Psychiatry - Theses

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    The role of adrenarche in shaping the mind: how adrenarcheal hormones contribute to the development of brain connectivity and internalising symptoms
    Barendse, Marjolein Eva Andrea ( 2018)
    The transition from childhood to adolescence is a particularly vulnerable period for the development of internalising symptoms and disorders. Hormonal changes as well as changes in brain structure and function may play a role in this increased vulnerability. Most of the research to date has focused on the hormonal and brain changes during gonadarche, whereas the literature is much more limited for adrenarche, an earlier pubertal phase that takes place prior to gonadarche. Therefore, this thesis aimed to examine how (changes in) adrenarcheal hormones relate to the development of brain structural and functional connectivity, and how that in turn affects internalising symptoms in late childhood to early adolescence. Data were used from two longitudinal community-based samples with two time points each (sample 1 M ages 9.5 and 12.2 years; sample 2 M ages 8.5 and 10 years). At each time point in each study, levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS) and testosterone were measured and averaged from morning saliva samples collected across several days. Participants also underwent Magnetic Resonance Imaging (MRI) scans, and completed self-report questionnaires, at both time points. Diffusion-weighted imaging scans were analysed to examine white matter structural connectivity. Functional Magnetic Resonance Imaging (fMRI) scans during an affective face processing paradigm were analysed to examine functional connectivity. Levels of internalising symptoms were based on self-report questionnaires: the Spence Children’s Anxiety Scale, the Children’s Depression Inventory, and the Positive And Negative Affect scale. Analyses were conducted to investigate associations between hormone levels (initial levels and changes in levels over time) and brain structural and functional connectivity (baseline and change over time). Analyses were also conducted to investigate whether hormone-related changes in structural/functional connectivity were associated with symptoms. The results showed that children with high DHEA levels at age 9 had higher mean diffusivity (cross-sectionally) in a wide range of white matter tracts, suggesting that relatively early exposure to DHEA might be negatively associated with white matter microstructure. Changes in testosterone from age 8.5 to 10 years were negatively associated with the development of white matter structure as quantified by fibre cross-section in posterior white matter tracts. Higher levels of testosterone at age 8.5 years, however, were related to stronger development of fibre cross-section from age 8.5 to age 10 years. These hormone-related changes in white matter structure were not significantly associated with levels of internalising symptoms. Analyses of functional connectivity during affective face processing focused on connectivity of the amygdala to the rest of the brain, because of the crucial role of the amygdala in emotion processing and consistent findings of its involvement in internalising disorders. Indirect effects were found of adrenarcheal hormone levels (controlled for age, potentially indicating a timing effect, i.e. maturation relative to same-age peers) on anxiety symptoms at age 9 years, mediated by amygdala connectivity to visual and limbic areas. Timing of adrenarcheal hormone exposure was also found to have indirect effects on anxiety symptoms longitudinally. Specifically, higher DHEA at age 9 years was indirectly related to more anxiety symptoms at age 12 years, controlling for symptoms at age 9 years, via more positive amygdala to inferior frontal gyrus connectivity. Thus, the findings in this thesis have demonstrated that elevated adrenarceal hormone levels (potentially reflecting early timing of adrenarche) are both cross-sectionally and longitudinally associated with anxiety symptoms through an effect on amygdala functional connectivity. We also showed that the hormonal processes of adrenarche have an impact on white matter microstructure development. These findings have implications for the understanding of how individual variation in adrenarcheal processes can impact children’s brain development and mental health. Future studies should examine whether effects of variation in adrenarcheal processes on brain development and mental health are persistent, as well as establish whether predictors found in the current thesis are also relevant in clinical samples.
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    Tau and beta-amyloid deposition, structural integrity, and cognitive function following traumatic brain injury in Australian war veterans
    Cummins, Tia ( 2018)
    Background: Traumatic brain injury (TBI), has been diagnosed in over 355,000 US military service personnel since 2000. Epidemiological research indicates that veterans with TBI are two-to-four times more likely to develop dementia than controls; however, mechanisms contributing to this relationship are poorly understood. The aim of this study was to investigate if Vietnam war veterans with a TBI show evidence of Alzheimer’s disease (AD) pathological markers, as assessed by A-amyloid, tau and glucose metabolism using PET, as well as structural MRI, including diffusion tensor imaging, and neuropsychological testing. Methods: Sixty-nine male veterans - 40 with TBI (aged 68.0±2.5 years) and 29 controls (aged 70.1±5.3 years) - underwent A-amyloid (18F-Florbetaben), tau (18F-AV1451) and 18F-FDG PET, MRI, psychiatric and neuropsychological assessment. The TBI cohort included 15 participants with mild, 16 with moderate, and 9 with severe injury. Fractional Anisotropy (FA) was employed as a measure of white matter tissue integrity. PET Standardized Uptake Value Ratios (SUVR) were calculated using the cerebellar cortex as reference region. Analyses were adjusted for IQ, age, ApoE status and psychiatric comorbidities. Results: Veterans with moderate-to-severe TBI performed significantly worse than controls on composite measures of memory and learning (M = -0.55  0.69, t(67) = 2.86, p=0.006, d=0.70) and attention and processing speed (M = -0.71  1.08, t(52) = 2.53, p=0.014, d=0.69). The moderate-to-severe TBI group had significantly lower FA than controls in the genu (F(3,36)=8.81, p<0.05, partial 2 = 0.17), and body (F(3,36)=4.39, p <0.05, partial 2=0.14) of the corpus callosum, as well as in global white matter (F(3,36)=5.35, p <0.05, partial 2=0.13). There were no significant differences in 18F-Florbetaben or 18F-AV1451 uptake amongst the groups, however the moderate-to-severe TBI group had significantly lower 18F-FDG retention than controls in the mesial temporal region (F(8,44) = 2.21, p <0.05, partial 2 = 0.13). No differences were found between the mTBI group and controls on any of the outcome measures. Conclusions: These findings indicate that moderate-to-severe TBI, but not mTBI, is associated with later-life cognitive deficits, and diminished global white matter integrity, specifically in the corpus callosum. However, these deficits are not associated with AD pathology. These results are consistent with current evidence of white matter axonal damage as the primary source of cognitive impairment in TBI, and are not reflective of a neurodegenerative process.
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    Examining the efficacy of Tuning Relationships with Music™ in helping parents with a history of interpersonal trauma reduce conflict and improve emotional responsiveness with their adolescent
    Colegrove, Vivienne Mary ( 2018)
    Parents who have experienced interpersonal trauma in childhood often struggle with relational functioning including difficulties with nonverbal communication (NVC), which may influence their ability to remain regulated during parent-child interaction. The challenges of parenting an adolescent may trigger memories of maltreatment, intensifying conflict, resulting in negative cycles of relating and poorer responsiveness to emotions when parenting. The thesis first explored existing knowledge about NVC in parent-child relationships. Then, the efficacy of Tuning Relationships with Music™ (TRM), an intervention developed by the author for parent- adolescent dyads experiencing heightened conflict where the parent has an interpersonal trauma history, was examined. TRM was expected to reduce conflict and adolescent mental health difficulties and improve parent responsiveness and emotion coaching. A randomised control (RCT) design was used where 26 parent-adolescent dyads were recruited from community services. Dyads were randomly allocated into intervention or wait-list control, completing self-report and observational measures at baseline, and again four months later. The thesis includes three studies. Study 1 reviews the literature about how nonverbal communication (NVC) is assessed and intervened with in parent-child relationships, in order to inform TRM development. Results showed that reliable and validated NVC assessment tools are not routinely used to inform intervention development or measure effectiveness, and that very few interventions directly target parent-child NVC. Study 2 reports on outcomes from the RCT of TRM, which found dyads that participated in TRM reported significantly reduced conflict, and parents were clinically observed to be less reactive and more responsive compared with dyads in the control condition. Although parents reported they were less dismissive and punitive, and more encouraging of their adolescent’s emotions, and both parents and adolescents reported improvements in the young person’s mental health, these were not statistically significant. Study 3 examined dyads as a single dynamic system during nonverbal conflict interaction, and aimed to examine relationships between parents’ trauma history, parent-adolescent conflict, parents’ reactivity and non-responsiveness, and dyads’ emotion regulation, consistency and predictability. A second aim was to discover whether TRM’s focus on NVC and emotion regulation would have an impact on post-intervention dyads’ nonverbal conflict interaction compared with controls. State space grid analyses showed that where parents reported higher levels of parent conflict this was correlated with predictable NVC sequences while dyads were emotionally dysregulated, and parents’ reactivity was correlated with dyads’ inconsistent NVC. Post-intervention dyads were more emotionally regulated, consistent and predictable during their nonverbal conflict interaction. Findings have important implications for intervention with parent-adolescent dyads where a parent has a childhood interpersonal trauma history, suggesting that a systemic focus on NVC and emotion regulation may assist dyads to reduce conflict and increase responsive interaction. This thesis makes a contribution to existing understandings of the systemic dynamics of parent-adolescent conflict where a parent has experienced interpersonal trauma, suggesting that using music to improve emotion regulation and NVC may reduce conflict and improve parents’ responsiveness in parent-adolescent relationships. Further research of TRM with a larger sample will be useful, to determine whether a focus on nonverbal processes may improve relational functioning.
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    Exploring candidate loci, genes, pathways, and evolutionary markers in schizophrenia by re-analyzing candidate gene and genome-wide association studies
    Liu, Chenxing ( 2018)
    In the last decade, consistent efforts have been made by psychiatric geneticists to elucidate the genetic mechanisms of schizophrenia, especially after the rise of genome-wide association studies (GWAS). However, the genetic etiology of schizophrenia has not been fully discovered, and enormous genetic datasets have been produced, allowing for additional investigation. In my PhD study, I have systematically identified candidate gene and GWAS in schizophrenia. Furthermore, I have re-analyzed these genetic datasets using meta-analyses, pathway analyses and evolutionary-based analyses. The results of these studies revealed new and supported current candidate loci, genes and pathways associated with increased risk of schizophrenia. I also provided evidence supporting a novel evolutionary mechanism for schizophrenia that extended the current conceptualizations of how schizophrenia emerged. In Chapter 1, I introduced the progress of genetic studies already achieved in schizophrenia, including family and twin studies, linkage studies, candidate gene association studies, genome-wide association studies, copy number variation studies and wholeexome/genome sequencing studies. A literature review of GWAS in schizophrenia and the aims of the thesis are included in this Chapter. Chapter 2 of this thesis provides a systematic review of genetic association studies in schizophrenia. In this study, I have reviewed more than 3000 association studies and merged them with the data from the existing schizophrenia knowledgebase (SzGene). Two rounds of meta-analyses, i.e. candidate-gene-only meta-analyses and expanded meta-analyses combined with samples from GWAS, have been conducted. In total, I have identified 21 Bonferroni significant single nucleotide polymorphisms (SNPs) in 14 Linkage disequilibrium (LD)-independent loci associated with schizophrenia susceptibility. Three of these loci, including methylenetetrahydrofolate reductase (MTHFR), D-amino acid oxidase activator (DAOA) and ARVCF, delta catenin family member (ARVCF), had never been implicated by a schizophrenia GWAS. Chapter 3 aimed to test the notion that schizophrenia is a pathway disorder. In this study, I conducted a pathway-wide association study, testing the association between schizophrenia and 255 biological pathways. Five independent GWAS datasets across three distinct ethnic populations were collected for pathway analyses. Almost half of biological pathways were associated with schizophrenia in each of three populations, and five of them (serotonergic synapse, ubiquitin mediated proteolysis, hedgehog signaling, adipocytokine signaling and renin secretion) were shared across three populations. These findings suggest schizophrenia is a poly-pathway disorder, and provide empirical support for that notion. In Chapter 4, I attempted to address the evolutionary paradox of schizophrenia: why negative genetic selection has not eliminated the deleterious alleles associated to schizophrenia susceptibility from the modern human genome? Using evolutionary markers in the genome, I showed that modern humans carried more protective SNPs for schizophrenia compared with our collateral ancestors: Neanderthals and Denisovans. Based on these findings, I proposed a novel framework to explain the evolutionary paradox and genetic origin of schizophrenia. In Chapter 5, the main findings and conclusion of my thesis are summarized. In addition, an expanded discussion of the meta-analyses of genetic association studies, the pathway-wide association study, and the evolutionary analysis are provided along with limitations and future directions.
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    The neuropsychiatric disorders of focal epilepsy
    Adams, Sophia Justine Lara ( 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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    Is the epidermal growth factor system a biomarker for clozapine response in schizophrenia?
    Sujeevan, Sinnatamby ( 2018)
    Schizophrenia is a severe neuropsychiatric disorder associated with significant disability. The antipsychotic drugs, the mainstay of treatment, are only effective in a proportion of patients. For those who do not respond, so-called treatment refractory schizophrenia (TRS) patients, the only available treatment is the atypical antipsychotic drug, clozapine. Although it has singular efficacy in treating TRS patients its use is restricted and delayed due to rare and potentially fatal side effects. Ability to predict response can help identify potential responders and introduce treatment early, but studies have so far not been able to identify any clinically useful biomarkers of response. A system that has been implicated in both schizophrenia and mechanism of action of clozapine is the epidermal growth factor (EGF) system. This study sought to examine the EGF system for potential predictors of response and did so by measuring peripheral EGF and betacellulin (BTC) levels in a prospective cohort of TRS patients commencing clozapine treatment. It also examined a larger cross-sectional sample of long-term clozapine treated patients for potential associations with EGF system single nucleotide polymorphisms (SNPs). The prospective sample of TRS patients were followed up over twenty-six weeks and clinical data and blood samples were collected at set time points. Symptom severity was measured using the Positive and Negative Syndrome Scale (PANSS). Additional clinical information was gathered using the Clinical Global Impression – Severity (CGI-S) scale, Global Assessment of Functioning (GAF) scale, Simpson Angus Scale (SAS) and the Calgary Depression Scale (CDS). Both EGF and BTC levels were determined using commercially available enzyme linked immuno-sorbent assay (ELISA) kits. Of the sixty-four patients who consented for the prospective study sixty entered the study and forty-nine completed the twenty-six weeks of clozapine treatment. Socio-demography of the patients revealed the significant disadvantages suffered by TRS patients. While 78.3% of the patients had completed more than ten years of education and 93.3% had been previously employed, at the time of the study 83.3% were dependent on the disability support pension. The average duration of illness of 11.2 years reflected the general reluctance and delay in introducing clozapine treatment. Although the response rate of 51.9% reiterated the unique efficacy of clozapine in treating TRS, the absence of any effect on negative symptoms highlighted this major gap in the treatment of schizophrenia. Significant improvement in both CGI-S and GAF scales in both responders and non-responders, while justifying continuation of treatment in the non-responders, also questions the current definition of response that is based solely on symptom improvement. Trends in smoking and psycho-active substance use, even though statistically not significant suggested possible additional advantages of clozapine. The low peripheral EGF and BTC levels in this study provide further support for an EGF system dysfunction in schizophrenia. Although clozapine treatment increased the EGF levels they still remained significantly lower than the healthy controls, implying that regardless of the duration of treatment, clozapine does not normalize EGF levels. Peripheral BTC levels were not affected by clozapine, but the correlation with positive symptoms suggest they could be a state marker. Neither EGF nor BTC levels predicted response to clozapine. The genetic analyses did not show any significant associations. Being an observational study, there was no provision to control for possible confounding factors, and having exclusively TRS patients limits its generalizability. Nevertheless, the findings of this study further implicate the EGF system both in schizophrenia and the mechanism of action of clozapine. Further exploration of this system would help better understand the pathogenesis of schizophrenia at the same time inform future development of antipsychotic medications.
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    An FMRI investigation of emotion regulation in youth depression
    Stephanou, Katerina ( 2018)
    The ability to regulate emotions plays an important role in social development during adolescence and young adulthood. Further, impaired ability to regulate emotions using cognitive strategies is a hallmark feature of major depressive disorder. Currently, there is a limited understanding of the neural underpinnings of emotion regulation in young people and how cognitive forms of emotion regulation (like cognitive reappraisal) develop. This issue is particularly pertinent to improving our understanding of depression in young people, given that the period from adolescence to young adulthood is associated with substantial brain maturational changes in regions associated with emotion–regulation and it is a time when most first episodes of depression occur. In the present study, a cognitive reappraisal paradigm containing social–stimuli was designed to probe the neural correlates of emotion regulation in depressed youth: in particular, to determine whether there were differences in the way that depressed and control participants regulated social–affective material, as well as developmental effects observed within the two groups. tudy participants—a large group of 15– to 25–year–old depressed participants and a matched control group—underwent fMRI where they used cognitive strategies to reinterpret negative social imagery. As expected, this cognitive reappraisal paradigm robustly activated regions involved in cognitive control and social–affective processing in both groups. Among healthy 15– to 25–year–olds (Study One), younger participants exhibited greater activation of temporal and occipital brain regions during reappraisal—implicated in processing social material—in combination with weaker suppression of amygdala reactivity. Further analyses demonstrated that these age–related influences on amygdala reactivity were specifically mediated by activation of the fusiform face area. Study Two revealed that depressed youth were significantly less able to reduce negative affect during reappraisal (compared to healthy individuals), which corresponded to blunted modulation of amygdala activity. Depressed youth also showed heightened activation of the ventromedial prefrontal cortex (vmPFC) and reduced activation of the dorsal midline cortex. Further, as distinct from the healthy youth, there was no relationship between development and modulation of amygdala activation in the depressed group. As the largest study of reappraisal in a young sample to date, our results in healthy controls highlight the importance of activation changes in social–processing and emotion processing networks, as being crucial to potential differences in the ability for adolescents to regulate their emotions. Enhanced neural sensitivity to social stimuli (e.g., facial stimuli) in younger individuals suggests a sensitivity to emotions of others during reappraisal that may be both adaptive in facilitating learning, but might also suggest difficulty disengaging from aversive social–cues. Findings in depressed youth are consistent with those in adults which suggest depression–related disturbances in both extended medial prefrontal (‘generative’) as well as dorsal (‘regulatory’) systems that contribute to adaptive emotional processing. Excessive engagement of the vmPFC—a region emphasised in contemporary neural systems models of MDD— may, in particular, be central to understanding how the process of assigning a new meaning to negative emotional material may be altered in depressed youth, with implications for treatment.
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    Functional brain networks in schizophrenia: mapping connectivity and topology at early and late psychotic illness stages
    Ganella, Eleni ( 2017)
    Schizophrenia is a severe mental disorder that is characterised by symptoms including hallucinations, delusions and disorganized thought. The cause of schizophrenia remains unknown; however, it is thought that a combination of genetics, environment and altered neurobiology play a role in the emergence and perpetuation of the disorder. Accumulating evidence suggests that disrupted brain network connectivity may in part underlie the pathophysiology of psychosis, and that network connectivity is to some extent genetically determined and heritable. However, there is still much to be learned surrounding the nature of network abnormalities and how they differ in early versus late psychosis. Exploring the underlying neurobiology at discrete clinical stages of psychotic illness creates a framework to evaluate the biological factors that may be contributing to the progression from early psychosis, to more advanced chronic stages of the disorder. This thesis used resting-state functional magnetic resonance imaging (fMRI) to characterise network functional connectivity and topology in early and late psychosis, as well as in a group of unaffected family members (UFM) of individuals with schizophrenia. Resting-state fMRI is a well validated and sensitive tool for probing the intrinsic functional integrity of the brain. Specifically, this thesis used a data-driven approach to map the temporal coherence of fMRI time series (functional connectivity) across the whole brain. To complement the resting-state functional connectivity (rs-FC) analysis, this thesis used graph theory to explore functional network topology. Network topology describes that brains ability to maintain a balance between local processing speed and global integration of information. These methodological approaches were used to investigate network abnormalities in three groups relative to healthy controls; a first-episode psychosis (FEP) group, a treatment-resistant schizophrenia (TRS) group and a group of UFM. This thesis aimed to investigate 1) whether rs-FC and network topology was abnormal in the early FEP stage of schizophrenia relative to healthy controls at two time-points (baseline and at 12-months follow-up); 2) whether rs-FC and network topology was impaired in a chronic TRS group relative to healthy controls; 3) whether abnormal rs-FC and network topology was evident in a group of UFM, and whether any network measure could be characterised as a marker of risk or resilience to psychosis in UFM. Firstly, results showed no evidence of abnormal rs-FC or topology in FEP individuals relative to healthy controls at baseline, or at the 12-months follow-up. Further, longitudinal changes in network properties over a 12-month period did not significantly differ between FEP individuals and healthy controls. Secondly, this thesis found widespread reductions in rs-FC in the TRS group that predominantly involved temporal, occipital and frontal brain regions. The TRS group also showed reduced global network efficiency and increased local efficiency relative to controls. Thirdly, TRS and UFM shared frontal and occipital rs-FC deficits, representing a ‘risk’ endophenotype. Additional reductions in frontal and temporal rs-FC appeared to be associated with risk that precipitates psychosis in vulnerable individuals, or may be due to other illness-related effects, such as medication. Functional brain networks were more topologically resilient in UFM compared to TRS, which may protect UFM from psychosis onset despite familial liability. Together, the body of work presented in this thesis provides a number of novel and unique findings that serve to advance the current state of knowledge regarding the pathophysiology and heritability of psychosis. Specifically, the work demonstrated that the latest most severe stage of psychosis, TRS, is associated with widespread reduced rs-FC, and that milder, yet similar patterns of dysconnectivity were observed in UFM, implying a genetic root to some, but not all of the observed network abnormalities. Network topology differed relative to healthy controls in both UFM and TRS patients, suggesting that functional network architecture is also disturbed in late psychosis, and again, results suggest a genetic/shared environmental basis for this characteristic. Our finding of no significant difference in rs-FC or network topology in our FEP sample suggests that there is a differentiation between biological processes occurring in early and late psychosis with a subgroup of individuals’ rs-FC potentially being unaffected in the FEP stage.
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    Concurrent treatment of mother-child relationship and mood disturbance within the context of postnatal depression
    Deans, Carolyn ( 2018)
    Aims. The aim of this study was to investigate the effect of the addition of an attachment-focussed mother and baby component to a standard group interpersonal therapy (IPT) treatment of postnatal depression. Specifically, the research looked at whether an intervention was capable of addressing both the mood disturbance and the relationship between the mother and baby concurrently. Methods. The research involved designing a new IPT protocol, which built on an existing model shown to address mood disturbance in new mothers. Elements of attachment theory and elaboration of the theoretical approach of IPT were used to guide the development of the new IPT-MC protocol. This therapy was then used with a group of mothers who were identified by a Maternal and Child Health Nurse (MCHN) as meeting criteria for major depressive disorder (post-natal onset) and requiring support. The group was compared with a group of mothers who received treatment-as-usual from their MCHN, including referral for GP, psychiatric, or psychological review and treatment as considered necessary. The mood disturbance and relationship changes were measured using a number of maternal self-report and observercoded variables. Results. The results indicated that the amendment of an evidence-based therapy for postnatal depression to include a mother-child focus did not affect the ability of the treatment to address mood disturbance. That is, there were no negative effects demonstrated that reduced its effectiveness, and it appeared to compare with the results of routine trials of IPT for postnatal depression. Due to the lack of exclusion criteria this study did not have the ability to determine whether the IPT-MC itself treated the mood disturbance. Results also indicated that IPT-MC has potential to address mother-child relational issues to a similar extent to existing treatments, and that these benefits can be shown at a moderate follow-up length (three months). IPT-MC improved the mother-child relationship significantly more than the treatment-as-usual condition. Conclusions. Clinical implications and limitations of the study are addressed. Further research extending the numbers and demographic of women involved would be warranted to confirm the findings.