Journal of neurotrauma
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Sleep disruption can occur after brain injury; however, insomnia prevalence and severity in adolescents with persistent post-concussion symptoms have not been investigated. This study examined: 1) some of the psychometric properties of the Insomnia Severity Index (ISI), 2) the prevalence and severity of insomnia symptoms, and 3) associations between insomnia symptoms and clinical measures of post-concussion symptoms, mental health symptoms, and cognitive tests in adolescents with slow recovery from concussion. Participants (N = 121) were adolescents 13-18 years of age (mean = 16.2; standard deviation [SD] = 1.2) and, on average, of 6.4 months (SD = 3.8) post-concussion. ⋯ Insomnia was significantly associated with more cognitive complaints and higher rates of failure on performance validity tests, but not with actual objectively measured cognitive abilities. Insomnia is common in adolescents with slow recovery from concussion and is associated with worse post-concussion symptoms, anxiety, depression, cognitive complaints, and performance validity concerns. Investigating evidence-based treatments for insomnia should be a priority in this population.
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Blood biomarker tests were recently approved for clinical diagnosis of traumatic brain injury (TBI), yet there are still fundamental questions that need attention. One such question is the stability of putative biomarkers in blood over the course of several days after injury if the sample is unable to be processed into serum or plasma and stored at low temperatures. Blood may not be able to be stored at ultra-low temperatures in austere combat or sports environments. ⋯ The amount of time whole blood and serum were refrigerated had no significant effect on GFAP concentration in plasma obtained from whole blood and in serum (p = 0.6256 and p = 0.3687, respectively), UCH-L1 concentration in plasma obtained from whole blood and in serum (p = 0.0611 and p = 0.5189, respectively), and S100B concentration in serum (p = 0.4663). Concentration levels of GFAP, UCH-L1, and S100B in blood collected from patients with TBI were found to be stable at 4-5°C for at least 3 days after blood draw. This study suggests that the levels of the three diagnostic markers above are still valid for diagnostic TBI tests if the sample is stored in 4-5°C refrigerated conditions.
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Journal of neurotrauma · Aug 2019
Serum Neurofilament Light Is Elevated Differentially in Older Adults with Uncomplicated Mild Traumatic Brain Injuries.
Neurofilament light (NF-L) might have diagnostic and prognostic potential as a blood biomarker for mild traumatic brain injury (mTBI). However, elevated NF-L is associated with several neurological disorders associated with older age, which could confound its usefulness as a traumatic brain injury biomarker. We examined whether NF-L is elevated differentially following uncomplicated mTBI in older adults with pre-injury neurological disorders. ⋯ A high correlation was found between age and NF-L levels in the total mTBI sample (r = 0.80), within the subgroups without pre-injury neurological diseases (r = 0.76) and with pre-injury neurological diseases (r = 0.68), and in the trauma control subjects (r = 0.76). Those with mTBIs and pre-injury neurological conditions had higher NF-L levels than those with no pre-injury neurological conditions (p < 0.001, Cohen's d = 1.01). Older age and pre-injury neurological diseases are associated with elevated serum NF-L levels in patients with head trauma and in orthopedically-injured control subjects.
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Journal of neurotrauma · Aug 2019
Observational StudyParoxysmal Sympathetic Hyperactivity rate in patients in vegetative or minimally conscious state due to severe acquired brain injury evaluated by PSH assessment measure.
The rate of paroxysmal sympathetic hyperactivity (PSH) was retrospectively assessed using the Paroxysmal Sympathetic Hyperactivity-Assessment Measure (PSH-AM) scale in patients with disorders of consciousness attributed to traumatic and non-traumatic acquired brain injury during the rehabilitation phase. These results were compared with previous studies carried out in the same clinical scenario, in order to verify the prevalence of PSH signs from 1998 to 2014. The entire sample consisted of 140 patients in vegetative state/unresponsive wakefulness syndrome or minimally conscious state admitted to a neurorehabilitation subacute unit from June 2010 to December 2014. ⋯ A comparison with previous studies revealed a reduction in the number of PSH cases in traumatic patients. This study provides evidence that PSH-AM can be used prospectively to detect the rate of PSH and stratify severity of signs. Further longitudinal analysis is warranted to confirm the prevalence of PSH signs in non-traumatic brain injured patients.
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Journal of neurotrauma · Aug 2019
Diazepam Inhibits Post-Traumatic Neurogenesis and Blocks Aberrant Dendritic Development.
Traumatic brain injury (TBI) triggers a robust increase in neurogenesis within the dentate gyrus of the hippocampus, but these new neurons undergo aberrant maturation and dendritic outgrowth. Because gamma-aminobutyric acid (GABA)A receptors (GABAARs) modulate dendritic outgrowth during constitutive neurogenesis and GABAAR-modulating sedatives are often administered to human patients after TBI, we investigated whether the benzodiazepine, diazepam (DZP), alters post-injury hippocampal neurogenesis. ⋯ DZP did not reduce cortical injury, reactive gliosis, or cell proliferation early after injury, but decreased c-Fos activation in the dentate gyrus at both early and late time-points after TBI, suggesting an association between neuronal activity and post-injury neurogenesis. Because DZP blocks post-injury neurogenesis, further studies are warranted to assess whether benzodiazepines alter cognitive recovery or the development of complications after TBI.