Prim Care Clin Office Pract

35 (2008) 81–103

Vocal Cord Dysfunction/Paradoxical

Vocal Fold Motion
Marcy Hicks, MSa,*, Susan M. Brugman, MDb,
Rohit Katial, MD, FAAAAI, FACPc
a
Department of Rehabilitation, National Jewish Medical and Research Center,
1400 Jackson Street, Denver, CO 80206, USA
b
Division of Pulmonology, National Jewish Medical and Research Center, The University
of Colorado Health Sciences Center, 1400 Jackson Street, Denver, CO 80206, USA
c
Division of Allergy and Clinical Immunology, National Jewish Medical and Research Center,
The University of Colorado Health Sciences Center, 1400 Jackson Street,
Denver, CO 80206, USA

Vocal cord dysfunction, often referred to as a mimicker of asthma [1–4],

is as confusing as the plethora of labels attached to this disorder. Each sub-
specialty reporting on vocal cord dysfunction has attached its own descrip-
tive name. For example, the medical community commonly refers to it as
‘‘vocal cord dysfunction,’’ whereas among speech-language pathologists it
is known as ‘‘paradoxical vocal fold motion’’ (PVFM). A large number of
labels (in excess of 70) have been used in the literature and include medical
terms (paradoxical vocal fold movement disorder, paradoxical vocal cord
movement, paradoxical vocal cord dysfunction, episodic paroxysmal laryng-
ospasm) [5–8] and psychologically based terms (factitious asthma, Mun-
chausen’s stridor, psychogenic stridor, and emotional laryngeal wheezing)
[9–14]. PVFM is probably a more accurate term because it describes the dy-
namic, dysfunctional, and paradoxical movements of the vocal folds and
better distinguishes this disorder from various organic pathologies that
have been termed ‘‘vocal cord dysfunction’’ [15,16]. PVFM is used through-
out this article.
PVFM is a laryngeal disorder that affects respiratory function and has
gained significant recognition over the past two decades. There are numer-
ous case studies reporting PVFM as a masquerader of asthma, allergies,
and severe upper airways obstruction with consequent misdiagnosis and
mismanagement. The literature is replete with descriptions of PVFM

* Corresponding author.
E-mail address: hicksm@njc.org (M. Hicks).

0095-4543/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2007.09.005 primarycare.theclinics.com
82 HICKS et al

presentations, patient profiles, and proposed etiologies. Unfortunately,

there is no unified understanding of this disorder, nor is there any consen-
sus on its evaluation, etiology, or treatment. This article addresses these is-
sues and presents a coherent discussion and interpretation of the relevant
literature and practice to date. It is hoped that the reader is left with use-
able knowledge and clinical decision-making skills to treat patients with
PVFM.

Description
PVFM is an upper airway obstruction associated with the paradoxical
adduction or closure of the vocal folds occurring primarily on inhalation
and sometimes during exhalation [4,17–20]. The clinical presentation of
PVFM ranges from mild dyspnea to acute, severe respiratory distress and
is often mistaken for an asthma attack [6]. Patients complain of sudden on-
set of difficulty breathing, usually on inhalation, air hunger, tightness local-
ized to the throat or neck, cough, and oftentimes stridor or laryngeal
wheezing [4,20–22]. Other symptoms and signs include dry cough; chest
tightness; neck or chest retractions; difficulty swallowing; globus pharyngeus
sensation (sensation of a lump in the throat); choking; suffocating; intermit-
tent aphonia (loss of voice) or dysphonia (deviant vocal quality); fatigue;
chest pain; and throat clearing [18–25]. The acute presentation is frequently
a frightening and emotional experience and may elicit panic and anxiety in
some patients. Rarely, patients may exhibit no distress whatsoever (‘‘la belle
indifference’’) while complaining of severe respiratory distress [26].
PVFM episodes frequently begin and end abruptly and may or may not
be attributed to identifiable triggers. Self-reported triggers include upper re-
spiratory infections; occupational exposures; eating; talking; laughing; sing-
ing; coughing; acid reflux; physical exertion; intense exercise; postnasal drip;
weather changes; emotional stressors; perfumes and strong scents; fumes;
solvents; smoke; air pollution; and, occasionally, unusual triggers (eg, cer-
tain brand of dry erase marker) [8,21]. Patients with PVFM may report a sin-
gle initiating trigger but then find that their PVFM is elicited by a number of
previously benign irritants (priming effect). In some cases, the trigger may be
a generalized exposure in a group setting, which sets off a mass hysteria-like
reaction [16,27].
PVFM patients are typically misdiagnosed as having refractory asthma
with resultant mistreatment [20]. Patients with PVFM generally do not re-
spond to pharmacologic treatment for asthma and frequently have severe
side effects from unnecessary medications and interventions including intu-
bation and tracheostomy [20,28–30]. The degree of iatrogenic complications
was well described by Newman and colleagues [20] in a group of 95 adults
with PVFM. Patients were misdiagnosed with asthma for an average of 4.8
years, with 81% of them having been treated with daily prednisone at an
average dose of 29.2 mg. Furthermore, these patients averaged 9.7
 VOCAL CORD DYSFUNCTION 83

emergency room visits and 5.9 hospital admissions in the year before pre-
sentation and 28% of them had been intubated. Similar finding were re-
ported by Andrianopoulos and colleagues [21] in 27 patients referred for
PVFM, with 44% of them needlessly treated with systemic steroids and
52% with bronchodilators. Similarly to the study by Newman and col-
leagues [20], 25% of these patients were treated in emergency rooms or hos-
pitalized and 7% underwent intubation or tracheostomy. The psychologic
effects of PVFM and the long-term prognosis may also be negatively
affected when the diagnosis is unrecognized and untreated [31]. The morbid-
ity of this disorder is substantial and emphasizes the need for awareness and
accurate diagnosis of PVFM.

Epidemiology
The incidence of PVFM is unknown, although the literature describes it
in subpopulations of patients. In a prospective study, Kenn and colleagues
[32] found PVFM in 2.8% of 1025 patients presenting to a pulmonary clinic
complaining of dyspnea. In a retrospective study of 236 patients admitted to
an inner city hospital asthma center for acute asthma exacerbations, Jain
and colleagues [33] found a 2% incidence of PVFM. Other authors have re-
ported various incidences in subgroups of patients. Newman and Dubester
[4] reported 40% of adults diagnosed with refractory asthma and referred to
a tertiary pulmonary center had PVFM, either as the sole diagnosis (10%)
or in combination with asthma (30%). In a similar population of severe,
asthmatic children, an incidence of PVFM was found in 14% [34]. Among
healthy, physically active adolescents and young adults, the incidence has
been variably reported to be 8% [35], 15% [30], and 27% [36]. PVFM is
probably more common than is generally appreciated and the true incidence
awaits further prospective research.
The breakdown of PVFM patients along age and gender lines is likewise
controversial. When first described by Christopher and coworkers [1] in
1983, PVFM was understood to be a psychiatric disorder of women between
20 and 40 years of age who were medically savvy and victims of childhood
or adult sexual abuse. A comprehensive review of the PVFM literature
paints a different picture [37]. Among the 1530 patients reported, 65%
were adults and 35% were children (defined as age !19 years). The age
range was quite wide (0.02–82 years old), with median ages for pediatric pa-
tients being 14 years and for adult patients 36.5 years. A female preponder-
ance was seen in all age groups with a ratio of 3:1 females to males. Another
review corroborated these findings among 1161 patients with PVFM and
found an even less impressive female preponderance (female/male ¼ 2:1)
[38]. Furthermore, the belief that psychologic dysfunction is an underlying
feature of all PVFM is not supported by the literature, which fails to docu-
ment a greater incidence of such dysfunction in PVFM than in the general
population [37]. Finally, the assumption that PVFM predominates among
84 HICKS et al

individuals with a medical background is also refuted by the data [37]. As

more thorough study is undertaken in this area, the clinical profile of pa-
tients will be further refined.

Pathophysiology
An understanding of PVFM is based on an appreciation for normal laryn-
geal physiology. The three basic functions of the larynx (protection, respira-
tion, and phonation) are controlled by a complex interrelationship of
neurosensory reflexes and the brainstem [39]. The protective function is solely
an automatic, reflexive action, whereas both respiration and phonation are
governed by involuntary (brainstem) and voluntary (cortical) neurons [39].
The most primitive and critical function of the larynx is pulmonary pro-
tection. This is subsumed by the glottic closure reflex, wherein the upper air-
way closes to prevent aspiration of food and liquid during deglutition and
noxious fumes and particulates during respiration [39,40]. This sphincteric
action involves adduction of three levels within the laryngeal framework
and occurs sequentially from bottom to top. The first level consists of the
aryepiglottic folds adducting toward the midline of the glottic chink while
the arytenoid cartilages fold in on the posterior glottis and the epiglottis in-
verts over the top of the anterior glottis. The second and third levels are then
activated as the true vocal cords and then the false vocal cords adduct force-
fully to seal the airway [39]. This highly choreographed reflex is mediated by
the superior laryngeal, recurrent laryngeal, and vagal nerves [41].
Another critical component of airway protection is the cough reflex [42].
This reflex is triggered by stimulation of upper aerodigestive tract sensory
receptors, which send afferent information to the brainstem mediated
through sensory neuropeptides [42]. Laryngeal sensory receptors fall into
four functional categories: (1) cold (flow) receptors, which respond to
changes in temperature; (2) irritant receptors, which respond to mechanical
deformation, and to irritants (including water) and aerosols; (3) pressure re-
ceptors, which respond to changes in laryngeal transmural pressure; and (4)
drive receptors, which respond to laryngeal motion [13]. The irritant recep-
tors are considered main players in the glottic reflex.
The vocal folds abduct (open) into a V-shaped aperture, called the glottic
‘‘chink,’’ during inspiration (Fig. 1A) and adduct (close) into a narrower V
or completely during expiration. Glottic widening begins just milliseconds
before diaphragmatic activation to ensure unimpeded airflow as the respira-
tory muscles start to contract. The glottic chink achieves maximum width at
mid-inspiration. This inspiratory movement is quite consistent within and
among individuals, whereas expiratory laryngeal motion is quite variable.
This vocal cord motion allows energy-efficient control of airflow (small la-
ryngeal muscles versus large respiratory muscles) and subtends other func-
tions of the larynx including breath-holding, abdominal straining,
vocalizing, and coughing [43].
 VOCAL CORD DYSFUNCTION 85

Fig. 1. (A) Normal cords at mid-inspiration. (B) Complete vocal cord adduction in mid-inspi-
ration (most common form of PVFM). (C) PVFM with chinking. (D) Periglottic structures
prolapsing (functional laryngomalacia). (Adapted from Perkner JJ, Fennelly KP, Balkisoon
R, et al. Irritant-associated vocal cord dysfunction. J Occup Environ Med 1998;40(2):136–43;
and Brugman SM, Simons ST. Vocal cord dysfunction: don’t mistake it for asthma. Physician
Sports Med 1998;26:36–4, 66, 67–74, 85; with permission.)

By definition, PVFM is the nonphysiologic, paradoxical closure of the

true vocal folds on inspiration, with or without concomitant closure on ex-
piration. The vocal folds may adduct along their entire length from anterior
to posterior (Fig. 1B) or may adduct along the anterior two thirds of their
length leaving a diamond-shaped posterior opening or chink (Fig. 1C)
[1,44]. This chink pattern, initially thought to be pathognomonic of
PVFM, has been seen in only 6% of cases reported in the literature [37]. Vo-
cal fold adduction may occur for part or all of inspiration, although closure
only at end-inspiration may be physiologic [45]. Expiratory-only closure of
the vocal folds has been described as a PVFM variant [9,12]. Because this
86 HICKS et al

pattern is physiologic during asthma, however, expiratory PVFM in the set-

ting of asthma is a questionable diagnosis [45].
Other patterns of PVFM have been reported and include pharyngeal
constriction [46], posterior arytenoids prolapse (Fig. 1D) [47], exercise-in-
duced laryngomalacia [48], and laryngochalasia [49]. There is some contro-
versy about whether these patterns are truly functional versus organic
derivatives of upper airway obstruction. Yet, it points to the lack of consen-
sus on the precise diagnostic features of PVFM, even though laryngoscopy
is still considered the gold standard. At present, there is no protocol for lar-
yngoscopy procedure or relevant findings in PVFM patients and there is
still debate over how to or who should perform laryngoscopy (otolaryngol-
ogists, speech pathologists, pulmonologists, and so forth). Until agreement
can be reached, PVFM diagnosis can be considered a multidisciplinary one
with laryngoscopy as a primary tool.

Differential diagnosis
It is important to eliminate organic causes of upper airway obstruction
when making a diagnosis of PVFM (Table 1). Most of these diseases can

Table 1
Differential diagnosis of PVFM
Infectious Croup, epiglottis, laryngeal papillomatosis, pertussis, laryngitis,
pharyngeal abscess, diphtheria, CMV
Inflammatory Rheumatoid cricoarytenoid arthritis, Wegner’s granulomatosis
Laryngeal sarcoid, relapsing polychondritis, Gulf War
laryngotracheitis, World Trade Center cough
Traumatic Vocal cord or upper airway hemorrhage, caustic ingestion,
thermal injuries, laryngeal fracture, inhalation injury
Neoplastic Carcinoma of larynx or upper aerodigestive tract, cystic
hygroma, hemangioma, rhabdomyosarcoma, teratoma,
lymphoma, papilloma, goiter
Allergic Spasmodic croup, hereditary angioedema, anaphylaxis, atypical
asthma, exercise-induced asthma, exercise-induced
anaphylaxis
Neurologic Brainstem anomalies or tumors, true laryngospasm, vocal cord
paralysis/paresis, tic disorders, multiple sclerosis, postpolio
syndrome, multiple system atrophy, myasthenia gravis,
Meige syndrome, Gerhardt’s disease, Parkinson’s disease,
diaphragmatic flutter syndrome, respiratory spasmodic
dysphonia, traction on recurrent laryngeal nerve (aortic
aneurysm)
Pulmonary Asthma, COPD, foreign body aspiration, gastric or
laryngopharyngeal aspiration, hyperventilation syndrome
Congenial anomalies Laryngomalacia, laryngeal cleft, intrathoracic vascular ring,
subglottic stenosis, laryngeal web
Psychiatric Munchausen’s syndrome, malingering, panic, anxiety disorder,
somatization disorder
Abbreviations: CMV, cytomegalovirus; COPD, chronic obstructive pulmonary disease.
 VOCAL CORD DYSFUNCTION 87

be easily differentiated on the basis of other corroborating findings. The char-

acteristic presentation of abrupt, transitory airway compromise without hypox-
emia that is typical of PVFM is rarely seen in these physical diseases. Perhaps
the greatest mimic is asthma. Even more confounding is the fact that PVFM
is frequently comorbid with asthma in as many as 40% of pediatric-aged pa-
tients and 38% of adults [20,50]. Sorting out these two diagnoses, particularly
during exercise, and determining which process is active at any one time is chal-
lenging. There are findings in the clinical presentation that are helpful (Table 2).
Neurologic abnormalities are the next most important class of diseases to
rule out. Certainly, peripheral or central nerve damage can result in vocal
cord paresis or paralysis and must be carefully sought. The importance of
laryngoscopy to ensure normal vocal cord function during an asymptomatic
period is essential. Tic disorders can also mimic PVFM, although a solitary
respiratory tic emanating from the larynx is highly unusual. On occasion,
Gillette de la Tourette’s syndrome can manifest as stridor as one element
of numerous motor and vocal tics. The neurologic disorder that most closely
approximates PVFM is respiratory laryngeal dystonia, which involves la-
ryngeal muscle tremor during breathing but does not produce classic stridor.
Another frequently mistaken diagnosis for PVFM is exercise-induced ana-
phylaxis. This rare disorder presents with angioedema, flushing, pruritus, hypo-
tension, urticaria, wheezing, and upper airway obstruction [51]. It is seen in
a minority of individuals who exercise after eating certain foods, specifically
shellfish, eggs, celery, grapes, wheat, and peaches. A lack of confirmatory history
or physical findings on supervised exercise testing is sufficient to rule this out.

Diagnosis
The diagnosis of PVFM relies on four areas: (1) clinical history and phys-
ical examination, (2) pulmonary function testing, (3) measures of oxygena-
tion, and (4) laryngoscopy (Box 1).
Table 2
Differentiating PVFM from asthma during exercise
PVFM Asthma
Female:male 3:1 1:1
Chest tightness  þ
Throat tightness þ 
Stridor þ 
Onset of symptoms after beginning exercise (min) !5 O10
Recovery period (min) 5–10 15–60
Refractory period  þ
Late-phase response  þ
Response to B2 agonists  þ
Nocturnal symptoms  þ
Abbreviation: PVFM, paradoxical vocal fold motion.
Data from Brugman SM, Simons ST. Vocal cord dysfunction: don’t mistake it for asthma.
Physician Sports Med 1998;26:36–4, 66, 67–74, 85.
88 HICKS et al

Box 1. Diagnostic indicators for PVFM

1. Clinical questionnaire
Do you have more trouble getting air in or getting air out?
Do you feel any tightness?
Where is the tightness located? (throat, upper chest, lower
chest)
Do you hear any noises when you breathe in?
Do you have numbness or tingling in your hands, feet, or lips?
Do you feel lightheaded or dizzy?
Have you passed out?
Do symptoms come on rapidly?
Do symptoms go away rapidly?
Do your asthma medicines help?
2. Spirometry
Saw-toothed, irregular, truncated, poorly reproducible
inspiratory flow loops
FEF50/FIF50 >1
Low FEV1 but normal FEV1/FVC ratio
3. Measures of oxygenation (during episodes)
Pulse oximetry >90%
Arterial PO >90 mm Hg
Alveolar-arterial oxygen difference >15 mm Hg
4. Response to treatment
No decrease in symptoms with >4 puffs of inhaled
bronchodilator
Worsening symptoms with inhaled medications
No significant response to escalating asthma treatment,
including inhaled corticosteroids
5. Presence of laryngopharyngeal irritants (gastroesophageal
reflux disease/laryngopharyngeal reflux, postnasal drip)

Clinical history
A careful clinical history may provide valuable information in diagnosing
PVFM [13]. Certain symptoms and signs are more suggestive of PVFM than
asthma or other respiratory conditions that have rapid onset and resolution
(Box 2). Many patients point to or grab their throat when describing their
respiratory symptoms, which may also differentiate upper from lower air-
way dysfunction [42,50]. Patients who have been treated for asthma may re-
port a worsening of their symptoms with metered dose or powder inhalers,
whereas nebulized medications can provide some relief [42]. Typically, pa-
tients are misdiagnosed as having asthma and are treated with intensive
 VOCAL CORD DYSFUNCTION 89

Box 2. Symptoms of PVFM

 Throat tightness
 Upper chest tightness
 Shortness of breath
 Tachypnea
 More difficulty getting air ‘‘in’’ than ‘‘out’’
 Sensation of choking or suffocation
 Stridor
 Neck or chest retractions
 Pallor (without cyanosis)
 Hoarseness or aphonia
 Cough
 Lightheadedness
 Dizziness
 Heaviness of extremities
 Paresthesias of hands, feet, around mouth
 Near or total loss of consciousness

antiasthma medications, including systemic steroids, without improvement

[20,37]. Symptoms of hyperventilation are quite common, occurring in
76% of patients diagnosed with PVFM in one study [52]. The clinical his-
tory may also point to risk factors and triggers for PVFM (Box 3), which
may also help narrow the diagnosis.

Pulmonary function testing

A characteristic finding of nonorganic extrathoracic airway obstruction is
a highly variable pattern of inspiratory flow configurations (Fig. 2) [13,41].

Box 3. Risk factors for PVFM

 Female gender
 Gastroesophageal reflux disease
 Upper airway inflammation (rhinitis, sinusitis, allergies,
recurrent viral infections)
 Prior traumatic event involving breathing (near-drowning,
suffocation, witnessing severe asthma attack, and so forth)
 Playing a wind instrument
 Competitive athletics
 Excessive voice demands (singing, drama, public speaking)
 Severe emotional distress
90 HICKS et al

Fig. 2. Flow volume loop showing forced expiratory flow at 50% of the vital capacity (FEF50)
and forced inspiratory flow at 50% of the vital capacity (FIF50). A normal FEF50/FIF50 is usually
!1 as shown by the line * to #. In PVFM, the FEF50/FIF50 ratio is O1, as shown by the line * to y.

A flattening or truncation of the inspiratory flow loop is often observed dur-

ing an acute PVFM attack [4,41,42] and, in an appropriate clinical context,
can differentiate PVFM from other laryngeal disorders [42]. Sequential in-
spiratory flow volume loops are also nonreproducible and highly variable,
which may be helpful in diagnosis [13,37]. The flow volume loop may also
be abnormal when patients are asymptomatic [20]. Organic laryngeal
obstructions typically present with a fixed truncation or flattening of both
inspiratory and expiratory loops [4]. Patients with asthma or accompanying
closure of the vocal folds during expiration may have blunting of expiratory
rather than inspiratory loops [41,53,54].
A helpful spirometric measure is the ratio between the forced expiratory
flow at 50% of the exhaled vital capacity and the forced inspiratory flow at
50% of the inhaled vital capacity (FEF50/FIF50). Because normal inspira-
tory flow is not limited by intrathoracic pressures like the expiratory flow,
this ratio is typically less than or equal to 1. In PVFM, this ratio often ex-
ceeds 1 and can frequently be estimated by observing the configuration of
the flow-volume (see Fig. 2). This ratio is not typically observed in patients
with both inspiratory and expiratory obstruction [13,55] and may be difficult
to interpret in cases of PVFM with comorbid asthma [13]. Another finding
in PVFM is a decrease of greater than 25% in the maximum inspiratory flow
during histamine inhalation challenge [56].
Spirometry may be difficult to interpret in patients with both PVFM and
asthma. Methacholine and histamine have been used as irritant stimuli to
provoke a PVFM attack separate from airway hyperactivity [17,57]. Patients
with PVFM may exhibit flattening of the inspiratory flow-volume loop and
 VOCAL CORD DYSFUNCTION 91

have a diagnostic laryngoscopy [41]. During bronchial provocation, lower

airways hyperresponsiveness characteristic of asthma is diagnosed if the
forced expiratory volume at 1 second (FEV1) is reduced by 20% or more
when compared with baseline [1]. If there is normal lower airway response
to methacholine challenge (PC20 FEV1 values of greater than 8 mg/mL)
in patients with PVFM, then asthma can be ruled out [41]. In those patients
who have both disorders, the bronchoprovocation is positive and the laryn-
goscopy can be positive or negative depending on whether associated PVFM
is also elicited. Needless to say, the overlap of these two disorders makes the
diagnosis complicated.
If methacholine challenge fails to elicit PVFM in patients with a compel-
ling history, a specific irritant challenge may be indicated [41,42]. Where ex-
ercise is the primary trigger, a graded exercise challenge on a bicycle
ergometer or treadmill is helpful [4,18,30].

Measures of oxygenation
A major differentiating feature of PVFM from other urgent respiratory
disorders is the lack of cyanosis or evidence of low oxygen tensions. Over
75% of PVFM patients reported in the literature had normal oxygenation
as measured by pulse oximetry or arterial blood gas sampling [37]. If a de-
creased PaO2 is seen on arterial blood gases, there is usually a corresponding
increase in PaCO2, indicative of a breath-hold. Conversely, a low PaCO2 can
be seen with an acute or compensated respiratory alkalosis because hyper-
ventilation is frequently seen in conjunction with PVFM. The alveolar-arte-
rial oxygen difference (PAO2-PaO2) calculated from arterial blood gases
confirms normal oxygen delivery and is typically less than 10 mm Hg [1].
This is in contrast to significant acute asthma where PaO2 decreases in direct
proportion to worsening airflow limitation and PAO2-PaO2 is elevated. The
discrepancy between the apparent severe respiratory distress and normal
measures of oxygenation may be a key discriminator for PVFM.

Flexible laryngoscopy
The gold standard for diagnosing PVFM is direct visualization using flex-
ible, transnasal laryngoscopy [13,17,20,29,38]. Paradoxic, inspiratory nar-
rowing of the vocal cords during acute attacks is the most frequent
finding. The controversy over the various patterns of inspiratory closure
has been discussed previously in this article. Newman and colleagues [20] re-
ported diagnostic laryngoscopic findings in 100% of PVFM patients while
symptomatic and 60% of patients while asymptomatic. There is argument
that flexible laryngoscopy is invasive, somewhat uncomfortable, and may in-
terfere with normal laryngeal function or induce PVFM. Until correlates of
laryngeal closure are determined or noninvasive methods of examining the
larynx are discovered, laryngoscopy remains the primary diagnostic tool.
92 HICKS et al

Pulmonary function tests may or may not show significant improvement

(greater than 12% increase in FEV) after inhaled bronchodilators and their
FEV and FEV/forced vital capacity ratio may be in the normal, low, or high
range [42]. In patients with predominantly inspiratory PVFM, the ratio of
forced expiratory to forced inspiratory flows (liters per minute) at 50% of
vital capacity is usually greater than 1 [13,28,42]. This ratio is not typically
observed in patients with both inspiratory and expiratory obstruction
[13,38,42] and may be difficult to interpret in cases of PVFM with comorbid
asthma [13]. Bucca and colleagues [56] demonstrated that a greater than
25% decrease in the maximum inspiratory flow during histamine inhalation
challenge was associated with changes in mid-inspiratory glottic area. Pa-
tients with pure PVFM have normal chest radiographs with no indication
of hyperinflation [41,42]. Most patients with PVFM have normal oxygena-
tion, as measured by pulse oximetry or arterial blood gas sampling [1,13] in
contrast to asthma, where the alveolar-arterial oxygen difference is elevated
[13]. The absence of an increase in PAO2-PaO2 gradient and when eosino-
philia is not present during an acute attack is a vital indicator of PVFM.
Both of these findings occur in greater than 90% of asthmatic attacks [53].
Methacholine or histamine may be used as irritant stimuli to invoke
a PVFM attack separate from airway hyperactivity [17,57]. Patients with
PVFM frequently show evidence of paradoxical vocal fold movement dur-
ing the inspiratory or expiratory phase of breathing during laryngoscopy
following methacholine challenge when compared with patients without
PVFM [41]. During bronchial provocation, the test is considered positive
for bronchial hyperactivity characteristic of asthma if the FEV1 is reduced
by 20% or more when compared with baseline [1]. In many cases there is
normal airway response to methacholine challenge with PC20 FEV, values
of greater than 8 mg/mL in patients with PVFM [42]. A negative bronchial
provocation helps to rule out asthma.
If methacholine challenge fails to elicit PVFM in patients with a compel-
ling history, a specific known irritant challenge may be indicated [41,58].
Provocation with exercise is required to elicit symptoms in those patients
with exercise-induced PVFM [4,18,30].

Etiology
The underpinnings of PVFM are poorly understood and more a matter
of conjecture than of science. It is probably best to categorize them as
a melding of psychologic, neurologic, and physiologic components. There
are several proposed etiologies that merit discussion (Box 4).

Upper airway hyperresponsiveness and exaggerated glottic closure reflex

The upper airway may be rendered hyperresponsive by a number of fac-
tors including viral infections, allergic and nonallergic inflammation,
 VOCAL CORD DYSFUNCTION 93

Box 4. Proposed etiologies of PVFM

A. Upper airway hyperresponsiveness (irritable larynx syndrome
[8]) secondary to
Laryngopharyngeal reflux
Inflammatory upper airway disease (allergic, nonallergic, viral
rhinitis, sinusitis, postnasal drip)
Toxic inhalation (occupational, accidental)
B. Exaggerated glottic closure reflex
C. Autonomic dysfunction of the larynx
D. Primary psychiatric disorder
Symptom amplification
Panic or anxiety disorder
Depression
Conversion disorder (unresolved psychiatric conflicts)
Stress

laryngopharyngeal or gastroesophageal reflux disease (GERD), prior epi-

sodic croup, and toxic inhalation exposures. Sensory receptors, particularly
irritant receptors, densely populate the upper airway and provoke glottic
closure and cough when stimulated [42]. It has been postulated that stimu-
lation of irritants by the olfactory nerve or by sensory afferent nerves in the
upper and lower respiratory tract trigger the glottic closure and other re-
flexes and then paradoxical movement in the vocal folds [41]. After a priming
insult, it is probable that the glottic closure reflex, which is initially adaptive,
becomes activated by nonspecific irritants (smoke, fumes, GERD, and so
forth) to perpetuate the clinical condition called PVFM [42].
Morrison and colleagues [8] defined this as the ‘‘irritable larynx syn-
drome,’’ which they described as ‘‘hyperkinetic laryngeal dysfunction result-
ing from an assorted collection of causes in response to a definitive
triggering stimulus.’’ They postulated that chronic noxious stimulation
could promote hyperfunctional laryngeal symptoms caused by neural plastic
changes in brainstem control centers. Although their theory has not been
rigorously studied, it does parallel other authors’ speculations about upper
airway hyperresponsiveness (UAWH).
Several studies have looked at the association of UAWH and inflamma-
tory or infectious conditions. Bucca and colleagues [59] studied UAWH and
bronchial hyperresponsiveness in 106 nonasthmatic adults with acute exac-
erbations of their chronic sinusitis. A remarkable 86% of them had UAWH
(termed ‘‘extrathoracic airways hyperresponsiveness’’), two thirds of whom
also had bronchial hyperresponsiveness. Following 2 weeks of treatment
with antibiotics and intranasal steroids, 76% of those with UAWH were
resolved and another 21% were improved. There was also significant
94 HICKS et al

resolution and improvement of corresponding bronchial hyperresponsive-

ness in these same patients. They proposed that both UAWH and bronchial
hyperresponsiveness ‘‘may be sustained by reflexes originating in pharyngeal
receptors made hypersensitive by local seeding of the inflammatory process’’
[59]. In a similar study of 37 patients with episodic dyspnea and 9 controls,
Bucca and colleagues [56] found that patients could be classified using his-
tamine challenges as asthma only, asthma with UAWH, and UAWH alone.
Those with UAWH as the only or contributing factor to their dyspnea had
sinusitis. In a larger study by the same authors of 441 patients with asth-
matic symptoms but without a prior diagnosis of asthma, 67% had
UAWH [60]. The influence of concurrent upper respiratory tract diseases
was also assessed and found to be substantial: postnasal drip (55%); phar-
yngitis (55%); laryngitis (40%); and sinusitis (32%). These studies provide
strong support for the theory that laryngeal and pharyngeal bombardment
by inflammatory cells and mediators from the upper airway causes mucosal
damage, irritant sensory stimulation, and the glottic closure and similar re-
flexes that result in UAWH and PVFM. Further study is needed to corrob-
orate and further elucidate this argument.
Inhalational exposures, both occupational and accidental, have also been
associated with PVFM [17,41,61,62]. The role of the upper airway as pri-
mary defender and gas filter places it in a vulnerable position when over-
whelmed by inhalational agents. Precipitants are varied and include
cleaning chemicals, soldering fumes, dust, organic solvents, machining fluid,
chlorine gas fumes, and smoke and particulates from fires. Cough is also
a frequent symptom in these cases. Perkner and colleagues [17] proposed
that chest pain, chest tightness, and GERD symptoms distinguish between
irritant and nonirritant PVFM.
Another important cause of UAWH is GERD, and there are numerous
studies to support this association. Canine models of GERD have indicated
that a pH of 2.5 or less provokes laryngospasm through vagally mediated
mechanisms and the sensitization of mucosal chemoreceptors [63]. Gastric
reflux and upper airway secretions have been implicated in apnea in infants
[64,65]. Likewise, Thatch [64] proposed that chronic or acute upper airway
inflammatory processes may be responsible for hyperresponsive laryngeal
chemoreflexes observed in infantile apnea.
If chronic cough is accepted as another manifestation of UAWH, then
several studies have confirmed the association of GERD and UAWH. Pal-
ombini and colleagues [55] proposed a pathogenic triad of asthma, postnasal
drip syndrome, and GERD as the most common causative factors of
chronic cough. Other authors have reported similar findings [66]. For exam-
ple, Altman and colleagues [42] found allergic rhinitis, cough-variant
asthma, and GERD as the cause of chronic cough in 86% of adult patients.
Vernigan and colleagues [24] reported on GERD and postnasal drip as un-
derlying factors in PVFM. It is likely that chronic cough along with PVFM
are manifestations of irritant-induced UAWH.
 VOCAL CORD DYSFUNCTION 95

Autonomic dysfunction
The role of viruses in inducing lower airways hyperresponsiveness is well
documented [67]. Likewise, there is reason to believe that viruses can also
induce UAWH. Ayres and Gabbott [68] proposed that PVFM may be
caused by autonomic imbalance provoked by an inflammatory process in
the upper airway. Laryngeal afferents, stimulated by inflammatory prod-
ucts, link to more central brain regions in the medulla, midbrain, and the
prefrontal cortex, causing a change in the sympathetic-parasympathetic ner-
vous output. This could lead to a persistent ‘‘autonomic preset’’ whereby
subsequent stimuli (eg, psychologic stressors, changes in ambient tempera-
ture, nonspecific irritants) induce cholinergically dominated reflexes. Such
reflexes result in airway narrowing in the upper airway or in the lower air-
ways in patients with asthma. Although only speculative at this point, such
a theory seems plausible [68].

Psychologic considerations
A number of studies suggest that psychologic factors may be operative in
some cases of PVFM. The first cases of psychologically driven PVFM may
have been those of Dunglison in 1842 who described patients with ‘‘hysteric
croup’’ (described disorders of the laryngeal musculature brought on by hys-
teria) [69]. Numerous other cases were reported in the late 1800s, then not
again until Patterson’s seminal paper of Munchausen’s stridor in 1975
[10]. Because all of the early literature associated this disorder with mental
diseases, it became known by a number of psychiatric names including psy-
chogenic stridor, emotional laryngeal wheezing, laryngoneurosis, and facti-
tious asthma [9–12]. In Christopher and coworkers’ [1] landmark citation in
1985, they reported on five patients with PVFM confirmed by laryngoscopy.
Evaluations on four of the five patients revealed psychiatric disorders rang-
ing from ‘‘mild stress-related exacerbation of symptoms to obsessive-com-
pulsive disorder.’’ Every one of these patients was reported to have
varying degrees of secondary gain from their symptoms and it was suggested
that they all suffered from a conversion disorder [1]. In a review of 48 PVFM
patients in the military, Lacy and McManis [11] found 45 individuals to
have a psychiatric disorder: 52% conversion disorder, 13% major depres-
sion, 10% factitious disorder, 4% obsessive-compulsive disorder, and 4%
adjustment disorder.
Several authors have postulated that the stridor in PVFM represents
‘‘unshed tears’’ or ‘‘symbolic crying’’ [70,71]. This supposition that PVFM
is primarily a conversion disorder (patients unconsciously ‘‘convert’’ unre-
solved psychological conflict into medical illness) has not been supported
in the literature. Neither has the belief that PVFM is a psychic accommoda-
tion to childhood abuse [1,72]. Some specific psychologic conditions have
been linked to PVFM. Anxiety is widely accepted to be comorbid with
96 HICKS et al

respiratory disorders with rates of 34% in adults and 25% in children

[73,74]. Gavin and colleagues [34] reported a higher incidence of anxiety
among adolescents with PVFM than among their age-matched peers with
asthma. Panic disorder and hyperventilation syndrome were more often
seen in PVFM patients as reported by Wamboldt and colleagues [75] in
an uncontrolled study.
Depression as a comorbid or underlying psychopathology has been re-
ported [1,20]. An extensive review of PVFM patients found depression in
only 13% and anxiety in 15%, although the number of patients who under-
went psychologic evaluation was admittedly small [37]. It is also possible
that symptoms of depression and anxiety are a result, rather than a cause,
of chronic respiratory illness [4,17,22].
A final psychologic cofactor with PVFM is stress. Certainly, other
chronic medical problems are known to be influenced by emotional stresses
including irritable bowel syndrome, migraine headaches, chronic abdominal
pain, and coronary artery disease. An estimated 20% of PVFM attacks are
triggered by stress in the general population and an indeterminate number
of soldiers have experienced PVFM, especially as a reaction to combat
[11,37]. Additionally, the achievement-oriented, competitive adolescents in
whom PVFM is often seen corroborate the stress-PVFM association [13,76].

Treatment of paradoxical vocal fold motion

Treatment for PVFM requires a multidisciplinary approach and is guided
by the comorbidities present. The team may include the primary care phy-
sician, pulmonologist, allergist, otolaryngologist, gastroenterologist, neurol-
ogist, psychiatrist or psychologist, speech-language pathologist, athletic
coach, or athletic trainer [5,42,77]. Medical intervention involves careful
and compassionate disclosure of the diagnosis. Patient education is an espe-
cially important component of treatment. Describing normal laryngeal
physiology and the paradoxical pattern of the vocal folds under various en-
vironmental exposures or stress augments the patient’s comprehension and
acceptance of the condition. If the PVFM was diagnosed by laryngoscopy,
viewing the videotape or DVD further enhances understanding and accep-
tance and allows the patient to visualize overcoming the laryngeal obstruc-
tion with breathing exercises [13].
Termination of unnecessary medications may be indicated for those pa-
tients misdiagnosed with asthma [1,22,38]. This should be done carefully,
however, under medical supervision if underlying airway hyperactivity is
suspected [38]. Medications can generally be tapered in those individuals
with overtreated coexisting asthma [53]. Pharmacologic treatment and life-
style modifications may be necessary when airway irritants, such as gastro-
esophageal reflux, laryngopharyngeal reflux, allergic and nonallergic
rhinitis, and sinusitis, are identified [22].
 VOCAL CORD DYSFUNCTION 97

Acute management
The acute management of PVFM requires a confirmed diagnosis and
treatment should be directed toward relieving the airway obstruction [38].
The first step is to reassure the patient that the condition is benign and
that their oxygen levels are normal despite the intense dyspnea, while calmly
validating their fears [2,13]. Morris and coworkers [38] found ample evi-
dence of the effectiveness of relieving acute airway symptoms with reassur-
ance alone. Various nonspeech tasks optimize a wide-open airway and
possibly abort PVFM attacks and include panting, sniffing, pursed lip
breathing on exhalation, and nasal inhalation [21,54,78,79]. Heliox is a mix-
ture of oxygen and helium in ratios of 80:20, 70:30, and 60:40 (helium to ox-
ygen) [80] that has been found to be dramatically effective in relieving acute
presentations of PVFM [1,28,80–82] but not in all cases [81,83]. Heliox takes
advantage of the lower density of helium compared with nitrogen and allows
oxygen to flow through occluded large airways by producing less turbulent
flow, hence decreasing the work of breathing [38,80]. As a therapeutic inter-
vention, heliox does not relax the vocal folds, but relaxes the patient by de-
creasing the work of breathing, which then leads to relaxation of the vocal
folds. In severe cases, sedation can be used because symptoms nearly always
disappear with sleep or anxiolysis [13]. The use of benzodiazepines can be
effective in terminating PVFM episodes in patients presenting with acute
symptoms [38]. A more invasive and least used treatment approach involves
intralaryngeal injection of botulinum toxin. Botulinum toxin type A acts at
nerve endings to prevent release of acetylcholine, resulting in chemical de-
nervation, which paralyzes the vocal fold in the abducted (open) position
[6,13,38]. Although this technique has been successful in treating adductor
laryngeal breathing dystonia and spasmodic dystonia [13,22], it is infre-
quently used in the treatment of PVFM [38]. It should only be considered
for the individual with severe protracted PVFM who does not respond to
other treatment and for whom intubation or tracheostomy presents as the
only option [6,13,84].

Chronic management
Speech therapy is regarded as the primary therapy for PVFM and is
considered by some physicians to be the cornerstone of treatment
[4,11,13,20,25,28,29,53]. Speech therapists and vocal pathologists play an
important role in long-term management of PVFM by providing respiratory
retraining; assessment and diagnostic input; patient education; supportive
counseling; management and suppression of laryngeal abusive behaviors
(ie, cough and throat clearing); voice therapy; and desensitization to specific
irritants [22,25,41]. Patients may also benefit from psychotherapy or psycho-
logic counseling and this is frequently used in conjunction with speech ther-
apy [38]. Psychotherapeutic intervention in PVFM lacks systematic study
98 HICKS et al

[13,22,38], but may be warranted in some PVFM cases and might range
from assisting patients with stress management to coping with underlying
psychopathology [22,85]. The use of surface electromyography biofeedback
and hypnosis have been found to be effective measures in some adolescents
with PVFM [85,86].

Speech-language pathology assessment

Assessment should begin with a comprehensive patient interview focusing
on the patient’s knowledge of his or her symptoms and reason for referral.
Many patients are unaware that speech-language pathologists specialize in
diseases and disorders of the larynx, including upper airway obstruction
and respiration. A careful and compassionate patient interview helps to es-
tablish rapport and trust between the patient and clinician [77]. Discrepant,
inconsistent, or unrealized but pertinent information can emerge from this
assessment [22]. The initial case history should also determine previously di-
agnosed or suspected respiratory disease; the patient’s knowledge of triggers
and symptoms; what the patient is currently doing to resolve his or her
symptoms; psychosocial aspects of the disorder (ie, anxiety or panic); effec-
tiveness of inhalers (when prescribed); changes in vocal quality; changes in
swallowing; existence of laryngeal abusive behaviors; presence of laryngo-
pharyngeal irritants (ie, postnasal drip, GERD, laryngopharyngeal reflux);
and any contribution of the patient’s lifestyle to the disorder (ie, hydration,
breathing pattern, vocal habits). The initial assessment should prompt any
referrals to physicians or counselors if indicated.
The patient should be provided education on normal laryngeal anatomy
and physiology as it relates to breathing, vocalizing, swallowing, coughing,
clearing, breath holding, and PVFM, and the paradoxical movement of the
vocal folds during PVFM attacks. Knowledge of normal and abnormal
physiology empowers the patient to accept and gain control over the
disorder.

Speech-language pathology treatment

Treatment provided by the speech-language pathologists at the National
Jewish Medical and Research Center is outlined next. It cannot be empha-
sized enough that treatment should be tailored to the specific needs of the
patient and any one given treatment may not be helpful or sufficient.
Patients are provided education on the role of laryngeal abusive behav-
iors (ie, cough and throat clearing) in PVFM and the rationale for pre-
vention or minimization of these behaviors. Patients are provided
demonstration of various cough suppression and throat clearing elimination
techniques and are provided ample practice for appropriate return demon-
stration. They are then provided education on what is believed to be hyper-
sensitivity in the larynx and hyperreaction of the protective nature of the
vocal folds that occurs with PVFM. The patients are taught various
 VOCAL CORD DYSFUNCTION 99

breathing techniques that are intended to provide immediate control or

quick release over paradoxical movement in the vocal folds. The following
techniques were developed by voice pathologist Fran Lowry, a revered col-
league at the authors’ facility. (1) The patient is cued to lower their shoul-
ders and place their hand on their mid-abdomen, which supports
abdominal breathing and decreases upper body tension. (2) The patient is
instructed to inhale quickly through the nose or the mouth for approxi-
mately 1 second. Patients are instructed to use whichever method of inhala-
tion feels best. Many patients have coexisting sinus disease and cannot
breathe in through their noses or sniff secretions back into their throats trig-
gering coughing or clearing. Sniffing in through the nose is noisy, so many
patients prefer inhalation through the mouth. This inhalation technique as-
sists with a forced abduction of the vocal folds. (3) Patients are instructed to
breathe out through tightly pursed lips for 2 to 3 seconds. This pursed lip
breathing technique creates a pressure behind the lips and through the phar-
ynx that forcibly abducts the vocal folds. The timing of this technique is im-
portant in that breathing in too long forces a longer exhalation, which may
create tension rather than release tension. The patients should be exhaling
what they inhale.
These techniques are then applied to symptom and trigger recognition,
which allows the patient to prevent or control PVFM attacks at their first
onset and during exposure to known triggers, the caveat being that aware-
ness of initial onset of symptoms and trigger identification precedes initia-
tion of these techniques. These techniques can provide immediate release
of the vocal folds and decrease anxiety and panic that often accompanies at-
tacks. Many patients can prevent or control their attacks during the first
visit. Patients are encouraged to practice five repetitions of this technique,
20 times daily when asymptomatic and at the first onset of difficulty. This
not only assists with laryngeal relaxation and retraining, but ensures an au-
tomatic response used by the patient during times of need. These techniques
are frequently tailored or tweaked to meet the individual needs of patients.
Patients who have a tendency toward hyperventilation or who have signifi-
cant anxiety or panic are instructed on controlled breathing exercises. These
exercises focus on a more controlled pursed lip breathing pattern using ab-
dominal support with focus directed at relaxation.
The quick-release techniques are also used for desensitization to specific
irritants and prevention or control during specific exercise triggers. Specific
irritant challenges are extremely beneficial because patients are taught con-
trol over and can frequently prevent episodes through progressive desensiti-
zation. Exercise challenges are provided for cycling, basketball, soccer,
swimming, and running. All techniques and skills taught during these chal-
lenges are tailored toward individual requirements. The setting should re-
semble the environment where their symptoms are triggered (ie, indoors
versus outdoors). Many athletes tax their bodies to physiologic limits and
beyond. Care is directed at relieving upper and lower body tension and
100 HICKS et al

any maladaptive patterns (ie, shallow breathing, posture, breath-holding)

during their challenges. Patients are taught paced breathing techniques us-
ing abdominal support with attention toward awareness of initial onset of
their symptoms. Patients use the quick-release techniques at initial onset
of their symptoms at their current pace. If symptoms do not resolve at
that pace, they back off until they can be resolved. Once symptoms subside,
patients can resume the faster pace. Pacing skills are an important aspect in
exercise challenges. Awareness of initial symptom onset ensures quick re-
solve and patients progress toward elimination or control of their
symptoms.

Summary
It is reasonable to suggest that there are subgroups of PVFM and that
one modality may not be sufficient in diagnosis or treatment. At the very
least, there is a need to come together as health care professionals in termi-
nology. There is a lack of sufficient knowledge regarding the relationship be-
tween psychologic and physiologic aspects of PVFM. Knowledge is needed
regarding laryngeal sensitivity and its role in this perplexing disorder. Fur-
ther research in treatment modalities is significantly needed. Prospective and
systematic study across disciplines and institutions is imperative.

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