Turkish Neurosurgery 2017 , Vol 27 , Num 6
Predictive Role of External Carotid Artery Vasospasm on Cerebral Ischemia After Subarachnoid Hemorrhage: Experimental Study
Nuriye Guzin OZDEMIR1,Mehmet Dumlu AYDIN2,Coskun YOLAS3,Ayhan KANAT4,Akin LEVENT5,Cemal GUNDOGDU6, Nazan AYDIN7
1Istanbul Training and Research Hospital, Neurosurgery Clinic, Istanbul, Turkey
2Ataturk University, Faculty of Medicine, Department of Neurosurgery, Erzurum, Turkey
3Erzurum Regional Training and Research Hospital, Neurosurgery Clinic, Erzurum, Turkey
4Recep Tayyip Erdogan University, Faculty of Medicine, Department of Neurosurgery, Rize, Turkey
5Ataturk University, Faculty of Medicine, Department of Radiology, Erzurum, Turkey
6Ataturk University, Faculty of Medicine, Department of Pathology, Erzurum, Turkey
7Bakırkoy Research and Training Hospital, Psychiatry Clinic, Istanbul, Turkey
DOI : 10.5137/1019-5149.JTN.17206-16.2 AIM: Cerebral vasospasm after subarachnoid hemorrhage (SAH) may lead to a devastating neurological outcome by inducing cerebral ischemia. However the role of external carotid artery (ECA) vasospasm has been rarely reported in the literature. The aim of this study was to elucidate the effect of ECA vasospasm on cerebral ischemia related neurodegeneration in the cerebral cortex after SAH.

MATERIAL and METHODS: This study was performed on 23 rabbits, divided into three groups: control (n=5), sham (n=5), and SAH (n=13). Experimental SAH was performed by injecting 0.75 mL auricular arterial homologous blood into the cisterna magna. After three weeks, the animals were decapitated and the common carotid arteries with their external and internal branches and the brains were examined histopathologically. Vasospasm indexes (VSI) of ECAs and internal carotid arteries (ICAs) and degenerated glial cell numbers of temporal cortices (n/mm3) were estimated stereologically and the results were compared statistically.

RESULTS: Temporal cortex glial cell density was estimated as 136.950±9.257/mm3 in normal rabbits, 131.324±7.987/mm3 in sham, 112.320±6.112/mm3 in light, and 97.543±5.432/mm3 in severe ECA vasospasm. The mean VSI values of ECA of all groups were 1.95±0.21, 2.15±0.29, 2.95±0.65 and 3.12±0.276, respectively. Statistical differences between the VSI values of ECA and degenerated neuron densities in temporal cortices were significant (p<0.005).

CONCLUSION: ECA vasospasm was observed to have a more important predictive role on the serious cerebral ischemia and neuronal degeneration after SAH. The mechanism may be related to ischemia of the parasympathetic ganglia of the lower cranial nerves and dorsal root ganglion. Keywords : Cerebral ischemia, Cerebral vasospasm, External carotid artery vasospasm, Subarachnoid hemorrhage

Corresponding author : Mehmet Dumlu Aydın, nmda11@hotmail.com