The primary aim of the present study was to evaluate the effectiveness of the intervention provided by Massey University Concussion Clinic for individuals following Mild Traumatic Brain Injury (MTBI). Concussion Clinics were set up across New Zealand to provide early intervention and assessment for individuals with MTBI to prevent long term complaints. Treatment outcomes at these clinics have not been empirically examined before. The current study compared the levels of post concussion symptoms, anxiety, depression, and psychosocial functioning between an intervention and a control group using a quasi-experimental design. In addition, reasons for nonattendance to the clinic, and participants’ perceptions of their recovery were also explored. The main outcome measures used were the Rivermead Postconcussion Symptoms Questionnaire, the Hospital Anxiety and Depression Scale, and the Sydney Psychosocial Reintegration Scale-2. Outcomes were initially assessed soon after injury or referral to the clinic and then three months later. Participants were recruited from the Palmerston North Hospital Emergency Department and the Massey University Concussion Clinic. With 20 participants in the intervention group and 15 in the control group, the main results showed that the Concussion Clinic intervention significantly decreased the level of anxiety and depression reported by participants in the intervention group over the control group. Greater improvements in post concussion symptoms and psychosocial functioning were also indicated in the intervention group. Additional findings suggest difficulty with transportation as a reason for nonattendance, which could be a potential barrier to recovery. Furthermore, participants highlighted the benefits of attending the service and its role in their recovery. Important issues relating to the referral processes were also identified. Findings of the current study suggest that the Concussion Clinic intervention is effective in improving recovery for those accessing the service. Nevertheless, these results must be interpreted with caution due to the small sample size. Further research is warranted to examine the effectiveness of the Concussion Clinics with larger samples, and the current study may serve as a valuable pilot for these future investigations.

One of the goals of cognitive rehabilitation following traumatic brain injury is to help people perform everyday tasks. However, options for the rigorous assessment of everyday cognitive effectiveness after rehabilitation are limited. Performance on neuropsychological tests is only moderately correlated with everyday functioning, while previous measures of everyday functioning include only fairly general estimates of overall cognitive functioning. The aim of the current study was to develop an ecologically valid measure that captured a number of subdomains of executive functioning, using systematic behavioural observation of an everyday task. The initial phase of the research involved identifying an everyday task that was sufficiently complex to ensure that executive functioning was utilised in the completion of the task. Participants with traumatic brain injury were then asked to prepare chocolate brownies, using a recipe provided, and a hot drink. Participants were allowed to use any compensatory strategy to help complete the task. Participant performance was directly observed by an examiner and videotaped for subsequent inter-rater reliability. Two independent raters assessed nine components of executive functioning. During this phase, the examiner manuals were modified improving inter-rater reliability. The final version of the measure was then trialled with participants with and without traumatic brain injury. Final inter-rater reliability indicated the approach had merit. Significant and moderate correlations were found between traditional measures of executive functioning and the everyday task. This study employed systematic behavioural observation to obtain fine-grained information regarding a person’s cognitive functioning. With further development, this approach may prove useful for targeting and monitoring specific functional difficulties during cognitive rehabilitation.

Conselho Nacional de Desenvolvimento Científico e Tecnológico / Traumatic brain injury (TBI) is a major cause of morbidity and mortality in industrialized countries leading to the motor and cognitive deficits. Evidence demonstrated that exercise is neuroprotective in traumatic brain injury. However, the effects of exercise before of the TBI at the cognitive function are unknown. Role of excitotoxicity and oxidative damage in secondary damage of TBI, however, until this moment, were not demonstrated if exists a relationship between early phase of damage and the late cognitive deficit. In the current study, we proposed that improvement cognitive response induced by exercise prior in rats after a TBI can be associated with the neuroprotection of early phase after injury. To demonstrate this hypotheses, adult rats practice swimming exercise during 6 weeks followed for TBI operation. We assessed the motor alterations of early phase, the glutamate uptake and antioxidant defense in twenty four hours (24 h) and 15 days after TBI. Acquisition of memory was assessed by recognition object task on days 15 post TBI. Moreover, we evaluated the brain-derived neurotrophic factor (BDNF) to assessement the synaptic plastic. In the present study, we showed that TBI induced by fluid percussion injury (FPI) in adult male Wistar rats induced early motor impairment 24 h, followed by learning retention deficit (2 weeks after neuronal injury). Previous swimming training improved the memory in object recognition task per se and protected against FPI-related disabilities. Although the FPI did not alter hippocampal expression of glutamate transporters (EAAT1 / EAAT2) and brain-derived neurotrophic factor (BDNF), the alterations in the redox status, herein characterized by DCFH-DA oxidation and SOD activity inhibition, led to marked impairment of protein functionally (Na+, K+-ATPase activity inhibition) and glutamate uptake inhibition 24 h after neuronal injury in sedentary injured rats. Indeed, the early increase of nuclear factor erythroid 2-related factor (pNRF2/NRF2 ratio) followed by a repair mechanism (protein HSP70 expression), 24 h and 2 weeks after neuronal injury, suggests that FPI-induced signal transduction may exert compensatory effect on pathophysiological processes. In this report we showed that previous physical exercise induced the increase of immune content of glutamate transporters (EAAT1/ EAAT2), pNrf2/Nrf2 ratio, SOD enzyme and HSP70 per se besides preventing against FPI-induced Na+, K+ - ATPase activity, glutamate uptake inhibition DCFH-DA oxidation 24 h after neuronal injury. The enhancement of hippocampal pNrf2/Nrf2 and HSP70 immune content in trained injured when compared with sedentary rats suggest that protein expression modulation associated to antioxidant defense elicited by previous physical exercise prevent against toxicity induced by TBI. The significant increase of BDNF levels in trained injured rats 24 h and 2 weeks strongly reinforce the idea that physical activity alters neuronal functions and thus delays or prevents secondary cascades that leave the neurobehavioral disability after TBI. / O traumatismo cranioencefálico (TCE) é uma das maiores causas de morte e morbidade nos países industrializados podendo levar ao comprometimento motor e déficits cognitivos. Evidências demonstram que o exercício físico é neuroprotetor na recuperação após o TCE. Porém, os efeitos do exercício físico antes do TCE na função cognitiva não são totalmente conhecidos. Sabe-se da participação da excitotoxicidade e do estresse oxidativo na cascata do dano secundário após o TCE, entretanto até o momento não foi demonstrado qual a relação da fase inicial após o TCE com os déficits cognitivos tardios. Portanto, no presente estudo, nós propomos que a melhora cognitiva tardia induzida pelo exercício prévio em ratos após o TCE pode estar associada com a neuroproteção da fase inicial após o dano. Para demonstrar esta hipótese, ratos adultos praticaram treinamento de natação durante 6 semanas e posteriormente foram submetidos a cirurgia para o TCE. Nós avaliamos as alterações motoras iniciais, a captação de glutamato e a defesa antioxidante em 24 horas (24 h) e 15 dias após o TCE. Aquisição da memória foi avaliada pela tarefa de reconhecimento de objetos em 15 dias após o TCE. Além disso, nós avaliamos o fator neurotrófico derivado do encéfalo (BDNF) para avaliar a plasticidade sináptica. No presente estudo, nós mostramos que o TCE induzido pela lesão de percussão de fluido (LPF) em ratos Wistar machos adultos induziu déficit motor inicial 24 h, seguido por déficit de aprendizagem (15 dias após o dano neuronal). O treinamento de natação prévio melhorou a memória na tarefa de reconhecimento de objeto per se e protegeu contra desabilidades relacionadas ao LPF. Embora o LPF não tenha alterado a expressão dos transportadores de glutamato (EAAT1/EAAT2) e de BDNF, causou uma alteração no estado redox, caracterizado pela oxidação de DCFH-DA e inibição da atividade da SOD. O LPF também causou prejuízo acentuado da funcionalidade de proteínas (inibição da atividade da enzima Na+, K+-ATPase) e inibição da captação de glutamato 24 h após o dano neuronal em ratos sedentários lesionados. De fato, o aumento inicial do fator de transcrição Nrf2 (relação pNrf2/Nrf2), 24 h após o TCE, seguido por um mecanismo de reparo (expressão da proteína Hsp70), 24 h e 15 dias após o dano neuronal, sugerem que a transdução de sinal induzida pelo LPF pode exercer um efeito compensatório em processos patofisiológicos. Neste trabalho, nós mostramos que o exercício físico prévio induziu o aumento do imunoconteúdo dos transportadores de glutamato (EAAT1/EAAT2), relação pNrf2/Nrf2, enzima SOD e a proteína Hsp70 per se, além de prevenir contra inibição da atividade da Na+, K+-ATPase, inibição da captação de glutamato e oxidação de DCFH-DA induzida pelo LPF, 24 h após o dano neuronal. O aumento do imunoconteúdo hipocampal de pNrf2/Nrf2 e Hsp70 em ratos treinados e lesionados quando comparado com ratos sedentários, sugerem que a modulação da expressão das proteínas associadas às defesas antioxidantes induzidas pelo exercício físico prévio preveniu contra a excitotoxicidade induzida pelo TCE. O significante aumento nos níveis de BDNF em ratos treinados e lesionados 24 h e 15 dias, reforçam fortemente a ideia que a atividade física altera a função neuronal e assim retarda ou previne as cascatas do dano secundário que levam a desabilidade neuronal após o TCE.

Syftet med studien var att beskriva användning av strategier och den betydelse de har för engagemang i aktivitet hos vuxna personer med förvärvad hjärnskada. En kvalitativ litteraturstudie har genomförts. Datainsamlingen skedde via sökning i lämpliga databaser utefter studiens syfte. Totalt 15 artiklar inkluderades till denna litteraturstudie. Insamlat data analyserades efter Fribergs anvisningar för kvalitativa litteraturstudier. Resultatet presenteras under ett övergripande tema; ”Strategier för engagemang i aktivitet” som innefattar de fyra huvudkategorierna ”Planering av aktiviteter i vardagen”, ”Selektera och prioritera aktiviteter utefter situation och sammanhang”, ”Planera det specifika utförandet” samt ”Omgivningens stöd för engagemang i aktiviteter”. Studien påvisade att personer med förvärvad hjärnskada använde sig av flera olika strategier för att möjliggöra engagemang i aktivitet men dess betydelse för individen skilde sig åt. Vissa strategier innebar att personerna själva kunde bemästra aktiviteter, medan andra strategier omfattade stöd från omgivning och personer i deras närhet för engagemang i aktiviteter. Samtidigt som stöd av andra personer främjade engagemang kunde detta upplevas som ett hinder för självständighet i aktivitet. Att planera sina aktiviteter kunde även förvärra symtom från skadan. Att tillämpa strategier kunde således medföra en problematik i aktivitet. Att samla denna kunskap har betydelse för det fortsatta arbetet inom arbetsterapi i att utforma mer precisa och individanpassade interventioner för personer med förvärvad hjärnskada och därmed bidra till en förbättrad rehabilitering. / The purpose of this study was to describe the use of strategies and its meaning for the engagement in activity for adults with acquired brain injuries. A qualitative study where used as method and 15 articles where included in this study. The collected data has been analyzed using Friberg’s suggestion for studying qualitative studies. The result is presented under an overall theme "Strategies for engagement in activities", which includes the four main categories “Planning of activities in the everyday”, “Select and prioritize activities according to the situation and context”, “Planning of the specific performance” and “The support from others for engagement in activities”. The study showed that people with acquired brain injury were using many strategies to enable engagement in activities but the value for the individual differed. Some strategies meant that the individuals independently were able to master activities, while other strategies included support from people in their environment for engagement in activities. While support from other people improved engagement, it could be perceived as a hindrance to independence in activity. Planning activities could also exacerbate their symptoms from injury. To apply strategies could thus cause problem in activity. This knowledge is important for the continued work in occupational therapy in designing more precise and individualized interventions for people with acquired brain injury and thereby improve rehabilitation.

La prise en charge des urgences vitales préhospitalières en France, est du ressort des SMUR sous l’autorité des SAMU, seuls responsables de l’organisation des soins, du lieu de survenue jusqu’à l’hôpital. L’accessibilité de la population aux équipes médicales des SMUR n’avait jamais été évaluée. Au travers de l’analyse prospective d’une cohorte de 500 patients traumatisés crâniens graves, pris en charge par les SAMU/SMUR en Ile de France, l’apport d’outils SIG a permis d’identifier les caractéristiques d’accessibilité et de disponibilité de l’organisation territoriale des SMUR franciliens. Des territoires ont été identifiés potentiellement à risque, en raison d’une accessibilité des moyens SMUR supérieure à 30 minutes. Cependant, le critère d’accessibilité pris isolément, masque de fortes inégalités dans l’organisation territoriale des SMUR. La disponibilité d’un SMUR est un critère essentiel, rarement évalué. La prise en charge du traumatisme crânien grave illustre parfaitement la situation. La réflexion géographique et l’utilisation des outils SIG permettent de pouvoir évaluer et visualiser objectivement les atouts et faiblesses de l’organisation territoriale d’un système de santé et de proposer des modèles d’organisation pertinents. / In France, the prehospital life threatning emergency are managed by mobile medical team (MMT) and an medical dispatcher service called SAMU. Access to medical mobile team, is a strong criterion but never has been estimated. Throughout a Paris regional study, who concerned five hundred severe traumatic head injury managed during two years by MMT, we perform, with tools GIS , an assessment of accessibility and availability to MMT in Paris area. We concluded that the SAMU organization made strong disparity in the area coverage.

Un dysfonctionnement du métabolisme cérébral est observé au décours d'un traumatisme crânien (TC). L’œdème cérébral et l’hypoxie cérébrale post-traumatiques sont des acteurs principaux de l’apparition des lésions ischémiques secondaires responsables en partie de la défaillance énergétique. Cette hypoxie tissulaire résulte de troubles macrocirculatoires, de troubles de la microcirculation et/ou de troubles de la diffusion de l’oxygène des capillaires sanguins aux tissus. La baisse de la consommation en oxygène est également liée à une dysfonction mitochondriale post traumatique de la chaine respiratoire. Ces phénomènes ischémiques ou hypoxiques aboutissent ainsi à une élévation de lactate endogène en condition anaérobie. Cependant, l'élévation de lactate endogène post traumatique est liée majoritairement à une crise métabolique conduisant à une hyperglycolyse en dehors de tout phénomène hypoxique ou ischémique. L'objectif de notre étude était donc d’étudier l'œdème cérébral, l'oxygénation cérébrale, la défaillance mitochondriale post traumatique et le métabolisme cérébral dans un modèle expérimental de traumatisme crânien diffus par impact accélération chez l'animal. Nous avons étudié les effets de différents neuroprotecteurs sur le métabolisme cérébral à l'aide d'un monitorage multimodal. Les effets de la rhEpo (5000UI/Kg), du mannitol (1g/kg) et du lactate de sodium molaire (1.5 ml/Kg soit 3mOsm/kg) ont été étudiés sur l'œdème cérébral (IRM, microscopie électronique), sur l'hypoxie cérébrale tissulaire (IRM BOLD, mesure de la pression tissulaire en O2, saturation veineuse en O2 du sinus longitudinal supérieur), sur le métabolisme cérébral (spectroRMN) et sur la mitochondrie (analyse de la capacité de rétention calcique, de la chaine respiratoire, microscopie électronique et mesure du calcium intramitochondrial) chez des rats wistar mâles. Notre hypothèse était que l’injection de différents neuroprotecteurs permettrait d’améliorer le métabolisme cérébral post traumatique par des effets bénéfiques sur l’hémodynamique cérébrale et l'œdème cérébral, sur l'hypoxie tissulaire ou sur la dysfonction mitochondriale post TC. Nos résultats ont démontré que la rhEpo avait un effet bénéfique sur l'hypoxie cérébrale post traumatique par le biais d'une diminution de l'œdème cérébral péri capillaire en phase aigue associée à une diminution de la dysfonction mitochondriale proapoptotique. Le mannitol améliore l'hypoxie cérébrale post traumatique en jouant sur la microvascularisation cérébrale perturbée par l'œdème astrocytaire péri capillaire. Enfin, le lactate de sodium molaire avait des effets bénéfiques anti œdémateux et sur la dysfonction mitochondriale post TC améliorant ainsi la crise métabolique post traumatique. Ces résultats permettent d'améliorer la compréhension de la physiopathologie des lésions survenant au décours du traumatisme crânien ainsi que les mécanismes d'action de différentes molécules neuroprotectrices. / Cerebral metabolism is impaired after a Traumatic Brain Injury (TBI). Post traumatic cerebral edema and hypoxia are mainly responsible of the development of secondary ischemic lesions after TBI leading to metabolic impairment. Tissular hypoxia can result from disorders in macro and microcirculation and/or disturbance in the diffusion of oxygen from the blood capillaries to tissue. The decrease in oxygen consumption observed after brain injury is also related to a post traumatic dysfunction of the mitochondrial respiratory chain. These ischemic or hypoxic phenomena may be responsible for metabolic disorders leading to elevated level of endogenous lactate under anaerobic conditions. However, the elevation of endogenous lactate is mainly the consequence of a metabolic crisis that led to a state of hyperglycolysis without cerebral hypoxia or ischemia after TBI. The aim of our study was to investigate cerebral edema, cerebral oxygenation, mitochondrial and metabolic impairment post TBI in an experimental model of impact acceleration diffuse brain injury in rats. We also analyzed the effects of various neuroprotective agents on cerebral metabolism using a multimodal monitoring. The effects of rhEpo (5000UI/Kg), mannitol (1g/Kg) and of molar sodium lactate (1.5 ml/Kg or 3mOsm/kg) were investigated on brain edema (MRI, electronic microscopy), on brain tissue hypoxia (BOLD MRI, measurement of the tissular pressure of O2, venous O2 saturation of the upper longitudinal sinus), on brain metabolism (Magnetic Resonance Spectroscopy) and on mitochondria (study of the calcium retention capacity, of the respiratory chain, morphological analysis with electronic microscopy and measurement of intramitochondrial calcium) in male wistar rats. We hypothesized that the injection of various neuroprotective agents would improve posttraumatic cerebral metabolism by restoring a better cerebral hemodynamic status, by improving cerebral edema, tissular oxygenation and/or mitochondrial function. On the early phase of TBI, we demonstrated that rhEpo had a beneficial effect on post traumatic cerebral hypoxia by decreasing post-traumatic cerebral capillaries collapse due to astrocytic end-foot swelling. This effect was associated with an improvement in cellular apoptosis induced by mitochondrial pathways. Mannitol improved brain hypoxia by decreasing peri vascular astrocytic edema. Sodium lactate had benefic effects on cerebral hypoxia by decreasing cerebral edema and improved mitochondrial and metabolic impairments after TBI. These results help understanding physiopathological events after TBI and the various effects of neuroprotective agents that can be used in future clinical research.

Le traumatisme cérébral (TC) touche des millions de personnes chaque année dans le monde. Les premières conséquences peuvent être une perte de conscience, des hémorragies et l’apparition d’un œdème cérébral. Cependant les personnes qui subissent un TC peuvent présenter des séquelles importantes à plus long terme. Ainsi le traitement préventif des pathologies post-traumatiques est devenu un réel problème de santé publique. La dépression représente la pathologie post-traumatique dont l’occurrence est la plus fréquente. Les origines connues de son apparition s’orientent vers une altération de la neurogenèse adulte hippocampique ainsi que des changements dans la neurotransmission GABAergique, qui est dépendante de l’homéostasie des ions chlorures. Mon travail de thèse suggère que la phase critique, responsable de l’apparition des pathologies post-traumatiques, survient au cours de la première semaine suivant le TC. Pendant cette période, mes résultats montrent que l’hyperexcitabilité des réseaux neuronaux hippocampiques est due à une perturbation des transporteurs des ions chlorure entraînant notamment, une diminution de l’inhibition neuronale. J’ai aussi pu mettre en évidence une altération de la neurogenèse adulte hippocampique liée à la perte d’interneurones dans le gyrus denté. Consécutivement à ces changements, vont s’installer des troubles dépressifs majeurs. Mes travaux indiquent également que la restauration précoce, de l’homéostasie des ions chlorure par un agent pharmacologique, prévient la mort des interneurones ainsi que les changements dans la neurogenèse et permet sur le long terme de réduire très fortement les troubles dépressifs majeurs. / Traumatic brain injury (TBI) affects annually millions of people over the world. The first major consequences include loss of consciousness, haemorrhage and the appearance of cerebral edema. However, people who experience TBI may have significant long-term sequelae and in the majority of cases develop major depressive disorders. In addition, debilitating effects of TBI substantially impair health-related quality of life and are associated with high health care costs. Hence, preventive treatment against posttraumatic pathologies has become a real public health concern. Increasing evidence points to an association between depressive disorders and changes in GABAergic neurotransmission as well as alteration of adult hippocampal neurogenesis.My thesis suggests that the critical phase of posttraumatic pathology occurs over the first week following the trauma. During this period, my results show that hippocampal network hyperexcitability is induced by a disruption of the chloride ion transporters, leading notably to a decrease in neuronal inhibition. Then my work highlighted an alteration of hippocampal neurogenesis related to the loss of interneurons in the dentate gyrus. After some latency, these changes will trigger major depressive disorders. My work also indicates that the early restoration, during this first post-traumatic week, of chloride ion homeostasis by a pharmacological agent, prevents cell death of interneurons as well as changes in neurogenesis and allows significant long-term reduction of major depressive disorders. This therefore suggests the possibility of developing new therapeutic strategies to prevent the emergence of posttraumatic pathologies.

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p. 1-243 / Submitted by Santiago Fabio (fabio.ssantiago@hotmail.com) on 2013-04-25T21:13:52Z No. of bitstreams: 1 222222.pdf: 3297140 bytes, checksum: 1291faff859d1a2fa3e097cac0f5f252 (MD5) / Approved for entry into archive by Maria Creuza Silva(mariakreuza@yahoo.com.br) on 2013-05-04T17:22:07Z (GMT) No. of bitstreams: 1 222222.pdf: 3297140 bytes, checksum: 1291faff859d1a2fa3e097cac0f5f252 (MD5) / Made available in DSpace on 2013-05-04T17:22:07Z (GMT). No. of bitstreams: 1 222222.pdf: 3297140 bytes, checksum: 1291faff859d1a2fa3e097cac0f5f252 (MD5) Previous issue date: 2010 / Esta tese apresenta o resultado da investigação sobre a funcionalidade de pacientes com traumatismo craniencefálico (TCE) que foram admitidos na unidade de referência estadual para este tipo de trauma na Região Metropolitana de Salvador, Bahia, Brasil no período de 1º de agosto de 2007 a 31 de julho de 2008. Inicialmente investigou-se o perfil epidemiológico dos pacientes e verificou-se que a distribuição por sexo foi uniforme de acordo com as faixas etárias, com exceção da faixa etária de 25 a 34 anos, cuja concentração de casos foi maior para homens e mulheres diferiram significativamente em relação à idade, local de ocorrência, atenção pré-hospitalar, etiologia do trauma, acidentes de transporte e quedas. A maior proporção dos traumas ocorreu em via pública, por atropelamento, espancamento e acidentes motociclísticos. Em seguida, analisou-se a distribuição espacial dos locais de ocorrência dos eventos e residência dos pacientes e constatou-se que muitos eventos ocorrem em locais distantes do hospital de referência dificultando o acesso e o socorro em tempo reduzido. Em função da magnitude do agravo observada para homens, um estudo de coorte foi conduzido para observar os fatores prognósticos da capacidade funcional e os relacionados com o retorno às atividades produtivas. Observou-se que idade, gravidade do trauma, fadiga, distúrbios da atenção e concentração, alteração no equilíbrio, presença de plegias ou fraturas estiveram significativamente associados com a incapacidade funcional global, assim como ter sido submetido a tratamentos multiprofissionais de reabilitação. Com relação às atividades produtivas prévias, observou-se que 91 (37,7%) indivíduos reassumiram antigas funções e que a média do tempo decorrido para o retorno às atividades produtivas foi de 225 dias, com 25% dos pacientes retornando em até 103 dias e 75% deles em até 390 dias. Os mais jovens que sofreram traumas mais graves, e concomitantes distúrbios motores, que evoluíram com sintomas somáticos ou cognitivo-comportamentais, além de incapacidade funcional global, apresentaram dificuldade para retomar suas atividades prévias ou não retornaram. Todavia, história pregressa de trabalho remunerado mostrou-se significativamente associado com mais rápido retorno à produtividade. / Salvador