Journal of neurotrauma
-
Journal of neurotrauma · Jul 2018
Adherence to Brain Trauma Foundation Guidelines for Management of Traumatic Brain Injury Patients and Its Effect on Outcomes: Systematic Review.
Traumatic brain injury (TBI) management based on Brain Trauma Foundation (BTF) guidelines is widely accepted and thought to improve outcome. The objectives of this study are to provide an overview of adherence to BTF guidelines and to explore which factors influence adherence. We conducted a search of relevant electronic bibliographic databases. ⋯ Treating patients with higher severity of injury as well as treatment in a Level I trauma center positively influenced adherence. Overall, adherence to BTF guidelines varies. Further research is required to strengthen the current evidence and to identify factors related to adherence to guidelines from a professional prospective.
-
Journal of neurotrauma · Jul 2018
Traumatic Brain Injury Disrupts Pain Signaling in the Brainstem and Spinal Cord.
Chronic pain is a common consequence of traumatic brain injury (TBI) that can increase the suffering of a patient and pose a significant challenge to rehabilitative efforts. Unfortunately, the mechanisms linking TBI to pain are poorly understood, and specific treatments for TBI-related pain are still lacking. Our laboratory has shown that TBI causes pain sensitization in areas distant to the site of primary injury, and that changes in spinal gene expression may underlie this sensitization. ⋯ Here we expand our knowledge of pain after TBI in two ways: (1) by outlining the neuropathology in pain-related centers of the brain and spinal cord involved in DNIC using the rat lateral fluid percussion (LFP) model of TBI, and (2) by evaluating the effects of a potent histone acetyl transferase inhibitor, anacardic acid (AA), on LFP-induced pain behaviors and neuropathology when administered for several days after TBI. The results revealed that TBI induces transient mechanical allodynia and a chronic persistent loss of DNIC. Further, while short-term AA treatment can block acute nociceptive sensitization and some early neuropathological changes, this treatment neither prevented the loss of DNIC nor did it alter long-term neuropathological changes in the brain or spinal cord.
-
Journal of neurotrauma · Jul 2018
Delayed Administration of BQ788, an ETB Antagonist, after Experimental Traumatic Brain Injury Promotes Recovery of Blood-Brain Barrier Function and a Reduction of Cerebral Edema in Mice.
Traumatic brain injury (TBI) is induced by immediate physical disruption of brain tissue, and causes death and disability. Studies on experimental TBI animal models show that disruption of the blood-brain barrier (BBB) underlies brain edema and neuroinflammation during the delayed phase of TBI. In neurological disorders, endothelin-1 (ET-1) is involved in BBB dysfunction and brain edema. ⋯ GFAP-positive astrocytes produced vascular endothelial growth factor-A (VEGF-A) and matrix metalloproteinase-9 (MMP9). FPI-induced increases in VEGF-A and MMP-9 production were reversed by BQ788. These results suggest that ETB receptor antagonism during the delayed phase of focal TBI promotes recovery of BBB function and reduction of brain edema.
-
Journal of neurotrauma · Jul 2018
Severe Traumatic Brain Injury Patients without Focal Lesion but with Behavioral Disorders: Shrinkage of Gray Matter Nuclei and Thalamus Revealed in a Pilot Voxel-Based MRI Study.
After a traumatic brain injury (TBI), behavioral disorders can occur without major focal brain lesion, and in these situations, their pathophysiology remains unclear. The aim of this study is to examine whether TBI patients with behavioral disorders but without any focal damage, as observed from an initial clinical CT scan, present subtle volumetric alterations that could be measured voxel-by-voxel in the whole brain with MRI. Eight male adults with severe TBI who had behavioral sequela but not major focal cerebral lesion and 17 age-matched controls underwent a volumetric T1-weighted 1.5T MRI. ⋯ WM volume was lower (p < 0.001, uncorrected) in the TBI group than in controls in the periventricular area and around the basal nuclei. We found shrinkage in the dorsomedial thalami in each of the TBI patients, and in the posterior part of the right putamen and caudate nuclei in seven TBI patients. Shrinkage in the dorsomedial thalami and in the posterior part of the right putamen and caudate nuclei may be a common effect of the disseminated microscopic lesions, and be associated with behavioral issues in severe TBI patients without major focal lesions.
-
Journal of neurotrauma · Jul 2018
Dimethyl Fumarate Attenuates Neuroinflammation and Neurobehavioral Deficits Induced by Experimental Traumatic Brain Injury.
Traumatic brain injury (TBI) is a serious neuropathology that causes secondary injury mechanisms, including dynamic interplay between ischemic, inflammatory, and cytotoxic processes. Fumaric acid esters (FAEs) showed beneficial effects in pre-clinical models of neuroinflammation and toxic oxidative stress, so the aim of the present work was to evaluate the potential beneficial effects of dimethyl fumarate (DMF), the most pharmacologically effective molecules among the FAEs, in a mouse model of TBI induced by controlled cortical impact (CCI). Mice were administered DMF orally at the doses of 1, 10, and 30 mg/kg 1 h and 4 h after CCI. ⋯ Further, DMF treatment up-regulated antioxidant Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor pathway, inducing activation of manganese superoxide dismutase and heme-oxygenase-1 and reducing 4-hydroxy-2-nonenal staining. Also, regulating the NF-κB pathway, DMF treatment decreased the severity of inflammation through a modulation of neuronal nitric oxide synthase, interleukin 1, tumor necrosis factor, cyclooxygenase 2, and myeloperoxidase activity, reducing ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein expression. Our results support the thesis that DMF may be an effective neuroprotectant after brain trauma and warrants further study.