Engaging Individuals with Neurological Conditions and Caregivers in Rural Communities in a Health Research Team.

Abstracts fromThe 32^nd AnnualNational Neurotrauma SymposiumJune 29–July 2, 2014San Francisco, California

Abstracts fromThe 33^rd AnnualNational Neurotrauma SymposiumJune 28–July 1, 2015Santa Fe, New Mexico

The data to put neurology on top of the public-health agenda

Abstracts from The 34(th) Annual National Neurotrauma Symposium June 26-29, 2016 Lexington, Kentucky.

Personal Bankruptcy After Traumatic Brain or Spinal Cord Injury: The Role of Medical Debt

Abstracts from The 35th Annual National Neurotrauma Symposium July 7-12, 2017 Snowbird, Utah.

Traumatic brain injury (TBI) and spinal cord injury (SCI) are acquired injuries to the central nervous system (CNS) caused by external forces that cause temporary or permanent sensory and motor impairments and the potential for long-term disability or even death. These conditions currently lack effective treatments and impose substantial physical, social, and economic burdens on millions of people and families worldwide. TBI and SCI involve intricate pathological mechanisms, and the inflammatory response contributes significantly to secondary injury in TBI and SCI. It plays a crucial role in prolonging the post-CNS trauma period and becomes a focal point for a potential therapeutic intervention. Previous research on the inflammatory response has traditionally concentrated on glial cells, such as astrocytes and microglia. However, increasing evidence highlights the crucial involvement of lymphocytes in the inflammatory response to CNS injury, particularly CD8+ T cells and NK cells, along with their downstream XCL1-XCR1 axis. This review aims to provide an overview of the role of the XCL1-XCR1 axis and the T-cell response in inflammation caused by TBI and SCI and identify potential targets for therapy. We conducted a comprehensive search of PubMed and Web of Science using relevant keywords related to the XCL1-XCR1 axis, T-cell response, TBI, and SCI. This study examines the upstream and downstream pathways involved in inflammation caused by TBI and SCI, including interleukin-15 (IL-15), interleukin-12 (IL-12), CD8+ T cells, CD4+ T cells, NK cells, XCL1, XCR1+ dendritic cells, interferon-gamma (IFN-γ), helper T0 cells (Th0 cells), helper T1 cells (Th1 cells), and helper T17 cells (Th17 cells). We describe their proinflammatory effect in TBI and SCI. The findings suggest that the XCL1-XCR1 axis and the T-cell response have great potential for preclinical investigations and treatments for TBI and SCI.

Combined SCI and TBI: Recovery of forelimb function after unilateral cervical spinal cord injury (SCI) is retarded by contralateral traumatic brain injury (TBI), and ipsilateral TBI balances the effects of SCI on paw placement

MicroRNA in the Pathophysiology of CNS Injury: Implication in Neuroregenerative Medicine.

Lipid profile analysis in spinal trauma patients shows severe distortion of AA/DHA after injury

Abstracts from The 37^th Annual National Neurotrauma Symposium June 29–July 3, 2019 Pittsburgh, Pennsylvania

Management of Mental Health Disorders, Substance Use Disorders, and Suicide in Adults with Spinal Cord Injury: Clinical Practice Guideline for Healthcare Providers.

Membrane resealing as a promising strategy for early treatment of neurotrauma

Traumatic brain and spinal cord injuries are significant causes of permanent disability and death. In 2010, 823,000 traumatic brain injuries were reported in the United States alone; in fact, the actual number is likely considerably higher because mild traumatic brain injuries and concussions are underreported. The number of new traumatic spinal cord injuries has been estimated at 12,000 annually. Survival from these injuries has increased due to improvements in medical care. This review covers mild traumatic brain injury and concussion, moderate to severe traumatic brain injury, and traumatic spinal cord injury. Figures include computed tomography scans showing a frontal contusion, diffuse cerebral edema and intracranial air from a gunshot wound, a subdural hematoma, an epidural hematoma, a skull fracture with epidural hematoma, and a spinal fracture from a gunshot wound. Tables list requirements for players with concussion, key guidelines for prehospital management of moderate to severe traumatic brain injury, key guidelines for management of moderate to severe traumatic brain injury, brain herniation brain code, key clinical practice guidelines for managing cervical spine and spinal cord injury, and the American Spinal Injury Association’s neurologic classification of spinal cord injury. This review contains 6 highly rendered figures, 12 tables, and 55 references.

Traumatic brain and spinal cord injuries are significant causes of permanent disability and death. In 2010, 823,000 traumatic brain injuries were reported in the United States alone; in fact, the actual number is likely considerably higher because mild traumatic brain injuries and concussions are underreported. The number of new traumatic spinal cord injuries has been estimated at 12,000 annually. Survival from these injuries has increased due to improvements in medical care. This review covers mild traumatic brain injury and concussion, moderate to severe traumatic brain injury, and traumatic spinal cord injury. Figures include computed tomography scans showing a frontal contusion, diffuse cerebral edema and intracranial air from a gunshot wound, a subdural hematoma, an epidural hematoma, a skull fracture with epidural hematoma, and a spinal fracture from a gunshot wound. Tables list requirements for players with concussion, key guidelines for prehospital management of moderate to severe traumatic brain injury, key guidelines for management of moderate to severe traumatic brain injury, brain herniation brain code, key clinical practice guidelines for managing cervical spine and spinal cord injury, and the American Spinal Injury Association’s neurologic classification of spinal cord injury. This review contains 6 highly rendered figures, 12 tables, and 55 references.