Metin Ant Atasoy

Management of glioblastoma multiforme: with special reference to recurrence

Between 1985 and 1995, 46 patients underwent craniotomy for glioblastoma multiforme. The mean age was 47, varying from 9 to 71 years. The influence of such prognostic factors as age, preoperative Karnofsky score, extent of resection, tumour site, tumour size, radiotherapy, reoperation as well as initial symptoms upon survival were studied. Of these, gross complete removal, radiotherapy, preoperative Karnofsky score, and reoperation were shown to be statistically significant to the survival time according to logrank and univariate tests. However, age, preoperative Karnofsky score, tumour size and temporal localisation remained as significant factors in multivariate analysis. The overall median survival was 53 weeks, with no patients surviving more than 3 years. Of the patients, 41% survived over a year and 8.6% lived over two years. Twenty-six patients developed a recurrent mass after an interval of 32 weeks. The median interval time from operation to recurrence was longer in those patients who underwent gross removal than in those who had a subtotal resection, 28.2 against 20 weeks (P < 0.05). Of patients who had a recurrent mass, 16 were reoperated on, with a subsequent median survival time of 26.5 weeks. Our experience suggests that the survival of patients with glioblastoma depends on many factors, including radical surgery as an initial step. In addition, the gross total removal of the tumour also delays the development of recurrence.

The importance of genomic copy number changes in the prognosis of glioblastoma multiforme

Glial tumors are the most common tumors of the nervous system, affecting individuals at any age. Since understanding of the molecular pathologies underlying human gliomas is still very poor, the treatment and therefore prognosis of this malignancy could not yet be improved. In order to determine whether different glioblastoma-associated genomic aberrations may serve as prognostic markers in combination with histopathological findings, 20 primary glioblastoma multiforme tumors were screened by comparative genomic hybridization, and the results were compared with histopathological and clinical features. All tumors showed genomic copy aberrations detected by comparative genomic hybridization. Regional and numerical increases in chromosome 7 copy number were the most frequently seen abnormality (10/20 tumors), followed by loss of chromosome 10 (8/20). Both of these aberrations were associated with shorter surveillance time. Chromosome 12q amplification was detected in seven tumors. Loss of 17p, 1p, and 19q in combination was seen in three cases. One of them was a giant cell GBM, whereas the remaining two cases were still alive. Combination of chromosome 1p and 19q deletions was also seen in a case with long surveillance. According to the preliminary findings of this study, in addition to the EGFR gene, amplification of other genes on chromosome 7 and the deletion of PTEN gene and other cancer-related genes on chromosome 10 appeared important to the development of glioblastoma multiforme and were associated with poor prognosis, whereas the combination of chromosome 1p and 19q deletions seems to be an informative molecular marker for better prognosis. The clinical features and genetic alterations of primary and secondary glioblastoma multiforme should be compared in large series to clarify the effective prognostic markers; and further molecular analyses focused on chromosomes 7 and 10 will be very helpful for understanding the molecular mechanisms underlying the progression of glioblastoma.

Genomic alterations in low-grade, anaplastic astrocytomas and glioblastomas.

To extend our understanding of potential stepwise genetic alterations that may underlie tumor progression from low-grade astrocytomas to glioblastomas, histopathologic and comparative genomic hybridization analyses were performed on tumor specimens from 68 primary lesions, including 40 glioblastomas, 10 anaplastic and 18 low-grade astrocytomas. The number of aberrations per case increased towards the higher grade tumors (grade II: 1.66±1.49; grade III: 2.80±1.68; grade IV: 3.02±1.07; F=6.955, p=0.002). A gain of 7/7q was common and the most frequently seen aberration in low-grade astrocytomas, whereas loss of 10q was the most frequently seen anomaly in anaplastic astrocytomas and glioblastomas. Chromosome 7p amplification was only detected in glioblastomas. Chromosome 10/10q deletion and combination of lp, 19q and 17p deletions were specific to high-grade astrocytic tumors. Sequences of chromosome 7 and 10 seem to have pivotal roles in the biology of human gliomas. The genomic copy deletions of chromosomes lp and 19q might provide an alternative mechanism in the genesis of astrocytomas.

Multiple nocardial abscesses of cerebrum, cerebellum and spinal cord, causing quadriplegia

In this paper we present a case of a diabetic patient with nocardial abscesses of cerebrum, cerebellum and the spinal cord. The present case is the first case in the literature of solitary intramedullary abscess in cervical spinal cord, causing tetraplegia. Nocardia asteroides grew in a culture of the abscess pus. After either surgical excision or drainage of lesions, a triple combination regimen of chemotherapy (amikacin, ceftriaxone and trimethoprim-sulfamethoxazole) was given, but the patient was lost in the postoperative period. This case gives suggestive evidence of an association between cervical spinal cord involvement and poor prognosis in CNS nocardiosis.

Diagnostic steps and staged operative approach in Currarino's triad: a case report and review of the literature

Abstract The Currarino triad is a combination of a presacral mass, a congenital sacral bony abnormality and an anorectal malformation. It mostly presents with constipation. Rectal examination, plain radiographs and magnetic resonance imaging are the main tools for the diagnosis. If the mass is a meningocele, colostomy and neurosurgical exploration should precede ano- plasty due to the risk of meningitis. A 14-month-old female patient with anal stenosis, a sacral scimitar defect and an anterior meningocele is presented in this report.

An unusual case of cervical clear-cell meningioma in pediatric age.

Introduction and backgroundA 4-year-old girl was admitted with complaints of diplegia, right lower limb monoplegia, and left lower limb monoparesia. Cervical magnetic resonance imaging revealed an intradural-extramedullary tumor at the level of C1–C2. The tumor was resected totally. Histopathologic diagnosis revealed clear-cell meningioma.DiscussionIntraspinal clear-cell meningioma (ICCM) is a rare aggressive variant of meningioma. There are only 25 cases reported to date, and only 13 of them are in pediatric age group. Of these 25 ICCM cases, only two are at cervical region. This report is the first ICCM case at upper cervical region (C1–C2) in both adult and pediatric age populations.

Erythropoietin prevents nitric oxide and cathepsin-mediated neuronal death in focal brain ischemia.

We examined the preventive effect of human recombinant erythropoietin (HrEPO) on nitric oxide (NO)-mediated toxicity to neurons and cysteine protease release into cytoplasm, which is attributed to neuronal death in brain ischemia. Focal cerebral ischemia was induced by permanent occlusion of middle cerebral artery in two sets of rat. The first set was used to monitor NO concentration and cathepsin activity, while the second was used for histological examination with hematoxylin and eosin, and TUNEL staining. A group in both set was administered human recombinant erythropoietin (HrEPO). NO content, cathepsins B and L activity increased significantly in the post-ischemic cerebral tissue (p<0.05). HrEPO treatment reduced NO concentration and cathepsin activity to control level (p>0.05). A significant increase in the number of necrotic and apoptotic neurons was observed in the post-ischemic cerebral cortex (p<0.05). HrEPO treatment was markedly lowered both of these (p<0.05). It is concluded that HrEPO prevents neuronal death by protecting neuronal liposomes from NO-mediated toxicity and suppressing the release of cathepsins.

Congenital cavernous hemangioma of the calvaria : Case report

The authors present the case of a 6-month-old infant with a cavernous hemangioma of the parietal bone and discuss the radiological, operative, and pathological features and differential diagnosis of these extremely rare lesions in infants. Only 1 case of an infant with a calvarial cavernous hemangioma without intracranial invasion has previously been reported, and that case involved a 4 month old. Although a cavernous hemangioma of the calvaria is extremely rare in the newborn, this condition should be included in the differential diagnosis of calvarial lesions. During surgical treatment of calvarial cavernous hemangiomas, utmost attention should be paid to avoid blood loss, which could be fatal in infants.

Spinal toxoplasmic arachnoiditis associated with osteoid formation: a rare presentation of toxoplasmosis.

Study Design. An extremely rare presentation of an isolated spinal toxoplasmic arachnoiditis is described. Objective. To draw attention to the fact that spinal arachnoid membranes may be a potential reservoir for Toxoplasma gondii. Summary of Background Data. Central nervous system toxoplasmosis is a common manifestation in patients who are immunodeficient. Reports on the spinal toxoplasmosis are rare and focused on spinal cord involvement. Methods. An adult patient presented with symptoms of spastic paraparesis that had begun 13 years before admission. Thoracic spinal magnetic resonance imaging showed small lesions in posterior subarachnoid space at Th7–Th8. A Th7–Th8 laminectomy was performed. Intradural-extramedullary lesions were excised. Results. Clinical, immunologic, and pathologic examinations showed adhesive spinal arachnoiditis associated with osteoid formation caused by past toxoplasmic infection. There was no impairment of the immunologic defense system. Conclusion. Where no causative factor is found in serious spinal adhesive arachnoiditis, the possibility of spinal toxoplasmosis should also be investigated.

Neuroprotective Effect of Resveratrol on Acute Brain Ischemia Reperfusion Injury by Measuring Annexin V, p53, Bcl-2 Levels in Rats

Background Cerebral ischemia is as a result of insufficient cerebral blood flow for cerebral metabolic functions. Resveratrol is a natural phytoalexin that can be extracted from grapes skin and had potent role in treating the cerebral ischemia. Apoptosis, a genetically programmed cellular event which occurs after ischemia and leads to biochemical and morphological changes in cells. There are some useful markers for apoptosis like Bcl-2, bax, and p53. The last reports, researchers verify the apoptosis with early markers like Annexin V. Methods We preferred in this experimental study a model of global cerebral infarction which was induced by bilateral common carotid artery occlusion method. Rats were randomly divided into 4 groups : sham, ischemia-reperfusion (I/R), I/R plus 20 mg/kg resveratrol and I/R plus 40 mg/kg resveratrol. Statistical analysis was performed using Sigmastat 3.5 ve IBM SPSS Statistics 20. We considered a result significant when p<0.001. Results After administration of resveratrol, Bcl-2 and Annexin levels were significantly increased (p<0.001). Depending on the dose of resveratrol, Bcl2 levels increased, p53 levels decreased but Annexin V did not effected. P53 levels were significantly increased in ishemia group, so apoptosis is higher compared to other groups. Conclusion In the acute period, Annexin V levels misleading us because the apoptotic cell counts could not reach a certain level. Therefore we should support our results with bcl-2 and p53.