Now recognized as vocal cord dysfunction (VCD), this syndrome is primarily characterized by paradoxical inspiratory vocal cord adduction and is frequently misdiagnosed and treated as asthma. Initially described in 1842 by Dunglison as 'hysteric croup', VCD was rarely mentioned in the medical literature until 30 years ago.2 In the early 1970s, Patterson and Schatz described a 33-year-old female with 15 hospital admissions for what they termed 'Munchausen's stridor'.3 The first modern series,'Vocal cord dysfunction presenting as asthma', published by Christopher et al. in 1983, reported their comprehensive evaluation of five patients treated for uncontrollable asthma.4 Although infrequently diagnosed prior to the early 1990s, increased awareness and recognition of VCD over the past decade has led to more insight into the various etiologies and treatment of this disorder.Psychiatric or emotional causes,asthma, exercise, airway irritants and gastroesophageal reflux disease (GERD) have all been implicated as a cause of VCD.5,6 An acute presentation of VCD closely resembles an asthma exacerbation with cough, wheezing, and dyspnea but is commonly characterized by the presence of inspiratory stridor. In numerous cases, the diagnosis is repeatedly unrecognized and many patients have been incorrectly treated for asthma for as long as 15 years.7 Understanding and recognizing the overlap between asthma and VCD is crucial to the proper treatment of patients with either disorder.

VCD is referred to by many terms describing a functional airway obstruction associated with predominantly inspiratory vocal cord adduction.

Paradoxical vocal cord (or fold) motion more correctly describes this syndrome, although several other terms, including pseudoasthma, non-organic or functional upper airway obstruction, factitious asthma, spasmodic croup and emotional laryngeal wheezing, have been used.8'14 There is a reported 2:1 female predominance, with 64% female patients and 36% male patients.

Seventy-one per cent of patients are adults and the remaining 29% are adolescents.15,16 The overall incidence of VCD in the general population is not well defined but it is relatively uncommon.A study of 1,025 patients with dyspnea evaluated 63 patients and found an overall 2.8% incidence of patients with VCD.17 A higher prevalence of 12% was noted in a smaller cohort of military patients evaluated for exertional dyspnea.18 Pathogenesis The pathogenesis of VCD is not well understood but is characterized by laryngeal hyper-responsiveness. Both organic (asthma, GERD, irritants, etc.) and non-organic (psychological disorders or emotional stressors) causes can precipitate episodes of VCD and may have different pathophysiology. Bucca et al. evaluated 441 patients with cough, wheeze, or dyspnea without documented asthma or bronchial obstruction and found extrathoracic airway hyper-responsiveness in 67% of patients.19 Other authors suggest that laryngeal hyper- responsiveness from an inflammatory component and altered autonomic balance may lead to an exaggeration and preservation of the laryngeal response.20 The hypothesis in irritant-induced VCD is that direct stimulation of sensory nerve endings in the respiratory tract may initiate local reflexes that lead to paradoxical laryngeal closure.21 The association between VCD and asthma is unclear and lacks sufficient prospective evaluation. The literature is replete with numerous case reports of VCD being misdiagnosed as asthma over long periods of time. Our review of the VCD literature of 1,200 patients found 33% were diagnosed with asthma prior to the correct diagnosis.22 In many instances, patients with VCD required no further asthma therapy after diagnosis and treatment. These reports do not clearly define whether patients had underlying reactive airways disease or, more importantly, whether underlying asthma is a trigger for VCD.The first large case series of 95 patients reported by Newman et al. found that 56% of patients had co-existent asthma based on broncho- provocation testing or peak flow variability.23 O'Connell et al. reported co-existent asthma in 35% of their cohort of 20 VCD patients.24 A study of exertional dyspnea noted that six of 10 patients with VCD also had Vocal Cord Dysfunction and Asthma Colonel Michael J Morris, MD, is Chief of the Department of Hospital Education at Brooke Army Medical Center in San Antonio, Texas, where he serves as affiliate faculty for the Pulmonary Disease/Critical Care Service. He is also Clinical Assistant Professor at the University of Texas Health Science Center at San Antonio. Dr Morris is a fellow of the American College of Physicians and American College of Chest Physicians. He is board-certified in internal medicine, pulmonary disease and critical care medicine.reactive methacholine challenge testing.18 In an emergency room evaluation of asthmatics, Jain et al.
found 10 of 50 patients with laryngoscopic evidence of VCD; 60% of these patients had co-existent asthma based on portable spirometry.25 Etiologies of VCD Numerous other causes of organic VCD have been identified, including exercise, GERD, upper respiratory infections, a variety of airway irritants and other conditions such as intubation,26 sleep,27 and anaphylaxis.28 Exercise is a commonly recognized precipitant of VCD and is reported as the underlying etiology in 18% of patients.22 It was first recognized as a cause of VCD in 1984, when McFadden and Zawadski reported seven elite athletes with a 'choking' sensation during exercise, normal spirometry, and negative bronchoprovocation testing.29 Landwehr et al., in the same year, diagnosed seven adolescent athletes with VCD based on post-exercise flow volume loop (FVL) inspiratory limb flattening.30 Other series have reported similar findings, with 5% noted in athletes, 52% of VCD patients evaluated in military facilities,31 and a series of 20 adolescent athletes all with exercise-induced VCD.32 These VCD patients are usually either elite competitive athletes or active-duty military who exercise regularly.

Irritant-induced VCD is hypothesized to be an accentuation of the glottic closure reflex and that various extrinsic and intrinsic stimuli trigger closure as a protective response.21 Numerous irritants have been implicated as a causative factor in the etiology of VCD and the largest series of 11 patients developed symptoms after exposure to agents such as ammonia, flux fumes, cleaning chemicals, smoke, and odors.33 Although not implicated as a causative factor in every patient, 18% of all VCD patients are reported to have underlying GERD. Powell et al. evaluated 22 adolescent VCD patients and noted posterior laryngeal changes typically seen in GERD.16 Morrison et al. reviewed 39 patients with the diagnosis of 'irritable larynx syndrome'; 25 patients were noted to have laryngospasm (not defined as inspiratory vocal cord adduction) and 92% of patients had the diagnosis of GERD.34 A less well defined trigger for VCD is upper respiratory infection or irritation. It has been suggested that allergic rhinitis with post-nasal drip can also cause upper airway irritation. Brugman reported a total of 213 VCD patients, or 19%, with allergic rhinitis and postnasal drip as a trigger for VCD.35 In 176 patients seen at military tertiary care facilities concomitant rhinosinusitis was noted in 31% of patients.31 Initial reports of VCD emphasized patients' underlying psychological conditions with this disorder.The initial terminology of 'hysteric croup','Munchausen's stridor, and 'emotional laryngeal wheezing' suggested an underlying psychological disorder as the etiology.2,3,14 Early VCD reviews described the condition as young females in the medical profession with significant emotional stress or psychiatric disease. A variety of functional disorders, including depression, sexual abuse, factitious disorder and conversion disorder, are now recognized to be associated with VCD. Newman et al. noted that the majority of their 95 VCD patients had underlying psychiatric disorders. Nine patients had prior psychiatric hospitalizations and 73% had an American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders ' Third Edition (DSM-III) diagnosis.23 A comparison of 12 adolescent VCD patients with controls found eight patients had significant psychiatric diagnoses, including major depression, separation anxiety, overanxious disorder, and dysthymia.36 Lacy and McManis performed a review of 48 VCD cases from the literature over a 30-year period and described 45 cases in which a psychiatric disorder was reported. Fifty-two per cent of patients were diagnosed with a conversion disorder, while other patients had either a major depression, a factitious disorder, obsessive-compulsive disorder, or adjustment disorder. Underlying all these diagnoses was the presence of significant emotional stress.37 Clinical Presentation The clinical presentation of VCD is well described.