Early decompressive surgery after combined intra-venous thrombolysis and endovascular stroke treatment.

BACKGROUND AND PURPOSE: The prognosis of malignant middle cerebral artery infarctions (MCA) is poor. The poor prognosis is attributable to the severe cerebral edema that causes a brain herniation and death. Decompressive surgery reduces mortality and may further improve patient outcomes. However, the safety and effectiveness of decompressive surgery in patients who underwent combined intravenous (IV) thrombolysis and endovascular stroke treatment are not certain. Moreover, the evidence on the timing of decompressive surgery is lacking. METHODS: The purpose of the open, prospective and non-randomized study was to compare the outcome and complication rates of patients with malignant MCA strokes who underwent early decompressive surgery after combined intravenous thrombolysis and endovascular treatment with those of decompressive surgery patients without prior recanalization treatment strategy. All patients underwent decompressive surgery within 24h of symptom onset. RESULTS: Thirty patients were included in the study. Twelve of the 30 patients were treated with combined IV thrombolysis and endovascular approach and 18 patients received standard treatment. The proportion of patients with a modified Rankin score ≤3 at the sixth month follow-up was 33% in the standard group and 44% in the combined treatment group (p=0.712). Mortality, and major and minor complications including symptomatic intracerebral hemorrhage after decompressive surgery did not differ between the two groups (p>0.05). CONCLUSION: Early decompressive surgery can be safely performed in patients who received combined IV thrombolysis and endovascular treatment and there was no difference in outcome of these patients compared with patients who did receive the standard medical treatment before early decompressive surgery.

Efficacy of prognostic factors on survival in patients with low grade glioma.

AIM: In this report, we aim to determine the prognostic factors influencing the length of survival in patients with low-grade gliomas. MATERIAL AND METHODS: In a retrospective evaluation, we have reviewed fiftythree patients who had been operated between the years of 1980 and 2006. The diagnoses of the patients were histopathologically verified as low-grade glioma(LGG). The medical records of the patients were reviewed for age, gender, tumor locations, extent of resection, and presence of seizure, the neurological status as defined by the Karnofsky Performance Scale (KPS) and radiotherapy treatment after surgery as possible prognostic factors. RESULTS: Median cumulative survival time for all the patients with LGG was 141+/-14.83 months. Median survival time was 216+/-78.52 months for astrocytoma Grade I; 115+/-8.22 months for astrocytoma Grade II, and 242+/-76.36 months for oligodendroglioma. Young age, histology subtype (oligodendroglioma) and preoperative KPS were determined to have positive influence on survival according to Log Rank Test. In contrast, age, histology type and the extent of resection remained independent prognostic factors upon survival when Cox Regression Backward Stepwise (Wald) method was performed. CONCLUSION: It can be concluded that surgery seems to be an appropriate first step option in the treatment of LGG.

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 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.

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.