The neuronal theory of experimental traumatic spinal cord dysfunction.
Previous studies by the author have demonstrated a hyperemia in the lateral funiculus of the Rhesus spinal cord following experimental traumatic spinal cord injury which has sufficient to render the animals permanently paraplegic. This absence of ischemia in the lateral funiculus, coupled with a reappraisal of available data from other investigators, has prompted the author to formulate a theory of primary neuronal dysfunction to explain the observed pathophysiology. It is suggested that the initial injury causes a pathologic biomolecular rearrangemant within the neuronal membrane which interferes with its ability to restrict sodium conductance at rest,nd in effect, makes the membrane nonexcitable.
D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D002463:Cell Membrane Permeability; D007773:Lactates / Q000097:blood; D008253:Macaca mulatta; D008564:Membrane Potentials; D008954:Models, Biological; D009119:Muscle Contraction; D009474:Neurons / Q000502:physiology*; D010264:Paraplegia / Q000209:etiology / Q000503:physiopathology; D012039:Regional Blood Flow; D013116:Spinal Cord / Q000098:blood supply; D013119:Spinal Cord Injuries / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D013256:Steroids / Q000494:pharmacology; D014882:Water-Electrolyte Balance
D007773:Lactates; D013256:Steroids