Neuroprotective Effects of Niacin on Ischemia/Reperfusion Injury of the Rabbit Spinal Cord.

OBJECTIVE: Previous studies have shown niacin has neuroprotective effects on the central nervous system. However, its specific effect on spinal cord ischemia/reperfusion injury has not yet been explored. This study aims to evaluate whether niacin can contribute neuroprotective effects on spinal cord ischemia/reperfusion injury. METHODS: Rabbits were randomized into 4 groups of 8 animals: group I (control), group II (ischemia), group III (30 mg/kg methylprednisolone, intraperitoneal), and group IV (500 mg/kg niacin, intraperitoneal). The rabbits in group IV were premedicated with niacin for 7 days prior to inducing ischemia/reperfusion injury. The control group was subjected only to a laparotomy, while the remaining groups underwent spinal cord ischemia through a 20-minute occlusion of the aorta caudal to the left renal artery. Following the procedure, levels of catalase, malondialdehyde, xanthine oxidase, myeloperoxidase, and caspase-3 were analyzed. Ultrastructural, histopathological, and neurological evaluations were also performed. RESULTS: Spinal cord ischemia/reperfusion injury resulted in increased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3, with a concomitant decrease in catalase levels. Treatment with methylprednisolone and niacin led to decreased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3 and an increase in catalase. Both methylprednisolone and niacin treatments demonstrated improvements in histopathological, ultrastructural, and neurological assessments. CONCLUSIONS: Our findings suggest that niacin has antiapoptotic, anti-inflammatory, antioxidant, and neuroprotective effects at least equal to methylprednisolone in ischemia/reperfusion injury of the spinal cord. This study is the first to report the neuroprotective impact of niacin on spinal cord ischemia/reperfusion injury. Further research is warranted to elucidate the role of niacin in this context.

Flow diverter stent treatment for unruptured supraclinoid segment internal carotid artery aneurysms: a Turkish multicenter study.

OBJECTIVE: Despite the relatively high success of surgical clipping of supraclinoid segment aneurysms of the internal carotid artery (ICA), flow diverter (FD) stent therapy is becoming increasingly used for these aneurysms. This study aims to evaluate the characteristics of FD placement for unruptured ICA supraclinoid segment aneurysms at 6 different centers with different experience levels in Türkiye. METHODS: In this retrospective, multicenter study, the authors reviewed the demographic information, aneurysm shape/dimensions (neck, aspect ratio, dome/neck ratio, and maximum diameter), preoperative antiplatelet regimen, FD stent brand, perioperative complications, intervention time, clinical (modified Rankin Scale) and radiological (O'Kelly-Marotta [OKM] grading scale) outcomes, and follow-up time of 54 patients. RESULTS: A total of 55 interventions for 61 aneurysms (58 supraclinoid ICA aneurysms) were performed in the 54 patients included in the study. The female/male ratio in this population was 44/10, and the mean age was 53.5 ± 13.6 (range 21-82) years. The most common form and location of the aneurysms were saccular 91.4% (53/58) and ophthalmic segment 69% (40/58), respectively. The preferred antiplatelet regimen was acetylsalicylic acid plus ticagrelor 50% (27/54). The overall complication rate was 25.5% (14/55), and the mean follow-up time was 25.76 ± 17.88 months. The successful radiological outcome (OKM grade C or D) rate at the 6-month follow-up was 92.6%. No perioperative complications led to any permanent or transient neurological deficit. CONCLUSIONS: The results of this first multicenter study evaluating FD stent use for unruptured ICA supraclinoid segment aneurysms showed that FD stent treatment is a feasible method for replacing clipping and coil embolization with manageable complications and a high success rate.

Biochemical, pathological and ultrastructural investigation of whether lamotrigine has neuroprotective efficacy against spinal cord ischemia reperfusion injury.

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.

Effects of Ganoderma lucidum Polysaccharides on Different Pathways Involved in the Development of Spinal Cord Ischemia Reperfusion Injury: Biochemical, Histopathologic, and Ultrastructural Analysis in a Rat Model.

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 1ß, 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 1ß, 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.

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.

Massive Intramedullary Hemorrhage After Subarachnoid Hemorrhage in Patient with Vertebrovertebral Arteriovenous Fistula.

BACKGROUND: Hemorrhagic presentations are rare in vertebrovertebral arteriovenous fistula (VVAVF). To the best of our knowledge, this is the first report of a patient initially presenting with subarachnoid hemorrhage and progressing to intramedullary hemorrhage. CASE DESCRIPTION: The authors report on a 59-year-old man with VVAVF who developed massive intramedullary hemorrhage. Twelve months before ictus, the patient presented with subarachnoid hemorrhage. Although we recommended endovascular surgery, the patient refused treatment. Twelve months after the initial attack, the massive intramedullary hemorrhage in cervical spinal cord caused complete spinal cord injury. Emergent endovascular intervention was performed after the intramedullary hemorrhage, but there was no neurologic improvement. CONCLUSIONS: Identification of this phenomenon is important in VVAVF because intramedullary hemorrhage dramatically degrades patient outcome. Prompt surgical intervention is mandatory for VVAVF cases presenting with subarachnoid hemorrhage.

Corticosteroid pre-treated primary CNS lymphoma: a detailed analysis of stereotactic biopsy findings and consideration of interobserver variability.

Prior corticosteroid therapy presents a major challenge in the diagnosis of CNS lymphomas, particularly in stereotactic biopsies. In this study we analysed the cytological, histopathological and immunohistochemical features in stereotactic biopsies of 25 primary CNS lymphoma cases pre-treated with corticosteroids. We documented the extent and the frequency of each finding. We also investigated the significance of subjectivity in evaluation of these biopsies in 3 seperate sessions including the final diagnostic decision. In 48% of our cases the diagnosis was straightforward. These cases were characterized by prominent blasts either in diffuse paranchymal infiltrates or in perivascular regions. The remaining 52% demonstrated some degree of variability among pathologists. Lymphoid atypia other than the typical blastic morphology appeared as a subjective finding and this was more pronounced in cytology preparations. In our study, corticosteroid pre-treatment in primary CNS lymphoma was associated with a large spectrum of histopathological, immunohistochemical and cytological findings. Combined use of an extended immunohistochemical panel would increase the possibility of conclusive diagnosis. Nevertheless some of these findings and therefore the diagnosis are open to subjectivity.

Osteopontin expressions correlate with WHO grades and predict recurrence in meningiomas.

Recurrence of meningiomas is a major prognostic issue. Although World Health Organization (WHO) histopathological grading correlates strongly with recurrence, it has some limitations, and predicting the biological behavior of grade I meningiomas is particularly difficult. Osteopontin (OPN) is a protein known to be involved in tumor progression. The purpose of this study is to determine expression of OPN in meningiomas and to investigate its correlation with WHO grades and tumor recurrence. Immunohistochemical (IHC) evaluation of expression of OPN was performed by two different methods to ensure reliability. OPN IHC and Allred scores were calculated on the basis of intensity and extent of staining. Both scores were in agreement and correlated significantly with meningioma grade and Ki-67 index. OPN scores were also significantly correlated with recurrence of WHO grade I meningiomas. Cut-off values for OPN IHC and OPN Allred scores between non-recurrent and recurrent grade I meningiomas were calculated as 70 and 5.5 respectively. We concluded that OPN is a valuable marker for grading meningiomas and for predicting the recurrence in WHO grade I tumors.

Spontaneous elevation of a ping-pong fracture: case report and review of the literature.

Depressed skull fractures compromise 7-10% of the children admitted to hospital with a head injury. Depressed skull fractures that occur in children younger than 1 year are different from those found in older children. In neonates and infants, a depressed fracture forms an inward buckling of the bones forming a 'cup shape', termed a 'ping-pong fracture'. In neonates, spontaneous elevation of a ping-pong fracture after birth trauma is well documented. However, in infants, spontaneous elevation of a ping-pong fracture following head injury is extremely rare. Here, we present the case of an 11-month-old child, in whom a ping-pong fracture was spontaneously elevated within 2 h. In addition, the relevant literature is reviewed and discussed.