Introduction
Background
Vocal cord dysfunction (VCD) 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.
VCD frequently mimics persistent asthma and is often treated with high-dose inhaled and/or systemic corticosteroids, bronchodilators, multiple emergency department visits, hospitalizations, and in some cases, tracheostomies and intubation.
This subset of patients has 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. The localization of airflow obstruction to the laryngeal pharynx is an important clinical discriminatory feature 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. They do not usually report nocturnal awakening due to breathlessness.
Objectively, the data reveal absence of hypoxemia in this subset as compared to compromised asthmatic persons.
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.
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. Additionally, 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, as does any reflex activity arising from pulmonary and laryngeal receptors.
The mechanism that causes glottic chink narrowing or intermittent closing during inspiration independent of any changes in lower airway caliber are unknown. Nevertheless, the integrated function of the vocal cords ceases episodically, and affected patients develop acute intermittent episodes of functional airway obstruction. These 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 shown other causes of vocal cord dysfunction, such as an inlet patch of heterotopic gastric mucosa in the upper esophagus and exposure to agents such as glutaraldehyde, chlorine, or even eucalyptus.
To summarize, the exact cause of this condition is not clearly evident, but the 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, laryngopharyngeal reflux, and neurologically-based dystonias.
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), persons with an increased body mass index and medical personnel. VCD may complicate true asthma in a small number of patients.
Mortality/Morbidity
Mortality rates are unknown, and 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.
Sex
This condition is predominantly observed in young adult females. The authors' review of the published literature indicates a female-to-male ratio of approximately 7:3.
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.
Clinical
History
- Wheezing
- Cough
- A feeling of tightness in the throat
- Hoarseness and voice change
- Stridor
- Shortness of breath
- Dyspnea on exertion
- Inspiratory difficulty
- Sudden episodes of shortness of breath
- Unresponsiveness to bronchodilators and corticosteroids
Physical
- Laryngeal auscultation may reveal harsh stridulous sounds during symptoms.
- Wheezing may be heard in the chest (transmitted from the upper airway).
Causes
Problems associated with VCD include the following:
- Gastroesophageal reflux disease, laryngopharyngeal reflux
- Sinusitis
- Postnasal drip
- Strenuous exercise
- Occupational exposure to irritant fumes
- Environmental allergens and/or pollutants
- Psychogenic causes
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Further Reading
Keywords
vocal cord dysfunction, VCD, paradoxical vocal cord motion, laryngeal dyskinesia, abnormal adduction of the vocal cords during the respiratory cycle, airflow obstruction, variable extrathoracic obstruction, inspiratory loop flattening, depression, obsessive-compulsive disorder, borderline personality disorder, neuroses induced by childhood sexual abuse, asthma
Overview: Vocal Cord Dysfunction