Getting a grip on Schizotypy: Elucidating dorsal stream deficits in Schizophrenia Spectrum Disorders
Creators: name: Shen, Elizabeth
Publisher: name: The Australian National University
Year: 2023

description: Schizophrenia Spectrum disorders (SDD) are associated with disproportionate dorsal visual stream dysfunction, relative to ventral visual stream function. However, there remains a gap in our understanding of the neuropsychology and functional implications of this deficit. Notably, the balance of evidence implicating dorsal stream deficits is from visual perception tasks (e.g., visual masking, contrast thresholds) and neglects another well-validated model of dorsal stream function - the Perception-Action Model (PAM). Within this framework, the dorsal visual stream performs the necessary transformations on visual information to guide movement (e.g., reaching, grasping). Accordingly, disorders with known dorsal stream impairment have been empirically associated with selective deficits in visually guided movement. However, whether such deficits also characterise SSD remains unclear. Moreover, recent neuroimaging experiments have identified two substreams within the dorsal stream, and the differential impact of SSD across these substreams is unknown. Furthermore, the vast majority of these studies have focussed on patients with Schizophrenia per se. While this population is likely to exhibit the most pronounced deficits, little is known about whether these deficits occur across the entire SSD spectrum and are, therefore, core to the condition or a result of confounding factors (e.g., medication use). This thesis aimed to investigate dorsal stream deficits in subclinical SSD using a visually guided movement paradigm. Subsequent to unexpected results from Study 1, the thesis undertook a comprehensive psychometric evaluation of the Oxford Liverpool Inventory of Feelings and Experiences (OLIFE) to validate its measurement of Schizotypy. Study 1 examined the nature of SSD-related dorsal stream deficits using PAM as an explanatory framework. It extended previous research by using visuomotor tasks with known neurobiological correlates to dorsal substreams (i.e., dorsomedial and dorsolateral substreams) and sampling from normative population varying on trait Schizotypy. Increased Schizotypy was hypothesised to correlate with increased errors in kinematic parameters of visually guided prehension. Moreover, the profile of errors across movement type (pointing versus grasping) and target type (stationary versus moving) were posited to more strongly implicate one dorsal substream over the other. Results showed no significant difference in the kinematics of visually guided movement as a function of Schizotypy. Given these unexpected results, coupled with ongoing debate about the construct of Schizotypy and its latent structure, Study 2 assessed the validity of the OLIFE; the measure used to quantify Schizotypy in Study 1. Past research has supported two-, three-, and four-factor models of Schizotypy, with little consensus over which architecture is valid. Specific criticisms of the OLIFE include validity of its factor structure, item content, and length. These shortcomings are likely to constrain the feasibility of finding the differential patterns of interest across kinematic measures as a function of Schizotypy, as hypothesised in Study 1. As such, Study 2 used Classical Test Theory and Item Response Theory to validate and revise the OLIFE. This resulted in a final 16-item short form; OLIFE16. Study 3 applied the OLIFE16 to the results from Study 1, however, this revealed no meaningful change from the original outcomes, i.e., no differences in kinematics measures were observed as a function of Schizotypy. These results suggest dorsal visual stream deficits in SSD may only be observed in clinical populations, which in turn, questions the validity of these deficits as core to the disorder. Nevertheless, the new OLIFE16 provides a valid and brief measure of Schizotypy and support for the three-factor structure of SSD. Future directions in differentiating dorsal substream deficits in SSD and further validation of the OLIFE16 are discussed.