Journal of neurotrauma
-
Journal of neurotrauma · Apr 2017
Longitudinal Study of Postconcussion Syndrome: Not Everyone Recovers.
We examined recovery from postconcussion syndrome (PCS) in a series of 285 patients diagnosed with concussion based on international sport concussion criteria who received a questionnaire regarding recovery. Of 141 respondents, those with postconcussion symptoms lasting less than 3 months, a positive computed tomography (CT) and/or magnetic resonance imaging (MRI), litigants, and known Test of Memory Malingering (TOMM)-positive cases were excluded, leaving 110 eligible respondents. We found that only 27% of our population eventually recovered and 67% of those who recovered did so within the first year. ⋯ PCS may be permanent if recovery has not occurred by 3 years. Symptoms appear in a predictable order, and each additional PCS symptom reduces recovery rate by 20%. More long-term follow-up studies are needed to examine recovery from PCS.
-
Journal of neurotrauma · Apr 2017
Natural History of Headache Five Years after Traumatic Brain Injury.
Headache is one of the most frequently reported symptoms following traumatic brain injury (TBI). Little is known about how these headaches change over time. We describe the natural history of headache in individuals with moderate to severe TBI over 5 years after injury. ⋯ More than half of classifiable headaches matched the profile of migraine or probable migraine. Headache is a substantial problem after TBI. Results suggest that ongoing assessment and treatment of headache after TBI is needed, as this symptom may be a problem up to 5 years post-injury.
-
Journal of neurotrauma · Apr 2017
Acute or delayed treatment with anatabine improves spatial memory and reduces pathological sequelae at chronic timepoints after repetitive mild TBI.
Traumatic brain injury (TBI) has chronic and long-term consequences for which there are currently no approved pharmacological treatments. We have previously characterized the chronic neurobehavioral and pathological sequelae of a mouse model of repetitive mild TBI (r-mTBI) through to 2 years post-TBI. Despite the mild nature of the initial insult, secondary injury processes are initiated that involve neuroinflammatory and neurodegenerative pathways persisting and progressing for weeks and months post-injury and providing a potential window of opportunity for therapeutic intervention. ⋯ Nine months following crossover the remaining mice showed no effect of injury on their spatial memory, and whereas pathological analysis showed improvements in mice that had received delayed treatment, corpus callosum IBA1 increased in post-crossover placebo r-mTBI mice. These data demonstrate efficacy of both early and late initiation of treatment with anatabine in improving long term behavioral and pathology outcomes after mild TBI. Future studies will characterize the treatment window, the time course of treatment needed, and the dose needed to achieve therapeutic levels of anatabine in humans after injury.
-
Journal of neurotrauma · Apr 2017
D-cycloserine restores experience-dependent neuroplasticity after TBI in the developing rat brain.
Traumatic brain injury (TBI) in children can cause persisting cognitive and behavioral dysfunction, and inevitably raises concerns about lost potential in these injured youth. Lateral fluid percussion injury (FPI) in weanling rats pathologically affects hippocampal N-methyl-d-aspartate receptor (NMDAR)- and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated glutamatergic neurotransmission subacutely within the first post-injury week. FPI to weanling rats has also been shown to impair enriched-environment (EE) induced enhancement of Morris water maze (MWM) learning and memory in adulthood. ⋯ EE significantly improved MWM performance in shams, regardless of treatment. In contrast, FPI-EE-Sal animals only performed to the level of standard housed animals, whereas FPI-EE-DCS animals were comparable with sham-EE counterparts. This study shows that NMDAR agonist use during reduced glutamatergic transmission after developmental TBI can reinstate early molecular and behavioral responses that subsequently manifest in experience-dependent plasticity and rescued potential.