Nuclear Medicine

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Browsing Nuclear Medicine by browse.metadata.advisor "Lochner, Christine"

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    Social anxiety disorder : Functional neuroimaging and social cognitive features
    (Stellenbosch : Stellenbosch University, 2018-03) Doruyter, Alexander Govert George; Warwick, James Matthew; Lochner, Christine; Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Medical Imaging and Clinical Oncology. Nuclear Medicine.
    ENGLISH SUMMARY : Neuroimaging has enabled important progress in understanding the neurobiology of social anxiety disorder (SAD). Functional neuroimaging experiments in SAD have mostly focused on regional neural activity in response to anxiety provocation or processing of emotional faces, and have found hyper-activations in limbic and paralimbic circuitry. Relatively little however, is known about resting-state conditions in SAD and how these are affected by pharmacotherapy. What is known is almost entirely based on functional magnetic resonance imaging (fMRI) techniques which, while powerful, have some important limitations. Similarly, there has been only limited work investigating the resting neural correlates of social cognitive biases in SAD; how reward processing is disrupted in the condition; and how these respective features are affected by therapy. This thesis presents the first work on SAD investigating resting functional connectivity (RFC) based on nuclear neuroimaging methods. In an experiment that analysed RFC based on single photon emission computed tomography with technetium-99m hexamethyl propylene amine oxime, it was found that RFC differences in SAD were largely consistent with a contemporary network model based on fMRI, as well as implicating disrupted connectivity of the cerebellum. Another novel finding was how pharmacotherapy in SAD increased RFC of the anterior cingulate cortex. Using graph theory and resting-state fMRI, the first evidence of reduced global efficiency and increased clustering coefficients within the theory-of-mind network in SAD as well as independent evidence of social attribution bias in the same sample were reported. In an experiment that investigated regional resting metabolism in the disorder, there was evidence of abnormality in SAD compared to controls, as well as evidence of pharmacotherapy effects, in several biologically relevant regions. These results merit further investigation. Finally, in an fMRI-based experiment on reward processing in SAD, initial results identified no evidence of disrupted processing on a monetary reward task. The findings here support a neurobiological model of SAD in which alterations in resting regional metabolism may underlie disruptions in resting brain networks that have been implicated as being important in social cognitive processing. The results also suggest that pharmacotherapy may affect resting-state conditions through compensatory effects. Finally, the provisional findings are consistent with the theory that reward deficits in SAD may be limited to the processing of social reward, and may not extend to the processing of other reward types. Future SAD research should focus on collaborative work, using pooled datasets, and place greater emphasis on molecular disruptions in neurotransmitter systems involved in the disorder.