There is a good deal of information available from both neuropsychology and cognitive psychology to support the contention that visual short term memory is functionally segregable from spatial short term memory, within the context of a working memory approach to cognitive functioning. However, relatively little is understood about the precise functional relationships between these segregated components or about the method in which they operate. One suggestion has been that the spatial system operates sequentially, in line with the idea that its output is mediated by movement of the body, whilst the visual short term memory system operates a more parallel manner, retaining input from the visual array in a more holistic fashion. In the research reported in this dissertation, methods originally used to research short term memory in experimental animals were adapted for use in adult humans. This was done with the aim of firstly clarifying the patterns of segregation of visual - spatial working memory and secondly beginning to understand the functional architecture of those segregated components. A series of experiments were conducted, initially based on Logie and Marchetti's (1991) demonstration of visuo-spatial segregation and later based on developments of the delayed response (DR) short term memory task used in experimental animals. In all of these experiments an interference paradigm was used to investigate segregation, with the assumption that segregation would manifest itself in differential effects of interference. For example, visual interference should impair visual but not spatial memory task performance, and vice versa for spatial interference. The results of these experiments clearly demonstrated segregation or visual and spatial processing. Furthermore they support the idea that spatial memory is a sequential process and visual memory a parallel one. However it was also observed that sequentially and parallelism were not the sole specifications of the two systems: memory for the appearance and location of items was also important.

Medulloblastoma is the most common malignant central nervous system (CNS) tumor in childhood. The cranio-spinal radiation (CSR) required to treat this disease results in long-term cognitive and neurologic impairments. Medulloblastoma was recently categorized into four genetic subgroups (WNT, SHH, Group 3, and Group 4). This study examined neuropsychological and intellectual functioning in 91 medulloblastoma patients (41 Group 4; 20 Group 3; 18 SHH; 12 WNT) following treatment, and examined the impact of several medical, treatment and demographic factors on functioning over time. Longitudinal growth curve analyses revealed hydrocephalus most clearly predisposes to poor neuropsychological functioning. Results also indicate medulloblastoma subgroups have heterogeneous intellectual outcomes following treatment. All subgroups experience intellectual declines following treatment; however, comparing between subgroups revealed Group 4 performs most poorly, and Group 3 has the best overall intellectual outcome. Lastly, qualitative analyses suggest treatment with a larger CSR dose may contribute to poor intellectual functioning.

Medulloblastoma is the most common malignant central nervous system (CNS) tumor in childhood. The cranio-spinal radiation (CSR) required to treat this disease results in long-term cognitive and neurologic impairments. Medulloblastoma was recently categorized into four genetic subgroups (WNT, SHH, Group 3, and Group 4). This study examined neuropsychological and intellectual functioning in 91 medulloblastoma patients (41 Group 4; 20 Group 3; 18 SHH; 12 WNT) following treatment, and examined the impact of several medical, treatment and demographic factors on functioning over time. Longitudinal growth curve analyses revealed hydrocephalus most clearly predisposes to poor neuropsychological functioning. Results also indicate medulloblastoma subgroups have heterogeneous intellectual outcomes following treatment. All subgroups experience intellectual declines following treatment; however, comparing between subgroups revealed Group 4 performs most poorly, and Group 3 has the best overall intellectual outcome. Lastly, qualitative analyses suggest treatment with a larger CSR dose may contribute to poor intellectual functioning.

No description available.

The overall objective of this dissertation was to increase scientific understanding of brain reserve. Chapter 1 describes how brain reserve has come to be viewed in two distinct ways: differential expression of brain injury on the basis of individual differences in gross brain properties (neurological), or on the basis of lifespan patterns of complex mental activity (behavioural). Evidence in the Alzheimer???s disease and ageing literature has been extensive, yet with conflicting reports. In order to better evaluate this evidence, a systematic review of cohort studies is the focus of Chapter 2. Complex mental activity was found to be associated with reduced incidence of dementia and slowed rate of cognitive decline. Neurological brain reserve evidence was limited. A major task of this dissertation was to develop a more standard and complete behavioural brain reserve instrument. Chapter 3 relates the development of the Lifetime of Experiences Questionnaire (LEQ) in a group of 86 healthy elderly. The LEQ had adequate levels of internal consistency and reliability. In a validation test, higher LEQ scores were also found to predict attenuated cognitive decline over 18 months independent of covariates including premorbid IQ. Chapter 4 describes how both LEQ (as a measure of behavioural brain reserve) and intracranial volume (as a measure of neurological brain reserve) significantly predicted cognitive decline over three years in a sample of 70 aged subjects. Total LEQ was furthermore significantly correlated with hippocampal volume independent of intracranial volume, and this association mediated the relationship with cognitive decline. Behavioural brain reserve may therefore work by protecting individuals from hippocampal atrophy. The fifth chapter explores therapeutic and neurobiological aspects of behavioural brain reserve in a preliminary fashion. A randomized-control mental activity trial was run with 20 healthy elderly who received repeat magnetic resonance spectroscopy. Mental activity subjects were found to have selective and sustained upregulation of phosphocreatine metabolism in the hippocampal region, a finding of potential neuroprotective significance. Experience-dependent neuroplasticity is proposed as a unifying framework in the final chapter, allowing synthesis of the present findings and reconciliation of the neurological and behavioural approaches to brain reserve.

The overall objective of this dissertation was to increase scientific understanding of brain reserve. Chapter 1 describes how brain reserve has come to be viewed in two distinct ways: differential expression of brain injury on the basis of individual differences in gross brain properties (neurological), or on the basis of lifespan patterns of complex mental activity (behavioural). Evidence in the Alzheimer???s disease and ageing literature has been extensive, yet with conflicting reports. In order to better evaluate this evidence, a systematic review of cohort studies is the focus of Chapter 2. Complex mental activity was found to be associated with reduced incidence of dementia and slowed rate of cognitive decline. Neurological brain reserve evidence was limited. A major task of this dissertation was to develop a more standard and complete behavioural brain reserve instrument. Chapter 3 relates the development of the Lifetime of Experiences Questionnaire (LEQ) in a group of 86 healthy elderly. The LEQ had adequate levels of internal consistency and reliability. In a validation test, higher LEQ scores were also found to predict attenuated cognitive decline over 18 months independent of covariates including premorbid IQ. Chapter 4 describes how both LEQ (as a measure of behavioural brain reserve) and intracranial volume (as a measure of neurological brain reserve) significantly predicted cognitive decline over three years in a sample of 70 aged subjects. Total LEQ was furthermore significantly correlated with hippocampal volume independent of intracranial volume, and this association mediated the relationship with cognitive decline. Behavioural brain reserve may therefore work by protecting individuals from hippocampal atrophy. The fifth chapter explores therapeutic and neurobiological aspects of behavioural brain reserve in a preliminary fashion. A randomized-control mental activity trial was run with 20 healthy elderly who received repeat magnetic resonance spectroscopy. Mental activity subjects were found to have selective and sustained upregulation of phosphocreatine metabolism in the hippocampal region, a finding of potential neuroprotective significance. Experience-dependent neuroplasticity is proposed as a unifying framework in the final chapter, allowing synthesis of the present findings and reconciliation of the neurological and behavioural approaches to brain reserve.

The overall objective of this dissertation was to increase scientific understanding of brain reserve. Chapter 1 describes how brain reserve has come to be viewed in two distinct ways: differential expression of brain injury on the basis of individual differences in gross brain properties (neurological), or on the basis of lifespan patterns of complex mental activity (behavioural). Evidence in the Alzheimer???s disease and ageing literature has been extensive, yet with conflicting reports. In order to better evaluate this evidence, a systematic review of cohort studies is the focus of Chapter 2. Complex mental activity was found to be associated with reduced incidence of dementia and slowed rate of cognitive decline. Neurological brain reserve evidence was limited. A major task of this dissertation was to develop a more standard and complete behavioural brain reserve instrument. Chapter 3 relates the development of the Lifetime of Experiences Questionnaire (LEQ) in a group of 86 healthy elderly. The LEQ had adequate levels of internal consistency and reliability. In a validation test, higher LEQ scores were also found to predict attenuated cognitive decline over 18 months independent of covariates including premorbid IQ. Chapter 4 describes how both LEQ (as a measure of behavioural brain reserve) and intracranial volume (as a measure of neurological brain reserve) significantly predicted cognitive decline over three years in a sample of 70 aged subjects. Total LEQ was furthermore significantly correlated with hippocampal volume independent of intracranial volume, and this association mediated the relationship with cognitive decline. Behavioural brain reserve may therefore work by protecting individuals from hippocampal atrophy. The fifth chapter explores therapeutic and neurobiological aspects of behavioural brain reserve in a preliminary fashion. A randomized-control mental activity trial was run with 20 healthy elderly who received repeat magnetic resonance spectroscopy. Mental activity subjects were found to have selective and sustained upregulation of phosphocreatine metabolism in the hippocampal region, a finding of potential neuroprotective significance. Experience-dependent neuroplasticity is proposed as a unifying framework in the final chapter, allowing synthesis of the present findings and reconciliation of the neurological and behavioural approaches to brain reserve.

Thesis (Ph. D.)--University of California, San Diego, and San Diego State University, 1998. / Vita. Includes bibliographical references (leaves 96-113).

Thesis (Ph. D.)--Drexel University, 2004. / Includes abstract and vita. Includes bibliographical references (leaves 54-60).

Thesis (Ph. D.)--University of Missouri-Columbia, 2002. / Typescript. Vita. Includes bibliographical references (leaves 66-76). Also available on the Internet.