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
Cortical Neuromodulation of Remote Regions after Experimental Traumatic Brain Injury Normalizes Forelimb Function but is Temporally Dependent.
Traumatic brain injury (TBI) results in well-known, significant alterations in structural and functional connectivity. Although this is especially likely to occur in areas of pathology, deficits in function to and from remotely connected brain areas, or diaschisis, also occur as a consequence to local deficits. As a result, consideration of the network wiring of the brain may be required to design the most efficacious rehabilitation therapy to target specific functional networks to improve outcome. ⋯ However, by conducting temporary contralesional cortex silencing in the same injured rats at 4 weeks post-injury, injury-affected limb function either remains unaffected and deficient or is worsened, indicating that circuit modifications are more permanently controlled or at least influenced by the contralesional cortex at extended post-injury times. We provide functional magnetic resonance imaging (MRI) evidence of the neuromodulatory effect of muscimol on forelimb-evoked function in the cortex. We discuss these findings in light of known changes in cortical connectivity and excitability that occur in this injury model, and postulate a mechanism to explain these findings.
-
Journal of neurotrauma · Mar 2019
Observational StudyNon-Invasive Pressure Reactivity Index Using Doppler Systolic Flow Parameters: A Pilot Analysis.
The goal was to predict pressure reactivity index (PRx) using non-invasive transcranial Doppler (TCD) based indices of cerebrovascular reactivity, systolic flow index (Sx_a), and mean flow index (Mx_a). Continuous extended duration time series recordings of middle cerebral artery cerebral blood flow velocity (CBFV) were obtained using robotic TCD in parallel with direct intracranial pressure (ICP). PRx, Sx_a, and Mx_a were derived from high frequency archived signals. ⋯ With application of ARIMA and LME modeling, it is possible to predict PRx using non-invasive TCD measures. These are the first and as well as being preliminary attempts at doing so. Much further work is required.
-
Journal of neurotrauma · Feb 2019
Immune Response Mediates Cardiac Dysfunction after Traumatic Brain Injury.
Cardiovascular complications are common after traumatic brain injury (TBI) and are associated with increased morbidity and mortality. In this study, we investigated the possible role of the immune system in mediating cardiac dysfunction post-TBI in mice. Adult male C57BL/6J mice were subjected to a TBI model of controlled cortical impact (CCI) with or without splenectomy (n = 20/group). ⋯ TBI induces immune cell infiltration and inflammatory factor expression in the heart as well as cardiac dysfunction. Splenectomy decreases heart inflammation and improves cardiac function after TBI. Immune response may contribute to TBI-induced cardiac dysfunction.
-
Journal of neurotrauma · Feb 2019
Estradiol to Androstenedione Ratios Moderate the Relationship between Neurological Injury Severity and Mortality Risk after Severe Traumatic Brain Injury.
Early declines in gonadotropin production, despite elevated serum estradiol, among some individuals with severe traumatic brain injury (TBI) suggests amplified systemic aromatization occurs post-injury. Our previous work identifies estradiol (E2) as a potent mortality marker. Androstenedione (A), a metabolic precursor to E2, estrone (E1), and testosterone (T), is a steroid hormone substrate for aromatization that has not been explored previously as a biomarker in TBI. ⋯ Multivariable Cox regression showed a significant E2:A*GCS interaction (p = 0.0129), wherein GCS predicted mortality only among those in the low aromatization group. E2:A may be a useful mortality biomarker representing enhanced aromatization after TBI. E2:A ratios may represent non-neurological organ dysfunction after TBI and may be useful in defining injury subgroups in which GCS has variable capacity to serve as an accurate early prognostic marker.