Radiofrequency Ablation and Augmentation in the Management of Spinal Metastases: Clinical Experience in 41 Patients.

OBJECTIVE: To evaluate functional outcome after combined radiofrequency ablation and vertebral augmentation in patients with metastatic spinal tumors using visual analog scale and Oswestry Disability Index scores. METHODS: This retrospective study included 41 patients with metastatic spinal tumors. There were 19 women and 22 men with a mean age of 67 years (range, 45-87 years). Visual analog scale and Oswestry Disability Index were used to assess the intensity of pain and quality of life. The assessments were performed before the procedure and at 1 week and 1, 2, 3, and 6 months after the procedure. RESULTS: No serious complications were seen in the periprocedural period. Two patients (4.8%) had transient neurological motor deficits without cement leakage, and 1 patient had a pulmonary embolism with transient mild symptoms. The comparison of preprocedural visual analog scale and Oswestry Disability Index scores with postprocedural scores up to 6 months after treatment revealed significant pain control and good functional state. CONCLUSIONS: Spinal metastasis is a frequent entity in the growing population of patients with cancer. A multidisciplinary approach using several nonsurgical and minimally invasive methods (e.g., radiofrequency ablation, vertebroplasty, balloon kyphoplasty) is key to successful management, and combining these procedures is effective against spinal metastatic pain.

Radiofrequency ablation may improve the beneficial results of vertebroplasty for vertebral hemangiomas: analysis of 46 patients.

OBJECTIVES: To evaluate the effect of vertebroplasty (VP) alone or combined therapy of radiofrequency ablation (RFA) with vertebroplasty on pain relief with visual analog scale (VAS) and Oswestry Disability Index (ODI) scores in vertebral hemangiomas. METHODS: Forty-six patients with hemangiomas were evaluated retrospectively: 20 males and 26 females were included. In group 1 (n = 25) only VP was performed, while RFA+VP were performed in the same treatment session in group 2 (n = 21). Radiological diagnosis was performed with X-ray, CT-scan and MRI images in all patients. The intensity of pain was assessed with the VAS together with the assesment of life quality with the ODI. The assesments were performed before, at first day, at first month and 6 months after treatment. RESULTS: There was no significant difference between mean preprocedural VAS and ODI scores, but a significant decrease was seen in postprocedural VAS and ODI scores between group 1 and 2, when compared with the preprocedural values. Although lack of a statistically significant difference in long term results, mean VAS score was 3.7 for group 1, while it was 1.8 for group 2, and the mean ODI score was 38 for group 1, and 22.48 for group 2 at 6th month assesment. DISCUSSION: Although minimally invasive percutaneous techniques are indicated as other modalities are ineffective or contraindicated, combining RFA with vertebral augmentation provide prevention of mechanical loading pain, and prevention of somatic pain in patients with spinal hemangiomas.

Modulation of Salubrinal-Mediated Endoplasmic Reticulum Stress in an Experimental Subarachnoid Hemorrhage Model.

BACKGROUND: Perfusion abnormalities due to vasospasm remain a major cause of morbidity and mortality in subarachnoid hemorrhage (SAH). Despite a large number of clinical trials, therapeutic options with strong evidence for prevention and treatment of cerebral vasospasm are rare. In this study, we aimed to evaluate the neuroprotective effect of salubrinal (SLB) in endoplasmic reticulum stress-induced apoptosis, a catastrophic consequence of vasospasm. METHODS: Thirty-two Wistar albino rats were divided into 4 groups of 8 rats each: control group, SAH, SAH+SLB, and SAH+nimodipine (NMN). In the SAH+SLB group, intraperitoneal SLB (1 mg/kg dose) administered 30 minutes after establishment of SAH, and in the SAH+NMN group, intraperitoneal NMN (0.1 mg/kg dose) was also administered 30 minutes after SAH. RESULTS: Higher total antioxidant status level, lower oxidative stress index, and significantly higher vascular endothelial growth factor-A (VEGF-A) level were detected in the SAH+SLB and SAH+NMN groups compared with the SAH group. There was a significant increase in eukaryotic translation initiation factor-2 alpha (elF2α) level in the SAH+SLB group compared with the SAH group. Histopathological evaluation revealed decrease in the subarachnoid hemorrhagic area, as well as in cortical edema and apoptotic bodies in the SAH+SLB and SAH+NMN groups. There was a significant decrease in caspase-3 staining in the SAH+SLB group, and the levels were significantly less in the SAH+NMN group than the SAH and SAH+SLB groups. CONCLUSIONS: SLB, selective inhibitor of eIF2α dephosphorylation, and NMN, a calcium channel blocker, can ameliorate SAH-induced damage. Inhibition of eIF2α dephosphorylation and enhanced VEGF-A production with SLB may protect brain tissue from apoptosis.

Pregabalin Protects Brain Tissue from Subarachnoid Hemorrhage by Enhancing HIF-1α/eNOS Signaling and VEGF Production.

OBJECTIVE: We investigated the effects of different doses of pregabalin on the pathophysiologic changes in early brain injury after subarachnoid hemorrhage (SAH) in rats. METHODS: Thirty-eight Wistar albino rats were divided into 4 groups: control (n = 8), SAH (n = 10), SAH plus 30 mg/kg/day of pregabalin (n = 10), and SAH plus 60 mg/kg/day of pregabalin (n = 10). SAH was induced with 0.3 mL of autologous blood injected to the cisterna magna of rats. Pregabalin was administered intraperitoneally. Oxidative stress markers, mRNA expression of endothelial nitric oxide synthase, hypoxia-inducible factor-1α, and vascular endothelial growth factor, and histopathological changes were evaluated. RESULTS: Pregabalin increased mRNA expression of endothelial nitric oxide synthase, hypoxia-inducible factor-1α, and vascular endothelial growth factor in a dose-dependent manner. Significant improvement in the histopathological parameters was observed at 60 mg/kg, including a decrease in diffuse hemorrhagic areas, edema and apoptotic bodies in the associated cortical area, evident vacuolization in the hippocampal area, and apoptotic bodies. However, these improvements were not observed with the lower dose (30 mg/kg). In contrast, the antioxidant effect was greater with 30 mg/kg of pregabalin than with 60 mg/kg. CONCLUSIONS: Although the antioxidant effect was significant with the lower dose of pregabalin, the anti-inflammatory effects via vasodilatation were more marked with the higher dose. Significant improvements in the histopathological changes were observed with the higher dose of pregabalin. The dose-dependent effects of pregabalin on SAH should be evaluated in animal studies as a function of time and in the acute and chronic phases.

Nimodipine can improve cerebral metabolism and outcome in patients with severe head trauma.

In the present study, the effect of nimodipine was investigated in a patient with severe head trauma. Nimodipine was administered into the peripheral vein to prevent secondary neuronal damages in patients. The five patients in control group were treated according to the standard procedures without nimodipine. Other five patients in nimodipine group were treated with standard procedures plus nimodipine. Cerebral perfusion pressure (CPP), intracranial pressure (ICP), jugular venous oxygen saturation (SjvO2), jugular lactate and glucose levels were measured. Additionally, all patients were evaluated with Glascow outcome score (GOS) before discharge. It was found that CPP (p<0.05) and SjvO2 (p<0.05) were significantly higher; but, ICP (p<0.001), jugular lactate (p<0.05) and jugular glucose (p<0.05) were lower in nimodipine than that of control groups. Again, GOS values were significantly higher in nimodipine than that of control groups (p<0.05). Results of this study revealed that nimodipine can improve cerebral metabolism and outcome in patient with severe head trauma. Thus, nimodipine may be considered as a protective agent against severe head trauma related neuronal injuries.