repressive effect. FOXP2, a transcription factor which is mutated in a rare speech and language disorder and implicated in autism pathogenesis, was found to repress transcription from the DISC1 promoter. Two pathogenic FOXP2 point mutations reduced this transcriptional repression. Preliminary evidence for a bi-directional regulatory relationship between DISC1 and FOXP2 was observed: a mouse model of schizophrenia that carries a Disc1 L100P amino acid substitution and shows altered developmental Disc1 expression was also found to show altered developmental expression of Foxp2. These results further understanding of two genes whose altered expression might contribute to the pathogenesis of psychiatric illness.

Traditional understandings of violence by the mentally disordered largely look to mental illness to explain such behaviour. More recently, research has begun to examine the role of alternative factors in driving violent offending in this context. Masculinity is one such factor to which little consideration has thus far been given, in spite of a wealth of literature which associates the construction and maintenance of a masculine identity with violence in the non-mentally disordered context. This thesis proceeds from these current understandings, and examines the nature of the relationship between mental illness, masculinity and violent behaviour. In order to examine this issue, interviews were conducted with a group of 10 male patients diagnosed with major mental illness and with violent offending histories, in a medium secure forensic psychiatric hospital in Scotland. A group of 10 male prisoners serving life sentences in a Scottish adult male prison following convictions for homicide offences were also interviewed, and acted as a comparator group. Following an analysis of these interviews, findings emerged in relation to three key areas of patients’ and prisoners’ accounts: past experiences of violent offending, present experiences of institutional settings, and future hopes for recovery and desistance. In particular, significant similarities and divergences in the experiences of the two groups were apparent, and this thesis advances two key arguments in light of this. Considering first the similarities in patients’ and prisoners’ experiences, it is posited here that for both the mentally ill and non-mentally ill male population the task of constructing and maintaining a masculine identity is a particularly pervasive force in their life histories. It will be demonstrated that for patients and prisoners in this study, masculinity plays a significant role in past violent offending, as well as having important implications for adaptation to present institutional settings, and the creation of a recovered and desisting identity for the future. Second, in looking to the divergences in patients’ and prisoners’ accounts, it is asserted that where major mental illness is present it serves to intercede in these three areas of men’s lives. Extracts from interviews with male patients will illustrate the interceding role of mental illness in violent scenarios from their pasts. In addition, it will be demonstrated that patients’ and prisoners’ respective present situations in institutional settings vary, as diagnosis of mental illness leads patients to be placed in a secure hospital rather than the prison, and the differing nature of these environments results in divergences in adaptation to these settings. Finally, in relation to the future, while prisoners focussed on their hopes for desistance from offending, the diagnosis of mental illness led patients to place recovery from such disorders as the primary process at this point.

The grief experienced by mothers and fathers when their child is diagnosed with a life threatening chronic-illness was investigated in order to validate the presence of grief in these parents and look at the factors that influence it. More specifically, I was interested in whether the grief experience differed for mothers and fathers and the impact that perceptions and coping have on both these gender differences in grief and on grief in general. The particular population investigated in this study were parents of children with Cystic Fibrosis. Participants were recruited through questionnaires randomly sent out by the National Cystic Fibrosis Association. In all, 37 mothers and 15 fathers took part. Results not only confirmed presence of grief in these parents but also indicated that this grief differs for mothers and fathers, with mothers reporting significantly higher levels of physical distress. In line with the literature no gender differences were found in regards to perception of impact parents felt their child's chronic-illness had had on their lives. Contrary to what was expected, however, no differences were found amongst the coping strategies used by mothers and fathers. In regards to the question of which factors have the greatest impact on the grief experienced by mothers and fathers combined, the coping strategy of self-blame was found to be the most important, followed closely by negative perceptions. The significance of these findings and their implications for parents and the people who work with them was discussed.

No description available.