Approximately half of Multiple Sclerosis (MS) patients experience cognitive deficits. Accessing neuropsychological assessment can be challenging due to the considerable time, expense, and expertise required for test administration. Computerized cognitive testing has been proposed as an alternative. The objective was to validate a computer generated cognitive screen for MS patients. Ninety-nine MS patients and 98 healthy controls completed the computerized battery consisting of the Stroop, Symbol Digit Modalities Test (C-SDMT), Paced Auditory Serial Addition Test (PVSAT-2, PVSAT-4), and simple and choice reaction time tests. The Minimal Assessment of Cognitive Function in MS (MACFIMS) was used to define cognitive impairment in the MS sample. A combination of the C-SDMT, PVSAT-2, PVSAT-4 had a sensitivity of 83.3% and specificity of 87.7% in detecting cognitive impairment. Each measure had good test-retest reliability (p < 0.001). High sensitivity and specificity, and brevity emphasize the usefulness of the computerized cognitive screen in busy MS clinics.

Cognitive impairment no dementia (CIND) is conceptualized as a stage of cognitive decline between normal aging and onset of dementia. As persons with CIND are at high risk of developing dementia, efforts to determine early predictors of cognitive decline are warranted to advance both clinical knowledge and practice. Recent evidence suggests persons with CIND may have changes in vascular function compared to non-impaired peers, which may have clinical potential to differentiate those with and without CIND. The purpose of this study is to determine whether vascular functioning, examined both by individual indicators and as an aggregate vascular factor, will be associated with cognitive impairment. It is expected that the individual vascular indicators of hypertension, diabetes, stroke, and heart problems will be related to cognitive status classification, with poorer vascular function being more strongly associated with CIND as compared to the control group. Further, it is expected that examining the aggregate vascular factor in a multivariate approach will be more strongly associated with cognitive status than examining the vascular indicators individually. Data for this study were collected in the Victoria Longitudinal Study (VLS), a large-scale longitudinal, sequential study of community-dwelling older adults in Victoria, British Columbia. Cognitive group status was determined by a distributional approach based on scores on 5 cognitive reference measures. The associations between all vascular factors and cognitive status groups were assessed using chi-square analyses. Univariate analyses were then carried out using ordinal logistic analysis. A multivariate approach using discriminant analysis was then used to determine if cognitive status group membership was associated with vascular function based on linear combinations of vascular indicators. Contrary to expected results, we did not find a significant association between any of the vascular indicators (i.e., blood pressure classification, severity of stroke, severity of heart troubles, and severity of diabetes) and the cognitive status classifications. Further, group membership was not associated with any of the individual vascular markers, or by a multivariate combination of the indicators. Several reasons for this study’s findings include discrepant definitions of cognitive impairment in the literature, sample characteristics (i.e. high education, low base rate of vascular problems), and methodological considerations. Future research objectives should address the longitudinal association of vascular function and cognitive status. / Graduate

Eight experiments tested priming in short-term memory as a model for latent inhibition and habituation. The model postulates that the two phenomena result from reduced processing when a representation of the target stimulus is already active (primed) in short-term memory at the time of its presentation. Priming is assumed to depend on the integrity of an association formed between the contextual stimuli and the conditional stimulus (CS) during exposure. Using a procedure that should have overshadowed the context, Experiment 1 found that latent inhibition and habituation were nevertheless maintained when a second CS of either equal or shorter duration overlapped with the target during exposure. Experiment 2 found no support for the priming of a configural stimulus when simultaneous compounds were preexposed. Experiment 3 ruled out sensitization and/or pseudoconditioning as an alternative explanation of latent inhibition. Experiments 4, 5 and 6 showed that sensory preconditioning as well as habituation and latent inhibition were obtained with compound exposure, providing evidence that the added CS was indeed processed along with the target. In Experiment 7, sequential pairings produced as much latent inhibition as compounds but less sensory preconditioning. Experiment 8 showed that retardation of conditioned inhibition was not attenuated by compound exposure. These results are interpreted as consistent with a correlational approach to classical conditioning.

Typescript (Photocopy) / Includes published papers coauthored by the author / Bibliography: leaves 387-428 / xx, 428 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Summary: Describes the use of a new measurement technique for the study of the facial expression of emotion. Based on a mathematical model of the face, a microcomputer approach is utilized to quantify facial movement / Thesis (Ph.D.)--University of Adelaide, Dept. of Psychiatry, 1993

Borderline Personality Disorder (BPD) is a serious psychiatric disorder characterised by turbulent interpersonal relationships, impaired self image, impulsivity, and a recurrent pattern of unstable affect which is usually evident by early adulthood. It has a community prevalence rate of two per cent, and approximately nine per cent of people diagnosed with BPD commit suicide. This suggests that BPD has one of the highest lethality rates of all psychiatric disorders. The course of the disorder shows a steady improvement over the course of early adulthood with the majority of cases remitting by middle age. This positive but incomplete long-term recovery is thought to be a naturalistic outcome that is independent of treatment effect. The reported study sought to test selected components of a multidimensional developmental neuropsychological model of executive functioning in BPD. The model proposed that BPD is characterised by impairments to four neuropsychological executive functions. These include working memory, response inhibition, affective-attentional bias, and problem-solving. The model further proposed that impaired executive functioning in BPD occurs as a result of the failure of ‘experience-dependent’ maturation of orbitofrontal structures. These structures are closely associated with the development of the ‘cognitive executive’. The study incorporated a cross-sectional design to analyse data from a BPD group, a Depressed Control Group, and a Medical Control Group. The overall findings of the study returned limited support for the original hypotheses. There was no evidence of deficits in working memory, response-inhibition, or problem-solving. In contrast, the BPD group returned some evidence of deficits in affective-attentional bias. Therefore, the results suggest that executive functioning remains largely intact in BPD. This also suggests that people with BPD have the working memory resources necessary to facilitate abstract cognition, have the capacity to effectively plan and execute future-oriented acts, and are able to perform appropriate problem-solving functions. These problem-solving returns are also particularly significant because a number of the tasks utilised in the study are known to be associated with so-called ‘frontal-executive’ function. These unremarkable findings challenge the view that people with BPD might experience some form of subtle neurological impairment associated with frontal-lobe compromise. The Stroop measure of affective-attentional bias provided the only supportive evidence for the proposed model, and these findings can be accounted for by at least two different explanations. The first suggests that BPD might be characterised by a hypervigilant attentional set. The specific cause of hypervigilance in BPD is unknown, but some candidate factors appear to be the often-reported abuse histories of borderlines, insecure attachment histories, and deficits in parental bonding. The second interpretation suggests that the Stroop findings reflect a form of ‘response conflict’ in which BPD participants experience difficulties overriding tasks that rely on the enunciation of automatic neural routines. As a result of these findings, further research on the role of arousal, priming, hypervigilance, and response-conflict in BPD is required. It is likely that the Stroop findings reflect a basic, ‘hard-wired’ attentional mechanism that consolidates by early adolescence at the latest. As a result, the Stroop findings have implications for both the prevention and treatment of BPD. A number of prevention strategies could be developed to address the attentional issues identified in the present study. These include assisting children to more effectively regulate arousal and affect, and assisting parents to communicate affectively with children in order to enhance self-regulation. The treatment implications suggest that interventions directed at affective-attentional processes are required, and further suggest the need for new pharmacotherapies and psychological treatments to modify dysfunctional attentional process. Affective neuroscience will have an increasingly important role to play in the understanding of BPD, and the next quarter century is likely to witness exciting advances in understanding this most problematic of disorders.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 4 uppsatser.

Thesis (Ph. D.)--University of Washington. / Bibliography: leaves [120]-123.

Thesis (Ph.D.)--McMaster University, 2006. / Supervisors: P.J. Bennett, A.B. Sekuler. Includes bibliographical references.

Thesis (Ph.D.)--City University of New York, 2003. / Includes bibliographical references (leaves 88-98).

Thesis (Ph.D.)--University of Adelaide, Dept. of Pathology, 2004? / Includes list of articles published or accepted for publication during the period of PhD candidature. "July, 2004" Includes bibliographical references (leaves 255-293).