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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 anoplasty 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.

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.

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 1p, 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 1p and 19q might provide an alternative mechanism in the genesis of astrocytomas.

AIM:The aim of this randomized study was to compare exercise program to control group regarding pain, back disability, behavioural outcomes, global health measures and back mobility who underwent microdiscectomy operation. MATErIAL and METHods:Thirty patients who underwent lumbar microdiscectomy were randomized into exercıse and control groups. After surgery, patients in the exercıse group undertook a 12-week home based exercise program, started immediately postsurgery and concentrated on improving strength and endurance of the back, abdominal muscles, lower extremities and mobility of the spine and hips. Outcome measures were: Oswestry Disability Index (ODI), Beck Depression scale, lumbar schober, Visual Analogue Scale (VAS), return to work (return-to-work status), generic functional status (SF-36).rEsuLTs: Treatment compliance was high in both groups. Surgery improved pain, disability, general health status, lumbar mobility and behavioural status. After the exercise program, the exercise group showed further improvements in these measures at 12 week after surgery. CoNCLusIoN:A 12-week postoperative exercise program starting immediately after surgery can improve pain, disability, and spinal function in patients who have undergone microdiscectomy.KEywords: Exercise therapy, Lumbosacral radicular syndrome, Microdiscectomy ÖZ AMAÇ: Çalışma, mikrodiskektomi ameliyatı sonrası egzersiz verilen grup ile verilmeyen kontrol grubunun ağrı, disabilite, duygu durumu, genel sağlık durumu ve bel mobilitesinin karşılaştırmasını amaçlamaktadır. yÖNTEM ve GErEÇLEr: 30 hasta çalışmaya alındı. Egzersiz grubuna ameliyat sonrası erken dönemde başlanılan, 12 hafta süren, ev tabanlı, bel, bacak, abdominal kasları kuvvetlendirici, enduransı arttırıcı ve bel mobilizasyonu artıran egzersiz tedavisi verildi. Ölçüm sonuçlarımız: Oswestry Disability Indeksi (ODI), Beck Depresyon Skalası, Lomber Schober, Visual Analogue Scale (VAS), işe dönüş zamanı, genel fonksiyonel durum (SF-36).BuLGuLAr: Her iki grupta da tedaviye iyi yanıt alındı. Cerrahi girişim ile ağrı, disablite, genel sağlık durumu, duygu durum ve bel mobilitesinde iyileşme gözlemlendi. Egzersiz programından sonra, egzersiz grubu, kontrol grubuna kıyasla 12 hafta sonra ağrı, disabilte ve genel sağlık durumunda anlamlı iyileşme gösterdi. soNuÇ: Operasyon sonrası erken dönemde başlanılan 12 haftalık egzersiz tedavisi, mikrodiskektomi geçiren hastalarda ağrının, disabiltenin azalması ve genel sağlık durumunun iyileşmesinde etkili olabilir.ANAHTAr sÖZCÜKLEr: Egzersiz tedavisi, Lumbosakral radiküler sendrom, Mikrodiskektomi

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.

BackgroundCerebral ischemia is as a result of insufficient cerebral blood flow for cerebral metabolic functions. Resveratrol is a natural phytoalexin that can be extracted from grape's 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.MethodsWe 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.ResultsAfter 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.ConclusionIn 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.

Little is known about genetic mutations during the malignant progression of spinal meningiomas. This study investigated genomic changes across the entire genome in spinal meningioma samples to determine possible mechanism(s) of tumorigenesis. Paraffin-embedded tissue sections of 16 spinal meningiomas were analyzed by the comparative genomic hybridization (CGH) technique. Lymphocytes of the patients were evaluated as controls. Genomic change was detected in 11 samples. Complete or partial loss of chromosome 22 was the most commonly seen abnormality in eight cases. Chromosome losses on 1p, 9p, and 10q and gains on 5p and 17q were the other abnormalities. These changes are all frequently seen in meningiomas, but are mostly specific to atypical and anaplastic meningiomas. However, in the present study, copy number changes on chromosomes 9p (3 samples), 17q (2 samples), and 1p (2 samples) were seen even in the benign tumors. Our results suggest that in addition to the neurofibromatosis type 2 tumor suppressor gene, other cancer-related genes located on 1p, 9p, 10q, and 17q might be involved in the etiology of spinal meningiomas.