Journal of neurotrauma
-
Journal of neurotrauma · Nov 2023
Observational StudyOptic nerve diameter on non-contrast computed tomography and intracranial hypertension in patients with acute brain injury: A validation study.
Intracranial hypertension is a feared complication of acute brain injury that can cause ischemic stroke, herniation, and death. Identifying those at risk is difficult, and the physical examination is often confounded. Given the widespread availability and use of computed tomography (CT) in patients with acute brain injury, prior work has attempted to use optic nerve diameter measurements to identify those at risk of intracranial hypertension. ⋯ When used to identify those with intracranial hypertension (> 20 mm Hg), the area under the receiver operator curve (AUROC) was 0.68. Using a previously proposed threshold of 0.6 cm, the sensitivity was 81%, specificity 43%, positive likelihood ratio 1.4, and negative likelihood ratio 0.45. CT-derived optic nerve diameter using a threshold of 0.6 cm is sensitive but not specific for intracranial hypertension, and the overall correlation is weak.
-
Journal of neurotrauma · Nov 2023
Neuropathological outcomes of traumatic brain injury and alcohol use in males and females: studies using preclinical rodent and clinical human specimens.
Traumatic brain injury (TBI) and alcohol misuse are inextricably linked and can increase the risk for development of neurodegenerative diseases, particularly in military veterans and contact sport athletes. Proteinopathy (defects in protein degradation) is considered an underlying factor in neurodegenerative diseases. Whether it contributes to TBI/alcohol-mediated neurodegeneration is unexplored, however. ⋯ We have previously demonstrated that ISGylation is increased in the LSCs of veterans with TBI/ALS (amyotrophic lateral sclerosis). Here, we show increased ISGylation of TDP-43 in the LSCs of TBI/ALS-afflicted female veterans compared with male veterans. Knowing that ISGylation induces proteinopathy, we suggest targeting ISGylation may prevent proteinopathy-mediated neurodegeneration post-TBI, particularly in women; however, causal studies are required to confirm this claim.
-
Journal of neurotrauma · Nov 2023
Mitochondrial dysfunction following repeated mild blast traumatic brain injury is attenuated by a mild mitochondrial uncoupling prodrug.
Mild traumatic brain injury (mTBI) results in impairment of brain metabolism, which is propagated by mitochondrial dysfunction in the brain. Mitochondrial dysfunction has been identified as a pathobiological therapeutic target to quell cellular dyshomeostasis. Further, therapeutic approaches targeting mitochondrial impairments, such as mild mitochondrial uncoupling, have been shown to alleviate behavioral alterations after TBI. ⋯ MP201 treatment alleviated elevated glia-enriched mitochondrial oxidative damage following rmbTBI. However, there was a lack of injury-associated differences in oxidative damage in synaptic mitochondria. Overall, our report demonstrates that rmbTBI results in mitochondrial impairment diffusely throughout the brain and mild mitochondrial uncoupling can restore mitochondrial bioenergetics and oxidative balance.
-
Journal of neurotrauma · Nov 2023
Predictors and Functional Outcomes Associated with Longitudinal Trajectories of Anxiety and Depression From 2 to 36+ Months After Moderate to Severe Traumatic Brain Injury.
This study investigated longitudinal trajectories of anxiety and depressive symptoms following moderate-severe traumatic brain injury (TBI), predictors of the trajectories, and associations with 1-year return to productivity. One hundred forty-eight patients with moderate-severe TBI were assessed at 2, 5, 12, and ≥36 months post-injury on the Beck Anxiety Inventory and the Beck Depression Inventory. Clinical interviews obtained information about demographics, injury characteristics, and 1-year return to productivity. ⋯ Those with worsening anxiety or depression were less likely to return to productivity by 1-year post-injury. There is a significant burden of anxiety (15%) and depression (20%) in the 3 years after moderate-severe TBI. Future research targeting at-risk patients may help to improve quality of life and functional recovery.
-
Journal of neurotrauma · Nov 2023
Randomized Controlled TrialIntegrating, Harmonizing, and Curating Studies with High-Frequency and Hourly Physiological Data: Proof of Concept from Seven Traumatic Brain Injury Datasets.
Research in severe traumatic brain injury (TBI) has historically been limited by studies with relatively small sample sizes that result in low power to detect small, yet clinically meaningful outcomes. Data sharing and integration from existing sources hold promise to yield larger more robust sample sizes that improve the potential signal and generalizability of important research questions. However, curation and harmonization of data of different types and of disparate provenance is challenging. ⋯ Our harmonized data set included data on 1536 patients from the Citicoline Brain Injury Treatment Trial (COBRIT), Effect of erythropoietin and transfusion threshold on neurological recovery after traumatic brain injury: a randomized clinical trial (EPO Severe TBI), BEST-TRIP, Progesterone for the Treatment of Traumatic Brain Injury III Clinical Trial (ProTECT III), Transforming Research and Clinical Knowledge in Traumatic brain Injury (TRACK-TBI), Brain Oxygen Optimization in Severe Traumatic Brain Injury Phase-II (BOOST-2), and Ben Taub General Hospital (BTGH) Research Database studies. We conclude with process recommendations for data acquisition for future prospective studies to aid integration of these data with existing studies. These recommendations include using common data elements whenever possible, a standardized recording system for labeling and timing of high-frequency physiological data, and secondary use of studies in systems such as Federal Interagency Traumatic Brain Injury Research Informatics System (FITBIR), to engage investigators who collected the original data.