Photochemically induced graded spinal cord infarction
- 1 November 1987
- journal article
- Published by Journal of Neurosurgery Publishing Group (JNSPG) in Journal of Neurosurgery
- Vol. 67 (5) , 745-753
- https://doi.org/10.3171/jns.1987.67.5.0745
Abstract
Neurological and morphological outcome was evaluated in a rat model of graded spinal cord infarction initiated by a photochemical reaction. In this model, light-dye interactions induce primary microvascular stasis, resulting in consistent patterns of tissue necrosis. Four groups of rats underwent photoinduction times ranging from 30 seconds to 10 minutes. Neurological and electrophysiological functions were assessed starting 1 week after irradiation and continuing for 8 weeks. A functional neurological score was obtained by combining results from sensory and motor tasks, and electrophysiological function was evaluated from the somatosensory evoked potential recordings. In rats irradiated for short periods (30 seconds and 1 minute) mild behavioral deficits were documented. In contrast, electrical conduction was suppressed acutely in both groups; this recovered by 8 weeks to baseline or near baseline in the 30-second group but not in the 1-minute group. In rats irradiated for longer periods (5 and 10 minutes), severe behavioral and conduction abnormalities were detected at both the subacute and chronic testing periods. Although no significant difference in behavior was documented between the 5- and 10-minute groups acutely, the rats with 5-minute photoinduction time demonstrated a significant improvement in behavior over time whereas the group with 10-minute photoinduction time showed no improvement. A severe conduction block was present in both animal groups during the course of the study. Histopathological examination combined with morphometric measurements of the lesion area in cross section revealed four different degrees of spinal cord necrosis which correlated significantly with photoinduction times and neurological scores at 8 weeks. Reproducible degrees of ischemic damage to spinal cord parenchyma following primary microvascular occlusion result in a predictable sequence of behavioral and functional abnormalities, which in some cases recover with time.Keywords
This publication has 19 references indexed in Scilit:
- Induction of reproducible brain infarction by photochemically initiated thrombosisAnnals of Neurology, 1985
- Spinal cord contusion in the rat: Behavioral analysis of functional neurologic impairment☆Experimental Neurology, 1985
- Ultrastructural alterations in blood vessels of the white matter after experimental spinal cord traumaJournal of Neurosurgery, 1984
- QUANTUM YIELD OF SINGLET OXYGEN PRODUCTION BY XANTHENE DERIVATIVESPhotochemistry and Photobiology, 1983
- Effect of sympathectomy on extracellular potassium ionic activity and blood flow in experimental spinal cord contusionBrain Research, 1982
- Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injuryCanadian Journal of Physiology and Pharmacology, 1982
- Structural and functional degradation of Ca2+:Mg2+-ATPase rich sarcoplasmic reticulum vesicles photosensitized by Erythrosin BChemico-Biological Interactions, 1982
- Inhibition of Na+-K+-activated ATPase activity following experimental spinal cord traumaJournal of Neurosurgery, 1978
- Objective clinical assessment of motor function after experimental spinal cord injury in the ratJournal of Neurosurgery, 1977
- Ultrastructural blood-brain barrier alterations and edema formation in acute spinal cord traumaJournal of Neurosurgery, 1976