No description available.

No description available.

The multidimensional nature of the frontal lobes serves to organize and coordinate brain functioning, playing a central and pervasive role in human cognition. The organizational and strategic nature of frontal lobe functioning affects memory processes by enhancing the organization of to-be-remembered information. Among the specific memory systems presumed to be based on anterior cerebral structures is the temporal organization of memory. An essential component of memory that involves temporal organization is sequential ordering. The acquisition of abilities thought to be mediated by the frontal lobes, including sequential memory, unfolds throughout childhood, serving to condition patterns of behavior for the rest of the brain. Development of the frontal regions of the brain is known to continue through late adolescence and into early adulthood, in contrast to the earlier maturation of other cortical regions. The purpose of the present study was to evaluate the development of sequential memory and to compare such findings to what currently is known regarding the development of frontal lobe functioning. Through an analysis of the previously collected standardization data of the Test of Memory and Learning (TOMAL; Reynolds & Bigler, 1994), a developmental function depicting the maturational process of sequential memory was derived. This model was then compared to an overall representative model of frontal lobe functioning. Results indicated a staging of development that begins in early childhood with the maturation of sequential memory continuing, although at a decreased rate, into early adolescence. The greatest period of development in sequential memory was evident between 5 and 8 years of age. The rate of development then decreased, and a continued deceleration of maturation continued throughout the age span examined. Gender was not found to be a significant predictor of developmental performance on sequential memory tasks. The results of the present study are consistent with previous findings that have suggested that the development of frontal functions occurs in a step-wise fashion with greatest period of development in frontal lobe functioning occurring at the 6- and 8-year old levels, with more moderate effects between the ages of 9 and 12 and performance approximating adult levels during adolescence.

Traumatic brain injury (TBI) is a leading cause of disability globally. Cognitive deficits represent the primary source of on-going disability in this population, yet the mechanisms of these deficits remain poorly understood. Here functional and diffusion-weighted imaging techniques were employed to characterize the mechanisms of neurofunctional change following TBI and their relationship to cognitive function. TBI subjects who had sustained moderate to severe brain injury, demonstrated good functional and neuropsychological recovery, and screened positive for diffuse axonal injury but negative for focal brain lesions were recruited for the project. TBI subjects and matched controls underwent structural, diffusion-weighted and functional MRI. The functional scanning paradigm consisted of a complex working memory task with both load and executive control manipulations. Study one demonstrated augmented functional engagement for TBI subjects relative to healthy controls associated with executive control processing but not maintenance operations within working memory. In study two, multivariate neuroimaging analyses demonstrated that activity within a network of bilateral prefrontal cortex (PFC) and posterior parietal regions was compensatory for task performance in the TBI sample. Functional connectivity analyses revealed that a common network of bilateral PFC regions was active in both groups during working memory performance, although this activity was behaviourally relevant at lower levels of task demand in TBI subjects relative to healthy controls. In study three, diffusion-imaging was used to characterize the impact of diffuse white matter pathology on these neurofunctional changes. Unexpectedly, decreased white matter integrity was not correlated with working memory performance following TBI. However, markers of white matter pathology did inversely correlate with the compensatory functional changes observed previously. These results implicate diffuse white matter pathology as a primary mechanism of functional brain change following TBI. Moreover, reactive neurofunctional changes appear to mediate the impact of diffuse injury following brain trauma, suggesting new avenues for neurorehabilitation in this population.

Traumatic brain injury (TBI) is a leading cause of disability globally. Cognitive deficits represent the primary source of on-going disability in this population, yet the mechanisms of these deficits remain poorly understood. Here functional and diffusion-weighted imaging techniques were employed to characterize the mechanisms of neurofunctional change following TBI and their relationship to cognitive function. TBI subjects who had sustained moderate to severe brain injury, demonstrated good functional and neuropsychological recovery, and screened positive for diffuse axonal injury but negative for focal brain lesions were recruited for the project. TBI subjects and matched controls underwent structural, diffusion-weighted and functional MRI. The functional scanning paradigm consisted of a complex working memory task with both load and executive control manipulations. Study one demonstrated augmented functional engagement for TBI subjects relative to healthy controls associated with executive control processing but not maintenance operations within working memory. In study two, multivariate neuroimaging analyses demonstrated that activity within a network of bilateral prefrontal cortex (PFC) and posterior parietal regions was compensatory for task performance in the TBI sample. Functional connectivity analyses revealed that a common network of bilateral PFC regions was active in both groups during working memory performance, although this activity was behaviourally relevant at lower levels of task demand in TBI subjects relative to healthy controls. In study three, diffusion-imaging was used to characterize the impact of diffuse white matter pathology on these neurofunctional changes. Unexpectedly, decreased white matter integrity was not correlated with working memory performance following TBI. However, markers of white matter pathology did inversely correlate with the compensatory functional changes observed previously. These results implicate diffuse white matter pathology as a primary mechanism of functional brain change following TBI. Moreover, reactive neurofunctional changes appear to mediate the impact of diffuse injury following brain trauma, suggesting new avenues for neurorehabilitation in this population.

Thesis (doctoral)--Westfälischen Wilhelms-Universität zu Münster, 1995. / Includes bibliographical references.

Time-based prospective memory has been found to be negatively affected by aging, possibly as a result of the declining frontal function that often accompanies aging. In the present study we investigated the role of the frontal lobes in prospective memory. Based upon their scores on a composite measure of frontal function, 32 older adults were characterized as possessing high- or low-frontal function, and were then tested on a time-based laboratory prospective memory task. Overall age effects were also assessed and each of the frontal groups was compared to a group of 32 younger adults. High-frontal functioning participants demonstrated better prospective memory than low-frontal functioning participants, and were not distinguishable from younger adults. The results of this study suggest that it is not aging per se that disrupts prospective memory performance, but it is instead the diminished frontal function seen in a subset of older adults.

Thesis (Ph. D.)--Cornell University, May, 2008. / Vita. Includes bibliographical references (leaves 147-159)

Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 189-196).

Thesis (M.S.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Not embargoed. Vita. Bibliography: 62-72.