Journal of neurotrauma
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Journal of neurotrauma · Dec 2012
Carvacrol together with TRPC1 elimination improve functional recovery after traumatic brain injury in mice.
Death of Central Nervous System (CNS) neurons following traumatic brain injury (TBI) is a complex process arising from a combination of factors, many of which are still unknown. It has been found that inhibition of transient receptor potential (TRP) channels constitutes an effective strategy for preventing death of CNS neurons following TBI. TRP channels are classified into seven related subfamilies, most of which are Ca(2+) permeable and involved in many cellular functions, including neuronal cell death. ⋯ To better define the type of the specific channel involved, the effect of carvacrol on the extent and speed of recovery after TBI was compared among mice lacking TRPC1, TRPC3, or TRPC5, relative to wild type controls. We found that neurological recovery after TBI was significantly enhanced by combining carvacrol with TRPC1 elimination, but not by the absence of TRPC3 or TRPC5, showing a synergistic effect between carvacrol application and TRPC1 elimination. We conclude that TRPC1-sensitive mechanisms are involved in TBI pathology, and that inhibition of this channel by carvacrol enhances recovery and should be considered for further studies in animal models and humans.
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In the clinical setting, skin temperature is both easily evaluated and useful in assessments of sympathetic dysfunction. The present study purposed to observe the serial skin temperature changes of both hindlimbs following several types of sciatic nerve injury (complete transection and ligation model [CTL], crush injury model [CRI], and chronic constriction injury model [CCI]) in Sprague-Dawley rats and, further, to delineate the possible mechanisms through various evaluation methods. The temperature differences between the intact and injured areas (ΔT) on the plantar surface and toes varied among the CTL, CRI, and CCI injury models during the acute stage (7 days post-injury). ⋯ The latency and amplitude of the compound muscle action potential (CMAP) in the involved plantar muscle was not found in the CTL group 4 weeks post-injury, but showed gradual restoration in the CRI and CCI models. Regression analysis revealed that the ΔT in the plantar area and toes were affected only by the CMAP amplitude in the involved plantar muscle; therefore, it can be said that the skin temperature on the injured area after sciatic nerve injury was influenced by the functional status of the involved muscle. Measurement of skin temperature can differentiate mild peripheral nerve injury from moderate-to-severe injuries, although its clinical significance might be limited.
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Journal of neurotrauma · Dec 2012
Degeneration of phrenic motor neurons induces long-term diaphragm deficits following mid-cervical spinal contusion in mice.
A primary cause of morbidity and mortality following cervical spinal cord injury (SCI) is respiratory compromise, regardless of the level of trauma. In particular, SCI at mid-cervical regions targets degeneration of both descending bulbospinal respiratory axons and cell bodies of phrenic motor neurons, resulting in deficits in the function of the diaphragm, the primary muscle of inspiration. Contusion-type trauma to the cervical spinal cord is one of the most common forms of human SCI; however, few studies have evaluated mid-cervical contusion in animal models or characterized consequent histopathological and functional effects of degeneration of phrenic motor neuron-diaphragm circuitry. ⋯ We report that phrenic motor neuron loss in cervical spinal cord, phrenic nerve axonal degeneration, and denervation at diaphragm neuromuscular junctions (NMJ) resulted in compromised ipsilateral diaphragm function, as demonstrated by persistent reduction in diaphragm compound muscle action potential amplitudes following phrenic nerve stimulation and abnormalities in spontaneous diaphragm electromyography (EMG) recordings. This injury paradigm is reproducible, does not require ventilatory assistance, and provides proof-of-principle that generation of unilateral cervical contusion is a feasible strategy for modeling diaphragmatic/respiratory deficits in mice. This study and its accompanying analyses pave the way for using transgenic mouse technology to explore the function of specific genes in the pathophysiology of phrenic motor neuron degeneration and respiratory dysfunction following cervical SCI.
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Journal of neurotrauma · Nov 2012
Randomized Controlled TrialThe effect of hyperbaric oxygen on symptoms after mild traumatic brain injury.
In this single-center, double-blind, randomized, sham-controlled, prospective trial at the U. S. Air Force School of Aerospace Medicine, the effects of 2.4 atmospheres absolute (ATA) hyperbaric oxygen (HBO₂) on post-concussion symptoms in 50 military service members with at least one combat-related, mild traumatic brain injury were examined. ⋯ Paired t-test results revealed 10 ImPACT scale scores in the sham-control group improved from pre- to post-testing, whereas two scale scores significantly improved in the HBO₂ group. One PCL-M measure improved from pre- to post-testing in both groups. This study showed that HBO₂ at 2.4 ATA pressure had no effect on post-concussive symptoms after mild TBI.
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Traumatic injury is a common cause of coagulopathy, primarily due to blood loss and hemodilution secondary to fluid resuscitation. Traumatic injury-associated coagulopathy often follows a course of transition from hyper- to hypocoagulable state exemplified in disseminated intravascular coagulation. The incidence of coagulopathy is significantly higher in patients with traumatic brain injury (TBI), especially those with penetrating trauma compared to injury to the trunk and limbs. ⋯ Studies in the past have shown that brain tissue is highly enriched in key procoagulant molecules. This review focuses on the biochemical and cellular characteristics of these molecules and pathways that could make brain uniquely procoagulant and prone to coagulopathy. Understanding this unique procoagulant environment will help to identify new therapeutic targets that could reverse a state of coagulopathy with minimal impacts on hemostasis, a critical requirement for neurosurgical treatments of TBI.