Spinal Cord Injury Damage Research Articles

An Experimental Model Combining Microdialysis with Electrophysiology, Histology, and Neurochemistry for Exploring Mechanisms of Secondary Damage in Spinal Cord Injury: Effects of Potassium

An experimental model for characterizing effects of agents suspected to cause damage secondary to spinal cord injury is presented. Microdialysis was used to administer candidate damaging agents and to sample the release of other substances in response to administered agents. Damage was assessed by monitoring the amplitudes of evoked potentials during candidate administration and by postmortem histologic examination. This approach enabled the correlation of electrophysiologic, histologic, and neurochemical parameters in the same experiment. Potassium was chosen as a candidate damaging agent, because (1) in high extracellular concentrations it destroys neurons and (2) its extracellular concentration rises substantially following impact injury to the spinal cord. A technique using parallel administering and collecting microdialysis fibers was developed to estimate the in vivo concentration of K+ outside the administering fiber. Administration of 100 mM KCl, 50 mM K2HPO4, or 100 mM potassium glucuronate in artificial cerebrospinal fluid blocked electrical conduction and destroyed cell bodies. Release of the neurotransmitter amino acids aspartate, glutamate, glycine, and gamma-aminobutyric acid (GABA) and the possible neurotransmitter taurine were dramatically increased by administration of 100 mM KCl. Levels of non-neurotransmitter amino acids increased to lesser degrees. Impairment of conduction, destruction of cell bodies, and release of excitotoxins were all consistent with elevated K+ serving as a secondary damaging agent in spinal cord injury.

Chemical and cellular mediators in spinal cord injury.

Journal of NeurotraumaVol. 9, No. 2 Chemical and Cellular Mediators in Spinal Cord InjuryDOUGLAS K. ANDERSONDOUGLAS K. ANDERSONSearch for more papers by this authorPublished Online:26 Mar 2009https://doi.org/10.1089/neu.1992.9.143AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited ByPredictors of intramedullary lesion expansion rate on MR images of patients with subaxial spinal cord injuryJournal of Neurosurgery: Spine, Vol. 22, No. 6Quercetin attenuates inflammatory processes after spinal cord injury in an animal model4 May 2010 | Spinal Cord, Vol. 48, No. 12Trauma3 January 2013Surgical Approaches for the Operative Management of Cervical Spine FracturesInvestigation of the dose-dependent neuroprotective effects of agmatine in experimental spinal cord injury: a prospective randomized and placebo–control trialJournal of Neurosurgery: Spine, Vol. 4, No. 5Spine Cord Injury: An UpdateSeminars in Spine Surgery, Vol. 17, No. 2Does early decompression improve neurological outcome of spinal cord injured patients? Appraisal of the literature using a meta-analytical approach6 July 2004 | Spinal Cord, Vol. 42, No. 9Management of Missile Head WoundsNeurosurgery Quarterly, Vol. 13, No. 2Non-surgical management of spinal cord injury24 February 2005 | Expert Opinion on Investigational Drugs, Vol. 11, No. 4Current developments in spinal cord injury researchThe Spine Journal, Vol. 2, No. 2Coadministration of Methylprednisolone with Hypertonic Saline Solution Improves Overall Neurological Function and Survival Rates in a Chronic Model of Spinal Cord InjuryNeurosurgery, Vol. 49, No. 6Tonicity of Resuscitative Fluids Influences Outcome after Spinal Cord InjuryNeurosurgery, Vol. 48, No. 1Chemokine antagonist infusion attenuates cellular infiltration following spinal cord contusion injury in ratJournal of Neuroscience Research, Vol. 59, No. 1Chemokine antagonist infusion attenuates cellular infiltration following spinal cord contusion injury in ratJournal of Neuroscience Research, Vol. 59, No. 1Characteristics of Human Fetal Spinal Cord Grafts in the Adult Rat Spinal Cord: Influences of Lesion and Grafting ConditionsExperimental Neurology, Vol. 148, No. 2The effects of taxol, methylprednisolone, and 4-aminopyridine in compressive spinal cord injury: A qualitative experimental studySurgical Neurology, Vol. 46, No. 4Traumatismos medulares experimentales: Revisión de la literatura y descripción de un modelo mediante compresión mantenida en la rataNeurocirugía, Vol. 7, No. 3Effect of a spinal cord photolesion injury on catalase16 December 1999 | International Journal of Developmental Neuroscience, Vol. 13, No. 6Treatment of Acute Injury of the Cervical SpineThe Journal of Bone & Joint Surgery, Vol. 76, No. 12Methylprednisolone and membrane properties of primary cultures of mouse spinal cordBrain Research, Vol. 637, No. 1-2An Experimental Model Combining Microdialysis with Electrophysiology, Histology, and Neurochemistry for Exploring Mechanisms of Secondary Damage in Spinal Cord Injury: Effects of Potassium DANXIA LIU and DAVID J. McADOO26 March 2009 | Journal of Neurotrauma, Vol. 10, No. 3 Volume 9Issue 2Jan 1992 To cite this article:DOUGLAS K. ANDERSON.Chemical and Cellular Mediators in Spinal Cord Injury.Journal of Neurotrauma.Jan 1992.143-146.http://doi.org/10.1089/neu.1992.9.143Published in Volume: 9 Issue 2: March 26, 2009PDF download

Delayed demyelination and macrophage invasion: a candidate for secondary cell damage in spinal cord injury.

Recent studies of the chronic morphology and physiology of experimental spinal cord injury (SCI) in the cat are reviewed and their conclusions outlined. In particular, variations in chronic dysmyelination of the lesion have been found to be largely independent of injury intensity, suggesting a secondary pathologic origin. New morphometric studies of the subacute development of contusion lesions are described. Using electron microscopy and light microscopic line-sampling of myelinated axons, it was found that demyelination of axons that survived the initial injury occurred largely between 2 and 7 days after contusion and did not accompany the much more rapid dissolution of myelin from those axons that degenerated within the first 2 days. The number of apparently intact axons at the center of the lesion declined by a factor of 2 or more in the same interval of 2-7 days. This secondary pathology was coincident with dense invasion of the lesion by macrophages and their phagocytosis of the membraneous debris remaining from the initial hemorrhagic necrosis. It is concluded that posttraumatic inflammation in the spinal cord should be investigated in more detail as a possible contributor to chronic deficits. In addition, these data emphasize the importance of defining the nature, time of occurrence, and proportional significance of secondary damage in order to evaluate those studies and hypotheses that attempt to differentiate acute secondary pathophysiology from primary degenerative processes.