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Vocal cord dysfunction: An uncommon cause of stridor
The Journal of Emergency Medicine, Vol. 28, No. 1, pp. 31–33, 2005 Copyright © 2005 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/05 $–see front matter
doi:10.1016/j.jemermed.2004.10.001
Clinical Communications
VOCAL CORD DYSFUNCTION: AN UNCOMMON CAUSE OF STRIDOR Carlo G. Soli,
MD*
and Alan J. Smally,
MD†‡
*Division of Emergency Medicine, The University of Connecticut, Farmington, Connecticut; †Division of Emergency Medicine, Hartford Hospital, Hartford, Connecticut; and ‡Department of Traumatology and Emergency Medicine, University of Connecticut School of Medicine, Hartford, Connecticut Reprint Address: Alan J Smally, MD, Medical Director, Emergency Department, Hartford Hospital, 80 Seymour Street, P.O. Box 5037, Hartford CT 06102-5037
e Abstract—We present a case of vocal cord dysfunction syndrome (VCDS) presenting as acute angioedema of the upper airway. The presentation of this syndrome and its differentiation from other upper airway conditions that require far different and more urgent treatment is discussed. © 2005 Elsevier Inc.
CASE REPORT A 23-year-old woman presented to the Emergency Department (ED) complaining of shortness of breath. She initially felt “anxious” and shortly afterward developed shortness of breath that progressed over an hour. The patient reported similar, less severe episodes in the past associated with hives and itching that resolved spontaneously. The patient also complained of “chest heaviness” but could not elaborate further. She denied dizziness, difficulty swallowing, sore throat, change in voice, recent upper respiratory tract infection, cough, palpitations, fever, chills, sweats, or itching. Her past medical history was significant only for the prior episodes of dyspnea/hives/itching that had been evaluated by both an allergist and otorhinolaryngologist (ENT) with no clear diagnosis. The patient’s medications were oral contraceptives and Fexofenadine as needed for hives and itching. She also had an Albuterol inhaler and an Epinephrine auto-injector at home, both of which she had never used. She had an allergy to cat dander but denied any food allergies such as peanuts, shellfish, or eggs. The patient was college educated and lived with her parents. She was a non-smoker and occasionally drank alcohol. She denied any family history of allergic reactions, asthma, or atopic dermatitis.
e Keywords—laryngeal diseases; voice disorders; vocal cords; angioneurotic edema; immediate hypersensitivity
INTRODUCTION Vocal cord dysfunction syndrome” (VCDS) is a respiratory disorder characterized by the abnormal adduction of the vocal cords upon inspiration, expiration, or both, leading to a diverse array of acute obstructive airway signs and symptoms. Although it was previously thought to be an uncommon disorder, recent literature suggests that it is relatively common (1,2). Although more frequently misdiagnosed as asthma, VCDS also has the potential to masquerade as an acute, life-threatening upper respiratory tract emergency. As such, it is important to raise awareness of this emerging syndrome.
Clinical Communications (Adults) is coordinated by Ron Walls, MD, of Brigham and Women’s Hospital and Harvard University Medical School, Boston, Massachusetts
RECEIVED: 2 June 2003; FINAL ACCEPTED: 14 April 2004
SUBMISSION RECEIVED:
19 March 2004; 31
32
C. G. Soli and A. J. Smally
On physical examination, the patient seemed to be in severe respiratory distress with audible inspiratory stridor. She did not seem toxic and was handling her secretions well. Curiously, between stridorous inspirations she was able to answer questions in full sentences and without any hoarseness in her voice. In fact, her stridor seemed to disappear when she was talking. Her initial vital signs were: temperature 36.2°C (97.1°F), pulse of 100 beats/min, blood pressure of 131/71 mm Hg, respiratory rate of 28 breaths/min, and an O2 saturation of 99% on room air. Head and neck examination revealed moist mucous membranes, no angioedema of the tongue, soft palate, or uvula, and no tracheal deviation. Examination of the heart and lungs revealed good air entry bilaterally with inspiratory stridor transmitted to the lower airways. There were no rales, rhonchi, or expiratory wheezes. Nor were there any murmurs, rubs, or gallops. The rest of the examination was unremarkable including examination of the skin, which did not reveal any cutaneous manifestations of an allergic reaction such as erythema or hives. Because the initial assessment suggested allergic angioedema of the upper airway, the patient was treated immediately with subcutaneous epinephrine and intravenous methylprednisolone succinate, diphenhydramine, and famotidine. In addition, racemic epinephrine was delivered via a nebulizer. Over the next 20 min she had partial resolution of her symptoms but continued to manifest noticeable absence of symptoms during speech and with distraction. For this reason the diagnosis of VCDS was entertained and ENT was consulted. While the patient was still partially symptomatic, direct fiberoptic laryngoscopy revealed the patient’s vocal cords paradoxically adducting during inspiration. Based on this finding the patient was diagnosed with VCDS. She was observed in the ED until her symptoms resolved completely and then discharged home with ENT follow up.
DISCUSSION During normal inspiration, vocal cord abduction occurs, allowing maximum flow of air into the lower airways. VCDS manifests as dyspnea due to paradoxical adduction of the vocal cords during respiration. A number of recent reports describe patients with VCDS presenting as apparent asthma or stridor (2–9). Our patient presented with a more uncommon manifestation of VCDS, symptomatology suggesting acute angioedema of the upper airway. The fact that she reported similar episodes in the past with associated dyspnea, hives, and itching was misleading, however, history of these symptoms may accompany patients with VCDS presenting to the Emergency Department (personal experience, A.J.S.).
Rather than being a specific pathologic process, VCDS is the manifestation of a spectrum of psychological (functional) and non-psychological diseases. Some of the psychological diseases associated with VCDS include depressive and anxiety disorders and personality disorders such as obsessive compulsive disorder (OCD) and borderline personality disorder (BPD) (3,10). It has been postulated that VCDS in these patients is a form of conversion disorder precipitated by stress (4). The main non-psychological diseases associated with VCDS are gastroesophageal reflux disease (GERD), environmental irritant exposure, and asthma. In the first two, direct irritation of the vocal cords by reflux of gastric contents and inhalation of chemical irritants, respectively, may focus the patient’s attention on his or her larynx, thereby predisposing the patient to develop vocal cord dysfunction in times of stress (1,11). The pathogenic mechanism of asthma-associated VCDS is less well understood. Asthmatics may use expiratory glottic narrowing to create auto-PEEP (positive endexpiratory pressure) in an attempt to improve alveolar ventilation. It is possible that this mechanism becomes a learned maneuver that is continued into inspiration causing respiratory distress of its own accord (5). When this happens, VCDS begins to coexist with asthma, producing apparently refractory disease of the lower airways. One study reported that VCDS could be responsible for as many as 40% of cases of treatment-resistant asthma (6). VCDS can also occur as a primary manifestation of one of the other psychological or non-psychological diseases described above. The respiratory signs and symptoms produced can lead to a misdiagnosis of bronchospasm or upper airway obstruction (as in our patient). This results in the inappropriate use of systemic steroids, frequent ED visits, hospitalization, and even unnecessary intubation or tracheostomy. There seem to be several psychosocial elements common to patients with VCDS. The process is most commonly observed in single women aged 20 – 40 years who have difficulty achieving independence of family and who exhibit anxiety, depression, and perfectionism (3). VCDS also seems to be more prevalent in health care workers (7). Given the diverse respiratory symptomatology produced by adduction of the vocal cords at various times during the respiratory cycle, the diagnosis of VCDS is not easy and requires a thoughtful diagnostic approach. Examination of the dyspneic patient should differentiate between abnormal sounds heard in the inspiratory and expiratory phases of respiration. Inspiratory stridor suggests obstruction in the extrathoracic airway, whereas expiratory wheezing most commonly suggests lower airway obstruction or asthma. When auscultation reveals abnormal inspiratory sounds that are interrupted by rel-
Vocal Cord Dysfunction
atively normal speech (an expiratory phase function), VCDS should be considered. This dichotomy is absent in all other conditions producing stridor (supraglottitis, angioedema, thermal injury, tumors, others). If VCDS is suspected, laryngoscopy while the patient is symptomatic is the preferred method of diagnosis. Classically, one will see the anterior two-thirds of the vocal cords adduct during inspiration, creating a posterior opening or “chink” (4). Other configurations of the vocal cords during inspiration or expiration also can be seen, however. One can also perform spirometry testing in symptomatic patients. The classic finding is blunting of the inspiratory flow volume loop, indicating extrathoracic obstruction (2). The expiratory flow volume loop also may be attenuated if there is an accompanying closure of the vocal cords during expiration or if there is simultaneous active asthma (2). There are a multitude of treatment options for VCDS, reflecting the fact that this is not a single disease process and there is no definitive treatment. In the Emergency Department, simply having the patient cough, pant or breathe against abdominal pressure may terminate an acute attack by helping the vocal cords abduct, thus widening the glottis and relieving symptoms (2). Diverting the patient’s attention from inspiration to expiration by asking the patient to make a soft “s” sound while exhaling may be helpful (2). Administering a mixture of 70% helium and 30% oxygen (“heliox”) may also help terminate an acute attack (12). Heliox is less dense than room air, producing less turbulent flow across the narrowed glottis. This reduces airflow noises such as stridor and wheezing, alleviating some of the perceived sense of dyspnea. Other options include supplemental O2, topical lidocaine spray, and sedatives such as Valium (2). A mask device designed to adjust resistance to inspiratory airflow while maintaining minimal resistance to expiratory airflow also has been used with some success (13). Long-term treatment of VCDS involves both speech therapy and psychotherapy. Speech therapy uses breathing exercises to train the patient to reduce the tension of the extrinsic laryngeal musculature and focus the attention away from the larynx. Patients first practice these techniques with a therapist and then use them on their own to abort an attack at the first sign of respiratory distress. Psychotherapy is also an integral part of the long-term treatment due to the functional nature of many cases of VCDS. Psychotherapy helps identify and elim-
33
inate any subconscious internal conflicts that may be at the root of the functional disorder. SUMMARY VCDS is a respiratory disorder characterized by abnormal vocal cord adduction leading to a variety of acute obstructive airway signs and symptoms. It is commonly misdiagnosed as asthma, but can also mimic an acute, life-threatening upper respiratory tract emergency. Recent literature suggests that it is much more common than previously thought. It is associated with a wide spectrum of psychological and non-psychological diseases. The gold standard for diagnosis is fiberoptic laryngoscopy while the patient is symptomatic. ED treatments include having the patient cough, pant, or breathe against abdominal pressure, benzodiazepines, or the use of heliox. Speech therapy and psychotherapy are the mainstays of long-term treatment. REFERENCES 1. Perkner JJ, Finelly KP, Balkissoon R, et al. Irritant associated vocal cord dysfunction. J Occup Environ Med 1998;40:136 – 43. 2. Bahrainwala AH, Simon MR. Wheezing and vocal cord dysfunction mimicking asthma. Curr Opin Pulm Med 2001;7:8 –13. 3. Martin RJ, Blager FB, Gay ML. Paradoxical vocal cord motion in presumed asthmatics. Semin Respir Med 1987;8:332–7. 4. Christopher KL, Wood RP, Eckert C, Blager FB, Raney RA, Souhrada KL. Vocal cord dysfunction presenting as asthma. N Engl J Med 1983;308:1566 –70. 5. Murray DM, Lawler PG. All that wheezes is not asthma. Paradoxical vocal cord movement presenting as severe acute asthma requiring ventilatory support. Anaesthesia 1998;53:1006 –11. 6. Newman KB, Dubester SN. Vocal cord dysfunction: masquerader of asthma. Semin Respir Crit Care Med 1994;15161–7. 7. Newman KB, Mason UG, Schmaling KB. Clinical features of vocal cord dysfunction. Am J Respir Crit Care Med 1995;152: 1382– 6. 8. Dinulos JG, Karas DE, Carey JP, Del Beccaro MA. Paradoxical vocal cord motion presenting as acute stridor. Ann Emerg Med 1997;29:815–7. 9. Heiser JM, Kahn ML, Schmidt TA. Functional airway obstruction presenting as stridor: a case report and literature review. J Emerg Med 1990;8:285–9. 10. Gavin LA, Wamboldt M, Brugman S, Roesler TA, Wamboldt F. Psychological and family characteristics of adolescents with vocal cord dysfunction. J Asthma 1998;35:409 –17. 11. Kellman RM, Leopold DA. Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 1982;92:58 – 60. 12. Weir M. Vocal cord dysfunction mimics asthma and may respond to heliox. Clin Pediatr (Phila) 2002;41:37– 41. 13. Archer GJ, Hoyle JL, McCluskey A. Inspiratory vocal cord dysfunction: a new approach in treatment. Eur Respir J 2000;15: 617– 8.
doi:10.1016/j.jemermed.2004.10.001
Clinical Communications
VOCAL CORD DYSFUNCTION: AN UNCOMMON CAUSE OF STRIDOR Carlo G. Soli,
MD*
and Alan J. Smally,
MD†‡
*Division of Emergency Medicine, The University of Connecticut, Farmington, Connecticut; †Division of Emergency Medicine, Hartford Hospital, Hartford, Connecticut; and ‡Department of Traumatology and Emergency Medicine, University of Connecticut School of Medicine, Hartford, Connecticut Reprint Address: Alan J Smally, MD, Medical Director, Emergency Department, Hartford Hospital, 80 Seymour Street, P.O. Box 5037, Hartford CT 06102-5037
e Abstract—We present a case of vocal cord dysfunction syndrome (VCDS) presenting as acute angioedema of the upper airway. The presentation of this syndrome and its differentiation from other upper airway conditions that require far different and more urgent treatment is discussed. © 2005 Elsevier Inc.
CASE REPORT A 23-year-old woman presented to the Emergency Department (ED) complaining of shortness of breath. She initially felt “anxious” and shortly afterward developed shortness of breath that progressed over an hour. The patient reported similar, less severe episodes in the past associated with hives and itching that resolved spontaneously. The patient also complained of “chest heaviness” but could not elaborate further. She denied dizziness, difficulty swallowing, sore throat, change in voice, recent upper respiratory tract infection, cough, palpitations, fever, chills, sweats, or itching. Her past medical history was significant only for the prior episodes of dyspnea/hives/itching that had been evaluated by both an allergist and otorhinolaryngologist (ENT) with no clear diagnosis. The patient’s medications were oral contraceptives and Fexofenadine as needed for hives and itching. She also had an Albuterol inhaler and an Epinephrine auto-injector at home, both of which she had never used. She had an allergy to cat dander but denied any food allergies such as peanuts, shellfish, or eggs. The patient was college educated and lived with her parents. She was a non-smoker and occasionally drank alcohol. She denied any family history of allergic reactions, asthma, or atopic dermatitis.
e Keywords—laryngeal diseases; voice disorders; vocal cords; angioneurotic edema; immediate hypersensitivity
INTRODUCTION Vocal cord dysfunction syndrome” (VCDS) is a respiratory disorder characterized by the abnormal adduction of the vocal cords upon inspiration, expiration, or both, leading to a diverse array of acute obstructive airway signs and symptoms. Although it was previously thought to be an uncommon disorder, recent literature suggests that it is relatively common (1,2). Although more frequently misdiagnosed as asthma, VCDS also has the potential to masquerade as an acute, life-threatening upper respiratory tract emergency. As such, it is important to raise awareness of this emerging syndrome.
Clinical Communications (Adults) is coordinated by Ron Walls, MD, of Brigham and Women’s Hospital and Harvard University Medical School, Boston, Massachusetts
RECEIVED: 2 June 2003; FINAL ACCEPTED: 14 April 2004
SUBMISSION RECEIVED:
19 March 2004; 31
32
C. G. Soli and A. J. Smally
On physical examination, the patient seemed to be in severe respiratory distress with audible inspiratory stridor. She did not seem toxic and was handling her secretions well. Curiously, between stridorous inspirations she was able to answer questions in full sentences and without any hoarseness in her voice. In fact, her stridor seemed to disappear when she was talking. Her initial vital signs were: temperature 36.2°C (97.1°F), pulse of 100 beats/min, blood pressure of 131/71 mm Hg, respiratory rate of 28 breaths/min, and an O2 saturation of 99% on room air. Head and neck examination revealed moist mucous membranes, no angioedema of the tongue, soft palate, or uvula, and no tracheal deviation. Examination of the heart and lungs revealed good air entry bilaterally with inspiratory stridor transmitted to the lower airways. There were no rales, rhonchi, or expiratory wheezes. Nor were there any murmurs, rubs, or gallops. The rest of the examination was unremarkable including examination of the skin, which did not reveal any cutaneous manifestations of an allergic reaction such as erythema or hives. Because the initial assessment suggested allergic angioedema of the upper airway, the patient was treated immediately with subcutaneous epinephrine and intravenous methylprednisolone succinate, diphenhydramine, and famotidine. In addition, racemic epinephrine was delivered via a nebulizer. Over the next 20 min she had partial resolution of her symptoms but continued to manifest noticeable absence of symptoms during speech and with distraction. For this reason the diagnosis of VCDS was entertained and ENT was consulted. While the patient was still partially symptomatic, direct fiberoptic laryngoscopy revealed the patient’s vocal cords paradoxically adducting during inspiration. Based on this finding the patient was diagnosed with VCDS. She was observed in the ED until her symptoms resolved completely and then discharged home with ENT follow up.
DISCUSSION During normal inspiration, vocal cord abduction occurs, allowing maximum flow of air into the lower airways. VCDS manifests as dyspnea due to paradoxical adduction of the vocal cords during respiration. A number of recent reports describe patients with VCDS presenting as apparent asthma or stridor (2–9). Our patient presented with a more uncommon manifestation of VCDS, symptomatology suggesting acute angioedema of the upper airway. The fact that she reported similar episodes in the past with associated dyspnea, hives, and itching was misleading, however, history of these symptoms may accompany patients with VCDS presenting to the Emergency Department (personal experience, A.J.S.).
Rather than being a specific pathologic process, VCDS is the manifestation of a spectrum of psychological (functional) and non-psychological diseases. Some of the psychological diseases associated with VCDS include depressive and anxiety disorders and personality disorders such as obsessive compulsive disorder (OCD) and borderline personality disorder (BPD) (3,10). It has been postulated that VCDS in these patients is a form of conversion disorder precipitated by stress (4). The main non-psychological diseases associated with VCDS are gastroesophageal reflux disease (GERD), environmental irritant exposure, and asthma. In the first two, direct irritation of the vocal cords by reflux of gastric contents and inhalation of chemical irritants, respectively, may focus the patient’s attention on his or her larynx, thereby predisposing the patient to develop vocal cord dysfunction in times of stress (1,11). The pathogenic mechanism of asthma-associated VCDS is less well understood. Asthmatics may use expiratory glottic narrowing to create auto-PEEP (positive endexpiratory pressure) in an attempt to improve alveolar ventilation. It is possible that this mechanism becomes a learned maneuver that is continued into inspiration causing respiratory distress of its own accord (5). When this happens, VCDS begins to coexist with asthma, producing apparently refractory disease of the lower airways. One study reported that VCDS could be responsible for as many as 40% of cases of treatment-resistant asthma (6). VCDS can also occur as a primary manifestation of one of the other psychological or non-psychological diseases described above. The respiratory signs and symptoms produced can lead to a misdiagnosis of bronchospasm or upper airway obstruction (as in our patient). This results in the inappropriate use of systemic steroids, frequent ED visits, hospitalization, and even unnecessary intubation or tracheostomy. There seem to be several psychosocial elements common to patients with VCDS. The process is most commonly observed in single women aged 20 – 40 years who have difficulty achieving independence of family and who exhibit anxiety, depression, and perfectionism (3). VCDS also seems to be more prevalent in health care workers (7). Given the diverse respiratory symptomatology produced by adduction of the vocal cords at various times during the respiratory cycle, the diagnosis of VCDS is not easy and requires a thoughtful diagnostic approach. Examination of the dyspneic patient should differentiate between abnormal sounds heard in the inspiratory and expiratory phases of respiration. Inspiratory stridor suggests obstruction in the extrathoracic airway, whereas expiratory wheezing most commonly suggests lower airway obstruction or asthma. When auscultation reveals abnormal inspiratory sounds that are interrupted by rel-
Vocal Cord Dysfunction
atively normal speech (an expiratory phase function), VCDS should be considered. This dichotomy is absent in all other conditions producing stridor (supraglottitis, angioedema, thermal injury, tumors, others). If VCDS is suspected, laryngoscopy while the patient is symptomatic is the preferred method of diagnosis. Classically, one will see the anterior two-thirds of the vocal cords adduct during inspiration, creating a posterior opening or “chink” (4). Other configurations of the vocal cords during inspiration or expiration also can be seen, however. One can also perform spirometry testing in symptomatic patients. The classic finding is blunting of the inspiratory flow volume loop, indicating extrathoracic obstruction (2). The expiratory flow volume loop also may be attenuated if there is an accompanying closure of the vocal cords during expiration or if there is simultaneous active asthma (2). There are a multitude of treatment options for VCDS, reflecting the fact that this is not a single disease process and there is no definitive treatment. In the Emergency Department, simply having the patient cough, pant or breathe against abdominal pressure may terminate an acute attack by helping the vocal cords abduct, thus widening the glottis and relieving symptoms (2). Diverting the patient’s attention from inspiration to expiration by asking the patient to make a soft “s” sound while exhaling may be helpful (2). Administering a mixture of 70% helium and 30% oxygen (“heliox”) may also help terminate an acute attack (12). Heliox is less dense than room air, producing less turbulent flow across the narrowed glottis. This reduces airflow noises such as stridor and wheezing, alleviating some of the perceived sense of dyspnea. Other options include supplemental O2, topical lidocaine spray, and sedatives such as Valium (2). A mask device designed to adjust resistance to inspiratory airflow while maintaining minimal resistance to expiratory airflow also has been used with some success (13). Long-term treatment of VCDS involves both speech therapy and psychotherapy. Speech therapy uses breathing exercises to train the patient to reduce the tension of the extrinsic laryngeal musculature and focus the attention away from the larynx. Patients first practice these techniques with a therapist and then use them on their own to abort an attack at the first sign of respiratory distress. Psychotherapy is also an integral part of the long-term treatment due to the functional nature of many cases of VCDS. Psychotherapy helps identify and elim-
33
inate any subconscious internal conflicts that may be at the root of the functional disorder. SUMMARY VCDS is a respiratory disorder characterized by abnormal vocal cord adduction leading to a variety of acute obstructive airway signs and symptoms. It is commonly misdiagnosed as asthma, but can also mimic an acute, life-threatening upper respiratory tract emergency. Recent literature suggests that it is much more common than previously thought. It is associated with a wide spectrum of psychological and non-psychological diseases. The gold standard for diagnosis is fiberoptic laryngoscopy while the patient is symptomatic. ED treatments include having the patient cough, pant, or breathe against abdominal pressure, benzodiazepines, or the use of heliox. Speech therapy and psychotherapy are the mainstays of long-term treatment. REFERENCES 1. Perkner JJ, Finelly KP, Balkissoon R, et al. Irritant associated vocal cord dysfunction. J Occup Environ Med 1998;40:136 – 43. 2. Bahrainwala AH, Simon MR. Wheezing and vocal cord dysfunction mimicking asthma. Curr Opin Pulm Med 2001;7:8 –13. 3. Martin RJ, Blager FB, Gay ML. Paradoxical vocal cord motion in presumed asthmatics. Semin Respir Med 1987;8:332–7. 4. Christopher KL, Wood RP, Eckert C, Blager FB, Raney RA, Souhrada KL. Vocal cord dysfunction presenting as asthma. N Engl J Med 1983;308:1566 –70. 5. Murray DM, Lawler PG. All that wheezes is not asthma. Paradoxical vocal cord movement presenting as severe acute asthma requiring ventilatory support. Anaesthesia 1998;53:1006 –11. 6. Newman KB, Dubester SN. Vocal cord dysfunction: masquerader of asthma. Semin Respir Crit Care Med 1994;15161–7. 7. Newman KB, Mason UG, Schmaling KB. Clinical features of vocal cord dysfunction. Am J Respir Crit Care Med 1995;152: 1382– 6. 8. Dinulos JG, Karas DE, Carey JP, Del Beccaro MA. Paradoxical vocal cord motion presenting as acute stridor. Ann Emerg Med 1997;29:815–7. 9. Heiser JM, Kahn ML, Schmidt TA. Functional airway obstruction presenting as stridor: a case report and literature review. J Emerg Med 1990;8:285–9. 10. Gavin LA, Wamboldt M, Brugman S, Roesler TA, Wamboldt F. Psychological and family characteristics of adolescents with vocal cord dysfunction. J Asthma 1998;35:409 –17. 11. Kellman RM, Leopold DA. Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 1982;92:58 – 60. 12. Weir M. Vocal cord dysfunction mimics asthma and may respond to heliox. Clin Pediatr (Phila) 2002;41:37– 41. 13. Archer GJ, Hoyle JL, McCluskey A. Inspiratory vocal cord dysfunction: a new approach in treatment. Eur Respir J 2000;15: 617– 8.