Protective Felix Culpa Effect of Superior Sympathetic Cervical Ganglion Degenerations on Prevention of Basilar Artery Spasm After Subarachnoid Hemorrhage: A Preliminary Experimental Study
World Neurosurgery, cilt.164, 2022 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 164
- Basım Tarihi: 2022
- Doi Numarası: 10.1016/j.wneu.2022.05.063
- Dergi Adı: World Neurosurgery
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, EMBASE, Index Islamicus, MEDLINE, Veterinary Science Database
- Anahtar Kelimeler: Basilar arteries, Degeneration, Subarachnoid hemorrhage, Superior cervical ganglion, Vasospasm
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
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/mm3 in severe vasospasm (n = 3), 841 ± 101/mm3 in moderate vasospasm (n = 4), and 1.921 ± 849/mm3 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.