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Background and Study Aim Basic neurophysiologic principles of the light reflex are well known. However, the effects of degenerated axon densities of oculomotor nerves (OMNs) secondary to posterior communicating artery (PComA) vasospasm following subarachnoid hemorrhage (SAH) have not been investigated. Our aim was to study this subject. Methods This study was conducted on 19 rabbits. There was a control group of five animals, a sham group of five animals in which saline was injected into the cisterna magna and a study group of nine animals in which homologous blood was injected into the cisterna magna. Pupillary diameters were measured for 1 week, then the animals were decapitated. The normal and degenerated axon densities of the OMNs were examined by stereological methods. Vasospasm indexes (VSIs) of posterior communicating arteries (PComAs) supplying OMNs were estimated and analyzed statistically. Results The pupillary diameter was 5.439 ± 368 µm, and the mean axon density of the OMNs was 0.924 ± 324/mm3 in the control group. The pupillary diameter and degenerated axon density of the OMNs in animals of the sham group were 6.980 ± 0.370 µm and 36 ± 8/mm3, respectively. The pupillary diameter was 9.942 ± 653 µm, and degenerated axon density of the OMNs was 265 ± 57/mm3 in animals with SAH. The mean VSI values of PComAs were 0.927 ± 0.224 in the control group, 1.542 ± 0.257 in the sham group, and 2.321 ± 0.324 in the SAH group. Conclusion We found a linear relationship between the axon density of the OMNs and pupillary diameters. High degenerated neuron density in the OMNs may be responsible for an unresponsive pupillary that has not been mentioned in the literature.

Background: The blood supply of the lower spinal cord is heavily dependent on the artery of Adamkiewicz. The goal of this study was to elucidate the effects of lumbar subarachnoid hemorrhage (SAH) on the lumbar 4 dorsal root ganglion (L4DRG) cells secondary to Adamkiewicz artery (AKA) vasospasm. Materials and Methods: This study was conducted on 20 rabbits, which were randomly divided into three groups: Spinal SAH (n = 8), serum saline (SS) (SS; n = 6) and control (n = 6) groups. Experimental spinal SAH was performed. After 20 days, volume values of AKA and neuron density of L4DRG were analyzed. Results: The mean alive neuron density of the L4DRG was 15420 ± 1240/mm3 and degenerated neuron density was 1045 ± 260/mm3 in the control group. Whereas, the density of living and degenerated neurons density were 12930 ± 1060/mm3 and 1365 ± 480/mm3 in serum saline (SS), 9845 ± 1028/mm3 and 4560 ± 1340/mm3 in the SAH group. The mean volume of imaginary AKAs was estimated as 1,250 ± 0,310 mm3 in the control group and 1,030 ± 0,240 mm3 in the SF group and 0,910 ± 0,170 mm3 in SAH group. Volume reduction of the AKAs and neuron density L4DRG were significantly different between the SAH and other two groups (P < 0.05). Conclusion: Decreased volume of the lumen of the artery of Adamkiewicz was observed in animals with SAH compared with controls. Increased degeneration the L4 dorsal root ganglion in animals with SAH was also noted. Our findings will aid in the planning of future experimental studies and determining the clinical relevance on such studies.

Background: Few case reports describe an increase in the size of syringomyelia and the worsening of neurologic symptoms after surgery for foramen magnum decompression. We report three such cases.Ma...

AIM To compare the clinical and radiological results of using synthetic bone graft versus autograft obtained from the spinous process in posterior lumbar interbody fusion. MATERIAL AND METHODS This retrospective study included 102 patients with degenerative lumbar spondylolisthesis who underwent one-segment posterior lumbar interbody fusion (PLIF) followed by one-segment posterior transpedicular instrumentation. PLIF surgery was performed using a local solid bone graft obtained from the spinous process in group A and using a synthetic solid calcium hydroxyapatite block in group B. The Oswestry Disability Index (ODI), visual analogue scale (VAS) scores, degree of bone formation, intervertebral disc heights at the operation segment, wound infection, and instrumentation complications were compared between the 6-month and 5-year follow-ups. RESULTS In both groups, ODI and VAS scores significantly improved at the 6-month and 5-year follow-up. Bone formation at both 6 months and 5 years were higher in group A than that in group B, but without a significant difference when compared. Moreover, the difference in maintaining the intervertebral disc heights was not significant between the two groups. Surgical wound infection more commonly occurred in group B, but without significant difference between the two groups, and rod fractures were observed in two patients in group B; however, no metal breakage was observed in group A. CONCLUSION Successful fusion of the intervertebral space and intervertebral height restoration can be achieved and maintained with an autograft from the patient's spinous processes.

Vagal nerves and their thermoreceptors could regulate temperature of brain. Cerebrospinal fluid (CSF) is increased in the early phases of subarachnoid hemorrhage (SAH). We hypothesised that choroid plexuses probably innervated by vagal nerves may play a role on the regulation of brain temperature and studied this subject.This study was conducted on 32 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 22 rabbits in the SAH group. In the SAH group, 7 of the animals were decapitated after 7 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 21 days of injections (Group IV). Brain temperature via laser thermometer 5 times a day during the experiment was measured. Normal and degenerated neuron density of nodose ganglia, water vesicles numbers of choroid plexuses were stereologicallyanalyzed. Statistical analysis was performed.At histopathologic analysis of present study, thermo regulator like structure was noted and the mean number of this structure was estimated.The mean number of water-filled vesicles, thermo regulator like structure, in SAH-induced animals,brain temperature and degenerated neuron density of nodose ganglia was statistically different between the early decapitated group (group III) and the late decapitated group (group IV) (P less then 0.05).We introduce a thermo regulator like structure, describe a new syndrome. In addition, it was noted thatwater-filled vesicles of CP are increased, brain temperature in nearly normal in the early phase of SAH due to likely irritation of vagal nerves. However in the late phase, mean number of water-filled vesicles numbers decreased in accordance with increased brain temperature with degenerative changes of the nodose ganglion.

Background Autonomous innervations of the lungs are maintained by cervical sympathetic and vagal nerves. Sympathetic overactivity-induced neurogenic pulmonary edema (NPE) is known as a serious complication of subarachnoid hemorrhage, but the rational neuronal mechanism of that overactivity has not yet been clarified fully. The aim of this study was to examine whether there is a relationship between vagal nerve ischemia related sympathetic overactivity and neurogenic pulmonary edema in subarachnoid hemorrhage. Methods This study was conducted on 27 rabbits. A control group was formed of 5 animals, a sham group of 7 to which saline was administered, and a study group of 15 animals that were injected with homologous arterial blood into the cisterna magna. Electrocardiography and respiratory rhythm parameters were monitored for 3 weeks and the animals were then decapitated. Statistical analysis was made of the numbers of degenerated axons in the pulmonary branches of the vagal nerves, the neuron density of stellate ganglions and the vasospasm index of the pulmonary arteries. Results In the control group, the normal respiration rate was 34 ± 6 bpm, total axon number was 1600 ± 270/mm 2 , degenerated axon number was 10 ± 3/mm 2 , and vasospasm index was 1.34 ± 0.25. The sham group values were 30 ± 3 bpm, 163 ± 47/mm 2 , and 1.95 ± 0.45 and the study group values were 45 ± 8 bpm, 530 ± 92/mm 2 , and 2.76 ± 0.83. The mean stellate ganglion neuron density was evaluated as 8.112 ± 1.230/mm 3 in all animals, as 7.420 ± 4.10/mm 3 in animals with slight NPE, and as 12.512 ± 1.236/mm 3 in animals that developed severe NPE. Conclusion High neuron density of stellate ganglion may have important roots in sympathetic overactivity-related NPE development in subarachnoid hemorrhage.

Objective The Adamkiewicz artery (AKA) supplies pudendal nerve roots and conus medullaris. The aim of this study was to elucidate if there is any relationship between neurodegenerative changes of the Onuf nucleus (ON)–pudendal nerve ganglia complex secondary to vasospasm of the AKA after spinal subarachnoid hemorrhage (SAH). Methods This study was conducted on 22 rabbits, which were randomly divided into 3 groups: control (n = 5), sham (n = 5), and spinal SAH (n = 12). Experimental spinal SAH was induced at the L2 level. After 2 weeks, the ON–pudendal nerve ganglia complex and AKA were examined histopathologically. Bladder volume values were estimated, and results were analyzed statistically. Results Two animals died within the first week of experiment. Histopathologically, severe vasospasm of the AKA and neuronal degeneration and neuronal apoptosis were observed in the ON–pudendal nerve ganglia complex in 5 animals of the SAH group. The mean volume of the imaginary AKA, mean bladder volumes, and degenerated neuron densities of ON and pudendal nerve ganglia were estimated. We found that vasospasm of the AKA led to numerous neuron degenerations in ON and pudendal ganglia and consequently urinary retention (P Conclusions ON–pudendal nerve ganglia complex degeneration secondary to vasospasm of the AKA may be a cause of urinary retention after spinal SAH.

Objective: The exact mechanism of phonophobia induced by subarachnoid hemorrhage (SAH) has not been understood well. This subject was investigated.Material and methods: This study was conducted on ...

Hematoma of the ligamentum flavum (LF) is a rare cause of neural compression and sciatica. Currently, the etiology and epidemiological characteristics of ligamentum flavum hematoma (LFH) are unknown and epidemiological investigations using rewieving of reported cases have not been performed. We report the case of a 63-year-old man with a LFH compressing the spinal canal at the left L2–L3 level, rewieved relevant literature. In Medline research, wefound a total of 50 reported cases with LFHs, and the interesting point of these cases were analyzed. Many of cases were old males. Interestingly, 39 of the 50 cases were reported from Asian countries. The ages of 42 patients could be verified. The youngest age was 45 years, oldest age was 81 years, and mean age was 66.07 years. Thirty-three out of these 42 patients (78.53%) were older than 60 years. An important aspect of the present review is to bring attention for occurrence in older Asian males. With an increasing number of elderly people in the general population, there is a need to investigate risk factors such as sexual gender, age, and geographic location for LFH.

Aim To examine ischemic neurodegeneration of the ciliospinal center on permanent miosis following subarachnoid hemorrhage (SAH). Material and methods Nineteen rabbits were examined in this study. The animals were divided into three groups, as control (GI, n=5), sham (GII, n=5) and study group (GIII, n=9). Pupil diameters were measured after giving 0.5 mL physiological saline for sham and autologous arterial blood for the study group into the cervico-thoracic subarachnoid space. After three weeks of follow up, the cervico-thoracic cord and bilateral superior cervical sympathetic ganglia were removed. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia and degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods. Results The mean pupil diameter was 5180 ± 370 µm and the mean degenerated neuron density of the ciliospinal center was 4 ± 1/mm3 in animals of the control group (GI). These values were 9850 ± 610 Iµm, 10 ± 3/mm3 in sham (GII), and 7.010 ± 440 Iµm and 98 ± 21/mm3 in the study (GIII) groups. There was an inverse relationship between degenerated neuron density of the ciliospinal nuclei and pupil diameters. Conclusion We showed and reported for the first time that ciliospinal sympathetic center ischemia-induced neurodegeneration may have been responsible for permanent miosis following SAH.

Aim: The morphologic mechanism of orgasmic sensation has not yet been understood. Taste roseas may be stimulated by fructose via pudendal nerves, which has not been studied yet.Methods: In this study, 27 male adult rabbits were used, which were divided into three groups: 5 as control; 5 as SHAM and 17 used as study group. We injected 0.2 cc of distilled water to SHAM and 0.2 cc of fructose solution to the study group of their urethral orifices, and examined the occurrence of penile erection. The relationship between erection and pudendal nerve ganglia and penile tissues was statistically compared.Results: In animals with high neuron density of pudendal ganglia, more erection phenomenon was observed than those animals with low neuron density. Interestingly, neuron density of pudendal ganglia was 9.243 ± 542 /mm3 in hypoactive and was 5.980 ± 463 /mm3 in non-active animals (p < 0.05).Conclusions: The seminal fructose may stimulate taste roseas of the urethra and glans penis via pudendal nerves. The ...

BACKGROUND Intradiploic epidermoid cysts (IEC) are rare, benign lesions derived from ectodermal remnants during neural tube closure. Their origin is still debated or unknown. OBJECTIVE Analyzing of the patients with intradiploic epidermoid cysts operated in the authors' department. METHODS The patients with IEC who were operated in the authors' department between January 2014 and December 2015 were investigated from data file. RESULTS Six patients with IEC were found, reviewed the literature, and noted that these cysts usually occur in adults. There are only 3 young cases that occurred after head injury. CONCLUSION It was shown that the nontraumatic IEC are more frequent in older ages. In youngs, it can generally be embryologic or rarely of mechanical origin following trauma. Cranial trauma may be important for developing of IEC. Trauma may lead to inclusion of epidermal cells into the diploe of the skull and may be a reason of intradiploic epidermoid cyst in older age. The effect of older age, and gender difference on occurrence should be investigated.

Introduction Although hyperglycemia is a serious complication of subarachnoid hemorrhage, its pathophysiologic mechanism based on neural circuitry has not been known. Materials and Methods Twenty-five rabbits were divided into 4 groups, with 5 in the control group. The SHAM and study groups received 1 mL saline and 1 mL autologous arterial blood into the sylvian cisterna, respectively. Blood glucose values (BGVs) of all animals were recorded 3 times weekly. After 2 weeks, animals were decapitated. BGVs, the number of normal and degenerated neuron densities (DNDs) of insular cortex (IC), and nodose ganglia, degenerated islands of Reil's surfaces values, were estimated by stereologically and analyzed statistically. Results The mean blood glucose values were measured as 101 ± 10 mg/dL in the control group ( n = 5), 114 ± 11 mg/dL in the SHAM group ( n = 5), and 137 ± 12 mg/dL in the subarachnoid hemorrhage (SAH) group ( n = 15). The DND of the nodose ganglion was 10 ± 3/mm 3 in the control group, while it was 45 ± 7/mm 3 in the SHAM group and 1688 ± 191/mm 3 in the SAH group. The DND of the IC was 65 ± 12/mm 3 in the control group, 689 ± 112/mm 3 in the SHAM group, and 3709 ± 643/mm 3 in the SAH group. In addition, the proportion of degenerated surface areas in the islet of Langerhans was 0.3% in the control group, 6% in the SHAM group, and 28% in the SAH group. Conclusion There is an important linear relationship among the blood glucose levels, DND of the IC, and nodose ganglia and degenerated surface areas of IL following experimentally induced sylvian SAH.

Objective The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insuts following subarachnoid hemorrhage (SAH)which may contribute to develop acidosis has not been investigated. Materials and Methods Twent-three hybrid rabbits were used.They divided into three groups; Five (n=5) as control group, five (n=5) as SHAM group, the remaining 13 (n=13) as study group. 1cc serum saline, 1cc autolog arterial blood into the cisterna magna were injected; in SHAM and study group, respectively. Blood pH values of all annimals were recorded. After two weeks, animal were decapitated. The number of normal and degenerated neuron density ofCBs were counted by stereological methods,analysed statistically. Results Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35±0.07 in control, 7.33±0.06 in SHAM, 7.29±0.05 in rabbits with slight acidisis (n=6) and 7.23±0.02 in in rabbits with prominent acidosis. In control groups, the average normal neuronal density of the CB was 6432±790/mm 3 and degenerated neuron density was 11±3/mm 3 while the degenerated neuronal density in CB was 35±8/mm 3 in SHAM group, 1034±112/mm 3 in slight acidis developed group (n=6; p 3 in the prominent acidosis developed animals (n=8; p 3 Conclusion Inverse relationship between neurodegeneration in the CB and PH values secondary to the disruption ofGPN-CBnetwork following SAH was foundwhich may contribute to develop acidosis.

Background Acute hydrocephalus (ventricular enlargement within 72 hours) is a common complication in patients with aneurysmal subarachnoid hemorrhage (SAH). Cerebrospinal fluid (CSF) secretion may be increased in the early phases of SAH, but it has not been proved definitively. We studied the histologic features of choroid plexus (CP) in the early and late phases of SAH. Methods This study was conducted on 20 rabbits, with 5 rabbits in the control group, 5 rabbits in the sham group, and 10 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 2 days of cisternal blood injections, and the other five animals were decapitated after 14 days of injections. The CP of lateral ventricles were obtained from coronary sections of brains at the level of the temporal horns of the lateral ventricles. Sections were stained with hematoxylin and eosin and Masson trichrome for SAH-related damage and examined stereologically to discern water-filled vesicles, which were counted. Sections were compared statistically. Results The mean numbers of water vesicles were different after SAH between the early decapitated group (group III) and the late decapitated group (group IV). The mean numbers of water vesicles were 2.80 (±0.05) in the control group (group I), 2.76 (±0.02) in the sham group (group II), 14.68 (±0.06) in the early decapitated group (group III), and 4.78 (±0.13) in the late decapitated group (group IV). Total number of fluid-filled vesicles of CP was also assessed stereologically; the total numbers were 840 (±16) in group I, 828 (±7) in group II, 4404 (±19) in group III, and 1434 (±41) in group IV. The numbers of water-filled cisterns were significantly increased in the early phases of SAH ( P Conclusions In SAH with aneurysm rupture, increased CSF secretion seems to be triggered by hemorrhage in the early phase, but it is not possible in the late phase because of CP degeneration. In the early phase of hemorrhage, CSF secretion may be stimulated by the irritant receptor glossopharyngeal and vagal nerve endings, which innervate the healthy CP epithelium and arteries. Our findings may be accepted as being causative. It is likewise possible that CSF blockage per se leads to hydrocephalus, and the morphologic changes are sequelae that occur later in the course of disease. This is the first study to show the water vesicles of CP as a causative factor in the development of acute hydrocephalus after SAH.

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.

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.

Background: Low back and leg pain due to lumbar discal hernia (LDH) is an important health issue. Current evidences support surgery in carefully selected patients who have failed conservative treatment and do not exhibit any psychosocial overlay. However, as known, sometimes it may be still very difficult to normalize the life qualities of patients for long times. Now different surgical methods for LDH are in use with new technological materials. One of them is lumbar disc prosthesis. In this study, the radiological and clinical effects of using lumbar disc prosthesis were evaluated with comparing patients underwent simple lumbar microdsicectomy. The purpose of this study is to reveal whether inserting the disc prosthesis into the intervertebral distance after lumbar microdiscectomy is beneficial or not both radiologically and clinically. Methods: A total of 114 patients were analyzed; the first cohort consisted of 57 patients who received a lumbar discectomy at a single level along with the implantation of a disc prosthesis and the second consisted of 57 patients only received a lumbar discectomy at a single level. These 2 groups were studied by comparing the disc space on the level of carried out operations with pain scales, foramen diameters of coming about related roots preoperatively and postoperatively at 3 years. Results: One of the significant results of the implementation of the disc prosthesis is fulfilment of a healthy disc height again after microdiscectomy due to LDH. We concluded that fulfilment of a healthy disc height with lumbar disc prosthesis was clinically beneficial for patients underwent microdiscectomy. Conclusions: Based on the results obtained in this study, it can be concluded that the implantation of a disc prosthesis in appropriate patients is more favorable regarding pain and spinal physiology when compared to simple microdiscectomy.

Gundogdu, Cemal/0000-0003-2857-923X; Kanat, Ayhan/0000-0002-8189-2877 WOS: 000370379200007 PubMed: 25972712 Context: Somato-sensitive innervation of bowels are maintained by lower segments of spinal cord and the blood supply of the lower spinal cord is heavily dependent on Adamkiewicz artery. Although bowel problems are sometimes seen in subarachnoid hemorrhage neither Adamkiewicz artery spasm nor spinal cord ischemia has not been elucidated as a cause of bowel dilatation so far. Aims: the goal of this study was to study the effects Adamkiewicz artery (AKA) vasospasm in lumbar subarachnoid hemorrhage (SAH) on bowel dilatation severity. Settings and Design: An experimental rabbit study. Materials and Methods: the study was conducted on 25 rabbits, which were randomly divided into three groups: Spinal SAH (N = 13), serum saline (SS) (SS; N = 7) and control (N = 5) groups. Experimental spinal SAH was performed. After 21 days, volume values of descending parts of large bowels and degenerated neuron density of L5DRG were analyzed. Statistical Analysis Used: Statistical analysis was performed using the PASW Statistics 18.0 for Windows (SPSS Inc., Chicago, Illinois). Two-tailed t-test and Mann-Whitney U-tests were used. the statistical significance was set at P < 0.05. Results: the mean volume of imaginary descending colons was estimated as 93 12 cm (3) in the control group and 121 26 cm (3) in the SS group and 176 49 cm (3) in SAH group. Volume augmentations of the descending colons and degenerated neuron density L5DRG were significantly different between the SAH and other two groups (P < 0.05). Conclusion: An inverse relationship between the living neuronal density of the L5DRG and the volume of imaginary descending colon values was occurred. Our findings will aid in the planning of future experimental studies and determining the clinical relevance on such studies.

Cerebrospinal fluid (CSF) secretion may be increased in the early phases of subarachnoid hemorrhage (SAH), possibly via ischemic glossopharyngeal nerve discharges, and decreased due to glossopharyngeal nerve degeneration in the late phase of SAH; but this reflex pathway has not been definitively investigated. We studied the relationship between petrous ganglion of the glossopharyngeal nerve (GPN) and water vesicles of the choroid plexus (CP) in the early and late phases of SAH. This study was conducted on 30 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 20 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 4 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 20 days of injections (Group IV). The Petrous Ganglia and CPs of lateral ventricles were removed and stained for stereological analysis. The mean number of follicles per cubic millimeter was 5.3 ± 1.2 the in control group (Group I), 4.5 ± 0.9 in the sham group (Group II), 16.60 ± 3.77 the in early decapitated group (Group III), and 4.30 ± 0.84 in the late decapitated group (Group IV). The mean number of degenerated neuron density of petrous ganglions was 6 ± 2, 50 ± 6, 742 ± 96, and 2.420 ± 350 in the control (Group I), sham (Group II), early decapitated (Group III), and late decapitated group (Group IV), respectively. The mean number of water vesicles was statistically different after SAH between the early decapitated group (group III) and the late decapitated group (group IV) (P

Object The glossopharyngeal nerves (GPNs) and carotid bodies (CBs) have an important role in the continuation of the cerebral autoregulation and cardiorespiratory functions. The relationship between degenerative injury of CB and the GPN in subarachnoid hemorrhage (SAH) was studied. Methods Twenty rabbits were included in this study. Five of them (n = 5) were used as control group. The remaining animals (n = 15) were exposed to experimental SAH. In the six animals of the SAH group, severe signs of illness were observed, and these six animals were killed in the first week after SAH. Others animals (n = 9) were followed for 20 days and then sacrificed. GPNs and CBs were examined and, the live and degenerated GPN axon number, and of CB neuron numbers were stereologically estimated. Results The mean number of live neurons in CBs was 4206.67 ± 148.35 and live axons of GPNs were 1211.66 ± 14.29 in the animals of the control group. The number of degenerated neurons of CBs was 2065 ± 110.27 and the number of degenerated axons of GPNs was 530.83 ± 43.48 in early killed animals with SAH. The number of degenerated neurons of CBs and the number of degenerated axons of GPNs were found as 1013.89 ± 4184 and 2270.5 ± 134.38 in the living animals with SAH, respectively. Conclusions High number of degenerated axons of GPN and neurons of CBs of the early killed animals suggest that the mortality in early SAH might be due to GPNs injury secondary to compression of their axons or supplying vessels by the probably herniated brainstem, and secondary denervation injury of CBs, and lung.

AYDIN, Nazan/0000-0003-3232-7713 WOS: 000249305600016 PubMed: 17786012 A 9-year-old male patient complaining of seizure attack was admitted to the neurosurgery department. Radiologic investigations revealed a 5-cm-long metallic sewing needle extending from the right frontal cortex to the right lateral ventricle. Burr hole surgery was performed and the needle was grasped with biopsy forceps and removed with endoscopic guidance. The patient recovered without any complications. Copyright (c) 2007 S. Karger AG, Basel.

We investigated the number of degenerated neurons in spinal roots of rabbits after spinal surgery to test if electrocauterization causes neuronal loss. The number of degenerated neurons was higher in study group than in control group, and the number of live neurons was higher in control group than in study group. These results suggest that electrocauterization applied during spinal surgery is hazardous to spinal neurons and should not be applied unless required.

✓ Four cases of alveolar hydatid disease of the brain encountered within 27 months in eastern Turkey are reported. All of the patients were male farmers who presented with signs of cerebral tumor. Two of the patients were shown to harbor hepatic lesions and one of them had pulmonary metastases. The cerebral lesions were removed in toto and neurological recovery was obtained in all four patients. A review of the literature revealed only five previously reported cases treated surgically. It is concluded that cerebral Echinococcus multilocularis lesions are amenable to surgery, and that their removal provides useful prolongation of life despite the presence of hepatic or pulmonary disease.

Cyst formation with meningioma is extremely rare. Two cases of large peritumoral cystic lesions associated with intracranial meningiomas that simulated astrocytomas are presented. In each of these young patients, the cyst caused misdiagnosis pre- and intraoperatively. However, total excision was accomplished in each case. The pertinent literature is reviewed. (Neurosurgery 16:87–89, 1985)