title: Altered cellular anatomy and physiology of acute brain injury and spinal cord injury.
abstract: The cellular elements and the chemical mediators in secondary injury following TBI or SCI do not act alone. The interconnections between the cellular elements and their secretions, the immune system, and the nervous system are highly regulated in normal physiology, which benefits the organism. When there is traumatic injury to cells in the CNS, the interconnections between the systems become more than tight; these systems act together to strangulate the tissue, depriving it of local control over microcirculation and necessary oxygen, rendering membrane potentials useless to modulate neuron function. Surgical intervention during the acute stages of TBI and SCI continues to advance as do biomechanical and bioelectric therapeutics during the chronic and rehabilitation stages. There is hope, too, for effective pharmacologic intervention at the initial stages, before secondary injury begins. The fact that the mediators of secondary injury are already resident in normal physiology, whether during development or adulthood, means that their activity can be modified by specific agonists and antagonists directed to restoring homeostasis or promoting pathways that can lead to regeneration. This is the direction of much current basic and clinical research.
authors.affiliation: School of Nursing and Health Studies, Department of Cell Biology, School of Medicine, Georgetown University, Washington, DC, USA.
authors.forename: L A
authors.initials: LA
authors.lastname: Zuccarelli
mesh_terms: D001369:Axons / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D001696:Biomechanical Phenomena; D001930:Brain Injuries / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D002118:Calcium / Q000502:physiology; D018846:Excitatory Amino Acids / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000502:physiology; D009410:Nerve Degeneration / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D017382:Reactive Oxygen Species / Q000276:immunology; D013119:Spinal Cord Injuries / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy
chemical_list: D018846:Excitatory Amino Acids; D005230:Fatty Acids, Nonesterified; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species; D002118:Calcium