ABSTRACT
BACKGROUND: Navigated transcranial magnetic stimulation (nTMS) has been established as a preoperative diagnostic procedure in glioma surgery, increasing the extent of resection and preserving functional outcome. nTMS motor mapping for the resection of motor eloquent meningiomas has not been evaluated in a comparative analysis, yet. METHODS: We conducted a retrospective matched-pair analysis for tumor location and size in meningioma patients with tumors located over or close to the primary motor cortex. Half of the study population received nTMS motor mapping preoperatively (nTMS-group). The primary endpoint were permanent surgery-related motor deficits. Additional factors associated with new motor deficits were evaluated apart from nTMS. RESULTS: 62 patients (mean age 62 ± 15.8 years) were evaluated. 31 patients received preoperative nTMS motor mapping. In this group, motor thresholds (rMT) corresponded with tumor location and preoperative motor status, but could not predict motor outcome. No patient with preoperative intact motor function had a surgery-related permanent deficit in the nTMS group whereas four patients in the non-TMS group with preoperative intact motor status harbored from permanent deficits. 13 patients (21.3%) had a permanent motor deficit postoperatively with no difference between the nTMS and the non-TMS-group. Worsening in motor function was associated with higher patient age (p = 0.01) and contact to the superior sagittal sinus (p = 0.027). CONCLUSION: nTMSmotor mapping did not lead to postoperative preservation in motorfunction. nTMS data corresponded well with the preoperative motorstatus and were associated with postoperative permanent deficits if tumors were located over the motor hotspot according to nTMS.
ABSTRACT
In glioblastoma (GBM), the interplay of different immune cell subtypes, cytokines, and/or drugs shows high context-dependencies. Interrelations between the routinely applied dexamethasone (Dex) and microglia remain elusive. Here, we exploited rat organotypic brain slice co-cultures (OBSC) to examine the effects on a rat GBM cell line (S635) outgrowth resulting from the presence of Dex and pretreatment with the colony-stimulating factor receptor 1 (CSF1-R) inhibitor PLX5622: in native OBSC (without PLX5622-pretreatment), a diminished S635 spheroid outgrowth was observable, whereas Dex-treatment enhanced outgrowth in this condition compared to PLX5622-pretreated OBSC. Screening the supernatants of our model with a proteome profiler, we found that CXCL2 was differentially secreted in a Dex- and PLX5622-dependent fashion. To analyze causal interrelations, we interrupted the CXCL2/CXCR2-axis: in the native OBSC condition, CXCR2-blocking resulted in increased outgrowth, in combination with Dex, we found potentiated outgrowth. No effect was found in the PLX5622-pretreated. Our method allowed us to study the influence of three different factors-dexamethasone, PLX5622, and CXCL2-in a well-controlled, simplified, and straight-forward mechanistic manner, and at the same time in a more realistic ex vivo scenario compared to in vitro studies. In our model, we showed a GBM outgrowth enhancing synergism between CXCR2-blocking and Dex-treatment in the native condition, which was levelled by PLX5622-pretreatment.