Midpoint of C7 Lateral Mass Serves as an Accurate Reference Point for the Placement of T1 Pedicle Screws: An Anatomic Study.

BACKGROUND AND OBJECTIVES: Free-hand placement of T1 pedicle screws can often be challenging. A reliable free-hand technique for placement of T1 pedicle screws can overcome some of the difficulties associated with poor fluoroscopy in this region. The purpose of this study was to propose a novel anatomic landmark for accurate identification of the T1 entry point using the midpoint of the C7 lateral mass as a reference point. Our hypothesis is that the midpoint of the C7 lateral mass is within 1-2 mm of the center of the T1 pedicle. METHODS: Using 3-dimensional reconstruction software, the pedicle of T1 and the lateral mass of C7 were isolated to assess the location of the T1 pedicle relative to the C7 lateral mass. Specifically, the distance between the center of the T1 pedicle and the center of the C7 lateral mass was measured on 40 computed tomography scans. Furthermore, a clinical validation of this technique was performed by assessing the postoperative computed tomography scans of 53 patients undergoing cervicothoracic instrumentation. The Gertzbein and Robbins classification system was used to grade the accuracy of T1 pedicle screw placements in all patients using this technique. RESULTS: The average horizontal deviation + SD from centers of the T1 pedicle and the C7 lateral mass was 0.398 mm ± 0.953 mm. The T1 pedicle on average was slightly medial to the center of the C7 lateral mass. A total of 98.1% of T1 pedicle screws placed in vivo using the free-hand technique were of Grade A. CONCLUSION: In this article, we demonstrate that the center of the C7 lateral mass overlays the T1 pedicle and the optimal entry point is immediately below the midpoint of the C7 lateral mass. This approach provides a practical and accurate landmark in posterior cervicothoracic spine procedures that reduce the need for additional radiation exposure or increased operative time with image-guided techniques.

Astrocyte- and Neuron-Derived Extracellular Vesicles from Alzheimer's Disease Patients Effect Complement-Mediated Neurotoxicity.

We have previously shown that blood astrocytic-origin extracellular vesicles (AEVs) from Alzheimer's disease (AD) patients contain high complement levels. To test the hypothesis that circulating EVs from AD patients can induce complement-mediated neurotoxicity involving Membrane Attack Complex (MAC) formation, we assessed the effects of immunocaptured AEVs (using anti-GLAST antibody), in comparison with neuronal-origin (N)EVs (using anti-L1CAM antibody), and nonspecific CD81+ EVs (using anti-CD81 antibody), from the plasma of AD, frontotemporal lobar degeneration (FTLD), and control participants. AEVs (and, less effectively, NEVs) of AD participants induced Membrane Attack Complex (MAC) expression on recipient neurons (by immunohistochemistry), membrane disruption (by EthD-1 assay), reduced neurite density (by Tuj-1 immunohistochemistry), and decreased cell viability (by MTT assay) in rat cortical neurons and human iPSC-derived neurons. Demonstration of decreased cell viability was replicated in a separate cohort of autopsy-confirmed AD patients. These effects were not produced by CD81+ EVs from AD participants or AEVs/NEVs from FTLD or control participants, and were suppressed by the MAC inhibitor CD59 and other complement inhibitors. Our results support the stated hypothesis and should motivate future studies on the roles of neuronal MAC deposition and AEV/NEV uptake, as effectors of neurodegeneration in AD.