Traumatic brain injury (TBI) affects 3.2 to 5.3 million persons in the United States (U.S.), and the impact in the U.S. military is proportionally higher. Consensus is lacking regarding an accepted outcome to measure the effectiveness of interventions to improve the symptoms associated with TBI, and no standard-of-care treatment exists for mild TBI (mTBI). A recent literature review evaluated hyperbaric oxygen therapy (HBO₂) interventions, and findings were mixed. We conducted a systematic review of non-HBO₂ mTBI interventional trials published in 2005-2015 in military and civilian populations. A total of 154 abstracts, seven randomized controlled trials (RCTs) and five pilot studies were reviewed. RCTs were evaluated using Consolidated Standards of Reporting Trials criteria. Results indicated that studies published within the period of review were small pilot studies for rehabilitation therapy and motion capture or virtual reality gaming interventions. Neuropsychological assessments were commonly specified outcomes, and most studies included a combination of symptom and neuropsychological assessments. Findings indicated a lack of large-scale, well-controlled trials to address the symptoms and sequelae of this condition, but results of small exploratory studies show evidence of potentially promising interventions.
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Neurourol Urodyn
January 2025
Department of Neurology, Hochzirl Hospital, Zirl, Austria.
Introduction: Neurogenic bladder dysfunction is a prevalent condition characterized by impaired bladder control resulting from neurological conditions, for example, spinal cord injury or traumatic brain injury (TBI). Detrusor overactivity is a typical symptom of central nervous system damage. A lesion affecting the pontine neural network typically results in loss of tonic inhibition exerted by the pontine micturition center and causes involuntary detrusor contractions.
View Article and Find Full Text PDFJ Zhejiang Univ Sci B
July 2024
Department of Psychiatry, the First Affiliated Hospital, Zhejiang University School of Medicine; Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou 310003, China.
Acute stress disorder (ASD) is a transient psychiatric disorder that may arise subsequent to abrupt, extreme trauma exposure, and serves as a reliable indicator for the subsequent development of posttraumatic stress disorder (PTSD) (Bryant, 2011; Battle, 2013). It exhibits rapid progression in the aftermath of trauma and persists for a duration of days or weeks (not exceeding one month), manifesting symptoms of dissociation, re-experiencing, avoidance, and hyperarousal (Bielas et al., 2018).
View Article and Find Full Text PDFClin Neuropsychol
January 2025
Department of Internal Medicine (Pulmonary, Critical Care, and Sleep Medicine Division), University of South Florida, Tampa, FL, USA.
Obstructive sleep apnea (OSA) has been associated with structural and functional brain changes and cognitive impairment in sleep clinic samples. Persons with traumatic brain injury (TBI) are at increased risk of OSA compared to community samples, and many experience chronic cognitive disability. However, the impact of OSA on cognitive outcome after TBI is unknown.
View Article and Find Full Text PDFCrit Care
January 2025
Department of Critical Care Medicine, Cumming School of Medicine, Health Research Innovation Center (HRIC), University of Calgary, Room 4C64, 3280 Hospital Drive N.W., Calgary, AB, T2N 4Z6, Canada.
Background: Traumatic brain injury (TBI) is a major public health concern worldwide, contributing to high rates of injury-related death and disability. Severe traumatic brain injury (sTBI), although it accounts for only 10% of all TBI cases, results in a mortality rate of 30-40% and a significant burden of disability in those that survive. This study explored the potential of metabolomics in the diagnosis of sTBI and explored the potential of metabolomics to examine probable primary and secondary brain injury in sTBI.
View Article and Find Full Text PDFNature
January 2025
Department of Physiology and Biophysics, University of California, Irvine, Irvine, CA, USA.
The zeta inhibitory peptide (ZIP) interferes with memory maintenance and long-term potentiation (LTP) when administered to mice. However, mice lacking its putative target, protein kinase PKMζ, exhibit normal learning and memory as well as LTP, making the mechanism of ZIP unclear. Here we show that ZIP disrupts LTP by removing surface AMPA receptors through its cationic charge alone.
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