The Role of Trigeminal Ganglion Neuron Density in the Prevention of Subarachnoid Hemorrhage-induced Basilar Artery Vasospasm: An Experimental Study

Abstract

Objective Cerebral arteries innervated by several systems contribute to the control of cerebral blood flow. Sensory fibers of the trigeminal nerve have a vasodilatory effect on the basilar artery. Subarachnoid hemorrhage (SAH) causes severe cerebral vasospasm by various neurochemical mechanisms. We examined possible relationships between the neuron density of the trigeminal ganglion and the severity of basilar artery vasospasm in SAH. Methods In this study, 28 rabbits were used. The animals were randomly divided into 3 groups: SAH (n=18), serum physiologic (n=5) and control (n=5) groups. Experimental SAH was induced by injecting homologous blood into the cisterna magna. After 20 days, the basilar arteries and trigeminal ganglions were examined histopathologically. Basilar artery volumes and the neuron density of the ophthalmic divisions of the trigeminal ganglions were estimated stereologically, and the results were statistically analyzed. Results The mean basilar artery volume was 4.15±0.19 mm3 and the mean neuronal density of the trigeminal ganglion was 6500±750/mm3 for the control group. These values were 4.05±0.29 mm3 and 6400±584/mm3 for the serum physiologic group, 3.80±0.35 mm3 and 4600±300/mm3 for living animals in the SAH group, and 2.26±0.29 mm3 and 2950±618/mm3 for dead animals in SAH group, respectively. A linear relationship was found between the neuronal density of the trigeminal ganglion and basilar artery volumes. Conclusions The neuron density of the trigeminal ganglion may be an important factor in the regulation of basilar artery volume and for the continuation of cerebral blood flow. The low neuron density of the trigeminal ganglion may be involved in the pathogenesis of severe basilar artery vasospasm induced by SAH.