Journal of neurotrauma
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Journal of neurotrauma · Feb 2018
Observational StudyEffect of History of Mild Traumatic Brain Injury on Optic Nerve Sheath Diameter Changes after Valsalva Maneuver.
Optic nerve sheath diameter (ONSD) measured by transocular ultrasound is a marker of real-time intracranial pressure (ICP). The objective of this study was to evaluate the association between optic nerve sheath (ONS) dilation after a Valsalva maneuver and a prior history of mild to moderate traumatic brain injury (mTBI) in a heterogeneous sample of participants. Participants were excluded if they had had a recent brain injury, were symptomatic from a prior brain injury, had a history consistent with severe TBI and/or had undergone intracranial surgery. ⋯ Following Valsalva, participants with a history of mTBI had a statistically significant increase in the ONSD compared with participants with no history of mTBI. This significant difference persisted after controlling for age, race, and sex. This study demonstrated an association between a prior history of mTBI and dilation of the ONS after Valsalva maneuver in a sample of asymptomatic participants, which was not seen in participants without a history of mTBI.
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Journal of neurotrauma · Feb 2018
Exacerbation of Acute Traumatic Brain Injury by Circulating Extracellular Vesicles.
Inflammatory lesions in the brain activate a systemic acute-phase response (APR), which is dependent on the release of extracellular vesicles (EVs) into the circulation. The resulting APR is responsible for regulating leukocyte mobilization and subsequent recruitment to the brain. Factors that either exacerbate or inhibit the APR will also exacerbate or inhibit central nervous system (CNS) inflammation as a consequence and have the potential to influence ongoing secondary damage. ⋯ By manipulating the circulating EV population, we were able to demonstrate that each population of transferred EVs increased the APR. However, the characteristics of the response were dependent on the nature of the EVs; specifically, it was significantly increased when animals were challenged with macrophage-derived EVs, suggesting that the cellular origins of EVs may determine their function. Selectively targeting EVs from macrophage/monocyte populations is likely to be of value in reducing the impact of the systemic inflammatory response on the outcome of traumatic CNS injury.
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Journal of neurotrauma · Feb 2018
Erythropoietin Attenuates the Brain Edema Response after Experimental Traumatic Brain Injury.
Erythropoietin (EPO) has neuroprotective effects in multiple central nervous system (CNS) injury models; however EPO's effects on traumatic brain edema are elusive. To explore EPO as an intervention in traumatic brain edema, male Sprague-Dawley (SD) rats were subjected to blunt, controlled traumatic brain injury (TBI). Animals were randomized to EPO 5000 IU/kg or saline (control group) intraperitoneally within 30 min after trauma and once daily for 4 consecutive days. ⋯ Animals treated with EPO demonstrated conserved levels of aquaporin 4 (AQP4) protein expression in the perilesional area, whereas control animals showed a reduction of AQP4. We show that post TBI administration of EPO decreases early cytotoxic brain edema and preserves structural and functional properties of the BBB, leading to attenuation of the vasogenic edema response. The data support that the mechanisms involve preservation of the tight junction protein ZO-1 and the water channel AQP4, and indicate that treatment with EPO may have beneficial effects on the brain edema response following TBI.
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Journal of neurotrauma · Feb 2018
Effects of intrathecal injection of the conditioned medium of bone marrow stromal cells on spinal cord injury of rats.
Bone marrow stromal cells (BMSCs) have been studied for the treatment of spinal cord injury (SCI). In previous studies, we showed that the transplantation of BMSCs, even though they disappeared from the host spinal cord within 1-3 weeks after transplantation, improved locomotor behaviors and promoted axonal regeneration. This result led to the hypothesis that BMSCs might release some neurotrophic factors effective for the treatment of SCI. ⋯ The density of axons extending through the astrocyte-devoid area was higher in the CM-injection group, compared with the control group. CM injection had beneficial effects on locomotor improvements and tissue repair, including axonal regeneration, meaning that the BMSC-CM stimulated the intrinsic ability of the spinal cord to regenerate. Activation of the intrinsic ability of the spinal cord to regenerate by the injection of neurotrophic factors such as BMSC-CM is considered to be a safe and preferable method for the clinical treatment of SCI.
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Journal of neurotrauma · Feb 2018
Spinal cord injury causes systolic dysfunction and cardiomyocyte atrophy.
Individuals with spinal cord injury (SCI) have been shown to exhibit systolic, and to a lesser extent, diastolic cardiac dysfunction. However, previous reports of cardiac dysfunction in this population are confounded by the changing loading conditions after SCI and as such, whether cardiac dysfunction per se is present is still unknown. Therefore, our aim was to establish if load-independent cardiac dysfunction is present after SCI, to understand the functional cardiac response to SCI, and to explore the changes within the cellular milieu of the myocardium. ⋯ The reduction in contractile indices is accompanied by a reduction in width and length of cardiomyocytes as well as alterations in the LV extracellular matrix. Importantly, we demonstrate that the reduction in the rate (dP/dtmax) of LV pressure rise can be offset with beta-adrenergic stimulation, thereby experimentally implicating the loss of descending sympatho-excitatory control of the heart as a principle cause of LV dysfunction in SCI. Our data provide evidence that SCI induces systolic cardiac dysfunction independent of loading conditions and concomitant cardiomyocyte atrophy that may be underpinned by changes in the genes regulating the cardiac extracellular matrix.