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.

Effects of Benidipine Hydrochloride on Ischemia Reperfusion Injury of Rat Brain.

AIM: To evaluate the neuroprotective effects of benidipine hydrochloride on the cerebral cortex tissues in rats exposed to cerebral ischemia-reperfusion (I/R) injury. MATERIAL AND METHODS: Twenty-four male Wistar albino rats were randomly divided into three groups, and administered benidipine hydrochloride (10 ?g/kg/day) orally through a catheter for 2 h to form the study group (BIR group, n=8). The I/R procedure was performed in the rats of the IR group (n=8), and a sham group was formed to determine the normal structure of the cerebral cortex (n=8). Transient ischemia was performed by clamping the left common carotid artery for 2 h. Subsequently, reperfusion was applied for 12 h. Cerebral infarct volumes were measured and cerebral cortex tissue samples were analyzed histopathologically and biochemically by measuring malondialdehyde (MDA), total glutathione, cyclooxygenase 1 (COX-1), COX-2 and superoxide dismutase (SOD) RESULTS: The infarct area was markedly reduced in the BIR group vs. the IR group. Histopathologically, neuroprotective effects of benidipine hydrochloride were observed in the cerebral cortex tissues. The mean malondialdehyde and COX-2 levels were statistically higher in the IR group; however, in the BIR group, these levels were within the normal limits. Furthermore, the mean total glutathione, COX-1 and SOD levels were markedly lower in the IR group, and within the normal limits in the BIR group. CONCLUSION: Benidipine hydrochloride may play a certain protective role in cerebral I/R injury. This effect may be related to improvement in the antioxidant capacity of brain tissue, and the inhibition of overproduction of inflammatory cytokines.

Relationship between subarachnoid and central canal hemorrhage and spasticity: A first experimental study.

Objective: Spastic disorders are considered as important cerebral complications of subarachnoid hemorrhage (SAH). However, there has been no research concerning the pathophysiological mechanism of its link with the spinal cord. The present study aimed to assess the relationship between the development of spasticity and neuronal degeneration after SAH and increase in spinal cord pressure after central canal hemorrhage (CCH).Participants: Twenty-three rabbits were included.Outcome measures: Of all rabbits, 5, 5, and 13 were allocated in the control, SHAM and study groups, respectively. Moreover, 1 cc of saline and 1 cc of autologous arterial blood were injected into the cisterna magna of the SHAM and study groups, respectively. The Muscle spasticity tension values (MSTVs) were determined according to the modified Ashworth scale. Degenerated neuron densities (DND) in the gray matter (GM) of each animal's spinal cord were stereologically calculated.Results: The average MSTV of each group was as follows: control group (n = 5) 2; SHAM group (n = 5) 3-5; and study group (n = 13) 8-10. The DND values of the spinal cord of each group were as follows: control group, 2 ± 1/mm3; SHAM group, 12 ± 3/mm3; and study group, 34 ± 9/mm3. Results showed an important linear relationship between the MSTVs and the DND of the spinal cord (P < 0.001).Conclusion: Spasticity may be attributed to other causes such as ischemic neurodegenerative process that develops after spinal SAH and the de-synchronization of the flexor-extensor muscles due to the spontaneous discharge of interneuronal structures, which are crossed within the spinal cord owing to the build-up of pressure after CCH.

The Effects of Agomelatine on The Biochemical and Pathological Features of Cisplatin-Induced Peripheral Neuropathy: The First Experimental Study in Rats.

AIM: To evaluate the effects of agomelatine on the biochemical and pathological features of cisplatin-induced peripheral neuropathy. MATERIAL AND METHODS: This study included a total of 30 male Wistar albino rats that weighed 285â€"300 grams and were divided into three groups: healthy controls (HC, n=10); cisplatin group (CIS, n=10) and agomelatine plus cisplatin group (AC, n=10). The CIS group received only cisplatin (EbeweLiba, Turkey) at a dose of 2.5 mg/kg, whereas the AC group received both agomelatine (25 mg/kg, Les Laboratoires Servier, France) and cisplatin (2.5 mg/kg). The animals were sacrificed by thiopental anaesthesia (50 mg/ kg, IE Ulagay, Turkey) and sciatic nerves were dissected. The sciatic nerve tissue was analysed for the levels of malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH) and superoxide dismutase (SOD) and was examined histopathologically. RESULTS: The mean levels of MDA, MPO, tGSH and SOD were 34.90 ± 13.83, 41.30 ± 18.03, 15.40 ± 6.06 and 48.60 ± 18.19, respectively. MDA and MPO were significantly lower in the AC group than in the CIS group (p < 0.001 for both). However, the antioxidative parameters tGSH and SOD were significantly higher in the AC group than in the CIS group (p < 0.001 for both). Pathological examinations revealed swollen myelinated nerve fibres and evident myelin sheath degeneration in the CIS group; in the AC group, the myelin sheath degeneration was less and the blood vessels were normal. CONCLUSION: Agomelatine decreased the oxidative status in an experimental rat model of cisplatin-induced peripheral neuropathy. Myelin sheath degeneration was less in the AC group than in the CIS group. To our knowledge, this was the first study that showed the positive effects of agomelatine on cisplatin-induced neuropathy in rats.

Effect of Vasa Vasorum on Basilar Artery Vasospasm Following Subarachnoid Hemorrhage.

BACKGROUND: A well-documented association exists between the vasa vasorum and vasopathologies, including atherosclerosis. However, information on the role of the vasa vasorum during vascular degenerative changes of vasospasm after subarachnoid hemorrhage (SAH) is insufficient. METHODS: In this study, 34 rabbits were divided into 3 groups: basal group (N = 8), sham group (N = 8), and SAH group (N = 18). Experimental SAH was formed using a double-injection model. During follow-up, the neurologic status of the rabbits was observed. All rabbits were euthanized after 2 weeks, and the vasopathologic degeneration was categorized as normal, mild, moderate, and severe according to the changes in the basilar arteries. The numbers, locations, and spasms of the vasa vasorum and their relation to the vasodegenerative changes of the basilar artery were investigated. RESULTS: The basilar arteries were graded as normal in the basal and sham groups. In the SAH group, 6 rabbits had mild, 7 had moderate, and 5 had severe degeneration. Neurologic deficits were prominent in the SAH group, and deficit grades correlated with vascular degeneration. The number of the vasa vasorum were significantly higher in the SAH group, and an enhanced formation of the vasa vasorum was noted in which severe degenerative changes were present. Moreover, the vasospasm index of the vasa vasorum, which increased with the aggravation of vascular degenerative changes, was significantly higher in the SAH group. CONCLUSIONS: The vasa vasorum and their vasospasm play a crucial role in the pathogenesis of basilar artery degeneration in the vasospasm following SAH.

Aortic Injury by Thoracic Pedicle Screw. When Is Aortic Repair Required? Literature Review and Three New Cases.

PURPOSE: Aortic injury by pedicle screw is rare but can cause serious complications. It has not been clearly determined when aortic repair is necessary in cases of screw impingement without perforation of the aortic wall. In this article, we review the treatment and clinical course of pedicle screw aortic impingement and attempt to clarify this issue. METHODS: Cases of aortic injury during thoracic screw procedures were found using a MEDLINE search and analyzed together with 3 new cases that we present. RESULTS: Nineteen cases collected from the literature and 3 new cases were included in the study. In 7 of the cases, aortic impingement by the pedicle screw was detected during postoperative follow-up (day 1) radiologic examinations. In the other cases, time to presentation of aortic impingement ranged between 2 weeks and 60 months after fixation. The main indications for thoracic spinal fixation were post-traumatic vertebral fracture and kyphoscoliosis/scoliosis. Repair of the aortic damage ranged from primary repair to stent and tube graft placement by the thoracic endovascular aortic repair method. CONCLUSIONS: In cases in which the screw impinges less than 5 mm into the aortic wall, hardware revision without aortic repair may be sufficient if recognized early and there are no sign of aortic leakage in vascular imaging. However, cases with more than 5 mm of screw impingement should undergo aortic repair first, even in the absence of aortic leakage, following by screw revision.

Decreased catalase expression is associated with ligamentum flavum hypertrophy due to lumbar spinal canal stenosis.

BACKGROUND: This is an immunohistologic study of gene expression between patients and controls.This study aims to evaluate expression of the catalase gene in hypertrophied ligamentum flavum (LF) specimens obtained from patients with lumbar spinal canal stenosis (LSCS).LSCS is one of the most common spinal disorders. It is well known that LF hypertrophy plays an important role in the onset of LSCS. Although degenerative changes, aging, and mechanical stress are all thought to contribute to hypertrophy and fibrosis of the LF, the precise pathogenesis of LF hypertrophy remains unknown. Previous genetic studies have tried to determine the mechanism of LF hypertrophy. However, the association between catalase gene expression and LF hypertrophy has not yet been explored. METHODS: LF specimens were surgically obtained from 30 patients with spinal stenosis (LSCS group) and from 30 controls with lumbar disc herniation (LDH group). LF thickness was measured at the thickest point using calipers to an accuracy of 0.01 mm during surgical intervention. The extent of LF elastin degradation and fibrosis were graded (grades 0-4) by hematoxylin and eosin staining and Masson trichrome staining, respectively. The resulting LF measurements, histologic data, and immunohistologic results were then compared between the 2 groups. RESULTS: The average LF thickness was significantly higher in the LSCS group than in the LDH group (5.99 and 2.95 mm, respectively, P = .004). Elastin degradation and fibrosis of the LF were significantly more severe in spinal stenosis samples than in the disc herniation samples (3.04 ±â€Š0.50 vs 0.79 ±â€Š0.60, P = .007; 3.01 ±â€Š0.47 vs 0.66 ±â€Š0.42, P = .009, respectively). Significantly lower expression of catalase was observed in the perivascular area of LF samples obtained from patients with LSCS compared with controls (61.80 ±â€Š31.10 vs 152.80 ±â€Š41.13, respectively, P = .009). CONCLUSION: Our findings suggest that decreased expression of catalase is associated with LF hypertrophy in patients with LSCS.

Brachial Artery Vasospasm Caused by Cervical Dorsal Root Ganglion Degeneration After Subarachnoid Hemorrhage: An Experimental Study.

PURPOSE: Subarachnoid hemorrhage (SAH) may lead to vasospasm in various vessels. The cervical nerves have a vasodilatory effect on the upper extremity arteries. The aim of this study was to investigate if there is a relationship between C6 dorsal root ganglion (DRG) degeneration and brachial artery (BA) vasospasm after spinal SAH. METHODS: This experimental study was conducted on 23 rabbits. The animals were divided into 3 groups: control (n = 5), SHAM (n = 5), and study group (n = 13). One cubic centimeter (cc) of serum saline was injected into the cisterna magna of animals of the SHAM group; the same procedure was performed by 1 cc of homologous blood in the study group. Degenerated neuron densities (DNDs) of DRGs (n/mm3) at C6 levels and BA vasospasm indexes (VSI; wall surface/lumen surface) of all animals were determined and results were analyzed statistically. RESULTS: Mean VSI values of BAs and DNDs of C6DRGs of the control, SHAM, and study groups were estimated as 10 ± 3/1.12 ± 0.11 n/mm3, 34 ± 9/1.27 ± 0.24 n/mm3, and 1031 ± 145/2.93 ± 0.78 n/mm3, respectively. Mean DNDs and VSI values were statistically significantly different between the control and study groups (P < 0.0001). CONCLUSIONS: C6DRG degeneration may be considered as an important factor in the etiopathogenesis of severe BA vasospasm after SAH.

A New Neuropathologic Mechanism of Blood pH Irregularities After Neck Trauma: Importance of Carotid Body-Glossopharyngeal Nerve Network Degeneration.

OBJECTIVE: We created a neck trauma model by injecting blood into the sheath of rabbits' carotid bodies (CBs). Then we determined the relationship between neuronal degeneration of the CB due to hemorrhage of this organ and its clinical effects such as blood pH and heart rhythm. METHODS: The present study included 24 adult male New Zealand rabbits. The animals were divided into 3 groups: control (n = 5); sham (0.5 mL saline injected into CBs; n = 5); and study (CB trauma model; n = 14). pH values and heart rhythms were recorded before the experiment to determine the values under normal conditions, and measurements were repeated thrice in the days following the experiment. The number of normal and degenerated neuron density of CBs was counted. The relationship between the blood pH values, heart rhythms, and degenerated neuron densities was analyzed. RESULTS: Heart rhythms were 218 ± 20 in the control group, 197 ± 16 in the sham group (P = 0.09), and 167 ± 13 in the study group (P < 0.0005). pH values were 7.40 ± 0.041 in the control group, 7.321 ± 0.062 in the sham group (P = 0.203), and 7.23 ± 0.02 in study group (P < 0.0005). Degenerated neuron densities were 12 ± 4/mm3 in the control group, 430 ± 74/mm3 in the sham group (P < 0.005), and 7434 ± 810/mm3 in the study group (P < 0.0001). CONCLUSIONS: A high degenerate neuron density in the CB can decrease blood pH and hearth rhythm after neck trauma, and there might be a close relationship between the number of degenerated neurons and clinical findings (such as heart rhythm and blood pH). This relationship suggests that injury to the glossopharyngeal nerve-CB network can cause acidosis by disturbing the breathing-circulating reflex and results in respiratory acidosis.

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.