Vocal Cord Dysfunction

Updated: Mar 30, 2016
  • Author: Praveen Buddiga, MD; Chief Editor: Michael A Kaliner, MD  more...
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Overview

Background

Vocal cord dysfunction (VCD), also commonly known as paradoxical vocal fold motion, can be characterized as an abnormal adduction of the vocal cords during the respiratory cycle (especially during the inspiratory phase) that produces airflow obstruction at the level of the larynx. [1, 2, 3]

The larynx receives very extensive sensory and motor innervation. With repeated stimulation and excitation by noxious intrinsic and extrinsic irritants, these nerve fibers may become hyperexcitable and hyperresponsive. Consequently, the threshold for activation of the reflex responsible for vocal cords closure is lowered. The underlying pathophysiology of VCD involves a hyperfunctional and inappropriate laryngeal closure reflex. [66, 67]

VCD frequently mimics persistent asthma and is often treated with high-dose inhaled or systemic corticosteroids, bronchodilators, multiple emergency department visits, hospitalizations, and, in some cases, tracheostomies and intubation. [2, 4, 5, 6]

The patients considered here have problems associated with abnormal vocal cord movement without an organic basis. Flow-volume loops obtained during symptomatic periods of wheezing show a limitation of inspiratory flow suggestive of variable extrathoracic obstruction (inspiratory loop flattening). Paradoxical vocal cord motion can be confirmed on laryngoscopy performed when patients are symptomatic.

The clinical history provides limited opportunity to distinguish between patients with VCD and patients with asthma because both groups present with symptoms of wheezing, cough, and dyspnea. [7, 8] The localization of airflow obstruction to the laryngeal area is an important clinical discriminatory feature in patients with VCD.

Another clinical clue may be that patients with VCD often seem to have refractory asthma with poor response to beta-agonists or inhaled corticosteroids. [9, 10] They do not usually report nocturnal awakening due to breathlessness.

Objectively, the data reveal absence of hypoxemia in this subset as compared to compromised persons with asthma. [10]

The hallmark of diagnosis is noted on direct rhinolaryngoscopy; a glottic chink is present along the posterior portion of the vocal cords, while the anterior portion of the vocal cords is adducted.

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Pathophysiology

During the normal respiratory cycle, the vocal cords partially abduct with inhalation and partially adduct with end-exhalation. This phasic vocal cord movement is physiologic, and it allows the unimpeded movement of air inward to the lungs and outward to the atmosphere while maintaining the alveolar patency of the lungs by providing positive airway pressure during expiration (ie, positive end-expiratory pressure [PEEP]).

The larynx, therefore, serves as an upper airway valve to help keep the lungs expanded. For this function, the larynx is richly innervated, and its size is regulated by the activation of striated muscles that are under voluntary and reflexive control. Both laryngeal and respiratory motor neurons influence glottic size, and they, in turn, may be influenced by vagal reflex activity arising from pulmonary and laryngeal receptors.

The mechanisms that cause glottic chink narrowing or intermittent closing during inspiration independent of any changes in lower airway caliber are unknown. In affected patients, the integrated function of the vocal cords ceases episodically, leading to acute intermittent episodes of functional airway obstruction. The clinical signs and symptoms resemble those observed in disorders such as vocal cord paralysis, asthma, epiglottitis, laryngospasm, and angioedema secondary to anaphylaxis.

Recent case reports have described other causes of VCD, such as an inlet patch of heterotopic gastric mucosa in the upper esophagus [11] and exposure to agents such as glutaraldehyde and chlorine inhalation by swimmers or divers.

VCD appears to be part of the spectrum of airway disorders caused by occupational exposures, including irritant exposures and psychological stressors, at the World Trade Center disaster. A recent study evaluating the role of formal psychological testing in patients with paradoxical vocal cord dysfunction found a pattern consistent with conversion disorder in some patients; however, a subset of patients did not appear to be associated with psychopathology. [12]

To summarize, the exact cause of this condition is not clearly evident and may be multifactorial. [10, 13] A hypothesis is that mediation of the vagus nerve may alter the laryngeal tone and lower the threshold for stimuli to produce vocal cord spasm or to precipitate the abnormal adduction of vocal cords. Recent literature suggests a greater emphasis on organic causes such as gastroesophageal reflux and laryngopharyngeal reflux since the laryngopharynx is highly sensitive to gastric acid irritation.

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Epidemiology

Frequency

United States

This condition is observed in up to 10% of patients at referral centers seeking evaluation of asthma that is unresponsive to aggressive therapy. The literature reveals a high incidence of VCD in persons with psychiatric conditions (eg, depression, obsessive-compulsive disorder, borderline personality disorder, neuroses induced by childhood sexual abuse), [1, 14] persons with an increased body mass index [6] and medical personnel. VCD may complicate true asthma in a small number of patients.

Mortality/Morbidity

Mortality rates are unknown, but morbidity is often significant from years of corticosteroid use, resulting in iatrogenic Cushing-like syndrome, bone density loss, and growth suppression in the pediatric population. [10]

Misdiagnosis of VCD as asthma may lead to significant morbidity and increased costs, and misuse of measures of asthma control may be contributing to these findings. [72]

Sex

This condition is predominantly observed in females. [12] The authors' review of the published literature indicates a female-to-male ratio of approximately 3:1.

Age

This condition predominates in people aged 20-40 years, but it can occur in people aged 6-83 years. Recent literature suggests an increase of this condition in children and adolescents.

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