Journal of neurotrauma
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Journal of neurotrauma · Dec 2021
Network Analysis of Neurobehavioral and Post-Traumatic Stress Disorder Symptoms One Year after Traumatic Brain Injury: A Veterans Affairs Traumatic Brain Injury Model Systems Study.
Traumatic brain injury (TBI) is often experienced under stressful circumstances that can lead to symptoms of post-traumatic stress disorder (PTSD) and neurobehavioral symptoms of brain injury. There is considerable symptom overlap in the behavioral expression of these conditions. Psychometric network analysis is a useful approach to investigate the role of specific symptoms in connecting these two disorders and is well suited to explore their interrelatedness. ⋯ Hyperarousal appears to play a key role in holding together this network of distress and thus represents a prime target for intervention among individuals with elevated symptoms of PTSD and a history of TBI. Network analysis offers an empirical approach to visualizing and quantifying the associations among symptoms. The identification of symptoms that are central to connecting multiple conditions can inform diagnostic precision and treatment selection.
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Journal of neurotrauma · Dec 2021
Supraspinal sensorimotor and pain-related reorganization after a hemicontusion rat cervical spinal cord injury.
Because the presence of pain impedes motor recovery in individuals with spinal cord injury (SCI), it is necessary to understand their supraspinal substrates in translational animal models. Using functional magnetic resonance imaging (fMRI) in a rat model of hemicontusion cervical SCI, supraspinal changes were mapped and correlated with sensorimotor behavioral outcomes. Female adult rats underwent sham or SCI using a 2.5 mm impactor and 150 kdyn force. ⋯ Hippocampus, amygdala, and thalamus showed decreased RSFC with most cortical regions and between themselves except the hippocampus-amygdala network, which showed increased RSFC after SCI. Whereas select nociceptive region's intrinsic activity associated strongly with evoked pain behaviors after SCI (e.g., PFC, ACC, hippocampus, thalamus, hypothalamus, M1, and S1BF) other nociceptive regions had weaker associations (e.g., amygdala, insula, auditory cortex, S1FL, S1HL, S2, and M2), but differed significantly in their intrinsic activities between sham and SCI. The weaker associated nociceptive regions may possibly encode both the evoked and affective components of pain.
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Journal of neurotrauma · Dec 2021
Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics.
Nociceptive input diminishes recovery and increases lesion area after a spinal cord injury (SCI). Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure (BP) and/or flow. ⋯ Further, inducing a rise in BP/flow using norepinephrine undermined long-term recovery and increased tissue loss. Mediational analyses suggest that the pain-induced rise in blood flow may foster hemorrhage after SCI. Increased BP appears to act through an independent process to adversely affect locomotor performance, tissue sparing, and long-term recovery.
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Journal of neurotrauma · Dec 2021
Fetal and perinatal expression profiles of proinflammatory cytokines in the neuroplacodes of rats with myelomeningoceles: A contribution to the understanding of secondary spinal cord injury in open spinal dysraphism.
The cellular and molecular mechanisms that presumably underlie the progressive functional decline of the myelomeningocele (MMC) placode are not well understood. We previously identified key players in post-traumatic spinal cord injury cascades in human MMC tissues obtained during postnatal repair. In this study, we conducted experiments to further investigate these mediators in the prenatal time course under standardized conditions in a retinoic acid-induced MMC rat model. ⋯ C-X3-C motif ligand 1 mRNA was lower in MMC tissues than in control tissues on E16. The presented findings contribute to the concept that pathophysiological mechanisms, such as cytokine induction in the neuroplacode, in addition to the "first hit," promote secondary spinal cord injury with functional loss in the late fetal time course. Further, these mediators should be taken into consideration in the development of new therapeutic approaches for open spinal dysraphism.