From Nose to Lumbar Spinal Cord - Reduced Sperm Numbers Occur by Olfactory Bulbectomy-Related Onuf's Nucleus Degeneration: New Experimental Evidence for Kallmann Syndrome.

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 (OBX) 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-2; n = 6), and 16 as the study group (G-3; n = 16) in which OBX was performed. The animals were followed for 2 months. After the decapitation of the animals, olfactory bulb (OB) volumes (mm3), the neuron density of the Onuf's nucleus (n/mm3), and sperm density (n/mm3) were estimated stereologically and analyzed. RESULTS: OB 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-1; 3.5 ± 0.7; 14 ± 4 and 96.891 ± 9.569 in G-2; and 1.3 ± 0.3; 91 ± 17 and 73.561 ± 6.324 in G-3. The statistical results of degenerated neuron density of Onuf's nucleus and sperm numbers between groups are p < 0.005 for G-1/G-2; p < 0.0005 for G-2/G-3; and p < 0.00001 for G-1/G-3. DISCUSSION: This study first time indicates that Onuf's nucleus degeneration secondary to OBX seems to be responsible for reduced sperm numbers.

Synthetic Bone Graft versus Autograft Obtained from the Spinous Process in Posterior Lumbar Interbody Fusion.

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.

Recrudescence of the syringomyelia after surgery of Chiari malformation type 1 with duraplasty.

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.Material and method: Retrospective review of patients with Chiari malformation (CM) and syringomyelia operated at the Erzurum Regional Hospital, Department of Neurosurgery between 1 January 2008 and 18 June 2018.Results: A total of 118 patients were operated during the study period. Of the 118 patients, 81 were females, 37 were males. Ages range between 4 and 82 years, mean 38 years. Cervical or thoracic syringomyelia was found in 81 patients. Decompressive surgery with duraplasty was performed in all patients, and the patients were followed at least 2 years. The syrinx was the same or smaller in volume in 74 patients postoperatively, however, in three patients (3.7% of all patients with syringomyelia), the syrinx increased in volume.Conclusions: In this study, it was observed that an improvement or resolution of syringomyelia in 74 patients (91.3%) after decompression. There were no changes in the cavity in 4 and increased size in 3.

New insights of the fever following subarachnoid hemorrhage and introducing a new thermoregulator like structure in choroid plexuses; preliminary study.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Spinal Subarachnoid Hemorrhage Induced Intractable Miotic Pupil. A Reminder of Ciliospinal Sympathetic Center Ischemia Based Miosis: An Experimental Study.

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 εm, 10 ± 3/mm3 in sham (GII), and 7.010 ± 440 εm 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.

First emerging objective experimental evidence of hearing impairment following subarachnoid haemorrhage; Felix culpa, phonophobia, and elucidation of the role of trigeminal ganglion.

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 25 rabbits. They divided into three groups: Five as control, five as SHAM, 20 as SAH group. All animals objected to 85 dB impulse noise by daily periods, and their phonophobic score values were examined by daily periods for 20 days. Their brains, trigeminal ganglia were extracted bilaterally. The normal and degenerated neuron densities of trigeminal ganglia were examined by stereological methods and compared with phonophobia scores. Results: Phonophobic score was 19-17, mean live neuron density (LND) of the trigeminal ganglia was 16.321 ± 2.430/mm3, and degenerated neuron density (DND) was 1.15 ± 0.120/mm3 in animals of control groups (n = 5). The phonophobic score was 17-14, LND: 14.345 ± 1.913/mm3, DND of the trigeminal ganglia was 1.150 ± 0.110/mm3 in SHAM group (n = 5). The phonophobic score was 14-8, LND: 12.987 ± 1.966/mm3, mean DND of the trigeminal ganglia was 2.520 ± 510/mm3 in animals with high phonophobia scores (n = 6). The phonophobic score was 7-4, LND: 9.122 ± 1.006, mean DND of the trigeminal ganglia was 5.820 ± 1.610/mm3, in animals with fever phonophobia scores (n = 9). Conclusion: An inverse relationship between DND trigeminal ganglion (TGG) and phonopobic score was found. The paralysis of tensor tympani muscle owing to trigeminal ganglia ischemia may be responsible for phonophobic clinical state in animals with SAH. In addition, there seems to be an important concern for the verbal component of GCS in SAH. These two important findings have not been published previously.

Single level discectomy with and without disc prosthesis: A comparative study of 114 patients.

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.

How Reliable Is Pupillary Evaluation Following Subarachnoid Hemorrhage? Effect of Oculomotor Nerve Degeneration Secondary to Posterior Communicating Artery Vasospasm: First Experimental Study.

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.

The sooth beneath the taste roseas in the urethra and first description of neuro-morpho-chemical mechanism of penile erectile posture in males: an experimental study.

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 present study describes a new neuro-morpho-chemical mechanism of orgasmic sensation with its neurosurgical aspect.

Nontraumatic Intradiploic Epidermoid Cyst and Older Age: Association or Causality?

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.

New Evidence for Causal Central Mechanism of Hyperglycemia in Subarachnoid Hemorrhage Secondary to Ischemic Degenerative Disruption of Circuitry Among Insular Cortex, Nodose Ganglion, and Pancreas: Experimental Study.

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/mm3 in the control group, while it was 45 ± 7/mm3 in the SHAM group and 1688 ± 191/mm3 in the SAH group. The DND of the IC was 65 ± 12/mm3 in the control group, 689 ± 112/mm3 in the SHAM group, and 3709 ± 643/mm3 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.

A New Determinant of Poor Outcome After Spontaneous Subarachnoid Hemorrhage: Blood pH and the Disruption of Glossopharyngeal Nerve-Carotid Body Network: First Experimental Study.

OBJECTIVE: The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insults after subarachnoid hemorrhage (SAH), which may contribute to acidosis, have not been investigated. METHODS: Twenty-three hybrid rabbits were used. They were divided into 3 groups: 5 as a control group, 5 as a sham group, and the remaining 13 as the study group. Injections included 1 cm3 serum saline and 1 cm3 autolog arterial blood into the cisterna magna in the sham and study group, respectively. Blood pH values of all animals were recorded. After 2 weeks, animals were euthanized. The number of normal and degenerated neurons of the carotid bodies (CBs) was counted by stereologic methods and analyzed statistically. RESULTS: Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35 ± 0.07 in the control group (n = 5), 7.33 ± 0.06 in the sham group (n = 5), 7.29 ± 0.05 in rabbits with slight acidosis (n = 6), and 7.23 ± 0.02 in rabbits with prominent acidosis (n = 7). In the control group, the average normal neuronal density of the CBs was 6432 ± 790/mm3 and the degenerated neuron density was 11 ± 3/mm3, whereas the degenerated neuronal density in CBs was 35 ± 8/mm3 in the sham group and 1034 ± 112/mm3 in the slight acidosis-developed group (n = 6; P < 0.05). Conversely, degenerated neuron density of CBs was 2134 ± 251/mm3 in the prominent acidosis-developed animals (n = 7; P < 0.005). Interestingly, in the rabbits who died, the degenerated neuron density of the CB was 3160 ± 840/mm3. CONCLUSION: An inverse relationship between neurodegeneration in the CB and pH values secondary to the disruption of the GPN-CB network after SAH was found, which may contribute to developing acidosis.

First report of important causal relationship between the Adamkiewicz artery vasospasm and dorsal root ganglion cell degeneration in spinal subarachnoid hemorrhage: An experimental study using a rabbit model.

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.

Predictive Role of External Carotid Artery Vasospasm on Cerebral Ischemia After Subarachnoid Hemorrhage: Experimental Study.

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.

Cervical disc hernia operations through posterior laminoforaminotomy.

OBJECTIVE: The most common used technique for posterolateral cervical disc herniations is anterior approach. However, posterior cervical laminotoforaminomy can provide excellent results in appropriately selected patients with foraminal stenosis in either soft disc prolapse or cervical spondylosis. The purpose of this study was to present the clinical outcomes following posterior laminoforaminotomy in patients with radiculopathy. MATERIALS AND METHODS: We retrospectively evaluated 35 patients diagnosed with posterolateral cervical disc herniation and cervical spondylosis with foraminal stenosis causing radiculopathy operated by the posterior cervical keyhole laminoforaminotomy between the years 2010 and 2015. RESULTS: The file records and the radiographic images of the 35 patients were assessed retrospectively. The mean age was 46.4 years (range: 34-66 years). Of the patients, 19 were males and 16 were females. In all of the patients, the neurologic deficit observed was radiculopathy. The posterolaterally localized disc herniations and the osteophytic structures were on the left side in 18 cases and on the right in 17 cases. In 10 of the patients, the disc level was at C5-6, in 18 at C6-7, in 2 at C3-4, in 2 at C4-5, in 1 at C7-T1, in 1 patient at both C5-6 and C6-7, and in 1 at both C4-5 and C5-6. In 14 of these 35 patients, both osteophytic structures and protruded disc herniation were present. Intervertebral foramen stenosis was present in all of the patients with osteophytes. Postoperatively, in 31 patients the complaints were relieved completely and four patients had complaints of neck pain and paresthesia radiating to the arm (the success of operation was 88.5%). On control examinations, there was no finding of instability or cervical kyphosis. CONCLUSION: Posterior cervical laminoforaminotomy is an alternative appropriate choice in both cervical soft disc herniations and cervical stenosis.

Rational Roots of Sympathetic Overactivity by Neurogenic Pulmonary Edema Modeling Arising from Sympathyco-Vagal Imbalance in Subarachnoid Hemorrhage: An Experimental Study.

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.

Ligamentum flavum hematomas: Why does it mostly occur in old Asian males? Interesting point of reported cases: Review and case report.

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.

Uncovering a New Cause of Obstructive Hydrocephalus Following Subarachnoid Hemorrhage: Choroidal Artery Vasospasm-Related Ependymal Cell Degeneration and Aqueductal Stenosis-First Experimental Study.

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 < 0.05). CONCLUSIONS: Ependymal cell desquamation and subependymal basal membrane destruction related to choroidal artery vasospasm may lead to aqueductal stenosis and hydrocephalus after SAH.

The Important Liaison Between Onuf Nucleus-Pudendal Nerve Ganglia Complex Degeneration and Urinary Retention in Spinal Subarachnoid Hemorrhage: An Experimental Study.

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 < 0.005). CONCLUSIONS: ON-pudendal nerve ganglia complex degeneration secondary to vasospasm of the AKA may be a cause of urinary retention after spinal SAH.

Unraveling of the Effect of Nodose Ganglion Degeneration on the Coronary Artery Vasospasm After Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: Cardiac arrest is a major life-threatening complication of subarachnoid hemorrhage (SAH). Although medullary cardiocirculatuar center injury and central sympathetic overactivity have been suspected of initiating coronary artery spasm-induced cardiac arrest, we aimed to elucidate the effects of vagal ischemia at the brainstem on coronary vasospasm and sudden death in SAH. METHODS: Twenty-six rabbits were randomly divided into 3 groups. Control (n = 5); SHAM (n = 8), and SAH group (n = 13). Experimental SAH was applied by injecting homologous blood into the cisterna magna, and the SHAM group was injected with isotonic saline solution also in the cisterna magna., Twenty-one days after the injection, histopathologic changes of the neuron density of nodose ganglia, the vasospasm index values of the coronary arteries, and the electrocardiographic events were analyzed. RESULTS: Increased vasospasm index of the coronary arteries and degenerated neuron density of nodose ganglion were significantly different between animals with SAH, control, and SHAM groups (P < 0.005). If neurons of the nodose ganglia are lesioned due to ischemic insult during SAH, the heart rhythm regulation by vagus afferent reflexes is disturbed. CONCLUSIONS: We found that there is causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with SAH. Vagal pathway paralysis induced by indirect sympathetic overactivity may trigger coronary vasospasm and heart rhythm disturbances. Our findings will aid in the planning of future experimental studies and in determining the clinical relevance of such studies.