Melbourne School of Psychological Sciences - Theses
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ItemCharacterising changes in brain structure and neuropsychological function in the psychoses of epilepsy( 2018)Psychosis of epilepsy (POE) is a poorly understood condition which can have a devastating impact on people with epilepsy. Despite over a century of investigation into the relationship between epilepsy and psychosis, the structural neurobiological basis and neuropsychological deficits of POE remain unclear. Research in schizophrenia, the paradigmatic psychotic disorder, strongly suggests that psychosis is underpinned by abnormal neurodevelopmental processes which lead to altered brain structure and psychotic symptoms in later life. Moreover, both epilepsy and psychosis are increasingly understood as disorders of large-scale brain networks such as the default mode network (DMN) and the cognitive control network (CCN). The neurodevelopmental model of psychosis on the one hand, and the contemporary understanding of epilepsy and psychosis as network disorders on the other, underpin the primary aim of this thesis, which was to investigate changes in brain structure and neuropsychological function in POE. Understanding the structural neurobiological and neuropsychological deficits of POE is critical as it may provide insights into its neurobiological and developmental mechanisms. Following the introductory chapters (1-3), a systematic review of the neuroimaging literature in POE was undertaken. The results of this review informed the 3 structural neuroimaging studies and 1 neuropsychological study that followed. Study 1 comprised the first examination of volumetric changes in hippocampal subregions in POE, undertaken in the largest POE sample to date (n = 50). It addresses the methodological limitations of past studies of the hippocampus in POE, which were identified via the systematic review. The results of Study 1 showed hippocampal volume loss on a postero-anterior gradient, with severe decreases in the tail, and moderate volume decreases in the body, but no difference in the hippocampal head in POE relative to matched epilepsy controls (EC). These findings suggest that posterior hippocampal atrophy may be a structural biomarker of POE. The hippocampus can be further subdivided into distinct subfields which, along with the hippocampal fissure, were not captured by the assessment of hippocampal subregions undertaken in Study 1. Specific subfields, and the hippocampal fissure, have been shown to be affected in other non-epilepsy related psychotic disorders, and have not previously been examined in POE. Therefore, Study 2 comprised the first assessment of hippocampal subfields and the hippocampal fissure in POE. The results revealed an enlarged right hippocampal fissure in POE, with no difference in subfield volumes relative to EC. Moreover, because the volume of the right hippocampal fissure was not related to duration of epilepsy or age of habitual seizure onset, hippocampal fissure enlargement is likely underpinned by abnormal neurodevelopment. Together, Studies 1 and 2 provide strong evidence for structural hippocampal abnormalities in POE. Study 3 examined changes in cortical thickness, area, and volume in POE relative to EC, comparing patients with postictal psychosis (PIP) and interictal psychosis (IP) - the two main POE subtypes. This study was also motivated by the findings of the systematic review, which highlighted that only two studies have examined cortical changes in POE, one showing cortical thickening in PIP and the other showing cortical thinning in IP. Study 3 directly investigated this distinction, revealing cortical thickening in nodes of the CCN and DMN in POE overall, with more extensive thickening in visual processing regions in IP. Study 4 comprised an examination of the neuropsychological performance of POE patients and was informed by the structural changes identified in Studies 1-3. The results revealed that patients with POE displayed significantly poorer performance on tasks supported by nodes of the DMN (verbal memory and visual memory) relative to EC and healthy controls (HC), and on tasks supported by the CCN (working memory and verbal fluency), relative to HC. Considered together, the results of this thesis advance our knowledge of the structural neurobiological basis and neuropsychological deficits of POE. Specifically, they suggest that hippocampal abnormalities and cortical thickening in nodes of key brain networks are involved in its neuropathogenesis, and underpin altered neuropsychological function. The findings of this thesis also provide initial evidence that these structural changes may reflect the impact of epilepsy on neurodevelopmental processes, and provide some new insights into the neurobiological mechanisms underpinning POE. A neurodevelopmental model of POE is proposed, wherein altered hippocampal development and interruption of normal synaptic pruning leads to cortical thickening within specific large-scale brain networks. These structural changes may underpin the cognitive deficits and psychiatric symptoms of POE.
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ItemTrauma and psychosis: investigating the role of post-traumatic intrusions, schemas and avoidance( 2016)Increasing evidence suggests that childhood trauma may play a role in the aetiology of psychosis, leading to suggestions that trauma-related symptoms may be mechanisms in the process. Two prominent cognitive models implicate post-traumatic intrusions and trauma-related schemas and emotion as key mechanisms. Neither of the models has been extensively tested, and both have implications for the content of hallucinations and delusions in relation to traumatic experiences. The aims of the current study are to 1) investigate statistical associations between the severity of trauma and psychosis, 2) investigate phenomenological associations between trauma, post-traumatic intrusions, hallucinations and delusions, and 3) explore the relationship between trauma-related avoidance and psychosis. Sixty-six people with first episode psychosis aged between 15 and 24 years were assessed for childhood trauma, post-traumatic stress disorder (PTSD) symptoms, psychotic symptoms and experiential avoidance. The content of hallucinations, delusions, post-traumatic intrusions and traumatic experiences (up to five of each) was assessed. Content relationships between hallucinations, trauma and post-traumatic intrusions were categorised as ‘direct’ (where hallucination content was identical to trauma or intrusion content), ‘indirect’ (where hallucinations contained elements of trauma/intrusion-specific content but were not exact representations of traumas/intrusions) or ‘thematic’ (where hallucinations were related to trauma or intrusions at the level of broader, schema-related themes). Sixty-five percent of the sample had experienced childhood trauma, and 26% met diagnostic criteria for PTSD. Childhood trauma severity was correlated with hallucination and delusion severity with moderate effect sizes (although the correlation with hallucinations did not reach significance). Post-traumatic intrusions correlated with both hallucinations and delusions with moderate to large effect sizes. In terms of hallucination content, 78% of people with hallucinations and childhood trauma had hallucinations related in content to their trauma. These relationships were primarily thematic, although a notable minority (25%) had hallucination content directly representative of their trauma. Sixty-four percent of people had more than one type of relationship (direct, indirect, thematic, or no relationship) between their trauma and hallucination content. Of those with hallucinations and post-traumatic intrusions, 73% experienced hallucinations related in content to their post-traumatic intrusions. For delusion content, 89% of people with delusions and trauma had delusional content related to their trauma. Relationships between childhood trauma, avoidance, hallucinations and delusions were investigated, and it was found that childhood trauma was correlated with experiential avoidance (with a moderate effect size), and that both experiential avoidance and post-traumatic avoidance were correlated with hallucinations and delusions (with moderate effect sizes). In a series of multiple linear regressions, post-traumatic intrusions (but not childhood trauma, post-traumatic avoidance, experiential avoidance or maladaptive schemas) were independently associated with hallucination severity and explained 13% of the variance in hallucinations. Post-traumatic intrusions and maladaptive schemas (but not childhood trauma, post-traumatic avoidance or experiential avoidance) were independently associated with delusion severity, and explained 14% and 5-8% of the variance in delusion severity respectively. These findings suggest that post-traumatic intrusions and maladaptive schemas may be particularly important mechanisms in the relationship between trauma and psychosis, and may be playing a stronger role than avoidance. This has implications for the treatment of trauma and PTSD symptoms in people with psychosis. Research trialling interventions that specifically target post-traumatic intrusions and schemas in people with early psychosis who have experienced childhood trauma is recommended.
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ItemThe CARE project: improving physical health outcomes for young people with first episode psychosis( 2016)People with psychotic disorders have 2-3 times the risk of dying early compared to the general population. This is primarily due to modifiable risk factors for cardiovascular disease, including increased smoking, poor diet and low physical activity contributing to overweight and obesity. Previous non-pharmacological physical health interventions have largely been atheoretical and have typically only included people with chronic schizophrenia. Although these interventions have generally resulted in weight loss, it is usually not clinically significant and there is a lack of evidence suggesting outcomes persist beyond the end of intervention. There is also limited evidence that non-pharmacological interventions for smoking cessation are successful in the chronic schizophrenia population. Physical health deterioration occurs in the first years following initial treatment with antipsychotic medication. It is therefore likely that intervening early in the course of a psychotic illness to prevent weight gain and promote early smoking cessation attempts will be more effective than interventions for weight loss and smoking cessation at later stages of illness. The present thesis sought to overcome challenges related to treatment effects by adopting Self-Determination Theory (SDT) to frame the development and evaluation of a physical health intervention development, and its subsequent analysis, allowing for clearer targeting of mechanisms of action. SDT emphasises autonomy, competence and relatedness as being core psychological needs that energise intrinsic motivation for health behaviour. Study One examined mental health clinicians’ motivation towards physical health intervention with a mixed methods design. Clinicians described a lack of perceived autonomy and competence as barriers to addressing physical health concerns of consumers with first episode psychosis (FEP). Study Two examined the feasibility and acceptability of the Competence, Autonomy, Relatedness and Experiential (CARE) intervention using a single group repeated measures design for 16 participants with FEP. The intervention was associated with improved symptoms and quality of life, and seven of nine the participants who completed the intervention did not experience significant weight gain at two-month follow-up. Participants also reported increased perceived autonomy support for physical health change, but no difference in intrinsic motivation and competence for physical health change. While participants described the CARE intervention as acceptable, accessibility contributed to low attendance and completion rate. Study Three examined the perspectives of participants in Study Two in relation to physical health intervention preferences. Participants reported the need for accessible interventions that are easy to follow and involve active participation. SDT provided a useful framework for understanding both clinician motivation for physical health intervention, and participants’ experience of the CARE intervention and challenges engaging in behaviour change.
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ItemAre auditory verbal hallucinations related to auditory processing deficits and prosodic impairment in schizophrenia?( 2015)The ability to interpret affect and linguistic intent based on the intonation, rhythm, and stress of speech, is known as receptive prosody. As an auditory communicative function, receptive prosody is ultimately reliant on the processing of its constituent perceptual elements, namely, pitch, tone duration, and loudness. Previous research clearly demonstrates that receptive affective prosody is impaired in schizophrenia; however, the findings as regards linguistic prosody are mixed. Similarly, research shows robust impairments for pitch and tone duration processing in schizophrenia samples, yet loudness processing remains relatively unexplored. Recent findings indicates that the pitch and prosodic processing impairments observed in schizophrenia may be linked. Moreover, a small body of recent research suggests a possible relationship between auditory and prosodic impairments, and the experience of auditory verbal hallucination (AVH) in schizophrenia; however, these associations are yet to be thoroughly examined. To this end, this thesis aimed to comprehensively investigate auditory and prosodic processing impairment as a function of the experience of AVH in a schizophrenia patient sample. 15 AVH schizophrenia patients, 15 non-AVH schizophrenia patients and 34 non- psychiatric controls were compared on auditory and prosodic processing tasks, as well as a number of clinical and neurocognitive measures. The auditory processing tasks indexed participants’ sensitivity to differences in the pitch, duration, and loudness of simple tones. The prosodic processing tasks included an affective prosody labeling task, a linguistic prosody labeling task, and a novel affective prosody labeling task comprising speech waveforms that were systematically modulated such that pitch, loudness, or duration cues were singularly available for prosodic decoding. Results indicated that schizophrenia patients had impaired sensitivity to differences in pitch and tone duration but not loudness, when compared with non-psychiatric controls. Overall, AVH schizophrenia patients showed the greatest impairments in tone discrimination when compared with non-psychiatric controls. Schizophrenia patients were also observed to display deficits in prosodic decoding. Again, the AVH schizophrenia patient group showed the largest impairments in affective prosody decoding relative to the non-psychiatric control group. Next, the novel prosody task based on modulated speech waveforms revealed that AVH patients alone were impaired in prosodic decoding based on duration and loudness cues. Moreover, AVH patients but not non-AVH patients were observed to be impaired in decoding interrogative linguistic prosody in speech. Numerous associations between tone discrimination and prosodic decoding were observed within the schizophrenia groups based on percent correct performance data; however, these associations were largely lost when performance was instead measured with a measure of performance that is independent of response bias, namely, d’ (d-prime). The findings from the current study suggest that AVH schizophrenia patients in particular have a profile of noteworthy impairments in auditory and prosodic processing. However, the findings from the modulated affective prosody task and correlational analyses based on d’ data suggest that the relationship between impairments in tone processing and prosodic decoding in schizophrenia may be more subtle and complex than previously suggested.
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ItemCognitive processing associated with hallucinations for At Risk Mental State( 2013)To date there has been limited investigation of cognitive factors associated with the experience of hallucinations for individuals identified as being at Ultra-High Risk (UHR) for psychosis. This study is the first to comprehensively examine the relationship between auditory hallucinations within a UHR population and prominent cognitive models of perceptual disturbances. Source monitoring, appraisal of cognitive intrusions and metacognition were compared between three groups: a UHR group reporting auditory hallucinations, a UHR comparison group without hallucinations and a non-patient comparison group. The UHR group reporting auditory hallucinations displayed distinct deficits in source monitoring and appraisal of cognitive intrusions, indicating that biases in cognitive processing appear to be associated with the development of hallucinations for UHR populations. Additionally, follow up of the UHR participants was conducted in order to examine the association between cognitive processing biases and persistence of hallucinations. Source monitoring deficits as well as beliefs about the omnipotence of voices were strongly associated with the persistence of hallucinations over the follow up period. This is the first study to demonstrate that distinct cognitive biases are associated with the development of hallucinations during the UHR period. These results provide evidence that cognitive biases may contribute to the emergence of hallucinations, prior to the onset of frank psychosis.
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ItemEvaluation of a continuum model of psychotic symptoms: evidence from neuroanatomical, neuropsychological and clinical correlates( 2012)The fully dimensional model of psychosis posits that schizotypal personality traits in psychologically healthy people lie on a continuum with the psychotic symptoms experienced by people with a psychotic illness. Therefore, it was anticipated that psychotic and psychotic-like symptoms would show similar correlates for both individuals with a psychotic illness and psychologically healthy individuals. The validity of this notion was evaluated across three studies, which examined relationships between positive symptom traits and a range of neuroanatomical, neuropsychological and psychological variables. Case participants involved in the three studies had a diagnosis of schizophrenia or schizoaffective disorder, and control participants were psychologically healthy. In Study 1, comprehensive phenomenological information was acquired from cases (n = 20 and controls (n = 30) regarding the nature and frequency of positive symptom traits. Significant differences were identified between groups in terms of how they responded to and appraised their own positive psychotic and psychotic-like experiences. Four of these responses (immersion, external and impersonal attributions, and lack of social understanding) were also associated with the frequency and severity of positive psychotic and psychotic-like experiences across all participants’ lifetimes. Study 2 examined both between-group differences and within-group relationships in relation to neurocognitive functioning. Cases (n = 167) had significantly lower mean scores than controls (n = 222) on measures of Full Scale IQ, immediate memory, visual construction, language, attention, delayed memory and working memory. Participants’ scores on a measure of working memory were negatively associated with the frequency and severity of positive psychotic and psychotic-like experiences across their lifetimes. In Study 3, diffusion weighted MRI was used to assess whether groups differed according to structural brain connectivity, and whether connectivity was related to the frequency and severity of psychotic and psychotic-like experiences. One measure of white matter connectivity (fractional anisotropy) was significantly lower for cases (n = 93) as compared to controls (n = 80) across diffuse areas of the brain. For control participants, fractional anisotropy measurements in the corpus callosum and inferior frontal and temporal areas were negatively associated with the frequency and severity of positive psychotic and psychotic-like experiences across participants’ lifetimes. The findings of the three studies identified similar relationships for both cases and controls between positive symptom traits and a range of neuroanatomical, neuropsychological and psychological variables. These were taken to broadly support a fully dimensional model of schizotypy and psychosis.
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ItemWhy transition is not the whole story: neurocognitive function and risk for psychosis( 2010)“Ultra-high risk” (UHR) refers to individuals thought to be in the prodromal phase of psychotic disorder. The neurobiological mechanisms underlying progression from UHR to frank psychosis remains unclear, although neurocognition has been shown to be a promising endophenotypic marker. The aim of this project was to investigate baseline neurocognitive markers of transition to psychosis and poor functional outcome in a cohort identified as UHR between two and 14 years prior. Extensive tracking was used to trace all individuals who participated in research at the PACE Clinic in Melbourne from 1994-2005 (N = 416). Seventy five percent of the sample was assessed by interview. Transition status was established for all 416 participants. There were three main aspects to this research project: the examination of transition to psychosis, poor functional outcome and change in performance over time in relation to neurocognitive function. This study is the longest follow-up of any UHR sample to date, with a mean follow-up period of 7.52 years (SD 3.26). It was demonstrated that 29.3% of the sample transitioned to psychosis and that transition occurred up to five years and more after identification as UHR. When all baseline neurocognitive scores were modelled together, none significantly predicted transition. Conversely, lower functioning and psychotic symptom scores significantly predicting the development of frank psychosis. Of the individuals who experienced poor functional outcome (defined by low scores on the Quality of Life Scale and Social and Occupational Functioning Assessment Scale), less than two thirds of them had ever experienced a frank psychotic episode and less than one third had schizophrenia. The poor outcome group showed impaired neurocognitive performance at baseline, particularly on the task of logical memory. Poor performance on this task was still the strongest predictor of later poor functioning when modelled with baseline functioning and symptom scores. This model correctly classified 75% of poor outcome cases. Very poor Verbal IQ and verbal learning and memory at baseline significantly increased the odds of poor functioning at follow-up. In general, the neurocognitive performance of the cohort improved over the follow-up period. There were no significant interactions of transition group by time, indicating that individuals who transitioned did not show a significant reduction in neurocognition relative to those who did not. However, interactions of functional outcome group by time were significant on Verbal and Full-scale IQ, and a task of attention and processing speed. The poor outcome group showed decrements in performance on these measures, while the good outcome group improved over time. The current results indicate a need to shift the traditional notion of outcome in UHR investigation. It may no longer be sufficient to focus only on transition to psychosis because there is a group of individuals who never transition to threshold level psychosis, but continue to demonstrate very poor social and occupational functioning. The results also bring into question the validity of comparing individuals who transition to psychosis with those who do not in the search for biomarkers and endophenotypes for schizophrenia.