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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 mm, 1.87 ± 0.19; 65.0 ± 12.0 mm, 1.91 ± 0.34; and 986.0 ± 112.0 mm, 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

BACKGROUND Spinal meningiomas are benign, well-circumscribed and slowly-growing intradural tumors that compress the spinal cord. Hereby, a retrospective review of 61 spinal meningioma cases evaluated in terms of demographic, clinical, pathological and radiological features to predict the early postoperative functional outcomes. METHODS Patients' records and MRI images of all the histologically confirmed spinal meningioma cases that underwent surgical resection at two university hospitals from January 2005 to June 2016 were retrospectively reviewed. Demographic data, clinical findings, radiological features and pathology reports were reviewed. Univariate and multivariate logistic regression analyses were used to evaluate the impact of each factor on the early 3-month post-surgical functional outcome. A receiver operating characteristic (ROC) curve was used to predict the power of the model. RESULTS Sixty-one cases of spinal meningiomas were operated: 13 males (21%) and 48 females (79%). Mean age was 60.5 years and ranged from 24 to 92 years. Patients presented with back pain (57%), motor deficits (47.5%), sensory deficits (18%) and sphincteric dysfunction (11.5%). One case (1.6%) showed an additional extradural growth. There were 40 thoracic, nine cervical, five cervicothoracic, five thoracolumbar, and two lumbar cases. Only four cases (6.6%) showed atypical pathological features (WHO grade II). At 3-month follow-up, 46 patients (75.4%) had either functionally improved or remained stable. Fifteen patients (24.6%) had "worse" functional outcome. Three variables showed statistically significant odds ratio for improved outcomes (OR): pre-surgical motor deficit (OR=5; P=0.005); presurgical sensory disturbance (OR=3.5; P=0.026); pre-surgical myelopathy (OR=3.5; P=0.026). Multivariate analysis showed increased OR for cross-sectional ratio, pre-surgical myelopathy, pre-surgical radiculopathy and non-cervical location of tumor (1.59, 3.46, 3.2, 1.63/3.56, respectively). Although none has reached statistical significance (P>0.05), the receiver operating characteristic (ROC) curve showed an area under the curve (AUC) of 0.74. CONCLUSIONS The independent predictors of the early postoperative functional outcomes of spinal meningioma resections may include pre-surgical motor deficit, sensory deficit and myelopathy.

Background Hydrocephalus is a serious complication of subarachnoid hemorrhage (SAH). Obstruction of the cerebral aqueduct may cause hydrocephalus after SAH. Although various etiologic theories have been put forward, choroidal artery vasospasm–related ependymal desquamation and subependymal basal membrane rupture as mechanisms of aqueductal stenosis have not been suggested in the literature. Methods This study was conducted on 26 hybrid rabbits. Five rabbits were placed in a control group, 5 were placed in a sham group, and the remaining rabbits ( n = 16) were placed in the SAH group. In the first 2 weeks, 5 animals in the SAH group died. The other 21 animals were decapitated after the 4-week follow-up period. Choroidal artery changes resulting from vasospasm, aqueduct volume, ependymal cell density, and Evans index values of brain ventricles were obtained and compared statistically. Results Mean aqueduct volume was 1.137 mm 3 ± 0.096, normal ependymal cell density was 4560/mm 2 ± 745, and Evans index was 0.32 ± 0.05 in control animals ( n = 5); these values were 1.247 mm 3 ± 0.112, 3568/mm 2 ± 612, and 0.34 ± 0.15 in sham animals ( n = 5); 1.676 mm 3 ± 0.123, 2923/mm 2 ± 591, and 0.43 ± 0.09 in animals without aqueductal stenosis ( n = 5); and 0.650 mm 3 ± 0.011, 1234/mm 2 ± 498, and 0.60 ± 0.18 in animals with severe aqueductal stenosis ( n = 6). The choroidal vasospasm index values were 1.160 ± 0.040 in the control group, 1.150 ± 0.175 in the sham group, 1.760 ± 0.125 in the nonstenotic group, and 2.262 ± 0.160 in the stenotic group. Aqueduct volumes, ependymal cell densities, Evans index, and choroidal artery vasospasm index values were statistically significantly different between groups ( P Conclusions Ependymal cell desquamation and subependymal basal membrane destruction related to choroidal artery vasospasm may lead to aqueductal stenosis and hydrocephalus after SAH.