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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
171

Inter-professional Clinical Practice Guideline for Vocational Evaluation following Traumatic Brain Injury

Stergiou-Kita, Mary Melpomeni 11 January 2012 (has links)
Due to physical, cognitive and emotional impairments, many individuals are unemployed or under-employed following a traumatic brain injury. The research evidence links the rigour of a vocational evaluation to future employment outcomes. Despite this link, no specific guidelines exist for vocational evaluations. Using the research evidence and a diverse panel of clinical and academic experts, the primary objective of this doctoral research was to develop an inter-professional clinical practice guideline for vocational evaluation following traumatic brain injury. The objective of the guideline is to make explicit the processes and factors relevant to vocational evaluation, to assist evaluators (i.e. clients, health and vocational professionals, and employers) in collaboratively determining clients’ work abilities and developing recommendations for work entry, re-entry or vocational planning. The steps outlined in the Canadian Medical Association's Handbook on Clinical Practice Guidelines were utilized to develop the guideline and include the following: 1) identifying the guideline’s objective/questions; 2) performing a systematic literature review; 3) gathering a panel; 4) developing recommendations; 4) guideline writing; 5) pilot testing. The resulting guideline includes 17 key recommendations within the following seven domains: 1) evaluation purpose and rationale; 2) initial intake process; 3) assessment of the personal domain; 4) assessment of the environment; 5) assessment of occupational/job requirements; 6) analysis and synthesis of assessment results; and 7) development of evaluation recommendations. Results from an exploratory study of the guideline’s implementation by occupational therapists in their daily practices revealed that clinicians used the guideline to identify practice gaps, systematize their evaluation processes, enhance inter-professional and inter-stakeholder communication, and re-conceptualize their vocational evaluations across disability groups. Statistically significant improvements were also noted in clients’ participation scores on the Mayo-Portland Adaptability Inventory–4 following guideline use. This guideline may be applicable to individuals with TBI, clinicians, health and vocational professionals, employers, professional organizations, administrators, policy makers and insurers.
172

Inter-professional Clinical Practice Guideline for Vocational Evaluation following Traumatic Brain Injury

Stergiou-Kita, Mary Melpomeni 11 January 2012 (has links)
Due to physical, cognitive and emotional impairments, many individuals are unemployed or under-employed following a traumatic brain injury. The research evidence links the rigour of a vocational evaluation to future employment outcomes. Despite this link, no specific guidelines exist for vocational evaluations. Using the research evidence and a diverse panel of clinical and academic experts, the primary objective of this doctoral research was to develop an inter-professional clinical practice guideline for vocational evaluation following traumatic brain injury. The objective of the guideline is to make explicit the processes and factors relevant to vocational evaluation, to assist evaluators (i.e. clients, health and vocational professionals, and employers) in collaboratively determining clients’ work abilities and developing recommendations for work entry, re-entry or vocational planning. The steps outlined in the Canadian Medical Association's Handbook on Clinical Practice Guidelines were utilized to develop the guideline and include the following: 1) identifying the guideline’s objective/questions; 2) performing a systematic literature review; 3) gathering a panel; 4) developing recommendations; 4) guideline writing; 5) pilot testing. The resulting guideline includes 17 key recommendations within the following seven domains: 1) evaluation purpose and rationale; 2) initial intake process; 3) assessment of the personal domain; 4) assessment of the environment; 5) assessment of occupational/job requirements; 6) analysis and synthesis of assessment results; and 7) development of evaluation recommendations. Results from an exploratory study of the guideline’s implementation by occupational therapists in their daily practices revealed that clinicians used the guideline to identify practice gaps, systematize their evaluation processes, enhance inter-professional and inter-stakeholder communication, and re-conceptualize their vocational evaluations across disability groups. Statistically significant improvements were also noted in clients’ participation scores on the Mayo-Portland Adaptability Inventory–4 following guideline use. This guideline may be applicable to individuals with TBI, clinicians, health and vocational professionals, employers, professional organizations, administrators, policy makers and insurers.
173

Алгоритам ургентног лечења трауматског можданог оштећења дизајниран кроз мултиваријантну анализу прогностичких фактора / Algoritam urgentnog lečenja traumatskog moždanog oštećenja dizajniran kroz multivarijantnu analizu prognostičkih faktora / Algorithm of emergency treatment of traumatic brain injury designed through multivariate analysis of prognostic factors

Golubović Jagoš 06 January 2020 (has links)
<p>Трауматско оштећење мозга (ТОМ) настаје услед дејства спољашње мехничке силе на кранијум и ендокранијални садржај, које се карактерише привременим или трајним неуролошким оштећењем, функционалном онеспособљеношћу или психосоцијалном неприлагођеношћу. Најчешће коришћени предиктори исхода су године повређеног, иницијални Гласгов кома скор (ГКС), статус зеница на пријему, време протекло од момента повређивања до неурохируршког збрињавања, удружене повреде, хипоксија, хипертензија и налаз компјутерско-томографског снимања. Основни циљ истраживања је израда алгоритма ургентног лечења трауматског можданог оштећења и дизајн скале за рану предикцију исхода ТОМ уз додатну анализу појединих фактора на пријему (ГКС, неуролошки налаз, радиолошки налаз, клинички симптоми). Спроведено је ретроспективно и проспективно истраживање којим је обухваћено 568 испитаника који су у периоду од 1.6.2018. до 31.05.2019. лечени унутар Клиничког центра Војводине у Новом Саду због трауматске озледе мозга. Узорак је чинило 34,3% жена и 65,7 % мушкараца. Старосна структура узорка је од 18-96 године (М=56,56; SD=20,17). Свим пацијентима је по пријему начињена радиолошка дијагностика компјутеризованом томографијом (ЦТ), начињен је детаљан физикални и неуролошки преглед, те је детаљно узета анамнеза. Нотирани су следећи подаци: витални параметри (артеријски крвни притисак, сатурација крви кисеоником), статус и повреде других система органа, знаци повређивања главе и врата. За неуролошки преглед је коришћена ГКС скала. За ЦТ преглед је нотирано присуство интракранијалних трауматских лезија и прелома лобање. Резултати овог истраживања указали су на неопходност пажљивог разматрања бројних фактора (радиолошких и клиничких) који се могу испољити већ на самом пријему. Иако ЦТ има висок појединачни допринос предвиђању исхода у моделу са више варијабли није се издвојио као значајан. Пацијенти који су имали дужи период између времена протеклог од момента повређивања до неурохируршког збрињавања имали су бољи исход лечења. Предпоставља се да су пацијенти који су стизали раније у здравствену установу имали тежа трауматска оштећења мозга и самим тим исход је био лошији, док су пацијенти са благим оштећењима долазили касније управо из разлога што манифестације проблема нису биле хитне. Ротердам скала се издвојила добром дискриминативном способношћу када се користи као изолован инструмент. Као најјачи предиктори издвојили су се следећи предиктори: нису показане цистерне на ЦТ-у, присутан САХ, померање више од 5 mm, присутан мали субдурални хематом, присутна велика контузија, примена антиагрегациона тераpија. Успешност предвиђања на основу новог модела је 96%. Резултати студије се могу искористити за боље разумевање ТОМ у смислу лакшег решавања дијагностичких дилема и терапијских, креирање ефикаснијих дијагностичких протокола и прецизније процене исхода након повређивања. Предикција исхода лечења је од великог значаја како би се благовермено направио алгоритам лечења и праћења ових пацијената.</p> / <p>Traumatsko oštećenje mozga (TOM) nastaje usled dejstva spoljašnje mehničke sile na kranijum i endokranijalni sadržaj, koje se karakteriše privremenim ili trajnim neurološkim oštećenjem, funkcionalnom onesposobljenošću ili psihosocijalnom neprilagođenošću. Najčešće korišćeni prediktori ishoda su godine povređenog, inicijalni Glasgov koma skor (GKS), status zenica na prijemu, vreme proteklo od momenta povređivanja do neurohirurškog zbrinjavanja, udružene povrede, hipoksija, hipertenzija i nalaz kompjutersko-tomografskog snimanja. Osnovni cilj istraživanja je izrada algoritma urgentnog lečenja traumatskog moždanog oštećenja i dizajn skale za ranu predikciju ishoda TOM uz dodatnu analizu pojedinih faktora na prijemu (GKS, neurološki nalaz, radiološki nalaz, klinički simptomi). Sprovedeno je retrospektivno i prospektivno istraživanje kojim je obuhvaćeno 568 ispitanika koji su u periodu od 1.6.2018. do 31.05.2019. lečeni unutar Kliničkog centra Vojvodine u Novom Sadu zbog traumatske ozlede mozga. Uzorak je činilo 34,3% žena i 65,7 % muškaraca. Starosna struktura uzorka je od 18-96 godine (M=56,56; SD=20,17). Svim pacijentima je po prijemu načinjena radiološka dijagnostika kompjuterizovanom tomografijom (CT), načinjen je detaljan fizikalni i neurološki pregled, te je detaljno uzeta anamneza. Notirani su sledeći podaci: vitalni parametri (arterijski krvni pritisak, saturacija krvi kiseonikom), status i povrede drugih sistema organa, znaci povređivanja glave i vrata. Za neurološki pregled je korišćena GKS skala. Za CT pregled je notirano prisustvo intrakranijalnih traumatskih lezija i preloma lobanje. Rezultati ovog istraživanja ukazali su na neophodnost pažljivog razmatranja brojnih faktora (radioloških i kliničkih) koji se mogu ispoljiti već na samom prijemu. Iako CT ima visok pojedinačni doprinos predviđanju ishoda u modelu sa više varijabli nije se izdvojio kao značajan. Pacijenti koji su imali duži period između vremena proteklog od momenta povređivanja do neurohirurškog zbrinjavanja imali su bolji ishod lečenja. Predpostavlja se da su pacijenti koji su stizali ranije u zdravstvenu ustanovu imali teža traumatska oštećenja mozga i samim tim ishod je bio lošiji, dok su pacijenti sa blagim oštećenjima dolazili kasnije upravo iz razloga što manifestacije problema nisu bile hitne. Roterdam skala se izdvojila dobrom diskriminativnom sposobnošću kada se koristi kao izolovan instrument. Kao najjači prediktori izdvojili su se sledeći prediktori: nisu pokazane cisterne na CT-u, prisutan SAH, pomeranje više od 5 mm, prisutan mali subduralni hematom, prisutna velika kontuzija, primena antiagregaciona terapija. Uspešnost predviđanja na osnovu novog modela je 96%. Rezultati studije se mogu iskoristiti za bolje razumevanje TOM u smislu lakšeg rešavanja dijagnostičkih dilema i terapijskih, kreiranje efikasnijih dijagnostičkih protokola i preciznije procene ishoda nakon povređivanja. Predikcija ishoda lečenja je od velikog značaja kako bi se blagovermeno napravio algoritam lečenja i praćenja ovih pacijenata.</p> / <p>Traumatic brain injury (TBI) Is defined as temporary or permanent neurological damage, functional disability or psychosocial inadaptability occurring due to effects of external mechanical force to brain and cranium. Mostly used predictors are age, Glasgow coma scale score, pupillary reactivity, time from injury to neurosurgical intervention, combined injuries, hypoxia, hypertension and computed tomography (CT) findings. Basic goal of this research was to analyse TBI and design early outcome prediction scale together with the analysis of individual factors on admission (GCS, neurological status, radiological findings). This research was both retro and prospective and included 568 patients treated for TBI at Clinical centre of Vojvodina in Novi Sad from 01.06.2018. to 31.05.2019. Sample was made out of 34,3% females and 65,7 % males aged from 18 to 96 years ( M=56,56; SD=20,17). All patients had CT diagnostics preformed upon admission, had undergone detailed general and neurological examination and patient&rsquo;s history was taken. Physical examination included: vitals (arterial blood pressure, blood oxygenation), status and injuries of other organs, signs of injury to head and neck. GCS scale was used for neurological examination Computed tomography (CT) included presence of intracranial lesions and skull fractures. Results of this research showed importance of careful observation of multiple factors (radiological and clinical) that can be present at the time of admission. Despite CT having high individual predictive power for outcome, in multiple variable model it was not significant. Patients with longer time elapsed to treatment had better outcome. It is assumed that patients who arrived shortly after injury had severe TBI thus having worse outcome, while patients suffering from mild TBI arrived later and thus had better outcome right because their symptoms of TBI were not very symptomatic. Rotterdam scale showed good disciminative power. The strongest predictors were: CT absence of cisterns, present subarachnoid haemorrhage, midline shift over 5mm, presence of small subdural haematoma, presence of large contusion, presence of antiaggregational therapy. Predictive power based on primary model was 96%. Results of this study can be used for better understanding of TBI in order to solve some diagnostic dilemma, create more efficient diagnostic protocols and facilitate more precise outcome assessment after TBI. Prediction of treatment outcome is very important in order to timely design treatment algorithm of treatment and follow up of TBI patients.</p>
174

Inhibiting Axon Degeneration in a Mouse Model of Acute Brain Injury Through Deletion of Sarm1

Henninger, Nils 24 May 2017 (has links)
Traumatic brain injury (TBI) is a leading cause of disability worldwide. Annually, 150 to 200/1,000,000 people become disabled as a result of brain trauma. Axonal degeneration is a critical, early event following TBI of all severities but whether axon degeneration is a driver of TBI remains unclear. Molecular pathways underlying the pathology of TBI have not been defined and there is no efficacious treatment for TBI. Despite this significant societal impact, surprisingly little is known about the molecular mechanisms that actively drive axon degeneration in any context and particularly following TBI. Although severe brain injury may cause immediate disruption of axons (primary axotomy), it is now recognized that the most frequent form of traumatic axonal injury (TAI) is mediated by a cascade of events that ultimately result in secondary axonal disconnection (secondary axotomy) within hours to days. Proposed mechanisms include immediate post-traumatic cytoskeletal destabilization as a direct result of mechanical breakage of microtubules, as well as catastrophic local calcium dysregulation resulting in microtubule depolymerization, impaired axonal transport, unmitigated accumulation of cargoes, local axonal swelling, and finally disconnection. The portion of the axon that is distal to the axotomy site remains initially morphologically intact. However, it undergoes sudden rapid fragmentation along its full distal length ~72 h after the original axotomy, a process termed Wallerian degeneration. Remarkably, mice mutant for the Wallerian degeneration slow (Wlds) protein exhibit ~tenfold (for 2–3 weeks) suppressed Wallerian degeneration. Yet, pharmacological replication of the Wlds mechanism has proven difficult. Further, no one has studied whether Wlds protects from TAI. Lastly, owing to Wlds presumed gain-of-function and its absence in wild-type animals, direct evidence in support of a putative endogenous axon death signaling pathway is lacking, which is critical to identify original treatment targets and the development of viable therapeutic approaches. Novel insight into the pathophysiology of Wallerian degeneration was gained by the discovery that mutant Drosophila flies lacking dSarm (sterile a/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously recapitulated the Wlds phenotype. The pro-degenerative function of the dSarm gene (and its mouse homolog Sarm1) is widespread in mammals as shown by in vitro protection of superior cervical ganglion, dorsal root ganglion, and cortical neuron axons, as well as remarkable in-vivo long-term survival (>2 weeks) of transected sciatic mouse Sarm1 null axons. Although the molecular mechanism of function remains to be clarified, its discovery provides direct evidence that Sarm1 is the first endogenous gene required for Wallerian degeneration, driving a highly conserved genetic axon death program. The central goals of this thesis were to determine (1) whether post-traumatic axonal integrity is preserved in mice lacking Sarm1, and (2) whether loss of Sarm1 is associated with improved functional outcome after TBI. I show that mice lacking the mouse Toll receptor adaptor Sarm1 gene demonstrate multiple improved TBI-associated phenotypes after injury in a closed-head mild TBI model. Sarm1-/- mice developed fewer beta amyloid precursor protein (βAPP) aggregates in axons of the corpus callosum after TBI as compared to Sarm1+/+ mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phosphorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after TBI. Strikingly, whereas wild type mice exhibited a number of behavioral deficits after TBI, I observed a strong, early preservation of neurological function in Sarm1-/- animals. Finally, using in vivo proton magnetic resonance spectroscopy, I found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1-/- mice compared to controls immediately following TBI. My results indicate that the Sarm1-mediated prodegenerative pathway promotes pathogenesis in TBI and suggest that anti-Sarm1 therapeutics are a viable approach for preserving neurological function after TBI.

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