• Evaluation of the glottis at rest for tremor or paradoxical motion during quiet breathing
• Evaluation for pooling of secretions
• Evaluation of glottal closure pattern, vocal fold motion and supraglottic hyperfunction
• Evaluation of agility and fatigability of vocal folds
• Repeat vocal tasks during visualisation and included
– “Sniff” manoeuvre alternates adduction with abduction and will emphasise movement abnormalities such as a subtle paresis
2.4 Vocal Cord Dysfunction
Vocal cord dysfunction (VCD) is characterised by an intermittent extrathoracic airway obstruction mainly during inspiration; the leading symptom is dyspnoea of varying intensity. In Europe, otolaryngologists sometimes use the term VCD incorrectly to describe various voice disorders, such as spastic dysphonia.
The first case report was published in 1974 by Patterson [3] who demonstrated laryngoscopic evidence of VCD, which he named “Munchausen’s stridor”. Since the early studies, there has been increased awareness and interest in understanding this condition.
Until now, there exists no international definition of the disease; due to this, lack of uniformity studies of the incidence, prevalence and risk factors is problematic. There have been no prospective cohort studies to assess the development of new cases, so a true incidence is missing. Several studies, prospective as well as retrospective, reported a prevalence range from 2.5 to 22%. Dyspnoea is the leading symptom. It occurs in children as well and seems more common in females [4].
Regarding the pathogenesis of VCD, a lack of understanding still exists. VCD is often observed associated with GER, laryngopharyngeal reflux (LPR), postnasal drip, asthma and psychological factors [5].
Sensory receptors from the nose to the bronchi exist, detecting irritant stimuli, leading to glottic closure reflexes to protect the lungs from exogenous agents. The laryngopharynx coordinates the four basic physiologic functions of the upper aerodigestive tract: airway protection, breathing, swallowing and phonation. Given the role of the larynx to protect the lungs, it is understandable that chronic postnasal drip as well as GER (retrograde flow of gastric contents into the oesophagus) may lead to increased laryngeal sensitivity and consequent laryngeal hyperresponsiveness [4, 5].
Another discussed mechanism is pathological alterations of olfactory chemoreception. It is hypothesised that olfactory triggers may activate the glottic closure reflex and thereby trigger a VCD.
Other reports suggest that the larynx can become hypersensitive due to a sensory neuropathy. Some patients with VCD may have had primarily a functional disorder of the larynx.
2.4.1 Diagnostic Work Flow in Case of VCD
The typical dyspnoea is characterised by sudden onset, short duration and self-limitation. Most VCD patients will have been given a diagnosis of asthma as described before. Specific attention should be given to detecting the possible evidence of postnasal drip, GER and LPR. The reported presence of allergies, nasal congestion, throat clearing, hoarseness, chronic cough, heartburn, indigestion, throat burning and cough worse is reported. Psychological assessment should include a query regarding any history of psychological distress or any history of abuse [4].
Spirometry in-between attacks is mostly completely normal. During an attack, spirometry can show variable extrathoracic airway obstruction on the flow-volume loop. A maximal inspiratory flow at 50% of forced vital capacity (MIF50)/maximal expiratory flow at 50% of forced vital capacity (MEF50) ratio of <1 suggests a VCD-related problem (Figs. 2.1 and 2.2). The utility of this non-invasive measurement requires validation. Radiographic studies are generally useless in establishing the diagnosis.
Fig. 2.1
Lung function of a VCD case (maximal inspiratory flow at 50% of forced vital capacity (MIF50) (− −)/maximal expiratory flow at 50% of forced vital capacity (MEF50) (−) <1)
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