Objectives: The purpose of this study was to document and analyze intraneural vascular flow within the median nerve using power and spectral Doppler sonography and to determine the relationship of this vascular flow with diagnosis of carpal tunnel syndrome based on electrodiagnostic testing.
Methods: Power and spectral Doppler sonograms in the median nerve were prospectively collected in 47 symptomatic and 44 asymptomatic subjects. Doppler studies were conducted with a 12-MHz linear transducer. Strict inclusion criteria were established for postexamination assessment of waveforms; routine quality assurance was completed; electrodiagnostic tests were conducted on the same day as sonographic measurements; and the skin temperature was controlled. Included waveforms were categorized by location and averaged by individual for comparative analysis to electrodiagnostic testing.
Results: A total of 416 waveforms were collected, and 245 were retained for statistical analysis based on strict inclusion criteria. The mean spectral peak velocity among all waveforms was 4.42 (SD, 2.15) cm/s. At the level of the pisiform, the most consistent data point, mean peak systole, was 3.75 cm/s in symptomatic patients versus 4.26 cm/s in asymptomatic controls. Statistical trending showed an initial increase in the mean spectral peak velocity in symptomatic but diagnostically negative cases, with decreasing velocity as diagnostic categories progressed from mild to severe.
Conclusions: An inverse relationship may exist between intraneural vascular flow in the median nerve and an increasing severity of carpal tunnel syndrome based on nerve conduction results. Randomized controlled trials are needed to determine whether spectral Doppler sonography can provide an additive benefit for diagnosing the severity of carpal tunnel syndrome.
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http://dx.doi.org/10.7863/jum.2012.31.5.729 | DOI Listing |
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Angiology and Vascular Surgery, Unidade Local de Saúde de São João; Surgery and Physiology, Faculdade de Medicina da Universidade do Porto, Portugal.
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Department of Biomedicine - Unit of Anatomy, Faculty of Medicine, University of Porto; RISE@Health, Porto, Portugal.
Background: Aortoiliac disease (AID) is a variant of peripheral artery disease involving the infrarenal aorta and iliac arteries. Similar to other arterial diseases, aortoiliac disease obstructs blood flow through narrowed lumens or by embolization of plaques. AID, when symptomatic, may present with a triad of claudication, impotence, and absence of femoral pulses, a triad also referred as Leriche Syndrome (LS).
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January 2025
Department of Surgery, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA 15219, United States; Department of Surgery, Indiana Center for Regenerative Medicine and Engineering, Indiana University School of Medicine, Indianapolis, IN 46202, United States. Electronic address:
Diabetic wounds are complicated by underlying peripheral vasculopathy. Reliance on vascular endothelial growth factor (VEGF) therapy to improve perfusion makes logical sense, yet clinical study outcomes on rescuing diabetic wound vascularization have yielded disappointing results. Our previous work has identified that low endothelial phospholipase Cγ2 (PLCγ2) expression hinders the therapeutic effect of VEGF on the diabetic ischemic limb.
View Article and Find Full Text PDFSci Rep
January 2025
University of Ulsan, 93 Daehak-ro, Nam-gu, Ulsan, 680-749, Republic of Korea.
This study employed large eddy simulation (LES) with the wall-adapting local eddy-viscosity (WALE) model to investigate transitional flow characteristics in an idealized model of a healthy thoracic aorta. The OpenFOAM solver pimpleFoam was used to simulate blood flow as an incompressible Newtonian fluid, with the aortic walls treated as rigid boundaries. Simulations were conducted for 30 cardiac cycles and ensemble averaging was employed to ensure statistically reliable results.
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January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
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