Steven M. Zeitels, MD, Robert E. Hillman, PhD
Glenn W. Bunting, MS, Traci Vaughn
Reinke's edema (RE) has been associated typically with smoking and sometimes
with vocal abuse, but aspects of the pathophysiology of RE remain unclear.
To gain new insights into phonatory mechanisms associated with RE pathophysiology,
we used an integrated battery of objective vocal function tests to analyze
20 patients (19 women) who underwent phonomicrosurgical resection. Preoperative
stroboscopic examinations demonstrated that the superficial lamina propria
is distended primarily on the superior vocal fold surface. Acoustically,
these individuals have an abnormal I y low average speaking fundamental
frequency (123 Hz),and they generate abnormally high average subglottal
pressures (9.7 cm H20). The presence of elevated aerodynamic driving pressures
reflects difficulties in producing vocal fold vibration that are most likely
the result of mass loading associated with RE, and possibly vocal hyperfunction.
Furthermore, it is hypothesized that in the environment of chronic glottal
mucositis secondary to smoking and reflux, the cephalad force on tile vocal
folds by the subglottal driving pressure contributes to the superior distention
of the superficial lamina propria. Surgical reduction of the volume of
the superficial lamina propria resulted in a significant elevation in fundamental
frequency (154 Hz) and improvement in perturbation measures. In almost
all instances, both the clinician and the patient perceived the voice as
improved. However,these patients continued to generate elevated subglottal
pressure (probably a sign of persistent hyperfunction) that was accompanied
by visually observed supraglottal strain despite the normal-sized vocal
folds. This finding suggests that persistent hyperfunctional vocal behaviors
may contribute to postsurgical RE recurrence if therapeutic strategies
are not instituted to modify such behavior.
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