Page 14 - Škrgat, Sabina, ed. 2023. Severe Asthma Forum - Monitoring and Treatable Traits in Severe Asthma. Koper: University of Primorska Press. Severe Asthma Forum, 2
P. 14
up to 22% of patients with recurrent emer- Pathogenesis of VCD
gency department visits for dyspnea8. Patients
severe asthma forum 2: severe asthma - monitoring and treatable traits in severe asthma with exertional dyspnea are reported to have The etiology of VCD is complex and multi-
VCD in 12%, and patients with exercise-in- factorial. VCD is a functional disorder. In the
duced asthma in 9%. Patients with “refracto- pathogenesis of VCD, there are several patho-
ry asthma” have VCD in 10% alone, 30% of genetic mechanisms. The essential patho-
them have both VCD and asthma36. VCD af- physiology is that of a hyper-functional la-
fects mainly children, young adults, and ath- ryngeal reflex to protect the lower airways 21.
letes, with female predominance (65%: 35%). The sensitivity of the laryngeal sensory recep-
Family history was not proven18. tors is increased and the response of the glot-
tic closure and cough reflex to several triggers
Vocal cord anatomy and function is heightened. It is analogous to bronchial or
nasal hyper-responsiveness. Direct stimula-
The larynx is a valve separating the trachea tion of the sensory nerve endings in the up-
from the upper aero-digestive tract. The glot- per or lower respiratory tract and hyperventi-
tis consists of the true and false vocal cords lation may also lead to glottic narrowing due
and an opening between them, the rima glot- to underlying laryngeal hyper-responsive-
tidis. The principal muscle for vocal cord ab- ness. Another possible etiology of VCD is neu-
duction is the posterior cricoarytenoid (PCA). rological, where autonomic neurophysiologic
Adduction is performed mainly by the lateral balance is altered. Central brain regions such
cricoarytenoid muscle (LCA). During normal as the medulla, midbrain, and prefrontal cor-
inspiration, the glottic opening is controlled tex are polysynaptic linked with the larynx
through the medullary respiratory center, via and the balance can be altered37. The hypoth-
the vagus nerve, which leads to contraction of esis is, that there is an initial inflammatory in-
the PCA muscle and therefore to vocal cord sult, which causes laryngeal hyper-respon-
abduction. During normal expiration there siveness and/or altered autonomic balance,
is a decrease in the tonic activity of the PCA which may be short or persistent. Subsequent
muscle and contraction of the LCA muscle, stimuli (psychological stresses or cold air and
resulting in a 10-40% narrowing of the rima irritants) induce local presynaptic reflexes
glottides, allowing air movement to and out causing airway narrowing18. While the etiol-
of the lungs18. The larynx has the function of ogy of this disease is still unclear, many sup-
protection the lower airway, which is strictly port the theory that VCD has a psychiatric
reflective. The other functions of the larynx basis6,9,25,36.
are respiration and phonation, which are reg-
ulated partially by involuntary brainstem re- Specific triggers of VCD
flexes and may be initiated voluntarily. Pul-
monary protection is mediated by the glottic Specific triggers are not always identified, be-
closure and cough reflexes, to protect the low- cause VCD episodes quickly begin and end.
er airway from noxious inhaled stimuli and VCD triggers are classified into three groups:
aspiration of foreign material during respira- irritants, psychological and emotional, and
tion. The cough reflex is initiated by an ad- exertional6. Initially, one patient has a single
verse stimulus triggering one of the many sen- trigger, then develop multiple triggers, that
sory receptors of the larynx1,9. In VCD there were previously benign. Self-reported triggers
is a brief inappropriate adduction of the vo- are upper respiratory tract infection, occupa-
cal folds during inspiration. This may mani- tional exposures, talking, laughing, singing,
fest with audible inspiratory sounds32. acid reflux, cough, different foods, physi-
cal exertion, exercise, postnasal drip, weath-
er changes, emotional stressors, odors, strong
gency department visits for dyspnea8. Patients
severe asthma forum 2: severe asthma - monitoring and treatable traits in severe asthma with exertional dyspnea are reported to have The etiology of VCD is complex and multi-
VCD in 12%, and patients with exercise-in- factorial. VCD is a functional disorder. In the
duced asthma in 9%. Patients with “refracto- pathogenesis of VCD, there are several patho-
ry asthma” have VCD in 10% alone, 30% of genetic mechanisms. The essential patho-
them have both VCD and asthma36. VCD af- physiology is that of a hyper-functional la-
fects mainly children, young adults, and ath- ryngeal reflex to protect the lower airways 21.
letes, with female predominance (65%: 35%). The sensitivity of the laryngeal sensory recep-
Family history was not proven18. tors is increased and the response of the glot-
tic closure and cough reflex to several triggers
Vocal cord anatomy and function is heightened. It is analogous to bronchial or
nasal hyper-responsiveness. Direct stimula-
The larynx is a valve separating the trachea tion of the sensory nerve endings in the up-
from the upper aero-digestive tract. The glot- per or lower respiratory tract and hyperventi-
tis consists of the true and false vocal cords lation may also lead to glottic narrowing due
and an opening between them, the rima glot- to underlying laryngeal hyper-responsive-
tidis. The principal muscle for vocal cord ab- ness. Another possible etiology of VCD is neu-
duction is the posterior cricoarytenoid (PCA). rological, where autonomic neurophysiologic
Adduction is performed mainly by the lateral balance is altered. Central brain regions such
cricoarytenoid muscle (LCA). During normal as the medulla, midbrain, and prefrontal cor-
inspiration, the glottic opening is controlled tex are polysynaptic linked with the larynx
through the medullary respiratory center, via and the balance can be altered37. The hypoth-
the vagus nerve, which leads to contraction of esis is, that there is an initial inflammatory in-
the PCA muscle and therefore to vocal cord sult, which causes laryngeal hyper-respon-
abduction. During normal expiration there siveness and/or altered autonomic balance,
is a decrease in the tonic activity of the PCA which may be short or persistent. Subsequent
muscle and contraction of the LCA muscle, stimuli (psychological stresses or cold air and
resulting in a 10-40% narrowing of the rima irritants) induce local presynaptic reflexes
glottides, allowing air movement to and out causing airway narrowing18. While the etiol-
of the lungs18. The larynx has the function of ogy of this disease is still unclear, many sup-
protection the lower airway, which is strictly port the theory that VCD has a psychiatric
reflective. The other functions of the larynx basis6,9,25,36.
are respiration and phonation, which are reg-
ulated partially by involuntary brainstem re- Specific triggers of VCD
flexes and may be initiated voluntarily. Pul-
monary protection is mediated by the glottic Specific triggers are not always identified, be-
closure and cough reflexes, to protect the low- cause VCD episodes quickly begin and end.
er airway from noxious inhaled stimuli and VCD triggers are classified into three groups:
aspiration of foreign material during respira- irritants, psychological and emotional, and
tion. The cough reflex is initiated by an ad- exertional6. Initially, one patient has a single
verse stimulus triggering one of the many sen- trigger, then develop multiple triggers, that
sory receptors of the larynx1,9. In VCD there were previously benign. Self-reported triggers
is a brief inappropriate adduction of the vo- are upper respiratory tract infection, occupa-
cal folds during inspiration. This may mani- tional exposures, talking, laughing, singing,
fest with audible inspiratory sounds32. acid reflux, cough, different foods, physi-
cal exertion, exercise, postnasal drip, weath-
er changes, emotional stressors, odors, strong
