Browsing by Author "Stevens, Sydney"

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    Decreasing Phantom Limb Pain for Amputees with Phantom Limb Pain and Brachial Plexus Avulsions Through Various Therapy Interventions: A Systematic Review
    (2021-04-30) Stevens, Sydney; Hoseinpour, Niki; Martin, Kylee; Stuckwisch, Devin; Barker, Haylee; Kramer, Martina; Chase, Tony; Department of Occupational Therapy, School of Health and Human Sciences
    This rapid systematic review of the literature discusses the evidence of studies related to effective occupational therapy interventions in reducing phantom limb pain (PLP) due to amputations and brachial plexus avulsions (BPA). This review provides a comprehensive overview and analysis of 30 studies that addressed many of the interventions commonly used in phantom limb pain rehabilitation. Phantom limb pain is a painful sensation perceived in the absence of a limb or in a deafferented limb. Suffering from acute or chronic pain can decrease engagement and performance in meaningful occupations. Overall, we found moderate evidence to support the effectiveness of various therapy interventions for decreasing PLP in individuals with amputations and BPAs.
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    Pulmonary vascular mechanical consequences of ischemic heart failure and implications for right ventricular function
    (American Physiological Society, 2019-02-15) Philip, Jennifer L.; Murphy, Thomas M.; Schreier, David A.; Stevens, Sydney; Tabima, Diana M.; Albrecht, Margie; Frump, Andrea L.; Hacker, Timothy A.; Lahm, Tim; Chesler, Naomi C.; Medicine, School of Medicine
    Left heart failure (LHF) is the most common cause of pulmonary hypertension, which confers an increase in morbidity and mortality in this context. Pulmonary vascular resistance has prognostic value in LHF, but otherwise the mechanical consequences of LHF for the pulmonary vasculature and right ventricle (RV) remain unknown. We sought to investigate mechanical mechanisms of pulmonary vascular and RV dysfunction in a rodent model of LHF to address the knowledge gaps in understanding disease pathophysiology. LHF was created using a left anterior descending artery ligation to cause myocardial infarction (MI) in mice. Sham animals underwent thoracotomy alone. Echocardiography demonstrated increased left ventricle (LV) volumes and decreased ejection fraction at 4 wk post-MI that did not normalize by 12 wk post-MI. Elevation of LV diastolic pressure and RV systolic pressure at 12 wk post-MI demonstrated pulmonary hypertension (PH) due to LHF. There was increased pulmonary arterial elastance and pulmonary vascular resistance associated with perivascular fibrosis without other remodeling. There was also RV contractile dysfunction with a 35% decrease in RV end-systolic elastance and 66% decrease in ventricular-vascular coupling. In this model of PH due to LHF with reduced ejection fraction, pulmonary fibrosis contributes to increased RV afterload, and loss of RV contractility contributes to RV dysfunction. These are key pathologic features of human PH secondary to LHF. In the future, novel therapeutic strategies aimed at preventing pulmonary vascular mechanical changes and RV dysfunction in the context of LHF can be tested using this model.