Journal of neurotrauma
-
Journal of neurotrauma · Jun 2021
Hippocampal-Dependent Cognitive Dysfunction Following Repeated Diffuse Rotational Brain Injury in Male and Female Mice.
Cognitive dysfunction is a common, often long-term complaint following acquired traumatic brain injury (TBI). Cognitive deficits suggest dysfunction in hippocampal circuits. The goal of the studies described here is to phenotype in both male and female mice the hippocampal-dependent learning and memory deficits resulting from TBI sustained by the Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA) device-a model that delivers both a contact-concussion injury as well as unrestrained rotational head movement. ⋯ Pathologically, the injury was characterized by white matter damage as observed by silver staining and glial fibrillary acidic protein (astrogliosis) in the optic tracts, with milder damage seen in the corpus callosum, and fimbria and brainstem (cerebral peduncles) of some animals. No changes in the density of GABAergic parvalbumin-expressing cells in the hippocampus, amygdala, or parietal cortex were found. This experiment confirmed significant sexually dimorphic cognitive impairments following a repeated, diffuse brain injury.
-
Journal of neurotrauma · Jun 2021
Acid-ion sensing channel 1a deletion reduces chronic brain damage and neurological deficits after experimental traumatic brain injury.
Traumatic brain injury (TBI) causes long-lasting neurodegeneration and cognitive impairments; however, the underlying mechanisms of these processes are not fully understood. Acid-sensing ion channels 1a (ASIC1a) are voltage-gated Na+- and Ca2+-channels shown to be involved in neuronal cell death; however, their role for chronic post-traumatic brain damage is largely unknown. To address this issue, we used ASIC1a-deficient mice and investigated their outcome up to 6 months after TBI. ⋯ Microglial activation was significantly reduced in ASIC1a-/- mice. In conclusion, ASIC1a deficiency resulted in reduced edema formation acutely after TBI and less brain damage, functional impairments, and neuroinflammation up to 6 months after injury. Hence, ASIC1a seems to be involved in chronic neurodegeneration after TBI.
-
Journal of neurotrauma · Jun 2021
Unexpected findings from a pilot study on vision training as a potential intervention to reduce sub-concussive head impacts during a collegiate ice hockey season.
Player-to-player contact is the most frequent head impact mechanism in collegiate ice hockey. Training with three-dimensional multiple-object tracking (3D-MOT) could potentially reduce the quantity and severity of head impacts by enhancing player anticipation of these impacts. The purpose of this study was to evaluate the efficacy of 3D-MOT training to reduce the numbers of head impacts sustained by National Collegiate Athletic Association Division III men's and women's ice hockey players. ⋯ Conversely, 3D-MOT defensemen sustained head impacts with a mean peak rotational velocity less than that of C defensemen (3D-MOT = 11.54 ± 6.76 rad.sec-1; C = 13.65 ± 8.43 rad.sec-1). There was no significant difference for all other parameters analyzed between 3D-MOT and C groups. Player position may play an important role in future interventions to reduce head impacts in collegiate ice hockey.
-
Journal of neurotrauma · Jun 2021
Meta AnalysisThe effect of growth hormone on neuropsychological outcomes and quality of life of patients with traumatic brain injury: a systematic review.
One of the most devastating chronic consequences of traumatic brain injury (TBI) is cognitive impairment. One of the possible underlying causes is growth hormone deficiency (GHD) caused by TBI-induced hypopituitarism. Currently, TBI patients are not routinely screened for pituitary function, and there are no standard therapies when GHD is diagnosed. ⋯ After TBI, regardless of GCS, 6-12 months of GH therapy, started in the chronic phase post-TBI, induced a moderate improvement in processing speed and memory capacities, decreased the severity of depression, and led to a marked improvement in quality of life. Limitations include the relatively low number of patients involved and the divergent neuropsychological tests used. These results indicate the need for further multi-centric controlled studies to substantiate the use of GH replacement therapy as a potential tool to alleviate TBI-related cognitive impairment and improve quality of life.
-
Journal of neurotrauma · Jun 2021
Serum neuron-specific enolase levels associated with connectivity alterations in anterior default mode network after mild traumatic brain injury.
Mild traumatic brain injury (mTBI) is the most prevalent neurological insult and leads to long-lasting cognitive impairment. Neuroimaging studies have discovered abnormalities in brain network connectivity following mTBI as the underlying neural basis of cognitive deficits. However, the pathophysiologic mechanisms involved in imaging alterations remain elusive. ⋯ In addition, efficiency and degree centrality of anterior DMN were negatively associated with working memory. Our study showed neuronal injury was associated with alterations in brain network connectivity after mTBI. These findings can facilitate capability to predict the brain functional outcomes and cognitive recovery in mTBI.