Understanding of Dry Eye in Subarachnoid Hemorrhage: An Experimental Study on the Role of Facial Nerve Ischemia

Özet

AIM: To understand possible mechanisms underlying lacrimal gland degeneration when facial nerve root ischemia inducespterygopalatine ganglion injury and subsequent dry eye in a rabbit model of subarachnoid hemorrhage.MATERIAL and METHODS: Rabbits were divided into four groups: control, sham, moderate subarachnoid hemorrhage, and severesubarachnoid hemorrhage. Autologous blood recovered from the auricular artery was injected into the cisterna magna to inducesubarachnoid hemorrhage in the two subarachnoid hemorrhage groups; animals were then monitored for dry eye development over21 days before removal of their facial nerve roots, pterygopalatine ganglia, and lacrimal glands for immunohistochemical analyses.Neuronal viability in the pterygopalatine ganglia was measured; lacrimal gland vesicles were counted by stereological methods.RESULTS: The mean tear-filled vesicle number and lacrimal gland volumes significantly decreased with an increase in facial nerveroot injury severity and damaged neuron numbers in the pterygopalatine ganglion. Increase in injury severity most significantlydecreased the tear-filled vesicle numbers in the pterygopalatine ganglion.CONCLUSION: Subarachnoid hemorrhage degenerates facial nerve parasympathetic branches entering the pterygopalatineganglion, and neuronal density in this ganglion may be correlated with tear secretion. Our data suggest that pterygopalatine gangliondegeneration following subarachnoid hemorrhage induces dry eye.