There is considerable evidence that working memory/executive dysfunction is a common feature of schizophrenia. A popular cognitive model of working memory comprises three elements, a controlling central executive and at least two slave systems - the articulatory or phonological loop and visuospatial sketchpad (Baddeley & Hitch, 1974), and is considered a dynamic system in which information is both stored and actively processed. Research evidence suggests that working memory engages both cortical and subcortical regions. At least five semi-independent, firontal-subcortical circuits have been proposed (Weiner, 1997; Alexander et al., 1986) the skeleto-motor, oculomotor, dorsolateral prefrontal, lateral orbitofrontal, and anterior cingluate circuits (Bradshaw, 2001). The present dissertation sought to investigate a model of working memory/executive function, and relate this to research concerning the neuroanatomy and neurophysiology of schizophrenia. A sample of 68 participants meeting criteria for schizophrenia of the International Classification of Diseases - Tenth Edition (ICD-10), and a group of 54 control participants completed the research protocol. The initial chapter of this thesis reviews relevant literature on the neuropsychological assessment of schizophrenia, methodological issues that impinge on the interpretation of neuropsychological research data, and proposed underlying brain pathology. Three studies are presented in four empirical chapters. The first empirical chapter (Chapter 3) reports a replication and extension of previous neuropsychological studies of schizophrenia. A variety of measures of executive functioning was examined between the groups. Participants with schizophrenia were significantly impaired on all standardised measures of executive functioning with the exception of a composite measure of the Trail Making Test. Results for dual task measures demonstrated that participants with schizophrenia crossed fewer boxes when they were required to simultaneously recall digit strings, than when crossing boxes alone. Since the group did not differ in the dual task decrement on recall of digit strings, but patients with schizophrenia crossed significantly fewer boxes in the dual task condition, a restricted impairment of the working memory system is implicated. The impairment occurs only for tasks in which the visuospatial sketchpad slave system requires central executive control. The second empirical chapter (chapter 4) examined whether discrete working memory/executive deficits underlie positive, negative and disorganised symptoms (as measured by the Positive and Negative Syndrome Scale; Kay et al., 1987) of schizophrenia. Negative and disorganised symptomatology was associated with distinct patterns of working memory dysfunction, with identifiable neuroanatomical substrates. In contrast, positive symptoms were unrelated to working memory impairment. The third and final empirical chapters more closely assess one aspect of cognitive impairment in schizophrenia - sustained attention and suppression of pre-potent motor responses, and its relation to symptom dimensions using the Sustained Attention to Response Task (SART). Chapter 5 demonstrated that the transition between controlled and automatic processing remained intact in patients with schizophrenia. Deficits were however evident in the patient group's accuracy and speed of responses, and number of errors. Chapter 6 showed that higher negative symptom scores were related to increased miss errors on the SART, while higher disorganised and positive symptom scores were unrelated to SART performance. This result implicates increased lapses of attention and psychomotor slowing among patients with predominantly negative symptoms. The final chapter provides a general discussion and synthesis of findings. Results from the current studies implicated the anterior cingulate, dorsolateral prefrontal, lateral orbitofirontal and motor circuits in the pathophysiology of schizophrenia. In addition subsequent research has implicated the dorsolateral prefrontal (e.g. Cameron et al., 2002) and oculomotor circuits (e.g. Levy et al., 1993; MacAvoy & Bruce, 1995, Ross et al., 1995). Thus overall it appears that the cognitive deficits evident in schizophrenia are consistent with the underlying neural circuits. Since all 5 circuits were identified as dysfunctional, a common component, namely the thalamus and its re-entrant loop to the cortex, was given as a plausible explanation for the results. In addition, differential patterns of cognitive impairment implicated the role of different frontostriatal circuits in symptom expression in schizophrenia. Negative and disorganised symptomatology implicated dysfunction of the dorsolateral prefrontal, lateral orbitofrontal and anterior cingluate circuits. In contrast, positive symptoms were unrelated to working memory impairment, thus considered unrelated to disruption of the frontostriatal circuitry.