Journal of neurotrauma
-
Journal of neurotrauma · Mar 2019
Blast Exposure Impairs Sensory Gating: Evidence from Measures of Acoustic Startle and Auditory Event-Related Potentials.
Many military service members and veterans who have been exposed to high-intensity blast waves experience traumatic brain injury (TBI), resulting in chronic auditory deficits despite normal hearing sensitivity. The current study sought to examine the neurological cause of this chronic dysfunction by testing the hypothesis that blast exposure leads to impaired filtering of sensory information at brainstem and early cortical levels. Groups of blast-exposed and non-blast-exposed participants completed self-report measures of auditory and neurobehavioral status, auditory perceptual tasks involving degraded and competing speech stimuli, and physiological measures of sensory gating, including pre-pulse inhibition and habituation of the acoustic startle reflex and electrophysiological assessment of a paired-click sensory gating paradigm. ⋯ Multiple linear regression analyses revealed that poorer sensory gating at the cortical level was primarily influenced by a diagnosis of TBI, whereas reduced habituation was primarily influenced by a diagnosis of post-traumatic stress disorder. A statistical model was created including cortical sensory gating and habituation to acoustic startle, which strongly predicted performance on a degraded speech task. These results support the hypothesis that blast exposure impairs central auditory processing via impairment of neural mechanisms underlying habituation and sensory gating.
-
Journal of neurotrauma · Mar 2019
Development of a Model of Hemispheric Hypodensity ("Big Black Brain").
Subdural hematoma (SDH) is the most common finding after abusive head trauma (AHT). Hemispheric hypodensity (HH) is a radiological indicator of severe brain damage that encompasses multiple vascular territories, and may develop in the hemisphere(s) underlying the SDH. In some instances where the SDH is predominantly unilateral, the widespread damage is unilateral underlying the SDH. ⋯ Pathological examination revealed a hypoxic-ischemic injury-type pattern with vasogenic edema through much of the cortical ribbon with relative sparing of deep gray matter. The percentage of the hemisphere that was damaged was greater on the ipsilateral versus contralateral side and was positively correlated with SDH area and estimated seizure duration. Further studies are needed to parse out the pathophysiology of this injury and to determine if multiple injuries and insults act synergistically to induce a metabolic mismatch or if the mechanism of trauma induces severe seizures that drive this distinctive pattern of injury.
-
Journal of neurotrauma · Mar 2019
Cerebral Glucose Metabolism in Patients with Chronic Mental and Cognitive Sequelae after a Single Blunt Mild Traumatic Brain Injury without Visible Brain Lesions.
The aim of this study is to investigate glucose uptake on 18F-fluorodeoxyglucose positron emission tomography positron emission tomography (FDG-PET) in patients with chronic mental and cognitive symptoms following a single blunt mild traumatic brain injury (TBI) and without visible brain lesions on computed tomography (CT)/magnetic resonance imaging (MRI). Eighty-nine consecutive patients (mean age 43.8 ± 10.75 years) who had a single blunt mild TBI from a traffic accident and suffering from chronic mental and cognitive symptoms without visible brain lesions on CT/MRI were enrolled in the study. Patients underwent FDG-PET imaging, and the mean interval between the TBI and FDG-PET was 50.0 months. ⋯ Glucose uptake was significantly decreased in the bilateral prefrontal area and significantly increased around the limbic system in the patient group compared with normal controls. This topographical pattern of glucose uptake is different from that reported previously in patients with diffuse axonal injury (DAI), but may be similar to that seen in patients with major depression disorder. These results suggest that the pathological mechanism causing chronic mental and cognitive symptoms in patients with a single blunt mild TBI and without visible brain lesions might be different from that due to primary axonopathy in patients with DAI.
-
Journal of neurotrauma · Mar 2019
Multicenter StudyPredicting Psychological Distress after Pediatric Concussion.
A significant proportion of children and adolescents report psychological distress following concussion, but little is known about the predictors of these problems. The purpose of this study was to examine predictive factors of psychological distress following pediatric concussion. It was hypothesized that the presence of pre-injury psychological distress would be the strongest predictor of psychological distress post-concussion, with other demographic and acute injury factors adding incrementally to prediction. ⋯ A pre-injury diagnosis of anxiety and acutely forgetting recent information were significant predictors of psychological distress at 4 weeks, whereas worse acute orientation assessment in the ED predicted psychological distress at 12 weeks. Nearly one of four youth experienced psychological distress after concussion. Clinicians in acute care settings should screen for the factors (pre-injury anxiety, acute mental status) associated with post-injury psychological distress and consider proactively referring patients for further assistance.
-
Journal of neurotrauma · Mar 2019
Outcomes of Subjective Sleep-Wake Disturbances Twenty Years after Traumatic Brain Injury in Childhood.
Sleep-wake disturbances (SWD) are frequent following traumatic brain injury (TBI) in childhood. However, outcomes of SWD following transition into young adulthood remain unknown. This study investigated prevalence and factors associated with subjective sleep quality, insomnia, and excessive daytime sleepiness in young adults with a history of childhood TBI. ⋯ Poor sleep quality in young adults with TBI was associated with high levels of anxiety and pain, and pain was also associated with higher risk of insomnia and excessive daytime sleepiness. Our findings indicate that sustaining TBI in childhood can increase risk of SWD in young adulthood, particularly following moderate TBI. Routine assessments and treatment of SWD, as well as anxiety and pain in children with TBI, should therefore continue into adulthood.