The cervical spinal canal in syringomyelia.
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Obstruction of cerebrospinal fluid pathways produces changes in the parenchyma of the brain and spinal cord. A murine model of hydrocephalus (hy-3) used to study changes in the central canal of the spinal cord and these changes are correlated with events occurring in the intracranial compartment. The central canal is enlarged and subependymal interstitial edema is produced by cerebrospinal fluid at the same time as the intracranial ventricular system is expanding. Plugging of the obex results in collapse of the central canal. Ferritin tracer studies demonstrate transependymal flow of cerebrospinal fluid throughout the central canal.
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Occlusion and reopening of the lumen of the spinal cord, two processes believed to be involved in early brain enlargement, were examined in chick embryos to determine what morphological features characterize these events. Occlusion begins at a particular craniocaudal level near the time that the neural folds become apposed in the dorsal midline and blocklike somites form from the segmental plates. During occlusion, the apical sides of the lateral walls of the neural tube are in close apposition. Interdigitating apical surface protrusions, cross-luminal intercellular junctions, and abundant cell-surface materials are lacking. Reopening has occurred by about stage 20 throughout most of the craniocaudal extent of the spinal cord. A lumen suddenly appears during this process, but correlated structural changes that might account for such a dramatic change in morphology were undetectable. Reopening involves the release of the forces that previously maintained occlusion, or the generation of new forces that overcome those causing occlusion, but what these forces are remains to be determined. Observations suggest that forces generated outside of the neural tube might be largely responsible for occlusion, and experiments are in progress to test this possibility.
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