Turkish Neurosurgery
Predictive Role of External Carotid Artery Vasospasm on Cerebral Ischemia in Subarachnoid Hemorrhage: Experimental Study
Nuriye Güzin Özdemir1, Mehmet Dumlu Aydın2, Coşkun Yolaş3, Ayhan Kanat4, Akın Levent5, Cemal Gündoğdu6, Nazan Aydın7
1İstanbul Training and Research Hospital, Neurosurgery, İSTANBUL,
2Erzurum Atatürk University, Faculty of Medicine, Neurosurgery, ERZURUM,
3Erzurum Regional Training and Research Hospital, Neurosurgery, ERZURUM,
4Recep Tayyip Erdoğan University, Faculty of Medicine, Neurosurgery, RİZE,
5Erzurum Atatürk University, Faculty of Medicine, Radiology, ERZURUM,
6Erzurum Atatürk University, Faculty of Medicine, Pathology, ERZURUM,
7Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, Psychiatry, İSTANBUL,
DOI: 10.5137/1019-5149.JTN.17206-16.2

Aim:Cerebral vasospasm after subarachnoid hemorrhage (SAH) may lead to 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 is 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 (SF; n = 5), and SAH (n = 13). Experimental SAH was performed by injecting of 0.75 mL auricular arterial homologous blood into cisterna magna. After three weeks, animals were decapitated and common carotid arteries with their external and internal branches, and brains were examined histopathologically. Vasospasm indexes (VSI) of ECAs and internal carotid arteries (ICA) and degenerated glial cell numbers of temporal cortices (n/mm3) were estimated stereologically and results were analysed 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 analysis 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.

Full text PDF