Affiliations: University of Massachusetts Medical School
Correspondence to: Gregory J. Gallivan, MD, FCCP,
Associate Professor of Clinical Surgery, 299 Carew St, Suite 404,
Springfield, MA 01104-2361; e-mail: email@example.com
Maillard and coworkers (September 2000)1
are to be commended for bringing to the readership of CHEST
the concepts of paradoxical vocal cord movement (PVCM) and
intralaryngeal injection of botulinum toxin type A in the intensive
care setting. Their statements that identification remains difficult,
and that use of inhaled corticosteroids, IV injected sedatives, and
speech therapy or psychotherapy cannot be used efficiently during the
acute presentation prompt other viewpoints.
The terms vocal folds and vocal cords are
synonymous, as are the terms paradoxical vocal fold movement
(PVFM) and episodic paroxysmal laryngospasm (EPL). The
choking, stridor, and wheezing in this condition occur primarily on
inhalation, rather than on exhalation, differentiating it from the
asthma it often mimics. While the problem sometimes involves the entire
respiratory cycle, the patient will often point to the larynx as the
site of difficulty. Auscultatory differentiation of inspiratory from
expiratory stridor is useful as are chest and soft-tissue neck
The two pathognomonic diagnostic criteria that need to be assessed
during an acute presentation are strobovideolaryngoscopy and pulmonary
function testing. There is a classic pattern of inspiratory adduction
of the anterior two thirds of the vocal folds, with a posterior
diamond-shaped glottic chink or gap and attenuation of the inspiratory
portion of the flow-volume loops.2Panting, sniffing, and
encouraging breath holding may release laryngospasm and be effective
Sedating such patients may cloud the sensorium and precipitate acute
respiratory acidosis. Inhaled corticosteroids are often irritative to
the larynx and should be withheld. Should syncope occur in patients not
subjected to invasive interventions, it will automatically result in an
open airway. Once there has been misdiagnosis and mistreatment with
endotracheal intubation and tracheostomy, acute and chronic glottic
changes exacerbating upper airway obstruction occur.4,5
Most of these patients have a tremendous emotional, psychological, and
stress burden, while a small subgroup may have laryngeal and
respiratory true dystonias. It is essential to acutely empower the
patient with breathing techniques and to intervene with specific
speech/language pathology therapy and noninsight
psychotherapy.2–3 The presence of other dystonias and a
clinical response to empiric botulinum toxin therapy may distinguish
those PVCM/PVFM/EPL patients who primarily have a dystonic rather than
a psychogenic etiology.3
Recognition of this entity is critical to appropriate medical and
behavioral management of these syndromes, avoiding unnecessary
polypharmacotherapy, emergency department and inpatient
hospitalizations, endotracheal intubations, tracheostomies, and the
creation of unnecessary comorbidities.3
We have read with interest the comments by Dr. Gallivan about
our article in the September 2000 issue of CHEST. We
essentially agree with his statements. However, we wish to emphasize
the extremely variable severity of clinical presentation in patients
with paradoxical vocal cord movement (PVCM). In the patient described
in our case report, well-established techniques of speech therapy and
psychotherapy could not be used efficiently during the acute
presentation as they are in other patients. In this case, acute
respiratory acidosis was present since the arrival of the patient to
the hospital before the administration of IV sedatives. We believe that
the acute effects of hypercapnia as well as the extreme anxiety of the
patient did not allow the implementation of these therapeutic
approaches. Only a small subset of patients with PVCM displays such a
severe clinical presentation. It is precisely in this group of patients
that unnecessary endotracheal intubations or tracheostomies are likely
to be performed. We think that intralaryngeal injection of botulinum
toxin type A in such patients might be a bridge towards increased
stability and towards the later use of behavioral and psychological
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