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Objective: Dexpanthenol (DXP) reportedly protects tissues against oxidative damage in various inflammation models. This study aimed to evaluate its effects on oxidative stress, inflammation, apoptosis, and neurological recovery in an experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. Methods: Rabbits were randomized into five groups of eight animals each: group 1 (control), group 2 (ischemia), group 3 (vehicle), group 4 (methylprednisolone, 30 mg/kg), and group 5 (DXP, 500 mg/kg). The control group underwent laparotomy only, whereas other groups were subjected to spinal cord ischemia by aortic occlusion (just caudal to the two renal arteries) for 20 min. After 24 h, a modified Tarlov scale was employed to record neurological examination results. Malondialdehyde and caspase-3 levels and catalase and myeloperoxidase activities were analyzed in tissue and serum samples. Xanthine oxidase activity was measured in the serum. Histopathological and ultrastructural evaluations were also performed on the spinal cord. Results: After SCIRI, serum and tissue malondialdehyde and caspase-3 levels and myeloperoxidase activity and serum xanthine oxidase activity were increased (p

Hydatid cyst disease as a zoonosis usually infests the liver and lungs, and it rarely affects muscles. Here, we presented a 36-year-old female patient with low back pain. Radiological evaluation revealed a soft tissue lesion located at the left paravertebral region without vertebral invasion. Surgical exploration and removal of the cyst were performed. The pathological diagnosis was hydatid cyst. After the surgery, the patient was treated with albendazole which is used to decrease the consequences of spillage and the possibility of recurrence. Hydatid cyst disease is rarely seen in paravertebral muscle tissue and needs to be correctly managed. Primary muscle involvement of hydatid cyst must be kept in mind for differential diagnosis of paravertebral cystic mass lesions.

Trauma-induced primary damage is followed by secondary damage, exacerbating traumatic brain injury (TBI). Dexpanthenol has been shown to protect tissues against oxidative damage in various inflammation models. This study aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI. Wistar albino male rats were randomly assigned to control (n = 16), trauma (n = 16) and dexpanthenol (500 mg/kg; n = 14) groups. TBI was induced under anesthesia by dropping a 300 g weight from 70-cm height onto the skulls of the rats. Twenty-four hours after the trauma, the rats were decapitated and myeloperoxidase (MPO) levels, luminol- and lucigenin-enhanced chemiluminescence (CL), malondialdehyde (MDA) levels, superoxide dismutase (SOD) levels, and catalase (CAT) and caspase-3 activities were measured in brain tissues. Following transcardiac paraformaldehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. In the trauma group, MPO level, caspase-3 activity and luminol-lucigenin CL levels were elevated (p < 0.05–0.001) when compared to controls; meanwhile in the dexpanthenol group these increases were not seen (p < 0.05–0.001) and MDA levels were decreased (p < 0.05). Decreased SOD and CAT activities (p < 0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol group (p < 0.05–0.001). in the dexpanthenol group there was relatively less neuronal damage observed microscopically in the cortices after TBI. Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI.

Objective: Apigenin is a plant flavone proven with biological properties such as anti-inflammatory, antioxidant, and antimicrobial effects. This study, it was aimed to examine the possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of the mild traumatic brain injury (TBI) model. Methods: Wistar albino male rats were randomly assigned to groups: control (n = 9), TBI (n = 9), TBI + vehicle (n = 8), and TBI + apigenin (20 and 40 mg/kg, immediately after trauma; n = 6 and n = 7). TBI was performed by dropping a 300 g weight from a height of 1 m onto the skull under anesthesia. Neurological examination and tail suspension tests were applied before and 24 h after trauma, as well as Y-maze and object recognition tests, after that rats were decapitated. In brain tissue, luminol- and lucigenin-enhanced chemiluminescence levels and cytokine ELISA levels were measured. Histological damage was scored. Data were analyzed with one-way ANOVA. Results: After TBI, luminol (p

Objective Inflammation and oxidative stress are 2 important factors in the emergence of paraplegia associated with spinal cord ischemia-reperfusion injury (SCIRI) after thoracoabdominal aortic surgery. Here it is aimed to investigate the effects of Ganoderma lucidum polysaccharide (GLPS) on SCIRI. Methods Rats were randomly selected into 4 groups of 8 animals each: sham, ischemia, methylprednisolone, and GLPS. To research the impacts of various pathways that are efficacious in formation of SCIRI, tumor necrosis factor α, interleukin 1β, nitric oxide, superoxide dismutase levels, and catalase, glutathione peroxidase activities, malondialdehyde levels, and caspase-3 activity were measured in tissues taken from the spinal cord of rats in all groups killed 24 hours after ischemia reperfusion injury. The Basso, Beattie, and Bresnahan locomotor scale and inclined plane test were used for neurologic assessment before and after SCIRI. In addition, histologic and ultrastructural analyses of tissue samples in all groups were performed. Results SCIRI also caused marked increase in tissue tumor necrosis factor α, interleukin 1β, nitric oxide, malondialdehyde levels, and caspase-3 activity, because of inflammation, increased free radical generation, lipid peroxidation, and apoptosis, respectively. On the other hand, SCIRI caused significant reduction in tissue superoxide dismutase, glutathione peroxidase, and catalase activities. Pretreatment with GLPS likewise diminished the level of the spinal cord edema, inflammation, and tissue injury shown by pathologic and ultrastructural examination. Pretreatment with GLPS reversed all these biochemical changes and improved the altered neurologic status. Conclusions These outcomes propose that pretreatment with GLPS prevents progression of SCIRI by alleviating inflammation, oxidation, and apoptosis.

Objectives:Traumatic brain injury (TBI) is a major cause of disability and mortality that induces oxidative stress and apoptosis causing cellular damage. Several animal models have shown paeonol to be a powerful antioxidant, antiapoptotic, and neuroprotective substance. This study aimed to investigate possible neuroprotective effects of paeonol in a rat TBI model.Materials and Methods:Thirty-two male rats were divided into four groups: control, trauma, vehicle, and paeonol groups. Trauma, vehicle, and paeonol groups were subjected to closed-head, contusive weight-drop injuries. The vehicle (saline) or paeonol (50 mg/kg) was orally administered as premedication for 15 days. Brain samples were obtained 24 hours after trauma. Histomorphological evaluation of the cerebral cortex was performed using electron and light microscopy.Results:Histopathological examination revealed that the TBI-induced cerebral cortex damage was less in the paeonol group.Conclusion:Paeonol exhibited neuroprotective and anti-edematous effects against TBI.

Cerebrospinal fluid is an essential, clear, and colorless liquid for the homeostasis of the brain and neuronal functioning. It circulates in the brain ventricles, the cranial and spinal subarachnoid spaces. The mean cerebrospinal fluid volume is 150 ml, with 125 ml in subarachnoid spaces and 25 ml in the ventricles. Cerebrospinal fluid is mainly secreted by the choroid plexuses. Cerebrospinal fluid secretion in adults ranges between 400 and 600 ml per day and it is renewed about four or five times a day. Cerebrospinal fluid is mainly reabsorbed from arachnoid granulations. Any disruption in this well-regulated system from overproduction to decreased absorption or obstruction could lead to hydrocephalus.

Traumatic brain injury (TBI) is one of the most common preventable causes of mortality and morbidity. Inflammation, apoptosis, oxidative stress, and ischemia are some of the important pathophysiological mechanisms underlying neuronal loss after TBI. Mildronate is demonstrated to be beneficial in various experimental models of ischemic diseases via anti-inflammatory, antioxidant, and neuroprotective mechanisms. This study aimed to investigate possible antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of mildronate in a rat model of TBI.A total of 46 male rats were divided into three groups of control, saline-treated TBI, and mildronate-treated TBI. Both TBI groups were subjected to closed-head contusive weight-drop injuries followed by treatment with saline or mildronate (100 mg/kg) administered intraperitoneally. The forebrain was removed 24 h after trauma induction, the activities of myeloperoxidase (MPO) and caspase-3, levels of superoxide dismutase (SOD), luminol- and lucigenin-enhanced chemiluminescence were measured, and histomorphological evaluation of cerebral tissues was performed.Increased MPO and caspase-3 activities in the vehicle-treated TBI group (p 0.001) were suppressed in the mildronate-treated TBI group (p 0.001). Similarly, increase in luminol and lucigenin levels (p 0.001 and p 0.01, respectively) in the vehicle-treated TBI group were decreased in the mildronate-treated TBI group (p 0.001). Concomitantly, in the vehicle-treated TBI group, TBI-induced decrease in SOD activity (p 0.01) was reversed with mildronate treatment (p 0.05). On histopathological examination, TBI-induced damage in the cerebral cortex was lesser in the mildronate-treated TBI group than that in other groups.This study revealed for the first time that mildronate, exhibits neuroprotective effects against TBI because of its anti-inflammatory, antiapoptotic, and antioxidant activities.

The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The cross-sectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.

Objective: The aim of this study was to investigate the possible neuroprotective effects of cinnamaldehyde (CA) on secondary brain injury after traumatic brain injury (TBI) in a rat model. Methods: Rats were randomly divided into 4 groups: control (n = 9), TBI (n = 9), vehicle (0.1% Tween 80; n = 8), and CA (100 mg/kg) (n = 9). TBI was induced by the weight-drop model. In brain tissues, myeloperoxidase activity and the levels of luminol-enhanced and lucigenin-enhanced chemiluminescence were measured. Interleukin 1β, interleukin 6, tumor necrosis factor α, tumor growth factor β, caspase-3, and cleaved caspase-3 were evaluated with an enzyme-linked immunosorbent assay method. Brain injury was histopathologically graded after hematoxylin-eosin staining. Y-maze and novel object recognition tests were performed before TBI and within 24 hours of TBI. Results: Higher myeloperoxidase activity levels in the TBI group (P < 0.001) were suppressed in the CA group (P < 0.05). Luminol-enhanced and lucigenin-enhanced chemiluminescence, which were increased in the TBI group (P < 0.001, for both), were decreased in the group that received CA treatment (P < 0.001 for both). Compared with the increased histologic damage scores in the cerebral cortex and dentate gyrus of the TBI group (P < 0.001), scores of the CA group were lower (P < 0.001). Decreased number of entries and spontaneous alternation percentage in the Y-maze test of the TBI group (P < 0.05 and P < 0.01, respectively) were not evident in the CA group. Conclusions: CA has shown neuroprotective effects by limiting neutrophil recruitment, suppressing reactive oxygen species and reducing histologic damage and acute hippocampal dysfunction. WOS:000687942800033 34224887 Q3

Introduction: Lamotrigine, an anticonvulsant drug with inhibition properties of multi-ion channels, has been shown to be able to attenuates secondary neuronal damage by influencing different pathways. The aim of this study was to look into whether lamotrigine treatment could protect the spinal cord from experimental spinal cord ischemia-reperfusion injury. Materials and methods: Thirty-two rats, eight rats per group, were randomly assigned to the sham group in which only laparotomy was performed, and to the ischemia, methylprednisolone and lamotrigine groups, where the infrarenal aorta was clamped for thirty minutes to induce spinal cord ischemia-reperfusion injury. Tissue samples belonging to spinal cords were harvested from sacrificed animals twenty-four hours after reperfusion. Tumor necrosis factor-alpha levels, interleukin-1 beta levels, nitric oxide levels, superoxide dismutase activity, catalase activity, glutathione peroxidase activity, malondialdehyde levels and caspase-3 activity were studied. Light and electron microscopic evaluations were also performed to reveal the pathological alterations. Basso, Beattie, and Bresnahan locomotor scale and the inclined-plane test was used to evaluate neurofunctional status at the beginning of the study and just before the animals were sacrificed. Results: Lamotrigine treatment provided significant improvement in the neurofunctional status by preventing the increase in cytokine expression, increased lipid peroxidation and oxidative stress, depletion of antioxidant enzymes activity and increased apoptosis, all of which contributing to spinal cord damage through different paths after ischemia reperfusion injury. Furthermore, lamotrigine treatment has shown improved results concerning the histopathological and ultrastructural scores and the functional tests. Conclusion: These results proposed that lamotrigine may be a useful therapeutic agent to prevent the neuronal damage developing after spinal cord ischemia-reperfusion injury. WOS:000715855800021 34391576 Q2

WOS: 000457328100119, PubMed ID: 30399469, BACKGROUND: Epidural fibrosis is a major problem after spine surgery, with some patients having recurrent symptoms secondary to excessive formation of scar tissue resulting in neurologic compression. We used a rat laminectomy model to determine if topical application of boric acid could be helpful in the prevention of epidural fibrosis. METHODS: Rats were randomly assigned to 2 control and 2 experimental groups (n = 8 for each group). The negative control group received no surgery, and the positive control group underwent laminectomy only. Experimental groups were classified according to the study agents applied onto the dura mater after laminectomy at the L3 level: 2.5% boric acid solution and 5% boric acid solution. The extent of epidural fibrosis was assessed 4 weeks later macroscopically and histopathologically. RESULTS: Boric acid reduced epidural fibrosis in rats after laminectomy. The effect of 5% boric acid solution was more pronounced (P < 0.05) compared with the 2.5% solution. CONCLUSIONS: The antifibrotic effect of boric acid solution for the prevention of epidural fibrosis suggests that boric acid should be further evaluated in future studies for the prevention of epidural fibrosis.

Vigabatrin, an antiepileptic drug, increases the level of gamma aminobutyric acid in the brain by inhibiting its catabolism. Because gamma aminobutyric acid has been proved to have vasodilatory effects, in the present study, we investigated the effect of vigabatrin to treat experimental subarachnoid hemorrhage (SAH)-induced vasospasm.A total of 30 New Zealand white rabbits were divided into 3 groups of 10 each: the control group, SAH group, and vigabatrin group. Experimental SAH was established by injection of autologous arterial blood into the cisterna magna. In the vigabatrin group, the rabbits were administered vigabatrin for 3 days after induction of the SAH. The first dose of vigabatrin was given 2 hours after SAH induction. A daily dose of 500 mg/kg vigabatrin was administered intraperitoneally. After 3 days, the rabbits were sacrificed, and the brains were removed, together with the cerebellum and brainstem. The basilar artery wall thickness and lumen areas were measured. The neuronal degeneration in the hippocampus (CA1, CA3, and dentate gyrus) was also evaluated.The arterial wall thickness of the vigabatrin group was less than that in the SAH group (P0.001), and the mean luminal area of the vigabatrin group was greater than that in the SAH group (P0.001). Additionally, the hippocampal neuronal degeneration score of the vigabatrin group was lower than that of the SAH group (P0.001).These findings have indicated that vigabatrin has a vasodilatory effect in an experimental SAH model in the rabbit. Moreover, it showed a neuroprotective effect in the hippocampal neurons against secondary injury induced by SAH.

Recent studies have demonstrated the neuroprotective and immunomodulatory effects of 1,25-dihydroxyvitamin D3 (calcitriol), but no previous study has examined these effects on spinal cord ischemia/reperfusion (I/R) injury. Therefore, the present study aimed to evaluate whether calcitriol protects the spinal cord from I/R injury.Rabbits were randomized into four groups of eight animals: group 1 (laparotomy control), group 2 (ischemia control), group 3 (30mg/kg intraperitoneal methylprednisolone at surgery), and group 4 (0.5μg/kg, intraperitoneal calcitriol for 7 days before I/R injury). The rabbits in the laparotomy control group underwent laparotomy only, whereas all rabbits in the other groups were subject to spinal cord ischemia by aortic occlusion for 20min, just caudal to the renal artery. Malondialdehyde and catalase levels, myeloperoxidase and xanthine oxidase activities, and caspase-3 concentrations were analyzed. Finally, histopathological, ultrastructural, and neurological evaluations were performed.After I/R injury, increases in malondialdehyde levels, myeloperoxidase and xanthine oxidase activities, and caspase-3 concentrations were found (p0.001 for all); by contrast, catalase levels decreased (p0.001). Calcitriol pretreatment was associated with lower malondialdehyde levels (p0.001), reduced myeloperoxidase (serum, p=0.018; tissue, p0.001) and xanthine oxidase (p0.001) activities, and caspase-3 concentrations (p0.001), but increased catalase levels (p0.001). Furthermore, calcitriol pretreatment was associated with better histopathological, ultrastructural, and neurological scores.Calcitriol pretreatment provided significant neuroprotective benefits following spinal cord I/R injury.

Introduction: Atherosclerosis might diminish the nutrient supply to intervertebral discs (IVD), leading to disc herniation. Therefore, there is interest in determining the possible association between the blood lipid profile and lumbar disc herniation (LDH). We aimed to evaluate the association between blood lipids and LDH in a homogeneous group of patients, controlling for age- and sex-specific effects. Material and methods: This is a case-control study which consisted of 100 individuals (mean age: 41.25 ±9.09; 50 men and 50 women), classified into two groups, as follows. Group I (G-I) consisted of 50 patients who underwent surgery for symptomatic LDH, while group II (G-II) consisted of 50 patients with nonspecific complaints of a headache, but with no previous history of back and/or leg pain, recruited among patients admitted to the outpatient clinic at the time of the study, and whose age and sex were matched to the study group. Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), fasting blood glucose, and hemoglobin A1c levels were measured. The TC/HDL-C ratio was calculated. Blood pressure, waist circumference, body mass index, and the history of smoking were included in the analysis. Results: The mean values of the TC, TG, LDL-C, HDL-C levels and TC/HDL-C ratio were 198.38, 132.76, 131.9, 40.38 mg/dl and 5.09, respectively. No statistically significant relationship between the blood lipid profile and LDH was identified in this population. Conclusions: Blood lipid levels in this young adult Turkish population did not predict LDH, and may not be a leading cause of IVD ischemia and IVD degeneration.

Background This study aims to investigate the factors affecting the survival of operated non-small cell lung cancer patients with synchronous brain metastasis. Methods Clinical outcomes of a total of 16 patients (14 males, 2 females; mean age 60 years; range, 41 to 71 years) who were diagnosed with non-small cell lung cancer and concomitant solitary/oligo brain metastasis and who underwent an intervention primarily for cranium, followed by lung resection in our clinic between January 2012 and January 2016 were retrospectively analyzed. Cranial surgery or gamma-knife radiosurgery was performed in the treatment of brain metastases. Results Twelve patients with solitary brain metastasis underwent cranial surgery, while four patients with solitary/oligo metastases underwent gamma-knife radiosurgery prior to pulmonary resection. Definitive pathological examination revealed adenocarcinoma in 13 patients and squamous-cell lung carcinoma in three patients. Mean survival time was 15.3±8.6 months. One-year and two-year survival rates were 56.2% and 32%, respectively. The number of brain metastases, treatment type, tumor cell type, resection type, and status of lymph nodes were not statistically significantly associated with survival (p>0.05). Conclusion Cranial surgery or gamma-knife radiosurgery followed by aggressive lung resection can be effectively applied in selected non-small cell lung cancer patients with synchronous brain metastasis. However, the suitability of the primary tumor and brain metastases for complete resection is of utmost importance in patient selection.

Context: Internal rigid fixation provides immediate stability of the occipito-cervical (OC) junction for treatment of instability; however, in current practice, the optimal OC junction stabilization method is debatable. Aims: The aim of this study to test the safety and efficacy of a newly designed modified inside-outside occipito-cervical (MIOOC) plate system for the treatment of instability. Settings and Design: This was a feasibility study of MIOCC plate system. Subjects and Methods: Five male and four female patients with OC instability were treated using MIOOC plate system. Stabilization rate, safety, and efficacy were evaluated radiologically and clinically. Results: Mean age of the patients was 35 ± 11 (range: 22–58) years. Etiology of OC instability included trauma, neoplasm, congenital abnormalities, and iatrogenic. The fusion levels ranged from occiput-C3 to occiput-C6. Mean follow-up duration was 22 ± 10 (range: 6–46) months. There were neither complication nor was there any need for plate revision or screw pullout. Mortality occurred in one patient due to primary malignancy at 6 months; otherwise, no morbidity was observed. During the follow-up, no recurrent subluxation or newly developed instability at adjacent levels occurred. All patients showed a satisfactory union at the most recent follow-up examination. Conclusions: These preliminary results suggest that the MIOCC plate system is a useful and safe method for providing immediate internal stability of the OC junction. Using a multi-piece plate design in this plate system provided easy implantation and a better interface between plate and OC bones. Further, clinical studies and long-term results are needed to determine the reliability of the MIOOC plate system.

Operative management of intrinsic brainstem lesions remains challenging despite advances in electrophysiological monitoring, neuroimaging, and neuroanatomical knowledge. Surgical intervention in this region requires detailed knowledge of adjacent critical white matter tracts, brainstem nuclei, brainstem vessels, and risks associated with each surgical approach. Our aim was to systematically verify internal anatomy associated with each brainstem safety entry zone (BSEZ) via neuroimaging modalities commonly used in pre-operative planning, namely high-resolution magnetic resonance imaging (MRI) and diffusion tensor tractography (DTT). Twelve BSEZs were simulated in eight, formalin-fixed, cadaveric brains. Specimens then underwent radiological investigation including T2-weighted imaging and DTT using 4.7 T MRI to verify internal anatomic relationships between simulated BSEZs and adjacent critical white matter tracts and nuclei. The distance between simulated BSEZs and pre-defined, adjacent critical structures was systemically recorded. Entry points and anatomic limits on the surface of the brainstem are described for each BSEZ, along with description of potential neurological sequelae if such limits are violated. With high-resolution imaging, we verified a maximal depth for each BSEZ. The relationship between proposed safe entry corridors and adjacent critical structures within the brainstem is quantified. In combination with tissue dissection, high-resolution MR diffusion tensor imaging allows the surgeon to develop a better understanding of the internal architecture of the brainstem, particularly as related to BSEZs, prior to surgical intervention. Through a careful study of such imaging and use of optimal surgical corridors, a more accurate and safe surgery of brainstem lesions may be achieved.

Gurer, Bora/0000-0003-1500-6184; Sargon, Mustafa Fevzi/0000-0001-6360-6008 WOS: 000363901600010 PubMed: 26298021 Introduction: Ganoderma lucidum (G. lucidum) is a mushroom belonging to the polyporaceae family of Basidiomycota and has widely been used as a traditional medicine for thousands of years. G. lucidum has never been studied in traumatic spinal cord injury. The aim of this study is to investigate whether G. lucidum polysaccharides (GLPS) can protect the spinal cord after experimental spinal cord injury. Materials and methods: Rats were randomized into five groups of eight animals each: control, sham, trauma, GLPS, and methylprednisolone. In the control group, no surgical intervention was performed. In the sham group, only a laminectomy was performed. In all the other groups, the spinal cord trauma model was created by the occlusion of the spinal cord with an aneurysm clip. In the spinal cord tissue, caspase-3 activity, tumour necrosis factor-alpha levels, myeloperoxidase activity, malondialdehyde levels, nitric oxide levels, and superoxide dismutase levels were analysed. Histopathological and ultrastructural evaluations were also performed. Neurological evaluation was performed using the Basso, Beattie, and Bresnahan locomotor scale and the inclined-plane test. Results: After traumatic spinal cord injury, increases in caspase-3 activity, tumour necrosis factor-alpha levels, myeloperoxidase activity, malondialdehyde levels, and nitric oxide levels were detected. After the administration of GLPS, decreases were observed in tissue caspase-3 activity, tumour necrosis factor-alpha levels, myeloperoxidase activity, malondialdehyde levels, and nitric oxide levels. Furthermore, GLPS treatment showed improved results in histopathological scores, ultrastructural scores, and functional tests. Conclusions: Biochemical, histopathological, and ultrastructural analyses and functional tests reveal that GLPS exhibits meaningful neuroprotective effects against spinal cord injury. (C) 2015 Elsevier Ltd. All rights reserved.

Gurer, Bora/0000-0003-1500-6184 WOS: 000349987000023 PubMed: 25452015 BACKGROUND CONTEXT: Epidural fibrosis is a major challenge in spine surgery, with some patients having recurrent symptoms secondary to excessive formation of scar tissue resulting in neurologic compression. One of the most important factors initiating the epidural fibrosis is assumed to be the transforming growth factor-1 beta (TGF-1 beta). Rosuvastatin (ROS) has shown to demonstrate preventive effects over fibrosis via inhibiting the TGF-1 beta. PURPOSE: We hypothesized that ROS might have preventive effects over epidural fibrosis through the inhibition of TGF-1 beta pathways. STUDY DESIGN: Experimental animal study. METHODS: Forty-eight adult male Wistar Albino rats were equally and randomly divided into four groups (laminectomy, spongostan, topical ROS, and systemic ROS). Laminectomy was performed at the L3 level in all rats. Four weeks later, the extent of epidural fibrosis was assessed both macroscopically and histopathologically. RESULTS: Our data revealed that topical application and systemic administration of ROS both were effective in reducing epidural fibrosis formation. Furthermore, the systemic administration of ROS yielded better results than topical application. CONCLUSIONS: Both topical application and systemic administration of ROS show meaningful preventive effects over epidural fibrosis through multiple mechanisms. The results of our study provide the first experimental evidence of the preventive effects of ROS over epidural fibrosis. (C) 2015 Elsevier Inc. All rights reserved.

Introduction: Liponeurocytomas are mostly localized in cerebellar hemispheres and the second most common location is the vermis. It is rarely observed within the intracranial ventricles. Here, we present a case of liponeurocytoma located in the right lateral ventricle and the systematic review of the literature. State of the art: We searched PubMed with keyword 'central liponeurocytoma' and the references of the related articles. There were no language or year restrictions. We included articles focusing on liponeurocytomas located in the central nervous system leaving a total of 17 articles and 21 reported cases[2TD$DIF]. Clinical implications: A 62-year-old female presented with confusion and mental disorientation without any other neurological deficit. Her magnetic resonance imaging (MRI) revealed a lateral ventricle located mass lesion which was hypointense on T1-weighted images (WI) and heterogeneously hyperintense on T2-WI with cystic component. Via craniotomy, yellow-beige colored, soft and moderately vascularized mass lesion was gross totally resected. Despite postoperative MRI revealed total resection, patient had left-sided hemiparesis. The patient recovered well in her postoperative period and there was no recurrence on her 6th month follow-up MRI. Future directions: Intraventricular liponeurocytoma has a favorable clinical course, and radiological features may be useful in the diagnosis of this rare tumor before surgery. Supratentorial intraventricular location should be kept in mind in the differential diagnosis of the lateral ventricular tumors.

AIM To investigate the effects of an anti-ischemic agent, mildronate, on subarachnoid hemorrhage-induced vasospasm. MATERIAL AND METHODS Rabbits were randomly divided into four groups: control, subarachnoid hemorrhage (SAH), vehicle, and mildronate (n=8 animals per group). In the treatment group, 200 mg/kg of mildronate were intraperitoneally administered 5 minutes after the procedure and continued for 3 days as daily administrations of the same dose. At the end of the third day, the cerebrum, cerebellum, and brain stem were perfused, fixated, and removed for histopathological examination. Tissues were examined for arterial wall thickness, luminal area, and hippocampal neuronal degeneration. RESULTS Mildronate group showed significantly increased luminal area and reduced wall thickness of the basilar artery compared with the subarachnoid hemorrhage group. In addition, the hippocampal cell degeneration score was significantly lower in the mildronate group than in the SAH and vehicle groups. CONCLUSION These results show that mildronate exerts protective effects against SAH-induced vasospasm and secondary neural injury.

WOS: 000448045000028, PubMed ID: 30393502, Introduction: Tetracosactide is an engineered peptide that applies the same biological impacts as the endogenous adrenocorticotropic hormone. Previous studies indicated that tetracosactide has anti-inflammatory, antioxidant and neurotrophic activity. In this study, we hypothesized that tetracosactide may have protective effects in spinal cord ischemia-reperfusion injury. Material and methods: Rabbits were randomized into the accompanying four groups of eight animals each: group 1 (control), group 2 (ischemia), group 3 (methylprednisolone) and group 4 (tetracosactide). In the control group, just a laparotomy was performed. In the various groups, the spinal cord ischemia model was made by the impediment of the aorta only caudal to the renal vein. Neurological assessment was conducted with the Tarlov scoring system. Levels of myeloperoxidase, malondialdehyde and catalase were analyzed, similar to the activities of xanthine oxidase and caspase-3. Histopathological and ultrastructural assessments were additionally performed. Results: After ischemia-reperfusion injury, increments were found in the tissue myeloperoxidase levels (p < 0.001), malondialdehyde levels (p < 0.001), xanthine oxidase action (p < 0.001) and caspase-3 movement (p < 0.001). Conversely, both serum and tissue catalase levels were diminished (p < 0.001 for both). After the administration of tetracosactide, declines were seen in the tissue myeloperoxidase levels (p < 0.001), malondialdehyde levels (p = 0.003), xanthine oxidase action (p < 0.001) and caspase-3 movement (p < 0.001). Conversely, both the serum and tissue catalase levels were expanded (p < 0.001). Besides, tetracosactide treatment indicated enhanced results related to the histopathological scores (p < 0.001), the ultra-structural score (p = 0.008) and the Tarlov scores (p < 0.001). Conclusions: The findings showed for the first time that tetracosactide shows significant neuroprotective activity against ischemia-reperfusion injury of the spinal cord.

INTRODUCTION Spinal anesthesia is a widely used technique of the modern practice of anesthesia. Spinal cord ischemia is a rare but catastrophic complication of spinal anesthesia which may be caused by a direct vasoconstrictive effect of the local anesthetic. Although the vasoconstrictive effects of levobupivacaine have been widely studied, the vasoconstrictive effects of this drug on the intradural arteries have never been studied. The aim of this study is to evaluate whether levobupivacaine has vasoconstrictive effects on the basilar artery in rabbits. MATERIAL AND METHODS Thirty male New Zealand white rabbits were divided randomly into three groups of ten rabbits each: group 1 (control); group 2 (0.125% levobupivacaine); group 3 (0.25% levobupivacaine). The cisterna magna was punctured as described below, then 1 ml of saline or 0.125% or 0.25% levobupivacaine was injected into the cisterna magna in 10 min by an infusion pump in groups 1, 2 and 3 respectively. All animals were euthanized by perfusion-fixation 30 min after the procedure. The luminal area and the size of the cross-sectional area for each basilar artery were measured. RESULTS Both 0.125% and 0.25% levobupivacaine infusion caused significant vasoconstriction. Vasoconstriction was more significant for the 0.125% concentration. CONCLUSIONS The results of this study indicated that both 0.125% and 0.25% concentrations of levobupivacaine caused significant vasoconstriction of the basilar artery when administered into the subarachnoid space. This may constitute proof that subarachnoid administration of levobupivacaine may diminish the spinal cord blood flow, causing ischemia.

Background The development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is a well-known entity. Consequently, the aim of the present study was to evaluate the role of omeprazole (OM) on rat model of TBI. Methods A total of 24 male rats were used and divided into 4 groups as follows; control, trauma, OM, and methylprednisolone (MP). The trauma, OM, and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with saline, OM, or MP, respectively. All the animals were sacrificed at 24 hours after trauma and brain tissues were extracted. The oxidant/antioxidant parameters (malondialdehyde, glutathione peroxidase, superoxide dismutase, nitric oxide) and caspase-3 in the cerebral tissue were analyzed, and histomorphologic evaluation of the cerebral tissue was performed. Results Levels of MDA and activity of caspase-3 were significantly reduced in the OM and MP groups compared with the trauma group. Glutathione peroxidase and superoxide dismutase levels were increased both in the OM and MP groups compared with the trauma group. The pathology scores were statistically lower in the OM and MP groups than the trauma group. Conclusions The results of the present study showed that OM was as effective as MP in protecting brain from oxidative stress, and apoptosis in the early phase of TBI.

The aim of this study was to analyze the topographical anatomy of the dorsal spinal cord (SC) in relation to the posterior median septum (PMS). This included the course and variations in the PMS, and its relationship to and distance from other dorsal spinal landmarks. Microsurgical anatomy of the PMS was examined in 12 formalin-fixed adult cadaveric SCs. Surface landmarks such as the dorsal root entry zone (DREZ), the denticulate ligament, the architecture of the leptomeninges and pial vascular distribution were noted. The PMS was examined histologically in all spinal segments. The PMS extended most deeply at spinal segments C7 and S4. This was statistically significant for all spinal segments except C5. The PMS was shallowest at segments T4 and T6, where it was statistically significantly thinner than at any other segment. In 80% of the SCs, small blood vessels were identified that traveled in a rostrocaudal direction in the PMS. The longest distance between the PMS and the DREZ was at the C1–C4 vertebral levels and the shortest distance was at the S5 level. Prevention of deficits following a dorsal midline neurosurgical approach to deep-seated SC lesions requires careful identification of the midline of the cord. The PMS and septum define the midline on the dorsum of the SC and their accurate identification is essential for a safe midline surgical approach. In this anatomical study, we describe the surface anatomy of the dorsal SC and its relationship with the PMS, which can be used to determine a safe entry zone into the SC. Clin. Anat. 28:45–51, 2015. © 2014 Wiley Periodicals, Inc.

Foot drop is defined as the weakness of the foot and ankle dorsiflexion. Acute unilateral foot drop is a well-documented entity, whereas bilateral foot drop is rarely documented. Slowly progressing bilateral foot drop may occur with various metabolic causes, parasagittal intracranial pathologies, and cauda equina syndrome. Acute onset of bilateral foot drop due to disc herniation is extremely rare. Here we present two cases of acute bilateral foot drop due to disc herniation. The first patient was a 45-year-old man presented with acute bilateral foot drop, without any sign of the cauda equina syndrome. Lumbar magnetic resonance imaging of the patient revealed L4-5 disc herniation. To our knowledge, this is the first presented case of acute bilateral foot drop without any signs of cauda equina syndrome caused by L4-5 disc herniation. The second patient was a 50-year-old man who was also presented with acute bilateral foot drop, and had T12-L1 disc herniation with intradural extension. Also this is the first presented case of T12-L1 disc herniation with intradural extension causing acute bilateral foot drop. We performed emergent decompressive laminectomy to both of the patients and extrude disc materials were excised. Both of the patients were recovered with favorable outcome.

Darbepoetin alpha is a hypersialylated analogue of erythropoietin effective for activating erythropoietin-receptors. This study investigated the vasodilator and neuroprotective effects of darbepoetin alpha on an experimental subarachnoid hemorrhage model and compared it with erythropoietin. Forty adult male New Zealand white rabbits were randomly divided into four groups of ten rabbits each: group 1 (control), group 2 (subarachnoid hemorrhage), group 3 (erythropoietin), and group 4 (darbepoetin alpha). Recombinant human erythropoietin was administered at a dose of 1,000 U/kg intraperitoneally after the induction of subarachnoid hemorrhage and continued every 8 h up to 72 h. Darbepoetin alpha was administered at a single intraperitoneal dose of 30 μg/kg. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, hippocampal degeneration scores and biochemical analyses were measured in all groups. Both erythropoietin and darbepoetin alpha treatments were found to attenuate cerebral vasospasm and provide neuroprotection after subarachnoid hemorrhage in rabbits. Darbepoetin alpha revealed better morphometric and histopathological results than erythropoietin among experimental subarachnoid hemorrhage-induced vasospasm. Our findings, for the first time, showed that darbepoetin alpha can prevent vasospasm and provides neuroprotection following experimental subarachnoid hemorrhage. Moreover, darbepoetin alpha showed better results when compared with erythropoietin.

Low grade gliomas (LGGs) are slow-growing primary brain tumors with heterogeneous clinical behaviors. The aim of our study is to review the treatment outcome of 63 patients with LGGs focusing on surgical outcome and the current therapeutic strategy.We retrospectively enrolled 63 patients surgically treated for LGGs. The gross total resection (GTR) was performed in 35 patients (60.3%), subtotal resection (STR) was performed in 19 patients (31.7%) and partial resection (PR) or biopsy was performed in 9 patients (14.3%). We analyzed their progression-free survival (PFS), overall survival (OS), and malignant transformation with regard to age, gender, Karnofsky performance score (KPS), clinical presentation, tumor location, radiologic pattern, contrast enhancement, extent of removal, pathologic subtype, chemotherapy (CT) and radiotherapy (RT) treatment.Among all LGGs, the 3-year OS rate was 80% and the 5-year OS was 76%. The 3-year PFS rate was 83.6% and the 5-year PFS was 25%. The non-eloquent area location showed a longer PFS than the eloquent area location (p=0.05). Oligodendroglial pathology showed a longer PFS compared to oligoastrocytomas and astrocytomas (p=0.02). Patients older than 60 years had poorer OS than younger patients (p0.05). Female gender had a shorter OS than male gender (p0.05), and a KPS of 90 or 100 had a longer OS than a KPS of 80 (p0.05). Oligodendroglial pathology statistically correlated with a longer OS (p0.05).The findings from our study, which were confirmed by uni- and multivariate analyses, demonstrated that radical tumor resection was associated with better long-term outcomes and tumor progression for patients with LGG.

The denticulate ligaments (DL), 20 or 21 pairs of meningeal extensions, spread from the lateral aspect of the spinal cord to the internal aspect of the spinal dura mater. The aim of this study is to define the specific relationship of the DL with adjacent axilla of the spinal nerve roots and to investigate the anatomical features of the DLs and their variations. The topographical anatomy of the DLs and their relationships with the adjacent axilla of the spinal nerve roots was examined on 16 formalin-fixed adult cadaveric spinal cords. The distances from the dural attachment of the DL to the axilla of the superior and inferior spinal nerve roots were measured bilaterally at every spinal level. Also the distances from the dural attachment of the DL to the lateral aspect of the spinal cord were measured bilaterally. Cervical DLs showed a triangular shape, while in the thoracic segment the ligament changes the shape to "Y." Also the most caudal DL was identified to be at the L1-2 level. Our study revealed that the distances from the dural attachment of the DL to the superior and inferior spinal nerve root axilla were different at the cervical, upper thoracic and the lower thoracic segments. Both distances to the superior and inferior spinal nerve root axilla were shown to increase from cervical to lower thoracic segments. This study provides a detailed anatomy of the DLs and their relationship with the adjacent spinal nerve root axilla.

The subparietal and parietooccipital sulci are both located on the medial surface of the brain. Both of these sulci reveal significant variability in pattern and complexity. Both subparietal and parietooccipital sulci play an important role as surgical landmarks using posterior interhemispheric parietooccipital approach to lesions located adjacent to the ventricular trigon deep to the cingulate gyrus. The aim of this study is to analyze variations in the patterns of the subparietal and parietooccipital sulci and to emphasize their surgical importance. Fifty-six formalin-fixed cadaveric cerebral hemispheres from 28 adult humans are examined. Subparietal and parietal sulci patterns, variations and their relationship with the cingulate sulcus are studied according to the terminology introduced by Ono et al. The H-pattern was observed in 50% (n = 28) of all hemispheres, being the most common pattern of the subparietal sulcus. The Straight pattern was observed in the 30.4% (n = 17) of all hemispheres, being the most common pattern of the parietooccipital sulcus. Furthermore, more detailed results among the patterns, connections, side branches and the relationship with the adjacent sulci are given. Our study further confirms the complexities in the patterns of the subparietal and parietooccipital sulci and demonstrates that these sulci fall within an expected range of variations. Better knowledge of these variations will further help neurosurgeons to navigate easily during approaches involving the medial surface of the parietal lobe. Clin. Anat. 26:667-674, 2013. © 2013 Wiley Periodicals, Inc.

Segments of the spinal cord generally do not correspond to the respective vertebral level and there are many anatomical variations in terms of the segment and the level of vertebra. The aim of this study is to investigate the variations and levels of lumbar and sacral spinal cord segments with reference to the axilla of the T11, T12, and L1 spinal nerve roots and adjacent vertebrae. Morphometric measurements were made on 16 formalin fixed adult cadaveric spinal cords. We observed termination of the spinal cord between the axilla of the L1 and L2 spinal nerve roots in 15 specimens (93.8%). In all cadavers the emergence of the T11, T12, and the L1 spinal nerve roots was at the level of the lower one-third of the same vertebral body. In 15 specimens (93.8%), the beginning of the lumbar spinal cord segment was found to be above the T11 spinal nerve root axilla and corresponded to the upper one-third of the T11 vertebral body. The beginning of the sacral spinal cord segment occurred above the L1 spinal nerve root axilla and corresponded to the upper one-third of the L1 vertebral body. The results of this study showed that when the conus medullaris is located at the L1-L2 level, the beginning of the lumbar spinal cord segment always corresponds to the body of T11 vertebra. This study provides detailed information about the correspondence of the spinal cord segments with reference to the axilla of the spinal nerve roots.

Glioblastoma multiforme (GBM) is a highly malignant primary brain tumor and is the most common primary malignancy of the central nervous system (CNS). It is also locally aggressive, invasive, and resistant to therapy. Extracranial seeding of GBM is very rare, but cerebrospinal fluid (CSF) seeding is observed in approximately 15–25 % of supratentorial GBM cases [1–3]. Spinal seeding of GBM metastasis is frequently observed in autopsy series, whilst symptomatic spinal metastases from primary GBM are rarely reported [3–5]. Here, we report the clinical features, radiographic findings, and management of a unique supratentorial GBM case presented with paraplegia secondary to massive spinal metastases.

Arteriovenous fistulas (AVFs) are relatively uncommon lesions f the spine. Despite their low overall incidence, AVFs are the most ommon vascular anomaly of the spinal cord [1]. AVFs between the ertebral artery (VA) and the jugular vein (JV) are a rare subgroup f spinal AVFs. Most are post-traumatic in origin, following direct njury or iatrogenic manipulations. Spontaneous fistulas are often ssociated with neurofibromatosis or fibromuscular dysplasia [2]. In this article, we present a unique case of a spontaneous verterojugular fistula that manifested as a diffusely enhancing lesion on he cervical spine, which mimicked an intradural extramedullary ass lesion such as a schwannoma.

Aim: The aim of this study was to assess the surgical outcome and prognostic importance of clinical and radiological data from children operated on under emergency conditions due to an extra-axial hematoma causing brain herniation. Methods: This retrospective study included 25 children operated on due to herniated traumatic extra-axial hematomas from January 2000 to December 2010. Results: Of those 25 children, 17 (68%) were diagnosed with subdural hematoma (SDH), 7 (28%) with epidural hematoma (EDH) and only 1 patient (4%) suffered from both SDH and EDH. Overall mortality from a herniated extra-axial hematoma was 44%. The mortality rate for herniated SDH patients was 52.9%, and only 1 patient died from a herniated EDH (14.2%). Low Glasgow coma scale scores at admission, high postoperative intracranial pressure (ICP) values, longer intervals from trauma to surgery, longer durations of brain herniation, the presence of intraoperative brain swelling, larger and thicker hematomas and more displacement of the midline structures and obliteration of the basal cisterns were all correlated with mortality and an unfavorable outcome. Conclusions: Brain herniation is a serious consequence of traumatic extra-axial hematomas in children, and approximately one third of these patients have the potential for a favorable outcome. We recommend postoperative ICP monitoring to predict outcome and early decompressive surgery when possible for promising results.

Introduction Tetracosactide is an engineered peptide that applies the same biological impacts as the endogenous adrenocorticotropic hormone. Previous studies indicated that tetracosactide has anti-inflammatory, antioxidant and neurotrophic activity. In this study, we hypothesized that tetracosactide may have protective effects in spinal cord ischemia-reperfusion injury. Material and methods Rabbits were randomized into the accompanying four groups of eight animals each: group 1 (control), group 2 (ischemia), group 3 (methylprednisolone) and group 4 (tetracosactide). In the control group, just a laparotomy was performed. In the various groups, the spinal cord ischemia model was made by the impediment of the aorta only caudal to the renal vein. Neurological assessment was conducted with the Tarlov scoring system. Levels of myeloperoxidase, malondialdehyde and catalase were analyzed, similar to the activities of xanthine oxidase and caspase-3. Histopathological and ultrastructural assessments were additionally performed. Results After ischemia-reperfusion injury, increments were found in the tissue myeloperoxidase levels (p < 0.001), malondialdehyde levels (p < 0.001), xanthine oxidase action (p < 0.001) and caspase-3 movement (p < 0.001). Conversely, both serum and tissue catalase levels were diminished (p < 0.001 for both). After the administration of tetracosactide, declines were seen in the tissue myeloperoxidase levels (p < 0.001), malondialdehyde levels (p = 0.003), xanthine oxidase action (p < 0.001) and caspase-3 movement (p < 0.001). Conversely, both the serum and tissue catalase levels were expanded (p < 0.001). Besides, tetracosactide treatment indicated enhanced results related to the histopathological scores (p < 0.001), the ultra-structural score (p = 0.008) and the Tarlov scores (p < 0.001). Conclusions The findings showed for the first time that tetracosactide shows significant neuroprotective activity against ischemia-reperfusion injury of the spinal cord.

Background The development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is well known. Decorin (DC) inactivates transforming growth factor β1, complement system, and tumor necrosis factor α, which are related to oxidative stress and apoptosis. Consequently, the aim of the present study was to evaluate the role of DC on TBI. Methods A total of 24 male rats were used and divided into 4 groups as follows; control, trauma, DC, and methylprednisolone (MP). The trauma, DC, and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with intraperitoneal saline, DC, or MP, respectively. All the animals were killed at the 24th hour after trauma and brain tissues were extracted. The oxidant/antioxidant parameters (malondialdehyde, glutathione peroxidase, superoxide dismutase, and NO) and caspase 3 in the cerebral tissue were analyzed, and histomorphologic evaluation of the cerebral tissue was performed. Results Levels of malondialdehyde, NO, and activity of caspase 3 were significantly reduced, and in addition glutathione peroxidase and superoxide dismutase levels were increased in the DC and MP groups compared with the trauma group. The pathology scores and the percentage of degenerated neurons were statistically lower in the DC and MP groups than in the trauma group. Conclusions The results of the present study showed that DC inactivates transforming growth factor β1 and protects the brain tissue and neuronal cells after TBI.