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Subarachnoid hemorrhage-induced hydrocephalus (SAIH) can affect the prognosis of subarachnoid hemorrhage (SAH). The relationship between hydromyelia and SAIH has been rarely investigated. This experimental model aimed to identify the pathophysiological changes developed in the SAH and elucidate the relationship between hydromyelia and SAIH. 25 female rabbits were randomly divided into three groups. The SAH group (n = 15), sham group (n = 5), and control group (n = 5). In the former group, the injection of 0.5 mL/kg of autologous blood was carried out into the cisterna magna on days 0 and 2. All animals were decapitated 21 days thereafter. Histological examinations of the medulla spinalis and brain samples were performed. The mean volumes of the central channel were 1.054, 1.287, and 1.776 mm 3  in the control, sham, and SAH groups, respectively (p = 0.028). The mean normal ependymal cell densities were 4.210, 3.602, and 2.923 cells/mm 2  in the control, sham, and SAH groups, respectively (p = 0.002). The mean ventricular Evans’ indices were 0.31, 0.34, and 0.41, in the control, sham, and SAH groups, respectively (p = 0.006). Basement membrane rupture, desquamated ependymal cells, and central channel occlusion were observed on histological examinations of the SAH group. Subependymal basement membrane destruction, blood cell accumulation on it, ependymal cell desquamation, increased cerebrospinal fluid (CSF) secretion, and increased ICP in the central channel that causes hydromyelia. When these pathological changes are chronically apparent, they may reflect on CSF pathways and cause permanent SAIH. Preventing long-time SAH-induced hydromyelia is believed to reduce the high rate of treatment-requiring SAIH.

Association between subarachnoid hemorrhage-induced hydrocephalus and hydromyelia: pathophysiological changes developed in an experimental model