Protective felix culpa effect of superior sympathetic cervical ganglion degenerations on prevention of basilar artery spasm after subarachnoid hemorrhage: A preliminary experimental study

Abstract

BACKGROUND: Posterior cerebral blood flow is regulated by the basilar arteries (BAs). Vasospasm of BAs can occur after subarachnoid hemorrhage (SAH). Superior cervical sympathetic ganglia (SCG) fibers have a vasoconstrictor effect on the BA. We aimed to investigate the relationship between the degenerated neuron density of the SCG and the severity of BA vasospasm after experimental SAH.

METHODS: Twenty-four rabbits were used. Five were used as the control group, and 5 were used as the sham group. Experimental SAHs were performed in the remaining 14 animals (study group) by injecting homologous blood into the cisterna magna. After 3 weeks of injection, neuron densities of SCG and the severity of BA vasospasm index values (VSI) were examined histopathologically and compared statistically.

RESULTS: The mean VSI was 0.669 +/- 0.1129 in the control group, 0.981 +/- 0.159 in the sham group, and 1.512 +/- 0.298 in the study group. The mean degenerated neuronal density of SCG was 436 +/- 79/mm(3) in severe vasospasm (n = 3), 841 +/- 101/mm(3) in moderate vasospasm (n = 4), and 1.921 +/- 849/mm(3) in the less vasospasm detected animals (n = 6).

CONCLUSIONS: This study shows an inverse relationship between the degenerated neuronal density in the SCG and VSI values. This finding indicates a diminished sympathetic input from the SCG, resulting in a beneficial effect the felix culpa) by dilating the lumen diameter of the BA, so SCG degeneration after SAH protects the BA spasm.