Trigeminal ganglion neuron density and regulation of anterior choroid artery vasospasm: In a rabbit model of subarachnoid hemorrhage

Abstract

Background:Subarachnoid hemorrhage (SAH) is associated with severe vasospasm caused by a variety of neurochemical mechanisms. The anterior choroid arteries (AChAs) are innervated by vasodilated fibers of the trigeminal ganglion (TGG). The goal of this study was to determine whether there is a relationship between the neuron density of the TGG and the severity of AChAs vasospasm with SAH.Methods:Thirty-two rabbits were used for the study; eight served as the baseline control group, seven as a SHAM group, with injections of 1 cc of isotonic saline solution, and 17 rabbits were included in the experimental SAH group, with injection of homologous blood into the cisterna magna. After 10 days, the histopathology of the AChAs and TGGs were examined. The AChAs vasospasm index (VSI) of the external/internal diameter and the neuron density of the ophthalmic root of the TGGs were evaluated stereologically. The AChAs VSI was preferred -- a measure of the degree of vasospasm. As the VSI increased, the degree of arterial vasospasm increased. The results were statistically analyzed.Results:The mean AChAs VSI was significantly higher and the mean neuronal density of the ophthalmic root of the TGG was significantly lower in the group with severe vasospasm associated with SAH compared to the controls, SHAM, and the group with mild vasospasm associated with SAH (P< 0.05). The ophthalmic root of the TGG neuron density in the 7 rabbits that developed severe vasospasm was statistically less than that observed in the 10 rabbits with mild vasospasm. There was a linear relationship between the low neuronal density in the ophthalmic root of the TGG and the severity of the AChA vasospasm.Conclusions:The trigeminal ganglion neuron density may be an important factor in the regulation of AChAs diameter and cerebral blood flow. Low neuron density of the ophthalmic root of the TGG may play a role in the pathogenesis of AChAs vasospasm associated with SAH.