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.

A rare complication of esophageal dilatation: Brain abscess.

Brain abscess is an uncommon serious disease, which has been reported as a rare complication of repeated esophageal dilations; however, routine periprocedural antibiotic prophylaxis is not currently recommended. Herein, we present a brain abscess that developed after esophageal dilatation for the treatment of induced caustic esophageal strictures. The clinical presentation is non-specific, the most reported signs are high fever and neurologic findings. Cases have been reported in the literature in adult and pediatric patients. Cranial imaging is essential for diagnosis, drainage and antibiotics are essential in its treatment. Clinical improvement was achieved with antibiotic therapy and surgical drainage. This serious complication should be kept in mind when treatment of corrosive strictures though repeated esophageal dilatation is planned and prophylaxis should be considered in selected patients.

A Rare Parasitic Infection: Primary Intradural Extramedullary Hydatid Cyst.

Echinococcus granulosus infrequently induces spinal hydatid cysts, and intradural hydatid cysts are extremely rare among these spinal hydatid cysts. We report a 30-year-old man with a history of progressive back pain caused by a previous back injury. Magnetic resonance imaging revealed a spinal intradural cystic lesion. After surgical removal, histopathological diagnosis was a hydatid cyst. The patient had no other symptoms of systemic hydatid cyst disease. Diagnosis of hydatid cyst should be considered prior to surgery, especially in young patients with spinal intradural cystic lesions, as leakage of the hydatid cyst's fluid during surgery is a frequent case of recurrence.

Hypericum perforatum Attenuates Spinal Cord Injury-Induced Oxidative Stress and Apoptosis in the Dorsal Root Ganglion of Rats: Involvement of TRPM2 and TRPV1 Channels.

Oxidative stress and cytosolic Ca(2+) overload have important roles on apoptosis in dorsal root ganglion (DRG) neurons after spinal cord injury (SCI). Hypericum perforatum (HP) has an antioxidant property in the DRGs due to its ability to modulate NADPH oxidase and protein kinase C pathways. We aimed to investigate the protective property of HP on oxidative stress, apoptosis, and Ca(2+) entry through transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels in SCI-induced DRG neurons of rats. Rats were divided into four groups as control, HP, SCI, and SCI + HP. The HP groups received 30 mg/kg HP for three concessive days after SCI induction. The SCI-induced TRPM2 and TRPV1 currents and cytosolic free Ca(2+) concentration were reduced by HP. The SCI-induced decrease in glutathione peroxidase and cell viability values were ameliorated by HP treatment, and the SCI-induced increase in apoptosis, caspase 3, caspase 9, cytosolic reactive oxygen species (ROS) production, and mitochondrial membrane depolarization values in DRG of SCI group were overcome by HP treatment. In conclusion, we observed a protective role of HP on SCI-induced oxidative stress, apoptosis, and Ca(2+) entry through TRPM2 and TRPV1 in the DRG neurons. Our findings may be relevant to the etiology and treatment of SCI by HP. Graphical Abstract Possible molecular pathways of involvement of Hypericum perforatum (HP) on apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in DRG neurons of SCI-induced rats. The TRPM2 channel is activated by ADP-ribose and oxidative stress through activation of ADP-ribose pyrophosphate although it was inhibited by N-(p-amylcinnamoyl) anthranilic acid (ACA) and 2-aminoethyl diphenylborinate (2APB). The TRPV1 channel is activated by oxidative stress and capsaicin and it is blocked by capsazepine. Injury in the DRG can result in augmented ROS release, leading to Ca(2+) uptake through TRPM2 and TRPV1 channels. Mitochondria were reported to accumulate Ca(2+), provided intracellular Ca(2+) rises, thereby leading to depolarization of mitochondrial membranes and release of apoptosis-inducing factors such as caspase 3 and caspase 9. HP via regulation of NADPH oxidase and PKC inhibits TRPM2 and TRPV1 channels. The molecular pathway may be a cause of SCI-induced pain and neuronal death, and the subject should be urgently investigated.

A rare type of peripheral nerve sheath tumor: radial nerve schwannoma.

Schwannomas, also known as neurilemmomas, are generally benign peripheral nerve sheath tumors developing from Schwann cells. Peripheral nerve sheath tumors account for less than 8% of soft tissue neoplasms. Schwannomas are characterized by a slow-growing and non-infiltrating pattern. We report a 21-year-old, right-handed male, with a mass at his right elbow anterolateral region, that was slowly enlarging and became more painful over time. Magnetic resonance imaging of the right upper extremity revealed a 2.5x2 cm mass with heterogeneous contrast enhancement. The patient underwent complete removal of the lesion. The histopathological diagnosis was schwannoma. The postoperative course was uneventful. Clinically, these tumors may be misdiagnosed as other benign tumors, such as lipomas, synovial cysts or hemangiomas. During surgery, care should be taken to protect the nerve. Schwannomas in the upper extremities can be excised completely with preservation of nerve function and total removal lowers the risk of recurrence.

Quality of life outcomes after revision lumbar discectomy.

OBJECT: The authors investigated quality of life (QOL) outcomes after primary versus revision discectomy. METHODS: A retrospective review was performed for all patients who had undergone a primary or revision discectomy at the Cleveland Clinic Center for Spine Health from January 2008 through December 2011. Among patients in the revision cohort, they identified those who needed a second revision discectomy. Patient QOL measures were recorded before and after surgery. These measures included responses to the EQ-5D health questionnaire, Patient Health Questionnaire-9, Pain and Disability Questionnaire, and quality-adjusted life years (QALYs). Cohorts were compared by using independent-sample t-tests and Fisher exact tests for continuous and categorical variables, respectively. Multivariable logistic regression was performed to adjust for confounding. RESULTS: A total of 196 patients were identified (116 who underwent primary discectomy and 80 who underwent revision discectomy); average follow-up time was 150 days. There were no preoperative QOL differences between groups. Postoperatively, both groups improved significantly in all QOL measures. For QALYs, the primary cohort improved by 0.25 points (p<0.001) and the revision cohort improved by 0.18 points (p<0.001). QALYs improved for significantly more patients in the primary than in the revision cohort (76% vs 59%, respectively; p=0.02), and improvement exceeded the minimum clinically important difference for more patients in the primary cohort (62% vs 45%, respectively; p=0.03). Of the 80 patients who underwent revision discectomy, yet another recurrent herniation (third herniation) occurred in 14 (17.5%). Of these, 4 patients (28.6%) chose to undergo a second revision discectomy and the other 10 (71.4%) underwent conservative management. For those who underwent a second revision discectomy, QOL worsened according to all questionnaire scores. CONCLUSIONS: QOL, pain and disability, and psychosocial outcomes improved after primary and revision discectomy, but the improvement diminished after revision discectomy.

Reduction in traumatic brain injury-induced oxidative stress, apoptosis, and calcium entry in rat hippocampus by melatonin: Possible involvement of TRPM2 channels.

Melatonin, which is a very effective reactive oxygen species (ROS) scavenger, acts through a direct reaction with free radicals. Ca(2+) entry induced by traumatic brain injury (TBI) has deleterious effects on human hippocampal function. TRPM2 is a Ca(2+) permeable non-selective channel in hippocampal neurons, and its activation of during oxidative stress has been linked to cell death. Despite the importance of oxidative stress in TBI, its role in apoptosis and Ca(2+) entry in TBI is poorly understood. Therefore, we tested the effects of melatonin on apoptosis, oxidative stress, and Ca(2+) entry through the TRPM2 channel in the hippocampal neurons of TBI-induced rats. Thirty-two rats were divided into the following four groups: control, melatonin, TBI, and TBI + melatonin groups. Melatonin (5 mg/kg body weight) was intraperitoneally given to animals in the melatonin group and the TBI + melatonin group after 1 h of brain trauma. Hippocampal neurons were freshly isolated from the four groups, incubated with a nonspecific TRPM2 blocker (2-aminoethyl diphenylborinate, 2-APB), and then stimulated with cumene hydroperoxide. Apoptosis, caspase-3, caspase-9, intracellular ROS production, mitochondrial membrane depolarization and intracellular free Ca(2+) ([Ca(2+)]i) values were high in the TBI group, and low in the TBI + melatonin group. The [Ca(2+)]i concentration was decreased in the four groups by 2-APB. In our TBI experimental model, TRPM2 channels were involved in Ca(2+) entry-induced neuronal death, and the negative modulation of the activity of this channel by melatonin pretreatment may account for the neuroprotective activity of TRPM2 channels against oxidative stress, apoptosis, and Ca(2+) entry.

Melatonin reduces traumatic brain injury-induced oxidative stress in the cerebral cortex and blood of rats.

Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We investigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex ß-carotene, vitamin C, vitamin E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain injury-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system.

Quality of life outcomes following surgery for patients with coexistent cervical stenosis and multiple sclerosis.

PURPOSE: To investigate the quality of life outcomes following surgical treatment of patients with coexisting multiple sclerosis (MS) and cervical stenosis with associated myelopathy (CS). METHODS: A retrospective review of the medical records and of prospectively acquired quality of life (QOL) data was performed for all patients with symptoms of myelopathy and coexisting diagnoses of MS and CS that underwent cervical decompression surgery between 2008 and 2011. The study population was matched (1:4) to a control cohort of patients that did not have MS but presented with similar myelopathic symptoms due to cervical stenosis, were of the same age and gender, and underwent the same cervical decompression procedure within the same year. RESULTS: Sixty-five patients were reviewed, including 13 in the MS group and 52 in the control group that were followed for an average of 22 and 18 months, respectively. Whereas patients in the MS cohort remained at a Quality-Adjusted Life-Year (QALY) gain of 0.51 both pre- and post-operatively (p = 0.96), patients in the matched control cohort improved from a preoperative QALY of 0.50 to a postoperative QALY of 0.64 (p < 0.0001). The latter represents an improvement that exceeds the minimum clinically important difference. Overall, 70% of patients in the control group experienced an improvement in QALY, compared to only 54% in the MS group (p = 0.4). CONCLUSION: Patients in the control cohort had clinically and statistically significant improvements in QALY outcomes. Those in the MS cohort averaged no change in QALY. However, only a minority of MS/CS patients had worsening QALY following surgery, and as such surgery may still be considered for these patients. It is imperative that there are preoperative discussions with the MS/CS patient regarding the likelihood that surgery will only provide limited, if any, improvements in QOL.

Neuroprotection induced by N-acetylcysteine and selenium against traumatic brain injury-induced apoptosis and calcium entry in hippocampus of rat.

Neurodegeneration associated with acute central nervous system injuries and diseases such as spinal cord injury and traumatic brain injury (TBI) are reported to be mediated by the regulation of apoptosis and oxidative stress through Ca(2+) influx. The thiol redox system antioxidants, such as N-acetylcysteine (NAC) and selenium (Se), display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties. However, there are no reports on hippocampal apoptosis, cytosolic reactive oxygen species (ROS), or Ca(2+) values in rats with an induced TBI. Therefore, we tested the effects of Se and NAC administration on apoptosis, oxidative stress, and Ca(2+) influx through TRPV1 channel activations in the hippocampus of TBI-induced rats. The 32 rats were divided into four groups: control, TBI, TBI + NAC, and TBI + Se groups. Intraperitoneal administrations of NAC and Se were performed at 1, 24, 48, and 72 h after TBI induction. After 3 days, the hippocampal neurons were freshly isolated from the rats. In cytosolic-free Ca(2+) analyses, the neurons were stimulated with the TRPV1 channel agonist capsaicin, a pungent compound found in hot chili peppers. Cytosolic-free Ca(2+), apoptosis, cytosolic ROS levels, and caspase-3 and -9 activities were higher in the TBI group than control. The values in the hippocampus were decreased by Se and NAC administrations. In conclusion, we observed that NAC and Se have protective effects on oxidative stress, apoptosis, and Ca(2+) entry via TRPV1 channel activation in the hippocampus of this TBI model, but the effect of NAC appears to be much greater than that of Se. They are both interesting candidates for studying the amelioration of TBIs.

N-acetylcysteine and selenium modulate oxidative stress, antioxidant vitamin and cytokine values in traumatic brain injury-induced rats.

It has been suggested that oxidative stress plays an important role in the pathophysiology of traumatic brain injury (TBI). N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1ß and IL-4 levels in brain and blood of TBI-induced rats. We investigated effects of NAC and Se administration on physical injury-induced brain toxicity in rats. Thirty-six male Sprague-Dawley rats were equally divided into four groups. First and second groups were used as control and TBI groups, respectively. NAC and Se were administrated to rats constituting third and forth groups at 1, 24, 48 and 72 h after TBI induction, respectively. At the end of 72 h, plasma, erythrocytes and brain cortex samples were taken. TBI resulted in significant increase in brain cortex, erythrocytes and plasma lipid peroxidation, total oxidant status (TOS) in brain cortex, and plasma IL-1ß values although brain cortex vitamin A, ß-carotene, vitamin C, vitamin E, reduced glutathione (GSH) and total antioxidant status (TAS) values, and plasma vitamin E concentrations, plasma IL-4 level and brain cortex and erythrocyte glutathione peroxidase (GSH-Px) activities decreased by TBI. The lipid peroxidation and IL-1ß values were decreased by NAC and Se treatments. Plasma IL-4, brain cortex GSH, TAS, vitamin C and vitamin E values were increased by NAC and Se treatments although the brain cortex vitamin A and erythrocyte GSH-Px values were increased through NAC only. In conclusion, NAC and Se caused protective effects on the TBI-induced oxidative brain injury and interleukin production by inhibiting free radical production, regulation of cytokine-dependent processes and supporting antioxidant redox system.

Bilateral ophthalmic-ethmoidal dural arteriovenous fistula presenting with intracranial hemorrhage: a rare entity.

Dural arteriovenous fistulas (DAVFs) are rare lesions. The most common locations of DAVFs are cavernous, sigmoid and transverse sinuses. Anterior cranial fossa is one of the less frequent placement for DAVFs and the risk of hemorrhage in this region is increased. Reported hemorrhage risks have been ranged from 62 to 91 %, and an aggressive clinical course is more likely than a benign clinical course. A 47-year-old man was admitted to our emergency room with headache and the computed tomography revealed frontal hemorrhage. Neurological examination was normal. We applied cerebral angiography in our interventional neurology department and an anterior cranial fossa DAVFs, supplied by bilateral ophthalmic-ethmoidal arteries, was determined. DAVFs are a rare cause of intracranial hemorrhages and in the literature anterior cranial fossa DAVFs have been reported scarcely, so that we aimed to present this rare entity.

Aspirin increases NMDA receptor subunit 2A concentrations in rat hippocampus.

The N-methyl-d-aspartate receptor (NMDAR), a heteromeric protein, is a glutamate receptor that has three classes of subunits: NR1, NR2, and NR3. It has been reported that these receptors are involved in synaptogenesis, synaptic plasticity, and many other processes in the central nervous system. The aim of this study is to investigate the efficacy of aspirin on hippocampal NMDARs. Sixteen rats were studied in two groups, with eight animals in each group. The first group was the control group, and the second one was the aspirin-given group. Aspirin (acetylsalicylic acid) was administered orally to the rats (200 mg/kg). Tissue samples were obtained after 3 h. The brain was removed, and both hippocampi were dissected out for evaluation. It was found that acute doses of aspirin caused increases on the levels of NMDAR 2A (NR2A) receptors and malondialdehyde (MDA), the end product of lipid peroxidation. Production was significantly increased in the aspirin-given group. We know that MDA is a marker for free radical-mediated tissue damage. In conclusion, lipid peroxidation, caused by acute doses of aspirin may lead to excitotoxicity effects by a hippocampal NR2A-mediated mechanism.

Spinal extradural arachnoid cyst.

BACKGROUND CONTEXT: Spinal extradural arachnoid cysts are uncommon expanding lesions. Idiopathic arachnoid cysts are not associated with trauma or other inflammatory insults. If they enlarge, they usually present with progressive signs and symptoms of neural compression. PURPOSE: Total removal of the cyst and repair of the dural defect is the primary treatment for large thoracolumbar spinal extradural arachnoid cysts causing neurogenic claudication. Laminoplasty may prevent spinal deformities in long segmental involvement. STUDY DESIGN: A clinical case was performed. PATIENT SAMPLE: We report a case of 25-year-old man with 1-year history of progressive back pain radiating to both legs. His diagnosis was dorsal intraspinal extradural cystic lesion longing from the level of T11 to L2 on magnetic resonance imaging. OUTCOME MEASURES: The patient's pain levels were noted as he reported. Physiologic outcome was assessed on pre- and postoperative motor and sensory examination. METHODS: The patient underwent a T11-L2 laminotomy and radical cyst wall resection was performed. A small communication with the subarachnoid space was seen at the level of T12. It was sealed with tissue fibrinogen after repair with primary suture. Titanium miniplates were used for laminoplasty. RESULTS: Follow-up magnetic resonance imaging demonstrated cyst resolution, and neurologic examination revealed no sensory and motor deficit. CONCLUSION: Extradural arachnoid cysts are primarily treated with total removal of the cyst wall and closure of the dural defect. Surgical treatment is curative for this rare lesion.

Gangliocytoma associated with focal cortical dysplasia in a young-adult: a case report.

Neoplasms and (non-neoplastic) focal dysplasias may coexist as a cause of seizures in both the developing and mature brain. Low grade neoplastic lesions (ganglioglioma/gangliocytoma) may present with seizures, and distinction of these lesions from focal cortial dysplasia is difficult on standard radiological imaging. We report a 24-year-old man who had complaints of tonic-clonic seizures for one week duration and was admitted to department of neurosurgery. He did not have any neurological deficit on his examination. Cranial computerized tomography and magnetic resonance imaging of the patient revealed a calcified, cystic lesion with contrast enhancement, in the left temporoparietal region. Subtotal resection of the mass was performed. Pathological examination revealed focal cortical dysplasia associated with gangliocytoma.