Browsing by Subject "Brain Injuries"
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Item Anxiety Trajectories the First 10 Years After a Traumatic Brain Injury (TBI): A TBI Model Systems Study(Elsevier, 2022-11) Neumann, Dawn; Juengst, Shannon B.; Bombardier, Charles H.; Finn, Jacob A.; Miles, Shannon R.; Zhang, Yue; Kennedy, Richard; Rabinowitz, Amanda R.; Thomas, Amber; Dreer, Laura E.; Physical Medicine and Rehabilitation, School of MedicineObjective Determine anxiety trajectories and predictors up to 10 years posttraumatic brain injury (TBI). Design Prospective longitudinal, observational study. Setting Inpatient rehabilitation centers. Participants 2836 participants with moderate to severe TBI enrolled in the TBI Model Systems National Database who had ≥2 anxiety data collection points (N=2836). Main Outcome Measure Generalized Anxiety Disorder-7 (GAD-7) at 1, 2, 5, and 10-year follow-ups. Results Linear mixed models showed higher GAD-7 scores were associated with Black race (P<.001), public insurance (P<.001), pre-injury mental health treatment (P<.001), 2 additional TBIs with loss of consciousness (P=.003), violent injury (P=.047), and more years post-TBI (P=.023). An interaction between follow-up year and age was also related to GAD-7 scores (P=.006). A latent class mixed model identified 3 anxiety trajectories: low-stable (n=2195), high-increasing (n=289), and high-decreasing (n=352). The high-increasing and high-decreasing groups had mild or higher GAD-7 scores up to 10 years. Compared to the low-stable group, the high-decreasing group was more likely to be Black (OR=2.25), have public insurance (OR=2.13), have had pre-injury mental health treatment (OR=1.77), and have had 2 prior TBIs (OR=3.16). Conclusions A substantial minority of participants had anxiety symptoms that either increased (10%) or decreased (13%) over 10 years but never decreased below mild anxiety. Risk factors of anxiety included indicators of socioeconomic disadvantage (public insurance) and racial inequities (Black race) as well as having had pre-injury mental health treatment and 2 prior TBIs. Awareness of these risk factors may lead to identifying and proactively referring susceptible individuals to mental health services.Item Assessing Negative Attributions After Brain Injury With the Ambiguous Intentions Hostility Questionnaire(Wolters Kluwer, 2020-09) Neumann, Dawn; Sander, Angelle M.; Perkins, Susan M.; Bhamidipalli, Surya Sruthi; Witwer, Noelle; Combs, Dennis; Hammond, Flora M.; Physical Medicine and Rehabilitation, School of MedicineOBJECTIVES: (1) To explore the construct validity of the Ambiguous Intentions Hostility Questionnaire (AIHQ) in participants with traumatic brain injury (TBI) (ie, confirm negative attributions are associated with anger and aggression); and (2) use the AIHQ to examine negative attribution differences between participants with and without TBI. SETTING: Two rehabilitation hospitals. PARTICIPANTS: Eighty-five adults with TBI and 86 healthy controls (HCs). DESIGN: Cross-sectional survey. MAIN MEASURES: The AIHQ, a measure of negative attributions (intent, hostility, and blame), anger, and aggressive responses to hypothetical scenarios. RESULTS: Attributions were significantly correlated with anticipated anger and aggressive responses to AIHQ scenarios. Compared with HCs, participants with TBI reported stronger negative attributions (P ≤ .001), anger (P = .021), and aggressive responses (P = .002) to the scenarios. CONCLUSION: Negative attributions were associated with anger and aggression responses, demonstrating construct validity of the AIHQ in the TBI population. Participants with TBI judged others' behaviors more severely than HCs, similar to prior research using a different attribution measure. The AIHQ has promise as a practical instrument for assessing negative attributions after TBI.Item Clinical Practice Guideline to Improve Locomotor Function Following Chronic Stroke, Incomplete Spinal Cord Injury, and Brain Injury(Wolters Kluwer, 2020-01) Hornby, T. George; Reisman, Darcy S.; Ward, Irene G.; Scheets, Patricia L.; Miller, Allison; Haddad, David; Fox, Emily J.; Fritz, Nora E.; Hawkins, Kelly; Henderson, Christopher E.; Hendron, Kathryn L.; Holleran, Carey L.; Lynskey, James E.; Walter, Amber; Physical Medicine and Rehabilitation, School of MedicineBackground: Individuals with acute-onset central nervous system (CNS) injury, including stroke, motor incomplete spinal cord injury, or traumatic brain injury, often experience lasting locomotor deficits, as quantified by decreases in gait speed and distance walked over a specific duration (timed distance). The goal of the present clinical practice guideline was to delineate the relative efficacy of various interventions to improve walking speed and timed distance in ambulatory individuals greater than 6 months following these specific diagnoses. Methods: A systematic review of the literature published between 1995 and 2016 was performed in 4 databases for randomized controlled clinical trials focused on these specific patient populations, at least 6 months postinjury and with specific outcomes of walking speed and timed distance. For all studies, specific parameters of training interventions including frequency, intensity, time, and type were detailed as possible. Recommendations were determined on the basis of the strength of the evidence and the potential harm, risks, or costs of providing a specific training paradigm, particularly when another intervention may be available and can provide greater benefit. Results: Strong evidence indicates that clinicians should offer walking training at moderate to high intensities or virtual reality–based training to ambulatory individuals greater than 6 months following acute-onset CNS injury to improve walking speed or distance. In contrast, weak evidence suggests that strength training, circuit (ie, combined) training or cycling training at moderate to high intensities, and virtual reality–based balance training may improve walking speed and distance in these patient groups. Finally, strong evidence suggests that body weight–supported treadmill training, robotic-assisted training, or sitting/standing balance training without virtual reality should not be performed to improve walking speed or distance in ambulatory individuals greater than 6 months following acute-onset CNS injury to improve walking speed or distance. Discussion: The collective findings suggest that large amounts of task-specific (ie, locomotor) practice may be critical for improvements in walking function, although only at higher cardiovascular intensities or with augmented feedback to increase patient's engagement. Lower-intensity walking interventions or impairment-based training strategies demonstrated equivocal or limited efficacy. Limitations: As walking speed and distance were primary outcomes, the research participants included in the studies walked without substantial physical assistance. This guideline may not apply to patients with limited ambulatory function, where provision of walking training may require substantial physical assistance. Summary: The guideline suggests that task-specific walking training should be performed to improve walking speed and distance in those with acute-onset CNS injury although only at higher intensities or with augmented feedback. Future studies should clarify the potential utility of specific training parameters that lead to improved walking speed and distance in these populations in both chronic and subacute stages following injury. Disclaimer: These recommendations are intended as a guide for clinicians to optimize rehabilitation outcomes for persons with chronic stroke, incomplete spinal cord injury, and traumatic brain injury to improve walking speed and distance.Item Effects of traumatic brain injury and posttraumatic stress disorder on Alzheimer's disease in veterans, using the Alzheimer's Disease Neuroimaging Initiative(Elsevier, 2014-06) Weiner, Michael W.; Veitch, Dallas P.; Hayes, Jacqueline; Neylan, Thomas; Grafman, Jordan; Aisen, Paul S.; Petersen, Ronald C.; Jack, Clifford; Jagust, William; Trojanowski, John Q.; Shaw, Leslie M.; Saykin, Andrew J.; Green, Robert C.; Harvey, Danielle; Toga, Arthur W.; Friedl, Karl E.; Pacifico, Anthony; Sheline, Yvette; Yaffe, Kristine; Mohlenoff, Brian; Department of Medicine, IU School of MedicineBoth traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) are common problems resulting from military service, and both have been associated with increased risk of cognitive decline and dementia resulting from Alzheimer's disease (AD) or other causes. This study aims to use imaging techniques and biomarker analysis to determine whether traumatic brain injury (TBI) and/or PTSD resulting from combat or other traumas increase the risk for AD and decrease cognitive reserve in Veteran subjects, after accounting for age. Using military and Department of Veterans Affairs records, 65 Vietnam War veterans with a history of moderate or severe TBI with or without PTSD, 65 with ongoing PTSD without TBI, and 65 control subjects are being enrolled in this study at 19 sites. The study aims to select subject groups that are comparable in age, gender, ethnicity, and education. Subjects with mild cognitive impairment (MCI) or dementia are being excluded. However, a new study just beginning, and similar in size, will study subjects with TBI, subjects with PTSD, and control subjects with MCI. Baseline measurements of cognition, function, blood, and cerebrospinal fluid biomarkers; magnetic resonance images (structural, diffusion tensor, and resting state blood-level oxygen dependent (BOLD) functional magnetic resonance imaging); and amyloid positron emission tomographic (PET) images with florbetapir are being obtained. One-year follow-up measurements will be collected for most of the baseline procedures, with the exception of the lumbar puncture, the PET imaging, and apolipoprotein E genotyping. To date, 19 subjects with TBI only, 46 with PTSD only, and 15 with TBI and PTSD have been recruited and referred to 13 clinics to undergo the study protocol. It is expected that cohorts will be fully recruited by October 2014. This study is a first step toward the design and statistical powering of an AD prevention trial using at-risk veterans as subjects, and provides the basis for a larger, more comprehensive study of dementia risk factors in veterans.Item The HMGB1-RAGE axis mediates traumatic brain injury-induced pulmonary dysfunction in lung transplantation(American Association for the Advancement of Science, 2014-09-03) Weber, Daniel J.; Gracon, Adam S.A.; Ripsch, Matthew S.; Fisher, Amanda J.; Cheon, Bo M.; Pandya, Pankita H.; Vittal, Ragini; Capitano, Maegan L.; Kim, Youngsong; Allete, Yohance M.; Riley, Amanda A.; McCarthy, Brian P.; Territo, Paul R.; Hutchins, Gary D.; Broxmeyer, Hal E.; Sandusky, George E.; White, Fletcher A.; Wilkes, David S.; Medicine, School of MedicineTraumatic brain injury (TBI) results in systemic inflammatory responses that affect the lung. This is especially critical in the setting of lung transplantation, where more than half of donor allografts are obtained postmortem from individuals with TBI. The mechanism by which TBI causes pulmonary dysfunction remains unclear but may involve the interaction of high-mobility group box-1 (HMGB1) protein with the receptor for advanced glycation end products (RAGE). To investigate the role of HMGB1 and RAGE in TBI-induced lung dysfunction, RAGE-sufficient (wild-type) or RAGE-deficient (RAGE(-/-)) C57BL/6 mice were subjected to TBI through controlled cortical impact and studied for cardiopulmonary injury. Compared to control animals, TBI induced systemic hypoxia, acute lung injury, pulmonary neutrophilia, and decreased compliance (a measure of the lungs' ability to expand), all of which were attenuated in RAGE(-/-) mice. Neutralizing systemic HMGB1 induced by TBI reversed hypoxia and improved lung compliance. Compared to wild-type donors, lungs from RAGE(-/-) TBI donors did not develop acute lung injury after transplantation. In a study of clinical transplantation, elevated systemic HMGB1 in donors correlated with impaired systemic oxygenation of the donor lung before transplantation and predicted impaired oxygenation after transplantation. These data suggest that the HMGB1-RAGE axis plays a role in the mechanism by which TBI induces lung dysfunction and that targeting this pathway before transplant may improve recipient outcomes after lung transplantation.Item Incretin mimetics as pharmacological tools to elucidate and as a new drug strategy to treat traumatic brain injury(Elsevier, 2014-02) Greig, Nigel H.; Tweedie, David; Rachmany, Lital; Li, Yazhou; Rubovitch, Vardit; Schreiber, Shaul; Chiang, Yung-Hsiao; Hoffer, Barry J.; Miller, Jonathan; Lahiri, Debomoy K.; Sambamurti, Kumar; Becker, Robert E.; Pick, Chaim G.; Department of Psychiatry, IU School of MedicineTraumatic brain injury (TBI), either as an isolated injury or in conjunction with other injuries, is an increasingly common occurring event. An estimated 1.7 million injuries occur within the US each year and 10 million people are affected annually worldwide. Indeed, some one-third (30.5%) of all injury-related deaths in the U.S. are associated with TBI, which will soon outstrip many common diseases as the major cause of death and disability. Associated with a high morbidity and mortality, and no specific therapeutic treatment, TBI has become a pressing public health and medical problem. The highest incidence of TBI occurs among young adults (15 to 24 years age) as well as in the elderly (75 years and older) who are particularly vulnerable as injury, often associated with falls, carries an increased mortality and worse functional outcome following lower initial injury severity. Added to this, a new and growing form of TBI, blast injury, associated with the detonation of improvised explosive devices in the war theaters of Iraq and Afghanistan, are inflicting a wave of unique casualties of immediate impact to both military personnel and civilians, for which long-term consequences remain unknown and may potentially be catastrophic. The neuropathology underpinning head injury is becoming increasingly better understood. Depending on severity, TBI induces immediate neuropathological effects that for the mildest form may be transient but with increasing severity cause cumulative neural damage and degeneration. Even with mild TBI, which represents the majority of cases, a broad spectrum of neurological deficits, including cognitive impairments, can manifest that may significantly influence quality of life. In addition, TBI can act as a conduit to longer-term neurodegenerative disorders. Prior studies of glucagon-like peptide-1 (GLP-1) and long-acting GLP-1 receptor agonists have demonstrated neurotrophic/neuroprotective activities across a broad spectrum of cellular and animal models of chronic neurodegenerative (Alzheimer's and Parkinson's diseases) and acute cerebrovascular (stroke) disorders. In line with the commonality in mechanisms underpinning these disorders as well as TBI, the current article reviews this literature and recent studies assessing GLP-1 receptor agonists as a potential treatment strategy for mild to moderate TBI.Item Long-term survival after traumatic brain injury: a population-based analysis controlled for nonhead trauma(Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins, 2014-01) Brown, Allen W.; Leibson, Cynthia L.; Mandrekar, Jay; Ransom, Jeanine E.; Malec, James F.; Department of Physical Medicine and Rehabilitation, IU School of MedicineOBJECTIVE: To examine the contribution of co-occurring nonhead injuries to hazard of death after traumatic brain injury (TBI). PARTICIPANTS: A random sample of Olmsted County, Minnesota, residents with confirmed TBI from 1987 through 1999 was identified. DESIGN: Each case was assigned an age- and sex-matched, non-TBI "regular control" from the population. For "special cases" with accompanying nonhead injuries, 2 matched "special controls" with nonhead injuries of similar severity were assigned. MEASURES: Vital status was followed from baseline (ie, injury date for cases, comparable dates for controls) through 2008. Cases were compared first with regular controls and second with regular or special controls, depending on case type. RESULTS: In total, 1257 cases were identified (including 221 special cases). For both cases versus regular controls and cases versus regular or special controls, the hazard ratio was increased from baseline to 6 months (10.82 [2.86-40.89] and 7.13 [3.10-16.39], respectively) and from baseline through study end (2.92 [1.74-4.91] and 1.48 [1.09-2.02], respectively). Among 6-month survivors, the hazard ratio was increased for cases versus regular controls (1.43 [1.06-2.15]) but not for cases versus regular or special controls (1.05 [0.80-1.38]). CONCLUSIONS: Among 6-month survivors, accounting for nonhead injuries resulted in a nonsignificant effect of TBI on long-term mortality.Item The Small-Molecule TrkB Agonist 7, 8-Dihydroxyflavone Decreases Hippocampal Newborn Neuron Death After Traumatic Brain Injury(Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins, 2015-06) Chen, Liang; Gao, Xiang; Zhao, Shu; Hu, Weipeng; Chen, Jinhui; Department of Neurological Surgery, IU School of MedicinePrevious studies in rodents have shown that after a moderate traumatic brain injury (TBI) with a controlled cortical impact (CCI) device, the adult-born immature granular neurons in the dentate gyrus are the most vulnerable cell type in the hippocampus. There is no effective approach for preventing immature neuron death after TBI. We found that tyrosine-related kinase B (TrkB), a receptor of brain-derived neurotrophic factor (BDNF), is highly expressed in adult-born immature neurons. We determined that the small molecule imitating BDNF, 7, 8-dihydroxyflavone (DHF), increased phosphorylation of TrkB in immature neurons both in vitro and in vivo. Pretreatment with DHF protected immature neurons from excitotoxicity-mediated death in vitro, and systemic administration of DHF before moderate CCI injury reduced the death of adult-born immature neurons in the hippocampus 24 hours after injury. By contrast, inhibiting BDNF signaling using the TrkB antagonist ANA12 attenuated the neuroprotective effects of DHF. These data indicate that DHF may be a promising chemical compound that promotes immature neuron survival after TBI through activation of the BDNF signaling pathway.