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ItemThe hyper-ordinary depression hypothesis, and mechanisms of cognitive rigidity in depression (or zen and art of reducing depressive cycle maintenance)( 2017)This thesis is comprised of two related parts: a theoretical inquiry into the antidepressant mechanisms of a range of Non-ordinary States of Consciousness (NSCs), alongside the development of a novel mechanistic account of depression; and a set of four empirical studies that investigated aspects of cognitive rigidity in depression that relate to this novel account. In Chapter 1, I show that various disparate induction procedures (e.g., mindfulness practice, psychedelics, brain entrainment, and endurance exercise) are associated with both the production of NSCs and the reduction of depressive symptoms. Interestingly, these NSCs have in common many core neurological, psychological, and phenomenological features that are antithetical to core features of depression. I suggest that these features of NSCs represent potential therapeutic mechanisms, and that the production of certain NSCs mediates the reduction in depressive symptoms. I argue that two related superordinate features underlie these changes – enhanced Receptivity (e.g., perceptual, particular, absorbed, suggestible, flexible, open) and enhanced Projectivity (e.g., self-efficacious, intimate, relational, self-transcendent), that together represent elevated Interdependence between the individual and the world. In contrast, I argue that numerous features of depression appear to represent a fundamental deficiency in Interdependent processing, and that this deficiency extends into the most basic level of minimal subjectivity, representing a global qualitative change that satisfies criteria for an altered state of consciousness. Consequently, I argue that depression is associated with a ‘Hyper-ordinary’ state of consciousness. I suggest that the degree to which an NSC can reduce depression is a function of the degree to which Interdependent processing occurs within the state, and endures thereafter. Chapters 2, 3, and 4 report on a set of four empirical studies that investigated cognitive abnormalities in depression associated with the Receptivity aspect of the Hyper-ordinary account of depression. These tasks explored the link between depressive symptoms and three related processes that fall under the rubric of ‘cognitive flexibility’ – the ability for unexpected information to gain access to awareness; the ability to generate divergent representations for that information; and the ability to abandon extant representations in favour of those that are more compatible with unexpected information. As depression is associated with various forms of cognitive rigidity, including biased beliefs and interpretations that resist change, these studies investigated processing abnormalities in depression that might account for such rigidities. Additionally, as cognitive rigidity in depression is typically confined to specific forms of information processing, the tasks all employed stimuli that are highly relevant to the level of construal, the thematic content, and the rhetorical mode of depressotypic thinking, thereby increasing their sensitivity to detect differences, and their ability to reveal potential therapeutic targets. Results showed that depressive symptoms were related to slower access to awareness for unexpected positive information (Chapter 4), deficits in producing diverse categories of response, with no relation to the total number of responses generated (Chapter 3), and deficits in updating interpretations, regardless of whether updating resulted in a more positive or negative interpretation (Chapter 2). Together, this thesis offers a novel account of the depression experience, argues for a set of plausible therapeutic candidates for the antidepressant effects of certain NSCs, and reports on three novel tasks that probe ecologically relevant features of cognitive rigidity in depression, thereby revealing novel therapeutic targets. The picture of depression that emerges from the theoretical account is of a profoundly isolated state characterised by a fundamental deficit in the individual’s susceptibility to be affected by their context, and the perception that one’s context cannot be affected by the individual. The empirical studies show how this deficiency relates to the diminished influence of contextual factors over interpretations and expectations in depression. The hope is that this work can improve and extend the current understanding of depression and its causes, and lead to new methods of recovery.
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ItemSubjective and objective sleep outcomes in young adults who sustained traumatic brain injury in childhood: relationship with fatigue, depression, and quality of life( 2019)Background: Traumatic Brain Injury (TBI) is highly prevalent in children and often associated with impairments in several functional domains including sleep. Sleep-wake disturbances (SWD) are common in children with TBI and are associated with functional impairments in several domains. While some children may recover from SWD in the short-term postinjury, others may experience persistent symptoms, until late adolescence. Although not explored in children with TBI, studies involving adults with TBI have associated SWD with fatigue and depression symptoms, with these symptoms often co-occurring and impacting quality of life (QoL). In addition, no study has investigated sleep-wake outcomes in adulthood following childhood TBI. This thesis is aimed at evaluating outcomes of subjective and objective sleep, fatigue, depression, and QoL, and the relationship between these outcomes in a sample of young adults with a history of childhood TBI. Also examined were the relationships between sleep outcomes and injury-related factors, socio-demographic factors, mental health, lifestyle factors, and medication use. Methods: The study used a longitudinal prospective design with a cross-sectional assessment of sleep outcomes. Participants included 54 young adults with childhood TBI (mild, moderate, and severe) and 13 typically developing control (TDC) participants matched to the TBI group on age, sex, and socioeconomic status at the time of recruitment. SWD were assessed subjectively with questionnaires and objectively using 14 days actigraphy recording, and all other evaluations were subjective. Results: At 20 years postinjury, subjective sleep outcomes were generally favorable in young adults who sustained TBI in childhood, although moderate TBI was associated with poorer subjective sleep quality compared to severe TBI. With the exception of objective sleep duration, no other objective sleep parameter was significantly associated with history of childhood TBI or TBI severity. Fatigue, depression, and QoL outcomes were also similar between study groups. Nonetheless, poor subjective sleep quality was significantly associated with evening chronotype, increased use of tobacco and psychotropic medications, greater symptoms of anxiety and pain, as well as increased symptoms of fatigue and depression, and reduced health status in the TBI group. Conclusions: Evidence from this first evaluation of SWD in young adulthood following childhood TBI revealed favorable outcomes in SWD, fatigue, depression, and QoL at this developmental stage postinjury, although a subgroup of this TBI sample presented with problems in these domains. Poor subjective sleep quality in the TBI group was associated with less severe TBI, mental health and physiological factors, behavioural factors, and QoL. These findings provide preliminary insight into these outcomes at this stage postinjury and highlight the important influence of sleep in these related domains, particularly, fatigue, depression, and QoL. Clinicians are encouraged to routinely assess sleep and these related outcomes in young adults who have sustained TBI in childhood to identify those at risk of poor outcomes and improve very-long-term outcomes in this TBI population.
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ItemPsychological outcomes of those experiencing early pregnancy loss( 2019)Early Pregnancy Loss (EPL), a loss occurring before 14 weeks gestation, is a relatively common event, occurring in about 20% of pregnancies. Although many women and their partners do not experience psychological difficulties associated with this loss, a significant minority experience intense and sustained grief, depression and anxiety symptoms. Reliable prevalence rates of serious psychological consequences for women are not well established, and those of partners are largely unknown. Furthermore, it is unclear what factors increase the risk for developing serious psychological symptoms. A range of potential risk factors have been identified, but remain under-researched and have not been rigorously studied. According to Cognitive Behavioural Theory, it is possible that cognitions surrounding the loss may be a particularly relevant risk factor. Yet this topic has rarely been examined and the studies that have are characterised by major methodological shortcomings. Importantly, partners are rarely included in these studies. This study aimed to determine prevalence rates for grief depression and anxiety over the first three and a half months after EPL. It also investigated cognitions after EPL through the Common-Sense Model of Illness Representation, and their link with grief, depression and anxiety symptoms. This study included 28 male partners and 68 women diagnosed with EPL who attended the Early Pregnancy Assessment Service at the Royal Women’s Hospital in Melbourne, Australia. Participants completed self-report measures two weeks (T1), and three months (T2) post-loss. These included the Perinatal Grief Scale, the Centre for Epidemiological Studies-Depression scale, the State Trait Anxiety Inventory, and the Illness Perception Questionnaire-Revised. Results showed that the prevalence of grief, depression and anxiety symptoms for women at T1 were 20.6%, 54.4%, and 52.9%, respectively. For partners, the prevalence rates were 0% for grief, 32.1% for depression, and 25% for anxiety. These rates decreased by T2. Illness perceptions were found to significantly predict grief, depression and anxiety. Unexpectedly, it was often better perceptions of the loss that predicted worse psychological outcomes. These findings provide new information about the experience of EPL and suggest that critical timing for assessment and treatment would be within the first 3 months after EPL. Treatment options, particularly in terms of grief theories presented in the introduction, are discussed. Considering the surprising results and that this is the first study to examine illness perceptions among this sample, replication of these results is needed.
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ItemEnvironment-by-brain development interactions as predictors of adolescent depressive symptoms and psychological well-being: structural brain development as a marker of responsivity to maternal parenting and socioeconomic status( 2019)Background Adolescence is widely reported to be a time of increased risk for depression and lower well-being. Importantly, however, outcomes are heterogeneous, and most adolescents do not develop mental health problems. In order to understand how these differences emerge, both environmental and biological factors have been examined in the literature. Evidence indicates that parenting behaviour, socioeconomic status and neurobiology may contribute and, further, that individual differences in brain development may moderate the extent to which contextual factors influence adolescents. That is, individual differences in brain development may confer ‘responsivity’ to context. Several developmental and evolutionary-developmental models provide frameworks with which to interpret such brain-by-environment interactions, and to describe biological responsivity – these are broadly associated with diathesis-stress and differential susceptibility/biological sensitivity frameworks. Broad PhD aim This thesis aims to investigate whether structural brain development moderates adolescent sensitivity to maternal parenting behaviour in the prediction of adolescent depressive symptoms and psychological well-being. Two empirical studies were completed to address this aim. Study 1 examined whether longitudinal change in brain structure modified adolescent vulnerability or susceptibility to aggressive and positive maternal parenting. Effects were assessed to infer evidence in support of either diathesis-stress or differential susceptibility frameworks. Study 2, in light of evidence that positive parenting protects against adversity, considered whether brain development moderated adolescent sensitivity to positive parenting, and whether this association was more pronounced for adolescents with low-socioeconomic status (SES). Methodology During early adolescence (age 13 years), participants completed observed interactions with their mothers, and the frequency of positive maternal behaviour was coded. At three time points (mean ages 13, 17 and 19 years), participants completed structural magnetic resonance imaging (MRI) scans. During late adolescence (age 19 years), participants completed self-report measures of depressive symptoms and psychological well-being. Two separate analyses (studies) were conducted in predicting late adolescent (age 19) outcomes (depressive symptoms and psychological well-being). For both studies, longitudinal brain development was indexed by changes in cortical thickness of structures within the frontal lobe, and volumetric changes of subcortical structures, from early to late adolescence. Study 1: Regression models analysed interactions between maternal behaviour and longitudinal brain development in the prediction of adolescent outcomes. Indices designed to distinguish between diathesis-stress and differential susceptibility effects were employed. Study 2: Regression models were used to investigate interactions between SES (parental occupation), positive maternal behaviour, and longitudinal brain development in the prediction of adolescent outcomes. Results Study 1: Results supported differential susceptibility, whereby less thinning of frontal regions (the left medial orbitofrontal, rostral middle frontal and superior frontal cortices, and the right pars opercularis) was associated with higher well-being in the context of low levels of aggressive maternal behaviour, and lower well-being in the context of high levels of aggressive maternal behaviour. Study 2: Results indicated that individual differences in structural brain development moderated the extent to which positive parenting impacted adolescents dependent on SES. High levels of positive parenting were associated with reduced depressive symptoms for low-SES adolescents with greater volumetric reduction of the right putamen. Further, low positive parenting was associated with reduced psychological well-being for individuals with greater neurobiological sensitivity, however, patterns of brain development that were associated with sensitivity differed by SES. Specifically, low positive parenting was associated with reduced psychological well-being for individuals with more thinning in the context of low-SES, but for individuals with less thinning in the context of high-SES. Significance Results across studies suggested that structural brain development may be associated with individual differences in how sensitive adolescents are to context. Study 1 indicated that reduced frontal cortical thinning during adolescence increased susceptibility to maternal aggressive behaviour in the prediction of well-being, for better and for worse. This finding is significant because it suggests that neither more or less cortical thinning is consistently good or bad for mental health. Results from Study 2 indicated that, although brain change was associated with responsivity to parenting behaviour, patterns of brain development associated with heightened responsivity to parenting were different for high- and low-SES. These results suggested that responsivity functions in a context dependent fashion and highlights the complex interactions that may occur across biological and multilevel environment factors. Results from these studies suggest that structural brain development may be a marker of responsivity to environmental influence. They also emphasise the importance of examining how brain development moderates the impact of multilevel environmental factors on mental health outcomes. Such study designs may better reflect the social settings in which adolescents develop.
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ItemThe SENSE Study (Sleep and Education: learning New Skills Early): long-term outcomes of a randomised controlled trial of a cognitive-behavioural and mindfulness-based group sleep intervention to prevent depression and improve anxiety in at-risk adolescents( 2019)Objective: Depression is one of the most common and debilitating mental health problems and its incidence dramatically increases during adolescence. Accumulating evidence suggests that adolescent depression can be prevented with psychosocial interventions, but there is still insufficient evidence to support their widespread implementation. Notably, there is a need for randomised controlled trials of novel interventions that are delivered to community-based adolescents identified to be at-risk for developing depression (i.e., targeted prevention) rather than the general adolescent population (i.e., universal prevention). Improving sleep represents a promising and innovative therapeutic target for the prevention of adolescent depression. Not only are sleep problems, including insufficient and poor-quality sleep, common during adolescence, they also tend to precipitate the onset of depression. Further, sleep interventions may be especially effective if they are delivered to adolescents experiencing anxiety. Anxiety, particularly generalised anxiety, and sleep problems often co-occur, and anxiety is also a risk factor for the development of depression. Evidence from a small but growing number of studies indicates that multicomponent cognitive-behavioural and mindfulness-based sleep interventions can improve sleep in adolescent samples. However, few studies have investigated depression and anxiety outcomes, particularly using randomised controlled designs, active control comparison conditions, extended follow-up periods, a multi-method assessment of sleep (i.e., subjective and objective measures) and mental health (i.e., diagnosis and symptoms) outcomes, and in community-based samples. Notably, no randomised controlled trial has investigated whether a sleep intervention can prevent the first onset of major depressive disorder (MDD) in adolescents. The current study was designed to address these gaps in the literature. The primary aim of the study was to investigate the long-term efficacy of a seven-week cognitive-behavioural and mindfulness-based group sleep intervention for the targeted prevention of first onset MDD and improvement of depressive symptoms over a two-year follow-up period in community-based adolescents experiencing concurrent high levels of anxiety symptoms and sleep problems (i.e., ‘at-risk’ for depression). Given the association between sleep and anxiety, notably generalised anxiety disorder (GAD), and dearth of adolescent sleep intervention studies investigating anxiety outcomes, the secondary and exploratory aim of the study was to investigate the long-term efficacy of the sleep intervention for preventing the incidence of GAD and improving anxiety symptoms over a two-year follow-up period. Importantly, the study aimed to demonstrate that any beneficial effects to depression and/or anxiety outcomes occurred via the putative mechanism of improvements to subjective and objective indices of sleep. As best can be determined, the research reported in this thesis represents the only attempt to date to prevent first onset MDD by improving sleep in an adolescent sample, and the only randomised controlled trial of an adolescent sleep intervention to examine anxiety outcomes over a two-year follow-up period. It was predicted that, compared to adolescents allocated to the active control (study skills) intervention, adolescents allocated to the sleep treatment intervention would: show greater improvements in subjective and objective indices of sleep (i.e., reduced sleep onset latency, increased total sleep time, better overall sleep quality, and reduced weekday bedtime intra-individual variability and weekday-to-weekend bedtime shift) immediately following the intervention and over the two-year follow-up period; be less likely to develop first onset MDD during, and would report lower levels of depressive symptoms at, the two-year follow-up (primary outcomes); and would be less likely to develop new onset GAD during, and would report lower levels of anxiety symptoms at, the two-year follow-up (secondary outcomes). Further, it was predicted that any beneficial long-term effects for depression and anxiety outcomes (i.e., lower incidence of MDD or GAD and/or reduction in depressive and anxiety symptoms) would be significantly mediated by improvements in sleep associated with the sleep treatment intervention (i.e., sleep improvements immediately post-intervention and/or over the two-year follow-up period). Methods: Participant recruitment and eligibility assessments occurred from January 2013 to June 2014. A school-based screening (n = 1491) was conducted at 23 secondary schools (14 Government, 4 Catholic, 5 Independent) in metropolitan Melbourne, Australia, to identify community-based adolescents with high levels of self-reported sleeping problems (score > 4 on the Pittsburgh Sleep Quality Index; PSQI) and anxiety symptoms (score > 32 males/ > 38 female on the Spence Children’s Anxiety Scale; SCAS). Consenting participants who met screening criteria (n = 218) completed semi-structured diagnostic clinical interview (Kiddie-Schedule for Affective Disorders and Schizophrenia for school-age children-Present and Lifetime version; K-SADS-PL) at the University of Melbourne, primarily to exclude individuals (n = 30) with a lifetime history of MDD, consistent with the study’s aim to prevent first onset depression. Eligible participants (n = 144) were randomised (1:1 allocation on an individual basis, and conditions were balanced for age, gender and presence or absence of current anxiety disorder at baseline) to either a seven-week, face-to-face, multicomponent cognitive-behavioural and mindfulness-based group sleep improvement treatment intervention (Sleep SENSE; n = 71) or an attention-matched active control study skills intervention (Study SENSE; n = 73). The Sleep SENSE intervention aimed to address common sleep problems including insufficient sleep duration, prolonged sleep onset, and variability in sleep timing, and included anxiety management components to assist with managing anxiety during the pre-sleep period. Mental health and sleep were assessed using: the K-SADS-PL (for MDD and GAD diagnosis); the Center for Epidemiologic Studies-Depression scale (CES-D; depressive symptoms); the SCAS (anxiety symptoms); the PSQI (self-reported sleep onset latency, total sleep time, overall sleep quality); and week-long actigraphy with sleep diary (objective sleep onset latency, total sleep time, weekday bedtime intra-individual variability, and weekday-to-weekend bedtime shift). Assessments occurred on three occasions–pre-intervention, post-intervention, and two-years after the completion of the intervention. All outcome assessments were administered by researchers who were blind to participants’ intervention assignment. Statistical analyses: All analyses used a modified intention-to-treat approach. Specifically, the final analysed sample (n = 122, sleep treatment n = 62, control intervention n = 60; 60% female; M age = 14.5 years, SD = 0.95, range 12.04 to 16.31 years) included participants who were eligible for and started the interventions, including those who dropped out of the interventions or were lost to follow-up (n = 13) but excluded participants who were identified as ineligible after randomisation (n = 2) and those who were randomised but never started the interventions (sleep treatment n = 10, control intervention n = 10). Latent growth curve modelling with multiple mediation analysis was used to test the effect of condition (i.e., sleep treatment or control intervention) on the long-term depression (i.e., presence or absence of MDD diagnosis, and severity of depressive symptoms) and anxiety (i.e., presence or absence of GAD diagnosis, and severity of anxiety symptoms) outcomes via improvements in the seven sleep variables immediately post-intervention (i.e., ‘initial status’ which was centred at the post-intervention time point) and over the two-year follow-up period (i.e., average linear ‘rate of change’ scaled to represent change per year). That is, the latent growth process of a sleep variable (i.e., the latent variables of initial status and rate of change) was used the mediator in the tested models. In total, 28 separate models were estimated using Mplus (Version 7) software using maximum likelihood estimation with robust standard errors. Results: Regarding the primary outcomes, there was no statistical evidence that the sleep treatment intervention improved subjective or objective indices of sleep immediately post-intervention or over the two-year follow-up period, or significantly predicted the presence or absence of major depressive disorder during, or reductions in depressive symptoms at, the two-year follow-up, relative to the active control intervention. Regarding the secondary outcome, the sleep treatment intervention did not significantly predict reductions on anxiety symptoms at two-year follow-up. However, the sleep treatment intervention significantly reduced the conditional odds of having GAD during the two-year follow-up period by a factor of seven on average, relative to the active control intervention, although confidence intervals suggested a small effect. There were no statistically significant indirect effects in any of the model investigated. Regardless of condition, participants’ subjective (B = -1.77, 95% CI [-3.47, -0.07]) and objective (B = -4.53, 95% CI [-7.96, -1.10]) sleep onset latency and subjective total sleep time (B = -0.18, 95% CI [-0.31, -0.05]) decreased over time, and weekday bedtime intra-individual variability increased over time (B = 7.99, 95% CI [2.11, 13.86]). In addition, poorer subjective sleep quality (B = 1.46, 95% CI [0.38, 2.54]) and less objective total sleep time (B = -3.31, 95% CI [-6.33, -0.28]) immediately post-intervention predicted depressive symptoms at two-year follow-up, and reductions in weekday bedtime intra-individual variability over time were associated with a decreased likelihood of GAD during the two-year follow-up (B = -0.52, 95% CI [-0.86, -0.18]). Conclusions: Together, the findings do not support the long-term efficacy of a targeted multicomponent cognitive-behavioural and mindfulness-based group sleep intervention for the improvement of sleep problems and prevention of first onset major depressive disorder in a community-based sample of at-risk adolescents. However, they tentatively suggest that anxiety may be more responsive to the sleep intervention than depression. In the context of a robust study design, the findings are hypothesis-generating and raise important considerations for the design of future clinical trials investigating the role of adolescent sleep interventions on emerging psychopathology. Funding: Australian National Health and Medical Research Council Grant (APP1027076). Trial Registration: Australian New Zealand Clinical Trials Registry (ACTRN12612001177842; prospectively registered on 6th November 2012).
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ItemThe psychological significance of different adolescent perfectionist profiles( 2018)Perfectionism has historically been regarded as a significant risk factor in the development and maintenance of psychological disorders. However, perfectionism is not always associated with poor psychological outcomes. Indeed, contemporary multidimensional perfectionism questionnaires include both adaptive and maladaptive dimensions, and recent research suggests a better understanding of perfectionism is achieved by focusing on combinations of these dimensions (rather than individual dimensions) to identify adaptive and maladaptive perfectionist subgroups/profiles. The purpose of the research reported herein was to investigate the nature of these subgroups in adolescents. Study 1 (n = 105, 17-year-olds) (Sironic & Reeve, 2012) examined perfectionist subgroups based on the Almost Perfect Scale-Revised (APS-R: Slaney, Rice, Mobley, Trippi, & Ashby, 2001), as well as the Depression Anxiety Stress Scales (DASS: Lovibond & Lovibond, 1995) and Motivated Strategies for Learning Questionnaire (Pintrich, Smith, Garcia, & McKeachie, 1991). It was hypothesised that four meaningful perfectionist subgroups could be derived from the APS-R’s High Standards and Discrepancy dimensions, and that each subgroup would rate their anxiety, depression, stress, and learning metacognitive beliefs differently. As predicted, cluster analysis of High Standards and Discrepancy dimension responses yielded four subgroup profiles: (1) high High Standards/low Discrepancy; (2) high High Standards/high Discrepancy; (3) low High Standards/high Discrepancy, and; (4) low High Standards/low Discrepancy). Subgroups were related to psychopathological symptoms and learning metacognitions in predictable ways. The low High Standards/high Discrepancy subgroup claimed to use metacognitive self-regulation significantly less often than the high High Standards/low Discrepancy and high High Standards/High Discrepancy subgroups; and the two high Discrepancy subgroups exhibited significantly higher depression ratings than the high High Standards/low Discrepancy subgroup. These findings support a four-subgroup account of perfectionism. The findings were interpreted as suggesting that the low High Standards/high Discrepancy subgroup might lack insight into (or deny) their perfectionistic tendencies—a tendency often associated with psychological disorders. Some suggest that perfectionism may be either externally and/or internally motivated. Insofar as this is correct, it is possible that students in this fourth subgroup are not seeking their own high standards but adopting the standards of significant others. Study 2 was designed to investigate this possibility. In Study 2 (n = 938, 14- to 17-year-olds) (Sironic & Reeve, 2015), high school students completed three commonly used perfectionism questionnaires (i.e., the Frost Multidimensional Perfectionism Scale, FMPS: Frost, Marten, Lahart, & Rosenblate, 1990; Child and Adolescent Perfectionism Scale, CAPS: Flett, Hewitt, Boucher, Davidson Munro, 2000; and APS-R), as well as the DASS. Preliminary analyses revealed commonly observed factor structures for each perfectionism questionnaire. Exploratory factor analysis of item responses from the three questionnaires (combined) yielded a four-factor solution (factors were labelled High Personal Standards, Concerns, Doubts and Discrepancy, Externally Motivated Perfectionism, and Organisation and Order). A latent class analysis of individuals’ mean ratings on each of the four factors yielded a six-class solution. Three of the six classes represented perfectionist subgroups (labelled adaptive perfectionist, externally motivated maladaptive perfectionist, and mixed maladaptive perfectionist) and three non-perfectionist subgroups (labelled non-perfectionist A, non-perfectionist B, and order and organisation non-perfectionist). Each subgroup was meaningfully associated with depression, anxiety, and stress symptoms. The mixed maladaptive perfectionist and externally motivated maladaptive perfectionist subgroups reported significantly higher levels of self-reported depression, anxiety, and stress compared with the adaptive perfectionist and non-perfectionist subgroups. The mixed maladaptive perfectionist and externally motivated maladaptive perfectionist subgroups did not differ in their depression and anxiety ratings, but the mixed maladaptive perfectionist subgroup reported significantly greater levels of stress than the externally motivated maladaptive perfectionist subgroup. The same three perfectionism questionnaires used in Study 2 were used in Study 3 (n = 299, 19-year-olds) (Sironic, Paul, & Reeve, under review at the time of thesis submission). Study 3 sought to establish whether externally motivated perfectionism was also an important aspect in a university undergraduate sample, and whether perfectionists’ beliefs about thinking (their clinical metacognitive beliefs, as measured by the Meta-Cognitions Questionniare-30 Shortened Version (MCQ-30: Wells & Cartwright-Hatton, 2004)) may differentiate perfectionist subgroups and help better explain their DASS depression, anxiety, and stress symptoms. Study 2’s four-factor solution was confirmed by factor analysis of items from the three perfectionism questionnaires, and the same three perfectionist subgroups were identified using latent class analysis of individuals’ average ratings on each factor. Clinical metacognitive beliefs and depression, anxiety, and stress ratings varied in expected ways in the different subgroups, with the externally motivated maladaptive perfectionists at greatest risk of poor psychological outcomes. Overall, the findings of the three studies offer new insights into the conceptualisation of adolescent perfectionism. Support was found for the existence of three perfectionist subgroups (one adaptive, two maladaptive) in adolescence. Findings showed that three out of 10 students were classified as maladaptive perfectionists, and that maladaptive perfectionists were more prevalent than adaptive perfectionists. Notably, the externally motivated maladaptive perfectionist subgroup seemed to possess the poorest metacognitive skills and be most at risk of experiencing psychopathology symptoms. These findings have implications for the treatment of perfectionists. They suggest that intervention strategies are needed to address issues associated with externally motivated perfectionism (i.e., the impact of parents, teachers or significant others); and that enhancing metacognitive skills could be included as part of an intervention strategy.
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ItemThe neuropsychiatric disorders of focal epilepsy( 2017)Neuropsychiatric disorders commonly co-exist with focal epilepsy. Despite intense investigation there remains significant limitations to our current understanding of the aetiological relationship between these conditions, as well as the clinical and radiological factors that are associated with the development of mental illness in epileptic patients. To address these questions I assembled a large cohort of consecutive focal epilepsy patients reviewed at a large tertiary referral centre over an 11-year period, and analysed relevant clinical, radiological and demographic findings using both cross-sectional (baseline evaluation) and longitudinal (serial assessments) study designs. For cross-sectional analyses, psychiatric and epilepsy comorbidity were comprehensively identified and compared to baseline MRI-determined Deep Brain Structure (DSB) volumes. In the prospective study, standardised psychiatric and quality of life assessments were obtained in a subset of patients and the development of mental illness compared to interval changes in DSB volumes. I focus on depression and psychosis, as they represent the two most prevalent psychiatric disorders identified, and classify focal epilepsy patients according to the site of seizure origin and presence of a lesion. Contrary to the common medical belief, I found that the rates of neuropsychiatric disorders in temporal lobe epilepsy were equivalent to those in extratemporal lobe epilepsy. There were no differences between those with and without psychiatric disorder by age, gender, and laterality of seizure, epilepsy severity or duration. Patients with non-lesional epilepsy, both temporal and extratemporal, have double the rate of depression compared to those with lesional focal epilepsy. There were high rates of quality of life difficulties in people with epilepsy and comorbid psychiatric disorders but the pattern of subjective concerns does not match objective clinician ratings. The hippocampal and amygdalae volumes of epilepsy patients were reduced compared to normal controls. People with co-existing epilepsy and depression had a trend towards smaller reductions in temporal lobe structures, which may represent differential expressions of progression through inflammation, trauma or emotional processing needs with either relative sparing or volumetric increases. People with psychosis and epilepsy have bilaterally reduced hippocampi compared to those with epilepsy, where reductions are predominantly ipsilateral to seizure focus. There is less evidence for amygdala change in psychosis, but a small relative increased volume was observed compared to those with epilepsy alone. There was no evidence of progression over time at a population level over 3.9 years, although there was greater variability in size in all epilepsy subjects compared to normal controls. These results convincingly argue against assumptions about the primary role of temporal lobe foci in the pathogenesis of psychiatric comorbidities in patients with epilepsy, whilst allowing for the possibility that disruption to frontotemporal networks may be a component in the development of psychiatric disorders. Progression is not an inevitable part of the natural history, at least over a 4 year period but it is possible that individuals may exhibit marked changes. They highlight the as yet unexplored possibility that the absence of a lesion as an epileptic site may be associated with greater risks of neuropsychiatric illness and allow for speculation that this may be related to inhibitory surround impacts, more extensive underlying diffuse abnormalities and disruption to frontotemporal connectivity.
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ItemVitamin D status and related health in young women: the Safe-D study( 2017)Background: Vitamin D deficiency is emerging as a global public health issue in all age groups and public interest in vitamin D has increased significantly over the past decade. Deficiency is associated with increased risk of a number of adverse health outcomes, including poor musculoskeletal health, cardiovascular disease, autoimmune diseases, infectious disease, mental ill-health and several cancers. In Australia, vitamin D deficiency affects one in three adults and up to 50% of young women. Despite this, few studies have examined vitamin D status in late adolescent and young adult women. Aims: The Safe-D study was a cross-sectional study examining the association between vitamin D status and related health outcomes and aimed to define the prevalence of vitamin D deficiency in young women. The objectives of this doctoral research included examining predictors and correlates of vitamin D status, exploring potential associations between vitamin D status, mental and musculoskeletal health in young women, defining reference data for bone turnover markers (BTMs) in young women and examining determinants of bone health, including BTMs. Exploratory aims included examining potential interrelationships between these health domains. Methods: Females aged 16-25 years, living in Victoria, Australia were recruited into the Safe-D study, via Facebook advertisements. Participants were required to complete a comprehensive, online questionnaire, wear an ultraviolet dosimeter for two weeks to measure personal sun exposure and attend a site visit. Data collected through the study questionnaire included: participant demographics, medical history, sun-related behaviours, mental health, physical activity, nutrition, behavioural risk factors and lifestyle choices. Site visit measures included: serum 25-hydroxyvitamin D (25OHD) assayed by liquid-chromatography tandem-mass spectrometry, various serum biochemistry measures (including BTMs), areal bone mineral density and body composition by dual-energy X-ray absorptiometry, volumetric bone mineral density and measures of bone quality by peripheral quantitative computed tomography and muscle function by Leonardo mechanography®. Results: A total of 557 young women were recruited into the Safe-D study, of whom 410 completed site visits and 407 had serum 25OHD results. The prevalence of vitamin D deficiency (serum 25OHD <50 nmol/L) was 26%. Mean (± standard deviation) serum 25OHD was 68 ± 27 nmol/L. Factors associated with serum 25OHD, such as sex hormone-binding globulin and iron levels, sun exposure, season, multivitamin use and anthropometry, were able to explain 56% of the variation in 25OHD levels. Reference intervals for CTX and P1NP were calculated as 230–1000 ng/L and 27–131 μg/L, respectively, and both markers were found to be strongly associated with age and contraceptive use. No association was found between vitamin D status and health domains highly-relevant to women, mental and musculoskeletal health. Conclusion: Although vitamin D deficiency was found to be common in young Victorian women, it did not appear to be a major health risk for the majority in the immediate period. Further investigation of temporal relationships between vitamin D status and relevant health outcomes using longitudinal data, in addition to exploring the effects of improving vitamin D status in young women is warranted.
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ItemDissociating therapeutic effects of exercise and environmental enrichment in mouse models of serotonergic dysfunction( 2017)Serotonergic (5-HTergic) signaling is implicated in the manifestation of psychiatric disorders and regulates hippocampus-dependent cognitive and emotional processing that can underpin them. Clinical evidence indicates that serotonin 1A receptor (5-HT1AR) and serotonin transporter (5-HTT) gene polymorphisms are associated with anxiety disorders and deficits in cognition. In animal models, exercise and environmental enrichment (EE) can change emotionality-related behaviours as well as enhance some aspects of cognition. We aimed to determine the therapeutic effects of exercise versus EE (which does not include running wheels) on constitutive 5-HT1AR and 5-HTT knock-out (KO) mice phenotypes. 5-HT1AR KO mice have an anxiety-like phenotype as well as hippocampus-dependent learning and memory deficits. In addition to increased anxiety-like behaviour, 5-HTT KO mice also have a depression-like phenotype. The Morris water maze (MWM) is one of the most widely cited behavioural tasks in neuroscience. It measures the capability of the hippocampus to create a viewpoint invariant cognitive map of a distal cue array to find a hidden platform escape goal. Using a Matlab classification algorithm of the search strategy utilised to find the escape during MWM spatial learning, we have shown that increases in the odds of more hippocampus-dependent (allocentric) strategy selection is the key measure indicating the formation of this map to the escape location. Furthermore, using this measure we demonstrated a novel cognitive enhancement due to exercise (but not EE) for the first time. We also showed that 5-HT1AR KO mice had a significant reduction in the likelihood of an allocentric strategy selection. This deficit provides a novel explanation for their impaired long-term memory on the MWM retention probe. Strikingly, we found that these increases in spatial strategy selection through exercise corrected the long-term spatial memory deficits displayed by the 5-HT1AR KO mice. Assessing emotionality-related behaviours in both models dissociated further therapeutic effects of exercise from EE. Exercise (but not EE) had an antidepressant-like effect in 5-HTT KO mice, rescuing their deficit on the forced-swim test. In contrast, our EE paradigm (but not exercise access) reduced anxiety-like behaviours in both 5-HT1AR and 5-HTT KO mice. Furthermore, we report that 5-HTT KO mice had impaired synaptic plasticity by measuring long term potentiation (LTP) in the hippocampus and exercise also rescued this deficit. Exercise elicited robust increases in adult-born cell survival in wild-type (WT) mice. Exercising 5-HTT KO mice did also have increased adult-born cell survival but had a 3-fold decrease in the level compared to exercising WT mice. LTP and adult neurogenesis are both hypothesised to contribute to antidepressant effects, so our study adds support to the hypothesis that LTP and neurogenesis changes drive the antidepressant-like effect of exercise in 5-HTT KO mice. Surprisingly, in 5-HTT HET mice exercise induced a deficit in LTP compared to WT control mice and there were no exercise-induced increases in adult-born cell survival. 5-HTT HET mice in the standard-housing condition displayed enhanced cognitive flexibility and this behaviour was not present in exercising 5-HTT HET mice. Prevalent 5-HT1AR or 5-HTT targeted drugs are established treatments in various psychiatric disorders. Functional polymorphisms in both the 5-HT1AR and the 5-HTT genes are associated with increased risk of developing various psychiatric disorders as well as with increased insensitivity to their unique sets of targeted pharmacology. Unfortunately, for this and for other reasons, not all patients have efficacious responses to these established interventions, so novel therapies are required. The therapeutic effects of exercise and EE we uncovered do not seem to require one of either the 5-HT1AR or the 5-HTT, although further mechanistic studies are required to substantiate that conclusion. Therefore, the preclinical evidence contained herein adds support for clinically employing analogous environmental manipulations, such as brief durations of cognitive-behavioural therapy and/or exercise regimes, as viable therapeutic alternatives for such patients.
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ItemPsychological and neurobiological mechanisms underpinning chronic tinnitus( 2017)Chronic tinnitus, the phenomenon of a ringing, buzzing or hissing type sound in the ears or head is a prevalent health condition affecting 10-15% of the general population (Henry, Dennis, & Schechter, 2005a). It can have significant negative effects on an individual’s health and wellbeing and is associated with significant economic burden (Maes, Cima, Vlaeyen, Anteunis, & Joore, 2013; Tyler & Baker, 1983). At present, there is no cure for chronic tinnitus, likely due to the lack of consensus regarding the mechanisms maintaining the presence or impact of chronic tinnitus on individuals experiencing this condition. This thesis aimed to determine if psychological factors, and associated neural networks, could be maintaining awareness of the tinnitus sound and the severity of its impact. To achieve this objective, four studies were conducted utilising meta-analytic, questionnaire, cognitive and neuroimaging techniques. The first study comprehensively and systematically reviewed current literature regarding the psychological functioning of adults with chronic tinnitus. Results suggest that a heterogeneous array of psychological functions may be involved in the experience of chronic tinnitus, particularly emotional and cognitive functions, with meta-analyses providing consistent evidence for a role of reduced emotional wellbeing in both the presence and impact of chronic tinnitus. Study 2 and 3 further investigated the role of emotional and cognitive factors respectively in chronic tinnitus. Specifically, Study 2 investigated possible interactions between psychological factors and the vicious cycle of hypervigilance to the tinnitus sound in a heterogeneous community sample of 81 adults with chronic tinnitus. While analyses replicated the presence of the vicious cycle, this was conditional on the experience of depressive symptoms. Study 3 aimed to determine the contribution of cognitive functioning to chronic tinnitus. Compared to healthy-hearing individuals (n=26) people with chronic tinnitus (n=26) showed significant impairments in cognitive control, inhibitory control and increased symptoms of depression, with depressive symptoms and cognitive control successfully discriminating between people with and without chronic tinnitus. Combined, these studies suggest that disruption of specific large-scale neurocognitive networks proposed to underpin a range of psychological and cognitive symptoms; particularly those associated with depression may also underpin chronic tinnitus. As such, the final study of this thesis investigated the functioning of our stable neurocognitive networks, specifically the cognitive control network, in people with chronic tinnitus (n=15) and matched controls (n=15). While both groups successfully engaged the cognitive control network, the chronic tinnitus group exhibited subtle disruptions to a core node of this network, namely the right middle frontal gyrus, revealing both attenuated activation during cognitive engagement. This region also showed decreased connectivity with a node of the salience network, the right anterior insula, and increased connectivity with nodes of the autobiographical memory network, namely left posterior cingulate cortex and left medial prefrontal cortex. Together, the results of this thesis identify a failure in the process of attention-switching and the associated neurocognitive networks as a core mechanism underpinning the persistent awareness and pervasive impact of chronic tinnitus. This provides a novel framework, the Attention-Switching Model, for investigating both the experience of tinnitus, and potential treatments to help people with chronic tinnitus.