Vocal Cord Dysfunction: Don't Mistake It for Asthma

Susan M. Brugman, MD; Stephen M. Simons, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 5 - May 98

In Brief: Vocal cord dysfunction (VCD), with its symptoms of stridor, air hunger, and chest or throat tightness, occurs primarily in active adolescents and young adults and may mimic exercise-induced asthma. Suspicions of VCD will be borne out by a mostly inspiratory stridor, abrupt onset and resolution of symptoms, an unpredictable symptom pattern, and the failure of usual asthma medications to resolve attacks. Laryngoscopy during acute symptoms is the definitive diagnostic tool. Panting can often stop an attack, and preventive treatment consists of patient education, speech therapy, and, when needed, psychological measures.

High-pitched wheezing is common at competitive events. Trained personnel, therefore, are likely to be on the alert for the characteristic breath sounds of exercise-induced asthma (EIA) so that prompt intervention can avert respiratory failure. But some of these episodes may not be asthma at all.

A variety of upper-airway obstructions can produce a high-pitched inspiratory sound that is easily mistaken for the wheezing of asthma. The cause might be the aspiration of a foreign body such as an insect. Other possibilities include exercise-induced anaphylaxis (a rare phenomenon) and poor-performance stridor, the factitious simulation of an asthma attack that diverts attention from substandard performance. It is perhaps more likely that the respiratory stridor and distress represent vocal cord dysfunction (VCD), a frequently unrecognized medical condition.

Mistaking VCD for asthma has resulted in significant unnecessary morbidity, including intubation (1-4), tracheostomy (5-8), high-dose corticosteroid use with attendant adverse effects (9,10), multiple hospitalizations (10,11), and long-term psychological and behavioral dysfunction (1,12,13). Among active patients, suboptimal performance and discontinuation of sports are unfortunate additional consequences of misdiagnosis.

VCD is operationally defined as the paradoxical closure or adduction of the vocal cords occurring during inspiration, when they are normally open. This maladaptive motion causes partial and sometimes severe airflow obstruction. Symptoms of VCD include sensations of throat tightness, air hunger and suffocation, and literal choking. Often, inspiratory stridor is heard. Coughing and hoarseness may or may not be present.

Patients Often Young, Female

VCD has been reported in ages 9 to 43, but mostly occurs in adolescents and young adults (table 1). Although there is a strong female preponderance (14), males constitute one third of adolescent patients with VCD (15) and a similar percentage of the 32 reported cases among athletes (5,6,16-30).

Table 1. Exercise-Induced Vocal Cord Dysfunction in Athletes—Literature Review (5,6,16-30)
Years reviewed	1983-1996
Number of articles	17
Number of subjects	32
Male-to-female ratio	12/20
Median age of subjects (yr)	16
Age range of subjects (yr)	9-43
Mean duration of symptoms (yr)	2.4
Range of duration of symptoms (yr)	0.2-13

The incidence of VCD in the population at large is unknown. However, among adult patients referred to a tertiary care facility with what was thought to be intractable asthma, VCD was the sole diagnosis in 10% and comorbid with asthma in an additional 30% (9). In 84 adolescents at the same center, 14% (12) had VCD and comorbid asthma (31). Other investigators have found a prevalence of approximately 2.5% among adults presenting with suspected asthma or exacerbation of chronic obstructive pulmonary disease (32,33).

Studies regarding the incidence of VCD among athletes are lacking. Evidence suggests that it may occur in approximately 3% of intercollegiate athletes who have a history of exercise-induced respiratory distress: A study (34) of 983 athletes with suspected EIA revealed a subgroup who, on exercise provocation, had significant symptoms but none of the pulmonary function changes of asthma.

There is no sport-specific predilection for VCD. It has been observed in skiing, swimming, track and cross-country, figure skating, boxing, wrestling, soccer, basketball, softball, football, baseball, racquetball, and tae kwon do.

Important Diagnostic Steps

Diagnosing vocal cord dysfunction requires a high index of suspicion along with a careful history, physical examination, and, if possible, direct fiberoptic laryngoscopy and pulmonary function evaluation while the patient is symptomatic.

History. Any active patient who has exercise-induced respiratory distress should be asked specific questions regarding the upper airway (table 2). Such information will help to differentiate VCD from EIA even when the two are concurrent (table 3).

Table 2. Questions for Active Patients if Vocal Cord Dysfunction Is Suspected Do you have more trouble breathing in than breathing out? Do you experience throat tightness? Do you have a sensation of choking or suffocation? Do you have hoarseness? Do you make a breathing-in noise (stridor) when you are having symptoms? How soon after exercise starts do your symptoms begin? How quickly do symptoms subside? Do symptoms recur to the same degree when you resume exercise? Do inhaled bronchodilators prevent or abort attacks? Do you experience numbness and/or tingling in your hands or feet or around your mouth with attacks? Do symptoms ever occur during sleep? Do you routinely experience nasal symptoms (eg, postnasal drip, nasal congestion, runny nose, sneezing)?

Clinical features. Pertinent features of VCD triggered by exercise include an abrupt onset and equally abrupt resolution of symptoms (see "Vocal Cord Dysfunction in a Teenage Girl," below). The pattern of VCD symptoms is unpredictable and not readily reproducible at similar levels of intensity. In contrast, EIA typically occurs after 6 to 12 minutes of high-intensity exertion or after exercise has ceased and, without treatment, lasts for approximately 60 minutes (35).

Table 3. Features of Vocal Cord Dysfunction (VCD) and Exercise-Induced Asthma (EIA) Compared
Feature	VCD	EIA
Female preponderance	+	-
Chest tightness	+/-	+
Throat tightness	+	-
Stridor	+	-
Usual onset of symptoms after beginning exercise (min)	<5*	>5-10
Recovery period (min)	5-10	15-60
Refractory period	-	+
Late-phase response	-	+
Response to beta-agonist	-	+
* Onset can be variable.

In addition, an episode of EIA is usually followed by a refractory period lasting 2 to 4 hours, during which identical exertion levels result in lessened respiratory symptoms. VCD has no such refractory period, and some patients have severe repeat attacks immediately on restarting activity. Inhaled bronchodilators are quite effective in both treating and preventing EIA, but this therapy has little if any benefit to patients who have VCD.

Physical examination. The physical examination is usually normal when patients are not experiencing an acute attack. However, evidence of upper-airway inflammation, such as rhinitis, postnasal drip, allergic shiners (swelling and discoloration around the eyes), or pharyngeal erythema may be a clue to allergic rhinitis or sinusitis, gastroesophageal reflux, or other underlying processes that may predispose the larynx to be "twitchy" (36).

When symptomatic, VCD patients usually exhibit anxiety and/or panic, hyperventilation, and suprasternal and neck muscle retraction. Interestingly, they are almost never cyanotic or demonstrably hypoxemic despite their apparently severe respiratory distress.

Inducing symptoms. Because most patients will not experience VCD attacks at the time of evaluation, acute symptoms of VCD need to be provoked in the pulmonary function laboratory. To trigger VCD, a standard, 10-minute, graded treadmill or bicycle exercise regimen similar to that used to provoke asthma should be performed. Extending the duration and intensity of the workout is frequently necessary to accommodate an active patient's high level of fitness and to more closely approximate practice or competition.

Patients are instructed to exercise until they rate the severity of their symptoms at 8 out of a possible 10. The challenge is then stopped, and, with the patient seated, laryngoscopy is performed while the patient is symptomatic. Pulmonary function tests are performed following laryngoscopy.

If symptoms are not provoked by exercise, patients undergo methacholine inhalation testing. Unfortunately, symptoms can be provoked in only 40% to 50% of patients in whom VCD is highly suspected (15,32).

Laryngoscopy. The gold standard for diagnosing VCD is direct laryngoscopy while the patient is symptomatic. This procedure can demonstrate various configurations of inspiratory vocal cord adduction. A primary care physician trained in laryngoscopy could successfully perform this test with a rhinolaryngoscope.

Three main configurations of VCD occur: complete closure, chinking, and periglottic tissue prolapse. Conversely, normal vocal cords allow air to pass through freely at midinspiration (figure 1: not shown).

Complete vocal cord closure (figure 2: not shown) is the most common form of dysfunction. Another configuration, the chinking phenomenon, is the result of adduction of the anterior two-thirds of the vocal cords, by which a posterior diamond-shaped opening is formed (figure 3: not shown). While it is described as pathognomonic in several reports (8,29,37), chinking is not uniformly found (15,20), and its absence does not rule out the diagnosis.

Vocal cord closure during the expiratory as well as the inspiratory phase of respiration (ie, biphasic VCD) may be present in up to 50% of VCD patients during attacks (21) and in 35% of patients who are asymptomatic (1). Although described as a variation of VCD (1,38), vocal cord closure occurring only during expiration is not necessarily abnormal, especially in the presence of asthma. This laryngeal motion, sometimes referred to as auto positive end-expiratory pressure (auto-PEEP), has been well described as a physiologic adaptive mechanism to stent open small airways during lower-airway obstruction (39). Thus, while inspiratory vocal cord closure is clearly paradoxical, expiratory vocal cord closure may be an adaptive physiologic response to bronchial obstruction.

A third variant of VCD involves prolapse of some or all of the periglottic tissues through the glottic opening during inspiration (figure 4: not shown) (27,28,40). Although technically not a vocal cord disorder, this functional form of laryngomalacia occurs during athletic endeavors and resembles in all other respects the paradoxical physiology of VCD.

Pulmonary function evaluation. Spirometry is essential in the evaluation of VCD. Flow-volume loops are generally normal when the patient is asymptomatic but reveal a blunted or flattened inspiratory curve when the patient is symptomatic (figure 5). Inspiratory flow curves that are highly varied from breath to breath also suggest a dynamic upper airway obstruction. In addition, the expiratory portion of the loop may be blunted if there is biphasic closure of the vocal cords, which occurs in some VCD patients, or if there is simultaneous asthma.

Routine measurements of airflow obstruction such as the forced expiratory volume in the first second (FEV1)and peak expiratory flow rate can be normal in VCD if the vocal cords close only on inspiration. However, the ratio of forced expiratory to inspiratory flow at 50% of vital capacity (FEF50/FIF50) is typically reversed from the normal value of less than or equal to 1.0, indicating primary inspiratory obstruction (9,15,41).

When vocal cord closure is biphasic, the FEV1 can be decreased, but this is usually accompanied by a comparable decrease in forced vital capacity (FVC), making the FEV1/FVC ratio normal. This helps to differentiate pure VCD from VCD combined with asthma, in which the FEV1 is reduced to a greater extent than the FVC, thus resulting in a low FEV1/FVC ratio.

Objective measurements of hypoxemia, typically present during acute asthma (42), are seen only rarely in attacks of VCD. Pulse oximetry and arterial oxygen partial pressure (Pao2), typically performed in the emergency department to evaluate the acutely dyspneic patient, are usually normal (8,43,44). If the Pao2 is low, the arterial carbon dioxide partial pressure (Paco2) is proportionately elevated, resembling a breath-hold pattern. The alveolar-arterial oxygen difference (A-aDo2), a measure of oxygen delivery from the lung calculated from the arterial blood gases, is typically normal. The discrepancy between observed levels of respiratory distress and objective measures of oxygenation is very suggestive of VCD.

Radiography. Chest radiographs are not helpful in diagnosing VCD or in helping discriminate it from asthma, since they are usually normal in both entities (15,45). Hyperinflation and peribronchial thickening raise suspicion of asthma but do not rule out concurrent VCD. Airway imaging with fluoroscopy may show paradoxical vocal cord motion, although this technique has only recently been used. While it is noninvasive and readily available, the usefulness of this technique is limited because results must be interpreted by a radiologist in real time, it has not been standardized against laryngoscopy, and it cannot rule out organic lesions of the vocal cords (46,47).

Differential diagnosis. Eliminating other causes of upper-airway obstruction during acute attacks of VCD is usually not difficult (table 4). Most of the disorders do not present the peculiar picture of acute-onset airway compromise that is transient and unassociated with hypoxemia. In addition, other physical findings corroborate suspicions of organic disease. In any event, most of these disorders have a low probability in the active individual.

Table 4. Differential Diagnosis of Vocal Cord Dysfunction (48) Anaphylactic laryngeal edema Bilateral vocal cord paralysis Exercise-induced asthma Extrinsic airway compression Foreign body aspiration Infectious croup Laryngomalacia Myasthenia gravis Neoplasms Spastic dysphonia and other neuropathies Subglottic stenosis Traumatic edema or hemorrhage

It should also be noted that VCD is often misdiagnosed as exercise-induced anaphylaxis. This rare disorder causes angioedema, flushing, pruritus, hypotension, hives, wheezing, and upper-airway obstruction (49). It is seen in individuals who exercise after eating certain foods, especially shellfish, eggs, celery, grapes, wheat, and peaches (50). A lack of confirmatory physical findings should make this diagnosis easy to rule out.

The Psychological Dimension

Emotional stress appears to play a significant role in VCD, although presuming a psychosomatic cause in all individuals has caused needless misunderstanding and distrust between patients and their caregivers. The terms used to describe VCD reveal the pejorative psychological perspective held in the literature: factitious asthma, emotional laryngeal wheezing, laryngoneurosis, pseudoasthma, psychogenic stridor, and Munchausen's stridor, to name a few (3,14,51). Although some of these terms imply a volitional component, it is generally agreed that patients do not manipulate or control their upper-airway obstruction and usually feel helpless and terrified during attacks (8).

VCD has been described in conjunction with several psychiatric disorders, sexual abuse, and wartime military service (8,19,52), and some authors consider the condition a conversion disorder (in which emotional distress or unconscious conflict is converted into a physical symptom) (38,53,54). It must be assumed that there are multiple psychological features of VCD and that no one profile typifies all affected individuals.

It appears that active patients who have VCD often fit the profile of the "type A" individual who is intolerant of personal failure and perceives family pressure to achieve a high level of success (21,29). Psychological testing has identified significantly higher levels of anxiety in adolescent VCD patients as compared with matched asthmatic controls (55). As suggested by McFadden and Zawadski (21), an athlete may subconsciously convert performance anxiety into laryngeal closure and literally "choke" under the pressure of high expectations. Appreciating this psychological dimension to VCD will help to guide treatment.

Acute Management

Some measures found to be helpful in acute attacks include panting, coughing, and breathing against pressure, such as a hand placed on the abdomen (table 5) (14,56). Panting is the most practical on-site maneuver to abort a VCD attack. It activates the posterior cricoarytenoid muscle (the principal abductor of the vocal cords) and widens the glottic aperture to near maximal diameter (56). Although a risk of hyperventilation exists, panting may be quite successful in resynchronizing the respiratory cycle.

Table 5. Treatment Modalities for Vocal Cord Dysfunction Acute Treatment Ask the patient to pant or cough Administer inhaled oxygen or heliox Long-Term Treatment and Prevention Disclose the diagnosis carefully Discontinue unnecessary medications Refer for speech therapy Refer for psychotherapy, if indicated Refer for relaxation therapy/biofeedback

A calm, reassuring manner during an acute attack cannot be overrated. When the diagnosis of VCD is strongly suspected and pulse oximetry is normal, it is helpful to eliminate all unnecessary activity and people from the immediate environment. An empathetic approach that validates the patient's fear while reassuring him or her of normal gas exchange will help to decrease anxiety and allow the attack to subside.

Asking the patient to focus on making a soft "s" sound while exhaling has the dual effect of diverting attention from inhalation while giving auditory feedback on air movement.

Gas inhalation therapy. Providing oxygen for acute VCD can be additionally beneficial. The feeling of air blowing on the face reinforces the idea that the patient is getting enough.

Other therapeutic modalities have also been used for acute VCD. The most common and effective of these is inhalation of "heliox" (a 70% to 80% helium and 20% to 30% oxygen gas mixture) through a mask (57). Because helium is less dense than nitrogen, air flow turbulence across the partially obstructed glottis is reduced. Heliox inhalation for as little as 10 minutes can improve respiratory distress dramatically and halt a VCD attack.

This therapy should be reserved for emergency department use, however, as the gas is expensive and not readily available. Furthermore, a patient's reliance on an extrinsic therapy can be counterproductive to the long-term success of intrinsic therapy such as speech exercises. Since heliox can also alleviate lower-airway obstruction, improvement in respiratory symptoms with its use does not differentiate VCD from asthma (58).

Medications. Sedatives and psychotropic medications, including hydroxyzine hydrochloride, diphenhydramine hydrochloride, desipramine hydrochloride, and diazepam, have been reported to be beneficial in acute episodes (14). It is reasonable to try these drugs acutely in patients who are extremely anxious and in whom other therapies fail to stop the attack. Long-term use is discouraged.

Overcoming Dysfunction

Patient education. The first tenet of treatment is careful and compassionate disclosure of the diagnosis. Communicating to a patient the idea that the symptoms are "all in your head" misrepresents the disorder and rarely helps treatment. Although the precise physiology of VCD remains uncertain, it seems reasonable to tell patients that their breathing process becomes asynchronous under stress and that this results in their vocal cords closing at the very moment they need to open wide to maximize airflow.

Viewing the laryngoscopy videotape with patients augments understanding and acceptance of this concept and allows them to visualize overcoming the laryngeal obstruction with breathing strategies. In addition, it may help to explain the mind-body connection of VCD by drawing parallels with such stress-induced disorders as migraine headaches and irritable colon. In VCD, the larynx, rather than the brain or intestinal tract, becomes the target for stress.

Most active patients are relieved to learn the diagnosis and will cooperate with speech therapy. Those who have trouble accepting the functional nature of VCD are often unable to successfully implement the breathing techniques and may have serious conflicts about competition or other psychological issues. Some patients are angry that their diagnosis was delayed or missed entirely, or that they missed out on athletic opportunities and suffered adverse drug effects. It is often therapeutic for them to express this anger in a supportive environment so they can move on.

If concurrent asthma cannot be documented, all asthma therapy should be discontinued. Patients should be weaned from systemic corticosteroids to allow recovery of the pituitary-adrenal axis, but usual doses of inhaled corticosteroids can be stopped abruptly without ill effect.

Speech therapy. Speech therapy is the cornerstone of treatment for VCD (tables 6 and 7: not shown). With this therapy, patients receive validation of their feelings of helplessness and fear and instruction in ways to remedy dysfunctional breathing patterns.

Three to four sessions with a trained therapist are usually required for a patient to feel confident in the techniques, which must be practiced during asymptomatic periods to ensure success during attacks. Patients should be told that they have to retrain their bodies to breathe under stress and deprogram the maladaptive pattern of VCD. With early institution of breathing exercises and a focus on pacing their exertion, most athletes can resume their previous levels of competition.

Psychological therapies. Most patients who have VCD could benefit from some form of stress reduction. Whether any one modality (eg, autohypnosis, yoga, biofeedback, psychotherapy, pharmacotherapy) is more beneficial than others is not known and has not been systematically studied.

For individuals in whom psychological problems are obvious or speech therapy alone is ineffective, psychological evaluation and treatment are highly recommended. This may include individual and/or family therapy. Drug treatment for given psychological conditions may alleviate some of the patient's stress and improve VCD, although no pharmacotherapy at present specifically targets dysfunction of the vocal cords.

Vocal cord injections. While a literature search reveals no formal studies on the use of botulinum toxin, its injection into the vocal cords reportedly has been effective in VCD (24). Botulinum toxin therapy blocks acetylcholine release at the motor endplate to achieve muscle weakness, and it has been used successfully in treating spasmodic dysphonia (60). Its use in VCD must at present be considered experimental and of questionable value.

Surgery. Surgery has almost no place in the therapeutic armamentarium against VCD. Tracheostomy has been performed in several patients reported in the literature, but the functional nature of VCD was not typically recognized beforehand (5,7,8,61-67). Epiglottoplasty was deemed essential in two children who had exercise-induced laryngomalacia; however, conventional speech and psychotherapeutic modalities were not attempted, and the necessity for this procedure is debatable (27,28).

Synchronizing for Success

For many high-achieving, active adolescents and young adults, the larynx is the end-organ for stress, and acute on-field management to stop the respiratory distress of VCD can be as simple as asking the patient to pant. Most active patients should be able to continue or resume their sport with correct diagnosis, patient education in a supportive environment, speech therapy, and, possibly, psychological therapies. Physician awareness of VCD will place it appropriately in the differential diagnosis of acute respiratory distress in the active patient.

References

1. Newman KB, Mason UG III, Schmaling KB: Clinical features of vocal cord dysfunction. Am J Respir Crit Care Med 1995;152(4 pt 1):1382-1386
2. Niven RM, Roberts T, Pickering CA, et al: Functional upper airways obstruction presenting as asthma. Respir Med 1992;86(6):513-516
3. Corren J, Newman KB: Vocal cord dysfunction mimicking bronchial asthma. Postgrad Med 1992;92(6):153-156
4. Heiser JM, Kahn ML, Schmidt TA: Functional airway obstruction presenting as stridor: a case report and literature review. J Emerg Med 1990;8(3):285-289
5. Myears DW, Martin RJ, Eckert RC, et al: Functional versus organic vocal cord paralysis: rapid diagnosis and decannulation. Laryngoscope 1985;95(10):1235-1237
6. McGrath K, Greenberger P, Zeiss C, et al: Factitious allergic disease: multiple factitious illness and familial Munchausen's stridor. Immunol Allergy Prac 1984;VI(7):41-49
7. Appelblatt NH, Baker SR: Functional upper airway obstruction: a new syndrome. Arch Otolaryngol 1981;107(5):305-306
8. Christopher KL, Wood RP II, Eckert RC, et al: Vocal cord dysfunction presenting as asthma. N Engl J Med 1983;308(26):1566-1570
9. Newman KB, Dubester SN: Vocal cord dysfunction: masquerader of asthma. Semin Respir Crit Care Med 1994;15(2):161-167
10. Sim TC, McClean SP, Lee JL, et al: Functional laryngeal obstruction: a somatization disorder. Am J Med 1990;88(3):293-295
11. Logvinoff MM, Lau KY, Weinstein DB, et al: Episodic stridor in a child secondary to vocal cord dysfunction. Pediatr Pulmonol 1990;9(1):46-48
12. Meltzer EO, Orgel HA, Kemp JP, et al: Vocal cord dysfunction in a child with asthma. J Asthma 1991;28(2):141-145
13. Hayes JP, Nolan MT, Brennan N, et al: Three cases of paradoxical vocal cord adduction followed up over a 10-year period. Chest 1993;104(3):678-680
14. Patterson DL, O'Connell EJ: Vocal cord dysfunction: what have we learned in 150 years? Insights Allergy 1994;9(6):1-12
15. Brugman SM, Howell JH, Mahler JL, et al: A prospective study of the diagnostic features of adolescent vocal cord dysfunction, abstracted. Am J Respir Crit Care Med 1997;155(4):A973
16. Kivity S, Bibi H, Schwarz Y, et al: Variable vocal cord dysfunction presenting as wheezing and exercise-induced asthma. J Asthma 1986;23(5):241-244
17. Liistro G, Stanescu D, Dejonckere P, et al. Exercise-induced laryngospasm of emotional origin. Pediatr Pulmonol 1990;8(1):58-60
18. Balasubramaniam SK, O'Connell EJ, Sachs MI, et al: Recurrent exercise-induced stridor in an adolescent. Ann Allergy 1986;57(4):243,287-288
19. Craig T, Sitz K, Squire E, et al: Vocal cord dysfunction during wartime. Mil Med 1992;157(11):614-616
20. Wood RP II, Jafek BW, Cherniack RM: Laryngeal dysfunction and pulmonary disorder. Otolaryngol Head Neck Surg 1986;94(3):374-378
21. McFadden ER Jr, Zawadski DK: Vocal cord dysfunction masquerading as exercise-induced asthma: a physiologic cause for "choking" during athletic activities. Am J Respir Crit Care Med 1996;153(3):942-947
22. Lakin RC, Metzger WJ, Haughey BH: Upper airway obstruction presenting as exercise-induced asthma. Chest 1984;86(3):499-501
23. Gallivan GJ, Hoffman L, Gallivan KH: Episodic paroxysmal laryngospasm: voice and pulmonary function assessment and management. J Voice 1996;10(1):93-105
24. Garibaldi E, LaBlance G, Hibbett A, et al: Exercise-induced paradoxical vocal cord dysfunction: diagnosis with videostroboscopic endoscopy and treatment with clostridium toxin, abstracted. J Allergy Clin Immunol 1993;91(1 pt 1):200
25. Kissoon N, Kronick JB, Frewen TC: Psychogenic upper airway obstruction. Pediatrics 1988;81(5):714-717
26. Smith MS: Acute psychogenic stridor in an adolescent athlete treated with hypnosis. Pediatrics 1983;72(2):247-248
27. Smith RJ, Bauman NM, Bent JP, et al: Exercise-induced laryngomalacia. Ann Otol Rhinol Laryngol 1995;104(7):537-541
28. Bent JP III, Miller DA, Kim JW, et al: Pediatric exercise-induced laryngomalacia. Ann Otol Rhinol Laryngol 1996;105(3):169-175
29. Landwehr LP, Wood RP II, Blager FB, et al: Vocal cord dysfunction mimicking exercise-induced bronchospasm in adolescents. Pediatrics 1996;98(5):971-974
30. Bittleman DB, Smith RJ, Weiler JM: Abnormal movement of the arytenoid region during exercise presenting as exercise-induced asthma in an adolescent athlete. Chest 1994;106(2):615-616
31. Wamboldt FS, Wamboldt MZ, Gavin LA, et al: Parental criticism and treatment outcome in adolescents hospitalized for severe, chronic asthma. J Psychosom Res 1995;39(8):995-1005
32. Kenn K, Willer G, Bizer C, et al: Prevalence of vocal cord dysfunction in patients with dyspnea: first prospective clinical study, abstracted. Am J Respir Crit Care Med 1997;155(4):A965
33. Ciccolella DE, Brennan KJ, Borbely B, et al: Identification of vocal cord dysfunction (VCD) and other diagnoses in patients admitted to an inner city university hospital asthma center, abstracted. Am J Respir Crit Care Med 1997;155(4):A82
34. Rice SG, Bierman CW, Shapiro GG, et al: Identification of exercise-induced asthma among intercollegiate athletes. Ann Allergy 1985;55(6):790-793
35. Spector SL: Update on exercise-induced asthma. Ann Allergy 1993;71(6):571-577
36. Bucca C, Rolla G, Scappaticci E, et al: Extrathoracic and intrathoracic airway responsiveness in sinusitis. J Allergy Clin Immunol 1995;95(1 pt 1):52-59
37. O'Connell MA, Sklarew PR, Goodman DL: Spectrum of presentation of paradoxical vocal cord motion in ambulatory patients. Ann Allergy Asthma Immunol 1995;74(4):341-344
38. Rodenstein DO, Francis C, Stanescu DC: Emotional laryngeal wheezing: a new syndrome. Am Rev Respir Dis 1983;127(3):354-356
39. Collett PW, Brancatisano T, Engel LA: Changes in the glottic aperture during bronchial asthma. Am Rev Respir Dis 1983;128(4):719-723
40. Nagai A, Kanemura T, Konno K: Abnormal movement of the arytenoid region as a cause of upper airway obstruction. Thorax 1992;47(10):840-841
41. Rotman HH, Liss HP, Weg JG: Diagnosis of upper airway obstruction by pulmonary function testing. Chest 1975;68(6):796-799
42. McFadden ER Jr, Lyons HA: Arterial-blood gas tension in asthma. N Engl J Med 1968;278(19):1027-1032
43. Cormier YF, Camus P, Desmeules MJ: Non-organic acute upper airway obstruction: description and a diagnostic approach. Am Rev Respir Dis 1980;121(1):147-150
44. Collett PW, Brancatisano T, Engel LA: Spasmodic croup in the adult. Am Rev Respir Dis 1983;127(4):500-504
45. Eggleston PA, Ward BH, Pierson WE, et al: Radiographic abnormalities in acute asthma in children. Pediatrics 1974;54(4):442-449
46. Shao W, Chung T, Berdon WE, et al: Fluoroscopic diagnosis of laryngeal asthma (paradoxical vocal cord motion). AJR Am J Roentgenol 1995;165(5):1229-1231
47. Nastasi KJ, Howard DA, Raby RB, et al: Airway fluoroscopic diagnosis of vocal cord dysfunction syndrome. Ann Allergy Asthma Immunol 1997;78(6):586-588
48. Rothrock SG, Perkin R: Stridor: a review, update, and current management recommendations. Pediatr Emergency Med Reports 1996;1(4):29-40
49. Maulitz RM, Pratt DS, Schocket AL: Exercise-induced anaphylactic reaction to shellfish. J Allergy Clin Immunol 1979;63(6):433-434
50. Tilles S, Schocket A, Milgrom H: Exercise-induced anaphylaxis related to specific foods. J Pediatr 1995;127(4):587-589
51. Fields CL, Roy TM, Ossorio MA: Variable vocal cord dysfunction: an asthma variant. South Med J 1992;85(4):422-424
52. Freedman MR, Rosenberg SJ, Schmaling KB: Childhood sexual abuse in patients with paradoxical vocal cord dysfunction. J Nerv Ment Dis 1991;179(5):295-298
53. Kattan M, Ben-Zvi Z: Stridor caused by vocal cord malfunction associated with emotional factors. Clin Pediatr (Phila) 1985;24(3):158-160
54. Selner JC, Staudenmayer H, Koepke JW, et al: Vocal cord dysfunction: the importance of psychologic factors and provocation challenge testing. J Allergy Clin Immunol 1987;79(5):726-733
55. Gavin LA, Wamboldt M, Roesler T, et al: Psychological and family characteristics of adolescents with vocal cord dysfunction. J Asthma 1997; to be published
56. Pitchenik AE: Functional laryngeal obstruction relieved by panting. Chest 1991;100(5):1465-1467
57. Reisner C, Borish L: Heliox therapy for acute vocal cord dysfunction. Chest 1995;108(5):1477
58. Corbridge TC, Hall JB: The assessment and management of adults with status asthmaticus. Am J Respir Crit Care Med 1995;151(5):1296-1316
59. Martin RJ, Blager FB, Gay ML, et al: Paradoxic vocal cord motion in presumed asthmatics. Semin Resp Med 1987;8(4):332-337
60. Whurr R, Lorch M, Fontana H, et al: The use of botulinum toxin in the treatment of adductor spasmodic dysphonia. J Neurol Neurosurg Psychiatry 1993;56(5):526-530
61. Skinner DW, Bradley PJ: Psychogenic stridor. J Laryngol Otol 1989;103(4):383-385
62. Chawla SS, Upadhyay BK, MacDonnell KF: Laryngeal spasm mimicking bronchial asthma. Ann Allergy 1984;53(4):319-321
63. George MK, O'Connell JE, Batch AJ: Paradoxical vocal cord motion: an unusual cause of stridor. J Laryngol Otol 1991;105(4):312-314
64. Tousignant G, Kleiman SJ: Functional stridor diagnosed by the anaesthetist. Can J Anaesth 1992;39(3):286-289
65. Starkman MN, Appelblatt NH: Functional upper airway obstruction: a possible somatization disorder. Psychosomatics 1984;25(4):327-333
66. Kellman RM, Leopold DA: Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 1982;92(1):58-60
67. Hammer G, Schwinn D, Wollman H: Postoperative complications due to paradoxical vocal cord motion. Anesthesiology 1987;66(5):686-687

Vocal Cord Dysfunction in a Teenage Girl

A 13-year-old girl experienced recurrent dyspnea and chest tightness. The first episode had occurred 5 years earlier after a physical education class at school. She had a sudden onset of substernal chest pain, accentuated on inspiration, which resolved on the way to the physician's office. A second episode 2 years later, provoked by running at recess, was similar. Her physician made the diagnosis of exercise-induced asthma, and she was treated with inhaled beta-agonists as needed.

In the 2 months before evaluation, she was having weekly episodes of dyspnea, stridor, tachypnea, a burning sensation in her throat, hoarseness, and chest tightness. She was hospitalized once for presumed croup and asthma and was being treated with multiple asthma medications with limited success. In addition to exercise, she identified fatigue and stress as well as exposure to dust, hair spray, tobacco smoke, and sagebrush as triggers for her attacks.

Pertinent medical history included milk intolerance in infancy and nasal and ocular allergy symptoms in the spring and fall. She also had chronic fatigue, recurrent headaches, and abdominal pain. In addition, multiple extended-family members had early-onset heart disease, her maternal grandmother died of lung cancer, and her own mother sustained a serious injury from chlorine gas inhalation. Stressors in the previous year included a move to a new city, a difficult school adjustment, and poor academic performance. Onset of menses had occurred 2 years prior to the examination.

The patient had been treated with oral corticosteroids briefly and was using chronic inhaled corticosteroids and beta-agonists. In spite of this, she reported two to three episodes of respiratory distress per week. The episodes were transient and frequently resolved when she rested and drank warm water. Her peak expiratory flow rates showed fluctuations between 70 and 400 L/min.

Allergy skin testing was positive to several grasses and one weed, a paranasal sinus series was normal, psychiatric evaluation indicated mild to moderate depression, pulmonary function tests were normal at rest, and a treadmill exercise study revealed a drop in flows and truncation of the inspiratory flow-volume loop after 15 minutes of exercise (figure A). The patient had loud inspiratory stridor with no expiratory wheezing. A saline nebulization was administered, and her clinical condition and pulmonary function abnormalities returned to normal. Asthma could not be proven.

The patient was diagnosed as having vocal cord dysfunction, seasonal allergic rhinitis, and depression. All asthma medications were discontinued, and she was treated with several sessions of speech therapy and intranasal corticosteroids for rhinitis. It was suggested that she pursue psychotherapy, but no pharmacotherapy was recommended.

Dr Brugman is an associate faculty member at the National Jewish Medical and Research Center and an associate professor of pediatrics at the University of Colorado Health Sciences Center, both in Denver. Dr Simons is associate director of the family practice residency at St Joseph's Medical Center in South Bend, Indiana, a fellow of the American College of Sports Medicine, and a charter member of the American Medical Society for Sports Medicine. Address correspondence to Stephen M. Simons, MD, 837 E. Cedar, Ste 125, South Bend, IN 46617; e-mail to simonss@sjcg.org.

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