The elderly are a rapidly growing population in the United States and have the highest rate of TBI-related hospitalization. Across all levels of severity, elderly persons have uniformly poorer outcomes including quality of life, community integration, disability, and mortality, but there is a significant lack of published research regarding communication outcome in the elderly population. The likelihood that speech-language pathologists (SLPs) will clinically treat elderly clients with TBI is great; understanding the effects that age of injury has on communication may inform clinicians’ abilities to accurately and efficiently assess, diagnose, and treat the elderly. The present study examined the relationship between age of onset of injury and severity of communication deficits following traumatic brain injury (TBI); the study included a review of published research and a survey of SLP estimates of severity of impairment. Limitations of the study and directions for further research are discussed. / text

Boredom is a common human experience, yet little is known about its underlying neural mechanisms. This thesis first set out to investigate the construct of boredom and more closely examined its relationship to phenomenologically similar mood states of depression, apathy and anhedonia. Next, deficits in sustained attention, and novelty seeking were examined in patients with traumatic brain injury (TBI), who are characterized by atypically high levels of boredom. Study 1 established that although related to varying degrees to apathy, anhedonia, and depression, boredom is indeed a distinct emotional experience. Furthermore, two boredom proneness subtypes - agitated and apathetic - were identified which varied in their relationships to depression. The relationship between boredom and depression was found to be high only in the agitated boredom prone subtype, which is characterised by a high degree of motivation to engage in meaningful, stimulating activities despite the fact that all attempts to do so fail to satisfy. In Study 2, the relationship between boredom proneness and depression was found to be greater in TBI patients than in healthy controls. Using a behavioral measure of sustained attention (SART; Robertson et al., 1997), Study 3 demonstrated a relationship between boredom proneness and sustained attention in healthy controls, such that RTs were faster and commission errors more prevalent in the agitated boredom prone subtype. No relationship between boredom proneness and sustained attention was found in TBI patients. So while attention and boredom show a clear relationship in the healthy brain, this relationship may be disrupted in TBI patients. Finally, Study 4 demonstrated an association between agitated boredom proneness and a preference for novel stimuli across participant groups. In addition, patients had a poorer ability to discriminate between similar and dissimilar stimuli than controls, which was more evident in the agitated boredom prone group. It may be the case then that agitated boredom prone individuals fail to satisfy their desire to engage in stimulating activities in part because they fail to accurately identify when something is indeed novel. Taken together, these results highlight important distinctions between apathetic and agitated boredom proneness, and the way in which these subtypes relate to depression, attention, and novelty seeking, in brain injured patients and healthy controls. More work is needed to determine the role played by boredom in TBI, particularly as this evolves from acute to chronic stages of the illness. Importantly, identifying boredom as a key element in depressive mood disorders, attention deficits (e.g., attention deficit hyperactivity disorder), and novelty seeking behaviour, facilitates the design and implementation of appropriate intervention strategies. For example, it will become increasingly important to deal with boredom as a significant component of depression. Thus, the work presented here represents a novel and important contribution to the study of boredom in that it brings the field one step closer to understanding and treating the experience. Further investigation with greater numbers of patients is necessary to fully explicate the relationship between boredom and depression, attention, and novelty seeking in TBI.

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No description available.

A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.

Vascular endothelial growth factor (VEGF) may play a role in neuroprotection after traumatic brain injury (TBI) in addition to being a regulator of angiogenesis. Gene therapy using an adenovirus carrying an engineered zinc-finger protein (Adv-ZFP) and transcription factor construct targeted to the VEGF gene, has been shown to upregulate genomic expression of VEGF-A isoforms in skeletal muscle. Our objective was to use this gene therapy to explore cell survival in TBI. Rats were subjected to a unilateral fluid percussion injury (FPI) in the cortex. Groups consisted of control, injured and injured-treated animals. Adv-ZFP-VEGF was injected into the cortex and hippocampus. Engineered ZFP-VEGF increases VEGF-A protein levels and correlates with increased CA2 hippocampal cell survival and reduction in apoptotic cell death following TBI. NF200 expression in TBI+VEGF animals was comparable to levels in naive animals. This study suggests a therapeutic strategy to treat delayed cell death in a model of TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.