Wheezing and vocal cord dysfunction mimicking asthma Abdul H. Bahrainwala, MD,* and Michael R. Simon, MD*

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1 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 2001, 7: Lippincott Williams & Wilkins, Inc. *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; abahrain@pol.net Current Opinion in Pulmonary Medicine 2001, 7:8 13 Abbreviation VCD vocal cord dysfunction ISSN Lippincott Williams & Wilkins, Inc. 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]. 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]. 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 ]. 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

2 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 (VE 50 /VI 50 ) [36]. Forced expiratory volume in the first second (FEV 1 ) and peak expiratory flow rate are normal in inspiratory VCD. The ratio of FEV 1 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

3 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. 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. 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. 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

4 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

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