BACKGROUND: Acute hydrocephalus (ventricular enlargement within 72 hours) is a common complication in patients with aneurysmal subarachnoid hemorrhage (SAH). Cerebrospinal fluid (CSF) secretion may be increased in the early phases of SAH, but it has not been proved definitively. We studied the histologic features of choroid plexus (CP) in the early and late phases of SAH.
METHODS: This study was conducted on 20 rabbits, with 5 rabbits in the control group, 5 rabbits in the sham group, and 10 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 2 days of cisternal blood injections, and the other five animals were decapitated after 14 days of injections. The CP of lateral ventricles were obtained from coronary sections of brains at the level of the temporal horns of the lateral ventricles. Sections were stained with hematoxylin and eosin and Masson trichrome for SAH-related damage and examined stereologically to discern water-filled vesicles, which were counted. Sections were compared statistically.
RESULTS: The mean numbers of water vesicles were different after SAH between the early decapitated group (group III) and the late decapitated group (group IV). The mean numbers of water vesicles were 2.80 (±0.05) in the control group (group I), 2.76 (±0.02) in the sham group (group II), 14.68 (±0.06) in the early decapitated group (group III), and 4.78 (±0.13) in the late decapitated group (group IV). Total number of fluid-filled vesicles of CP was also assessed stereologically; the total numbers were 840 (±16) in group I, 828 (±7) in group II, 4404 (±19) in group III, and 1434 (±41) in group IV. The numbers of water-filled cisterns were significantly increased in the early phases of SAH (P < 0.05).
CONCLUSIONS: In SAH with aneurysm rupture, increased CSF secretion seems to be triggered by hemorrhage in the early phase, but it is not possible in the late phase because of CP degeneration. In the early phase of hemorrhage, CSF secretion may be stimulated by the irritant receptor glossopharyngeal and vagal nerve endings, which innervate the healthy CP epithelium and arteries. Our findings may be accepted as being causative. It is likewise possible that CSF blockage per se leads to hydrocephalus, and the morphologic changes are sequelae that occur later in the course of disease. This is the first study to show the water vesicles of CP as a causative factor in the development of acute hydrocephalus after SAH.