Split cord malformation concomitant with spinal teratoma without open spinal dysraphism.

PURPOSE: Split cord malformation (SCM) presenting concomitant with spinal teratoma without any open spinal dysraphism has rarely been reported in the literature. We aimed to make a systematic review and qualitative analysis of the literature about the topic and present the first case of SCM concomitant with spinal teratoma harboring papillary thyroid carcinoma (PTC) component. METHODS: Two big search tools (Pubmed/MEDLINE) and Scopus were used. The search strategy was compatible to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). An exemplary case of ours was also presented. RESULTS: There were 30 patients (15 pediatric and 15 adult). Female and male distribution was even. Median age of the patients was 18 years (range = 0-66 years). The most common presenting symptoms were back pain and lower limb weakness. Spinal teratoma and SCM mostly presented at thoracic/thoracolumbar region in children and lumbar region in adults. Surgical outcome was better in the children compared to the adults. CONCLUSION: Thoracolumbar region is the most common location for such entity in children, whereas lumbar region for the adults. Surgical resection should be done as much as possible under neuromonitorization. The resected material should be evaluated thoroughly not to miss any malign pathology. Surgical outcome is better when it is done at an early age.

Amelioration of Cerebral Vasospasm and Secondary Injury by Vigabatrin After Experimental Subarachnoid Hemorrhage in the Rabbit.

BACKGROUND: 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. METHODS: 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. RESULTS: The arterial wall thickness of the vigabatrin group was less than that in the SAH group (P < 0.001), and the mean luminal area of the vigabatrin group was greater than that in the SAH group (P < 0.001). Additionally, the hippocampal neuronal degeneration score of the vigabatrin group was lower than that of the SAH group (P < 0.001). CONCLUSION: 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.

The Vasorelaxant and Neuroprotective Effects of Mildronate in A Rabbit Subarachnoid Hemorrhage Model.

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.

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits.

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.

Antidepressant Prescriptions in Neurosurgical Practice: A Survey of Current Trends.

AIM: To better understand the indications and the impact of antidepressant drugs on the field of neurosurgery in terms of risks and benefits in Turkey. MATERIAL AND METHODS: A national survey was conducted among neurosurgeons in current practice in Turkey to report routine prescription trends of antidepressant drugs. Gender, neurosurgical subspecialty, city, type of practice, years of experience, antidepressant agent, indications and reasons not to prescribe were ascertained. A brief review of literature was done to show clinical and research evidence. RESULTS: A total of 336 neurosurgeons took the survey; 53% of them prescribe antidepressants routinely, whereas 47% of them do not. Of the 72% non-prescribers prefer to refer their patients to a psychiatrist and 22% of them believe that antidepressants have no role in neurosurgery. Vascular and pediatric neurosurgeons as well as neurosurgeons at research hospitals showed the lowest prescription proportion, while general and brain tumor neurosurgeons and ones in private practice showed the highest prescription proportion. Surgeons with more than 20 year-experience had the lowest prescription proportion (43%). Type of practice and years of experience showed a statistically significant association with the prescription of antidepressant drugs across (p=0.002 and p=0.025, respectively). CONCLUSION: Type of practice and years of experience showed a statistically significant association with the proportion of antidepressants' prescribers in Turkish neurosurgery practice at the time of this survey. Non-prescriber neurosurgeons need to recognize the indications, whereas prescribers have to understand the risks of using antidepressants.

Antifibrotic Effect of Boric Acid in Rats with Epidural Fibrosis.

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.

Comparative effects of methylprednisolone and tetracosactide (ACTH1-24) on ischemia/reperfusion injury of the rabbit spinal cord.

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.

Comparative effects of vitamin D and methylprednisolone against ischemia/reperfusion injury of rabbit spinal cords.

INTRODUCTION: 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. METHODS: 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. RESULTS: After I/R injury, increases in malondialdehyde levels, myeloperoxidase and xanthine oxidase activities, and caspase-3 concentrations were found (p<0.001 for all); by contrast, catalase levels decreased (p<0.001). Calcitriol pretreatment was associated with lower malondialdehyde levels (p<0.001), reduced myeloperoxidase (serum, p=0.018; tissue, p<0.001) and xanthine oxidase (p<0.001) activities, and caspase-3 concentrations (p<0.001), but increased catalase levels (p<0.001). Furthermore, calcitriol pretreatment was associated with better histopathological, ultrastructural, and neurological scores. CONCLUSION: Calcitriol pretreatment provided significant neuroprotective benefits following spinal cord I/R injury.