Shalabi, Abdulrhman
(2023)
Neural mechanisms of treatment for mental disorders.
PhD thesis, University of Nottingham.
Abstract
“Cognitive control” refers to the ability to regulate thoughts and actions in the service of goals or plans (Braver, 2012). Coordination between the central and peripheral autonomic nervous systems (ANS) maintains arousal and attention levels, which are essential for effective cognitive control. Diamond (2013) proposed a cognitive control model that builds on three core cognitive functions: cognitive flexibility, inhibitory control, and working memory. Abnormality in active inhibitory cognitive control is implicated in a broad range of psychiatric and personality disorders, including schizophrenia, attention deficit hyperactivity disorder (ADHD), impulsivity, and substance abuse, among many others. Transcranial direct current stimulation (tDCS) and cognitive training are two neuromodulation techniques which have the potential to modulate cortical functions to introduce long-lasting neuronal plasticity. The antisaccade task is a visual inhibitory control task frequently used to assess cognitive control. It requires the participant to suppress an automatic stimulus-driven saccadic eye movement and instead make a goal-driven saccade in the opposite direction.
In this thesis, by conducting two separate studies, we used the antisaccade task to examine the effect of tDCS and computerised cognitive training on inducing neuroplastic changes for the oculomotor control network (OCN). Chapter 1¢introduces relevant concepts to the subject of this thesis with a technical account of the methods used. The details of the first study are discussed in Chapter 2 - Chapter 4, where we used eye-tracking during antisaccade performance with the continuous assessment of cortical activity using Magnetoencephalography (MEG). Chapter 2 will discuss the short-term neuroplastic changes introduced by the tDCS on the functional connectivity within the resting state networks assessed using MEG. We found evidence of increased connectivity following the engagement in the antisaccade task for both active tDCS and sham conditions, but with different spatial patterns. Following tDCS delivered over the frontal cortex, there was increased connectivity with the frontal cortex. In contrast, in the sham condition there was increased connectivity with the posterior cortex. The effects of tDCS stimulation on the ANS activity during the task performance were further assessed via pupillometry as a measure of Locus Coeruleus (LC) activity in Chapter 3. Our results showed that faster pupil dilation, reflecting increased arousal and sympathetic activity, was associated with faster saccade reaction times. In Chapter 4, we investigated the immediate effects of tDCS stimulation on the cerebral cortex during active cognitive inhibition followed by a correct saccadic response. The tDCS introduced neuromodulatory changes in the putative Alpha and low-Beta band during the anticipatory and post-stimulus periods, reflecting enhanced cortical engagement in a task-beneficial pattern.
Chapter 5 reports on the second study in which we used functional magnetic resonance imaging (fMRI) to evaluate the neuromodulatory effects of prolonged computerised cognitive training games (RECOGNeyes) on the resting state functional connectivity of the OCN and pupil dilation. Following gaze-control training, the connectivity within the left hemisphere was strengthened, while the intra-right hemisphere and the interhemispheric connectivity were diminished. Chapter 6 provides a summary of the findings and concluding remarks. Our result furthers our knowledge of the processes involved in the performance of the antisaccade task, the mechanisms of action and the neuroplastic effects of two neuromodulation techniques. However, the exact mechanisms underlying these methods' beneficial effects demand further exploration.
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