Address correspondence and reprint requests to Alison Behrman, PhD, Department of Otolaryngology, The New York Eye
and Ear Infirmary, 310 East 14th Street, New York, NY 10003.
E-mail: abehrman@nyee.com
Journal of Voice, Vol. 17, No. 3, pp. 403410
2003 The Voice Foundation
0892-1997/2003 $30.000
doi:10.1067/S0892-1997(03)00018-3
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ALISON BEHRMAN ET AL
INTRODUCTION
Nonorganic dysphonia is predominantly a diagnosis of exclusion in which voice production is impaired without discernable morphologic or
neurological abnormalities of the larynx. Diagnosis
is confounded by a lack of uniform terminology.
Labels include functional dysphonia,13 muscle
misuse dysphonia,4 muscle tension dysphonia,14
and psychogenic dysphonia.5 The nomenclature is
derived from a complexity of diagnostic classifications that are based primarily on endoscopic signs of
glottic and supraglottic postures.15 Other diagnostic
signs are also frequently included, such as specific vocal qualities, voice use patterns, or psychogenic factors. However, many of these diagnostic
features overlap more than one category, adding additional complexity to classification. Cooccurring organic lesions are often included, either
as a precipitating cause of the functional component2
or as a reactive inflammatory response,14 further
confounding application of these classification systems to diagnosis.
Two vocal tract postures commonly identified as
diagnostic hallmarks of nonorganic dysphonia are
anteriorposterior compression of the supraglottis
and medial compression of the ventricular folds.
These postures define the two types of primary
muscle tension dysphonia proposed by Rosen and
Murry,3 two of the six types of muscle misuse disorder identified by Morrison and Rammage,4 three of
the six features of vocal hyperfunction identified by
Van Lawrence,6 and the main types of supraglottic
laryngeal postures of muscle tension dysphonia described by Koufman and Blalock.2 Despite the apparent widespread acceptance of these postures as
endoscopic signs of vocal dysfunction, there is little
empirical data to support their diagnostic utility.
Sama et al7 assessed prevalence of the six features
of functional dysphonia as defined by Morrison and
Rammage5 and the six features of hyperfunction
defined by Van Lawrence6 in 51 subjects found to
have functional (nonorganic) dysphonia and 52
normal controls. Categorical data were obtained
from qualitative judgments of the fiber-optic examinations. No feature had significantly greater prevalence in the dysphonic group as compared to the
normals. Stager et al8 also obtained categorical data
Journal of Voice, Vol. 17, No. 3, 2003
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Measurements
Quantification of the relative degree of anteriorposterior and medial compression of the supraglottis was achieved as follows. The anterior to
posterior distance was measured midline between
the vocal folds from anterior commissure or petiole
of the epiglottis to the interarytenoid mucosa in
pixels, and this distance was denoted AP (Figure 1).
To capture the medial compression of the ventricular
folds, the medial distance was measured as the width
of the true folds at their mid-membranous point from
the medial-most point of each ventricular fold in
pixels, and this width distance was denoted W
(Figure 2). All measures derived from endoscopic
images must be relative quantities normalized to
some known constant or to another quantity measured from the same image, primarily due to the
unknown and variable distance of the endoscope tip
to the larynx. Both the AP and W distances were
normalized to the LO, a measure recently described
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DISCUSSION
The inconsistent nomenclature and lack of uniform diagnostic classification systems of nonorganic
dysphonia reflect an uncertain pathophysiology.
Morrison et al1 hypothesized that the underlying
mechanism of functional dysphonia is incomplete
relaxation of the posterior cricoarytenoid muscle,
which causes incomplete vocal fold adduction.
The authors indicate that this results in hyperfunction of thyroarytenoid as a compensatory mechanism
to achieve phonatory glottal closure. In a later publication, Morrison and Rammage4 represent functional dysphonia as the manifestation of excessive
activity of intrinsic and extrinsic laryngeal muscles
during phonation. Rosen and Murry3 posit that the
underlying mechanism may be the in-coordination
of respiratory effort with vocal fold position or
Journal of Voice, Vol. 17, No. 3, 2003
tension. Koufman and Blalock2 note that occult underlying disease may be present, such as glottal
incompetence, and therefore, the functional dysphonia may represent a maladaptive compensatory
strategy.
The presumption of muscle hyperfunction that
underlies these theoretical constructs of abnormal
laryngeal and vocal tract biomechanics cannot be
measured directly. Therefore, diagnosis must rely
on signs that are presumed manifestations of hyperfunction, such as anteriorposterior and medial compression of the supraglottis observed on endoscopic
evaluation. The data from this study add to the growing body of evidence79 that these laryngeal postures
may not be signs of phonatory dysfunction.
The finding of this study are consistent with both
of the Stager et al studies.8,9 Those studies sought to
distinguish between vocal tract postures associated
with dysphonia, termed static postures, and dynamic
postures, those that may be a normal articulatory
feature associated with connected speech. Their earlier study,8 using categorical, qualitative assessment,
demonstrated no task dependence (eg, sustained
vowel or speech) for anteriorposterior compression, whereas there were statistically significant differences among tasks by group for medial
compression of the ventricular folds. The authors
concluded that the medial compression of the ventricular folds appeared to be more of a dynamic
articulatory feature, whereas anteriorposterior
compression, a static posture across all tasks, might
be suggestive of dysfunction. In the subsequent
study of Stager et al,9 using interval data from quantitative measures, the authors found significantly
less anteriorposterior compression in the normal
controls, whereas no group differences were found
in degree of medial compression. The lack of a statistically significant difference between groups for
the LOw measure found in this study supports their
conclusion that medial compression is largely a
normal articulatory posture rather than one of dysfunction. Another finding from this study, significantly lesser degree of LOAP for the normal controls,
also supports their conclusion that anteriorposterior
compression may be abnormal. Further supporting
their conclusions is the finding in this study of a
lack of a robust correlation between the LOw and
LOAP measures, because a correlation between a
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was not sensitive to all types of nonorganic hyperfunction. Many patients exhibit hyperfunction in
most phonatory contexts. In those cases, anterior
posterior or medial compression of the suprgalottis
would likely be visualized during the endoscopic
task assessed in this study. Other patients, however,
may exhibit abnormal vocal tract postures only
under conditions of physiologic or linguistic stress
and not during routine endoscopic examination.
Therefore, it is possible that the prevalence of supraglottal postures associated with hyperfunction was
underestimated in the patient population due to the
nature of the task.
CONCLUSIONS
Much information is lost when the three-dimensional vocal tract is viewed through an endoscopic
image. As such, endoscopic assessment of laryngeal
and vocal tract postures reveals little about the underlying pathophysiology. The results of this study
demonstrate a significant presence of medial compression of the ventricular folds in normal voiced
individuals, as quantified by the LOw measure. Despite the greater range of values obtained for the
dysphonic group, the lack of significant group
differences and overlap in values between the two
groups implies that medial compression of the supraglottis is of limited clinical utility in the diagnosis
of nonorganic dysphonia. Anteriorposterior compression, as captured by the LOAP measure, was
found to occur in significantly greater degree in the
dysphonic group. Some overlap in this measure of
anteriorposterior compression was demonstrated
across groups, and therefore, this measure is of uncertain diagnostic utility relative to nonorganic dysphonia. The findings of this and other studies79
strongly suggest that some of the assumptions about
the nature (and, hence, diagnosis) of functional dysphonia may not be correct, and certainly additional
empirical data are needed. The pathophysiology and
clinical findings that are diagnostic of nonorganic
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