Histopathological Investigation of the Effectiveness of Collagen Matrix in the Repair of Experimental Spinal Dura Mater Defects.

OBJECTIVE: This study investigated the suitability of the collagen matrix as a dural graft in the repair of experimental spinal dura mater defects. MATERIALS AND METHODS: In the study, 30 New Zealand white rabbits were used. The rabbits were divided into a study and control group. In both groups, following exact laminectomy (Th 10 and 11) in rabbits under the isoflorane anesthesia, a spinal dural defect 1×0.5 cm in size was formed. In the study group, the dura mater defect was covered with collagen matrix; in the control group, the excised dura was sutured back to its original position. At the end of the follow-up period, the rabbits were sacrificed. In all subjects, the vertebral colon was excised completely, and it was fixed in 10% formaldehyde solution. Sections 3 pm thick were taken from the specimens, stained with hematoxylin and eosin, and examined under a light microscope. The stained sections were evaluated under light microscopy with regard to the cellular inflammatory response, fibroblastic proliferation, foreign body reaction, and capsule formation. RESULTS: The collagen matrix was completely absorbed, and it was easy to use since it did not require sutures. Foreign body reactions were minimal in the early period and were resolved entirely in the end. Inflammatory response against the collagen matrix was no greater than in the control group in which the dura was sutured primarily and then closed, eventually disappearing entirely, and no adhesion formation resulted. Collagen permits successful regeneration by combining with the dura mater. No capsule formation was observed in either group. CONCLUSION: This study shows that collagen is suitable for duraplastic procedures and that it may be a useful agent in patients in whom the dura cannot be closed primarily due to retraction, constriction, or excision.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study1.

PURPOSE: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. METHODS: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. RESULTS: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). CONCLUSION: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

A new described mechanisms of intestinal glandular atrophy induced by vagal nerve/Auerbach network degeneration following subarachnoid hemorrhage: The first experimental study.

Stress ulcers is a trouble complication of subarachnoid hemorrhage (SAH). Although gastrointestinal ulcerations may be attributed to increased HCL secretion in SAH; the exact mechanism of that complication has not been investigated definitively. We studied if vagal network degeneration may cause intestinal atrophy following SAH. Study was conducted on 25 rabbits, with 5 control group (Group-A), 5 SHAM group (Group-B), and 15 SAH group via injection of autologue blood to cisterna magna. Seven animals followed for seven days (Early Decapitated-Group-C) and eight animals followed 21 days (Late Decapitated-Group-D). The vagal nodosal ganglia (NGs), Auerbach plexuses and goblet cells of duodenums were examined by current stereological methods and compared statistically. The mean numbers of degenerated axon density/mm2 of gastric branches of vagal nerves was 8 ±â€¯2, 34 ±â€¯11, 189 ±â€¯49 and 322 ±â€¯81 in the Group A, B, C, and D respectively. The mean numbers of degenerated neuron density/mm3 of NGs was 5 ±â€¯2, 54 ±â€¯7, 691 ±â€¯87 and 2930 ±â€¯410 in the Group A, B, C, and D respectively. The mean numbers of degenerated Auerbach neurons 2 ±â€¯1, 4 ±â€¯1, 12 ±â€¯3 and 27 ±â€¯5/mm3 in the Group A, B, C, and D respectively. The mean numbers of degenerated goblet cells/mm3 were 4.3 ±â€¯1.02, 11.5 ±â€¯0.26, 143 ±â€¯26 and 937 ±â€¯65 Group A, B, C, and D respectively. Statistical analysis showed that vagal network ischemia could cause intestinal bleeding and so atrophy in SAH progression. Statistical analyses of groups were; Group-D/Group-A < 0.001, Group-D/Group-B < 0.005, Group-C/Group-A < 0.005. Undiscovered effect of ischemic vagal network injuries should be regarded as a major cause of stress ulcerations following SAH which has not been mentioned in the literature.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study

Abstract Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

Open Discectomy vs. Microdiscectomy: Results from 519 Patients Operated for Lumbar Disc Herniation.

OBJECTIVE: The aim of this study was to evaluate the outcomes of patients with lumbar disk hernia operated between 2012 January and 2017 August and to compare the differences between open discectomy (OD) and microdiscectomy (MD). MATERIALS AND METHODS: Files of 519 patients who presented at our neurosurgical department with lumbar disk herniation were retrospectively reviewed and recorded. Preoperatively, all patients routinely underwent spinal lumbar magnetic resonance imaging (MRI) and anteroposterior as well as lateral lumbar vertebrae X-rays. During the early postoperative period, there was no need for imaging. Surgical interventions were performed using the two currently accepted OD and MD methods. RESULTS: We reviewed 519 patients with lumbar disk herniation who were operated in our clinic between 2012 and 2017. The mean age of 276 patients who underwent OD was 44.85±9.92 y, and that of the remaining 243 patients who underwent MD was 47.69±12.87 y. There was no difference in the demographic distributions of patients; levels of lumbar disk herniations; postoperative clinical outcomes; and long-term reoperation rates due to root injury, wound infection, dural tear, or the recurrence of lumbar disk herniation (p>0.05). The duration of operation was significantly shorter for OD (37.82±7.15 vs. 49.07±6.88 min; t=-18.184, p<0.001). CONCLUSION: The long-term results of patients who underwent OD and MD for lumbar disk herniation were similar. We believe that both methods can be safely used under appropriate conditions and surgical experience and that surgical experience has an impact on their outcomes.

A Rare Complication of Subdural-peritoneal Shunt: Migration of Catheter Components through the Pelvic Inlet into the Subdural Space.

Subdural-peritoneal (SP) shunting is a simple procedure to treat subdural hygromas; however, several rare complications such as shunt migration exist. A 15-year-old boy presented with headache, nausea, and vomiting, and underwent SP shunting for left frontoparietal chronic subdural effusion. Six weeks later, radiographic examinations revealed total migration of the shunt through the pelvic inlet. The migrated shunt was replaced with a new SP shunt. Four weeks later, radiographic examinations revealed shunt migration into the subdural space. The shunt catheter was removed and the subdural effusion was evacuated. Shunt migration may result from pressure differences between the abdomen and the cranium or from head movement, and insufficient fixation and/or large burr holes can facilitate shunt migration. Double firm anchoring and small-sized burr holes can prevent this complication. SP shunt is a simple procedure, and its assumed complications can be prevented through precaution.

Should we use the serum vaspin level for the diagnosis and/or prognosis of subarachnoid hemorrhage?

BACKGROUND: We aimed to investigate whether vaspin, a member of the serine protease family, could be used as a marker for the severity and prognosis of subarachnoid hemorrhage (SAH). METHODS: Fifty-two consecutive patients (mean age, 51.46±3.2 years; 61.5% male) admitted to the emergency service of our hospital and hospitalized at our clinic with the diagnosis of aneurysmal SAH between 2012 and 2014 were included in the study and followed up for six months for outcome. The control group consisted of 52 healthy individuals of similar age and gender. RESULTS: During the 6-month follow-up, 8 of 52 patients died, and 18 (34.6%) patients had poor the Glasgow Outcome Score (GOS) scores. In 20 (38.46%) patients, acute hydrocephalus developed, and external ventricular drainage was performed. In the study group, the mean vaspin level was significantly higher than control group (157.88±33.6 pg/mL and 109.59±45.68 pg/mL, respectively; P<0.01). The mean vaspin level was 215.18±12.36 pg/mL in the non-survival group and 147.47±24.43 pg/mL in the survival group. Furthermore, it was 195.99±21.10 pg/mL in patients with poor outcome in terms of GOS, and 137.71±17.61 pg/mL in those with good outcome. The vaspin levels significantly increased with worsening of GOS, the World Federation of Neurological Surgeons (WFNS) grading system, and Fisher scores and increasing plasma C-reactive protein levels (P<0.01 for all). CONCLUSIONS: In conclusion, vaspin can play a role as a new marker in the diagnosis, severity assessment, and prognosis of SAH.

Serum nesfatin-1 levels: a potential new biomarker in patients with subarachnoid hemorrhage.

BACKGROUND: Acute subarachnoid hemorrhage (SAH) is a neurological emergency with significant potential for long-term morbidity and mortality. Nesfatin-1 is a polypeptide which is found in various regions of the brain that play role in the feeding and metabolic regulation. OBJECTIVE: So this study aimed to investigate if nesfatin-1 levels in patients with SAH, could be used as a marker for the severity and prognosis. METHOD: Forty-eight consecutive patients (except those excluded) admitted to the emergency service of our hospital and hospitalized at our clinic with the diagnosis of aneurysmal SAH between 2011 and 2013 were included in the study and followed up for six months for outcome. The control group consisted of 48 healthy individuals of similar age and gender. RESULTS: During the 6-month follow-up, 7 of 48 patients died and 16 (33.3%) patients had poor Glasgow Outcome Score (GOS) scores. In the study group, the mean nesfatin-1 level was significantly higher than the control group (7.36 ± 2.5 pg/ml and 4.29 ± 2.02 pg/ml, respectively; p < 0.01). The mean nesfatin-1 level was 11.58 ± 0.87 pg/ml in the non-survival group and 6.64 ± 1.89 pg/ml in the survival group. Furthermore, it was 10.22 ± 1.42 pg/ml in patients with poor outcome in terms of GOS and 5.93 ± 1.46 pg/ml in those with good outcome. The nesfatin-1 levels significantly increased with worsening of GOS, the World Federation of Neurological Surgeons grading system, and Fisher scores and increasing plasma C-reactive protein levels (p < 0.01 for all). CONCLUSION: The present study is the first that shows the mortality/poor outcome of the SAH with assessing serum nesfatin-1 levels. So levels of nesfatin-1 might be useful in SAH management.

A Very Rare Complication of Cerebral Hydatid Cyst Surgery: Cortical Collapse.

Hydatid diseases are still endemic pathologies in developing countries which generally needs surgical treatment. The main aim of the treatment is total cyst evacuation without rupture. Dowling technique is preferable for this aim. There are various complications of hydatid disease surgery which include cortical collapse which is very serious and can be mortal. Our case was a 6-year-old boy diagnosed with a solitary isointense cystic mass in the left parietal region. There was no surrounding edema. The cyst was completely evacuated with Dowling technique without rupture. In about 10 min after evacuation, hemispheric cortical collapse occurred, and the patient developed cardiac arrest. Although cortical collapse is a rare complication, it can cause perioperative mortality. Special care and efforts should be taken as not to form large defects after cyst evacuation to prevent cortical collapse and related mortality.

Once the Light Touch to the Brain: Cytotoxic Effects of Low-Dose Gamma-Ray, Laser Light, and Visible Light on Rat Neuronal Cell Culture.

OBJECTIVE: We aimed to evaluate the effects of gamma-ray, laser light, and visible light, which neurons are commonly exposed to during treatment of various cranial diseases, on the viability of neurons. MATERIALS AND METHODS: Neuronal cell culture was prepared from the frontal cortex of 9 newborn rats. Cultured cells were irradiated with gamma-ray for 1-10 min by (152)Eu, (241)Am, and (132)Ba isotopes, visible light for 1-160 min, and laser light for 0.2-2 seconds. The MTT tetrazolium reduction assay was used to assess the number of viable cells in the neuronal cell cultures. Wavelength dispersive X-ray fluorescence spectrometer was used to determine Na, K, and Ca levels in cellular fluid obtained from neuronal cell culture plaques. RESULTS: Under low-dose radiation with (152)Eu, (241)Am, and (132)Ba isotopes, cell viability insignificantly decreased with time (p>0.05). On the other hand, exposure to visible light produced statistically significant decrease in cell viability at both short- (1-10 min) and long-term (20-160 min). Cell viability did not change with 2 seconds of laser exposure. Na, K, and Ca levels significantly decreased with gamma-ray and visible light. The level of oxidative stress markers significantly changed with gamma-ray. CONCLUSION: In conclusion, while low dose gamma-ray has slight to moderate apoptotic effect in neuronal cell cultures by oxidative stress, long-term visible light induces remarkable apoptosis and cell death. Laser light has no significant effect on neurons. Further genetic studies are needed to clarify the chronic effect of visible light on neuronal development and functions.

The feasibility of dual-energy CT in differentiation of vertebral compression fractures.

OBJECTIVE: To prospectively evaluate the ability of dual-energy CT (DECT), compared with MRI, to identify vertebral compression fractures in acute trauma patients. METHODS: This institutional review board-approved study included 23 consecutive patients with 32 vertebral fractures who underwent both DECT and MRI of the spine between February 2014 and September 2014. A total of 209 vertebrae were evaluated for the presence of abnormal bone marrow attenuation on DECT and signal on MRI by five experienced radiologists. The specificity, sensitivity, predictive values and intraobserver and interobserver agreements were calculated. RESULTS: MRI revealed a total of 47 vertebrae (22.4% of all vertebrae) and DECT revealed 44 vertebrae (21.0% of all vertebrae) with oedema. Using MRI as the reference standard, DECT had sensitivity, specificity, positive-predictive value, negative-predictive value and accuracy of 89.3, 98.7, 95.4, 96.9 and 96.6%, respectively. With respect to establishing the presence of oedema, the interobserver agreement was almost perfect (k = 0.82), and the intraobserver agreement was substantial (k = 0.80). CONCLUSION: Compared with MRI, DECT can provide an accurate demonstration of acute vertebral fractures and can be used as an alternative imaging modality for the assessment of vertebral fractures in patients with contraindications for MRI. ADVANCES IN KNOWLEDGE: Distinguishing of acute and chronic vertebral compression fracture is important for treatment choices. DECT is very fast compared with MRI and is an alternative imaging modality for the assessment of vertebral fractures in patients with contraindications for MRI.

Preventive Role of Hilar Parasympathetic Ganglia on Pulmonary Artery Vasospasm in Subarachnoid Hemorrhage: An Experimental Study.

AIM: Pulmonary arteries are mainly innervated by sympathetic vasoconstrictor and parasympathetic vasodilatory fibers. We examined whether there is a relationship between the neuron densities of hilar parasympathetic ganglia and pulmonary vasospasm in subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: Twenty-four rabbits were divided into two groups: control (n=8) and SAH (n=16). The animals were observed for 20 days following experimental SAH. The number of hilar parasympathetic ganglia and their neuron densities were determined. Proportion of pulmonary artery ring surface to lumen surface values was accepted as vasospasm index (VSI). Neuron densities of the hilar ganglia and VSI values were compared statistically. RESULTS: Animals in the SAH group experienced either mild (n=6) or severe (n=10) pulmonary artery vasospasm. In the control group, the mean VSI of pulmonary arteries was 0.777±0.048 and the hilar ganglion neuron density was estimated as 12.100±2.010/mm < sup > 3 < /sup > . In SAH animals with mild vasospasm, VSI=1.148±0.090 and neuron density was estimated as 10.110±1.430/mm < sup > 3 < /sup > ; in animals with severe vasospasm, VSI=1.500±0.120 and neuron density was estimated as 7.340±990/mm < sup > 3 < /sup > . CONCLUSION: There was an inverse correlation between quantity and neuron density of hilar ganglia and vasospasm index value. The low numbers and low density of hilar parasympathetic ganglia may be responsible for the more severe artery vasospasm in SAH.

Effect of pregabalin in preventing secondary damage in traumatic brain injury: an experimental study.

BACKGROUND: In this study we aimed to explore the effects of pregabalin on a traumatic brain injury model in rats. MATERIAL AND METHODS: This study included 40 adult male Sprague-Dawley rats randomized into 4 groups, each of which contained equal numbers of animals. The control group had no head trauma and thus was not treated. The trauma group had head trauma but was not treated. The pregabalin group had no head trauma but was treated by pregabalin. The trauma + pregabalin group had head trauma treated with pregabalin. The biopsy samples taken from the study animals were histopathologically examined for the presence of edema, inflammation, and neuronal damage. RESULTS: All animals in the trauma group had edema, inflammation, and neuronal damage. Four subjects in the control group, 6 in the pregabalin group, and 4 in the trauma + pregabalin group had edema; inflammation was present in 1 subject in the control group, 3 subjects in the pregabalin group, and 3 subjects in the trauma + pregabalin group; neuronal damage existed in 1 subject in the control group, 1 subject in the pregabalin group, and 6 subjects in the trauma+pregabalin group. The trauma group had significantly higher edema and neuronal damage scores than the other groups. Similarly, inflammation was significantly more prevalent in the trauma group than the control and trauma+pregabalin groups. CONCLUSIONS: The results of the present study indicated anti-edema, anti-inflammatory, and neuroprotective effects of pregabalin in an experimental head trauma model in rats. Pregabalin may thus be beneficial in humans with acute TBI by relieving concomitant edema and inflammation.