No description available.

<p>This dissertation recruited 24 premature infants born less than 32 weeks gestational age over a one year time period from October 2010 to 2011. The goals were to longitudinally measure cerebral oxygen saturation, evaluate how environmental variables controlled by nursing, positioning and noise, affect cerebral oxygen saturations, and examine the relationship between cerebral oxygen saturation and two currently measured vital signs.</p><p>Using mixed general linear models, findings from this dissertation showed the developmental trajectory of cerebral oxygen saturation values in premature infants' began in the high 70s during the first two days of life and then significantly decreased into the mid-60s over several weeks during hospitalization in a neonatal intensive care unit (NICU). The trajectory of cerebral oxygen saturation during the first week of life in those infants who developed an IVH did not significantly differ from those infants without IVH. At this time, use of cerebral oxygen saturation to identify those infants at risk for IVH during the first week of life cannot be supported, but findings may indicate that cerebral oxygen saturation monitoring could potentially monitor the severity of the impact of IVH later during hospitalization as those infants with an IVH had significantly lower cerebral oxygen saturation values after the third week of life. In this case, cerebral oxygen saturation might help to understand the long-term degree of neurological damage. </p><p>Heart rate and peripheral oxygenation were chosen as the two physiologic variables to compare to cerebral oxygen saturation and average cerebral oxygen saturation was lower with higher heart rate and higher with higher peripheral oxygenation. Peripheral oxygenation that is already routinely measured in premature infants appears to not provide an accurate measure of the changes in cerebral oxygen saturation. Cerebral oxygen saturation monitoring is highly suggested for those infants who are at risk for neurological damage such as infants with hypoxic-ischemic encephalopathy or seizures since peripheral oxygenation does not appear to be an appropriate proxy for cerebral oxygenation.</p><p>Finally, sound and positioning were chosen to represent two frequently encountered components of the neonatal intensive care environment that also influence infant cerebral oxygen saturation. A peak in sound from the ambient sound level was only 5 decibels and found to not significantly affect cerebral oxygen saturation values. A neutral position considered the gold standard-- supine, head midline--was compared to five other positions widely used by NICU nurses. However, results showed positions with a turned head did not significantly change cerebral oxygen saturation from the neutral position. Yet, differences in cerebral oxygen saturation were found between two lateral positions (left lateral and right lateral, head elevated 15°) with an elevated head measuring lower cerebral oxygen saturation levels.</p> / Dissertation

There has been extensive research investigating the differences between global and local feature discrimination. The role that global and local feature discrimination has in sustained attention tasks however has been relatively neglected. In the current research, participants were required to perform a sustained attention task requiring them to engage in either global or local shape stimuli discrimination. Reaction times to local feature discrimination revealed a quadratic trend with time-on-task, with performance levels showing a decline before returning to initial levels towards the end of the task. This trend was not found in the global shape discrimination condition. Functional near-infrared spectroscopy (fNIRS) was employed to assess hemispheric cerebral oxygenation during the tasks. It was found in both conditions that there was greater oxygenation in the right hemisphere compared to the left hemisphere. It was also found that right hemisphere oxygenation increased with time-on-task. Left hemisphere oxygenation decreased during the global task, while it increased during the local task with time on task. Total cerebral oxygenation, collapsed over both hemispheres, increased more over time in the local discrimination task than the global discrimination task. The performance data and the fNIRS results suggest an increased utilization of bilateral cognitive resources with time-on-task in the local discrimination condition, but not in the global discrimination condition. Results and implications are discussed.

PROBLEM: Expanding knowledge of how the brain responds to various exercise types may allow for investigation and development of individualized methods of concussion management. PURPOSE: Identify differences in cerebral oxygenation recovery following bouts of maximal anaerobic, resistance and aerobic exercise. METHODS: Twenty-eight active adults were recruited, each partaking in two sessions. At the first, anthropometric measures and leg press 1-RM were determined. During the second session, cerebral oxygenation and ventilatory gas exchange variables were recorded while participants completed maximal anaerobic, resistance, and aerobic tests, and for 15-minutes of recovery. RESULTS: Anaerobic (637.41s ± 330.42s) and aerobic (689.29s ± 311.05s) exercise resulted in longer durations of time to return to baseline compared to resistance (363.07s ± 366.34s). CONCLUSION: Anaerobic and aerobic exercise taking longer than resistance to return to baseline indicates prolonged activity. Expecting equivalent outcomes as concussion management tools from differing exercise methods may be misguided and requires additional research. / February 2017

The overall aim of the present thesis was to study post-resuscitation care of cardiac arrest (CA) patients treated with target temperature management 33°C with a focus on evaluation of two prognostic tools: variations in cerebral venous saturation and acute magnetic resonance imaging (MRI) findings on the brain post-CA. An additional aim was to investigate patients’ neurological outcome and relatives’ experiences 6 months after the event. Paper I describes the cerebral oxygen saturation of blood obtained from a jugular bulb (SjvO2) catheter The results showed that patients with poor outcome tended to have higher SjvO2values,but this difference was only significant at 96 and108 hours post-CA. The main findings of Paper II were that patients with good outcome displayed a pathological pattern mainly in the frontal and parietal lobes on MRI of the brain. Patients with poor outcome had an extensive pathological pattern in several brain regions. Furthermore, very low apparent diffusion coefficient (ADC) values were associated with poor outcome regardless of brain region. Paper III investigated physical and cognitive function over time, between one month and 6 months post-CA, as well as d life satisfaction at 6 months. The results showed that impairment in physical and cognitive function is common in CA survivors but tends to decrease over time. Despite a severe illness, which has impaired the physical and cognitive functions, satisfaction with life as a whole was reported by 70% of CA survivors. In Paper IV, relatives described their experiences 6 months after a significant others CA. The analysis resulted in three themes reflecting relatives’ everyday life 6 months after the event: Difficulties managing a changed life situation, Feeling like I come second and Feeling new hope for the future. In conclusion, the results of the present thesis have increased our understanding of the two prognostic tools that were investigated; they have generated new and revealed aspects that should be taken into account during prognostication and assessing neurological outcome of this group of patients. The thesis has also shown that the healthcare needs to improve its routines for follow-ups and information provision to both patients and their relatives.

No description available.

No description available.

La drépanocytose est une hémoglobinopathie aux formes et aux sévérités cliniques très hétérogènes qui affectent de nombreux organes chez les patients touchés. Pour cette raison le terme de syndrome drépanocytaire majeur est généralement employé. Tous les syndromes drépanocytaires majeurs ont en commun une mutation ponctuelle du gène β-globine appelée mutation βs . Cette mutation βs conduit à la synthèse de la protéine d'hémoglobine S (HbS) caractérisée par sa capacité à polymériser dans sa forme désoxygénée. La polymérisation de l'HbS est l'élément déclencheur de la falciformation du globule rouge et conduit à de nombreuses altérations hématologiques et hémorhéologiques. Ces dernières sont à l'origine de troubles de l'hémodynamique, de l'oxygénation sanguine et de la perfusion tissulaire en oxygène. Il en résulte de nombreuses complications aigues (crise vaso-occlusive, accident vasculaire cérébral, syndrome thoracique aigu etc.) et/ou chroniques (glomérulopathie, ostéonécrose de la tête fémorale etc.) causés par un défaut d'oxygénation des tissus. / Sickle cell anemia is a hemoglobinopathy forms and severities very heterogeneous clinical affecting many organs in affected patients. For this reason the term major sickle cell syndrome is generally used. All major sickle cell syndromes have a common point mutation in the gene called β-globin mutation βs. This βs mutation leads to the synthesis of the protein hemoglobin S (HbS) is characterized by its ability to polymerize in its deoxygenated form. The polymerization of HbS is the trigger for the sickling of red blood cells and leads to many Hematological and hemorheological. These are at the origin of disorders hemodynamics, blood oxygenation and tissue perfusion with oxygen. This results in many acute complications (vaso-occlusive crisis, stroke, acute chest syndrome, etc..) And / or chronic (glomerulopathy, osteonecrosis of the femoral head etc.). Caused by a defect of tissue oxygenation.

Implication de l’oxygénation cérébrale dans les limitations à l’exercice musculaire des personnes non-entraînées et sportifs d’endurance. L’objectif général de ce travail était de déterminer si l’oxygénation cérébrale était un facteur de la limitation à l’exercice de type aérobie. Dans un premier temps, nous nous sommes attachés à étudier le rôle de l’oxygénation cérébrale mesurée par la Spectroscopie dans le proche Infra-Rouge (NIRS) dans la limitation de l’exercice progressif maximal en rampe. Nous avons montré l’existence d’un seuil de déclin de l’oxygénation cérébrale associé au point de compensation respiratoire (RCP). L’amélioration de la performance avec une supplémentation d’O2 était liée au décalage de ce seuil à de plus hautes intensités d’exercice chez des sujets actifs (étude 1). Dans un second temps, nous avons montré que ce seuil de déclin de l’oxygénation, retrouvé aussi chez des sportifs entraînés en endurance apparaîssait à de plus hautes intensités d’exercice que chez des sujets non-entraînés (étude 2). Enfin, nous avons déterminé l’impact de l’hypoxémie artérielle induite par l’exercice (HIE) des sportifs d’endurance sur l’oxygénation cérébrale au cours d’un exercice maximal en rampe et d’un exercice de temps limite à charge constante. Nous avons ainsi montré que l’oxygénation cérébrale était augmentée avec la HIE suggérant un effet compensatoire à l’hypoxémie artérielle au cours de l’exercice progressif maximal en rampe. Ceci, n’existait pas au cours de l’exercice de temps limite ne supportant pas l’implication de l’oxygénation cérébrale dans ce type d’exercice (étude 3). Ces travaux ont donc mis en évidence l’implication de l’oxygénation cérébrale dans la limitation de l’exercice maximal en rampe chez des sujets actifs et des sportifs entraînés en endurance présentant ou pas une HIE. Toutefois, elle ne semble pas être un facteur majeur de limitation de l’exercice de temps limite. / Involvement of cerebral oxygenation in muscular exercice limitation in untrained and trained endurance men. A decrease in oxygen availability in the brain could be a physiological mechanism limiting aerobic fitness. We first studied the role of cerebral oxygenation measured by Near Infra-Red Spectroscopy (NIRS ) in maximal cycle ramp exercise limitation. We showed a cerebral oxygenation threshold decline associated with respiratory compensation point (RCP). This threshold appeared for higher exercise intensities -related to performance improvement with hyperoxia in untrained endurance men (study 1). Secondly , we showed that the cerebral oxygenation threshold in athletes occurred for higher sub-maximal exercise intensities than untrained (study 2). Finally , we determined the involvement of exercise-induced arterial hypoxemia (EIH) in endurance athletes on cerebral oxygenation during maximal cycle ramp exercice and exercice time to exhaustion. We showed that cerebral oxygenation was improved by EIH suggesting a compensatory effect of EIH during the maximal cycle ramp. This did not occur during exercise time to exhaustion, and does not support the involvment of cerebral oxygenation in this type of exercise (study 3). This work has therefore highlighted the involvement of cerebral oxygenation in maximal cycle ramp exercice limitation in untrained and trained endurance men with or without EIH. However, it was unlikely been the major factor limiting the exercise time to exhaustion.

There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S cvO2), cerebro-vascular carbon dioxide reactivity (δScvO2), and brain structural damage (β-amyloid precursor protein [βAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 ± 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better ScvO2 (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO2 evoked a 16 ± 4% increase in ScvO2, indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in βAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO2 reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.