Melbourne School of Psychological Sciences - Theses
Permanent URI for this collection
Search Results
1 - 3 of 3
-
ItemBrain and behavioural correlates of emotional voice processing in autism and its broader phenotype( 2019)Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterised by impairments in two core domains of social communication deficits and restricted, repetitive behaviours or interests. A milder variant of autism-like characteristics, known as the Broader Autism Phenotype (BAP), is present at higher rates in relatives of individuals with ASD than the general population, indicating a genetic liability for ASD. There is a wealth of social cognitive research documenting theory of mind, empathising, and emotional face processing deficits in ASD and the BAP, which correspond to abnormal brain function in the “social brain”. However, less research has been conducted on the brain and behavioural correlates of emotional voice processing in ASD and the BAP, despite its significance for social cognition. This thesis aimed to profile emotional voice processing abilities in ASD and the BAP in relatives and the general population, specifically relating to non-linguistic vocalisations known as vocal affect bursts (e.g., laughter, cries, screams). This thesis also aimed to identify the neurobiological substrates of emotional voice processing in individuals with ASD and relatives with the BAP. Three studies were performed to address these aims, each using the same purpose-built, web-based and/or functional MRI (fMRI) task to assess behavioural performance and elicit brain activation. Whole-brain activation elicited by the fMRI task was assessed using random- and fixed-effects analyses (RFX and FFX), which allowed inferences to be made on the population and sample levels, respectively. Study 1 examined vocal affect burst recognition and its neurobiological correlates in individuals with high-functioning ASD (n = 16) compared to typically-developing controls (n = 16). The ASD group demonstrated a vocal emotion recognition deficit on the web-based task, where they misclassified neutral non-linguistic voices as expressing basic emotions at a higher rate than controls. RFX analyses revealed no significant group differences in brain activation, whereas FFX analyses revealed that the ASD group demonstrated higher activation relative to controls in widely distributed regions associated with emotional voice processing, executive function, memory, motor and somatosensory processing, and visual processing. These findings enable atypical brain activation to be inferred for this specific ASD cohort, but not for the wider ASD population. Although cohort-specific, such information may facilitate hypothesis generation for future investigations of neurobiological compensation in ASD. Study 2 addressed the same research questions as Study 1 in relatives of individuals with ASD (n = 13) who were determined to have the BAP on clinical assessment. The BAP group demonstrated no vocal emotion recognition deficit relative to controls (n = 13) on the web-based task. Under FFX analyses alone (not RFX analyses), the BAP group demonstrated significantly higher activation in the left lateral occipital cortex relative to controls. Inferences about the FFX findings are limited to the specific BAP cohort assessed here, and cannot be extended to the wider population of ASD-relatives with the BAP. Nonetheless, these findings may inform new hypotheses exploring endophenotypes (i.e., intermediate phenotypes) of ASD, characterised by a similar expression of neurobiological compensation in ASD and the BAP. Study 3 used the web-based task to assess the association between vocal affect burst recognition and the continuous distribution of BAP traits in the general population of individuals without a family history of ASD. It was hypothesised that lower recognition accuracy for the six basic emotions would correlate with higher self-ratings of BAP traits. In contrast to expectations, higher classification accuracy (and emotional intensity ratings) for angry voices correlated significantly with higher self-ratings of rigid BAP traits. The specific anger-rigid association indicates that enhanced auditory threat detection constitutes an aspect of the BAP in the general population. Further research is recommended to examine whether this relationship is mediated by underlying personality factors like neuroticism or trait anxiety. Overall, different behavioural profiles of emotional voice processing abilities were observed in individuals with ASD (deficit—misclassifying neutral voices as being emotional), relatives with the BAP (no deficit—intact performance), and individuals from the general population with higher levels of BAP traits (advantage—enhanced sensitivity to angry voices). The neuroimaging findings of enhanced activation in the specific ASD and BAP cohorts assessed here may have implications for future research investigating the role of neurobiological compensation for emotional voice processing in their respective populations, potentially including the exploration of endophenotypes of ASD. Such studies would ideally include larger ASD and BAP (relatives) samples that enable the assessment of more homogenous, identifiable subgroups who may be susceptible to increased cognitive demands for emotional voice processing. This thesis extends research on social cognition within the voice modality in ASD and the BAP, and may have wider implications for understanding the genetic aetiology of social communication impairments in ASD.
-
ItemEffects of reward and punishment on learning from errors in smokers : bold response and task-based functional connectivity( 2019)Nicotine dependence is the main cause of preventable mortality and morbidity worldwide. Besides health detriments, nicotine dependence appears associated with impairments in emotional and cognitive processes. Dependent smokers have shown hypersensitivity to reward and hyposensitivity to punishment, along with impairments in learning from errors. The underlying neural mechanisms for the failure to adapt performance following an error, particularly when receiving negative feedback, remain unclear. Smokers were hypothesized to have significantly poorer error learning following monetary punishment, but increased motivation by high reward. Smokers’ impaired learning from punished errors was expected to be associated with hypoactivation in the insula, dorsal anterior cingulate cortex and hippocampal regions. Differences between smokers and controls in task-based functional connectivity were expected between regions that have previously been found to be engaged in feedback-based associative learning tasks. Two versions of a feedback-based spatial associative-learning task were administered to different sets of 30 dependent smokers (abstinent more than 3h) and 30 matched controls. One of the tasks was administered during functional magnetic imaging (fMRI) data collection to 23 smokers and 23 matched controls. Whole-brain conventional blood-oxygen level dependent (BOLD) responses and region-of-interest task-based functional connectivity were analysed. Smokers learned less from small rewards and large punishments than controls. The three-way interaction between feedback magnitude, feedback type (reward, punishment) and group was significant, F(1,48) = 5.288, p = 0.026, ɳ2p = 0.099. In the Avoid Learning from Errors task (AvLFE), neither participant group corrected locations offering reward more often than those offering avoidance of punishment and the interaction between group and feedback condition (reward, avoid punishment) was not significant, F(1,58) = 0.0, p = 0.99, ɳ2p =0.001. None of the hypothesized brain regions showed differences between groups. Smokers showed hyperactivity in the right dorsolateral prefrontal cortex during recall and re-encoding epochs. Hyperactivity in the re-encoding period was associated with future error-correction in smokers only. While controls showed higher deactivation of the sensorimotor cortex during high punishment, smokers showed higher deactivation during low punishment. Task-based functional connectivity demonstrated increased connectivity between nucleus accumbens (NAcc) and anterior cingulate cortex (ACC) in smokers. Smokers’ connectivity was increased during both recall of corrected and repeated errors, while controls’ connectivity increased, although less than smokers’, during corrected errors but decreased during repeated errors. The results suggest that smokers have poorer learning from errors when receiving negative feedback. Larger rewards reinforced smokers’ behaviour more than smaller rewards, whereas this effect was not present in controls. Conventional BOLD response analysis supports the notion of impaired error-learning in smokers, increased reward anticipation, and decreased attentional control associated with hyperactivity in the dorsolateral prefrontal cortex. Smokers exhibited decreased punishment sensitivity which appeared to limit their ability to learn when facing repeated punishment. Task-based functional connectivity analysis supported conventional BOLD response findings of increased reward anticipation in smokers, suggesting that increased reward anticipation facilitated impaired negative-feedback processing and reduced error-learning. The findings support the hypothesis that smokers better respond to positively framed and rewarded anti-smoking programs when compared to those relying on negative feedback or punishment.
-
ItemQuantifying variation in brain structure and function in autism spectrum disorders (ASD)( 2019)Neurodevelopmental abnormalities in autism spectrum disorders (ASD) are not well defined. In particular, the link between altered neurodevelopment and ASD symptomatology remains poorly characterised. A key challenge is the high degree of heterogeneity in the phenotypic expression of ASD. Consequently, neuroimaging findings across multiple studies demonstrate poor generalisability and often fail to replicate. Emerging evidence suggests that heterogeneity in ASD is related to subject-specific variation. Such patterns of individualised alterations in ASD within the population could explain the inconsistency of previous findings. In the present thesis, it is hypothesised that individual differences in brain structure and function would predict individual variation in ASD symptom severity. A novel subject-level distance-based method was used to quantify individual variation in subject-specific attributes of neurodevelopment and severity of social dysfunction. The first study on brain structural morphometry from magnetic resonance imaging (MRI) investigated this hypothesis in 200 individuals with ASD and controls in a large multi-centre cohort of singletons, strictly matched at the subject-level on key confound variables. Individual differences in 19 cortical thickness and 10 surface area features selected by machine learning demonstrated out-of-sample prediction of ASD symptom severity variation. As expected, conventional group-averaged approaches showed poor prediction performance by comparison. In the second study, the subject-level distance-based method was applied to a different imaging modality of functional connectivity data from task-free functional MRI (fMRI) in the same subjects. Intrinsic brain network components were extracted with an unsupervised machine learning method for network decomposition. Individual differences in the strength of an intrinsic subnetwork predicted individual differences in social impairment severity. The subnetwork comprised of hubs of the salience network and the occipital-temporal face perception network. In the third study, we replicated and validated findings from both studies on brain structural morphometry and intrinsic connectivity in an independent monozygotic twin cohort of six locally recruited twin pairs concordant or discordant for ASD. For structural morphometry, surface area but not cortical thickness of regional features identified in the singleton cohort significantly predicted symptom severity variation in the independent twin validation cohort. For functional connectivity, the same salience and face-perception subnetwork was reproducible as a predictor of individual differences in severity of social deficits. Together, these empirical findings provide strong evidence implicating the salience network and occipital-parietal-temporal regions underlying individual differences in social dysfunction in ASD. The identified networks and cortical regions subserve typical functions of salience detection and face perception that are highly consistent with symptom domains of ASD. Given the lack of consistent and reliable findings in ASD neuroimaging literature, the robustness of present results validated across independent multi-site cohorts of singleton and twin populations is promising, and advances current knowledge and methods for investigating the neural basis of ASD. Because monozygotic twins share identical genes and environmental influences, non-shared environmental exposures are further implicated in within-twin-pair differences on identified cortical region and intrinsic network features of ASD. Subject-level variation in the neural correlates of symptom severity is an important feature in heterogeneous neurodevelopmental disorders such as ASD that should be further investigated.