5 resultados para Tbi

em Brock University, Canada


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Traumatic brain injury (TBI) often affects social adaptive functioning and these changes in social adaptability are usually associated with general damage to the frontal cortex. Recent evidence suggests that certain neurons within the orbitofrontal cortex appear to be specialized for the processing of faces and facial expressions. The orbitofrontal cortex also appears to be involved in self-initiated somatic activation to emotionally-charged stimuli. According to Somatic Marker Theory (Damasio, 1994), the reduced physiological activation fails to provide an individual with appropriate somatic cues to personally-relevant stimuli and this, in turn, may result in maladaptive behaviour. Given the susceptibility of the orbitofrontal cortex in TBI, it was hypothesized that impaired perception and reactivity to socially-relevant information might be responsible for some of the social difficulties encountered after TBL Fifteen persons who sustained a moderate to severe brain injury were compared to age and education matched Control participants. In the first study, both groups were presented with photographs of models displaying the major emotions and either asked to identify the emotions or simply view the faces passively. In a second study, participants were asked to select cards from decks that varied in terms of how much money could be won or lost. Those decks with higher losses were considered to be high-risk decks. Electrodermal activity was measured concurrently in both situations. Relative to Controls, TBI participants were found to have difficulty identifying expressions of surprise, sadness, anger, and fear. TBI persons were also found to be under-reactive, as measured by electrodermal activity, while passively viewing slides of negative expressions. No group difference,in reactivity to high-risk card decks was observed. The ability to identify emotions in the face and electrodermal reactivity to faces and to high-risk decks in the card game were examined in relationship to social monitoring and empathy as described by family members or friends on the Brock Adaptive Functioning Questionnaire (BAFQ). Difficulties identifying negative expressions (i.e., sadness, anger, fear, and disgust) predicted problems in monitoring social situations. As well, a modest relationship was observed between hypo-arousal to negative faces and problems with social monitoring. Finally, hypo-arousal in the anticipation of risk during the card game related to problems in empathy. In summary, these data are consistent with the view that alterations in the ability to perceive emotional expressions in the face and the disruption in arousal to personally-relevant information may be accounting for some of the difficulties in social adaptation often observed in persons who have sustained a TBI. Furthermore, these data provide modest support for Damasio's Somatic Marker Theory in that physiological reactivity to socially-relevant information has some value in predicting social function. Therefore, the assessment of TBI persons, particularly those with adaptive behavioural problems, should be expanded to determine whether alterations in perception and reactivity to socially-relevant stimuli have occurred. When this is the case, rehabilitative strategies aimed more specifically at these difficulties should be considered.

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Vitamin D metabolites are important in the regulation of bone and calcium homeostasis, but also have a more ubiquitous role in the regulation of cell differentiation and immune function. Severely low circulating 25-dihydroxyvitamin D [25(OH)D] concentrations have been associated with the onset of active tuberculosis (TB) in immigrant populations, although the association with latent TB infection (LTBI) has not received much attention. A previous study identified the prevalence of LTBI among a sample of Mexican migrant workers enrolled in Canada's Seasonal Agricultural Workers Program (SA WP) in the Niagara Region of Ontario. The aim of the present study was to determine the vitamin D status of the same sample, and identify if a relationship existed with LTBI. Studies of vitamin D deficiency and active TB are most commonly carried out among immigrant populations to non-endemic regions, in which reactivation of LTBI has occurred. Currently, there is limited knowledge of the association between vitamin D deficiency and LTBI. Entry into Canada ensured that these individuals did not have active TB, and L TBI status was established previously by an interferon-gamma release assay (IGRA) (QuantiFERON-TB Gold In-Tube®, Cellestis Ltd., Australia). Awareness of vitamin D status may enable individuals at risk of deficiency to improve their nutritional health, and those with LTBI to be aware of this risk factor for disease. Prevalence of vitamin D insufficiency among the Mexican migrant workers was determined from serum samples collected in the summer of 2007 as part of the cross sectional LTBI study. Samples were measured for concentrations of the main circulating vitamin D metabolite, 25(OH)D, with a widely used 1251 250HD RIA (DiaSorin Inc.®, Stillwater, MN), and were categorized as deficient «37.5 nmoI/L), insufficient (>37.5 nmollL, < 80 nmol/L) or sufficient (2::80 nmoI/L). Fisher's exact tests and t tests were used to determine if vitamin D status (sufficiency or insufficiency) or 25(OH)D concentrations significantly differed by sex or age categories. Predictors of vitamin D insufficiency and 25(OH)D concentrations were taken from questionnaires carried out during the previous study, and analyzed in the present study using multiple regression prediction models. Fisher's exact test and t test was used to determine if vitamin D status or 25(OH)D concentration differed by LTBI status. Strength of the relationship between interferongamma (IFN-y) concentration (released by peripheral T cells in response to TB antigens) and 25(OH)D concentration was analyzed using a Spearman correlation. Out of 87 participants included in the study (78% male; mean age 38 years), 14 were identified as LTBI positive but none had any signs or symptoms of TB reactivation. Only 30% of the participants were vitamin D sufficient, whereas 68% were insufficient and 2% were deficient. Significant independent predictors of lower 25(OH)D concentrations were sex, number of years enrolled in the SA WP and length of stay in Canada. No significant differences were found between 25(OH)D concentrations and LTBI status. There was a significant moderate correlation between IFN-y and 25(OH)D concentrations ofLTBI-positive individuals. The majority of participants presented with Vitamin D insufficiency but none were severely deficient, indicating that 25(OH)D concentrations do not decrease dramatically in populations who temporarily reside in Canada but go back to their countries of origin during the Canadian winter. This study did not find a statistical relationship between low levels of vitamin D and LTBI which suggests that in the presence of overall good health, lower than ideal levels of 2S(OH)D, may still be exerting a protective immunological effect against LTBI reactivation. The challenge remains to determine a critical 2S(OH)D concentration at which reactivation is more likely to occur.

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Individuals who have sustained a traumatic brain injury (TBI) often complain of t roubl e sleeping and daytime fatigue but little is known about the neurophysiological underpinnings of the s e sleep difficulties. The fragile sleep of thos e with a TBI was predicted to be characterized by impairments in gating, hyperarousal and a breakdown in sleep homeostatic mechanisms. To test these hypotheses, 20 individuals with a TBI (18- 64 years old, 10 men) and 20 age-matched controls (18-61 years old, 9 men) took part in a comprehensive investigation of their sleep. While TBI participants were not recruited based on sleep complaint, the fmal sample was comprised of individuals with a variety of sleep complaints, across a range of injury severities. Rigorous screening procedures were used to reduce potential confounds (e.g., medication). Sleep and waking data were recorded with a 20-channel montage on three consecutive nights. Results showed dysregulation in sleep/wake mechanisms. The sleep of individuals with a TBI was less efficient than that of controls, as measured by sleep architecture variables. There was a clear breakdown in both spontaneous and evoked K-complexes in those with a TBI. Greater injury severities were associated with reductions in spindle density, though sleep spindles in slow wave sleep were longer for individuals with TBI than controls. Quantitative EEG revealed an impairment in sleep homeostatic mechanisms during sleep in the TBI group. As well, results showed the presence of hyper arousal based on quantitative EEG during sleep. In wakefulness, quantitative EEG showed a clear dissociation in arousal level between TBls with complaints of insomnia and TBls with daytime fatigue. In addition, ERPs indicated that the experience of hyper arousal in persons with a TBI was supported by neural evidence, particularly in wakefulness and Stage 2 sleep, and especially for those with insomnia symptoms. ERPs during sleep suggested that individuals with a TBI experienced impairments in information processing and sensory gating. Whereas neuropsychological testing and subjective data confirmed predicted deficits in the waking function of those with a TBI, particularly for those with more severe injuries, there were few group differences on laboratory computer-based tasks. Finally, the use of correlation analyses confirmed distinct sleep-wake relationships for each group. In sum, the mechanisms contributing to sleep disruption in TBI are particular to this condition, and unique neurobiological mechanisms predict the experience of insomnia versus daytime fatigue following a TBI. An understanding of how sleep becomes disrupted after a TBI is important to directing future research and neurorehabilitation.

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We examined the role of altered emotional functioning across the spectrum of injury severity (mild head injury [MHI], moderate/severe traumatic brain injury [TBI]), its implications for social behaviours, and the effect of modifying arousal and its relation to cognitive performance. In the first study (N = 230), students with self-reported MHI endorsed engaging in socially unacceptable and erratic behaviours significantly more often than did those with no MHI. We did not find significant differences between the groups in the measure of emotional intelligence (EI); however, for students who reported a MHI, scores on the EI measure significantly predicted reports of socially unacceptable behaviours such that lower scores predicted poorer social functioning, accounting for approximately 20% of the variance. Also, the experience of postconcussive symptoms was found to be significantly greater for students with MHI relative to their peers. In the second study (N = 85), we further examined emotional underarousal in terms of physiological (i.e., electrodermal activation [EDA]) and self-reported responsivity to emotionally-evocative picture stimuli. Although the valence ratings of the stimuli did not differ between students with and without MHI as we had expected, we found evidence of reduced and/or indiscriminate emotional responding to the stimuli for those with MHI which mimics that observed in other studies for persons with moderate/severe TBI. We also found that emotional underarousal followed a gradient of injury severity despite reporting a pattern of experiencing more life stressors. In the third study (N = 81), we replicated our findings of emotional underarousal for those with head trauma and also uniquely explored neuroendocrine aspects (salivary cortisol; cortisol awakening response [CAR]) and autonomic indices (EDA) of emotional dysregulation in terms of stress responsivity across the spectrum of injury severity (MHI [n = 32], moderate/severe TBI [n = 9], and age and education matched controls [n = 40]). Although the manipulation was effective in modifying arousal state in terms of autonomic and self-reported indices, we did not support our hypothesis that increased arousal would be related to improved performance on cognitive measures for those with prior injury. To our knowledge, this is the only study to examine the CAR with this population. Repeated measure analysis revealed that, upon awakening, students with no reported head trauma illustrated the typical CAR increase 45 minutes after waking, whereas, students who had a history of either mild head trauma or moderate/severe TBI demonstrated a blunted CAR. Thus, across the three studies we have provided evidence of emotional underarousal, its potential implications for social interactions, and also have identified potentially useful indices of dysregulated stress responsivity regardless of injury severity.

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Client-directed long-term rehabilitative goals and life satisfaction following head injury emphasize the importance of social inclusion, rather than cognitive or physical, outcomes. However, very little research has explored the socio-emotional factors that pose as barriers to social reintegration following injury. This study investigates social barriers following head injury (i.e., decision-making - Iowa Gambling Task [IGT] and mood – depression) and possible amelioration of those challenges (through treatment) in both highly functioning university students with and without mild head injury (MHI) and in individuals with moderate traumatic brain injury (TBI). An arousal manipulation using emotionally evocative stimuli was introduced to manipulate the subject’s physiological arousal state. Seventy-five university students (37.6% reporting a MHI) and 11 patients with documented moderate TBI were recruited to participate in this quasi-experimental study. Those with head injury were found to be physiologically underaroused (on measures of electrodermal activation [EDA] and pulse) and were less sensitive to the negative effects of punishment (i.e., losses) in the gambling task than those without head injury, with greater impairment being observed for the moderate TBI group. The arousal manipulation, while effective, was not able to maintain a higher state of arousal in the injury groups across trials (i.e., their arousal state returned to pre-manipulation levels more quickly than their non-injured cohort), and, subsequently, a performance improvement was not observed on the IGT. Lastly, head injury was found to contribute to the relationship between IGT performance and depressive symptom acknowledgment and mood status in persons with head injury. This study indicates the possible important role of physiological arousal on socio- emotional behaviours (decision-making, mood) in persons with even mild, non-complicated head injuries and across the injury severity continuum.