Abstract

Although the central canal is an integral component of the cerebral ventricular system, central canal dilation has not been examined adequately during the progression of subarachnoid hemorrhage–related hydrocephalus (SAH-H). Central canal dilation–associated ependymal cell desquamation or subependymal membrane rupture has been rarely reported. Herein, we try to describe possible mechanisms of central canal dilation “Hydromyelia,” developing after SAH. A total of 25 New Zealand hybrid female rabbits were recruited. Five served as controls, and five received sham operations. In the remaining animals (n = 15), 0.5 mL/kg of autologous blood was injected into the cisterna magna twice on 0 and 2nd days. Five of these animals died within a few days. A total of 10 survivor animals decapitated 3 weeks later, and the brains and cervical spinal cords were histologically examined. Central canal volumes, ependymal cell numbers on the canal surfaces, and the Evans’ indices of the ventricles were compared. On histological examination, central canal occlusion with desquamated ependymal cells and basement membrane rupture were evident. The mean Evans’ index of the brain ventricles was 0.31, the mean central canal volume was 1.054 mm3, and the normal ependymal cell density was 4.210/mm2 in control animals; the respective values were 0.34, 1.287 mm3, and 3.602/mm2 for sham-operated animals, and 0.41, 1.776 mm3, and 2.923/mm2 in the study group. The differences were statistically significant (p < 0.05). Hydromyelia, an ignored complication of SAH-H, features ependymal cell desquamation, subependymal basement membrane destruction, blood cell accumulation on the subependymal cell basement membrane, and increased CSF pressure. Hydromyelia may be a significant complication following SAH.

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