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The Neurocognitive Factors Underlying Anomalous Experience in the Non-Clinical Population

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The Neurocognitive Factors Underlying Anomalous Experience in the Non-Clinical Population THE NEUROCOGNITIVE FACTORS UNDERLYING ANOMALOUS EXPERIENCE IN THE NON-CLINICAL POPULATION by RACHEL ELLEN MARCHANT A thesis submitted to the University of Birmingham for the degree of DOCTOR OF PHILOSOPHY School of Psychology College of Life and Environmental Sciences University of Birmingham September 2019 Corrections submitted December 2020 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. You are free to: Share — copy and redistribute the material in any medium or format The licensor cannot revoke these freedoms as long as you follow the license terms. Under the following terms: Attribution — You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use. NonCommercial — You may not use the material for commercial purposes. NoDerivatives — If you remix, transform, or build upon the material, you may not distribute the modified material. No additional restrictions — You may not apply legal terms or technological measures that legally restrict others from doing anything the license permits. Notices: You do not have to comply with the license for elements of the material in the public domain or where your use is permitted by an applicable exception or limitation. No warranties are given. The license may not give you all of the permissions necessary for your intended use. For example, other rights such as publicity, privacy, or moral rights may limit how you use the material. Abstract Anomalous experiences (such as hallucinations) are known to occur in healthy, non-clinical groups. Despite this, the neurocognitive mechanisms underlying such experiences in these groups has received little attention. This thesis therefore aimed to explore the relationships between anomalous experience and one candidate neurocognitive mechanism, cortical hyperexcitability, in non- clinical samples. Chapters 2 and 3 explored the contribution of visual cortical excitability to anomalous experiences in multiple modalities, by investigating the relationship between trait (questionnaire) and state (pattern glare) anomalous experiences under transcranial direct current stimulation (tDCS) of different areas of extrastriate cortex; Brodmann’s areas 5 and 7, and 17-19 (targeted with electrode sites Pz and POz respectively). These chapters evidenced differential relationships between visual trait and state measures. Chapter 2 revealed a trait-state relationship a relationship that was influenced by anodal tDCS brain stimulation, but only in those predisposed to pattern glare (indicating cortical hyperexcitability). Chapters 2 and 3 evidenced significant interactions between state experiences of pattern glare and tDCS condition, suggesting that these anomalous experiences vary depending on baseline excitability. Chapter 4 explored whether the trait-state relationships observed within the visual modality in the previous chapters could be extended to auditory cortex. Trait and state anomalous experiences were again measured using questionnaires and pattern glare respectively. EEG-based sensory gating was used to index state 2 auditory cortex inhibition. Chapter 4 tentatively suggested a cross modal relationship, with greater trait predisposition to anomalous visual experiences associated with greater suppression of the auditory P2 component. Greater P2 suppression may lead to source labelling errors and so perceptual distortions. Overall, this thesis indicates intriguing subtleties in the relationships between trait and state measures of anomalous experience and cortical excitability, that are also modality-dependent. Main argument The main argument of this thesis is that cortical hyperexcitability is a possible “bottom-up” mechanism underlying anomalous experiences in the healthy non-clinical population (see Figure A1). Predisposition to these experiences may depend on baseline cortical excitability states, with those with heightened baseline excitability being more likely to have anomalous experiences. In contrast, those low to normal baseline excitability may be less predisposed to these experiences. If the heightened excitability occurs in visual cortex, individuals are more likely to have visual anomalous experiences – particularly those analogous to “positive” elementary hallucinations (see Figure A2). Considerable further work is needed to fully understand these relationships, such as teasing out the relationships between trait (predisposition to) and state (ongoing experience of) anomalous perceptions. Cortical hyperexcitability may also interfere with “top-down” forward processing to produce anomalous experiences in healthy groups. It is possible that cortical hyperexcitability within e.g. the visual network can spread to or influence 3 processing in other sensory networks, e.g. auditory. To move this research area forward, there is need to test and establish more precise measures or indicators of state cortical excitability in healthy groups. Visual abstract – Core concepts Figure A1 – Visual abstract of the proposed relationship between cortical excitability and perception. The top panel shows “normal” neuronal functioning, with balanced excitation and inhibition. This is associated with “normal” excitability in visual cortex and veridical everyday perception, and so little to no pattern-glare- type visual distortions. The bottom panel shows cortical hyperexcitability, where excitation and inhibition are not balanced. This is associated with increased excitability in visual cortex, and so increased pattern glare and anomalous experiences. 4 Figure A2 – Visual abstract of the proposed relationship between cortical excitability, pattern glare (PG), and transcranial direct current stimulation (tDCS). It may be that baseline excitability interacts with tDCS to produce different effects. The top panel shows proposed relationships for the “non-PG” groups studied here, with low to “normal” visual excitability (scoring <1 on the PG task). Here, anodal tDCS excites visual neurons and increases PG experiences, whilst cathodal tDCS may prime visual neurons to also increase PG experiences. The bottom panel shows proposed relationships for the “PG” groups (with high visual excitability, scoring 1 or more on the PG task). In contrast to the non-PG groups, here anodal tDCS may not be able to excite visual neurons or may cause reversal effects (due to combining tDCS and PG stimulation), leading to no change or decreases in PG experiences. Cathodal tDCS may not be able to exert inhibitory effects due to deficient inhibition, leading to no change in PG experiences. 5 Dedication This thesis is dedicated to anyone who has struggled with their mental health. You can do anything you set your mind to. I have, and I did. 6 Acknowledgements I am very grateful for the support of my supervisors, Dr Jason Braithwaite and Dr Ali Mazaheri. Jason, it was your research that inspired me to do a PhD, and without your support during my Masters I would not have been able to win my PhD studentship. I am very grateful for your many years of support, and the valuable lessons you have taught me. Ali, I am so grateful that you took me on late in my PhD. Thank you for supporting me to learn new skills, for your mentorship, and for always giving me some much-needed perspective. I would not have been able to complete this degree without you both, and will be forever thankful for your support. Thank you to all of my family, friends, and colleagues who have supported me throughout the PhD. Thank you to my family – Mum, Dad, Naomi – for supporting me in this long journey and always pushing me forward, even in tough times. Thank you to my wonderful partner, Lawrence, for providing the daily love I needed to get me through. Thank you to my lovely friends, who are always there for me – you’re all wonderful, and I’m so grateful for your friendship. Thank you to my fellow postgrads for all your support and help – only you can truly understand the PhD struggle! Thank you to my mentors for your wisdom. You have all kept me sane, and pushed me when I needed it most. I would also like to thank all of the participants who took part in my studies. Without you, this thesis would not have been possible. This work was supported by a full studentship from the Economic and Social Research Council. I am very grateful to the ESRC for their generous support of my PhD research. 7 Publications and Presentations During the course of my PhD in the School of Psychology, University of Birmingham, the following were submitted for publication or presented at conferences. Where listed, secondary authors contributed to the work through advice on study design, data analysis, and paper editing. Papers submitted for publication An edited version of Chapters 2 and 3 has been submitted as: Marchant, R., Mevorach, C., and Braithwaite, J.J. (Under review). Examining individual predisposition to anomalous experiences in the non-clinical population using transcranial direct current stimulation (tDCS) of extrastriate cortex. Cognitive, Affective, and Behavioral Neuroscience. Conference presentations Marchant, R. & Braithwaite, J. (2017, April). Using the Cortical Hyperexcitability index (CHi) to predict anomalous experience in psychologically-healthy young people. Oral presentation at the International Association for Youth
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