Biomechanical fixation properties of cortical versus transpedicular screws in the osteoporotic lumbar spine: an in vitro human cadaveric model.

OBJECTIVE Optimal strategies for fixation in the osteoporotic lumbar spine remain a clinical issue. Classic transpedicular fixation in the osteoporotic spine is frequently plagued with construct instability, often due to inadequate cortical screw-bone purchase. A cortical bone trajectory maximizes bony purchase and has been reported to provide increased screw pullout strength. The aim of the current investigation was to evaluate the biomechanical efficacy of cortical spinal fixation as a surgical alternative to transpedicular fixation in the osteoporotic lumbar spine under physiological loading. METHODS Eight fresh-frozen human spinopelvic specimens with low mean bone mineral densities (T score less than or equal to -2.5) underwent initial destabilization, consisting of laminectomy and bilateral facetectomies (L2-3 and L4-5), followed by pedicle or cortical reconstructions randomized between levels. The surgical constructs then underwent fatigue testing followed by tensile load to failure pullout testing to quantify screw pullout force. RESULTS When stratifying the pullout data with fixation technique and operative vertebral level, cortical screw fixation exhibited a marked increase in mean load at failure in the lower vertebral segments (p = 0.188, 625.6 ± 233.4 N vs 450.7 ± 204.3 N at L-4 and p = 0.219, 640.9 ± 207.4 N vs 519.3 ± 132.1 N at L-5) while transpedicular screw fixation demonstrated higher failure loads in the superior vertebral elements (p = 0.024, 783.0 ± 516.1 N vs 338.4 ± 168.2 N at L-2 and p = 0.220, 723.0 ± 492.9 N vs 469.8 ± 252.0 N at L-3). Although smaller in diameter and length, cortical fixation resulted in failures that were not significantly different from larger pedicle screws (p > 0.05, 449.4 ± 265.3 N and 541.2 ± 135.1 N vs 616.0 ± 384.5 N and 484.0 ± 137.1 N, respectively). CONCLUSIONS Cortical screw fixation exhibits a marked increase in mean load at failure in the lower vertebral segments and may offer a viable alternative to traditional pedicle screw fixation, particularly for stabilization of lower lumbar vertebral elements with definitive osteoporosis.

Glibenclamide for the treatment of acute CNS injury.

First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. During the last decade, glibenclamide has received renewed attention due to its pleiotropic protective effects in acute CNS injury. Acting via inhibition of the recently characterized Sur1-Trpm4 channel (formerly, the Sur1-regulated NCCa-ATP channel) and, in some cases, via brain KATP channels, glibenclamide has been shown to be beneficial in several clinically relevant rodent models of ischemic and hemorrhagic stroke, traumatic brain injury, spinal cord injury, neonatal encephalopathy of prematurity, and metastatic brain tumor. Glibenclamide acts on microvessels to reduce edema formation and secondary hemorrhage, it inhibits necrotic cell death, it exerts potent anti-inflammatory effects and it promotes neurogenesis-all via inhibition of Sur1. Two clinical trials, one in TBI and one in stroke, currently are underway. These recent findings, which implicate Sur1 in a number of acute pathological conditions involving the CNS, present new opportunities to use glibenclamide, a well-known, safe pharmaceutical agent, for medical conditions that heretofore had few or no treatment options.