The supplementary motor area (SMA) syndrome is a frequently encountered clinical phenomenon associated with surgery of the dorsomedial prefrontal lobe. The region has a known motor sequencing function and the dominant pre-SMA specifically is associated with more complex language functions; the SMA is furthermore incorporated in the negative motor network. The SMA has a rich interconnectivity with other cortical regions and subcortical structures using the frontal aslant tract (FAT) and the frontostriatal tract (FST). The development of the SMA syndrome is positively correlated with the extent of resection of the SMA region, especially its medial side. This may be due to interruption of the nearby callosal association fibres as the contralateral SMA has a particular important function in brain plasticity after SMA surgery. The syndrome is characterized by a profound decrease in interhemispheric connectivity of the motor network hubs. Clinical improvement is related to increasing connectivity between the contralateral SMA region and the ipsilateral motor hubs. Overall, most patients know a full recovery of the SMA syndrome, however a minority of patients might continue to suffer from mild motor and speech dysfunction. Rarely, no recovery of neurological function after SMA region resection is reported.
Background: Several studies show that subventricular zone (SVZ) contact of glioblastoma at diagnosis is a negative prognosticator of survival. In this report, we study glioblastoma patient survival, molecular biological and MRI-based volumetric findings according to SVZ contact. Patients and methods: We conducted a retrospective study of adult patients diagnosed with supratentorial glioblastoma and uniformly treated with temozolomide-based chemoradiotherapy after surgery. The patient cohort was dichotomized according to tumor contact with the SVZ at diagnosis as determined on preoperative MR imaging. Tumor volume was measured using semi-automated segmentation technique. MGMT-gene promoter methylation and IDH mutation status were determined on stored tumor tissue. Kaplan-Meier survival curves were constructed. Cox regression analysis was used to adjust for known confounding factors of glioblastoma patient survival. Results: A total of 214 patients were included in the study of whom 68% belonged to the SVZ pos group. Median tumor volume was significantly larger in the SVZ pos group (33,8 mL vs 15,6 mL; p < .001). MGMT-unmethylated glioblastoma was more frequent in the SVZ pos group (61.4% vs 44.9%; p ¼ .028). The overall survival and progression-free survival were 12.2 months and 5.9 months for the SVZ pos patient group but 16.9 months and 10.3 months for the SVZ neg group (log-rank p ¼ .016 and .007 respectively). In multivariate Cox survival analysis, SVZ contact proved a negative prognostic parameter, independent from age, KPS, extent of resection, MGMT-methylation and IDH mutation status. Conclusions: This study confirms SVZ contact at diagnosis as an independent negative prognostic factor for glioblastoma patient survival. SVZ pos glioblastoma had larger tumor size and a larger proportion of unmethylated tumors than SVZ neg glioblastoma. Further research is needed to establish whether the observed differences are solely explained by a different molecular profile of SVZ pos glioblastoma or by interaction of glioblastoma with the unique SVZ microenvironment.
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