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Ulaş Yener, Timucin Avsar, Emel Akgün, Aşkın Şeker, Yaşar Bayri and Türker Kılıç


Angiogenesis and the platelet-derived growth factor (PDGF) pathway are active in the pathogenesis of vestibular schwannomas (VSs). The purpose of this study was to test whether imatinib mesylate (Gleevec), a PDGF receptor (PDGFR) blocker, reduces angiogenic capacity in sporadic VS and in VS associated with neurofibromatosis Type 2 (NF2) using a corneal angiogenesis assay.


From 121 VS tissue samples stored in the tumor bank at the Marmara University Institute of Neurological Sciences, 10 samples (6 from sporadic cases, 4 from NF2-associated cases) were selected at random for use in this study. Expression of PDGF-A and PDGF-B and their receptors was evaluated in sporadic and NF2-associated VS as well as in glioblastoma (GBM) and normal brain tissue by means of immunohistochemistry and Western blot analysis. Corneal angiogenesis assay was then used to evaluate the angiogenic capacity of tissue specimens from sporadic and NF2-associated VS with and without imatinib treatment as well as positive and negative controls (GBM and normal brain tissue).


The angiogenic potential of the sporadic and NF2-associated VS tumor tissue differed significantly from that of the positive and negative control tissues (p <0.05). Furthermore, NF2-associated VS showed significantly lower angiogenic potential than sporadic VS (p <0.05). Imatinib treatment significantly reduced the angiogenic potential in both the sporadic VS and the NF2-associated VS groups. The level of PDGF-A and PDGFR-α as well as PDGF-B and PDGFR-β expression in sporadic VS and NF2-associated VS also differed significantly (p <0.05) from the levels in controls. Additionally the level of PDGFR-β was significantly higher in sporadic VS than in NF2-associated VS (p <0.05).


The findings of this study indicate that NF2-associated VS has significantly more angiogenic potential than sporadic VS and normal brain tissue. Additionally, imatinib reduces the angiogenic activity of both sporadic and NF2-associated VS. The authors conclude that imatinib may be a potential treatment for VS, especially for NF2-associated lesions that cannot be cured with resection or radiosurgery.

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Rebecca M. Burke, Thomas J. Buell, Dominic M. Maggio, Ulas Yener, Chun-Po Yen, Christopher I. Shaffrey and Justin S. Smith

Adolescent idiopathic scoliosis patients treated with spinal fusion may develop adjacent segment disease and curve progression into adulthood. Revision operations can be challenging, especially for adult patients treated with outdated instrumentation such as sublaminar hooks and/or wires. The authors demonstrate revision lumbar spine surgery in a 38-year-old female with scoliosis progression from junctional degeneration below a prior T5–L3 posterior instrumented arthrodesis with a hook-and-rod wire system. They also demonstrate safe application of an ultrasonic bone scalpel for completion of a Smith-Petersen osteotomy. The patient provided written, informed consent for all material presented in this case demonstration.

The video can be found here:

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Thomas J. Buell, Ulas Yener, Tony R. Wang, Avery L. Buchholz, Chun-Po Yen, Mark E. Shaffrey, Christopher I. Shaffrey and Justin S. Smith


Sacral insufficiency fracture after lumbosacral (LS) arthrodesis is an uncommon complication. The objective of this study was to report the authors’ operative experience managing this complication, review pertinent literature, and propose a treatment algorithm.


The authors analyzed consecutive adult patients treated at their institution from 2009 to 2018. Patients who underwent surgery for sacral insufficiency fractures after posterior instrumented LS arthrodesis were included. PubMed was queried to identify relevant articles detailing management of this complication.


Nine patients with a minimum 6-month follow-up were included (mean age 73 ± 6 years, BMI 30 ± 6 kg/m2, 56% women, mean follow-up 35 months, range 8–96 months). Six patients had osteopenia/osteoporosis (mean dual energy x-ray absorptiometry hip T-score −1.6 ± 0.5) and 3 received treatment. Index LS arthrodesis was performed for spinal stenosis (n = 6), proximal junctional kyphosis (n = 2), degenerative scoliosis (n = 1), and high-grade spondylolisthesis (n = 1). Presenting symptoms of back/leg pain (n = 9) or lower extremity weakness (n = 3) most commonly occurred within 4 weeks of index LS arthrodesis, which prompted CT for fracture diagnosis at a mean of 6 weeks postoperatively. All sacral fractures were adjacent or involved S1 screws and traversed the spinal canal (Denis zone III). H-, U-, or T-type sacral fracture morphology was identified in 7 patients. Most fractures (n = 8) were Roy-Camille type II (anterior displacement with kyphosis). All patients underwent lumbopelvic fixation via a posterior-only approach; mean operative duration and blood loss were 3.3 hours and 850 ml, respectively. Bilateral dual iliac screws were utilized in 8 patients. Back/leg pain and weakness improved postoperatively. Mean sacral fracture anterolisthesis and kyphotic angulation improved (from 8 mm/11° to 4 mm/5°, respectively) and all fractures were healed on radiographic follow-up (mean duration 29 months, range 8–90 months). Two patients underwent revision for rod fractures at 1 and 2 years postoperatively. A literature review found 17 studies describing 87 cases; potential risk factors were osteoporosis, longer fusions, high pelvic incidence (PI), and postoperative PI-to–lumbar lordosis (LL) mismatch.


A high index of suspicion is needed to diagnose sacral insufficiency fracture after LS arthrodesis. A trial of conservative management is reasonable for select patients; potential surgical indications include refractory pain, neurological deficit, fracture nonunion with anterolisthesis or kyphotic angulation, L5–S1 pseudarthrosis, and spinopelvic malalignment. Lumbopelvic fixation with iliac screws may be effective salvage treatment to allow fracture healing and symptom improvement. High-risk patients may benefit from prophylactic lumbopelvic fixation at the time of index LS arthrodesis.