956379
AORXXX10.1177/0003489420956379Annals of Otology, Rhinology & LaryngologyKridgen et al
research-article2020
Original Article
Patient-Reported Factors
Associated with the Onset of
Hyperfunctional Voice Disorders
Annals of Otology, Rhinology & Laryngology
1–6
© The Author(s) 2020
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https://doi.org/10.1177/0003489420956379
DOI: 10.1177/0003489420956379
journals.sagepub.com/home/aor
Samantha Kridgen, MS, CF-SLP1,2, Robert E. Hillman, PhD, CCC-SLP1,2,3,
Tara Stadelman-Cohen, MS, CCC-SLP1,2, Steven Zeitels, MD, FACS1,3,
James A. Burns, MD, FACS1,3, Tiffiny Hron, MD1,3,
Carol Krusemark, MS, CCC-SLP1,2, Jason Muise, MS, CCC-SLP1,2,
and Jarrad H. Van Stan, PhD, CCC-SLP1,2,3
Abstract
Objectives: Prevention, diagnosis, and treatment of hyperfunctional voice disorders would be improved by better
understanding their etiological contributing factors. Therefore, this study estimated the prevalence of etiological factors
using self-reported data about disorder onset from a large cohort of patients with Phonotraumatic Vocal Hyperfunction
(PVH) and Non-Phonotraumatic Vocal Hyperfunction (NPVH).
Methods: Retrospective chart review extracted the self-reported rate (gradual, sudden) and events associated (voice use,
anxiety/stress, upper respiratory infection [URI]) with disorder onset from 1,577 patients with PVH and 979 patients with
NPVH.
Results: Both patient groups reported a gradual onset more than a sudden onset. Voice use was the most frequently
reported event for PVH and the NPVH group self-reported all three events at equal frequency. The largest PVH subgroups
were associated with voice use while the NPVH subgroups were associated with only voice use, only URI, or only anxiety/
stress.
Conclusion: The results support the general clinical view that PVH is most strongly related to the gradual accumulated
effects of phonotrauma, while NPVH has a more heterogeneous etiology. The identified PVH and NPVH subgroups may
have clinical relevance and future work could investigate differences in treatment and outcomes among these subgroups.
Keywords
vocal fold nodules, muscle tension dysphonia, voice disorders, vocal hyperfunction
Introduction
Voice disorders have been estimated to affect approximately
6.6% to 7.6% of adults in the United States at any given
point in time1,2 and the most commonly treated voice disorders are associated with vocal hyperfunction.1 Vocal hyperfunction (VH) refers to chronic conditions of abuse and/or
misuse of the vocal mechanism due to excessive and/or
unbalanced muscular force.3 Generally, VH can be divided
into two subtypes: Phonotraumatic Vocal Hyperfunction
(PVH) and Non-Phonotraumatic Vocal Hyperfunction
(NPVH).4 PVH is associated with obvious signs of true
vocal fold trauma (eg, bilateral vocal fold nodules, polyps).
Non-Phonotraumatic Vocal Hyperfunction—also referred
to as functional dysphonia5 or primary muscle tension dysphonia6—is associated with symptoms such as chronic dysphonia and vocal fatigue in the absence of vocal fold tissue
trauma. Because NPVH is a diagnosis of exclusion (ie, no
physical or neurological disorder can account for the vocal
symptoms), this disorder is associated with a myriad of
potential etiologies (eg, stress, anxiety, upper respiratory
infections/URI, voice overuse).6-15 All voice disorders and
putative contributing factors are standardly labeled according to the Classification Manual for Voice Disorders.16
1
Center for Laryngeal Surgery and Voice Rehabilitation, Massachusetts
General Hospital, Boston, MA, USA
2
MGH Institute of Health Professions, Boston, MA, USA
3
Department of Surgery, Harvard Medical School, Boston, MA, USA
Corresponding Author:
Jarrad H. Van Stan, PhD, CCC-SLP, Department of Surgery, Harvard
Medical School, 25 Shattuck Street, Boston, MA 02115, USA.
Email: jvanstan@mgh.harvard.edu
2
The chronic VH state is thought to be caused by factors
such as transient periods of increased vocal demands with
inadequate vocal recovery time (eg, prolonged loud talking)3,17; increased psychological stress promoting non-volitional (autonomic nervous system) heightened activity of the
perilaryngeal and/or extralaryngeal muscles7-9,18; and environmental factors like URIs, laryngopharyngeal reflux (LPR),
irritants, and dehydration.19-24 Additionally, there are some
commonly held clinical notions that various eliciting factors
are more likely to be associated with PVH or NPVH. For
example, increased voice use is believed to play a larger role
in PVH than in NPVH and increased stress and anxiety are
assumed to play a more prominent role in NPVH than
PVH.7-9,11,16,18,25
Current knowledge regarding the causative factors of
hyperfunctional voice disorders relies mostly on clinical
impressions and empirical data acquired after disorder occurrence (measures of vocal function, personality/psychological
profiles, etc).6,19,26,27 Causative theories, when informed by
data collected after disorder formation, contain a high degree
of uncertainty because one cannot separate whether the measurements of interest pre-existed the voice disorder and/or
characterize compensatory behaviors due to the disorder.3,28 To
objectively evaluate causative factors, the gold standard would
be a prospective observational study of subjects in a high-risk
occupation.29 This study design is pragmatically impossible for
behaviorally-based voice disorders as the incidence is very
low, even in high-risk occupations (estimates 5-7%).2,30
However, as a starting point, patients can be asked to recall
what they thought was associated with the onset of their voice
disorder or how long they think it took for their disorder to
develop. Despite the limitations of self-report (eg, biases in
recall),31 collecting this subjective data in a large cohort of
patients has the potential to provide adequate power to detect
even small consistencies.32 Additionally, data regarding what
patients think was associated with the onset of their disorder
could provide valuable directions for further investigation.
Better information about the relative prevalence of factors
that have been cited as contributing to the etiologies of hyperfunctional voice disorders could ultimately lead to the development of more focused and effective approaches for
preventing, diagnosing, and treating these disorders. For
example, programs aimed at prevention of hyperfunctional
voice disorders in high risk populations or subgroups could
focus on those factors that are shown to be most often associated with disorder onset. Such knowledge would also help to
guide the gathering of salient information during the diagnostic interview. In terms of treatment, with the move toward personalized medicine, it has become increasingly clear that
treatment must be tailored to the individual patient or subgroups of a particular diagnosis.33 Since different singular
causes (or combinations of causes) of the same disorder often
necessitate different treatment approaches, patient reported
factors associated with disorder onset have the potential to
identify clinically meaningful subgroups that may attain
Annals of Otology, Rhinology & Laryngology 00(0)
greater benefit from treatments that are specifically tailored to
each subgroup.
Since, to the author’s knowledge, no study has formally
analyzed self-report data regarding what the patient believed
was associated with their disorder onset, this study attempted
to gain a better understanding of the relative prevalence of etiologic factors for PVH and NPVH and to use this information to
identify potentially useful clinically meaningful subgroups.
We hypothesized that (1) patients from both PVH and NPVH
will report gradual onsets more often than sudden onsets (supporting the hypothesized habitual nature of the disorders); (2)
patients with PVH would self-report voice use as the most frequent event associated with voice disorder onset and all large
subgroups will be associated with voice use (supporting “phonotrauma” as the putative causative factor of PVH); (3) the
NPVH group would equally self-report all associated events
and all subgroups will be unidimensional (supporting the
hypothesis that this group is etiologically heterogeneous).
Methods
Participant Recruitment
All research was approved by the hospitals’ Institutional
Review Boards. Patients with a primary diagnosis of vocal fold
nodules, vocal fold polyp(s), or muscle tension dysphonia
were retrospectively identified in an automated search of the
clinical database from the Massachusetts General Hospital
Center for Laryngeal Surgery and Voice Rehabilitation (MGH
Voice Center) from the years 2006 to 2017 and a deidentified
copy of the database from the Massachusetts Eye and Ear
Infirmary (MEEI) Voice and Speech Laboratory from the years
1994 to 2004. Diagnoses were based on a comprehensive team
evaluation (laryngologist and speech-language pathologist) at
the MEEI or MGH Voice Center that included (1) the collection of a complete case history, (2) endoscopic imaging of the
larynx and (3) instrumental aerodynamic and acoustic assessment of vocal function. After performing the automatic database search, each patient was included or excluded after
manually reading their laryngology evaluation. Patients with
NPVH (ie, primary muscle tension dysphonia) were included
in the study if they had secondary diagnoses of LPR and gastro-esophageal reflux disease (GERD). However, patients with
NPVH were excluded if they had any secondary diagnoses
related to structural or neurological disorders: specifically laryngitis, loss of superficial lamina propria, benign lesion, polyp,
cyst, dysphagia, sulci, paradoxical vocal fold motion, any
mention (confirmed or possible) of upper airway paralysis or
paresis, polypoid corditis, keratosis, presbylarynx, fibrovascular changes, leukoplakia, injury of the recurrent or superior
laryngeal nerve, or history of radiation or neurological
impairment.
Patients with PVH (ie, vocal fold nodules and polyps)
were included in the study if they had secondary diagnoses of
LPR and GERD as well as those commonly associated with
Kridgen et al
phonotrauma, specifically: erythema, edema, varices, ectasia, laryngitis, secondary/reactive muscle tension dysphonia,
hemorrhage. However, patients with PVH were excluded if
they displayed secondary diagnoses not related to phonotrauma, specifically: cyst, pseudocyst, unilateral (ie, the
lesions had to be bilateral), sulci, cancer, bamboo nodule,
anterior web, or paradoxical vocal fold motion.
Case History Form
The case history form was filled out after the laryngology
evaluation and before the speech-language pathology evaluation. It included two questions related to factors associated with the onset of the patient’s voice disorder:
1.
2.
Was the onset of your voice disorder: sudden, gradual, unsure, or not applicable (circle the most appropriate response).
Were there any events or circumstances that
occurred with the onset of your voice difficulty:
Anxiety/stress, increased voice use, vocal abuse
(yelling/screaming), URI, change in job, injury
(trauma), surgery, chemical exposure, accident,
none, other, and not applicable (circle all that apply).
All responses to the case history form questions were coded
as binary variables: 1 = the patient selected the response;
0 = the patient did not select the response.
Statistics and Analysis
Differences between the PVH and NPVH groups were evaluated for four onset variables (ie, gradual, sudden, unsure, not
applicable), six associated event variables (ie, voice use, anxiety/stress, URI, other, not applicable, and none), six combinations of variables to investigate interactions between
onset*event (ie, gradual or sudden onset and voice use, anxiety/stress, or URI), and (3) six patient subgroups (anxiety/
stress only, voice use only, URI only, anxiety/stress and voice
use, voice use and URI, and other only). Only three individual
associated events were statistically compared because Voice
Use and Vocal Abuse were combined into one category labeled
“Voice Use” and the categories of Voice Use, Anxiety/Stress,
and URI were the only ones to be reported by at least 10% of
patients. All other associated events were grouped into the
“Other” category. Two (group) by two (presence/absence of
category) Chi Square tests were performed to evaluate pairwise between-group differences (PVH vs NPVH). Significance
was Bonferroni-corrected to the level of P < .002 for each of
the 22 total 2 × 2 comparisons because of multiple hypothesis
testing. Odd’s ratios (OR) were used as an effect size metric to
help represent the potential clinical significance of any statistically significant pair-wise between-group differences. Patient
subgroups were identified when approximately 100 or more
patients reported only a single event or the same combination
of multiple events.
3
Table 1. Number of Patients (Percentage of Total Patients)
that Reported Duration of Onset Occurrence Within Each
Group.
Patient Groups
Onset Time
Course
PVH
Gradual
Sudden
Unsure
Not applicable
902 (57%)
321 (20%)
218 (14%)
136 (9%)
NPVH
Odds
Ratios
422 (43%)
293 (30%)
135 (14%)
129 (13%)
1.8*
1.7a
—
1.6a
Abbreviations: NPVH, non-phonotraumatic vocal hyperfunction; PVH,
phonotraumatic vocal hyperfunction.
Note. The “dash” under the “Odds Ratios” column represent nonsignificant differences. Odds ratios with * or “a” represent a higher
prevalence in PVH or NPVH, respectively.
Table 2. Frequency of Patient-Reported Associated Events
with the Onset of Disorder Within Each Group.
Patient Reported
Associated Event
Anxiety/Stress
Gradual onset
Sudden onset
Voice use
Gradual onset
Sudden onset
URI
Gradual onset
Sudden onset
Other
None
Not applicable
Patient Groups
PVH
291 (19%)
176 (11%)
60 (4%)
850 (54%)
544 (35%)
165 (11%)
307 (20%)
175 (11%)
83 (5%)
290 (18%)
108 (7%)
466 (20%)
NPVH
181 (19%)
100 (5%)
48 (5%)
227 (23%)
116 (12%)
57 (6%)
212 (22%)
93 (10%)
82 (4%)
316 (32%)
124 (13%)
317 (15%)
Odds
Ratios
—
—
—
3.9*
3.9*
1.9*
—
—
—
2.1a
2.0a
—
Abbreviations: NPVH, nonphonotraumatic vocal hyperfunction; PVH,
phonotraumatic vocal hyperfunction; URI, upper respiratory infection.
Note that some subjects selected multiple categories, so the
percentages will sum to >100% per patient group. The “dash” under
the “Odds Ratios” column represent non-significant differences. Odds
ratios with * or “a” represent a higher prevalence in PVH or NPVH,
respectively.
Results
The automatic database search identified 3,105 total patients
with a diagnosis of PVH or NPVH. After manual filtering,
2,556 were included in the analysis: 1,577 patients with
PVH and 979 patients with NPVH.
Table 1 shows the rate of onset for all groups. While both
groups reported gradual onset more often than sudden
onset, gradual onset was reported more frequently by
patients with PVH (57%) than NPVH (43%); χ2(1) = 48.0,
P < .001, OR = 1.8. Sudden onset was reported more frequently by patients with NPVH (30%) than those with PVH
(20%); χ2(1) = 30.3, P < .001, OR = 1.7.
Table 2 shows the events associated with disorder onset.
The most frequently reported event for both groups was
4
Annals of Otology, Rhinology & Laryngology 00(0)
Table 3. Frequency of Combinations of Patient-Reported
Associated Events with the Onset of Disorder Within Each
Group.
Associated Onset Patient
Clusters
Anxiety/Stress only
Voice use only
URI only
Anxiety/Stress and URI
Anxiety/Stress and voice use
Voice use and URI
Anxiety/Stress, voice use,
and URI
Other only
Patient Group
PVH
NPVH
Odds
Ratios
50 (3.2%)
505 (32.0%)
107 (6.8%)
21 (1.3%)
166 (10.5%)
125 (7.9%)
54 (3.4%)
98 (10.0%)
124 (12.7%)
130 (13.3%)
25 (2.6%)
46 (4.7%)
45 (4.6%)
12 (1.2%)
3.4a
3.2*
2.1a
n/a
2.4*
1.8*
n/a
124 (7.9%)
226 (23.1%)
3.5a
Abbreviations: NPVH, nonphonotraumatic vocal hyperfunction; PVH,
phonotraumatic vocal hyperfunction; URI, upper respiratory infection.
Note. “n/a” is denoted for patient groupings that did not have a large
enough sample size for reliable Chi Square analysis. Odds ratios with *
or “a” represent a higher prevalence in PVH or NPVH, respectively.
voice use, but it was more frequently reported by the PVH
group (54%) than the NPVH (23%) group; χ2(1) = 234.1,
P < .001, OR = 3.9, respectively. There was no significant
difference in self-reported anxiety/stress or URI between
the NPVH and PVH groups. The group-based differences
(or lack thereof) remained unchanged after separately evaluating gradual and sudden onsets associated with voice use,
anxiety/stress, or URI.
Table 3 shows all unique patient-reported combinations of
associated events. Besides the large amount of patients who
reported no associated events, not applicable, or only “Other,”
there were four large PVH subgroups (Voice use only = 505,
Voice use and anxiety/stress = 166, Voice use and URI = 125,
and URI only = 107), two large NPVH subgroups (URI
only = 130 and Voice use only = 124), and one borderline
large NPVH subgroup (Anxiety/stress only = 98). Three of
the four PVH subgroups occurred more frequently in the
PVH group than the NPVH group: Voice use only,
χ2(1) = 121.9, P < .001, OR = 3.2; Anxiety/stress and voice
use, χ2(1) = 30.0, P < .001, OR = 2.4; Voice use and URI,
χ2(1) = 10.8, P < .001, OR = 1.8. Two of the three NPVH subgroups occurred more frequently in the NPVH group than the
PVH group: URI only, χ2(1) = 30.3, P < .001, OR = 2.1;
Anxiety/stress only, χ2(1) = 51.8, P < .001, OR = 3.4.
Discussion
The purpose of this study was twofold: (1) to gain a better
understanding of the relative prevalence of etiologic factors
for PVH and NPVH and (2) to identify clinically meaningful patient subgroups. The patient-reported information
supported multiple commonly-held clinical notions about
the similarities and differences in disorder onset between
the two types of hyperfunctional voice disorders. For example, it is thought that PVH and NPVH are associated with
chronic, long-term vocal behaviors and the patients in both
groups more frequently self-reported their disorder onset as
gradual (~50%) than sudden (~25%). Furthermore, when
patients estimated in their case history form how long the
symptoms of their disorder were present before seeing a laryngologist, most reported months (49%) or years (46%) and
very few reported a timescale of weeks or less (5%).
Patient self-report data supported the clinical belief that
PVH is mainly caused and/or associated with habitual, chronic
voice use—specifically the accumulated effect of phonotrauma.3,28 Over half of the PVH group (54%) reported voice
use was associated with the beginning of their symptoms and
32% of the PVH group reported that voice use was the only
event associated with disorder onset. Additionally, three out of
four patient subgroups included voice use as an associated
event. The PVH subgroups have potential to guide research
into more refined conceptual models or frameworks of how
phonotraumatic lesions are formed. For example, although the
biggest patient subgroup reported only voice use and nothing
else associated with disorder onset, the next two largest subgroups (voice use and anxiety/stress; voice use and URI) suggest that excessive phonotrauma may not only result from too
much voice use. A large portion of phonotraumatic lesions
may form during periods of vocal fold tissue degradation
(URI) in the presence of “typical levels” of phonotrauma. This
is further reinforced by the smallest subgroup where the only
associated event was URI. Also, as supported by the Voice
Use and Anxiety/Stress subgroup, perhaps increased phonotrauma can occur because of anxiety- or stress-provoking situations (eg, shouting during arguments or social events). In the
patient subgroups where Voice Use is not the sole contributor,
prevention and treatment approaches focused on changing
how the patient generally produces voice would probably be
less effective than vocal hygiene education or practicing
“healthy/efficient” voicing under emotional situations.
Results for patients with diagnoses of nodules and polyps
were combined in the PVH category. This was done for two
reasons. First, diagnoses of patients in the databases were
determined by several different clinical teams that could
have employed different criteria for differentiating between
nodules and polyps, which are both associated with phonotrauma and can sometimes be challenging to definitively
classify (eg, differentiating bilateral nodules vs a polyp and
reactive nodule). Second, there were no differences between
the groups of patients diagnosed with nodules or polyps that
were meaningful enough to change the final interpretation of
the results, particularly with respect to comparisons with the
NPVH group.
As was expected, the self-report data from the NPVH
group were heterogeneous. The NPVH group equally
reported Voice Use, Anxiety/Stress, and URI (~20%) as
associated with the onset of their disorder; and the largest
Kridgen et al
subgroup reported only an “Other” event. The “Other”
events consisted of many infrequently (<100 patients
across both PVH and NPVH groups) reported events like
various surgeries, dysphagia, reflux, allergies, and job
change. Furthermore, this heterogeneity was mostly distributed in a unidimensional way, as 65% of patients with
NPVH reported only one category of associated onsets. The
large NPVH subgroups were also unidimensional, as 10%
of patients only reported Anxiety/Stress, 12% only reported
Voice Use, and 13% only reported URI. Perhaps these findings indicate that, in general, there are three subtypes of
NPVH patients; all of which have been mentioned sporadically throughout the existent literature. The “Voice Use”
subgroup (representing the traditional view of primary muscle tension dysphonia6) could be described as those who use
their voice a great deal, but are not vocally efficient enough
to fulfill their daily needs without vocal fatigue and/or deterioration. The “URI” subgroup could be described as those
who had no vocal difficulties until their upper respiratory
system was physically compromised. The vocal compensations used to communicate during the URI became habitual
and remained despite recovery from the infection. Recent
literature suggests that upper respiratory symptoms were
associated with a 49% to 75% increased odds of developing
a voice disorder in general.34 Finally, the “Anxiety/Stress”
subgroup could be described as those whose vocal function
deteriorates in association with a psychological state or
event that impacts voice production. There are multiple
commonly-used diagnostic labels and theories/frameworks
in the literature specifically referring to a psychological
association with NPVH (eg, psychogenic, functional).5-8,18,35
These three subgroups could also indicate the need for different behavioral treatment approaches; for example,
improving the efficiency of voicing for the “Voice Use”
subgroup, helping patients access the voice they had before
their infection for “URI” subgroup, and addressing how
psychologically stressful or anxious events relate to their
voice disorder in the “Anxiety/Stress” subgroup.
The chronic nature of these disorders and their relationship to events in daily life reinforce the clinical importance of
developing assessments that consider longer time periods
than traditional in-clinic measurements of vocal function/
behavior. Ambulatory voice monitoring technology can provide estimates of how patients are using their voice in daily
life over extended time scales (eg, hours, days, weeks).4,28,36,37
Additionally, the events or situations associated with disorder
onset can be difficult to replicate during a therapy session; for
example, artificially evoking a realistic level of stress is hard.
Therefore, ambulatory voice monitoring could potentially
measure vocal behavior in real-life stressful situations for
assessment purposes or to provide biofeedback to assist with
maintaining good vocal function during stressful events.
A limitation of the study is that the data consist entirely of
patient self-report. However, this is the closest empirical
5
measurement possible without directly observing subjects
before they experience any vocal difficulty. It is also possible
that the “Voice Use” event is over-reported since the patients’
disorders inherently affected their voice. All patients had seen
a laryngologist and were given a diagnosis before the case
history form was filled out, which could have influenced their
responses. However, the large number of subjects in each
group should mitigate the effect of noisy self-report metrics.
Conclusion
A large cohort of patients with PVH (n = 1,577) and NPVH
(n = 979) provided self-report data on the onset of their
voice disorder in terms of rate (sudden vs gradual) and associated events. The patient self-report data support the general clinical view that PVH is most strongly related to the
gradual accumulated effects of phonotrauma, while NPVH
has a more heterogeneous etiology. Subgroups of PVH and
NPVH patients were identified that may have clinical relevance and future work could investigate differences in treatment and outcomes among these subgroups.
Declaration of Conflicting Interests
The author(s) declared the following potential conflicts of interest
with respect to the research, authorship, and/or publication of this
article: Drs Robert Hillman and Steven Zeitels have a financial
interest in InnoVoyce LLC, a company focused on developing and
commercializing technologies for the prevention, diagnosis, and
treatment of voice-related disorders. Dr Hillman’s and Dr Zeitels’
interests were reviewed and are managed by Massachusetts
General Hospital and Partners HealthCare in accordance with their
conflict of interest policies.
Funding
The author(s) disclosed receipt of the following financial support
for the research, authorship, and/or publication of this article: This
work was supported by the Voice Health Institute and the National
Institutes of Health (NIH) National Institute on Deafness and Other
Communication Disorders under Grants R33 DC011588 (PI: Dr
Robert Hillman) and P50 DC015446 (PI: Dr Robert Hillman). The
article’s contents are solely the responsibility of the authors and do
not necessarily represent the official views of the NIH.
ORCID iD
Jarrad H. Van Stan
https://orcid.org/0000-0001-8932-3276
References
1. Bhattacharyya N. The prevalence of voice problems among adults
in the United States. Laryngoscope. 2014;124(10):2359-2362.
2. Roy N, Merrill RM, Gray SD, Smith EM. Voice disorders in
the general population: prevalence, risk factors, and occupational impact. Laryngoscope. 2005;115(11):1988-1995.
3. Hillman RE, Holmberg EB, Perkell JS, Walsh M, Vaughan
C. Objective assessment of vocal hyperfunction: an
6
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
Annals of Otology, Rhinology & Laryngology 00(0)
experimental framework and initial results. J Speech Hear
Res. 1989;32(2):373-392.
Mehta DD, Van Stan JH, Zañartu M, et al. Using ambulatory voice monitoring to investigate common voice disorders:
research update. Front Bioeng Biotechnol. 2015;3:155.
Roy N. Functional dysphonia. Curr Opin Otolaryngol Head
Neck Surg. 2003;11(3):144-148.
Kunduk M, Fink DS, McWhorter AJ. Primary muscle tension
dysphonia. Curr Otorhinolaryngol Rep. 2016;4(3):175-182.
Roy N, Bless DM. Personality traits and psychological factors
in voice pathology: a foundation for future research. J Speech
Lang Hear Res. 2000;43(3):737-748.
Roy N, Bless DM, Heisey D. Personality and voice disorders: a
multitrait-multidisorder analysis. J Voice. 2000;14(4):521-548.
Roy N, Bless DM, Heisey D. Personality and voice disorders: a superfactor trait analysis. J Speech Lang Hear Res.
2000;43(3):749-768.
Altman KW, Atkinson C, Lazarus C. Current and emerging
concepts in muscle tension dysphonia: a 30-month review. J
Voice. 2005;19(2):261-267.
Dworkin JP, Meleca RJ, Abkarian G. Muscle tension dysphonia.
Curr Opin Otolaryngol Head Neck Surg. 2000;8(3):169-173.
Lowell SY, Kelley RT, Colton RH, Smith PB, Portnoy JE.
Position of the hyoid and larynx in people with muscle tension
dysphonia. Laryngoscope. 2012;122(2):370-377.
Spencer ML. Muscle tension dysphonia: a rationale for
symptomatic subtypes, expedited treatment, and increased
therapy compliance. SIG 3 Perspect Voice Voice Disord.
2015;25(1):5-15.
Van Houtte E, Van Lierde K, Claeys S. Pathophysiology and
treatment of muscle tension dysphonia: a review of the current knowledge. J Voice. 2011;25(2):202-207.
Morrison MD, Nichol H, Rammage LA. Diagnostic criteria in
functional dysphonia. Laryngoscope. 1986;96(1):1-8.
Verdolini K, Rosen C, Branski RC (eds). Classification
Manual for Voice Disorders-I, Special Interest Division 3,
Voice and Voice Disorders, American Speech-Language
Hearing Division. Mahwah, NJ: Lawrence Erlbaum; 2006.
Bridger M, Epstein R. Functional voice disorders. J Laryngol
Otol. 1983;97(12):1145-1148.
Dietrich M, Verdolini Abbott K, Gartner-Schmidt J, Rosen
CA. The frequency of perceived stress, anxiety, and depression in patients with common pathologies affecting voice. J
Voice. 2008;22(4):472-488.
Karkos PD, McCormick M. The etiology of vocal fold nodules in adults. Curr Opin Otolaryngol Head Neck Surg.
2009;17(6):420-423.
Kuhn J, Toohill RJ, Ulualp SO, et al. Pharyngeal acid reflux
events in patients with vocal cord nodules. Laryngoscope.
1998;108(8):1146-1149.
Chung JH, Tae K, Lee YS, et al. The significance of laryngopharyngeal reflux in benign vocal mucosal lesions.
Otolaryngol Head Neck Surg. 2009;141(3):369-373.
22. Jiang J, Verdolini K, Aquino B, Ng J, Hanson D. Effects of
dehydration on phonation in excised canine larynges. Ann
Otol Rhinol Laryngol. 2000;109(6):568-575.
23. Sivasankar M, Leydon C. The role of hydration in vocal
fold physiology. Curr Opin Otolaryngol Head Neck Surg.
2010;18(3):171.
24. De Bodt M, Ketelslagers K, Peeters T, et al. Evolution of
vocal fold nodules from childhood to adolescence. J Voice.
2007;21(2):151-156.
25. McGrory JJ, Tasko SM, Bless DM, Heisey D, Ford CN.
Psychological correlates of functional dysphonia: an investigation using the Minnesota Multiphasic Personality Inventory.
J Voice. 1997;11(4):443-451.
26. Kunduk M, McWhorter AJ. True vocal fold nodules: the role
of differential diagnosis. Curr Opin Otolaryngol Head Neck
Surg. 2009;17(6):449-452.
27. Leonard R. Voice therapy and vocal nodules in adults.
Curr Opin Otolaryngol Head Neck Surg. 2009;17(6):453457.
28. Van Stan JH, Mehta DD, Ortiz AJ, et al. Differences in weeklong ambulatory vocal behavior between female patients with
phonotraumatic lesions and matched controls. J Speech Lang
Hear Res. 2020;63(2):372-384.
29. Saks M, Allsop J. Researching Health: Qualitative,
Quantitative and Mixed Methods. London: Sage; 2012.
30. Roy N, Merrill RM, Thibeault S, Parsa RA, Gray SD, Elaine
S. Prevalence of voice disorders in teachers and the general
population. J Speech Lang Hear Res. 2004;47(2):281-293.
31. Mehta DD, Van Stan JH, Masson MLV, Maffei M, Hillman
RE. Relating ambulatory voice measures with self-ratings of
vocal fatigue in individuals with phonotraumatic vocal hyperfunction. Paper presented at: Proceedings of the Acoustical
Society of America, Boston, USA; 2017.
32. Cohen J. Statistical Power Analysis for the Behavioral
Sciences. 2nd ed. Hillsdale: Lawrence Erlbaum; 1988.
33. Hamburg MA, Collins FS. The path to personalized medicine.
N Engl J Med. 2010;363(4):301-304.
34. Bainbridge KE, Roy N, Losonczy KG, Hoffman HJ, Cohen
SM. Voice disorders and associated risk markers among young
adults in the United States. Laryngoscope. 2017;127(9):20932099.
35. Van Mersbergen M, Patrick C, Glaze L. Functional dysphonia during mental imagery: testing the trait theory of
voice disorders. J Speech Lang Hear Res. 2008;51(6):
1405-1423.
36. Hillman RE, Heaton JT, Masaki A, Zeitels SM, Cheyne HA.
Ambulatory monitoring of disordered voices. Ann Otol Rhinol
Laryngol. 2006;115(11):795-801.
37. Van Stan JH, Mehta DD, Petit R, et al. Integration of motor
learning principles into real-time ambulatory voice biofeedback and example implementation via a clinical case
study with vocal fold nodules. Am J Speech Lang Pathol.
2017;26(1):1-10.