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

AIM: To understand possible mechanisms underlying lacrimal gland degeneration when facial nerve root ischemia induces pterygopalatine 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 severe subarachnoid hemorrhage. Autologous blood recovered from the auricular artery was injected into the cisterna magna to induce subarachnoid hemorrhage in the two subarachnoid hemorrhage groups; animals were then monitored for dry eye development over 21 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 nerve root injury severity and damaged neuron numbers in the pterygopalatine ganglion. Increase in injury severity most significantly decreased the tear-filled vesicle numbers in the pterygopalatine ganglion.

CONCLUSION

Subarachnoid hemorrhage degenerates facial nerve parasympathetic branches entering the pterygopalatine ganglion, and neuronal density in this ganglion may be correlated with tear secretion. Our data suggest that pterygopalatine ganglion degeneration following subarachnoid hemorrhage induces dry eye.