Eyebrow supraorbital keyhole craniotomy for olfactory groove meningiomas with endoscope assistance: case series and systematic review of extent of resection, quantification of postoperative frontal lobe injury, anosmia, and recurrence.

BACKGROUND: Olfactory groove meningiomas (OGMs) are commonly treated with open craniotomy. Endonasal approaches have also been described. OBJECTIVE: To present clinical and radiographic outcomes for the minimally invasive eyebrow incision supraorbital keyhole approach with endoscopic assistance for OGMs. METHODS: We performed a retrospective single-center cohort study and a systematic literature review. RESULTS: Fifteen patients were identified, all with Grade I meningiomas. Radiographic gross total resection of enhancing tumor was achieved in all patients. Mean frontal lobe fluid-attenuated inversion recovery volume decreased from 11.1 ± 18.3 cm3 preoperatively to 9.9 ± 11.4 cm3 immediately postoperatively, and there was minimal new restricted diffusion (3.2 ± 2.2 cm3; max 7.5 cm3). Median length of stay was 3 days (range 2-8). Vision was improved in 4 (80%) and stable in 1 (20%) of 5 patients with a preoperative deficit. New postoperative anosmia occurred in 3 (23%) of 13 patients with any preoperative olfaction. All patients were satisfied with their cosmetic result at 3 months. After a median follow-up of 32.2 months, there were 2 (13.3%) asymptomatic radiographic recurrences, 1 treated with radiosurgery and the other with endoscopic endonasal approach (EEA). No patients required further craniotomy. Systematic review revealed the present series to be the largest to date reporting disaggregated outcomes for the eyebrow approach to OGM. CONCLUSION: The eyebrow incision supraorbital keyhole craniotomy with endoscopic assistance is a safe and effective approach to OGM with tumor control rates similar to more invasive open approaches and better than the endonasal approach. Rates of frontal lobe injury, CSF leak and anosmia are comparatively low.

Lumbar Giant Disk Herniations Treated With a Unilateral Approach for Bilateral Decompression.

BACKGROUND: Disk herniations that obstruct the spinal canal by more than 50% are named "giant disk herniations" (GDHs). GDHs are challenging to treat from a surgical perspective because of their size and the risk of iatrogenic manipulation during resection resulting in additional neurological compromise. As a result, the appropriateness of minimally invasive tubular approaches for the treatment of lumbar GDHs remains controversial. OBJECTIVE: To report our experience in treating lumbar GDHs using tubular minimally invasive surgery. METHODS: A total number of 228 disk herniations were evaluated for the criteria of GDH. In addition, the presence of neurological deficits such as cauda equina syndrome, pain as measured by a visual analog scale, operating time, complications, estimated intraoperative blood loss, and number of surgical revisions were assessed. The standard tubular diskectomy technique was modified to include unilateral laminectomy for bilateral decompression before the diskectomy to create a sufficient working space for removal of the disk fragments. RESULTS: Twenty-three (10%) patients met the criteria for GDH. Clinically significant motor weakness was present in 21 patients (91.3%) before surgery, and 3 patients (13%) presented with cauda equina syndrome. The average mean visual analog scale (±SD) for the preoperative pain score was 8.3 and decreased to 2.4 at follow-up after surgery. All cases of cauda equina syndrome resolved postoperatively. CONCLUSION: Unilateral tubular minimally invasive surgery diskectomy seems to be a safe and effective treatment alternative for lumbar GDHs, combined with the "over-the-top" decompression, which provides bilateral decompression and working space.

Lineage-Restricted OLIG2-RTK Signaling Governs the Molecular Subtype of Glioma Stem-like Cells.

The basic helix-loop-helix (bHLH) transcription factor OLIG2 is a master regulator of oligodendroglial fate decisions and tumorigenic competence of glioma stem-like cells (GSCs). However, the molecular mechanisms underlying dysregulation of OLIG2 function during gliomagenesis remains poorly understood. Here, we show that OLIG2 modulates growth factor signaling in two distinct populations of GSCs, characterized by expression of either the epidermal growth factor receptor (EGFR) or platelet-derived growth factor receptor alpha (PDGFRα). Biochemical analyses of OLIG2 function in normal and malignant neural progenitors reveal a positive feedforward loop between OLIG2 and EGFR to sustain co-expression. Furthermore, loss of OLIG2 function results in mesenchymal transformation in PDGFRα(HIGH) GSCs, a phenomenon that appears to be circumscribed in EGFR(HIGH) GSCs. Exploitation of OLIG2's dual and antithetical, pro-mitotic (EGFR-driven), and lineage-specifying (PDGFRα-driven) functions by glioma cells appears to be critical for sustaining growth factor signaling and GSC molecular subtype.