Changes in number of water-filled vesicles of choroid plexus in early and late phase of experimental rabbit subarachnoid hemorrhage model; the role of petrous ganglion of glossopharyngeal nerve

Abstract

Cerebrospinal fluid (CSF) secretion may be increased in the early phases of subarachnoid hemorrhage (SAH), possibly via ischemic glossopharyngeal nerve discharges, and decreased due to glossopharyngeal nerve degeneration in the late phase of SAH; but this reflex pathway has not been definitively investigated. We studied the relationship between petrous ganglion of the glossopharyngeal nerve (GPN) and water vesicles of the choroid plexus (CP) in the early and late phases of SAH. This study was conducted on 30 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 20 rabbits in the SAH group. in the SAH group, five of the animals were decapitated after 4 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 20 days of injections (Group IV). the Petrous Ganglia and CPs of lateral ventricles were removed and stained for stereological analysis. the mean number of follicles per cubic millimeter was 5.3 +/- 1.2 the in control group (Group I), 4.5 +/- 0.9 in the sham group (Group II), 16.60 +/- 3.77 the in early decapitated group (Group III), and 4.30 +/- 0.84 in the late decapitated group (Group IV). the mean number of degenerated neuron density of petrous ganglions was 6 +/- 2, 50 +/- 6, 742 +/- 96, and 2.420 +/- 350 in the control (Group I), sham (Group II), early decapitated (Group III), and late decapitated group (Group IV), respectively. the mean number of water vesicles was statistically different after SAH between the early decapitated group (group III) and the late decapitated group (group IV) (P < 0.05). We studied the relationship between petrous ganglion cells of the GPN and water vesicles of CP in the early and late phases of SAH, and found that CP vesicles are increased in the early phase of SAH due to irritation of GPN, and decreased in the late phase due to ischemic insult of the petrous ganglion and parasympathetic innervation of the CP.