Dissertations / Theses on the topic 'Traumatic brain injury'
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Force, Lisa Marie. "Traumatic brain injury and acidosis /." view abstract or download text of file, 2006. http://hdl.handle.net/1794/3913.
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Singh, Rajiv K. "Depression after traumatic brain injury." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18730/.
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Background Depression is known to be common after traumatic brain injury (TBI) and associated with worse functional and psychosocial outcomes. However, there remains considerable uncertainty over the exact prevalence of the condition. Aims The aim of this study was to accurately assess the prevalence of post TBI depression and its changes over a period of one year. The associated demographic and injury features were also examined for possible association with risk of depression in the hope that those with higher susceptibility to depression may be identified. Methods The study population was a prospective cohort of TBI admissions to a teaching hospital emergency department over a two year period. Minimal exclusions were applied in order to recruit a representative TBI population who were then assessed in a specialist brain injury clinic at ten weeks and at one year post injury. Demographic and injury features were recorded to establish links with risk of depression which was recorded with a HADS (Hospital Anxiety and Depression Scale). Results Over a two year period, 774 individuals were recruited of whom 690 attended one year follow-up and 38 had died. Only 6% of the cohort was lost to follow-up after one year. The prevalence of depression at ten weeks was 56.3% [95% CI 52.8-59.8] and at one year 41.2% [95% CI 37.6-44.9] A multivariable analysis identified the independent predictors of depression; at ten weeks these were TBI severity, abnormal CT scan, past psychiatric history, alcohol intoxication at the time of injury, female gender and non-white ethnicity. At one year the independent predictors were; abnormal CT scan, past psychiatric history, alcohol intoxication at the time of injury and female gender. TBI severity was no longer significant. Features such as injury aetiology, social isolation, age, length of stay and medical comorbidity were not associated with depression risk. All other outcome measures in the study, including psychosocial function, symptom severity and global overall outcome showed very high correlations with depression. Discussion The prevalence of depression is very high after TBI and associated with a number of injury features. While the prevalence drops over a year it still remains considerably elevated. There is also evidence that features related to the injury itself, such as TBI severity, become less significant in long term outcome compared to the initial period. It is possible that other psychosocial features such as personality and coping mechanisms are more important in determining long term outcome than injury features such as severity and aetiology. Some population features have been identified that may allow targeting of susceptible populations for intervention. The close correlations between all 4 outcome measures including depression suggest that they might be measuring a similar construct of emotional distress. Future work will seek to reassess the prevalence of depression at three or five years as well as associated features, re-examining the relationship between various outcomes and use of interventions and treatments, especially in targeting at risk individuals.
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Perel, Pablo Andraes. "Prognosis in traumatic brain injury." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2009. http://researchonline.lshtm.ac.uk/1635515/.
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Introduction: The general purpose of this thesis was to study prognosis in traumatic brain injury (TBI) patients, with the aim of providing useful and practical information in clinical practice and clinical research. The specific objectives were: to develop and validate practical prognostic models for TBI patients and to assess the validity of the Modified Oxford Handicap Scale (mOHS) for predicting disability at six months. Methods: A survey was first conducted to understand the importance of prognostic information among physicians. A systematic review of prognostic models for TBI patients was then carried out. Prognostic models were developed using data from a cohort of 10,008 TBI patients (CRASH trial) and validated in a cohort of 8,509 TBI patients (IMPACT study). Two focus groups and a survey were conducted to develop a paper-based prognostic score card. The correlation between the mOHS and the Glasgow Outcome Scale (GOS) was assessed, the validity of different mOHS dichotomies was assessed, and the discriminative ability of the mOHS to predict GOS was evaluated. Results: Doctors considered prognostic information to be very important in the clinical management of TBI patients, and believed that an accurate prognostic model would change their current clinical practice. Many prognostic models for TBI have been published, but they have many methodological flaws which limit their validity. Valid prognostic models for patients from high income countries and low & middle income .countries were developed and made available as a web calculator, and as a paper based score card. The mOHS was strongly correlated with and was predictive of GOS at six months. Conclusion: The prognostic models developed are valid and practical to use in the clinical setting. The association between mOHS and GOS suggest that the mOHS could be used for interim analysis in randomised clinical trials in TBI patients, for dealing with loss to follow-up, or could be used as simple tool to inform patients and relatives about their prognosis at hospital discharge.
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Rowe, Rachel K. "POST-TRAUMATIC SLEEP FOLLOWING DIFFUSE TRAUMATIC BRAIN INJURY." UKnowledge, 2013. http://uknowledge.uky.edu/neurobio_etds/7.
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Traumatic brain injury (TBI) is a major cause of death and disability throughout the world with few pharmacological treatments available for individuals who suffer from neurological morbidities associated with TBI. Cellular and molecular pathological processes initiated at the time of injury develop into neurological impairments, with chronic sleep disorders (insomnia, hypersomnolence) being among the somatic, cognitive and emotional neurological impairments. Immediately post-injury, TBI patients report excessive daytime sleepiness, however, discordant opinions suggest that individuals should not be allowed to sleep or should be frequently awoken following brain injury. To provide adequate medical care, it is imperative to understand the role of acute post-traumatic sleep on the recovery of neurological function after TBI.
The aim of this thesis was to examine post-traumatic sleep after experimental TBI, defined as an increase in sleep during the first hours post-injury. In these studies, we non-invasively measured sleep activity following diffuse brain injury induced by midline fluid percussion injury to examine the architecture of post-traumatic sleep in mice. We detected significant injury-induced increases in acute sleep for six hours regardless of injury severity or time of day injury occurred. We found concurrent increases in cortical levels of the sleep promoting inflammatory cytokine interleukin 1-beta. We extended the timeline of post-injury sleep recording and found increases in post-traumatic sleep are distinctly acute with no changes in chronic sleep following diffuse TBI. Further, we investigated if post-traumatic sleep was beneficial to neurological outcome after brain-injury by disrupting post-traumatic sleep. Disruption of post-traumatic sleep did not worsen functional outcome (neuromotor, sensorimotor, cognition) at one week after diffuse TBI. With sufferers of TBI not always seeking medical attention, our final studies investigated over-the-counter analgesics and their effect on post-traumatic sleep and functional outcome. Acute administration of analgesics with varying anti-inflammatory properties had little effect on post-traumatic sleep and functional outcome.
Overall, these studies demonstrated translational potential and suggest sleep after a concussion is part of the natural recovery from injury. While disrupting sleep does not worsen outcome, it is in no way beneficial to recovery. Additionally, a single analgesic dose for pain management following concussion plays little role in short term outcome.
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Keller, Kristen Jo. "Challenges to Secondary Brain Injury Prevention in Severe Traumatic Brain Injury." Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/338712.
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BACKGROUND/AIMS: Inconsistency in the use of secondary brain injury prevention guidelines among US trauma centers after severe traumatic brain injury is prevalent in many literature sources. However, this phenomenon has not been thoroughly studied. The purpose of this DNP project is to identify the key barriers and challenges in compliance to the evidence-based guidelines for secondary brain injury prevention. DESIGN: An exploratory, emergent design was used to collect descriptive qualitative data through the use of a survey. SETTING: Six Phoenix Metropolitan Level 1 trauma centers. PARTICIPANTS: All survey participants who consented to survey completion, which had greater than six months of experience and directly worked with patients suffering from a severe TBI in the clinical setting. MEASUREMENTS: Participant demographics (work experience, area of work, job title), current awareness and use of Brain Trauma Foundation guidelines, and time duration for evidence based order set implementation. Narrative responses were also used to identify barriers to current use of the BTF guidelines and factors that may promote their use in the future. RESULTS: A total of 43 participants consented to the survey study, with completion by 35 participants. RNs (n=27), Physicians (n=2), NPs or PAs (n=5), with an average work experience of 6 to 14 years (42.86%). A total of n=22 (62%) of participants were unaware of the current BTF guidelines for severe TBI and only 25% (n=9) aware that their facility has a protocol based on the BTF guidelines for severe TBI, while 51% (n=18) were unsure if their facility had a protocol. Barriers were identified in narrative form and were consistent with awareness/education, provider congruence, communication, and order set/protocol process improvement. CONCLUSION: The understanding of current patient management for severe TBI based on the BTF guidelines is sporadic among the greater Phoenix area Level 1 trauma centers. Requiring proof of BTF guidelines compliance by the ACS at time of Level 1 certification may increase the consistent recommended use of the BTF guidelines for the care of severe TBIs.
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Al-Hasani, Omer Hussain. "Traumatic brain injury with particular reference to diffuse traumatic axonal injury subpopulations." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5569.
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Traumatic brain injury (TBI) remains an important cause of morbidity and mortality within society. TBI may result in both focal and diffuse brain injury. Diffuse traumatic axonal injury (TAI) is an important pathological substrate of TBI, and can be associated with a range of clinical states, ranging from concussion through to death, the clinical severity being associated with a number of factors related to the injury. A retrospective study was conducted using 406 cases with TBI, from the archive of the Academic Department of Pathology (Neuropathology) University of Edinburgh, during the period from1982 and 2005. This cohort was sequential and provided a unique description of the range of pathologies associated with fatal TBI within the Edinburgh catchment area. All the data was collected on a proforma and analysed to provide a description of the incidence in the injury patterns among the Edinburgh cohort. This cohort was then used to provide cases to try and critically assess the mechanisms of axonal injury in TBI. A study was undertaken to investigate TAI in an experimental model of non-impact head injury in a gyrencephalic mammalian model (piglet model) and in human autopsy materials using immunohistochemical analysis of a range of antibodies, and to define the distribution of axonal injury with flow and neurofilament markers in TAI. A further objective was to examine the expression of β-APP as an indicator of impaired axonal transport, three neurofilament markers targeting NF-160, NF-200, and the phosphorylated form of the neurofilament heavy chain (NFH), in different anatomical regions of piglet and human brains. The double immunofluorescence labelling method was then employed to investigate the hypothesis of co-localisation between β-APP and each one of the previous neurofilament markers. The animal studies showed significant differences in NF-160 between sham and injured 3-5 days old piglet cases (6 hour survival) and between 3-5 days sham and injured, when stained with SMI-34 antibody. In 4 weeks old piglet cases (6 hour survival), immunoreactivity of β-APP was significantly higher in injured than control. No other significant differences for any of the antibodies were noted, based on age, velocity, and survival time. Human results suggested that the brainstem had a higher level of β-APP and NF-160 than the corpus callosum and internal capsule. Co-localisation of β-APP with NFs was not a consistent feature of TAI in piglet and human brains, suggesting that markers of impaired axonal transport and neurofilament accumulation are sensitive to TAI, but may highlight different populations involved in the evolution of TAI.
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Malhotra, Rajiv. "GENE EXPRESSION FOLLOWING TRAUMATIC BRAIN INJURY." VCU Scholars Compass, 1998. http://scholarscompass.vcu.edu/etd/5082.
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The pathology which results from traumatic brain injury (TBI) have long been believed to be immediate and irreversible. However, recently it has been shown that, although the primary effects are virtually unavoidable, the secondary effects manifest themselves through biochemical processes set in motion at the time of the injury. These events are frequently mediated through the process of excitotoxicity, which results from a widespread release of excitatory neurotransmitters. These neurotransmitters go on to activate both ionotropic and metabotropic receptors. The signal transduction initiated through these receptor populations gives rise to changes in gene expression.
One result of this release of neurotransmitter is an influx of calcium by means of excitatory receptors on the cell. The neurotransmitters upon which most research is focused are glutamate, aspartate, and acetylcholine. Current research is aimed at investigating antagonists to this process as well as elucidating steps within the process. Antagonists primarily function to reduce the calcium toxicity through modulation of receptor activity. However, the therapeutic window for effective antagonist usage is short. Therefore, although they may represent a viable treatment option, they need to be administered as early as possible following the injury to have the greatest effect.
The purpose of this paper is to provide a summary of the available literature on TBI and excitotoxicity with a focus on changes in gene regulation. This paper will summarize information on the steps inVolved in the intracellular signaling cascade following brain injury and provide insight to further sites for regulation and treatment. This will also allow for development hypotheses on the possible roles of some of the genes whose expression is already known to be altered.
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Davies, Suzanne. "Personality change following traumatic brain injury." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397519.
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This thesis is submitted in partial fulfilment of the requirements for the degree of Clip. Psy, D. _ at the School of Psychology, University of Birmingham. It represents both the clinical work and research conducted over the course of the clinical training. Volume I contains the research components which are concerned with examining factors affecting adjustment following traumatic brain injury (TBI). The literature review explores-3 0 papers-written since 1998t hat examine the factors-purported to - affect the development of depression after a TBI. The empirical paper examines personality change following'TBI and includes the concurrent validation of a new measure of personality change in this population. Volume II contains five Clinical Practice Reports (CPRs) which were submitted over the course of the. clinical training. The first. four. reports represent the. core training components of the Clin. Psy. D. They include case examined from two psychological perspectives, a small-scale service-related report, a case study and a single-case experimental, design., The fifth report is a .case study from a. special t. paediatric neuropsychology placement. The fifth Clinical Practice Report was presented orally, therefore only-the abstract and references are presented.
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Macqueen, Ruth. "Masculine identity after traumatic brain injury." Thesis, University of East Anglia, 2016. https://ueaeprints.uea.ac.uk/60949/.
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Background: Men are twice as likely to experience a Traumatic Brain Injury (TBI) as women suggesting that aspects of masculine identity play an important role in how people acquire their brain injury. Research also suggests that masculine identity influences how people manage their health experiences. Masculine identity may therefore be an important consideration for neuropsychological therapy and rehabilitation more generally particularly because part of the process of rehabilitation concerns helping individuals with their sense of self. This research aimed to explore men’s experiences of masculine identity following TBI. Method: Individual interviews were conducted with 10 men age 21-67 who had experienced a TBI who were living in the community. Interpretative phenomenological analysis was used to consider lived experiences and to explore the meaning of the TBI experience in relation to masculine identity. Results: Three superordinate themes emerged from the analysis: Doing life and relationships differently: Participants identified changes in aspects of their role as a man within relationships, family, occupation and social groups. Self-perceptions and the perceived view of others: Self-perceptions and others perceptions of the ability to perform roles as a man resulted in experiences of shame and loss of self-confidence. The invisibility of the injury appeared to both accentuate and protect from the experience of shame. Managing the impact: Participants identified ways in which they thought about their lives and reformulated their behaviour in order to protect their identity as a man. Conclusions: The findings suggest that men experience changes in masculine identity following TBI, particularly when ideals about independence and roles were challenged. The findings highlight how masculine identity may be a valuable aspect of self in considering threats to and reconstruction of self-identity after TBI. Aspects of gender identity should be considered in order to promote engagement, support adjustment and achieve meaningful outcomes in rehabilitation.
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Helmy, Adel Ezzat. "Neuro-inflammation in traumatic brain injury." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610114.
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Nagulavancha, Sruthi. "Traumatic brain injury options web application." Kansas State University, 2010. http://hdl.handle.net/2097/4626.
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Master of ScienceDepartment of Computing and Information Sciences
Daniel A. Andresen
According to the Division of Injury Response, Centers for Disease Control and Prevention, approximately 1.4 million Americans sustain a traumatic brain injury each year. The aim of the project is to create a web interface to link survivors, family members, and caregivers of individuals suffering from traumatic brain injuries (TBI) to potentially helpful agencies or service centers within their local communities. Often the TBI service centers located in the remote places are difficult to trace hence this website mainly concentrates on small rural centers which are located in Kansas State. The portal will offer two-dimensional and basic information about traumatic brain injury centers and specifically about access of resources. Within the portal, a link to an interactive map will be provided. A form for data entry helps the service centers to publish about their presence and the regions they serve. A search distance feature is also added into the website which interactively searches the nearest latitude, longitude values (TBI service center) to the user’s location by using the haversine formula.
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LeMay, Carrie C., and Jill D. Stinson. "Sex Offenders With Traumatic Brain Injury." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/7906.
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Osterstock, Guillaume. "Hypothalamic defaults after traumatic brain injury." Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON1T017/document.
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Les travaux de cette thèse ont porté sur le contrôle des neurones à GHRH dans des conditions physiologiques et pathologiques. Le but étant de caractériser les mécanismes cellulaires et moléculaires impliqués dans le fonctionnement ou dérégulations du réseau de neurones à GHRH. Ces neurones sont les principaux stimulateurs de la libération de l’hormone de croissance (GH). Nous avons d’abord montré que l’axe de la croissance et de l’appétit peuvent être régulés indépendamment au niveau de l’hypothamus. En effet, la ghréline, seule hormone produite par le tractus gastro-intestinal et connue pour stimuler la libération de GH en agissant principalement sur les neurones GHRH, stimule ces derniers de manière uniquement directe. Ces effets sont indépendants de ceux qu’elle exerce sur les neurones voisins à NPY, orexigéniques. De plus, la ghréline et les GHS (agonistes sélectifs du récepteur de la ghréline) ne changent pas le mode de décharge électrique des neurones à GHRH ni ne les synchronise. Enfin, ces effets ne présentent pas de dimorphisme sexuel. Dans un second temps, la somatostatine, principal inhibiteur de l’axe GH, induit un rythme d’activité électrique des neurones à GHRH médié par les récepteurs de sous-type SST1 et SST2. Ces effets sont donc temps-dépendants, et aussi sexuellement dimorphiques. Ils sont probablement impliqués dans la modulation de la pulsatilité ultradienne de la libération de GH. Enfin, après un traumatisme crânien, nous observons un déficit de la libération de GH qui apparaît tôt et est soutenu, comme ceux observés chez l’humain. Aucune inflammation ni changement histologique n’a été observe dans l’hypophyse. Cependant, l’inflammation, impliquant une réaction tanycytaire, microgliale, astrocytaire, est présente dans le noyau arqué et l’éminence médiane (EM), ou sont respectivement présents les corps cellulaires et terminaisons des neurones à GHRH. Ceci est lié à des changements morpho-fonctionnels de l’EM (augmentation perméabilité, rupture des barrières tanycytaires). Aucun changement n’a été observé dans le noyau périventriculaire, où sont localisés les neurones à somatostatine. Enfin, les propriétés électriques passives des neurones à GHRH ne sont pas modifiées. En conclusion, une dérégulation de leur activité au niveau des terminaisons nerveuses doit expliquer les défauts posttraumatiques de libération de GHThe works of this thesis were interested in the control of the hypothalamic GHRH neurons in physiological and pathological conditions. The goal was to clarify the molecular and cellular mechanisms involved in the control or impairments of GHR neuronal network functions. These neurons are the main stimulators of the GH release. We first showed that the hypothalamic growth axis could be regulated independently from the feeding network. Indeed, GHRH neurons are directly stimulated by ghrelin, which is the only hormone produced by the gastrointestinal tract known to stimulate the GH release through acting mainly on GHRH neurons. These effects are independent from its orexigenic effects exerted on the neighbourings NPY neurons. In addition, ghrelin and GHS (synthetic ghrelin receptor agonists) don’t change neither the firing rate of GHRH neurons, nor synchronize them. These effects are not gender-dependant; by contrast, Somatostatin, the major GH axis inhibitor, generates a sexual dimorphic and rhythmic inhibition of the GHRH neurons electrical activity mediated by its SST1 and SST2 receptors subtypes. These effects are so time-dependant direct and indirect effects and can probably be involved in the generation of the ultradian rhythm of the GH release. After a traumatic brain injury, we found an early and sustained deficiency of the GH release, like those observed in human. No pathological changes are visible in the pituitary gland. Inflammation occurs at the arcuate nucleus, and mainly at the median eminence levels; it involves a strong astrocyte reaction, tanycytes, and microglial and (or) infiltrated immune cells activations. These changes elicit morpho-functional impairments of the median eminence, permeability and leakage of the tanycyte barrier between the blood, CSF and Arc; at the opposite, nothing occur at the periventricular level, where are located SST neurons. Neither the number of GHRH neurons, neither their passive electrophysiological properties changed. Impairments of the activities of the GHRH nerve terminals, maybe associated to impairments of their regulated activity, must explain a GH deficiency
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Moazzez, Lesko Mehdi. "Prognosis in traumatic brain injury (TBI)." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/prognosis-in-traumatic-brain-injury-tbi(8b69e340-7ecd-4890-9746-863089bf55f5).html.
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Introduction: Prognosis in Traumatic Brain Injury (TBI) can be made using prognostic models (the IMPACT and CRASH models) or brain injury biomarkers (S100B). Current prognostic models are derived from historic datasets recruited from heterogeneous countries in terms of trauma care and for the purpose of clinical trials. Objective: To construct a prognostic model suitable for British trauma care, to compare the prognostic performance of prognostic models with S100B and to assess the combination of prognosticators from the constructed models with S100B. Methods: A dataset of 802 TBI cases from the Trauma Audit and Research Network (TARN), Manchester, UK was used to construct the prognostic models.. During the modelling, criteria for well-developed models as per the literature review were followed such as the dataset being large, the variables being selected from the literature and missing information being imputed. A further dataset of TBI cases was used to validate these models Moreover, the resulting models were run on a dataset of 100 TBI cases who had their serum S100B recorded at 24 hours to compare their performance with S100B. Results: Two prognostic models were constructed (models A and B) to predict the discharge survival. Both models share age, admission Glasgow Coma Scale (GCS), admission pupillary reactivity and presence/absence of hypoxia and lowblood pressure (on admission) and brain stem injury. However, model A includes Injury Severity Score (ISS) which is replaced with cause of injury, extracranial injury, brain swelling and interaction of cause of injury and age in model B. Both models have high performance either on the derivation dataset (Area Under the ROC Curve (AUC) of model A: 0.92 and AUC of model B: 0.93) or the external validation set from a later time period in TARN (AUC of model A: 0.92 and AUC of model B: 0.82). Furthermore, in the S100B dataset, it appears that the performance of prognostic models is not significantly different to that of S100B (for example, AUC of model A in this dataset: 0.64 versus 0.69 of the model just including S100B for survival prediction). A combination of S100B and models prognosticators improved performance and S100 improved the performance of models A and B. Discussion: The proposed prognostic models have very high AUCs and since they have been validated on a different TBI dataset from TARN, they are valid to be used for the purpose of the British trauma care benchmarking. Unfortunately, the results of the analysis on the small S100B dataset are not adequately powerful to be conclusive. However, these findings highlight the importance of future research on this topic in larger datasets. Conclusion: Two prognostic models have been constructed which can be used for the British TBI patients.
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Arietta, Luca. "Clinical Data Mining: Traumatic Brain Injury." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amslaurea.unibo.it/3897/.
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Il trauma cranico é tra le piú importanti patologie traumatiche. Ogni anno 250 pazienti ogni 100.000 abitanti vengono ricoverati in Italia per un trauma cranico. La mortalitá é di circa 17 casi per 100.000 abitanti per anno. L’Italia si trova in piena “media” Europea considerando l’incidenza media in Europa di 232 casi per 100.000 abitanti ed una mortalitá di 15 casi per 100.000 abitanti.
Degli studi hanno indicato come una terapia anticoagulante é uno dei principali fattori di rischio di evolutiviá di una lesione emorragica. Al contrario della terapia anticoagulante, il rischio emorragico correlato ad una terapia antiaggregante é a tutt’oggi ancora in fase di verifica.
Il problema risulta rilevante in particolare nella popolazione occidentale in quanto l’impiego degli antiaggreganti é progressivamente sempre piú diffuso. Questo per la politica di prevenzione sostenuta dalle linee guida nazionali e internazionali in termini di prevenzione del rischio cardiovascolare, in particolare nelle fasce di popolazione di etá piú avanzata.
Per la prima volta, é stato dimostrato all’ospedale di Forlí[1], su una casistica sufficientemente ampia, che la terapia cronica con antiaggreganti, per la preven- zione del rischio cardiovascolare, puó rivelarsi un significativo fattore di rischio di complicanze emorragiche in un soggetto con trauma cranico, anche di grado lieve. L’ospedale per approfondire e convalidare i risultati della ricerca ha condotto, nell’anno 2009, una nuova indagine. La nuova indagine ha coinvolto oltre l’ospedale di Forlí altri trentuno centri ospedalieri italiani.
Questo lavoro di ricerca vuole, insieme ai ricercatori dell’ospedale di Forlí, verificare: “se una terapia con antiaggreganti influenzi l’evolutivitá, in senso peggiorativo, di una lesione emorragica conseguente a trauma cranico lieve - moderato - severo in un soggetto adulto”, grazie ai dati raccolti dai centri ospedalieri nel 2009.
Il documento é strutturato in due parti. La prima parte piú teorica, vuole fissare i concetti chiave riguardanti il contesto della ricerca e la metodologia usata per analizzare i dati. Mentre, la seconda parte piú pratica, vuole illustrare il lavoro fatto per rispondere al quesito della ricerca.
La prima parte é composta da due capitoli, che sono:
• Il capitolo 1: dove sono descritti i seguenti concetti: cos’é un trauma cra- nico, cos’é un farmaco di tipo anticoagulante e cos’é un farmaco di tipo antiaggregante;
• Il capitolo 2: dove é descritto cos’é il Data Mining e quali tecniche sono state usate per analizzare i dati.
La seconda parte é composta da quattro capitoli, che sono:
• Il capitolo 3: dove sono state descritte: la struttura dei dati raccolti dai trentadue centri ospedalieri, la fase di pre-processing e trasformazione dei dati. Inoltre in questo capitolo sono descritti anche gli strumenti utilizzati per analizzare i dati;
• Il capitolo 4: dove é stato descritto come é stata eseguita l’analisi esplorativa dei dati.
• Il capitolo 5: dove sono descritte le analisi svolte sui dati e soprattutto i risultati che le analisi, grazie alle tecniche di Data Mining, hanno prodotto per rispondere al quesito della ricerca;
• Il capitolo 6: dove sono descritte le conclusioni della ricerca.
Per una maggiore comprensione del lavoro sono state aggiunte due appendici. La prima tratta del software per data mining Weka, utilizzato per effettuare le analisi. Mentre, la seconda tratta dell’implementazione dei metodi per la creazione degli alberi decisionali.
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Akin, Faith W. "Vestibular Evaluation of Traumatic Brain Injury." Digital Commons @ East Tennessee State University, 2009. https://dc.etsu.edu/etsu-works/2448.
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Yin, Terry. "Neuroprotective strategies for traumatic brain injury." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1811.
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Traumatic brain injury (TBI) causes life-debilitating conditions. While patient survival after a TBI has improved, the outlook for quality of life after TBI currently remains poor. In order to address this problem, there is a significant unmet need for new therapeutic options to prevent progression of deficits associated with TBI. To this end, we investigated two strategies to combat the deleterious affect of TBI. First, we targeted cerebral acidosis associated with TBI by testing whether disruption of acid sensing ion channel 1a (ASIC1a) in CNS, or buffering acidosis with sodium bicarbonate, could prevent neurological deficits after TBI. We next tested whether treatment with the neovel class of aminopropyl carbozoles, known as the P7C3 series, could also prevent TBI-associated neurological decline.
Using the mouse fluid percussion injury model of TBI, we observed post-injury acidosis in the cortex, consistent with what has been shown in humans following brain injury. Administering HCO3- after fluid percussion injury prevented acidosis and reduced neurodegeneration. Because acidosis activates acid sensing ion channels (ASICs), we also studied AIC1a-/- mice and found reduced neurodegeneration after injury. Both HCO3-3 administration and loss of ASIC1a reduced functional deficits caused by fluid percussion injury. These results suggest that fluid percussion injury induces cerebral acidosis, which activates ASIC channels in the brain and contributes to neurodegeneration. Blocking ASIC1aactivity may thus offer a new therapeutic strategy to attenuate the adverse consequences of TBI.
We next applied the blast injury model of TBI to test whether the P7C3 class of neuroprotective aminopropyl carbazoles would be of therapeutic benefit. In addition to preventing neuronal cell death, P7C3 molecules also preserved axonal integrity before neuronal cell loss in this model. The mechanism of P7C3 neuroprotection may be linked to its ability to activate the enzyme, nicotinamide phosphoribosyltransferase, which catalyzed the rate limiting step of nicotinamide adenine dinucleotide salvage pathway. Administration of the lead compound in the series, P7C3-S243, 1 day after blast-mediated TBI blocked axonal degeneration and preserved normal synaptic activity. P7C3-S243 administration also reduced neuronal functional deficits, including impaired learning, memory, and motor coordination in mice. We additionally reported persistent neurologic deficits and acquisition of anxiety-like phenotype in untreated animals 8-months after blast-mediated TBI. Optimized variants of P7C3 thus offer hope for identifying neuroprotective agents for conditions involving axonal damage, neuronal cell death, or both. Together, the results of this body of work identify novel therapeutic interventions that may attenuate deficits associated with TBI, and thus improve the quality of life in people after TBI.
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Savicki, Laura Elizabeth. "Collaborative referencing in traumatic brain injury." Thesis, University of Iowa, 2012. https://ir.uiowa.edu/etd/2977.
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Traumatic brain injury (TBI) is a global health epidemic that has deleterious consequences for the individuals with the brain injury, their families, and society. The development and validation of effective treatments is imperative. The current study was inspired by Ylvisaker's collaborative intervention approach with individuals with TBI and draws on a line of work by Duff and colleagues (e.g., Duff et al., 2006; Gupta et al., 2011) documenting patterns of spared and impaired learning abilities in individuals with various types focal brain damage (e.g., hippocampus) and selective neuropsychological impairment (e.g., declarative memory) using a collaborative referencing paradigm. This study extends this line of work by examining the ability of individuals with mild to moderate traumatic brain injury to develop and use referential labels for novel picture cards across repeated interactions with a familiar partner as they complete a collaborative referencing task. Five TBI participant pairs (an individuals with TBI and their partner) and five healthy comparison pairs completed 24 trials (6 trials in each of 4 sessions) of the collaborative referencing task across two days. As a group, the performance of four of the five TBI pairs did not differ from healthy comparison pairs on the primary dependent variables of card placement accuracy, time to complete each trial, and reduction in communicative resources across trials. That is, despite having TBI, these individuals were able to develop and use unique and concise labels to reference the novel cards in collaboration with a familiar partner. The fifth TBI participant pair (3591) differed from the other TBI and healthy comparison pair on both quantitative and qualitative measures. Speculating that 3591's husband may have contributed to their poor performance, a follow-up study was conducted whereby 3591 was brought back to lab several months later and she complete one session of the collaborative referencing task with a new partner. The results of the follow-up study were striking. 3591 and her new partner were as successful as other pairs on all measures of learning in the study.
Given the complex nature of cognitive, neurological, behavioral, personality, and communicative impairments associated with TBI, the findings here, that all participants with TBI were successful in the task, are surprising and provides further evidence that these interactive sessions are potent learning environments. The results of the study support the idea that use of a social and collaborative interaction paradigm facilitates learning in adults at least one year time post injury with mild to moderate brain injuries. Aspects of the collaborative referencing task that exemplify Ylvisaker's contextualized invention approach are completion of a goal-directed task, working with a partner who was relevant to the participant's everyday life, supports were provided by the partner as needed, the task was repeated many times in order to increase chances of the pair's success, and skills were taught through collaboration rather than explicit instruction. Although this was not an intervention study, these findings provide further evidence supporting the use of Ylvisaker's social, interactive, and collaborative approach for individuals with TBI. This study is the first to our knowledge to investigate learning during a collaborative referencing task with individuals with TBI and the positive results obtained here suggest that this may be a fruitful way to deploy Ylvisaker's contextualized intervention approach in more controlled research settings.
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Akin, Faith W., and Owen D. Murnane. "Vestibular Consequences of Mild Traumatic Brain Injury (Blast Injury)." Digital Commons @ East Tennessee State University, 2008. https://dc.etsu.edu/etsu-works/1940.
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Lalani, Sanam Jivani. "Effects of Traumatic Brain Injury on Pediatric Brain Volume." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/6924.
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This study investigated the effects of lesion presence within larger brain networks (e.g., default mode network (DMN), salience network (SN), and mentalizing network (MN)) in the chronic phase of a pediatric traumatic brain injury (TBI) and the effect on social function. We compared children with a TBI to children with an orthopedic injury (OI) with three different aims. The first aim was to determine whether network volume differed by group (e.g., TBI vs. OI). Second, investigate if lesion presence in a sub component region of the network resulted in total network volume loss for that network. Finally, learn whether network volume would predict outcome on the Behavior Assessment System for Children, Second Edition (BASC-2). Approximately 184 participants (65% male; 70% Caucasian) between the ages of 6-17 years completed testing and a structural MRI scan in the chronic stage (at least one-year post-injury) of the injury. Injury severity included complicated mild, moderate, and severe TBI. Radiological findings were analyzed using recommendations from the Common Data Elements' core (presence or absence of a lesion) and supplementary (lesion type and location) recommendations. Volumetrics for all participants were obtained with FreeSurfer to quantify total network volumes for the DMN, SN, and MN. The parent of each participant completed a behavioral measure for externalizing and internalizing behaviors. Three sets of statistical analyses were completed, including multivariate analysis of covariance, analysis of covariance, and multiple regression, for each of the three aims of the study, respectively. There were significant differences in total DMN volume between the two groups and participants with lesions solely in the MN had lower total MN volume. Moreover, lower total MN volume was associated with worse functioning on measures of externalizing and internalizing behaviors. The larger implications, including developmental and social implications, of these findings are discussed.
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LaRoux, Charlene I. 1979. "Executive function deficits in traumatic brain injury." Thesis, University of Oregon, 2010. http://hdl.handle.net/1794/11063.
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xii, 98 p. : ill. (some col.)The short and long term pathophysiology of traumatic brain injury (TBI) has not been fully elucidated. Individuals recently suffering a mild TBI (mTBI) or having a history of TBI frequently suffer deficits in their ability to maintain and allocate attention within and between tasks. This dissertation examines the influence of mild and chronic TBI on performance of task switching. We employed spatial and numerical task switching paradigms to assess the behavioral deficits in mTBI, and we used an internally generated switching and an externally cued switching task along with functional Magnetic Resonance Imaging (fMRI) to assess the long term deficits in executive function resulting from chronic TBI. In the first experiment, individuals with mTBI were identified and tested within the first 48 hours of injury and then at a set interval 5, 14, and 28 days post injury. In the second investigation, individuals with chronic TBI were tested at least 12 months after their most recent injury. Healthy gender, age, and education matched controls were also tested in both studies. This research demonstrated that mTBI subjects display deficits in switching behavior within 48 hours of injury that failed to resolve a month post-injury; however, these costs did not generalize across the switching task types. Chronic TBI subjects performed internally generated and externally cued switching paradigms with a degree of success equivalent to that of healthy controls but displayed larger amounts of activation and recruited more areas of the brain at lower levels of difficulty and did not increase recruitment in a stepwise fashion at higher levels of difficulty. Mild TBI causes significant deficits in task switching, but there is specificity in these deficits. Chronic TBI patients performed at a level equivalent to that of controls but displayed different patterns and degree of activation. Taken together, these findings indicate that there may be a specific time frame during which task switching shows behavioral deficits, after which the subject may compensate for these deficits to produce normalized performance.
Committee in Charge: Dr. Paul van Donkelaar, Chair; Dr. Li-Shan Chou; Dr. Ulrich Mayr; Dr. Marjorie Woollacott
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Hånell, Anders. "Plasticity and Inflammation following Traumatic Brain Injury." Doctoral thesis, Uppsala universitet, Neurokirurgi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-146551.
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Traumatic Brain Injury (TBI) mainly affects young persons in traffic accidents and the elderly in fall accidents. Improvements in the clinical management have significantly improved the outcome following TBI but survivors still suffer from depression, memory problems, personality changes, epilepsy and fatigue. The initial injury starts a series of events that give rise to a secondary injury process and despite several clinical trials there is no drug available for clinical use that targets secondary brain injury mechanisms. Some recovery of function is seen during the first months following injury but is usually limited and there are no drugs that stimulate the recovery of lost function. Some of the recovery is attributed to plasticity, the brains ability to adapt to new circumstances, and enhancing plasticity via increased axonal growth has the potential to partly restore lost function. In this thesis mice were subjected to the controlled cortical impact model of TBI and functional outcome was evaluated using Morris water maze, the cylinder test and the rotarod. Brain tissue loss was measured in all Papers but the additional histological analyses differ among the Papers. Attempts to increase axonal growth were made by interfering with Nogo receptor function in Paper I and by conditional knockout of ephA4 in Paper II. Contrary to the hypothesis cognition was impaired in Paper I but otherwise no effects of treatment were detected in Paper I and II. Much is still unknown about plasticity and despite the discouraging results of Papers I and II this treatment approach is still worth further exploration. It is firmly established that TBI results in an inflammatory response and some aspects of it may damage brain tissue. In Papers III and IV the inflammatory response was attenuated using an IL-1β directed antibody which resulted in reduced tissue loss and edema while improving cognitive function. The results from Papers III and IV are encouraging and the possibility to find a treatment based on IL-1β inhibition appears promising.
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Van, der Merwe Jó-Marié. "Family needs following adult traumatic brain injury." Thesis, University of Port Elizabeth, 2004. http://hdl.handle.net/10948/335.
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Traumatic brain injury (TBI) represents a significant and growing type of disability in South Africa. Coping with the impact of traumatic brain injury is one of the most difficult tasks that can confront a family, and family members experience a wide range of needs as the injured person progresses through rehabilitation. In South Africa, research on family needs following traumatic brain injury has thus far been neglected and rehabilitation resources are sadly lacking. For this reason it is necessary to accumulate knowledge about these families’ needs so as to assist with the planning of future rehabilitation programmes. The study aimed to explore and describe the needs of a sample of families with adult traumatic brain injury individuals in the Eastern Cape utilizing the Family Needs Questionnaire (FNQ). The research approach followed could be described as descriptive and exploratory in nature and was conducted within a quantitative framework. A biographical questionnaire and the FNQ were administered to a heterogeneous sample of 32 family members, including significant others and primary caregivers, of 16 adult traumatically brain-injured individuals, who sustained the TBI one to three years previously, and who underwent rehabilitation treatment at a private rehabilitation hospital in Port Elizabeth. A non-probability, purposive, and convenient sampling method was used. Descriptive statistics were computed to determine the importance and the perceived fulfillment of the needs. The results of the present study indicated that all 40 needs were endorsed by at least half the sample as being important to very important. Furthermore, 52.50% of the needs were endorsed by more than two-thirds of the sample as being important to very important. The needs were rank-ordered according to their importance ratings and the 10 mostly rated as important or very important were identified. These 10 needs were endorsed by between 84.38% and 93.75% of the family members as being important to very important. Six of the important or very important needs related to health information, two to professional support, one to community support, and one to emotional support. The relation between various participant, traumatically brain-injured individual and brain injury characteristics and the 10 important or very important needs, as well as the 10 needs more frequently rated as met were investigated and found to either have a limited or varied relationship. The 10 needs most often rated as met were endorsed by between 43.75% and 56.25% of the family members. Six of the met needs related to health information, two to community support, one to instrumental support, and one to treatment decisions. The highest unmet need was endorsed by 46.88% of the participants and related to the need to discuss their feelings with someone who has gone through the same experience. Based on the findings of the present study, further research on family needs following traumatic brain injury is suggested. It is also recommended that the Family Needs Questionnaire be used to evaluate existing rehabilitation programmes so as to make suggestions as to how to improve them. The results of this study suggested that family members would benefit from receiving educational information material, as well as referrals to professionals for advice and support.
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Crawford, Maria Anne, and n/a. "Speed of retrieval after traumatic brain injury." University of Otago. Department of Psychology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20060830.115029.
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Although it is well established that persons with traumatic brain injury (TBI) experience word retrieval difficulties, the underlying cause of these deficits is not known. Difficulties with word retrieval have negative social implications as they can impact on the ability to converse with others. The overarching goal of this dissertation was to determine the underlying cause of problems with word retrieval after TBI.
To test word retrieval in this dissertation, participants were given a series of word fluency tasks and the speed of word generation was measured. In addition to measuring interresponse times, procedures used by Rohrer, Wixted, Salmon and Butters (1995) were also followed. This involved the calculation of parameter estimates to investigate whether slowed retrieval or degraded semantic stores were responsible for the patients� word retrieval difficulties. One parameter (N) was a measure of the total number of retrievable words and the second parameter (tau) was an estimate of mean latency.
Study 1 was designed to trial the procedure and equipment adopted throughout this dissertation to analyse speech. University students were presented with categories on a computer screen and asked to generate as many exemplars as possible in 60 seconds. A PowerLab Chart sound system was used to measure the time that each word was generated. The results of Study 1 showed that the methodology of previous research could be replicated using the PowerLab Chart sound system.
In Study 2, persons with postconcussion syndrome (PCS) and matched controls were given two word fluency tasks. Results showed that on both tasks patients recalled fewer words, had longer pauses between words, and took significantly longer to generate their first word than controls. Also, patients had a significantly reduced N relative to controls, but there was no difference in tau between patients and controls. Given that the participants had not finished responding and that parameter estimates require responses to be exhausted, Study 3 was designed to replicate the findings of Study 2 using an extended recall period.
In Study 3, patients with PCS and matched controls completed a series of word fluency tasks and were given extended periods of time to generate words. Results showed that the patients obtained significantly fewer words on two of the tasks, but no evidence of slowed retrieval was found. There was also no difference in the estimates of N and tau between patients and controls. As the patients in Study 3 sustained more minor injuries than those in Study 2, Study 4 tested patients with severe TBI.
In Study 4, patients with severe TBI and matched controls were given a series of word fluency tasks. Results showed that the patients generated fewer words and experienced slowed retrieval. Again, there was no difference in the estimates of N and tau between patients and controls. The results of Study 4 confirmed the hypothesis that slowed word retrieval is a consequence of TBI. Taken together, the results of this dissertation show that an underlying slowness of processing is the primary cause of problems with word retrieval in persons with TBI.
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Kruijk, Jelle de. "Mild traumatic brain injury intervention and prognosis /." [Maastricht] : Maastricht : UPM, Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 2001. http://arno.unimaas.nl/show.cgi?fid=7622.
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Israelsson, Charlotte. "Molecular Characterization of Experimental Traumatic Brain Injury." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7087.
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Johnson, Victoria E. "Progressive neuopathological changes following traumatic brain injury." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3162/.
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Whilst the acute effects of traumatic brain injury (TBI) may be devastating, growing evidence suggests TBI may initiate long-term neurodegenerative processes. Indeed, an epidemiological association between TBI and Alzheimer’s disease (AD) has been demonstrated. Here the link between TBI and chronic neurodegeneration is explored by examining associated pathologies in material from patients surviving TBI for varying intervals. Furthermore, the Aβ clearing enzyme, neprilysin, has emerged as important with regards to Aβ dynamics in AD and thus may be relevant to Aβ-plaque formation in TBI. Its influence on Aβ dynamics in TBI was explored in an animal model of TBI and in human TBI material. First, a potential association between acute-Aβ plaques post-TBI and a GT repeat polymorphism of the Aβ-degrading enzyme, neprilysin was investigated using DNA fragment sizing analysis (n=81). Results show there was an increased risk of Aβ plaques for patients with greater than 41 total repeats (p<0.0001, OR:10.1). In addition, the presence of 22 repeats in at least one allele was independently associated with plaque deposition (p=0.03, OR: 5.2). In contrast, the presence of 20 GT repeats in one allele was independently associated with a reduced incidence of Aβ plaques (p=0.003). These data suggest a genetically linked mechanism that determines which TBI patients will rapidly form Aβ plaques. The role of neprilysin in TBI was further examined using immunohistochemistry (IHC) to evaluate plaque formation in neprilysin knock-out mice at 2h, 48h and 4mo following a single controlled cortical impact in mice. Young (2mo) and older (8mo) mice were examined at each time point and compared to age-matched injured and uninjured wild-type mice (n=4 for all groups). No plaques were observed at any time point or in age group indicating that neprilysin deficiency alone is insufficient to recapitulate the plaque pathology observed in humans using this model. Next, post-mortem brains from long-term survivors of just a single TBI (1 to 47 years survival; n=39) versus uninjured, age-matched controls (n=47) were examined for hallmark AD pathologies, neurofibrillary tangles (NFTs) and Aβ plaques using IHC and thioflavin-S staining. NFTs were exceptionally rare in young, uninjured controls, yet were abundant and widely distributed in approximately one third of TBI cases. Moreover, thioflavin-S staining revealed that while plaque-positive control cases displayed predominantly diffuse plaques, 64% of plaque-positive TBI cases, displayed predominantly thioflavin-S positive plaques or a mixed positive / diffuse pattern. These data indicate that TBI may induce or accelerate the presence of neurodegeneration-associated pathologies many years following just a single injury. To explore potential mechanisms driving plaque formation post-TBI, IHC was used to examine amyloid-β’s precursor, APP in TBI cases with acute survival (10h to 1 week; n=20), moderate survival (1 week to 1 year; n=17) and long-term survival (>1 year; n=33), versus uninjured controls (n=47). Following TBI, increased somatic APP immunoreactivity (IR) was observed in all TBI cases (n=70; 100%) versus (n=47; 70%) of controls (Chi Sq; p=0.00001). Moreover, increased APP IR was present in all survival intervals examined, (10h to 10 days, p=0.001; 10 days to 1 year, p=0.0001; > 1 year; p=0.001; all Chi Sq) versus controls, and an increased extent / distribution of pathology was demonstrated in the TBI group regardless of survival time. Interestingly, APP IR was not associated with the presence of plaques suggesting increased APP alone is insufficient to drive post-traumatic plaque formation. The Tar-DNA binding protein, TDP-43 has emerged as an important pathological feature in various chronic neurodegenerative diseases including frontotemporal lobe dementia, and more recently in dementia pugilistica caused by repetitive TBI. Here we examined survivors of a single TBI using IHC specific for TDP-43. TBI cases were acute (n=23: Survival <2 weeks) and long-term (n=39; 1-47 years survival) and were compared to uninjured controls (n=47). No association was found between single TBI and pathological TDP-43 inclusions. Specifically, just 3 of 62 TBI cases displayed p-TDP-43 pathology versus 2 of 47 control cases. However, IR to phosphorylation-independent TDP-43 was commonly increased in the cytoplasm following TBI with both acute and long-term survival, potentially as part of a normal stress-response. Finally, acute and chronic inflammation was evaluated in the corpus callosum following TBI, a region highly susceptibility to injury. IHC specific for CR3/43 and CD68 was analysed using digital quantitation to determine the percentage area of positive staining in acute TBI cases (survival < 14 days; n=18) and compared to age-matched controls (n=18). Long-term survivors of TBI (surv >1 year; n=23) were compared to controls (n=23) and a further subset of acute TBI cases (survival < 10 days; n=12) compared to age-matched long-term survivors of TBI (survival >1 year; n=12). While no quantitative difference was demonstrated between groups, 44% of long-term survival TBI cases displayed extensive amoeboid cells versus 0% of controls (Chi Sq; p=0.0004), indicating a percentage of TBI patients may develop a chronic inflammatory response in a time-frame consistent with epidemiological associations linking TBI with AD.
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Craddock, Holly L. "Nursing interventions utilized in traumatic brain injury." Honors in the Major Thesis, University of Central Florida, 1998. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/27.
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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.Bachelors
Health and Public Affairs
Nursing
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Bradshaw, Douglas Robert Saunders. "Linear wave propagation in traumatic brain injury." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341646.
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Williams, Claire. "Emotion deficit disorders following traumatic brain injury." Thesis, Swansea University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678429.
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Herbert, Camilla. "Grief and loss following traumatic brain injury." Thesis, University of Sheffield, 1998. http://etheses.whiterose.ac.uk/10277/.
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Literature Review: The literature review summarises the main theoretical models of grief and illustrates how these have developed from intra- to inter-personal models and from clinical to psychosocial models of bereavement. The paper explores the concepts of pathological, anticipatory, and disenfranchised grief, and attempts to identify aspects that are relevant to grief in contexts other than bereavement. Finally an attempt is made to integrate themes from the literature that are applicable to the experience of loss amongst relatives of traumatically brain-injured patients. Some useful concepts are identified, but there is not yet an adequate description in the literature of the characteristics and time course of the experience of grief in this population. Research Paper: - This research paper seeks to contribute to our understanding of grief and loss in the relatives of brain injured people. The study investigated the utility of a modified form of the Inventory of Complicated Grief as an appropriate measure of grief, and explored the hypothesis that unresolved grief was associated with poor family adjustment following traumatic brain injury. The study found that the Inventory of Complicated Grief had potential to be a useful assessment tool, with some further modifications, but in this small study, it was not possible to identify a component of grief distinct from anxiety and depression that predicted family adjustment. Critical Appraisal: - The process of identifying and carrying out the research study is discussed. The direction of the study was influenced both by clinical questions and practical issues. Factors that assisted the process or made it more difficult are described. Finally, consideration is given to the question of future research in the light of the experience of carrying out this particular project.
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Khadr, Sophie N. "Neuroendocrine consequences of childhood traumatic brain injury." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/29194.
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Objectives: 1) To determine the prevalence, aetiology and clinical significance of pituitary dysfunction after moderate or severe childhood traumatic brain injury (TBI); and 2) to examine its impact on quality of life (QoL) and body composition. Subjects: Retrospective observational study of 33 survivors of accidental TBI (27 males) and two of inflicted TBI (both males). Accidental TBI group: mean (SD) age at study was 13.4y (3.7y) and interval since injury, 4.1y (1.6y). King's Outcome Scale for Childhood Head Injury (KOSCHI) rating: 15 good recovery, 16 moderate disability, 2 severe disability. Inflicted TBI group: ages at study were 5.0 and 3.7 years at 4.9 and 3.3 years post-injury with good recovery and moderate disability respectively. Methods: Early morning urine samples were obtained for osmolality. Basal hormone evaluation (0800-1000h) was followed by the gonadotropin-relasing hormone (GnRH) and insulin tolerance (ITT, n=26) or glucagon tests (if previous seizures, n=9). Subjects were not primed. Body composition was evaluated using bioelectrical impedance analysis. Standardised quality of life (QoL) questionnaires were completed. Head injury details were extracted from patient records. Results: There were no abnormal findings in the two survivors of inflicted TBI. Among the accidental TBI group, no subject had clinical evidence of impaired growth: mean height standard deviation score (SDS) was +0.5 (range -1.6 to +3.0 SD). Median peak growth hormone (GH) response to stimulation was 7.9 μg/L. Six peri-pubertal males had suboptimal GH responses (< 5 μg/L). Their height SDS at study ranged from -1.5 to +1.4; one had slow growth on follow-up. GH response was borderline low in one post-pubertal male (3.2 μg/L). Median peak Cortisol responses were 538 nmol/L (ITT) and 562 nmol/L (glucagon). 9/25 (ITT) and 2/8 (glucagon) subjects had sub-optimal responses. In two cases (one ITT, one glucagon test), basal Cortisol levels were high (624 and 722 nmol/L). For the rest, in 6/9, further testing or no action was advised; in 3/9, steroid cover was recommended for moderate or severe illness or injury. None required routine glucocorticoid replacement. No subject had diabetes insipidus. Thyroid function, IGF-I, oestradiol/testosterone, and baseline and GnRH-stimulated LH and FSH were appropriate for age, sex and pubertal stage. One male was prolactin deficient (< 50 mU/L). Abnormal endocrine findings were unrelated to severity of TBI, nature of primary or secondary brain injury, or KOSCHI rating. No significant difference in QoL was observed between those with normal or abnormal pituitary function < 16y. QoL was poorer in the post-pubertal male with GH deficiency than in other subjects >16y. Conclusions: Whilst mild pituitary 'dysfunction' was common (39%), no unequivocal clinically significant endocrinopathies were found, although the GH and hypothalamopituitary-adrenal axes may be vulnerable.
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Trenchard, Sian Olivia. "Traumatic brain injury in a paediatric population." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/traumatic-brain-injury-in-a-paediatric-population(cf299afa-75ff-4a58-9684-6b332d25715e).html.
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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.
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Donnelly, Joseph. "Intracranial monitoring after severe traumatic brain injury." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271422.
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Intracranial monitoring after severe traumatic brain injury offers the possibility for early detection and amelioration of physiological insults. In this thesis, I explore cerebral insults due raised intracranial pressure, decreased cerebral perfusion pressure and impaired cerebral pressure reactivity after traumatic brain injury. In chapter 2, the importance of intracranial pressure, cerebral perfusion pressure and pressure reactivity in regulating the cerebral circulation is elucidated along with a summary of the existing evidence supporting intracranial monitoring in traumatic brain injury. In chapter 4, intracranial pressure, cerebral perfusion pressure, and pressure reactivity insults are demonstrated to be common, prognostically important, and responsive to long-term changes in management policies. Further, while these insults often occur independently, coexisting insults portend worse prognosis. In chapter 5, I examine possible imaging antecedents of raised intracranial pressure and demonstrate that initial subarachnoid haemorrhage is associated with the subsequent development of elevated intracranial pressure. In addition, elevated glucose during the intensive care stay is associated with worse pressure reactivity. Cortical blood flow and brain tissue oxygenation are demonstrated to be sensitive to increases in intracranial pressure in chapter 6. In chapter 7, a method is proposed to estimate the cerebral perfusion pressure limits of reactivity in real-time, which may allow for more nuanced intensive care treatment. Finally, I explore a recently developed visualisation technique for intracranial physiological insults and apply it to the cerebral perfusion pressure limits of reactivity. Taken together, this thesis outlines the scope, risk factors and consequences of intracranial insults after severe traumatic brain injury. Novel signal processing applications are presented that may serve to facilitate a physiological, personalised and precision approach to patient therapy.
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Walk, Alexandra Elizabeth. "Traumatic Brain Injury: Teacher Knowledge and Skills." University of Dayton / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=dayton1312572728.
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Kinkela, Jessica H. "Diagnosis Threat in Mild Traumatic Brain Injury." Ohio University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1223597555.
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Szabó, Borbála L. "Families of adolescents with traumatic brain injury /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488196234911166.
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Wagner, Michael R. "The Nitroxidative Response to Traumatic Brain Injury." Ohio University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1584179902783766.
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Thomasz, Tennille Amanda. "Investigations of Friendship Following Traumatic Brain Injury." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/14916.
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This research is comprised of two studies, both conducted with the overarching aim of investigating friendships following traumatic brain injury (TBI). The first investigation was a survey study. Sixty-eight speech pathologists who work with clients who have sustained a TBI were surveyed. The survey aimed to answer specific queries surrounding the current perspective of speech pathologists when working with friends, the reason that speech pathologists work with friends, barriers to working with friends and why speech pathologists perceive that some friendships succeed post TBI. Responses were analysed using a combination of descriptive statistics and content analysis of the open-ended responses. Results showed that 39.71% of speech pathologists work with friends. In comparison 60.29% speech pathologists do not work with friends. Indirect work is the main type of work that is conducted surrounding friendship. Education is provided to friends more so than training. Speech pathologists worked on friendships for a variety of reasons. These reasons fell into two broad categories, including providing therapeutic benefits which positively affected the work conducted by the clinician and it benefiting the person with TBI directly in some way. Numerous barriers were identified to working with friends, however the major barriers included time constraints, difficulty accessing friends, the suitability of pre-injury friends for the person with TBI to be interacting with post TBI and the person with TBI choosing not to engage with friends. The reasons that speech pathologists attributed to success in the area of friendship post TBI could be considered within the framework provided in the International Classification of Functioning (ICF) (WHO, 2001). The responses that speech pathologists provided in this question mapped on to the ICF, providing a framework to report on these. Body structures and functions, activities and participation and environmental and personal factors were all considered to be important in the maintenance of friendship post TBI. The second study was a qualitative study. This study addressed the question, why do some friendships succeed post TBI? Nine individuals, who were identified as friends by four adults with TBI, were interviewed. Data collected via semi-structured interviews were analysed using a grounded theory approach. Open coding, focused coding, followed by theoretical coding was conducted to develop the proposed theory: Actively placing the self in the friendship. The model proposes that two processes exist simultaneously. These two processes are: making sense of the TBI and its consequences and maintaining normality in the friendship. It appears that friends engage in both of these processes, which allows them to actively find where they fit in the friendship once their friend with a TBI has sustained their injury. The proposed theory provides details of the types of consequences that friends find out about and how they engage in learning about these consequences. It also illustrates how normality is maintained in the friendship post TBI. Together, these studies provide a thorough and rich description of friendship post TBI from the perspective of both speech pathologists and friends of those who have sustained a TBI. The results provide building blocks to enable a more systematic approach to the current work that is conducted surrounding friendships post TBI. Importantly, the firsthand ideas and experiences of friends who have maintained their friendships with people with TBI are considered and can now be used when developing approaches to working with friends.
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Akin, Faith W. "Symposium: Vestibular Related Traumatic Brain Injury (TBI)." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/2428.
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Akin, Faith W., and Owen D. Murnane. "Vestibular Consequences of Mild Traumatic Brain Injury." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/1928.
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MacMillan, Pamela Jo. "Vulnerability to disability following traumatic brain injury." W&M ScholarWorks, 1999. https://scholarworks.wm.edu/etd/1550154124.
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PISCHIUTTA, FRANCESCA. "Mesenchymal stromal cells for traumatic brain injury." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/52353.
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The multiple pathological cascades activated after traumatic brain injury (TBI) and their extended nature offer the possibility for therapeutic interventions possibly affecting multiple injury mechanisms simultaneously. Mesenchymal stromal cell (MSC) therapy matches this need, being a bioreactor of a variety of molecules able to interact and modify the injured brain microenvironment.
Compared to autologous MSCs, bank stored GMP-graded allogenic MSCs appear to be a realistic choice for TBI in a translational perspective, due to the need of delivering cell therapy in the acute phase of the pathology and promptly interact with the damaged tissue and maximize neuroprotective and restorative processes. Allogenic transplant poses the risk of host rejection due to immunological mismatch and introduces the critical issue of immunosuppression. In TBI patients immunosuppression is associated with an increased susceptibility to infections which is directly related to unfavorable outcomes and thus deserves careful consideration. Today no direct comparison of MSC efficacy in immunocompetent and immunosuppressed hosts has been performed. In this thesis we analyzed whether long-term efficacy of human bone marrow MSCs in traumatized mice brain is dependent or not on immunosuppressive treatment, in order to address this important preclinical issue. By observing a similar degree of protection in immunocompetent compared to immunosuppressed mice our data represent a forward step towards the definition of a clinical protocol and provide a strong rational to further investigate the potential of human BM MSC in TBI.
In the second part of the thesis, using the same MSC source and the same injury/treatment protocol we focused on mechanistic insight of MSC effect after injury and analyzed the interaction between infused MSCs and resident/recruited immune cerebral cells. In particular we investigated the effects of MSC treatment on the activation and functional changes of microglia/macrophages after TBI and how these phenotypical changes are related to microenvironmental beneficial effects.
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Sauerbeck, Andrew David. "TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/133.
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The development of Parkinson's disease (PD) in humans has been linked to genetic and environmental factors for many years. However, finding common single insults which can produce pathology in humans has proved difficult. Exposure to trichloroethylene (TCE) or traumatic brain injury (TBI) has been shown to be linked to PD and it has also been proposed that multiple insults may be needed for disease development.
The present studies show that exposure to TCE prior to a TBI can result in pathology similar to early PD and that the interaction of both insults is required for impairment in behavioral function, and cell loss. Following exposure to TCE for 2 weeks there is a 75% impairment in mitochondrial function but it has yet to be shown if the addition of a TBI can make this worse. If the exposure to TCE is reduced to 1 week and combined with TBI a 50% reduction in mitochondrial function is observed following the dual injury which requires both insults. These studies provide further support for the hypothesis that PD may result from a multifactorial mechanism.
It had been established that regional differences exist in mitochondrial function across brain regions. The present studies indicate that previous findings are not likely to be the result of differences in individual mitochondria isolated from the cortex, striatum, and hippocampus. Further analysis of the effect of mitochondrial inhibitors on enzyme activity and oxygen consumption reveal that the different regions of the brain are similarly affected by the inhibitors. These results suggest that findings from previous studies indicating regionally specific deficits following systemic toxin exposure, such as with TCE, are not the result of regional differences in the individual mitochondria.
Given that TBI results in significant dysfunction, finding effective therapeutics for TBI will provide substantial benefits to individuals suffering an insult. Treatment with Pioglitazone following TBI reduced mitochondrial dysfunction, cognitive impairment, cortical tissue loss, and inflammation. These findings provide initial evidence that treatment with Pioglitazone may be an effective intervention for TBI.
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Carter-Allison, Samantha Natalie. "Diagnosis threat and injury beliefs after mid traumatic brain injury." Thesis, King's College London (University of London), 2015. https://kclpure.kcl.ac.uk/portal/en/theses/diagnosis-threat-and-injury-beliefs-after-mid-traumatic-brain-injury(c6ba3d52-13d9-46ea-aeee-d34ed2e43943).html.
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Background: Diagnosis threat is a form of stereotype threat, where individuals with a history of mild traumatic brain injury (mTBI) have shown performance decrements on cognitive tasks, owing to negative expectancies around cognitive ability elicited by cues in the environment. This study systematically reviews experimental studies to gauge the presence/absence of an effect of diagnosis threat on neuropsychological task performance in mTBI. It also investigates whether methodological variation and methodological quality contribute to variation in study findings. Method: A systematic search of four online databases (Medline, PyscINFO, SportDISCUS, PsycEXTRA) was conducted to identify diagnosis threat studies that employed an experimental paradigm. Neuropsychological test outcomes were extracted, along with information on inclusion criteria, mTBI diagnostic criteria, participant characteristics and study design. Methodological quality was assessed using modified Scottish Intercollegiate Guidelines Network (SIGN) criteria. Results: A total of nine studies were identified. Evidence for diagnosis threat was found, although there was considerable heterogeneity across study results. The most robust finding was the impact of diagnosis threat on the cognitive domain of attention/working memory. No clear associations between methodological variation, methodological quality and study outcome were noted. Conclusions: The review found evidence for diagnosis threat, although the strength of this effect may be smaller than previously thought. Although there was heterogeneity across elements of study design, there was no obvious relationship between these factors and outcome. However, the substantial variation makes comparison difficult. These issues are similar to findings in other examinations of stereotype threat. Further research is needed to replicate findings and add clarity to the impact of diagnosis threat on both objective and subjective measures, and to further investigate the role of possible moderating variables. A more formal meta-analysis in the area may also be helpful to clarify findings in the research field. Future studies should aim to create established operational definitions and outcomes to improve consistency and comparability between studies.
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Rossouw, Joanne Courtney. "Incidence of traumatic brain injury, prevalence of dysphagia, and factors predicting health outcomes following traumatic brain injury in adults." Master's thesis, University of Cape Town, 2015. http://hdl.handle.net/11427/16646.
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Includes bibliographical referencesSouth Africa has a high incidence of injury-related disorders, such as traumatic brain injury (TBI) as a result of motor vehicle accidents and assault. Dysphagia is a common sequela of TBI, which may result in malnutrition or aspiration pneumonia. There is limited epidemiological data available for TBI and dysphagia in South Africa which is important for health care planning. There is also inadequate literature reporting predictive factors for dysphagia and health outcomes of patients with TBI and swallowing disorders for the South African context, which would provide management guidelines for Speech-Language Pathologists (SLPs) for patients with TBI and dysphagia. This study aims to begin to provide up-to-date information regarding the incidence of TBI and the prevalence of dysphagia in the population with TBI in Bloemfontein, South Africa. Predictive factors for dysphagia and health outcomes were also investigated in order to provide management guidelines for TBI-related dysphagia for SLPs. A prospective cohort study followed 77 participants aged 18 to 68 years (M = 33.1) with mild to severe traumatic brain injury, admitted to 2 state and 2 private hospitals in the Bloemfontein metropole, South Africa, to investigate the incidence of TBI and the prevalence of TBI-related dysphagia in the adult population in 2013. Participants were tracked from admission to hospital to discharge. Demographic and medical data was collected for each participant, including: gender, age, TBI aetiology, means of nutritional intake, respiratory status, length of hospital stay, and number of speech therapy sessions. Glasgow Coma Scale (GCS) scores at time of admission, swallowing evaluation, and discharge were noted as an indicator of TBI severity and each participant was assessed with the Mann Assessment of Swallowing Ability on admission and prior to discharge to assess the presence of dysphagia. The incidence of TBI for the Bloemfontein metropole was 353 per 100,000 people and was greater in the male than in the female population (11.83:1). The main mechanism for TBI in Bloemfontein was interpersonal violence (67.53%), followed by road traffic accidents (motor and pedestrian vehicle accidents; 23.38%). The prevalence rate for dysphagia was 32%. Twenty-eight percent of those who presented with dysphagia also aspirated. Severe TBI (GCS ≤ 8) was identified as a predictive factor for dysphagia. Participants with dysphagia had longer hospital stays (days; M = 22.04, SD = 17.67) than those with normal swallowing (M = 6.23, SD = 4.28), t(75) = 6.13, p < .001, and took significantly more days to achieve oral intake (M = 6.23, SD = 10.32) than those without dysphagia (M = .31, SD = 1.41), t(75) = 4.08, p < .001. Ventilation was associated with longer hospital stays, rs(25) = -.47, p = .02 and longer duration until achievement of oral intake, rs(22) = -.80, p < .001. Tracheotomised participants also had significantly longer hospital stays, rs(25) = -.67, p < .001, and took longer to achieve oral intake, rs(22) = -.52, p = .01. An increased period of time with a tracheostomy was also significantly associated with mortality, χ2(2, n = 11) = 6.52, p = .04. Participants with dysphagia (M = 3.84, SD = 5.44) required significantly more therapy sessions with an SLP than those without dysphagia (M = .15, SD = .64), t(75) = 4.85, p < .001, and those with low GCS scores were significantly less likely to achieve oral intake prior to discharge, rs(25) = -.45, p = .02, and had longer hospital stays than participants with mild head injuries, rs(25) = -.49, p = .01. All participants who received nutrition via nasogastric tubes returned to oral intake; however, individuals who had percutaneous endoscopic gastrostomies did not achieve oral intake prior to discharge. It is recommended that objective swallowing evaluations be conducted for patients admitted with severe TBIs, and patients with mild and moderate TBIs be screened to determine the presence of dysphagia. TBI prevention initiatives should be developed to reduce the incidence of TBI, specifically in the young adult male population.
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Sacho, Raphael Hillel. "Brain temperature, inflammation and outcome after severe traumatic brain injury." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503675.
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Powell, Janet M. "Effectiveness of comprehensive inpatient rehabilitation following traumatic brain injury /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/10320.
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Reid, Louise Marie. "Traumatic brain injury, post-traumatic stress disorder symptom reporting and attentional bias : unravelling the misidentification of post-traumatic stress disorder in people with a traumatic brain injury." Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/1221/.
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Background: Post-traumatic stress disorder (PTSD) can occur following a traumatic event that has led to moderate to severe traumatic brain injury (TBI) even when there is little or no memory for the event. The incidence of PTSD is higher when diagnosed by self-report questionnaires compared to structured clinical interview. Previous studies suggest PTSD can be misdiagnosed in a significant proportion of cases and the incidence is in fact low. To explore this issue further there is a need to not only understand whether there are differences between cases that do and do not fulfill symptom criteria for PTSD, but also whether some cases have ‘partial PTSD’; that is to say they have PTSD symptoms but do not fulfill the DSM-IV symptom criteria exactly. Aims: The study aims to establish whether an attentional bias to trauma related words exists in people with TBI who report PTSD symptoms and to investigate the relationship between physiological arousal and attentional bias in people with a TBI reporting PTSD symptoms. Method: Forty-one participants with severe-extremely severe TBI were recruited from the community and completed measures of cognitive functioning. Attentional bias was measured using a Stroop task in which trauma, negative, neutral and positive words were administered randomly. Physiological reactivity (heart rate) was recorded and PTSD ‘caseness’ was established using a self-report questionnaire and a clinician-administered structured interview. Results: No significant relationship between PTSD symptom severities and attentional bias to trauma stimuli was apparent. Those with ‘PTSD’ demonstrated significantly slower reaction times to negative words however; this bias was associated with self-report of depression rather than PTSD symptomatology. Heart rate decreased throughout the interview and was not associated with PTSD symptom severities. Conclusions: Greater PTSD symptom reporting was not associated with an attentional bias to trauma words. Heart rate decreased over the course of the interview, independent of PTSD severity and diagnosis. This suggests that ‘partial’ PTSD was not present, and instead those who reported PTSD symptoms were curious about the gap in memory caused by amnesia without the associated fear response.
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Bellander, Bo-Michael. "On the role of complement activation following traumatic brain injury /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-929-3/.
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