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Objective Glioma patients often complain about problems in daily conversation with a negative impact on quality of life. Disorders in standardized language tests (e.g. naming and fluency), are frequently observed. Most studies claim recovery of language functions within 3 months. However, long-term effects of surgery on spontaneous speech remain unknown. Patients and Methods Eighteen glioma patients were compared to healthy controls in spontaneous speech variables: Type Token Ratio (TTR), Mean Length of Utterance words (MLUw), Incomplete Sentences, Self-corrections and Repetitions. Boston Naming Test (BNT) and Category Fluency (CF) were also assessed. We compared: pre- and 3 months postoperatively (T1-T2), 3 months and 1 year postoperatively (T2-T3), pre- and 1 year postoperatively (T1-T3). Correlations were computed between deviating variables and BNT/CF, tumor localization, and tumor grade. Results Patients had deficits in Incomplete sentences (T1, T2, T3), TTR (T2,T3), MLUw (T3) and Self-corrections (T2). Between T1-T2 no decline was present. Between T2-T3 and T1-T3, there was a decrease of MLUw, Self-corrections and Repetitions and an increase of Incomplete Sentences, BNT and CF were impaired (T1, T2, T3) without differences between test-moments. Most spontaneous speech variables did not correlate with standardized tests. Tumor localization and grade had no influence on spontaneous speech. Conclusion Glioma patients showed impaired spontaneous speech combined with naming and fluency deficits. Surgery appeared to have deteriorated the quality of spontaneous speech until long-term but not the performance at test-level. Hence, spontaneous speech has an added value to standardized tests for diagnosis of language impairments.

Background Patients with meningiomas carry an increased risk for postoperative venous thromboembolic complications (VTE) including deep venous thrombosis (DVT) and pulmonary embolism (PE). Objective In the present retrospective study we investigated the incidence of VTE and the risk factors involved, in a large cohort of patients surgically treated for an intracranial meningioma at our institution. Methods During the period from January 1997 to January 2009, 581 consecutive patients underwent craniotomy for intracranial meningioma. All patients received low-molecular weight heparins as thromboembolism prophylaxis. Patient demographics and tumor characteristics were gathered via retrospective chart review. Postoperative VTE and hemorrhages were noted. Backward stepwise logistic regression was used to determine the risk factors. Results 80.6% of meningiomas were WHO grade 1; 15.1% WHO grade 2; 4.3% WHO grade 3. Postoperative VTE were observed in 41 patients (7.2%). Of these, DVT was seen in 20 (3.5%) and PE in 26 patients (4.6%). The thromboembolic complication appeared on average 21.1 ± 29.2 days post surgery. The 90-day mortality rate after VTE was 11.2% (23.1% for PE and 5.0% for DVT). Postoperative hemorrhages requiring surgical treatment were found in 2.9% of patients. Risk factors for VTE were body mass index (p = 0.015) for DVT; weight (p = 0.001) and bedridden postoperatively (p = 0.001) for PE; and weight (p = 0.004) and bedridden postoperatively (p = 0.003) for VTE in general. There was no relation between tumor grade and thromboembolic complications. Conclusion The major risk factors for postoperative VTE found in our single center study are patient weight and a bedridden status postoperatively. Prophylactic intervention for this potentially fatal complication should be evaluated against the relative lower risk of postoperative hemorrhages.

Lessons from the history of cancer therapy inform that a multimodal approach offers the best potential to eradicate the tumor mass and prevent the recurrence after therapy. One of the most promising experimental therapies for cancer is the use of oncolytic adenoviruses as therapeutic agents. These biologic agents exert their function by directly infecting and killing tumor cells. The new progeny generated after the first infection round will spread, generating a therapeutic wave that will optimally eliminate every cancer cell. Recently, modifications in the virus genome have allowed for the designing of viruses that infect with more potency than wild-type adenoviruses, replicate exclusively in tumor cells, selectively target cellular receptors or molecular defects in the cancer cells, and deliver prodrug genes. In addition, these last-generation viruses can be combined with chemotherapy and other forms of cancer therapies to enhance the tumor killing capability. With the steady and fast pace of the progress in our knowledge of the genetics of tumors, we may soon fulfill our hope of reaching the final objective of an adenovirus-based personalized medicine for cancer.