Abstract
Anxiety disorders are the most common group of mental disorders in Aotearoa New Zealand. Despite the high disease burden associated with anxiety disorders, there are currently no objective biomarkers that can aid their diagnosis. Goal-conflict specific rhythmicity (GCSR) is proposed to be the first electroencephalographic (EEG) biomarker for a neural process contributing to clinical anxiety. Previous studies have shown GCSR to be anxiolytic sensitive and increased in clinically diagnosed patients, but no one has compared GCSR between patients and age-matched controls. The aim of the current thesis was to investigate the clinical validity of GCSR within patients diagnosed with DSM-IV-TR anxiety disorder diagnoses. We hypothesised that clinically diagnosed patients would show stronger GCSR than controls; high anxiety, indexed by Spielberger’s State-Trait Anxiety Inventory – Trait (STAI-T) items, would be linked to increased GCSR; and no specific DSM-IV-TR anxiety disorder diagnosis would show stronger GCSR than other diagnoses. Goal-conflict specific rhythmicity of 79 participants recruited from Student Job Search (SJS), 53 untreated patients from the community, and 35 healthy controls from the community were recorded at F8. The first analysis compared GCSR between SJS participants with high, medium, and low STAI-T scores. Participants with high STAI-T scores produced moderately stronger GCSR than the other two groups; the difference was statistically significant between the high STAI-T and medium STAI-T groups. In the second analysis, GCSR was compared between patients with DSM-IV-TR anxiety disorder diagnoses and healthy controls. Patients diagnosed with DSM-IV-TR anxiety disorder diagnoses showed stronger GCSR than the control group; however, no significant differences in GCSR were found between patients with different STAI-T scores. To investigate whether the lack of difference between the two patient groups was due to STAI-T not being a pure measure of anxiety, multiple regression analyses were carried out using the Anxiety and Depressivity scores from the Personality Inventory of DSM-IV-TR (PID-5) and the Neuroticism score from the Eysenck Personality Questionnaire Revised (EPQ-R) to predict STAI-T scores. In line with my prediction, Neuroticism, PID-Anxiety, and PID-Depressivity scores were found to be significant predictors of STAI-T. In the final analysis, GCSR was compared between patients with different primary DSM-IV-TR anxiety disorder diagnosis: pure generalised anxiety disorder (GAD), social anxiety disorder (SAD), comorbid GAD and major depressive disorder (MDD), and a group of pooled other diagnoses (e.g., panic disorder, post-traumatic stress disorder). Contrary to my expectations, patients diagnosed with comorbid GAD and MDD had significantly higher GCSR, different from the other diagnosis groups. Although this thesis is not without limitations, it is among the first to directly compare GCSR between DSM-IV-TR anxiety disorder diagnosed patients and controls. These results provide evidence that GCSR is a human biomarker for a process related to clinical anxiety.