Articles: traumatic-brain-injuries.
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Years following the insult, patients with traumatic brain injury often experience persistent motor control problems, including bimanual coordination deficits. Previous studies revealed that such deficits are related to brain structural white and grey matter abnormalities. Here, we assessed, for the first time, cerebral functional activation patterns during bimanual movement preparation and performance in patients with traumatic brain injury, using functional magnetic resonance imaging. ⋯ Moreover, a significant interaction effect between Feedback Condition and Group in the primary motor area (bilaterally) (P < 0.001), the cerebellum (left) (P < 0.001) and caudate (left) (P < 0.05), revealed that controls showed less overlap of activation patterns accompanying the two feedback conditions than patients with traumatic brain injury (i.e. decreased neural differentiation). In sum, our findings point towards poorer predictive control in traumatic brain injury patients in comparison to controls. Moreover, irrespective of the feedback condition, overactivations were observed in traumatically brain injured patients during movement execution, pointing to more controlled processing of motor task performance.
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Guidelines suggest that Traumatic Brain Injury (TBI) related hospitalizations are best treated at Level I or II trauma centers because of continuous neurosurgical care in these settings. This population-based study examines TBI hospitalization treatment paths by age groups. ⋯ Utilization of trauma center resources for hospitalized TBIs may be low considering the established lower mortality rate associated with treatment at Level I or II trauma centers. The higher transfer rate for older adults may suggest rapid decline amid an unrecognized initial need for a trauma center care. A better understanding of hospital destination decision making is needed for patients with TBI.
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OBJECTIVE The Brain Trauma Foundation recommendation regarding the timing of surgical evacuation of epidural hematomas and subdural hematomas is to perform the procedure as soon as possible. Indeed, faster evacuation is associated with better outcome. However, to the authors' knowledge, no study has looked at where delays in intrahospital care occurred for patients suffering from traumatic intracranial mass lesions. ⋯ CONCLUSIONS A long delay until surgery still exists for patients requiring urgent mass lesion evacuation. Many factors contribute to this delay, including performing imaging and transfer to and preparation in the OR. Strategies can be implemented to reduce delays and improve the delivery of care.
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Journal of neurotrauma · Sep 2016
Detection of Growth Hormone Deficiency in Adults with Chronic Traumatic Brain Injury.
This study examined the prevalence of growth hormone deficiency (GHD) in patients with traumatic brain injury (TBI) during the post-acute phase of recovery and whether GHD was associated with increased disability, decreased independence, and depression. A secondary objective was to determine the accuracy of insulin-like growth factor-1 (IGF-1) levels in predicting GHD in patients with TBI. Anterior pituitary function was assessed in 235 adult patients with TBI through evaluation of fasting morning hormone levels. ⋯ Symptoms of depression were also more prevalent in this group. In addition, patients with severe GHD had delayed admission to post-acute rehabilitation. This study confirms the high prevalence of GHD in patients with TBI and the necessity to monitor clinical symptoms and perform provocative testing to definitively diagnose GHD.
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Neural stem cells in the adult brain possess the ability to remain quiescent until needed in tissue homeostasis or repair. It was previously shown that traumatic brain injury (TBI) stimulated neural stem cell (NSC) proliferation in the adult hippocampus, indicating an innate repair mechanism, but it is unknown how TBI promotes NSC proliferation. In the present study, we observed dramatic activation of mammalian target of rapamycin complex 1 (mTORC1) in the hippocampus of mice with TBI from controlled cortical impact (CCI). ⋯ With 5-bromo-2'-deoxyuridine labeling, we observed that TBI increased mTORC1 activation in proliferating NSCs. Furthermore, administration of rapamycin abolished TBI-promoted NSC proliferation. Taken together, these data indicate that mTORC1 activation is required for NSC proliferation postinjury, and thus might serve as a therapeutic target for interventions to augment neurogenesis for brain repair after TBI.