Ali Arslantas

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.

Prevalence of dementia and associated risk factors in Middle Anatolia, Turkey.

This study aimed to investigate the prevalence of various cognitive disorders in the older population (age 55 years and above) of Eskisehir, Turkey, by conducting a cluster sampled door-to-door survey. A total of 3100 inhabitants were screened with the Mini-Mental State Examination (MMSE) and a questionnaire concerning demographic, occupational and social data. Individuals (n=320) with MMSE scores of 25 were assessed according to the 10th Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) and were investigated in the more detailed phase 2 study. The overall prevalence of dementia was 8.4%, although it ranged from 2.2% among those aged 55-59 years to 5.3% among those aged 60-64 years, and to 30.4% among those aged 75 or above. Vascular dementia was the most common type (51.1%), followed by Alzheimers dementia (48.8%). In a very small proportion of individuals (0.1%), dementia was due to other causes such as B12 deficiency, a tumour or hydrocephalus. Significant risk factors for dementia were female sex, low education, age, living in a rural area and a family history of dementia.

Erythropoietin improves oxidative stress following spinal cord trauma in rats

Spinal cord injury (SCI) is a very destructive process for both patients and society. Lipid peroxidation is the main cause of the further secondary damage which starts after mechanical destruction of tissues. Recent studies have shown that erythropoietin (EPO) has neuroprotective properties. In this study, we aimed to see the effect of EPO treatment after spinal cord injury on the oxidant and anti-oxidant enzyme systems and the relationship with the N-methyl-D-Aspartate (NMDA) blockage. Spinal cord injury was produced by epidural compression with a cerebral vascular clip that has a closing force of 40 g for 30s after a limited multilevel laminectomy (T9-11). Experiment was done in 5 groups: Group 1: Sham-operated untraumatised, Group 2: SCI untreated, Group 3: 150 i.u./kg EPO injected i.p. at the end of the first hour following the trauma. Group 4: NMDA receptor antagonist ketamine (100mg/kg) i.p. Group 5: EPO+ketamine i.p. The experiments were finished after 12h of the trauma. The spinal cords were excised for biochemical examinations. Anti-oxidant enzymes; catalase and reduced glutathione (GSH) levels increased and lipid peroxidation product, malonyldialdehyde (MDA) level decreased in EPO treated group when compared to the other groups. TNF-alpha levels decreased in EPO treated group. Application of ketamine before EPO treatment decreased effects of EPO. In conclusion, our results suggest that 150 i.u./kg i.p. EPO, a therapeutic dose in anaemic patients, applied after 1h of spinal cord injury significantly attenuated the oxidative damage of spinal cord injuries in rats. This activity is abolished via ketamine pretreatment.

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.

Inadvertent insertion of a nasogastric tube in a patient with head trauma

Abstract This is a report of a 3-year-old boy with intracranial penetration of a nasogastric tube causing brain damage in the left frontal lobe. A computed tomography (CT) showed passage of the nasogastric tube via a fracture of the cribriform plate into the intracranial cavity. The tube was manually removed under antibiotic prophylaxis. The patient then underwent dural repair for rinorrhoea and was discharged in good health.

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.

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.

IDH1 mutations is prognostic marker for primary glioblastoma multiforme but MGMT hypermethylation is not prognostic for primary glioblastoma multiforme

PURPOSE To establish the frequency of IDH1 mutations and MGMT methylation in primary glioblastomas. EXPERIMENTAL DESIGN We screened primary glioblastoma multiforme (GBM) in a population-based study for IDH1 mutations and MGMT methylation and correlated them with clinical data. RESULTS IDH1 mutations were detected in 5 of 40 primary glioblastomas (12,5%). Primary GBM patients carrying IDH1 mutations were significantly younger, mean age of 41±5.06years, than patients with wild-type IDH1, mean age of 57±2,29years, p=0.011. The mean survival time of all GBM patients with and without IDH1 mutations was 19months (5 cases) and 16months (35 cases), respectively (p>0,05). MGMT methylation was detected in 13 of the 40 patients (32,5%). MGMT-promoter methylation did not correlate with overall survival (OS; p>0,05). CONCLUSION In summary, our study is the first study to investigate the IDH1 mutation status and MGMT methylation in primary GBMs in Turkish population and confirmed IDH1 mutation as a genetic marker for also primary GBMs. Our data are still insufficient for definite ascertainment; and our preliminary results suggest: IDH1 status shows an association with younger age and there is a lack of association between IDH1 mutation and survival time. Furthermore MGMT promoter methylation had no prognostic value and lower frequency in primary glioblastomas.