Vocal Fold Self-Disruption After Phonotrauma

On A Lead Actor: A Case Presentation

*Mara Behlau, *Gisele Oliveira, and Paulo Pontes
Summary: It is well known that phonotraumatic events may produce laryngeal inflammation, vocal fold hemorrhage
and different types of mass lesions. This study describes a vocal fold self-disruption that occurred on stage to a lead actor
in the role of Richard III. The study design is as case presentation. A 43-year-old actor presented with a sudden voice
loss that first occurred on stage after a series of presentations. He also had a cold-like condition that had not been treated.
His past medical history included an average of ten cigarettes per day for ten years and a 10-year history of gastritis and
stomach ulcer. Perceptual, acoustic, and laryngeal analyses were performed following pharmacological and voice therapy. Perceptual and acoustic analyses showed mild deviations whereas laryngeal visual examination revealed a complete
right vocal fold detachment from the anterior commissure to the vocal process, with generalized hyperemia. A mild
diffuse Reinkes edema was observed on the left vocal fold. Mild discomfort was present only during the first day of
the acute period. Modified vocal rest was recommended and a series of vocal exercises were administered. The patient
performed again 4 days later, after following a series of behavioral modification techniques that included casting guidelines during the subsequent 15 days. Healing was exceptional and his voice returned to normal. This unique case with an
exceptional recovery emphasizes the etiological aspects of scar formation after phonotrauma. Positive contributing factors may include a good vocal technique and adequate training as well as the protective upregulated genes present in
Reinkes edema.
Key Words: PhonotraumaProfessional voiceReinkes EdemaVocal fold lesion.
INTRODUCTION
The concept underlying phonotrauma is the presence of a laryngeal injury directly associated with phonation.
Phonotraumatic events may produce laryngeal inflammation,
vocal fold hemorrhage and different mass lesions.15 Vocal deviations responsible for laryngeal acute inflammation are related to high subglottic pressure and dosage of vocal fold
vibration.6 A review of the literature presents a wide range of
possible lesions, such as vocal fold hemorrhage after extensive
crying,7 granuloma related to vocal behavior and tension,8,9
acute or soft vocal fold nodules,10 polyps,1 and even vocal
fold scar after repetitive trauma.7,11
A survey of forty world renowned voice specialists,12,13 including 20 laryngologists and 20 speech-language pathologists,
pointed out that aggressive vocal production was the main cause
of an acute phonotrauma (100%). Screaming and/or yelling
were identified as the most hazardous vocal behavior (55%),
particularly under inadequate acoustic or physical conditions.
The use of voice on a bout of laryngitis or any upper respiratory
infection was considered particularly dangerous (32.5%). Inadequate technique (20%) and use of voice under extreme tension
(12.5%) were also reported. In addition to the commonly cases
of vocal fold hemorrhage (65%), polyps (50%), and granulomas
(30%) already described as direct consequence of an acute vocal fold trauma, specialists also cited isolated cases of transient

Accepted for publication March 20, 2008.

This paper was presented at The Voice Foundations 36th Annual Symposium: Care of
the Professional Voice, 2007, Philadelphia, Pennsylvania.
From the *Centro de Estudos da Voz CEV, Sao Paulo, Brazil; and the yInstituto da
Laringe INLAR, Sao Paulo, Brazil.
Address correspondence and reprint requests to Mara Behlau, Centro de Estudos da Voz
CEV, Rua Machado Bittencourt 361, 10th Floor, SP 04044-001 Sao Paulo, Brazil. E-mail:
mbehlau@uol.com.br
Journal of Voice, Vol. 23, No. 6, pp. 726-732
0892-1997/$36.00
2009 The Voice Foundation
doi:10.1016/j.jvoice.2008.03.006

vocal fold paralysis and pseudocysts. The most common predisposing factor reported was recurrent inflammation or upper
respiratory infection (25%). According to the surveyed specialists, vocal rehabilitation plays a role even during the acute episode (30%) and may also prevent recurrence (100%).
There are several individual and environmental factors that
contribute to the development of a vocal fold lesion after a phonotrauma. Individual factors are gender (female),14,15 occupation, such as voice professional users1624; personality and
stress8,2427; histological characteristics14,28,29; high vocal demand or aggressive vocal behavior, such as yelling, screaming,
talking too loud and crying6,7,24,3033; weak voice33; inadequate
vocal training32; health conditions, such as, upper respiratory infections,5,33,34 allergies,35 laryngopharyngeal reflux,3638 and
hormonal imbalance3942; aspirin and nonsteroidal anti-inflammatory use42,43; and tobacco smokers.44 Environmental factors
such as background noise, poor room acoustics, distance among
speakers, lack of voice amplifiers, poor air quality, dust,6,24,33
and the presence on stage of artificial fogs and smokes45 can
also lead to the development of an acute or chronic voice problem.

CASE REPORT
This case report describes a vocal fold self-disruption that occurred to a 43-year-old lead actor (type I professional voice
user46) playing Richard III, with a negative past history of dysphonia. The actor presented a sudden loss of vocal quality on
stage after he had been performing for 5 consecutive days, including two shows the 2 previous days, with diffuse cold-like
symptoms (according to patients report). In an attempt to
achieve the needed volume for a scene, he used extreme effort,
which was followed by blood taste and a sudden vocal change
toward a release sensation. After a few minutes with a good
voice, the actor experienced a progressive vocal deterioration,

Mara Behlau, et al

Vocal Fold Self-Disruption After Phonotrauma

leading the conclusion of the play with severe difficulties, not

noticeable to the public but evident to his colleagues on stage.
Right after the show, the actor contacted the first author (MB)
who instructed him to remain under a strict voice rest until being examined by the otolaryngologist (PP). The patient refused
to follow these recommendations since he had to travel from
Sao Paulo to Rio de Janeiro to sign a contract. He was fully advised about the possibility of an acute severe condition.
The next day, the patient presented at the clinic with no further vocal deterioration. Perceptual analysis revealed a moderate roughness with instability in vocal quality and frequency.
Maximum phonation time was 18 seconds for the open /ae/
vowel, at the lower bottom of normal range for Brazilian
male adult speakers.47 Loudness was slightly reduced and
mean intensity at conversational level was at 62 dB with capture
at 1 m from the mouth (Realistic, Sound Level Meter). Dynamic
and phonatory ranges were not measured during the first evaluation due to the laryngeal condition, but his voice was clearly
restricted in modulation. The acoustic analysis (VoxMetria
2.5, CTS Informatica) revealed a low fundamental frequency
(86.12 Hz) and all other parameters were within the normal
range, including jitter, shimmer, and glottal-to-noise-excitation
measurement. Spectrographic trace analysis for the sustained
vowel /ae/, which was almost 8 seconds long, revealed a moderate trace of irregularity, presence of harmonics up to 4000 Hz,
nonsystematic vertical striations indicating the occasional presence of noise, breathy glottal attack and unsteady raise and decay times. Frequency distribution during the connected speech
task of counting numbers from 1 to 10 (FonoView 1.0, CTS Informatica) was mean frequency at 81.06 Hz, minimum and
maximum frequencies at 70.47 Hz and 94.30 Hz, respectively.
The maximum frequency limit was achieved with the first
word of the sequence of numbers (um, ie, one) and all
other numbers presented lower marks. The spectrogram is
shown on Figure 1A. The phonatory deviation diagram (Figure 2), also known as Hoarseness Diagram or Gottingen Diagram48,49 (VoxMetria, CTS Informatica) showed a horizontal
distribution with only some points out of the normal area, indicating a tendency to irregularity.
The laryngeal examination showed an unexpected right vocal
fold disruption, from the anterior commissure to the vocal process and generalized hyperemia (Figure 3A). There was no
presence of hemorrhagic tissue, hematoma, feeding vessel or
vascular ectasia. The contralateral vocal fold presented a mild
Reinkes edema. No sign of reduced vocal fold mobility was
noticed.
The vocal history of this patient included more than 20 years
of professional acting, with extensive vocal training for theater,
television and movies. No history of dysphonia was mentioned.
The only vocal symptoms prior to this episode were due to respiratory infections or colds that did not result in any chronic
condition. Previous history of gastritis, stomach ulcer, and
smoking of 10 cigarettes per day during the last 20 years
were reported. The patient also mentioned that a previous laryngological examination revealed the presence of a smoking
edema but no intervention was suggested, aside from the recommendation of quitting smoking.

727

The initial medical treatment was corticosteroid therapy that

included Deflazacort (30 mg/day) via the oral route, beclomethasone dipropionate (750 mcg/day) by inhalation, and an antibiotic therapy of Azitromicine (500 mg/day) via the oral route,
for 5 days. The voice team suggested a complete and strict voice
rest42 and the cancellation of the show for a week, followed by
a new examination and further intervention. The actor, who was
also the show producer, refused to follow these recommendations because the show was sold out and no supernumerary
was available for his role. The patient understood all of the possible consequences and he adopted an alternative regimen with
minimum usage of voice and selected vocal exercises. The vocal rehabilitation program consisted of (1) Vocal hygiene guidelines and tips for avoidance of voice usage (emails or instant
messages instead of phone calls, for example); (2) Cancellation
of any extra rehearsal, advertisement recording, professional,
and social meetings during a week; (3) Voice exercises. Five
regular sessions were conducted with three on-site visits to implement guidelines and monitoring at the theater and a longterm follow up after 9 months.
Vocal training started with gentle exercises. Nasal sounds
(sustained humming for 3 seconds, with no modulation) and
a voiced fricative (sustained z for 3 seconds, with no modulation) were used during the first session, following a simple body
stretching approach to release tension; 2 days later, during the
following session, modulation was included using the same selected sounds (m.. and z.) and a semi-occluded vocal
tract exercise50 with closed rounded lips and a prolonged sustained and modulated sound was added. In the course of the subsequent sessions, chant talk, along with sequences of nasal and
voiced fricative syllables, were included. During the last session, since most of the detached mucosa was already reabsorbed,
vocal vibration technique (tongue trills) was included in three
ways: sustained, modulated, and with vowels. A physiological
warm-up and cool-down program was developed for the patient.
Three days later, a new examination revealed partial reabsorption of the detached mucosa (Figure 3B). Despite the unusual finding, there was no sign of hematoma or fibrosis. The
voice was quasinormal, with mild reduced loudness (62 dB at
1 m distance). The second author (GO) went to the theater
and advised the rest of the cast of what was happening with
the lead actor. During this meeting, the actors agreed to introduce several modifications to reduce effortful phonation,
mainly by lowering the overall loudness, creating a more contained interpretation. After 4 days, the actor was back on stage,
using the suggested behavioral changes in interpretation and
a good adherence to the vocal program regimen. The suggestion
of using a microphone was not followed.
After a week, laryngeal videostroboscopy showed regular
vocal fold vibrations, with mild mucosal wave asymmetry
and complete vocal fold closure. The posterior redundant mucosa at the disrupted fold did not interfere in the vibrations. It
would have been interesting to have a high-speed digital imaging analysis for detailed view51 but the equipment is not currently available in Brazil. There were no signs of mucosal
scar formation or vibratory deficit significant enough to impair
the patients professional voice use.

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Journal of Voice, Vol. 23, No. 6, 2009

FIGURE 1. Spectrographic traces of connected speech, number counting from 1 to 10 (FonoView 1.0, CTS Informatica). A. Speech sample at
a day postphonotraumatic event; B. Speech sample after 9 months.
The patient is currently acting in a soap opera and has just recorded two movies. He is getting ready for a new theater play.
He considers his performance as normal as it was in the past.
Nine months following the acute episode, perceptual analysis
showed mild roughness, which was consistent with his preferred and habitual voice.52 Maximum phonation time was at
the same mark (vowel /ae/1800 ) and fundamental frequency
did not show any considerable displacement (88.88 Hz).
Acoustic evaluation was within normal limits, including the
distribution of the phonatory deviation diagram. Loudness
was normal and mean intensity at conversational level was
higher, measured at 64 dB with capture at 1 m from the mouth
(Realistic, Sound Level Meter). Dynamic range varied from 48

to 92 dB, excluding shouting. Frequency distribution during

a connected speech task (such as counting numbers from 1 to
10) showed a higher mean frequency at 90.87 Hz, minimum
frequency at the same level, 70.58 Hz and maximum frequency
displaced towards a higher level, at 115.17 Hz. The maximum
frequency limit was produced in the third end of the sequence
of numbers (word sete, ie, seven) and a more modulated
natural speech was observed (Figure 1B). Spectrographic trace
analysis for the a self-selected comfortable sustained vowel /ae/
presented a longer duration12.51 seconds, with mild irregularity of trace (particularly during the first third of the production), presence of harmonics up to 5500 Hz, no vertical
striations, normal glottal attack and a more stable raise and

Mara Behlau, et al

Vocal Fold Self-Disruption After Phonotrauma

729

FIGURE 2. Phonatory Deviation Diagram (VoxMetria 2.5, CTS Informatica) showing the graphic distribution at a day postphonotraumatic event
(dark blue lines) and after 9 months (light green lines).

decay times. The Phonatory Deviation Diagram48,49 showed

a horizontal distribution within the normal area (Figure 2).
Laryngeal evaluation showed only a discrete bilateral symmetrical Reinkes edema, with no scar formation or any organized stiff tissue. At the posterior third of the glottis, over the
arytenoid cartilages there was a small mucosal bulk corresponding to the residual detached tissue. It did not interfere with the
vibrations (Figure 3C).

DISCUSSION
Stage actors use their voices with special adjustments to
achieve projection, enhance interpretation, and avoid vocal fatigue or dysphonia.5357 During a Shakespeare production,
voice projection usually requires an increased subglottic pressure, rapid vocal fold closure and a prolonged closed phase to
achieve the desired vocal projection without electric amplification. Usually, vocal loading is high in Shakespearean tragedies

FIGURE 3. Laryngeal images during breathingA. at a day postphonotraumatic event; B. after 3 days; C. after 9 months.

730
and the Brazilian version of Richard III was almost 3 hours long
with the lead actor being on stage 90% of the time. The projection skills of stage actors performing Shakespearean plays rely
on their voices rather than amplification and, therefore, optimal
projection is crucial and the presence of an actors formant can
be of great help.58
A sudden loss of voice quality and vocal fatigue after a phonotraumatic event is usually associated with vocal fold hemorrhage.5,7 However, our initial suspicion was wrong and instead
of the expected vocal fold hemorrhage, a highly disturbing image of a torn superficial layer of the vocal fold was seen.
Therefore, the sequence followed for this case was (1) complete voice evaluation; (2) correlation among data from all
exams and decision on voice management: medication, relative
vocal rest associated with vocal rehabilitation, and play set-up
modification; (3) consecutive follow up over a period of 1 year.
The importance of vocal rest after a mucosal damage is still
not clear. Behrman and Sulica59 studied vocal rest after microsurgical removal of vocal fold nodules, polyps, and cysts. Results indicate that there is a preference for the use of voice
rest, with an average of seven days, regardless of the type of lesion. However, complete or relative rest remains controversial.
Because the patient did not agree to undergo complete vocal
rest, the voice team decided to associate relative rest with selected vocal exercises. The rational for this option was speculative but recently, Branski et al60 stated that low physiological
levels of mechanical forces might be beneficial to tissue healing. Therefore, exercises can even help to reduce inflammation
and to promote wound healing by inducing synthesis of matrixassociated proteins.
The process of vocal fold wound healing is still unclear. Various types of stress can elicit an acute and complex set of inflammatory responses that lead to healing but also to
a possible tissue dysfunction or death.61,62 Much of the wound
healing knowledge comes from research done on the skin and
from some preliminary data on biochemical markers associated
to laryngeal secretions.63 The vocal fold mucosa has special
properties and is subjected to extensive mechanical forces
like no other tissue in the body. Therefore, results cannot be
generalized from other organs. The interactions between components of inflammation and response to stress are complex and
not well defined. The overall sequence of a tissue repair after
being injured comprises of hemostasis, inflammation, mesenchymal cell migration and proliferation, angiogenesis, epithelialization, protein and proteoglycan synthesis, wound
contraction, and remodeling.64 Wound healing is a systematic
process involving the reorganization of the tissue matrix. It
may produce scar and loss of tissue function, the most severe
response to injury at the vocal fold level, with adverse consequences. A scar in a highly specialized structure65 such as the
vocal fold can produce a nonpleasant effortful and highpitched, extremely deviated voice and is a treatment challenge
both for the physician and the speech-language pathologist.11,66
Our main concern when evaluating the patient was the possibility of a scar formation that would impair his vocal function and
threaten his career. There is not a single typical wound-healing
paradigm for the vocal folds64 and the influence of etiological

Journal of Voice, Vol. 23, No. 6, 2009

aspects and baseline mucosal condition on the anatomical and

functional outcome is not clear.
The patients larynx also showed Reinkes edema. Heavy
smoking is traditionally associated with this condition and laryngopharyngeal reflux may be strongly implicated.67 Histologically, this lesion has been characterized by a chaotic
distribution of short, torn, and scattered connective fibers,
marked by an excess of extracellular matrix.68 This histologically loose structure may have been ripped apart due to high
subglottic pressure and vocal fold stress related to the vocal demand of the scene. The vascular characteristic and increased
permeability of blood vessels in the superficial layer28,69 may
explain the blood taste in the mouth right after the feeling of vocal release.
The presence of previous Reinkes edema, which is characterized by excessive extracellular matrix68 may have helped
to rebuild the superior lamina propria due to the component
of the lesion, because it was observed that both epithelial and
stromal cells were in a state of higher metabolic activity reflecting their role in the production of extracellular matrix. Moreover, Duflo et al70 recently identified a high expression level
of antioxidants in Reinkes edema tissue samples that may protect the cells against negative effects of oxidative stress. As well
as the upregulated genes that may confer cellular resistance
(MAP2K3, SOD1, GPX2, and GTSA2), the CASP9 gene, responsible for cellular apoptosis execution was also upregulated
in these lesions. These findings can be interpreted as an extra
protection to patients with Reinkes edema when submitted to
a phonotrauma. The conclusion of this study is that a cellular
defense mechanism may provide protection against oxidative
stress that can explain the reduced occurrence of tumor cell
growth in the larynx of these patients. Although specific data
on our subject was not available (because we did not have a mucosal sample for microarray analysis), hypothetically, the upregulated genes may have played a role in the rapid recovery
without scar formation.
Because the patient refused to undergo complete vocal rest,
the alternative regimen was administered.
This case report reinforces the notion of fragility of the vocal
apparatus under an acute condition such as a cold or upper respiratory infection. A high vocal demand71 in a patient with
health problems may result in severe damage to the vocal folds,
leading to mucosal disruption. Moreover, the course of the condition considering the lack of recommended complete vocal
rest may reveal the possibility of using gentle vocal exercises
with low levels of mechanical forces for enhancing wound healing in cases of acute phonotrauma.
Acknowledgment
The authors would like to recognize the contribution of our
friend Dr Thomas Murry for the detailed editing of the final
text.
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