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Progressive Dysphonia: Ortner Syndrome

A 68-year-old woman with known idiopathic heart failure and severe reduced ejection fraction was admitted for aggravation of dyspnea and recurrent dysphonia over the past 6 months, progressing to constant hoarseness.

Vitals signs were normal. Laboratory tests showed normal hemoglobin and white blood cell count, increased levels of N-terminal pro-brain natriuretic peptide (NT-proBNP; 10574 pg/mL), and stage-3 chronic kidney disease. Besides a first-degree atrioventricular block and a slightly long QTc, electrocardiogram results were normal.

A chest radiograph showed massive cardiomegaly (cardiothoracic ratio of 75%) with prominent left atrium and ventricle and splaying of the carina; signs of pulmonary congestion were also present. Contrast-enhanced axial computed tomography imaging confirmed the marked left atrial enlargement. Transthoracic echocardiography showed a severe mitral regurgitation. Ear, nose, and throat evaluation by direct laryngoscopy revealed a paralyzed left vocal fold fixed in the paramedian position (Figures A-D).

Ortner syndrome (or cardiovocal syndrome) refers to dysphonia resulting from left recurrent laryngeal nerve palsy secondary to nerve impingement, stretching, or compression at mediastinum. It represents 1%–3% of all cases of extralaryngeal dysphonia.1 The eponym is named after the Austrian internist Norbert Ortner who first described 3 patients with dysphonia due to left vocal fold palsy concomitant to left atrial enlargement (due to mitral valve stenosis).2 The pathophysiology of Ortner syndrome stems from the anatomy of the left recurrent laryngeal nerve. The left recurrent laryngeal nerve branches off the vagus nerve just below the aorta, then it loops around the ligamentum arteriosum (between the superior surface of the origin of the left pulmonary artery and the inferior surface of the aortic arch) and ascends to the larynx (hence the term recurrent in the name) along the tracheoesophageal groove. The nerve’s peculiar course at the aortopulmonary window makes it susceptible to compression by structures abutting this space.

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-Matteo Coen, MD, MD-PhD, Igor Leuchter, MD, MSc, Massimo Sussetto, MD, Carlo Banfi, MD, PhD, Raphaël Giraud, MD, Karim Bendjelid, MD, PhD

This article originally appeared in the December issue of The American Journal of Medicine.

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