Background: The Cushing response was first described in 1901. One of its components is elevated systemic blood pressure secondary to raised intracranial pressure. However, controversy still exists in its pathophysiologic mechanism. Hypertension is attributed to sympathetic overactivity and vagotomy increased renal-based hypertension. However, the role of the parasympathetic system in hypertension has not been investigated. This subject was investigated following subarachnoid hemorrhage (SAH). Methods: A total of 24 rabbits were used: control group (n = 5), SHAM group (n = 5), and an SAH group (n = 14; bolus injection of blood into the cisterna magna). Blood pressures were examined before, during, and after the experiment. After 3 weeks, animals were decapitated under general anesthesia. Vagal nodose ganglion, axonal degeneration, and renal artery vasospasm (RAV) indexes of all animals were determined histopathologically. Results: Significant degenerative changes were detected in the vagal axons and nodose ganglia following SAH in animals with severe hypertension. The mean degenerated neuron density of nodose ganglions, vasospasm index (VSI) values of renal arteries of control, SHAM, and study groups were estimated as 9.0 ± 2.0 mm3, 1.87 ± 0.19; 65.0 ± 12.0 mm3, 1.91 ± 0.34; and 986.0 ± 112.0 mm3, 2.32 ± 0.89, consecutively. Blood pressure was measured as 94.0 ± 10.0 mmHg in control group, 102.0 ± 12.0 mmHg in SHAM; 112.0 ± 14.0 mmHg in middle (n = 9); and >122.0 ± 10.0 mmHg in severe RAV-developed animals (n = 5). Differences VSI values and blood pressure between groups were statistically significant (P < 0.05). Conclusion: The degeneration of vagal nodose ganglion has an important role in RAV and the development of RAV and hypertension following SAH.

The authors believe that the balloon insertion technique may be a useful method to prevent brain collapse, cortical convolution, and complications associated with this condition. Further technical refinements of the system are needed for better results.

Background: Life-threatening basilar artery dissection (BAD) can be seen following subarachnoid hemorrhage (SAH), but it is not clear whether subarachnoid hemorrhage causes dissection, or not. This study aims to investigate the relationship between, degenerative changes in the superior cervical ganglia and the dissection rate of the basilar artery. Material and Method: In this article, after three weeks of experimental SAH, animals were decapitated. 18 rabbits were divided into three groups, according to their vasospasm indexes. The basilar arteries were examined by anatomical and histopathological methods. Results: Basilar dissection with high vasospasm index value (VSI>3) was detected in six animals (G-I, n=6); severe basilar edema and moderate vasospasm index value (VSI>2.4) in seven rabbits (G-II, n=7) and slight vasospasm (VSI<1.5) index value in five subjects (G-III, n=5) was detected. The degenerated neuron densities (n/mm3) of the superior cervical ganglia were detected as 12±4 in G-I, 41±8 in G-II; and 276±78 in G-III. The dissected surface values/lumen values were calculated as (42±1)/(64±11) in G-I; (21±6)/(89±17) in G-II; and (3±1)/(102±24) in G-III. If we look at these ratios as a percentage: 62%in G-I, 23% in G-II, and 5% in G-III. Conclusion: Inverse relationship between the degenerated neuron densities (n/mm3) of the superior cervical ganglia and the dissected surface values basilar artery was observed. The common knowledge is that basilar artery dissection may lead to SAH, however, this study indicates that SAH is the cause of basilar artery dissection.

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