The research process illustrates the interaction between the therapist and the neuropsychological impaired client in the therapeutic context where we utilised drawing and painting as a creative medium I descn'be the interaction from a systems paradigm New paradigm research is used as the researcher is included in the research findings. The focus is on new meanings that the therapist and clients generated. Three case studies are descn'bed in this study. A circular description is given of the use of drawing and painting in therapy. The losses that the clients suffer are described and explained to make sense of the interaction. The use of art is described and incorporated in the therapeutic process as creative exercises were important ways to connect with the clients. This study illustrates that creativity should always be part of the therapeutic endeavour, especially when understanding the verbal expression of the client is difficult. / Psychology / M.A. (Clinical Psychology)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / Traumatic brain injury (TBI) is a public health problem, and is considered a leading cause of death among children and young adults in industrialized countries. TBI can be defined as a mechanical external aggression to the brain, which may produce an altered state of consciousness leading the cognitive and / or motor impairment. In this context, the inflammatory process plays an important role in the development and exacerbation of secondary damage after TBI, mediating, through the release of cytokines, increased permeability of the blood brain barrier (BBB), edema formation and promoting the accumulation of leukocytes after TBI. Exercise provides protection on a variety of diseases and insults of the Central Nervous System (CNS). However, there are few studies showing the prophylactic effects of regular exercise on the damage caused by TBI. Therefore, the aim of this study was to investigate whether physical exercise protects against acute inflammatory response and motor impairment induced by TBI in rats. For this, the animals performed exercise for four weeks and then underwent the model of TBI by fluid percussion injury (FPI). Twenty-four hours after TBI the results showed that there was an impairment of motor function, followed by increased permeability of the BBB and brain inflammation characterized by increased levels of interleukin-1β (IL-1β ) of tumor necrosis factor-α (TNF-α) and by decreasing levels of interleukin-10 (IL-10). Furthermore, increased myeloperoxidase (MPO) and inhibition of enzyme activity Na+,K+-ATPase after TBI suggests that the opening of the BBB, followed by infiltration of neutrophils and brain inflammation may contribute to failure of selected targets leading to damage side. The results also demonstrated that physical exercise protected against motor impairment, BBB permeability and also protect against an increase in brain levels of IL-1β and TNF-α and decrease levels of IL-10 induced by fluid percussion injury (FPI) . This exercise protocol also protected the increase of MPO activity and inhibition of Na+,K+-ATPase after TBI. This protection correlated with decreased MPO activity, suggesting that a change in cerebral inflammatory profile, caused by physical exercise, may be reducing the initial injury and limiting secondary damage after TBI. / O traumatismo cranioencefálico (TCE) constitui um problema de saúde pública, sendo considerada uma das principais causas de morte entre crianças e jovens adultos em países desenvolvidos. O TCE pode ser definido como uma agressão mecânica externa ao encéfalo, que pode produzir um estado alterado de consciência levando ao comprometimento das habilidades cognitivas e/ou motoras. Neste contexto, o processo inflamatório tem papel importante do desenvolvimento e na exacerbação do dano secundário após o TCE, mediando, através da liberação de citocinas, o aumento da permeabilidade da barreira hematoencefálica (BHE), a formação de edema e promovendo o aumento da migração de leucócitos após o TCE. Sabe-se que o exercício físico oferece proteção sobre varias doenças e insultos do Sistema Nervoso Central (SNC). No entanto, poucos são os estudos que mostram os efeitos profiláticos da prática regular de exercício físico diante dos danos decorrentes do TCE. Portanto, o objetivo desta dissertação foi verificar se o exercício físico protege da resposta inflamatória aguda e do comprometimento motor induzido pelo TCE em ratos. Para isso, os animais realizaram exercício físico durante quatro semanas e posteriormente foram submetidos ao TCE pelo modelo de lesão por percussão de fluido (LPF). Vinte e quatro horas após o TCE os resultados obtidos mostraram que houve um comprometimento da função motora, seguido do aumento na permeabilidade da BHE e da inflamação cerebral, caracterizada pelo elevação nos níveis de interleucina-1β (IL -1β) , do fator de necrose tumoral-α (TNF-α) e pela diminuição nos níveis de interleucina-10 (IL-10). Além disso, houve um o aumento na atividade da enzima mieloperoxidase (MPO) e uma inibição na atividade da enzima Na+,K+-ATPase após o TCE sugerindo que a abertura da BHE, seguida pela infiltração de neutrófilos e inflamação cerebral podem contribuir para a falência dos alvos seletivos. Os resultados também demonstraram que o exercício físico prévio protegeu do comprometimento motor e do aumento na permeabilidade da BHE, bem como aumentou dos níveis de IL-10 e protegeu do aumento dos níveis cerebrais de IL-1β e TNF-α, indzidos pela lesão por percussão de fluido (LPF). Este protocolo de exercício também protegeu do aumento da atividade da MPO e da inibição da enzima Na+,K+-ATPase após o TCE. Esta proteção correlacionada com a diminuição da atividade da MPO, sugere que uma modificação no perfil inflamatório cerebral, provocada pelo exercício físico, pode estar reduzindo a lesão inicial e limitando o dano secundária após o TCE.

No description available.

INTRODUÇÃO: Evidências relevantes acerca dos benefícios da hipotermia terapêutica provieram da utilização de técnicas de resfriamento sistêmico. Essas técnicas, no entanto, podem causar complicações graves que poderiam ser evitadas com métodos de hipotermia encefálica seletiva. O presente estudo objetiva: 1) verificar a viabilidade da hipotermia encefálica exclusiva através de um sistema de resfriamento nasofaríngeo concomitante ao de preservação da temperatura corpórea em suínos e 2) investigar os efeitos da hipotermia encefálica exclusiva nas variáveis fisiológicas sistêmicas e encefálicas. MÉTODOS: Dez suínos híbridos foram submetidos a resfriamento nasofaríngeo durante 60 minutos e subsequente reaquecimento espontâneo. Foram obtidos dados referentes a: pressão arterial média, débito cardíaco, temperatura encefálica, pressão parcial de oxigênio do tecido encefálico (PbtO2, do inglês, pressure of brain tissue O2), velocidade do fluxo sanguíneo nas artérias encefálicas, índice de resistência e índice de pulsatilidade. RESULTADOS: O resfriamento nasofaríngeo associou-se à um decréscimo gradual da temperatura encefálica, que foi mais marcante no hemisfério cerebral esquerdo (p < 0,01). Neste hemisfério, houve redução de 1,47 ± 0,86°C nos primeiros 5 minutos (p < 0,01), 2,45 ± 1,03°C aos 10 minutos e 4,45 ± 1,36°C após 1 hora (p < 0,01). A diferença entre as temperaturas cerebral sistêmica foi 4,57 ± 0,87°C (p < 0,01). As temperaturas centrais (retal, esofágica e da artéria pulmonar), assim como a hemodinâmica encefálica e sistêmica, mantiveram-se estáveis durante o procedimento. Houve diminuição significativa da PbtO2, concomitantemente ao decréscimo da temperatura encefálica. CONCLUSÕES: A indução de hipotermia encefálica exclusiva é possível através de resfriamento nasofaríngeo associado a medidas de preservação da temperatura sistêmica. O resfriamento encefálico exclusivo não influencia as funções hemodinâmicas sistêmicas e encefálicas, contudo reduz significativamente a PbtO2 / INTRODUCTION: Relevant evidences for the use of therapeutic hypothermia derive from studies using whole body cooling methods. These methods can lead to serious complications. To avoid such complications, selective brain cooling methods were developed. The objective of this study was: 1) to verify the feasibility of exclusive brain hypothermia by means of nasopharyngeal cooling along with measures of systemic temperature preservation in an experimental swine model, and 2) to investigate the influence of the exclusive brain cooling on cerebral and systemic hemodynamics as well as on cerebral oxygenation. METHODS: Ten hybrid swine underwent nasopharyngeal cooling for 60 minutes, followed by spontaneous rewarming. A number of physiological variables were monitored: arterial blood pressure, cardiac output, temperature in the right and left cerebral hemispheres, pressure of brain tissue O2, cerebral blood flow velocities, resistance index, and pulsatility index. RESULTS: Nasopharyngeal cooling was associated with decrease in brain temperature, which was more significant in the left cerebral hemisphere (p < 0,01). There was a reduction of 1.47 ± 0.86°C in the first 5 minutes (p < 0.01), 2.45 ± 1.03°C within 10 min, and 4.45 ± 1.36°C after 1 hour (p < 0.01). The brain-core gradient was 4.57 ± 0.87°C (p < 0,001). Rectal, esophageal, and pulmonary artery temperatures, as well as brain and systemic hemodynamics, remained stable during the procedure. PbtO2 values significantly decreased following the brain cooling. CONCLUSION: Achievement of exclusive brain hypothermia is feasible by means of nasopharyngeal cooling associated with measures of systemic temperature preservation. Selective brain cooling does not influence both systemic and cerebral hemodynamics, except PbtO2, which decreased significantly

Mental fatigue is a complex hidden disability. This study investigates how people with mental fatigue assess the accessibility of various typical city environments. Specifically if they use spatial strategies to redress their disability and how they view interaction with other actors in the same space. The study also aims to offer tools for city planners in order to facilitate an understanding of how infrastructure can promote accessibility in public buildings and spaces. The study at hand is qualitative and was conducted as a virtual city tour which allowed the subjects to share their experience of accessibility. Labov's theory of narrative structure was used to analyse the data. The samples of narrative were collected from people who suffer from mental fatigue after a mild traumatic brain injury. The results show that stimuli intense environments increase the use of spatial strategies and complicate the accessibility as well as the interaction with others. The study finds that people with mental fatigue should fall under the protection of the availability impact act and therefore have a legal right to accessibility promoting actions.

La gravité du traumatisme crânien (TC) dépend de la sévérité immédiate des lésions primaires mais également de leur aggravation dans les heures et les jours qui suivent le TC, avec l’apparition de lésions secondaires. La neuro-inflammation constitue l’une des cascades physiopathologiques post-TC dont le contrôle a été décrit comme une stratégie neuroprotectrice potentielle. Elle compromet le taux de la forme soluble α du précurseur du peptide ß amyloÏde, sAPPα, un neuroprotecteur endogène issu de l’action des enzymes α-sécrétases (ADAMs). Dans ce contexte, mon travail de thèse a eu pour but d’étudier l’intérêt thérapeutique des composés pharmacologiques modulant le taux de sAPPα post-TC sur les conséquences biochimiques, histopathologiques et fonctionnelles, à court et à long terme, dans un modèle de TC par percussion mécanique chez la souris. Parmi les différents composés, la minocycline, une tetracycline de 2e génération aux effets anti-inflammatoires, et l’étazolate, une pyrazolopyridine récemment décrite comme activateur des α-sécrétases, ont été sélectionnés. Le traitement anti-inflammatoire par la minocycline permet de restaurer le taux de la sAPPα, et cet effet dans la phase précoce est accompagné d’une réduction des conséquences histopathologiques (atrophie callosale et striatale, lésion des bulbes olfactifs et ventriculomégalie) à 3 mois post-TC. Sur le plan fonctionnel, le test d’aversion olfactive a été pour la première fois mis au point sur un modèle expérimental de TC et a permis de révéler un déficit olfactif persistant dans notre modèle. De plus, un déficit cognitif persistant a été également mis en évidence par le test NORT « Novel Object Recognition Test ». Le même traitement par la minocycline a permis de corriger ces déficits olfactif et cognitif à court et à long terme (3 mois) post-TC. Les résultats obtenus sur l’étazolate (étude de fenêtre thérapeutique, étude d’effet-dose) ont montré, pour la première fois dans un modèle de lésion cérébrale, son potentiel anti-inflammatoire et anti-œdémateux, associé à la restauration du taux de la sAPPα, avec une fenêtre thérapeutique d’au moins de 2h. Le même traitement réduit les conséquences histopathologiques (activation microgliale, ventriculomégalie, lésion des bulbes olfactives) et fonctionnelles (hyperactivité locomotrice, déficit cognitif), à court à long terme (3 mois) post-TC. En conclusion, l’ensemble de ce travail a permis d’établir les bénéfices d’une stratégie pharmacologique s’opposant à la fois à la neuro-inflammation et à la chute du taux de la sAPPα dans la phase précoce de TC avec une amélioration histologique et fonctionnelle à long terme, soulignant son intérêt thérapeutique. Il est important de souligner que la minocycline est déjà entrée en essai clinique pour le traitement de TC, et que malgré le peu de données précliniques, l’étazolate (EHT-0202) est tout récemment entré en phase II pour le traitement de la maladie d’Alzheimer. / The severity of the sequelae of traumatic brain injury (TBI) depends on the extent of primary damage as well as the implication of secondary injury cascades that are triggered within the hours and days post- insult. Neuroinflammation is an important post-TBI cascade whose inhibition has been described as a potential neuroprotective strategy. Neuroinflammation has been associated to the decrease of an endogenous neuroprotector, the soluble form α of the amyloid precursor protein (sAPPα), generated by the activity of the enzymes α-secretases or ADAMs. The aim of this work was to evaluate the therapeutic interest of pharmacological compounds that restore sAPPα levels on short- and long-term biochemical, histological and functional outcome in a mouse model of TBI by mechanical percussion. Among the potential candidates, the compounds selected were minocycline, a tetracycline that exerts anti-inflammatory activity, and etazolate, a pyrazolopyridine that activates α-secretases. The anti-inflammatory treatment with minocycline was able to restore post-TBI sAPPα levels, and this acute effect was accompanied by lasting neuroprotection, namely reduction of lesion size (corpus callosum, striatum and olfactory bulbs) and ventriculomegaly and attenuation of glial reactivity. The olfactory aversion test, developped for the first time in experimental TBI, unraveled a persistant olfactory deficit. Moreover, a durable cognitive deficit was revealed by the Novel Object Recognition Task (NORT). Treatment with minocycline was able to attenuate both the olfactory and cognitive deficits in an effective manner. Moreover, the results obtained in the pharmacological study with etazolate (therapeutic window, dose-response) demonstrated, for the very first time, the anti-inflammatory and anti-oedematous efficacy of etazolate, when administered at least 2 hours post-TBI. The same treatment protocol was also able to attenuate sAPPα levels and offered persistent neuroprotection, namely reduction of lesion size (ventriculomegaly, olfactory bulb lesion) and microglial activation, and attenuation of functional deficits (hyperactivity, cognitive deficit). In conclusion, the findings of this work highlight the therapeutic efficacy of compounds that attenuate neuroinflammation and restore sAPPa levels within the acute and critical post-TBI aftermath, on histological and functional outcome. It is worth noting that minocycline is actually in a clinical trial for the treatment of traumatic brain injury and etazolate (EHT 0202), despite the poor experimental data available, has managed to enter a clinical trial for the treatment of Alzheimer’s disease.

Abstract Traumatic brain injury can be a catastrophe for an individual and a huge economic burden for a society. Such injuries are common especially among young men and as many as half of the patients are under the influence of alcohol at the time of injury. Traumatic brain injuries can also frequently cause epileptic seizures. On the other hand, epileptic seizures are often caused by alcohol. A significant reduction in the tax on alcohol in Finland in 2004 led to a 10% increase in its consumption at the population level and a considerable increase in mortality rate among patients with alcoholic liver diseases. The risk of subsequent epileptic seizures and traumatic brain injuries among intoxicated head trauma subjects has not been evaluated before. The present cohort consists of all subjects who were admitted to the emergency room at Oulu University Hospital in 1999 on account of head trauma. These subjects were then followed-up for 10 years, which enabled the effect of the tax reduction on the long-term outcome to be observed. The effect of being under the influence of alcohol at the time of the index head trauma on the onset of a new epileptic seizure problem and further traumatic brain injuries was investigated. The mortality rate among head trauma subjects with harmful drinking increased significantly after the reduction in the alcohol tax, and the subjects with recorded alcohol-related seizure problems experienced an increased risk of death after the price reduction. Head trauma under the influence of alcohol predicted both new-onset seizure problems and traumatic brain injury during the follow-up. The results are in accordance with the previous observations of a rapid increase in mortality among heavy drinkers following a sharp reduction in alcohol prices. Inebriated head trauma subjects have an increased risk of subsequent traumatic brain injury and epileptic seizure. / Tiivistelmä Traumaattinen aivovamma voi olla potilaalle katastrofi ja yhteiskunnalle valtava taloudellinen tappio. Aivovammat ovat yleisiä erityisesti nuorilla miehillä, ja jopa puolet niistä tapahtuu alkoholin vaikutuksen alaisena. Aivovammat aiheuttavat usein epileptisiä kohtauksia, jotka toisaalta usein johtuvat alkoholista. Vuonna 2004 Suomessa tapahtunut mittava alkoholiveron alennus lisäsi väestötasolla alkoholin kokonaiskulutusta 10&#160;% vuoden aikana. Kuolleisuus erityisesti alkoholimaksasairauksiin lisääntyi voimakkaasti. Aiemmin ei ole tiedetty humalassa ilmaantuneen pään vamman vaikutuksesta potilaan riskiin saada uusi aivovamma tai uusi epileptinen kohtaus. Tutkimuskohortin muodostivat vuonna 1999 Oulun yliopistollisen sairaalan päivystyksessä hoidetut päähän vammautuneet potilaat. Heitä seurattiin rekisteritietojen avulla vuoden 2009 loppuun, minkä ansiosta voitiin tutkia veronalennuksen vaikutusta potilaiden pitkäaikaisennusteeseen. Tutkimuksessa havainnoitiin humalassa tapahtuneen pään vamman vaikutusta epileptisen kohtauksen ja uuden aivovamman ilmaantumiseen seuranta-aikana. Haitallisesti alkoholia käyttävien päähän vammautuneiden potilaiden kuolleisuus lisääntyi merkitsevästi alkoholiveron alennuksen jälkeen. Myös alkoholiin liittyvän epileptisen kouristuksen sairastaneilla kuolleisuus lisääntyi merkitsevästi. Alkoholin vaikutuksen alaisena tapahtunut pään vamma oli riskitekijä uudelle epileptiselle kohtaukselle sekä uudelle aivovammalle seuranta-aikana. Tulokset vahvistavat aiempia havaintoja siitä, että alkoholin hinnan voimakas lasku lisää nopeasti alkoholin suurkuluttajien kuolleisuutta. Humalassa päätään loukanneella on lisääntynyt riski saada uusi aivovamma sekä uusi epileptinen kohtaus.

Le traumatisme craniocérébral (TCC) modéré à sévère constitue une cause majeure d’invalidité chez les jeunes adultes. Il entraine des séquelles physiologiques, comportementales, cognitives et affectives qui entravent le devenir fonctionnel et psychosocial des survivants. Les perturbations de la qualité du sommeil et de l’éveil figurent parmi les plaintes les plus fréquentes et persistantes à la suite d’un TCC modéré à sévère, mais on ignore si celles-ci sont associées à une atteinte de l’intégrité du sommeil. Cette question est primordiale puisque le sommeil est central pour maintenir les capacités d’éveil et un fonctionnement cognitif optimal, ce qui est d’autant plus essentiel lorsque le cerveau est lésé. Cette thèse vise ainsi à caractériser la nature et les corrélats des perturbations du sommeil et de l’éveil durant la phase chronique d’un TCC modéré à sévère. L’association entre les capacités d’apprentissage post-TCC et l’activité à ondes lentes, une caractéristique du sommeil lent connue pour jouer un rôle dans la plasticité synaptique et la mémoire, est également explorée. Pour ce faire, des mesures objectives (actigraphie, polysomnographie) et subjectives (agenda de sommeil et questionnaires) de sommeil-éveil ont été conduites chez des survivants d’un TCC modéré à sévère et des sujets contrôles en bonne santé. La sévérité du trauma, la présence de comorbidités (anxiété, dépression, douleur) et la prise de médicaments psychotropes ont aussi été documentées. La première étude a montré que comparativement aux contrôles, les personnes ayant subi un TCC modéré à sévère rapportent un niveau significativement plus élevé de difficultés d’endormissement, de mauvaise qualité de sommeil, de somnolence diurne et de fatigue. L’actigraphie enregistrée sur une semaine à domicile n’a en revanche pas montrée de perturbations de la qualité du sommeil nocturne. Au contraire, la durée de sommeil sur une période de 24h était significativement supérieure chez les participants TCC par rapport aux contrôles, et cela particulièrement dans un sous-groupe de participants TCC sous médication psychotrope et qui ont subi un trauma global plus sévère. La présence de comorbidités était par ailleurs associée aux plaintes de sommeil-éveil dans le groupe TCC. Dans la deuxième étude, l’architecture du sommeil telle que mesurée par la polysomnographie a été évaluée. Là encore, les résultats indiquent que malgré des plaintes significatives de sommeil-éveil chez le groupe TCC, la macro- et microarchitecture du sommeil étaient similaires chez ces derniers comparativement au groupe contrôle. Toutefois, une association a été montrée entre la qualité du sommeil et la cognition post-TCC, de sorte que plus i l’activité à ondes lentes est élevée au cours du sommeil lent, meilleures sont les performances d’apprentissage et de mémoire épisodique du lendemain. Cette association était plus forte à la suite de la survenue d’un TCC plus sévère par rapport à un TCC moins sévère, suggérant une plus forte dépendance des survivants ayant subi un TCC sévère à l’activité à ondes lentes au cours du sommeil pour apprendre de nouvelles informations. Cette thèse apporte de nouvelles évidences que le cerveau lésé à la suite d’un TCC modéré à sévère semble capable de produire une architecture de sommeil comparable à celle de sujets contrôles en santé. Les plaintes de sommeil-éveil persistantes à la suite d’un TCC modéré à sévère apparaissent influencées par d’autres facteurs, notamment la survenue d’un trauma plus complexe nécessitant une prise en charge pharmacologique, ainsi que des facteurs environnementaux et comorbides. En outre, cette thèse supporte le besoin d’explorer davantage le rôle du sommeil dans les capacités cognitives post-TCC. / Moderate to severe traumatic brain injury (TBI) is a major cause of disability in young adults. It causes physiological, behavioral, cognitive and emotional sequelae that hinder functional and psychosocial outcomes. Disturbances in sleep quality and wakefulness are among the most common and persistent complaints in moderate to severe TBI survivors. However it is unclear if these complaints are associated with impaired sleep integrity. This question is crucial as sleep is central in wakefulness-promoting and optimal cognitive functioning, which is particularly essential when the brain is injured. This thesis aims to characterize the nature and correlates of sleep and wakefulness disturbances during the chronic phase of moderate to severe TBI. The association between post-TBI learning capacity and slow-wave activity, a sleep characteristic known to play a role in synaptic plasticity and memory, is also explored. To do this, objective (actigraphy, polysomnography) and subjective (sleep diary and questionnaires) sleep-wake measures were used in moderate to severe TBI survivors and healthy control subjects. The severity of the trauma, the presence of comorbidities (anxiety, depression, pain) and the use of psychotropic medications have also been documented. The first study showed that compared to controls, people with moderate to severe TBI reported significantly lower sleep quality, and higher levels of daytime sleepiness and fatigue. Yet, a seven-day actigraphy recording did not show any disturbances in the nighttime sleep efficiency. Rather, sleep duration over a 24h period was significantly increased in participants with TBI compared to controls, particularly in a subgroup of TBI who used psychotropic medications and suffered a more severe overall trauma. The presence of comorbidities was also associated with sleep-wake complaints in TBI group. In the second study, the sleep architecture as measured by polysomnography was evaluated. Again, the results indicated that despite significant sleep-wake complaints in TBI group, the macro- and micro-architecture of sleep measured in the TBI group were similar to those in the control group. However, an association between sleep quality and post-TBI cognition was shown, as higher slow-wave-activity sleep was associated with better memory performance the day after. This association was stronger following more severe TBI compared to milder TBI, suggesting that adults who sustained more severe TBI are more dependent on sleep slow-wave-activity for next- day memory function. iii This thesis brings new evidence that the injured brain following moderate to severe TBI appears to be able to produce sleep architecture comparable to healthy control subjects. Persistent sleep- wake complaints following moderate-to-severe TBI appear to be influenced by other factors, including the occurrence of more complex trauma requiring pharmacological management, as well as environmental and comorbid factors. In addition, this thesis supports the need to further explore the role of sleep in post-TBI cognitive abilities.

Introduction : Il existe beaucoup d’hétérogénéité dans la prise en charge des patients se présentant au département d’urgence avec un traumatisme crâniocérébral léger (TCCL) et des lésions à la tomodensitométrie (TDM) cérébrale. L’objectif principal de cette étude est de valider des critères de gravité du saignement intracrânien afin de prédire le besoin d’intervention neurochirurgicale puis, en deuxième lieu, valider si ces mêmes critères peuvent également prédire le besoin d’admission en centre de neurotraumatologie. Méthodes : Cette étude est une analyse rétrospective d’une cohorte de patients adultes avec TCCL se présentant au département d’urgence d’un centre de neurotraumatologie, de 2008 à 2012. Le besoin d’intervention neurochirurgicale et d’admission était laissé à la discrétion du médecin traitant. La sensibilité et la spécificité des critères de gravité ont été calculées avec des intervalles de confiance à 95% (IC95%). Résultats : En tout, 678 patients (homme = 65.9%, âge moyen = 62.5 ans) ont été inclus. Parmi eux, 114 (16.8%) ont subi une intervention neurochirurgicale. Tous les patients ayant nécessité une intervention neurochirurgicale remplissaient des critères de lésions significatives à leur TDM initiale (sensibilité 100% [IC95% 96.8-100]). Par contre, la spécificité était faible, soit 34.8% (IC95% 30.8-38.8) : 196 (28.9%) patients n’ayant pas nécessité d’intervention neurochirurgicale n’avaient pas de critères de lésions significatives. Ces critères ont une sensibilité de 78.3% (IC95% 74.6-81.7) et une spécificité de 55.9% (IC95% 47.4-64.2) afin de prédire l’admission en centre de neurotraumatologie. Conclusion : Les critères de gravité du saignement intracrânien ont identifié tous les patients ayant requis une intervention neurochirurgicale, sans toutefois démontrer une forte spécificité. Ils étaient moins sensibles, mais plus spécifiques, pour prédire l’admission en centre de neurotraumatologie. / Background: There is variability in the management of patients presenting to the emergency department (ED) with mild traumatic brain injury (MTBI) and abnormal findings on their initial head computed tomography (CT). The main objective of this study was to validate the value of the Important Brain Injury (IBI) criteria, introduced by the Canadian CT-Head Rule, in predicting the need for surgical intervention. The secondary objective was to evaluate the usefulness of IBI criteria to predict admission to a tertiary care hospital. Methods: This is a post hoc analysis of a prospective cohort of adult patients presenting to the ED of one tertiary care, academic center, between 2008 and 2012, with MTBI and an abnormal initial head CT. Neurosurgical intervention and tertiary center admission were at the discretion of the treating physician. The sensitivity and specificity of the IBI criteria were calculated with their 95% confidence intervals (95%CI). Results: A total of 678 patients (male = 65.9%, mean age = 62.5 years) were included, of whom 114 (16.8%) required neurosurgical intervention. All patients requiring neurosurgical intervention met IBI criteria on their initial head CT (sensitivity of 100% [95%CI 96.8-100]). However, only 196 (28.9%) patients who did not require neurosurgical intervention were correctly identified using these criteria (specificity of 34.8% [95%CI 30.8-38.8]). The IBI criteria had sensitivity of 78.3% (CI 74.6-81.7) and specificity of 55.9% (CI 47.4-64.2) to predict admission to a tertiary care center. Conclusion: The IBI criteria for MTBI identified all patients who required neurosurgical intervention, but did not show a high specificity. They were less sensitive, but more specific, in predicting admission to a tertiary care center.

Introduction: This study evaluates the use of antibiotic prophylaxis for prevention and development of ventilator associated pneumonia (VAP) in pediatric patients with moderate to severe traumatic brain injury (TBI) in order to promote best practices and use the appropriate resources. Methods: A retrospective cohort study of all pediatric patients, between 1 and 18 years, who were admitted and had moderate or severe TBI diagnosis at the Pediatric Emergency Hospital, Lima-Peru. Results: One hundred and forty-five patients with diagnosis of traumatic brain injury (TBI), who received mechanical ventilation for at least 48 hours, were evaluated. We obtained an incidence density of 44.60/1000 ventilator days. No relationship was found between antibiotic prophylaxis and the development of VAP. Likewise, it was found that performing oral hygiene with chlorhexidine reduces the risk of developing VAP by 45% (p = 0.03, CI 0.33-0.95).In addition, the presence of purulent secretions (IC 2.23-11.45), solid (, IC 1.67-11.34) or dense ( IC 2.91-16.75) has a 3, 5 and 6 times higher risk of ventilator-associated pneumonia, respectively. Conclusions: Antibiotic prophylaxis did not show to have a positive effect on the prevention of ventilator associated pneumonia; However, other measures such as oral hygiene with chlorhexidine were associated with reducing the risk of developing VAP. The proportion of patients who received antibiotic prophylaxis was 81 (55.6%) and the incidence density of VAP found in the study is within the standards found in the available literature. Furthermore, the type of discharge was identified as a predictor of increased risk of ventilator-associated pneumonia. Even more studies focused on this population are required. / Introducción: Se evaluará el uso de antibióticos profilácticos para prevenir el desarrollo de neumonía asociada a ventilador (NAV) en la población pediátrica admitida con diagnóstico de traumatismo encéfalo craneano (TEC) moderado a grave. Métodos: Se realizó un estudio cohorte retrospectivo de todos los pacientes pediátricos, entre 1 y 18 años, que fueron admitidos con diagnóstico TEC moderado o grave y estuvieron con ventilación mecánica más de 48 horas en el Hospital de Emergencias Pediátricas, Lima-Perú. Resultados: Ciento cuarenta y cinco pacientes con TEC y que recibieron ventilación mecánica fueron evaluados. Se encontró una densidad de incidencia de neumonía asociada a ventilador (NAV) de 44.60/1000 días de ventilador. No se encontró relación entre la profilaxis antibiótica y el desarrollo de NAV. Asimismo, se obtuvo que la realización de higiene oral con clorhexidina disminuye en 45% el riesgo de desarrollar NAV (IC 0.33-0.95). Además, la presencia de secreciones purulentas (IC 2.23-11.45), sólidas (IC 1.67-11.34) o densas (IC 2.91-16.75) tiene 3, 5 y 6 veces más riesgo de neumonía asociada a ventilador, respectivamente. Conclusiones: La profilaxis antibiótica no mostró tener un efecto positivo en la prevención de neumonía asociada a ventilador; sin embargo, otras medidas como la higiene oral con clorhexidina sí estuvieron asociadas disminuyendo el riesgo de desarrollar NAV. La proporción de pacientes que recibieron profilaxis antibiótica fue 81 (55.6%) y la densidad de incidencia de NAV encontrada en el estudio se encuentra dentro de los estándares encontrados en la literatura disponible. Además, el tipo de secreción se identificó como un factor predictor de mayor riesgo de neumonía asociada a ventilador. Se requieren aún más estudios enfocados en esta población. / Tesis