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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.

Fatal pulmonary edema and hemorrhage are significant complications of endovascular treatment in steno-occlusive carotid artery disease; a rational mechanism has not been adequately examined in the literature so far. We investigated if cervical sympathetic ganglia ischemia prevents pulmonary vasospasm on the prognosis of bilateral common carotid artery ligation (BCCAL). Twenty-three adult New Zealand rabbits (4.2 AE 0.3 kg) were randomly divided into three groups: the control group (G1, n = 5), the sham group (G2, n = 6), and the BCCAL group (G3, n = 12). Common carotid arteries were dissected bilaterally in G2/G3, and permanent BCCAL was applied to only in G3. All animals were followed for 3 weeks and decapitated under general anesthesia. Histopathological changes in stellate ganglia and severity of pulmonary vasospasm-related lung edema and hemorrhage were investigated. Results were analyzed by the Kruskal-Wallis test. Two animals of G3 dead within three weeks and the remainder were sacrificed three weeks later. Subpleural petechial foci and an endotracheal bloody fluid collection were grossly observed in the lungs. Histopathologically, pulmonary artery vasospasm, perivascular and subintimal edema, interalveolar hemorrhage, and alveolar wall destructions were observed with less ischemic-degenerated neuron density-determined stellate ganglia animals. Neurodegeneration of stellate ganglia may have a beneficial effect on the prevention of lung injury during stenoocclusive carotid artery disease.

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Aim: Scalp hairs are mainly innervated by sensitive fibers of trigeminal nerves. Ischemic neurodegeneration of trigeminal ganglion can cause denervation injury of scalp hairs. We investigated if there is a relationship between the degenerated neuron densities of trigeminal ganglion neuron densities and the numbers of degenerated hair follicles numbers following subarachnoid hemorrhage (SAH). Material and Method: Five normal (n=5), five SHAM (n=5), and ten (n=10) male rabbits were chosen from formerly experimental SAH created by cisternal homologous blood injection (0.75cc) group, which followed for three weeks. Degenerated neuron numbers of trigeminal ganglion and atrophic hair follicles numbers in the frontal areas of the scalp were examined by stereological methods. Degenerated neuron densities of trigeminal ganglions and atrophic hair follicles numbers were analyzed by the Mann-Whitney U test. Results: The mean degenerated neuron densities trigeminal ganglions (n/mm3) and atrophic hair follicles (n/mm2) were determined as 5±2/m3 and12±4/mm2 in control; 12±3/m3 and 41±8/mm2 in Sham and, 168±23/m3 and 79±14/mm2 in the study group (p>0.001). In the post-hoc analysis, all groups differed significantly from each other. A linear association was observed between the degenerated neuron densities of trigeminal ganglions and atrophic hair follicles (r: 0.343, p: 0.007). Conclusion: Trigeminal ganglion neurodegeneration may be an essential factor in hair follicles atrophy after SAH, which has not been mentioned in the literature so far.

Somatosensitive innervation of lower abdominal region skin region (LARS) is mainly managed by somatosensitive fibers of lumbar spinal dorsal root ganglions (DRG). We investigated if there is a relationship between the degenerated neuron densities (DND) of the first lumbar DRG (L1) and LARS' total tissue viability score (TVS) following subarachnoid hemorrhage (SAH). Study was conducted on 20 rabbits. All animals divided in three groups as Control group (n=5), SHAM group (n=5) and study group (n=10). For SHAM group 0,5 cc saline solution injected into lumbar spinal subarachnoid space and for study group, 0.5cc autolog blood injected into lumbar spinal subarachnoid space under general anesthesia. All animals were followed up three weeks and sacrificed. DND of L1 DRG (n/mm3) and the histopathological changes of LARS examined histopathologically. A value determined for hair loss per square millimeter (n): 1 point(P); if n<5, 2P if 10>n>5; 3P if n>10. For skin thickness as micrometer (T m), it was scored as 1P if T>700 m, 2P if 600 m 400 m, and 3P if T<400 m. Evaluation was made on their total 12-points tissue viability score (TVS). If TVS>10, the skin is considered as normal; If 106, the moderately damaged; if TVS < 7, the was severely damaged. DND and TVS values analyzed by Mann Witney U test. The mean DND of LI DRG (n/mm3) and TVS values were determined as 13±3/11±1 in control; 34±8/8±2 in SHAM and 263±44/<6 in the study group. Statistical values were: p<0.05 (Control/SHAM), p<0.0005 (SHAM/Study) and p<0.0001 (Control/Study). Somatosensitive innervation deficiency resulting from DRG ischemia following SAH may lead to deterioration of LARS which may be important in reconstructive surgery.

Introduction: Olfaction and its relation to human health is an area of growing interest. Although olfaction disorders have been considered a part of Kallmann Syndrome, the role of olfactory dysfunction on spermatogenesis has not been studied yet. We studied if olfactory bulbectomy causes dysfunction in spermatogenesis as a result of Onuf’s nucleus damage. Methods: Twenty-eight male rats were divided into three groups: six as the control (G-1; n=6), six as the only frontal burr-hole applied animals SHAM (G-1I; n=6), and 16 as the study group (G-III; n=16) in which OBX was performed. The animals were followed for two months. After the decapitation of the animals, olfactory bulb (OB) volumes (mm3), the neuron density of the Onuf nucleus (n/mm3), and sperm density (n/mm3) were estimated stereologically, and analyzed. Results: Olfactory bulb volumes (mm3), degenerated neuron density of Onuf's nucleus (n/mm3), and sperm numbers of control, SHAM, and study groups were estimated as: 4±0.5; 6±2 and 103.245±10.841 in G-I; 3.5±0.7; 14±4 and 96.891±9.569 in G-II and 1.3±0.3; 91±17 and 73.561±6.324 in GIII. The statistical results of degenerated neuron density of Onuf's nucleus and sperm numbers between groups are as p<0.005 for GI/GII; p<0.0005 for GII/GIII and p<0.00001 for G-I/G-III. Discussion/Conclusion: This study first time indicates that Onuf's nucleus degeneration secondary to OBX seems to be responsible for reduced sperm numbers.