Nuclear Medicine
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Browsing Nuclear Medicine by Subject "Brain -- Neuroimaging"
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- ItemMethamphetamine dependence with and without psychotic symptoms : a multi-modal brain imaging study(Elsevier, 2018) Vuletica, Daniella; Dupontc, Patrick; Robertsond, Frances; Warwick, James M.; Zeevaartc, Jan Rijn; Steina, Dan J.Objective: Methamphetamine dependence can lead to psychotic symptoms which may be mediated by frontal, striatal, limbic, and thalamic regions. There are few neuroimaging data that allow comparison of individuals with methamphetamine dependence who do, and do not, have psychosis. Two complementary imaging techniques were employed to investigate neurocircuitry associated with methamphetamine dependence with and without psychotic symptoms. Methods: Three groups of participants were recruited: methamphetamine dependent (MAA) (N=11), methamphetamine dependent with psychotic symptoms (MAP) (N=14), and controls (N=14). Resting brain glucose metabolism was measured using [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) and cerebral perfusion was assessed using arterial spin labelling (ASL) magnetic resonance imaging. Results: Methamphetamine abusers (MAA and MAP groups) had decreased glucose metabolism compared to healthy controls in the left insula, left precentral gyrus, and the anterior cingulate cortex. Compared to MAA participants, MAP participants had 1) decreased glucose metabolism in the left precentral gyrus and the left inferior frontal gyrus and 2) increased glucose metabolism in the putamen and pallidum. MAP participants also had increased cerebral perfusion in the right putamen and right pallidum compared to MAA. Conclusion: Findings support the involvement of frontal, striatal, and limbic regions in methamphetamine dependence. Furthermore, they indicate that glucose metabolism and cerebral perfusion in these regions are disrupted in methamphetamine dependent individuals with psychotic symptoms.
- ItemSocial 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.