Traumatic brain injury is one of the leading causes of death and disability in the North America, and can result in long-term physical and psychological consequences, which over time change brain injury from a medical problem to an issue of quality of life. Various self-care activities can significantly improve the quality of life in people living with a chronic health condition. However, research on self-care in these populations has focused on the physical aspect of self-care, often excluding other domains of functioning. There is minimal self-care research involving people who had a traumatic brain injury; however, it is important to understand how they experience and make sense of their injury and its consequences in order to develop more effective approaches to their rehabilitation and support systems. In this study, I interviewed adults with traumatic brain injury who had their injury at least two years prior to the study. Narrative analysis of their stories revealed that the participants faced the following difficulties: constructing an explanation for the injury, dealing with losses and limitations, feeling misunderstood and insignificant, and dealing with memory deficits and physical problems. The ways in which participants tried to overcome these difficulties was understood as self-care. It manifested in a variety of ways, including deliberate health-related behaviours, changes in one’s way of thinking, emotional regulation strategies, and linguistic and paralinguistic means used in the narratives. I discuss ways to understand the findings using different theoretical models, such as illness narratives, social disenfranchisement, and social disability models. The results of the study strongly suggest that our understanding of self-care should encompass both physical and psychological health.

This study furthers our understanding of naturalistic strategy use by ABI survivors with executive dysfunction. Strategies used by 14 stroke survivors, 12 TBI survivors and 25 matched controls on the Baycrest Multiple Errands Test (BMET) were scored. Relationships between strategy use and BMET performance were found for all groups (rs=.30-.71). TBI participants experienced monitoring difficulties (rs=-.38 to -.71). Greater use of task setting strategies was associated with better performance for all participants. Results support the theory of fractionation of the prefrontal lobes and the suggestion for further fractionation of the task setting and monitoring processes. Strategy use was consistently correlated with scores on the AMPS (rs=.30-.75) indicating good ecological validity. Differences in patterns of strategy use between stroke and TBI participants suggest these types of ABIs do not affect real-world performance in the same way. This study indicates the importance of understanding naturalistic strategy use for cognitive rehabilitation after ABI.

This study furthers our understanding of naturalistic strategy use by ABI survivors with executive dysfunction. Strategies used by 14 stroke survivors, 12 TBI survivors and 25 matched controls on the Baycrest Multiple Errands Test (BMET) were scored. Relationships between strategy use and BMET performance were found for all groups (rs=.30-.71). TBI participants experienced monitoring difficulties (rs=-.38 to -.71). Greater use of task setting strategies was associated with better performance for all participants. Results support the theory of fractionation of the prefrontal lobes and the suggestion for further fractionation of the task setting and monitoring processes. Strategy use was consistently correlated with scores on the AMPS (rs=.30-.75) indicating good ecological validity. Differences in patterns of strategy use between stroke and TBI participants suggest these types of ABIs do not affect real-world performance in the same way. This study indicates the importance of understanding naturalistic strategy use for cognitive rehabilitation after ABI.

This work began with a review of visual spatial selective attention, from a behavioural perspective with particular emphasis placed upon the spotlight model. To complement the behavioural review, the physiological aspects of the visual system were studied to find possible loci of the spotlight. The literature pointed to the pulvinar nucleus of the thalamus, interacting with the parietal and frontal cortices. Some experimental work examined relationships between visual spatial selective attention and event-related potentials (ERPs) recorded from the scalp. The second section of this thesis reviewed the ERP measures relating specifically to the visual modality for their possible application in a visual attentional task. This yielded two independent findings. First, the Probe-ERP paradigm comprising an attentional task being performed by the subject, with a separate stimulus to probe the unused resources within the system. Second, the steady-state evoked response, with the stimulus presented as a small sinusoidal variation around a mean level of contrast. The combination of the Probe-ERP paradigm and the steady-state visually evoked potential (SSVEP) warranted experimental evaluation.

The purpose of this study was to evaluate the performance of adolescents with traumatic brain injury on a written persuasive discourse task. Nine adolescents with TBI (mean age = 14 years 4 months) and nine age, gender and education matched peers completed a written essay on the topic of whether trained animals in circuses should be allowed to perform for the public. Language measures included productivity (number of words, number of T-units and mean length of T-unit) and complexity (number of clauses, clause density and clause breakdown). Pragmatic measures were drawn from the developmental persuasive discourse literature and included essential elements of argument (claim, number of reasons, number of elaborations, conclusion, irrelevancies, repetition of information and attitude). In comparison to their age-matched peers, the TBI group produced significantly fewer reasons to support their claims, significantly more repetitions of information and failed to take alternative perspectives on the topic. There were no significant differences on any measures of language productivity or complexity, however the TBI group performed consistently below their peers on these measures. The results are discussed alongside current literature in the field of discourse production and persuasion. Implications for clinical practice and future directions for research in this area are also offered.

This thesis examined neuropsychological and psychological outcomes following paediatric traumatic brain injury (TBI). The introductory chapter provides an overview of the paediatric TBI literature, giving definitions of key terms and concepts and providing a description of the epidemiology of childhood head injury. Key models relevant to paediatric TBI are introduced, including developmental neurological, cognitive and psychological perspectives. This is followed by a discussion of factors pertinent to outcome after TBI, followed by a description of outcomes relating to cognitive, behavioural, psychological, adaptive and family functioning domains. Existing research demonstrates that poor outcomes are frequently observed in paediatric TBI populations across these domains and difficulties are persistent over time, particularly where children have sustained severe head injury. Thus, research has turned its focus to the prediction of outcomes which can assist clinicians in the identification of those individuals who will require rehabilitation in order to promote their long-term recovery. Whilst the literature has identified injury and demographic factors that can assist in this process, little attention has been given to the potential utility of psychological screening assessment. Given the prevalence of neuropsychological and psychosocial problems after paediatric TBI and lack of empirical data considering factors predictive of difficulty at the post-acute phase, this research aimed to consider the clinical utility of completing a pre-discharge screening assessment in children and adolescents with TBI. Specific areas of consideration included the potential impact of injury severity on neuropsychological functioning, psychosocial impairment and return to full-time schooling. The study design comprised a prospective case series of 11 children and adolescents with TBI (aged 7-15 years), who were assessed both pre- and post-discharge (3-6 month follow-up). Domains of intellectual, emotional, behavioural, and adaptive functioning, health-related quality of life and parenting stress were assessed at both time-points. Clinically significant findings were demonstrated in domains of neuropsychological and psychosocial functioning, particularly for those with a severe TBI. Specifically, ratings of self-reported emotional distress, and parental perceptions of child health-related quality of life were found to be within clinical ranges at pre- and post-discharge for more than half of the participants. The majority of participants with severe injury required further neuropsychological assessment and interventions relating to emotional and/or behavioural management. The post-discharge functioning of this cohort provided preliminary evidence for the clinical utility of cognitive and psychosocial screening after paediatric TBI. The observed level of clinical need, particularly in the severely-injured group indicated that screening was a useful tool for early identification of difficulties, and provided an opportunity for timely intervention. Without screening, children and adolescents with TBI may be discharged to the community without appropriate support in place; raising long-term concerns for the child, family, and the wider social and economic systems. Despite this, further research which explicates these findings within larger samples is required. The discussion chapter reviews these findings in relation to the wider literature, followed by consideration of this study's limitations. The thesis concludes with a description of the clinical implications of the findings and suggested future directions.

This project explored two main areas: the assessment of apraxia and the intervention effectiveness in rehabilitation of the apraxic condition. This was achieved through a group study and a series of single case designs. Three experimental groups were used to investigate clinical tests and the kinematics ofmovement~ apraxic (n=17) and non-apraxic (n=13) left hemisphere damaged patients, and normal control subjects (n=ll). Using computergraphic techniques, the data provided evidence of disruption to the temporalspatial aspects of movement in apraxic people, which was not related to modality of testing, though some normal kinematic profiles were found within the apraxic group. Clinical assessments used to identify apraxia showed no relationship one with another which suggested each was identifying different aspects, or sub-types of a heterogeneous condition. Some tests were found to have low internal consistency, though inter-rater reliability through the observer-judgment process was high. A test devised for identifying agnosia was shown to relate to possible cognitive-perceptual processes or intact vision-to-action routes in the apraxic movement output. Dissociations found between clinical assessments for apraxia and kinematics of movement were explained in relation to different compensatory movement strategies employed by the apraxic patients, and/or as evidence for possible 'sub-types' of the apraxic condition. Analysis also suggested that different task demands might determine compensatory movement strategies and produce altered movement kinematics. This group study was followed by a series of single cases, two of which charted the 'natural history' process in recovery of apraxia using task performance and kinematic analysis as outcome measures. Evidence for spontaneous recovery over a six week period was shown in one case. Four single case ABA design investigations were then carried out on individuals with ideomotor and ideational apraxia to determine the effectiveness of intervention strategies. Specific sensory stimulation protocols were evaluated with no convincing evidence for effectiveness of the intervention, though both natural recovery improvements and learning effects were seen in the outcome measures. Variability of performance was a feature of all cases studied and could be considered a feature of the apraxic condition. Task break-down strategies were also evaluated in functional activities and demonstrated some effectiveness in a case of ideomotor apraxia, though a case with an ideational component indicated a more intractable condition. The strategy was not seen to generalise to other unpracticed tasks. In conclusion, the associations and dissociations found between movement kinematics and the clinical assessment tests for apraxia suggested the presence of 'sub-types' within the blanket diagnosis of the condition. Identification of such sub-types might be facilitated by the development of the agnosia test newly devised for this project. Finally, research into intervention effectiveness in apraxia calls for further investigation to determine what procedures might be used with different sub-types of the condition.

Woodpeckers can withstand 1200-1400 g of force during repetitive pecking. The forces a woodpecker’s skull and brain are subjected to warrants an in-depth investigation for the possible existence of neuro-trauma. Dr. Philip May and colleagues in 1976 published a paper titled “Woodpeckers and Head Injury” detailing two woodpeckers and one toucan control. The group utilized ferrocyanide staining, a general stain used for detecting iron deposits, on the sections. The results of these stains were not reported in Dr. May’s paper, yet he and his colleagues conclude that “clearly the woodpecker’s brain is protected somehow from impact and vibration injury.” Close to 115 journal articles have cited this one paper as the standard for woodpeckers not incurring brain injury during pecking. Due to limited studies on the woodpecker brain and the fact the woodpecker is a model for advancing helmet technology, we set out to study the woodpecker’s brain for signs of injury. Taking 10 different ethanol preserved woodpeckers from all parts of the world in different climates, and five non-woodpecker, ethanol preserved red-winged black bird experimental controls, paraffin embedded sections were cut and stained. A piece of human Alzheimer’s disease cortex was also used as a positive control. We utilized Gallyas silver stain for the study of neurofibrillary tangles and tauopathies as well as anti-phospho-tau and anti-glial fibrillary acidic protein (GFAP) immunostaining to detect tau protein and GFAP respectively. The results demonstrated perivascular silver-positive deposits in the superficial cortex and axonal tract injury of eight out of the 10 woodpeckers. The anti-phospho-tau immunostaining stained axonal tract injury in two of the three woodpeckers studied. The red-winged back birds demonstrated no positivity for all three stains. The Alzheimer’s positive control showed silver positive and phospho-tau positive staining as expected. This is the first study of this kind to discover and label potential brain injury in the woodpecker model. The negative staining of the red-winged black bird controls contrasted with the positive staining woodpecker sections suggest pecking in the woodpecker may induce brain injury. When addressing the development of safety equipment, the use of the woodpecker model should be approached with caution. Moving forward, research into different immunostaining molecular targets and an age controlled woodpecker and experimental control study should be performed to determine if the brain injury seen with our research is age-dependent.

Traumatic brain injury (TBI) is a common event that can lead to profound consequences for the individual involved, and a considerable socio-economic cost. The initial injury event triggers a series of secondary brain injury mechanisms that lead to further mortality and contribute to morbidity. One classical injury pathology is termed traumatic axonal injury (TAI), which in clinical settings produces the picture of diffuse axonal injury. TAI occurs both as a primary insult, and as a consequence of secondary mechanisms. One secondary injury mechanism that worsens TAI may be Wallerian degeneration (WD), a cell-autonomous axonal death pathway. The relationship between traumatic axonal injury and WD is poorly characterised. This thesis explores the basic mechanisms by which a physical axonal trauma can lead to WD, and how modulation of the WD pathway can affect the cellular responses to a traumatic injury. This involves the development and characterisation of in vitro and in vivo models of traumatic axonal injury. These models are then used to explore the response of cellular cultures to injury when treated with pharmacological and genetic modulators of WD. Using a primary neuronal stretch-injury system we demonstrate that rates of neurite degeneration are altered by modulators of the WD pathway but that a purported neuroprotective compound ‘P7C3-A20’ did not protect primary cultures in vivo and did not act via a WD dependent mechanism. An organotypic hippocampal slice stretch injury model was then used to demonstrate genetic rescue of cellular death, and used to assess amyloidogenic responses to injury. Next we established a TBI model using Drosophila Melanogaster, and demonstrated that a loss of function mutation in a key WD gene ‘highwire’ which controls NMNAT levels, was capable of rescuing premature death and a range of behavioral deficits after a high impact trauma. The injury caused dopaminergic neuronal loss and this was rescued by highwire mutation. Furthermore, this dopaminergic neuronal protection extended to a genetic PINK1 model of Parkinsonism. Together these results help establish WD as an important secondary injury mechanism in TBI, and provide evidence that modulation of the WD pathways can improve outcomes in various model systems. This provides a foundation for future translational research into the fields of WD and TBI.

Previously, we have demonstrated that nicotinamide (NAm), a neuroprotective soluble B-group vitamin, improves recovery of function following traumatic brain injury (TBI). However, no prior studies have examined whether NAm is beneficial following continuous infusions over seven days post-TBI. The purpose of this study was to investigate the preclinical efficacy of NAm treatment as it might be delivered clinically; over several days by slow infusion. Rats were prepared with either unilateral controlled cortical impact (CCI) injuries over the somatosensory cortex (SMC) or sham procedures and divided into three groups: CCI-NAm, CCI-vehicle, and sham. Thirty minutes following CCI, Alzet osmotic mini-pumps were implanted subcutaneously. NAm was delivered at a rate of 50 mg/kg/day for seven days immediately post-CCI. On day seven following injury, the pumps were removed and blood draws were collected for serum NAm and nicotinamide adenine dinucleotide (NAD+) analyses. Starting on day two post-CCI, animals were tested on a battery of sensorimotor tests (bilateral tactile adhesive removal, locomotor placing, and limb-use asymmetry). Statistical analyses of the tactile removal and locomotor placing data revealed that continuous administration of NAm significantly reduced the initial magnitude of the injury deficit and improved overall recovery compared to the vehicle-treated animals. NAm treatment also significantly decreased limb-use asymmetry compared to vehicle-treated animals. Continuous infusion of NAm resulted in a significant serum elevation in NAm, but not NAD+, as well as significantly attenuated cortex tissue loss than un-treated animals. The NAm-treated group also had the lowest number of glial fibrillary acidic protein (GFAP) positive cells. No detrimental effects were seen following continuous infusion. The present results suggest that NAm delivered via a clinically relevant therapeutic regimen may truncate behavioral damage following TBI. Thus our results offer strong support for translation into the clinical population.