Journal of neurotrauma
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Journal of neurotrauma · Jan 2016
Traumatic Brain Injury Impairs SNARE Complex Formation and Alters Synaptic Vesicle Distribution in the Hippocampus.
Traumatic brain injury (TBI) impairs neuronal function and can culminate in lasting cognitive impairment. While impaired neurotransmitter release has been well established after experimental TBI, little is understood about the mechanisms underlying this consequence. In the synapse, vesicular docking and neurotransmitter release requires the formation of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. ⋯ Synapses in the hippocampus were imaged at 100k magnification, and vesicle distribution was assessed in pre-synaptic terminals at the active zone. CCI resulted in a significant reduction in vesicle number within 150 nm of the active zone. These findings provide the first evidence of TBI-induced impairments in synaptic vesicle docking, and suggest that reductions in the pool of readily releasable vesicles and impaired SNARE complex formation are two novel mechanisms contributing to impaired neurotransmission after TBI.
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Previous studies report that cavum septum pellucidum (CSP) is frequent among athletes with a history of repeated traumatic brain injury (TBI), such as boxers. Few studies of CSP in athletes, however, have assessed detailed features of the septum pellucidum in a case-control fashion. This is important because prevalence of CSP in the general population varies widely (2% to 85%) between studies. ⋯ Sixteen of 17 (94%) players had a CSP graded ≥2 compared with 3 of 17 (18%) controls. CSP was significantly higher grade (p<0.001) and longer in players than controls (mean length±standard deviation: 10.6 mm±5.4 vs. 1.1 mm±1.3, p<0.001). Among patients presenting to a memory clinic, long high-grade CSP was more frequent in retired pro-football players compared with patients without a history of TBI.
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Journal of neurotrauma · Jan 2016
Combination Therapies for Traumatic Brain Injury: Retrospective Considerations.
Patients enrolled in clinical trials for traumatic brain injury (TBI) may present with heterogeneous features over a range of injury severity, such as diffuse axonal injury, ischemia, edema, hemorrhage, oxidative damage, mitochondrial and metabolic dysfunction, excitotoxicity, inflammation, and other pathophysiological processes. To determine whether combination therapies might be more effective than monotherapy at attenuating moderate TBI or promoting recovery, the National Institutes of Health funded six preclinical studies in adult and immature male rats to evaluate promising acute treatments alone and in combination. ⋯ One study demonstrated worse results with the combination in comparison with monotherapies. While specific research findings are reported elsewhere, this article provides an overview of the study designs, insights, and recommendations for future research aimed at therapy development for TBI.
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Journal of neurotrauma · Dec 2015
Noninvasive Reactivation of Motor Descending Control after Paralysis.
The present prognosis for the recovery of voluntary control of movement in patients diagnosed as motor complete is generally poor. Herein we introduce a novel and noninvasive stimulation strategy of painless transcutaneous electrical enabling motor control and a pharmacological enabling motor control strategy to neuromodulate the physiological state of the spinal cord. This neuromodulation enabled the spinal locomotor networks of individuals with motor complete paralysis for 2-6 years American Spinal Cord Injury Association Impairment Scale (AIS) to be re-engaged and trained. ⋯ We also observed on-command selective activation of the gastrocnemius and soleus muscles when attempting to plantarflex. At the end of 18 weeks of weekly interventions the mean changes in the amplitude of voluntarily controlled movement without stimulation was as high as occurred when combined with electrical stimulation. Additionally, spinally evoked motor potentials were readily modulated in the presence of voluntary effort, providing electrophysiological evidence of the re-establishment of functional connectivity among neural networks between the brain and the spinal cord.
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Journal of neurotrauma · Dec 2015
Mean Arterial Blood Pressure Correlates With Neurological Recovery Following Human Spinal Cord Injury: Analysis of High Frequency Physiologic Data.
Current guidelines for the care of patients with acute spinal cord injuries (SCIs) recommend maintaining mean arterial pressure (MAP) values of 85-90 mm Hg for 7 days after an acute SCI however, little evidence supports this recommendation. We sought to better inform the relationship between MAP values and neurological recovery. A computer system automatically collected and stored q1 min physiological data from intensive care unit monitors on patients with SCI over a 6-year period. ⋯ Duration of hypotension may be more important than average MAP. It provides support for the notion of MAP thresholds in SCI recovery, and the highest MAP values correlated with the greatest degree of neurological recovery. The results are concordant with current guidelines in suggesting that MAP thresholds >85 mm Hg may be appropriate after acute SCI.