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Browsing by Subject "Brain Injuries, Traumatic"
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Item Demographic and Mental Health Predictors of Arrests Up to 10 Years Post-Traumatic Brain Injury: A Veterans Affairs TBI Model Systems Study(Wolters Kluwer, 2021-07) Miles, Shannon R.; Silva, Marc A.; Neumann, Dawn; Dillahunt-Aspillaga, Christina; Corrigan, John D.; Tang, Xinyu; Eapen, Blessen C.; Nakase-Richardson, Risa; Physical Medicine and Rehabilitation, School of MedicineOBJECTIVE: Examine rates and predictors of arrests in Veterans and Service Members (V/SM) who received inpatient rehabilitation for traumatic brain injury (TBI). SETTING: Veterans Administration (VA) Polytrauma Rehabilitation Centers. PARTICIPANTS: A total of 948 V/SM drawn from the VA TBI Model Systems cohort with arrest data up to 10 years post-TBI. DESIGN: Longitudinal cohort study; secondary analysis of pre-TBI characteristics predicting post-TBI arrests. MAIN MEASURES: Disclosure of arrests pre-TBI and up to10 years post-TBI. RESULTS: Thirty-six percent of the sample had been arrested prior to their TBI; 7% were arrested post-TBI. When considering all variables simultaneously in a multivariate model, pre-TBI mental health treatment (adjusted odds ratio [aOR] = 4.30; 95% confidence interval [CI]: 2.03-9.14), pre-TBI heavy alcohol use (aOR = 3.04; CI: 1.08-8.55), and number of follow-up interviews (aOR = 2.05; CI: 1.39-4.50) were significant predictors of post-TBI arrest. CONCLUSION: Arrest rates of V/SM prior to TBI were consistent with rates of arrest for people of similar ages in the United States. Post-TBI rates were lower for V/SM than published rates of post-TBI arrests in civilians with TBI. As part of rehabilitation planning for V/SM with TBI, providers should assess for preinjury mental health services and alcohol misuse to (1) identify those who may be at risk for postinjury arrests and (2) provide relevant resources and/or supports.Item The Minimal Clinically Important Difference for the Mayo-Portland Adaptability Inventory(Wolters Kluwer, 2017-07) Malec, James F.; Kean, Jacob; Monahan, Patrick O.; Physical Medicine and Rehabilitation, School of MedicineOBJECTIVES: To determine the Minimal Clinically Important Difference (MCID) and Robust Clinically Important Difference (RCID) of the Mayo-Portland Adaptability Inventory-4 (MPAI-4) as measures of response to intervention. METHODS: Retrospective analysis of existing data. Both distribution- and anchor-based methods were used to triangulate on the MCID and to identify a moderate, that is, more robust, level of change (RCID) for the MPAI-4. These were further evaluated with respect to clinical provider ratings. PARTICIPANTS: Data for individuals with acquired brain injury in rehabilitation programs throughout the United States in the OutcomeInfo Database (n = 3087) with 2 MPAI-4 ratings. MAIN MEASURES: MPAI-4, Supervision Rating Scale, Clinician Rating of Global Clinical Improvement. RESULTS: Initial analyses suggested 5 T-score points (5T) as the MCID and 9T as the RCID. Eighty-one percent to 87% of clinical raters considered a 5T change and 99% considered a 9T change to indicate meaningful improvement. CONCLUSIONS: 5T represents the MCID for the MPAI-4 and 9T, the RCID. Both values are notably less than the Reliable Change Index (RCI). While the RCI indicates change with a high level of statistical confidence, it may be insensitive to change that is considered meaningful by providers and participants as indicated by the MCID.Item Randomized Placebo-Controlled Trial of Methylphenidate or Galantamine for Persistent Emotional and Cognitive Symptoms Associated with PTSD and/or Traumatic Brain Injury(Nature Publishing Group, 2016-04) McAllister, Thomas W.; Zafonte, Ross; Jain, Sonia; Flashman, Laura A.; George, Mark S.; Grant, Gerald A.; He, Feng; Lohr, James B.; Andaluz, Norberto; Summerall, Lanier; Paulus, Martin P.; Raman, Rema; Stein, Murray B.; Department of Psychiatry, School of MedicineWe report findings from a 12-week randomized double-blinded placebo-controlled trial of methylphenidate or galantamine to treat emotional and cognitive complaints in individuals (n=32) with a history of PTSD, TBI, or both conditions. In this small pilot study, methylphenidate treatment was associated with clinically meaningful and statistically significant improvement compared with placebo on the primary outcome, a measure of cognitive complaints (Ruff Neurobehavioral Inventory-Postmorbid Cognitive Scale), as well as on the secondary outcomes reflecting post-concussive (Rivermead Post Concussive Symptom Questionnaire) and post-traumatic stress symptoms (Posttraumatic Stress Disorder Checklist). Treatment was well tolerated. These results suggest the need for a larger RCT to replicate and confirm these findings. Design considerations for such a trial should include the need for multiple sites to facilitate adequate recruitment and extension of the treatment and follow-up periods.Item Traumatic Brain Injury Severity Affects Neurogenesis in Adult Mouse Hippocampus(Mary Ann Liebert, 2016-04-15) Wang, Xiaoting; Gao, Xiang; Michalski, Stephanie; Zhao, Shu; Chen, Jinhui; Department of Neurological Surgery, School of MedicineTraumatic brain injury (TBI) has been proven to enhance neural stem cell (NSC) proliferation in the hippocampal dentate gyrus. However, various groups have reported contradictory results on whether TBI increases neurogenesis, partially due to a wide range in the severities of injuries seen with different TBI models. To address whether the severity of TBI affects neurogenesis in the injured brain, we assessed neurogenesis in mouse brains receiving different severities of controlled cortical impact (CCI) with the same injury device. The mice were subjected to mild, moderate, or severe TBI by a CCI device. The effects of TBI severity on neurogenesis were evaluated at three stages: NSC proliferation, immature neurons, and newly-generated mature neurons. The results showed that mild TBI did not affect neurogenesis at any of the three stages. Moderate TBI promoted NSC proliferation without increasing neurogenesis. Severe TBI increased neurogenesis at all three stages. Our data suggest that the severity of injury affects adult neurogenesis in the hippocampus, and thus it may partially explain the inconsistent results of different groups regarding neurogenesis following TBI. Further understanding the mechanism of TBI-induced neurogenesis may provide a potential approach for using endogenous NSCs to protect against neuronal loss after trauma.