Simona Mihaela Florea, Thomas Graillon, Thomas Cuny, Regis Gras, Thierry Brue and Henry Dufour
Ophthalmoplegia is a rare complication of transsphenoidal surgery, only noted in a few studies. The purpose of this study was to analyze the complications of cranial nerve III, IV, or VI palsy after transsphenoidal surgery for pituitary adenoma and understand its physiopathology and outcome.
The authors retrospectively analyzed 24 cases of postoperative ophthalmoplegia selected from the 1694 patients operated via a transsphenoidal route in their department.
Two patients were operated on via microscopy and 22 via endoscopy. Patients operated on endoscopically had a greater risk of presenting with an extraocular nerve deficit postoperatively (p = 0.0115). It was found that an extension into or an invasion of the cavernous sinus (Knosp grade 3 or 4 on MRI, 18/24 patients) was correlated with a higher risk of postoperative ophthalmoplegia (p < 0.0001). The deficit was apparent immediately after surgery in 2 patients. For these 2 patients, the mechanisms of ophthalmoplegia were compression or intraoperative nerve lesion. The other 22 patients became symptomatic in the 12–72 hours following the surgery. The mechanisms implied in these cases were intrasellar compressive hematoma (4/22 cases), intracavernous hemorrhagic suffusion, or incomplete resection of the intracavernous portion of the tumor. All patients who did not present with oculomotor palsy immediately after surgery completely recovered their deficits in the 3 months that followed, while the other 2 experienced permanent damage.
Extraocular nerve dysfunction after transsphenoidal pituitary surgery is a rare complication that occurs more frequently in the case of the invasion or an important extension into the cavernous sinus. In this series, it also appears to be significantly more frequent in patients operated on via an endoscopic approach. Most patients have deficits that appear with a delay of 12–72 hours postoperatively and they are most likely to completely recover.
Thomas Graillon, Patrick Rakotozanany, Benjamin Blondel, Tarek Adetchessi, Henry Dufour and Stéphane Fuentes
The optimal management of unstable thoracolumbar fractures remains unclear. The objective of the present study was to evaluate the results of using an expandable prosthetic vertebral body cage (EPVBC) in the management of unstable thoracolumbar fractures.
Eighty-five patients with unstable T7–L4 thoracolumbar fractures underwent implantation of an EPVBC via an anterior approach combined with posterior fixation. Long-term functional outcomes, including visual analog scale and Oswestry disability index scores, were evaluated.
In a mean follow-up period of 16 months, anterior fixation led to a significant increase in vertebral body height, with an average gain of 19%. However, the vertebral regional kyphosis angle was not significantly increased by anterior fixation alone. No significant difference was found between early postoperative, 3-month, and 1-year postoperative regional kyphosis angle and vertebral body height. Postoperative impaction of the prosthetic cage in adjacent endplates was observed in 35% of the cases, without worsening at last follow-up. Complete fusion was observed at 1 year postoperatively and no cases of infections or revisions were observed in relation to the anterior approach.
The use of EPVBCs for unstable thoracolumbar fractures is safe and effective in providing long-term vertebral body height restoration and kyphosis correction, with a moderate surgical and sepsis risk. Anterior cage implantation is an alternative to iliac bone graft fusion and is a viable option in association with a posterior approach, in a single operation without additional risks.
Thomas Graillon, David Romano, Céline Defilles, Alexandru Saveanu, Amira Mohamed, Dominique Figarella-Branger, Pierre-Hugues Roche, Stéphane Fuentes, Olivier Chinot, Henry Dufour and Anne Barlier
Meningiomas express somatostatin receptor subtype 2 (SST2), which is targeted by the somatostatin analog octreotide. However, to date, using somatostatin analog therapy for the treatment of these tumors in clinical practice has been debated. This study aims to clarify the in vitro effects of octreotide on meningiomas for precise clinical applications.
The effects of octreotide were analyzed in a large series of 80 meningiomas, including 31 World Health Organization (WHO) Grade II and 4 WHO Grade III tumors, using fresh primary cell cultures to study the impact on cell viability, apoptosis, and signal transduction pathways.
SST2 mRNA was detected in 100% of the tested meningiomas at levels similar to those observed in other SST2-expressing tumors, neuroendocrine tumors, or pituitary adenomas. Octreotide significantly decreased cell proliferation in 88% of meningiomas but did not induce cell death. On average, cell proliferation was more inhibited in the meningioma group expressing a high level of SST2 than in the low-SST2 group. Moreover, octreotide response was positively correlated to the level of merlin protein and inversely correlated to the level of phosphorylated p70-S6 kinase, a downstream effector of the PI3K/Akt/mammalian target of rapamycin (mTOR) pathway. Octreotide inhibited Akt phosphorylation and activated tyrosine phosphatase without impacting the extracellular regulated kinase (ERK) pathway.
Octreotide acts exclusively as an antiproliferative agent and does not promote apoptosis in meningioma in vitro. Therefore, in vivo, octreotide is likely to limit tumor growth rather than induce tumor shrinkage. A meta-analysis of the literature reveals an interest in octreotide for the treatment of WHO Grade I tumors, particularly those in the skull base for which the 6-month progression-free survival level reached 92%. Moreover, somatostatin analogs, which are well-tolerated drugs, could be of interest for use as co-targeting therapies for aggressive meningiomas.