Wheezing and vocal cord dysfunction mimicking asthma
Abdul H. Bahrainwala, MD,* and Michael R. Simon, MD*†‡
Vocal cord dysfunction (VCD) is a respiratory disorder characterized by paradoxical closure of the vocal cords during the
respiratory cycle leading to obstructive airway symptoms. The
presenting symptoms vary from stridor to wheezing. VCD may
coexist with asthma or masquerade as asthma. Misdiagnosis
of VCD as asthma leads to inappropriate use of systemic
steroids with its adverse effects, frequent emergency department visits, hospitalization, and, rarely, intubation and
tracheostomy. Attenuation of the inspiratory flow volume loop
on spirometry is suggestive of VCD. Laryngoscopic demonstration of the paradoxical vocal cord movements during an
acute attack is the gold standard for the diagnosis of VCD.
Patient education, speech therapy, and psychologic counseling are the therapeutic tools for treatment. Curr Opin Pulm Med
Vocal cord dysfunction (VCD) is not a new entity. The
clinical syndrome suggestive of VCD was described as
early as the mid-1800s [1–3]. Interest in VCD was rekindled by Patterson et al. in 1974 [4]. The recent literature
suggests that VCD is more common than previously
reported as observed in two studies from a single institution of 139 subjects with VCD [5,6].
2001, 7:8–13 © 2001 Lippincott Williams & Wilkins, Inc.
The community prevalence of VCD among children
and adults is unknown. It occurs at all ages, with the
highest rate being among adolescent girls [13,14•].
Otherwise men and women are equally affected [13,15].
Sexual abuse in women may be a predisposing factor
[16,17•]. VCD also seems to be more prevalent in health
care workers [5,9,17•].
*Department of Pediatrics, Children’s Hospital of Michigan; †Department of
Internal Medicine, Wayne State University School of Medicine; ‡John Dingell VA
Medical Center, Detroit, Michigan, USA.
Correspondence to Abdul H. Bahrainwala, MD, Division of Immunology, Allergy
& Rheumatology, Children’s Hospital of Michigan, 3901 Beaubien St., Detroit,
MI 48201, USA; e-mail: [email protected]
Current Opinion in Pulmonary Medicine 2001, 7:8–13
Abbreviation
VCD
vocal cord dysfunction
ISSN 1070–5287 © 2001 Lippincott Williams & Wilkins, Inc.
Vocal cord dysfunction has several synonyms, including
false croup [1], Munchausen stridor [4], psychogenic
stridor [7], hysterical stridor [8], factitious asthma [9],
emotional laryngeal wheezing [10], episodic laryngeal
dyskinesia [11], and paradoxical vocal cord motion [12].
Vocal cord dysfunction may occur by itself or may
coexist with asthma [18]. When this occurs, VCD
substantially contributes to the apparent refractory
nature of the asthma. In a series of 95 patients with
VCD, 53 also had asthma [5]. VCD may also masquerade as exercise-induced asthma [19,20••,21], with VCD
causing symptoms of cough and wheezing with any type
of exercise. Knowledge about the exact incidence of
VCD presenting as exercise-induced asthma is lacking,
but it is suspected to occur in approximately 3% of intercollegiate athletes having exercise-induced asthma, with
no particular sex bias or sport predilection [13].
Pathogenesis
Vocal cord dysfunction may represent a spectrum of
diseases with psychologic (functional) and nonpsychologic causes [11,22]. Neurologic diseases and gastroesophageal reflux with VCD represent some of the
nonpsychologic causes [22]. These are uncommon as
compared with psychologic causes. The pathogenic
mechanism for nonpsychologic VCD is not known.
Psychologic causes range from simple depression to a
subconscious conversion reaction [11,23]. Early literature described VCD as being exclusively due to a
conversion reaction [24]. However, a classic conversion
reaction is not always seen. A conversion reaction is
usually associated with an underlying subconscious
conflict with primary or secondary gains. Primary gain
8
Wheezing and vocal cord dysfunction mimicking asthma Bahrainwala and Simon 9
diverts an internal conflict or need into a psychologic or
physical symptom, thereby avoiding the anxiety that
would occur if that conflict were to surface into awareness. Secondary gain avoids a particular noxious condition, providing support, attention, sympathy, and material gain. It is important to note that VCD with
psychologic causes has its mechanism at the subconscious level. The symptoms cannot be reproduced
voluntarily. Therefore the patient is not malingering.
Evidence of a psychologic or psychiatric cause is seen
only in a subset of functional VCD patients. On numerous occasions there are affected individuals without
evidence of any psychopathology [25•].
The main trigger factor for VCD associated with psychologic causes is emotional stress. Nonpsychogenic trigger
factors include all common asthma triggers such as dust,
cigarette smoke, exercise, occupational or environmental
irritant exposure, and upper respiratory tract infection
[6,19,26]. These trigger factors do not cause VCD but act
to direct the patient’s attention toward the larynx [27].
Clinical features and diagnosis
Symptoms of airway obstruction, such as stridor, cough,
wheezing, and shortness of breath, are the main symptoms of VCD. Rarely, during an attack, a patient may
also experience neck pain, hoarseness, dysphonia, tightness in the throat and chest, and sometimes difficulty
swallowing [26]. The stridor of VCD may or may not be
accompanied by shortness of breath. On occasion,
chronic cough may be the sole manifestation of VCD
[28]. Symptoms of VCD usually, but not always, resolve
during sleep. However, VCD has been reported to cause
nocturnal cough and awakening in four patients [29].
Physical examination findings are usually normal when
the patient is asymptomatic. During symptoms, the
physical examination reveals inspiratory or expiratory
stridor or wheezing. The high-pitched wheezing
produced by the nearly apposed vocal cords is heard all
over the chest and is loudest over the larynx and large
airways. However, the wheezing may not be loudest
over the larynx or larger airways, may not always be high
pitched, and often mimics that of asthma [30]. The
degree of respiratory distress varies from minimal (“la
belle indifference”) [31] to severe. A flexed neck
posture may be assumed during acute attacks [8].
Despite signs and symptoms of upper airway obstruction or bronchospasm, arterial hypoxemia is usually
lacking. Patients have a normal oxygen saturation on
pulse oximetry and normal alveolar-arterial gradient
(< 20 mm Hg) [7,9,31,32]. The carbon dioxide tension is
usually normal, although there are case reports of both
hyper- and hypocapnea with VCD [31]. Chest radiography findings are normal, and unlike asthma, do not
reveal hyperinflation [33,34].
The diagnosis of VCD is not straightforward and
requires a high index of suspicion. Suspicion of VCD
should be raised when the degree of dyspnea is out of
proportion to the clinical signs and when there is little
response to standard treatment [35]. Pulmonary function
studies with recording of the inspiratory and expiratory
flow volume loops and laryngoscopy, both done when
the patient is symptomatic, are required for the diagnosis of VCD. Flow volume loops may be normal when the
patient is asymptomatic. However, 23% of VCD
patients had abnormal inspiratory flow volume loop
when asymptomatic [5]. When the patient is symptomatic, the classic finding on spirometry is the attenuation or flattening (“top hat”) of the inspiratory flow
volume loop [36]. The expiratory flow volume loop may
be blunted if there is an accompanying closure of the
vocal cords during expiration or if there is simultaneous
asthma. There is an increased ratio of the forced expiratory flow to forced inspiratory flow at 50% vital capacity
(VE50/VI50) [36]. Forced expiratory volume in the first
second (FEV1) and peak expiratory flow rate are normal
in inspiratory VCD. The ratio of FEV1 to forced vital
capacity, which is normal in isolated VCD, may be
reduced in VCD combined with asthma [13].
Pronounced variability in spirometric test results may
also be a clue to the diagnosis [36]. The gold standard
for the diagnosis of VCD is the visualization of the paradoxical motion of the vocal cords by laryngoscopy when
the patient is symptomatic. Laryngoscopy may be indirect or direct. Videolaryngoscopy is preferred, as the
patient can observe the anomalous motion of the vocal
cords while it is recorded. Laryngoscopy should be
performed without sedation or general anesthesia, as it
may prevent or resolve the abnormal vocal cord motion
[27]. Nebulized ipratropium bromide may interfere with
vocal cord motion by inhibiting the vagal nerve and
should also be avoided [31]. The characteristic finding
on laryngoscopy during inspiration is the closure of the
anterior two thirds of the glottis by the adduction of the
true vocal cords with the creation of a small diamondshaped chink in the posterior glottis [24]. This finding
has been described as pathognomonic of VCD [28,37].
However, chinking is not always observed and its
absence does not rule out VCD [13]. Other configurations of abnormal vocal cord movements include a
complete closure of the vocal cords [13] and adduction
during both the inspiratory and expiratory phase of
respiration (biphasic VCD) [19,38]. Mild vocal cord
adduction present only during expiration may be physiologically adaptive in asthma, providing positive endexpiratory pressure, and should not be mistaken for
vocal cord dysfunction [19,36].
Laryngoscopy allows assessment of vocal cord movements. Stroboscopy, which involves the addition of
strobe light to laryngoscopy, allows assessment of vocal
10 Asthma
cord vibration. Subtle stroboscopic abnormalities such
as an unstable zero phase, phase asymmetry,
decreased mucosal waves, and decreased amplitude of
vibration are seen during asymptomatic periods [39].
These findings suggest that VCD may be a continuum
of laryngeal instability that is exacerbated during
symptoms. Fluoroscopy combined with high-voltage
filtered radiography can also be used to demonstrate
the paradoxical vocal cord movement, providing a
noninvasive diagnostic alternative to laryngoscopy
[32]. Electromyographic recording of the laryngeal
muscle activity has been shown to be useful in differentiating functional from neurologic laryngeal disorders. It may become an important tool for diagnosis of
VCD in the future [40].
Due to the episodic nature of VCD, it is often difficult
to evaluate the patient and perform pulmonary function
tests and laryngoscopy during an acute attack. Thus,
some authors have suggested provocation challenges to
induce VCD. Provocation stimuli could be exercise
[13], methacholine [6,20•], histamine [6,41], or olfaction [42]. However, due to the functional etiology of
VCD in many patients, paradoxical vocal cord movements may occur only with the appropriate psychologic
milieu. Therefore a negative provocative challenge
does not rule out VCD [13]. In those circumstances, a
strong clinical suspicion with a normal flow volume loop
and normal laryngoscopy findings, when the patient is
asymptomatic, is strongly suggestive of VCD.
Once VCD is diagnosed, it is important to rule out a
pathologic cause. VCD can occur in brain stem compression (eg, Arnold-Chiari malformation, cerebral aqueductal stenosis); upper motor neuron injury (eg, encephalitis) [43]; nuclear or lower motor neuron injury (eg,
amyotrophic lateral sclerosis); or movement disorders
(eg, adductor laryngeal breathing dystonia, myoclonic
disorders, Parkinson-plus syndromes, drug-induced
brain stem dysfunction) [22]. A thorough history accompanied by a detailed neurologic examination will rule
out a neurologic disorder. Strobovideolaryngoscopy,
laryngeal muscle electromyography, or CT scanning or
magnetic resonance imaging of the brain may also be
indicated to rule out neurologic disease.
The association between gastroesophageal reflux and
VCD is controversial. Gastroesophageal reflux is
thought to induce VCD and VCD may aggravate
gastroesophageal reflux by increasing the degree of
negative inspiratory intrathoracic pressure [22].
Gastroesophageal reflux was diagnosed in eight of nine
infants with stridor and paradoxical vocal cord movements [44]. However, the stridor did not resolve with
antireflux treatment [44]. Eight of 22 juvenile patients
with VCD showed interarytenoid pachyderma, which is
typically associated with gastroesophageal reflux [14•].
However, no further investigations were done to prove
the gastroesophageal reflux. The presence of gastroesophageal reflux should be ruled out when VCD occurs
in young infants, older adults, or in the presence of
nocturnal symptoms.
Differential diagnosis
All conditions that cause obstructive airway symptoms
are included in the differential diagnosis of VCD. Two
important differential diagnoses are discussed here:
differentiation of VCD wheeze from asthmatic wheeze
and differentiation of functional VCD from VCD caused
by pathologic disorders.
As discussed earlier, VCD commonly masquerades as
asthma. A strong suspicion of VCD should be aroused
when symptoms are acute in onset in the presence of
psychologic trigger factors and when symptoms are
unresponsive to standard asthma management. It
becomes especially difficult to suspect VCD in a patient
with known asthma who develops VCD, as the wheezing could be easily explained by poor asthma control.
However, VCD should always be suspected in asthmatic
patients whose symptoms do not follow their usual
pattern, when there are changes in symptom character
or severity, or when the patient is unresponsive to previously effective anti-inflammatory medications. Other
clues to diagnosis of VCD during acute episodes are
normal oxygen saturation, normal alveolar-arterial
oxygen gradient, and the absence of hyperinflation on
chest radiography.
Acute management
A calm, reassuring, and sensitive approach is of utmost
importance. Once VCD is suspected and the oxygen
saturation by pulse oximetry is normal, all unnecessary
activity and personnel should be removed from the
patient’s room. Reassurance to the patient of his or her
normal blood oxygen levels and adequate gas exchange
should help decrease the patient’s fears and anxiety
and may allow the attack to subside. Diverting the
patient’s attention from inspiration to expiration by
asking the patient to make a soft “s” sound while
exhaling may be helpful [13]. Panting is a practical onsite maneuver to abort a VCD attack. Panting helps
abduct the vocal cord by activating the cricoarytenoid
muscle, thus widening the glottic aperture and relieving the symptoms [13]. Coughing and breathing against
pressure, such as a hand placed on the abdomen, may
be helpful [13]. Demonstrating to the patient his or her
abnormal vocal cord movements by videolaryngoscopy
and resolution of the abnormal movements by panting
or diaphragmatic breathing can not only help in resolving acute symptoms but also help in the long-term
management by allowing the patient to understand and
accept that breathing strategies can help open the
Wheezing and vocal cord dysfunction mimicking asthma Bahrainwala and Simon 11
glottis. It also demonstrates the patient’s ability to
control his or her own vocal cords.
Oxygen via nasal cannula or face mask at times may
resolve an attack. A mixture of helium:oxygen (70:30 or
80:20 mixture) inhalation can resolve an acute attack
[24,45]. Because helium is less dense than the nitrogen
in the air, helium-oxygen mixture creates less turbulence across the narrowed glottis, thus relieving some of
the perceived sense of dyspnea [40]. Sedatives,
hypnotics, and mask continuous positive airway pressure
also help resolve an acute VCD attack [8,11].
Long-term management
Once the functional nature of VCD is confirmed, the
first step in the long-term management is the disclosure of the functional nature of the diagnosis.
However, statements like “all of this is coming from
your head” are detrimental to the patient-physician
relationship and to future follow-up and management.
It is reasonable, with sympathy and care, to explain to
the patient that the movements of the vocal cords
have become asynchronous under stress. It is of
utmost importance to explain that this process is
occurring at a subconscious level and that the patient
is not to be blamed for its occurrence. The understanding and acceptance of the diagnosis by the
patient and his or her family lay the foundation for
long-term control of VCD. Speech therapy and
psychologic counseling are then the two main treatment modalities.
Speech therapy
Speech therapy trains the patient in diaphragmatic
breathing that diverts the conscious attention away
from the larynx and also helps focus on expiration as
compared with inspiration [24,46]. Wide open throat
breathing, practiced simultaneously with diaphragmatic
breathing, is also helpful. This method is practiced by
having the lips closed, tongue lying flat on the floor of
the mouth behind the incisors, jaw being held in a
gently open position (teeth not clenched), and taking
slow inspiration and expiration using diaphragm
muscles [47]. The patient should be educated in recognizing the symptoms of VCD and taught to apply the
breathing maneuvers to help resolve the symptoms.
Thus speech therapy helps educate the patient in selfcontrol of the vocal cord movement and helps abort the
symptoms as soon as they occur. One session of speech
therapy may be adequate for some patients in learning
the breathing exercise, but some need several sessions
for reinforcement.
Psychologic counseling
Because the root cause of functional VCD is due to an
underlying psychologic conflict, counseling is of utmost
importance in addressing and building up inner
defenses. Speech therapy helps resolve symptoms once
they occur. However, only psychologic counseling can
ultimately treat or prevent future episodes of VCD by
helping resolve the underlying conflict that led to VCD
in the first place [7,24,48]. Speech therapy alone rarely
leads to a cure of VCD, but the combination of the two
has a good success rate. Once the responsible subconscious conflict is resolved or the patient learns to cope
with it, VCD does not reoccur.
Other treatments
An innovative approach using simple anesthetic equipment consisting of a face mask and one-way inspiratoryexpiratory adjustable pressure-limiting valves proved
useful in treating a patient with chronic VCD in whom
speech therapy had failed [49•]. The device is thought
to work by slowing inspiration, which in turn decreases
the airflow across the vocal cord that in turn prevents
the abnormal adduction.
A self-hypnosis technique has been reported to help
treat VCD. Hypnosis induces relaxation and an altered
state of awareness and uses imagery, both specific and
nonspecific, to achieve a state of well-being that helps
resolve the VCD [50]. Biofeedback training also has
been reported to successfully treat VCD [26,51•].
Botulinum type A toxin injection is useful in the treatment of VCD due to adductor laryngeal breathing dystonia [52]. Its use in functional VCD has also been
reported [51•,53]. However, this latter use should still
be considered experimental [13].
Prognosis
Prognosis for VCD is excellent once the patient and the
family understand and accept the diagnosis and undertake speech therapy and psychologic counseling [24,27].
However, in one 10-year follow-up of three patients,
VCD proved to be refractory to speech therapy and
psychologic counseling [32]. It could be argued that
these patients represented the extreme end of the clinical spectrum of VCD [15]. Other long-term studies on
the success of therapy for VCD are not available.
Conclusions
Vocal cord dysfunction is an important, not uncommon,
respiratory disorder that should be included in the
differential diagnosis of refractory asthma. It is most
prevalent in teenage girls. Symptoms of VCD can
easily masquerade as asthma, leading to unnecessary
use of asthma medications with their concomitant side
effects. An abnormal inspiratory flow volume loop is
suggestive, and laryngoscopy showing paradoxical
vocal cord movements is diagnostic of VCD.
Treatment of functional VCD involves speech therapy
12 Asthma
and psychologic counseling. The subsequent prognosis
is excellent.
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••
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