Torrents of torment: turbulence as a mechanism of pulsatile tinnitus secondary to venous stenosis revealed by high-fidelity computational fluid dynamics.

BACKGROUND: Pulsatile tinnitus (PT) is a debilitating condition that can be caused by a vascular abnormality, such as an arterial or venous lesion. Although treatment of PT-related venous lesions has been shown to successfully cure patients of the associated 'tormenting' rhythmical sound, much controversy still exists regarding their role in the etiology of PT. METHODS: A patient presented with a history of worsening, unilateral PT. A partial venous sinus obstruction related to the large arachnoid granulation was detected on the right side, and subsequently stented at the right transverse sinus. High-fidelity computational fluid dynamics (CFD) was performed on a 3D model digitally segmented from the pre-stent venogram, with assumed pulsatile flow rates. A post-stent CFD model was also constructed from this. Data-driven sonification was performed on the CFD velocity data, blinded to the patient's self-reported sounds. RESULTS: The patient reported that the PT was completely resolved after stenting, and has had no recurrence of the symptoms after more than 2 years. CFD simulation revealed highly disturbed, turbulent-like flow at the sigmoid sinus close to auditory structures, producing a sonified audio signal that reproduced the subjective sonance of the patient's PT. No turbulence or sounds were evident at the stenosis, or anywhere in the post-stent model. CONCLUSIONS: For the first time, turbulence generated distal to a venous stenosis is shown to be a cause of PT. High-fidelity CFD may be useful for identifying patients with such 'torrents' of flow, to help guide treatment decision-making.

The Latest Lessons Learned from Retrieval Analyses of Ultra-High Molecular Weight Polyethylene, Metal-on-Metal, and Alternative Bearing Total Disc Replacements.

Knowledge regarding the in vivo performance and periposthetic tissue response of cervical and lumbar total disc replacements (TDRs) continues to expand. This review addresses the following four main questions: 1) What are the latest lessons learned from polyethylene in large joints and how are they relevant to current TDRs? 2) What are the latest lessons learned regarding adverse local tissue reactions from metal-on-metal, CoCr bearings in large joints and how are they relevant to current TDRs? 3) What advancements have been made in understanding the in vivo performance of alternative biomaterials, such as stainless steel and polycarbonate urethane, for TDRs in the past five years? 4) How has retrieval analysis of all these various artificial disc bearing technologies advanced the state of the art in preclinical testing of TDRs? The study of explanted artificial discs and their associated tissues can help inform bearing selection as well as the design of future generations of disc arthroplasty. Analyzing retrieved artificial discs is also essential for validating preclinical test methods.

Neoangiogenesis contributes to the development of hemophilic synovitis.

Joint arthropathy secondary to recurrent hemarthroses remains a debilitating complication of hemophilia despite the use of prophylactic factor concentrates. Increased vascularity and neoangiogenesis have been implicated in the progression of musculoskeletal disorders and tumor growth. We hypothesized that de novo blood vessel formation could play a major role in the pathogenesis of hemophilic joint disease (HJD). We observed a 4-fold elevation in proangiogenic factors (vascular endothelial growth factor-A [VEGF-A], stromal cell-derived factor-1, and matrix metalloprotease-9) and proangiogenic macrophage/monocyte cells (VEGF(+)/CD68(+) and VEGFR1(+)/CD11b(+)) in the synovium and peripheral blood of HJD subjects along with significantly increased numbers of VEGFR2(+)/AC133(+) endothelial progenitor cells and CD34(+)/VEGFR1(+) hematopoietic progenitor cells. Sera from HJD subjects induced an angiogenic response in endothelial cells that was abrogated by blocking VEGF, whereas peripheral blood mononuclear cells from HJD subjects stimulated synovial cell proliferation, which was blocked by a humanized anti-VEGF antibody (bevacizumab). Human synovial cells, when incubated with HJD sera, could elicit up-regulation of HIF-1α mRNA with HIF-1α expression in the synovium of HJD subjects, implicating hypoxia in the neoangiogenesis process. Our results provide evidence of local and systemic angiogenic response in hemophilic subjects with recurrent hemarthroses suggesting a potential to develop surrogate biologic markers to identify the onset and progression of hemophilic synovitis.