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Background: Lumbar facet nerve (medial branch) blocks are often used to diagnose facet joint-mediated pain. The authors recently described a new ultrasound-guided methodology. The current study determines its accuracy using computed tomography scan controls.

Methods: Fifty bilateral ultrasound-guided approaches to the lumbar facet nerves were performed in five embalmed cadavers. The target point was the groove at the cephalad margin of the transverse (or costal) process L1-L5 (medial branch T12-L4) adjacent to the superior articular process. Axial transverse computed tomography scans, with and without 1 ml contrast dye, followed to evaluate needle positions and spread of contrast medium.

Results: Forty-five of 50 needle tips were located at the exact target point. The remaining 5 were within 5 mm of the target. In 47 of 50 cases, the applied contrast dye reached the groove where the nerve is located, corresponding to a simulated block success rate of 94% (95% confidence interval, 84-98%). Seven of 50 cases showed paraforaminal spread, 5 of 50 showed epidural spread, and 2 of 50 showed intravascular spread. Despite the aberrant distribution, all of these approaches were successful, as indicated by contrast dye at the target point. Abnormal contrast spread was equally distributed among all lumbar levels. Contrast traces along the needle channels were frequently observed.  相似文献   

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BACKGROUND: Lumbar facet nerve (medial branch) block for pain relief in facet syndrome is currently performed under fluoroscopic or computed tomography scan guidance. In this three-part study, the authors developed a new ultrasound-guided methodology, described the necessary landmarks and views, assessed ultrasound-derived distances, and tested the clinical feasibility. METHODS: (1) A paravertebral cross-axis view and long-axis view were defined under high-resolution ultrasound (15 MHz). Three needles were guided to the target point at L3-L5 in a fresh, nonembalmed cadaver under ultrasound (2-6 MHz) and were subsequently traced by means of dissection. (2) The lumbar regions of 20 volunteers (9 women, 11 men; median age, 36 yr [23-67 yr]; median body mass index, 23 kg/m2 [19-36 kg/m2]) were studied with ultrasound (3.5 MHz) to assess visibility of landmarks and relevant distances at L3-L5 in a total of 240 views. (3) Twenty-eight ultrasound-guided blocks were performed in five patients (two women, three men; median age, 51 yr [31-68 yr]) and controlled under fluoroscopy. RESULTS: In the cadaver, needle positions were correct as revealed by dissection at all three levels. In the volunteers, ultrasound landmarks were delineated as good in 19 and of sufficient quality in one (body mass index, 36 kg/m2). Skin-target distances increased from L3 to L5, reaching statistical significance (*, **P < 0.05) between these levels on both sides: L3r, 45+/-6 mm*; L4r, 48+/-7 mm; L5r, 50+/-6 mm*; L3l, 44+/-5 mm**; L4l, 47+/-6 mm; L5l, 50+/-6 mm**. In patients, 25 of 28 ultrasound-guided needles were placed accurately, with the remaining three closer than 5 mm to the radiologically defined target point. CONCLUSION: Ultrasound guidance seems to be a promising new technique with clinical relevance and the potential to increase practicability while avoiding radiation in lumbar facet nerve block.  相似文献   
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Ischemia resulting from myocardial infarction (MI) promotes VEGF expression, leading to vascular permeability (VP) and edema, a process that we show here contributes to tissue injury throughout the ventricle. This permeability/edema can be assessed noninvasively by MRI and can be observed at the ultrastructural level as gaps between adjacent endothelial cells. Many of these gaps contain activated platelets adhering to exposed basement membrane, reducing vessel patency. Following MI, genetic or pharmacological blockade of Src preserves endothelial cell barrier function, suppressing VP and infarct volume, providing long-term improvement in cardiac function, fibrosis, and survival. To our surprise, an intravascular injection of VEGF into healthy animals, but not those deficient in Src, induced similar endothelial gaps, VP, platelet plugs, and some myocyte damage. Mechanistically, we show that quiescent blood vessels contain a complex involving Flk, VE-cadherin, and beta-catenin that is transiently disrupted by VEGF injection. Blockade of Src prevents disassociation of this complex with the same kinetics with which it prevents VEGF-mediated VP/edema. These findings define a molecular mechanism to account for the Src requirement in VEGF-mediated permeability and provide a basis for Src inhibition as a therapeutic option for patients with acute MI.  相似文献   
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