VOCAL CORD DYSFUNCTION - pediagenosis
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Saturday, July 4, 2020

VOCAL CORD DYSFUNCTION


VOCAL CORD DYSFUNCTION
Vocal cord dysfunction (VCD), also known as paradoxical vocal cord motion (PVCM), is a relatively poorly understood laryngeal disorder manifest by inappropriate adduction, or closing, of the vocal cords during inspiration. This is in contrast to the normal respiratory cycle, in which the vocal cords are abducted, or open, during inspiration and only begin to adduct toward the end of exhalation or with the onset of phonation. Physiologically, partial adduction of the vocal cords at the end of the expiratory phase maintains alveolar patency by generating positive end-expiratory pressure. Full adduction of the vocal cords occurs normally during phonation. As air expelled from the lungs encounters a closed glottis, subglottic air pressure increases, which in turn provides the force necessary to vibrate the vocal cords and produce voice. In contrast, paradoxical adduction of the vocal cords during inspiration in patients with VCD results in acute, intermittent episodes of functional airway obstruction.

VOCAL CORD DYSFUNCTION

The most common symptoms of VCD are inspiratory stridor, dyspnea, hoarseness, throat tightening, and cough. Unfortunately, these symptoms are relatively nonspecific and may mimic other conditions such as asthma, epiglottitis, angioedema, or anaphylaxis. Many patients with VCD will have been treated aggressively for presumed asthma without improvement. In contrast to asthma, the airway obstruction in VCD occurs with inspiration rather than expiration, and laryngeal stridor should not be mistaken for bronchial wheezing. Pulmonary function testing can help exclude asthma and support a diagnosis of VCD, with attenuation of the inspiratory flow rate on flow-volume loops. It is common to have both asthma and VCD, in which case methacholine challenge testing is often helpful.
A diagnosis of VCD can be further substantiated with transnasal flexible fiberoptic laryngoscopy. As with pulmonary function testing, this should be done while the patient is symptomatic. Because of the episodic nature of VCD, it may be necessary to first challenge the patient with exercise, sustained vocal tasks, or other known triggers to elicit an acute exacerbation. Flexible laryngoscopy demonstrates a structurally normal larynx with paradoxical adduction of the vocal cords during inspiration. This is more pronounced when breathing in through the mouth rather than the nose, which provides a stronger neural stimulus for vocal cord abduction. Adduction of the anterior two-thirds of the vocal cords with a diamond-shaped posterior glottic gap is most commonly described, although additional findings of false vocal cord adduction and anterior to posterior supraglottic constriction have been reported.
The cause of VCD is poorly understood. Because of the lack of clear organic pathology and the high incidence of underlying psychiatric conditions in these patients, VCD has historically been considered a psychogenic disorder, as evidenced by such antiquated terms as Munchausen’s stridor and factitious asthma. Although VCD may be a manifestation of a somatization or conversion disorder in some patients, nonpsychogenic causes must also be considered. Brainstem compression, upper or lower motor neuron injury, and movement disorders have been associated with VCD. Laryngeal hyperresponsiveness secondary to laryngopharyngeal reflux (LPR) has also been implicated as a potential causative factor in VCD. A diagnosis of LPR is supported by findings of posterior laryngeal erythema, interarytenoid mucosal pachydermy, and posterior pharyngeal cobblestoning on flexible laryngoscopy. The treatment of VCD involves a multifaceted approach, with identification and elimination of potential irritants or triggers, medical therapy for underlying psychogenic or pathologic conditions, and intensive behavioral therapy with an experienced speech-language pathologist focusing on laryngeal relaxation and diaphragmatic breathing techniques. If necessary, severe attacks may be managed acutely with anxiolytics, heliox, or continuous positive airway pressure ventilation. Most patients with VCD improve with proper treatment and time.

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