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Long-term Therapy for Spasmodic Dysphonia
Acoustic and Aerodynamic Outcomes
Ritvik P. Mehta, BS;
Stephen N. Goldman, MA;
Lisa A. Orloff, MD
Arch Otolaryngol Head Neck Surg. 2001;127:393-399.
ABSTRACT
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Objective To evaluate the long-term aerodynamic, acoustic, and electromyographic
effects of serial botulinum toxin (BT) injections in patients with adductor
spasmodic dysphonia.
Design Two-year, nonrandomized, controlled, before-after study.
Setting Ambulatory care clinic at a single academic medical center.
Patients A convenience sample of 91 patients with adductor spasmodic dysphonia
evaluated and treated during 2 years and 64 age- and sex-matched controls.
Interventions Injections of BT into the thyroarytenoid muscles in conjunction with
electromyographic evaluation and acoustic and aerodynamic evaluation before
and after serial BT injections.
Main Outcome Measures Translaryngeal airflow, jitter, shimmer, signal-to-noise ratio, fundamental
frequency, standard deviation of fundamental frequency, maximum phonation
time, and inappropriate muscle activity by electromyography.
Results Translaryngeal airflow, jitter, and shimmer improved significantly after
serial BT treatments and showed sustained improvement over time. Fundamental
frequency, standard deviation of fundamental frequency, and signal-to-noise
ratio did not change significantly after BT treatment. Electromyographic data
suggested decreased inappropriate muscle activity with repeated BT injections.
Conclusion Treatment with BT provides ongoing relief of voice perturbations in
patients with adductor spasmodic dysphonia who undergo long-term cumulative
therapy.
INTRODUCTION
DYSTONIAS are disorders of central motor processing that lead to abnormal
tonicity of muscles and thus dyskinetic movements or uncontrolled spasms.
These movements can be slow and sustained or rapid and uncoordinated. Focal
dystonias involve only one particular region of the body, whereas multifocal
dystonias, as the name implies, involve several regions or muscle groups.
In 1871, Traube1 first described the focal
laryngeal dystonia known as spasmodic dysphonia (SD).
Spasmodic dysphonia is characterized by spasms of the laryngeal muscles
that are active during vocal fold adduction (vocalis-thyroarytenoid muscle
complex) or, less commonly, those involved in vocal fold abduction (posterior
cricoarytenoid muscles). In the adductor type of SD, the voice is typically
hoarse, soft, and strained, with abrupt initiation and termination of voicing
causing breaks in phonation and variation in pitch. These symptoms are associated
with increased approximation of the vocal folds and decreased transglottic
airflow during phonation. The abductor variety of SD is characterized by a
whispery or weak, breathy voice, especially at the onset of voicing, with
associated decreased vocal fold approximation and increased airflow during
phonation. In addition, some patients might exhibit characteristics of both
forms of SD.
As with most dystonias, the cause of SD is unknown, although it is believed
to originate in the basal ganglia, a well-known motor nucleus in the brain.
It has also been determined that some forms of dystonia have a genetic origin.
The incidence of SD is about 1 in 10 000 adults and is more prevalent
in women than in men. The average age of onset of the disorder is 40 to 50
years. Although there is no known cure for SD, therapeutic interventions have
ranged from surgery to voice therapy to pharmacologic injections into the
laryngeal musculature. The most common surgical treatment involves sectioning
of the recurrent laryngeal nerve to induce vocal fold paralysis. Although
this approach was initially promising, high rates of recurrence of symptoms
(up to 64%) have been reported after surgery.2
A relatively new surgical treatment involving selective denervation of the
adductor branch of the recurrent laryngeal nerve has been attempted by Berke
et al.3 However, outcomes based on a large
series are not yet available for this procedure.3
Voice therapy has been aimed mainly at control of symptoms and does not alter
the underlying disorder.
Currently, the preferred treatment for patients with adductor and abductor
types of SD is localized injections of botulinum toxin (BT) directly into
the hyperfunctioning laryngeal muscles. Botulinum toxin is produced by the
anaerobic bacterium Clostridium botulinum and is
harvested from bacterial cultures for therapeutic use. Use of BT achieves
a temporary weakening or partial paralysis of the musculature controlling
the vocal folds by blocking the presynaptic release of the neurotransmitter
acetylcholine. The effect of BT treatment is eventually overcome as reinnervation
of the muscle occurs through the sprouting of new nerve terminals. Patients
with SD thus receive BT injections periodically an average of every 3 to 4
months. Botulinum toxin is typically injected into the hyperfunctional thyroarytenoid
muscles for adductor SD and into the posterior cricoarytenoid muscles for
abductor SD.
The aim of this study was to comprehensively and objectively document
the effects of repeated injections of BT on acoustic and aerodynamic voice
properties and laryngeal electromyographic (EMG) activity in patients with
adductor SD who undergo long-term treatment.
PATIENTS AND METHODS
PATIENTS
All patients with adductor SD evaluated at the University of California,
San Diego Medical Center between September 1, 1995, and December 31, 1998,
were invited to participate in this study. The diagnosis of SD was made by
an otolaryngologist (L.A.O.) in conjunction with a speech pathologist (S.N.G.)
based on the results of a detailed clinical history, fiberoptic laryngoscopy
with or without videostroboscopy, a complete neurological examination, and
an acoustic and aerodynamic analysis of each patient's voice. The fiberoptic
laryngoscopy confirmed the presence of abnormal spasms and hyperfunction of
the laryngeal musculature during speech. The voice analysis allowed an objective
confirmation of the patient's vocal symptoms. The proposed research protocol
was approved by the Human Subjects Committee at the University of California,
San Diego.
STUDY DESIGN
Patients who completed the entire protocol were studied for a minimum
of 2 years at 6 points: T1, entry into the study (before treatment or retreatment);
T2, 6 weeks after the first BT treatment or retreatment; T3, immediately before
the first BT treatment that occurred 12 months or more after T1; T4, 6 weeks
after the T3 measurement; T5, immediately before the first BT treatment that
occurred 12 months or more after the T3 injection (approximately 2 years after
study entry); and T6, 6 weeks after the T5 measurement. Some patients did
not complete all 6 data collection sessions, as described in the "Results"
section. Each pair of measurements (ie, T1 and T2, T3 and T4, and T5 and T6)
represented a preinjection and postinjection set of data.
In addition to patient data collection, normative data for all noninvasive
aerodynamic and acoustic measurements were obtained from 64 age- and sex-matched
control subjects without a voice disorder.
PROCEDURES
All BT injections were performed by one otolaryngologist (L.A.O.) using
a transcutaneous approach and EMG guidance into the laryngeal muscles. Immediately
before BT injection, patients received subcutaneous 1% lidocaine injections
to induce local anesthesia. Patients received unilateral or bilateral thyroarytenoid
injections at doses ranging from 0.75 to 30.00 U of BT (botulinum toxin type
A; Allergan Inc, Irvine, Calif) at each injection site. There are no concrete
guidelines for dosage, and each patient's injection dosage was determined
by evaluating individual responses to injections. The first few injections
for each patient typically varied in dose until an optimal therapeutic dose
was determined based on perceptual evaluation of the patient's vocal quality,
degree and duration of symptom relief, and incidence of adverse effects such
as breathiness, hoarseness, and dysphagia. There were no complications from
BT injections.
DATA COLLECTION
Aerodynamic Data: Phonatory Airflow
Each patient was fitted with a standard anesthesia face mask covering
the nose and mouth. Coupled to this mask was a pneumotachograph and a differential
pressure transducer, which in turn connected to a laboratory computer and
its accompanying software (Atlantis; Lakeshore Technologies, Chicago, Ill).
The system was calibrated by passing a continuous airstream through a rotameter
coupled to the pneumotachograph and differential pressure transducer. Airflow
was measured for each patient's sustained phonation of the vowel /a/. Three
samples of the /a/ were obtained at each data collection point. The airflow
rates of the first 3 seconds of each of the 3 samples were averaged, and this
value was used for analysis.
In the second year of the study, a new device for measuring airflow,
the Aerophone II model 6800 (Kay Elemetrics Corp, Lincoln Park, NJ), was acquired.
The Aerophone II consists of a handheld transducer module that gathers information
about airflow, air pressure, and sound pressure levels. The data collected
are transmitted to the Aerophone II software for numerical analysis. Airflow
is measured in a method similar to that described in the previous paragraph
using the pneumotachograph.
During the initial period when the Aerophone II was introduced into
the study, patients underwent airflow measurements with the pneumotachograph
and the Aerophone II; 83 measurements were obtained using both systems. A
correlation matrix between the values obtained revealed a correlation coefficient
of 0.654. A Fisher r-to-z transformation showed this value to be highly significant
(P<.001). Given this strong correlation between
the 2 systems, the old pneumotachograph system was dismantled, and all subsequent
airflow measurements were made using the Aerophone II.
Acoustic Measures
Acoustic data were gathered from voice samples of sustained phonation
of the vowel /a/ and repetition of the syllable /wun/. The voice signals were
recorded using a microphone (Audio Technica AT822; Sony, Tokyo, Japan) and
low-pass filtered with a sampling rate of 8 kHz. The acoustic signals were
digitally processed using the software program CspeechSP (Paul Milenkovic,
PhD, University of Wisconsin–Madison). The following acoustic measures
were recorded: (1) fundamental frequency (F0), in hertz; (2) shimmer, in percentage
(cycle-to-cycle variation in signal amplitude); (3) jitter, in milliseconds
(cycle-to-cycle variation in the period or frequency of the signal); (4) signal-to-noise
ratio (SNR), in decibels (ratio of energy in the signal vs the noise components
also contained in the acoustic spectrum); and (5) standard deviation of F0
(SDF0), in hertz (square root of the variance around the mean F0).
Maximum Phonation Time
At each data collection point, a voice recording consisting of the sustained
phonation of the vowel /a/ was obtained for each patient and used to calculate
the maximum phonation time (MPT).
EMG Studies
At the time of BT injection, the EMG signal was subjectively graded
by the otolaryngologist and the speech pathologist on a 3-point severity scale
of inappropriate muscle activity (IMA)4: 1
indicates little to no IMA; 2, low-amplitude IMA during phonation; and 3,
high-amplitude IMA during phonation.
The EMG signal observed was a function of the location of the needle
tip within the muscle being injected, which might have varied from one injection
to the next in a given patient. Nevertheless, effort was made at each injection
to identify and inject the site of maximum IMA within the vocal fold.
STATISTICAL ANALYSIS
The aerodynamic and acoustic variables were analyzed using analysis
of variance (ANOVA) at an overall significance level of P<.05. A Fisher protected least significant difference was computed
for all possible pairwise comparisons using data from T1 through T6. In addition,
a 1-factor repeated-measures ANOVA was performed on the subset of patients
who had complete data at each data collection point (T1-T6). Patient data
were compared with control data using an unpaired t
test. A separate analysis was conducted to evaluate whether there were any
significant differences between patients who had and those who had not been
treated with BT before study entry. This analysis revealed no significant
differences between the 2 groups in terms of the acoustic and aerodynamic
variables evaluated. The results presented in the following section thus represent
all patients in the study. Data are given as mean ± SD.
RESULTS
PATIENTS
Of 91 patients who underwent initial evaluation (T1), 70 were women
and 21 were men (age range, 26-93 years; median age, 62 years). Of these 91
patients, 61 (67%) had been treated previously with BT and the remaining 30
(33%) had their first BT injection as part of the study. At T2, 65 patients
had complete evaluations. At the remaining points, the following numbers of
patients underwent measurements: T3, 52 patients; T4, 36 patients; T5, 34
patients; and T6, 21 patients. Patient accrual continued during the study,
so the sample size at each data collection point from T1 to T6 is different.
Theoretically, preinjection measurements (T1, T3, and T5) were made
at a time when the patient's vocal symptoms were at their worst. Postinjection
measurements should be indicative of the amount of benefit a particular patient
received from BT therapy because the patient's voice had typically stabilized
within 6 weeks of treatment.
AERODYNAMIC MEASUREMENTS: PHONATORY AIRFLOW
Mean airflow at each data collection point is shown in Figure 1A and Table 1.
Overall, patients showed improvement in airflow after BT treatment, with the
overall difference between periods being statistically significant (P = .03). The most significant difference was between T1
and T2 (P = .008). When all pretreatment airflow
measurements (T1, T3, and T5) were averaged and compared with an average of
all posttreatment airflow measurements (T2, T4, and T6), the difference was
statistically significant (P = .007) (Figure 1B).
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Figure 1. Aerodynamic data: mean translaryngeal
airflow for all patients (A), average preinjection vs postinjection airflow
(B), and translaryngeal airflow for 16 patients who had data at all 6 data
collection points (C). Error bars represent SD. See the "Study Design" section
for definitions of the data collection points (T1-T6).
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Table 1. Mean Translaryngeal Airflow for Sustained Phonation of the
Vowel /a/ for Controls and All Patients at Each Data Collection Point*
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Repeated-measures ANOVA for 16 patients who had data at all 6 data collection
points (T1-T6) again showed the overall difference between periods to be statistically
significant (P = .006) (Figure 1C).
Control data for airflow yielded mean airflow of 187.14 ± 96.91
mL/s. The overall difference between this value and patient values at any
given data collection point (T1-T6) was not statistically significant. Comparing
the control group average to the pretreatment airflow average (T1, T3, and
T5), P>.10. Comparing average airflow for controls
with the posttreatment airflow average (T2, T4, and T6), borderline significance
was noted (P = .07). However, patients with SD showed
a trend in which they initially started with lower-than-normal airflow but
after BT treatment had higher-than-normal airflow, which was maintained with
subsequent injections.
ACOUSTIC MEASUREMENTS
Fundamental Frequency
Data for F0 were analyzed separately by sex owing to the distinct difference
in vocal pitch between men and women. Overall differences between data collection
points (ANOVA) and the repeated-measures ANOVA were not statistically significant
for either sex. Control data indicated a mean F0 of 170 ± 31.7 Hz for
women and 127.9 ± 36.5 Hz for men, which did not differ significantly
from patient data (Table 2).
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Table 2. Acoustic Data for Sustained Phonation of the Vowel /a/ for
Controls and All Patients at Each Data Collection Point*
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Standard Deviation of F0
Differences in mean values for SDF0 at each data collection point were
not statistically significant (Table 2).
Control data, however, showed a mean SDF0 of 2.32 ± 1.63 Hz, which
was significantly lower than patient data at each data collection point (P<.001). Thus, patients with SD have a higher SDF0 than
normal.
Shimmer
Mean values for shimmer at each data collection point are shown in Figure 2A and Table 2. Neither differences between data collection points for
all patients nor the repeated-measures ANOVA for the 14 patients with complete
shimmer data from T1 through T6 were statistically significant. Control data
for shimmer showed a mean value of 5.61% ± 3.83%. The overall difference
between control data and patient data at each data collection point was highly
statistically significant (P<.001). Thus, patients
with SD had higher than normal values for shimmer. The trend from T1 through
T6 suggests that shimmer tends to decrease after treatment with BT, although
it never reaches normal values.
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Figure 2. Acoustic data: shimmer (A), jitter
(B), signal-to-noise ratio (C), and maximum phonation time (D). Error bars
represent SD. See the "Study Design" section for definitions of the data collection
points (T1-T6).
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Jitter
Mean values for jitter at each data collection point are shown in Figure 2B and Table 2. The overall difference between periods was of borderline
statistical significance (P = .05). The pair contributing
most to the significance level was T1 and T2 (P =
.02). When all pretreatment jitter measurements (T1, T3, and T5) were averaged
and compared with an average of all posttreatment jitter measurements (T2,
T4, and T6), the difference was statistically significant (P = .02). Repeated-measures ANOVA for the 14 patients with complete
jitter data from T1 through T6 did not show overall significance (P>.05).
Control data for jitter showed a mean value of 0.046 ± 0.051
milliseconds. The overall difference between control data and patient data
at each data collection point was highly statistically significant (P<.001). As with shimmer, patients with SD had much-higher-than-normal
values of jitter that tended to decrease with treatment but never reached
normal values.
Signal-to-Noise Ratio
Mean values for SNR at each data collection point are shown in Figure 2C and Table 2. The overall difference between data collection points for
all patients and the repeated-measures ANOVA for the subset of patients with
complete SNR data from T1 through T6 were not statistically significant (P>.05). Control data showed a mean SNR of 17.50 ±
3.63 dB. The overall difference between control data and patient data at each
data collection point was statistically significant (P<.005).
Patients with SD had lower-than-normal SNR values, and there was no significant
increase in SNR after BT therapy.
PHONATION TIME
Mean MPT during sustained phonation of the vowel /a/ for each data collection
point is shown in Figure 2D and Table 2. The overall ANOVA was not statistically
significant. When all pretreatment MPT measurements (T1, T3, and T5) were
averaged and compared with an average of all posttreatment MPT measurements
(T2, T4, and T6), the difference was statistically significant (P = .03). The repeated-measures ANOVA for the subset of 14 patients
with MPT data at each data collection point did not show a significant change
(P>.05).
Control data showed a mean MPT of 15.46 ± 6.15 seconds. Patient
values at each data collection point were significantly lower than control
values (P<.05). Thus, patients with SD tend to
have lower-than-normal MPT values.
EMG DATA
Electromyographic data were recorded at each treatment period (ie, T1,
T3, and T5). The mean score on the 3-point IMA scale at T1 (n = 84) was 2.875
± 0.328, decreasing to 2.723 ± 0.513 at T3 (n = 56) and to 2.653
± 0.619 at T5 (n = 36). This downward trend suggests that decreased
IMA and lower-amplitude EMG signals are obtained with repeated BT injections.
Reasons that not all patients completed measurements at all 6 data collection
points included (1) late entry into the study, (2) unwillingness to return
for evaluation at a point that a BT injection would not be administered (T2,
T4, and T6), (3) doing well from the last BT injection and not believing it
was necessary to return for another injection before the study ended, and
(4) being lost to follow-up. For 26 patients lost to follow-up, a questionnaire
was mailed to determine their reasons for not returning for BT therapy or
evaluation. Of these, 6 patients subsequently returned for further therapy
or reported that their symptoms were manageable and that they would return
for further treatment if necessary; 8 cited geographic reasons for discontinuing
therapy; 4 cited financial reasons for being unable to continue with therapy;
and 7 did not return the questionnaires and we were unable to contact them.
Only 1 patient stated that BT treatment was not helpful.
COMMENT
Although BT therapy for SD has previously been shown to benefit patients
in the short term regarding their acoustic and aerodynamic characteristics,5 the results of the present study demonstrate that
the benefit of BT therapy is maintained in the long term and after repeated
injections. In a recent retrospective analysis of their long-term experience
with BT treatment of SD, Blitzer et al6 documented
subjective improvements in the symptoms of most patients. However, no objective
data have been previously documented for patients who receive long-term or
ongoing treatment of SD.
Given that adductor SD is essentially a disorder of phonatory airflow
secondary to overclosure of the vocal folds, the efficacy of BT in treating
SD primarily results from the improvement in translaryngeal airflow after
treatment. Most studies5, 7, 8
of airflow in patients with SD report lower-than-normal airflow rates. Hirano
et al9 reported airflow rates within the reference
range in patients with SD. Normal airflow rates also vary based on the source
of information. The Aerophone II device manual reports that normal mean airflow
in adults is 140 mL/s. Zwirner et al5 found
controls to have mean airflow of 177mL/s. In this study, control subjects
had mean airflow of 187 mL/s. It is clear in this study that patients with
SD have lower-than-normal airflow and that airflow typically increases to
higher than normal after therapy with BT. This increase in airflow can be
maintained with repeated injections of BT.
The lowest airflow rate occurred at the T1 baseline measurement. Subsequent
pretreatment measurements (ie, T3 and T5) show higher airflow rates than at
baseline, which might be due to patients returning for injections before severe
deterioration of their voice.
The ideal study would measure airflow in many patients who received
the same dose of BT through serial injections over time. However, variation
in dosage among patients was occasionally necessary because the optimal balance
between degree and duration of symptom relief and the incidence of adverse
effects was patient specific. Feedback from patients regarding their experience
throughout the interval between injections was incorporated into the decision
regarding successive BT doses. Rather than having an ideal quantitative end
point for aerodynamic values, a qualitative end point of "optimal voice" with
minimal adverse effects was pursued through treatment with BT injections,
and the resultant or quantitative airflow values were evaluated to see how
they corresponded to a voice that had reduced or resolved symptoms.
Objective acoustic measures are other important tools used widely in
the clinical management of voice disorders.10
The variables evaluated in this study are related to the salient perceptual
characteristics of the voice, namely, vocal pitch, loudness, and quality.
The F0 measurements, before and after treatment, did not differ significantly
compared with control measurements, suggesting that vocal pitch itself is
not significantly altered in SD. In a double-blind controlled study of BT
treatment in 13 patients with adductor SD, Truong et al11
also noted that F0 did not differ between BT- and placebo-treated patients.
However, they noted that the range of vocal F0 decreased in patients treated
with BT compared with placebo. This might suggest that BT diminishes spasmodic
movements of the vocal folds even though the overall F0 remains unchanged.
Although F0 in patients with SD is comparable to that of controls, the
SDF0 differs significantly between patients with SD and controls. The SDF0
is a reflection of laryngeal stability and has been noted to be significantly
higher in patients with SD than controls in previous studies.5, 12
Both of these studies also showed that BT therapy resulted in a significant
decrease in SDF0, suggesting increased laryngeal stability. In our study,
SDF0 was also significantly higher in patients with SD compared with the control
group. However, the expected trend of decreases in SDF0 after treatment were
seen only for the first 2 rounds of measurements, ie, through T4. The final
measurements actually showed a marginal increase in SDF0 from T5 to T6. These
differences were not statistically significant (P>.05)
and thus might be due to chance. One limitation of this analysis is that the
sample size decreased at each successive data collection point. Thus, not
all patients received measurements of SDF0, as reflected in Table 2. The initial trend of decreases in SDF0, however, suggests
increased laryngeal stability after BT therapy.
Jitter and shimmer are measures of vocal perturbation that can be used
to detect vocal abnormalities. The idea of using jitter and shimmer to detect
or monitor vocal abnormalities is based on the hypothesis (for which there
is growing evidence) that healthy vocal folds form a well-balanced system
that produces nearly periodic oscillations. Vocal abnormalities might perturb
this mechanical balance, producing oscillations that change from period to
period in frequency and amplitude. Measurements of jitter and shimmer thus
provide an index of the perturbation present within the vocal system. Higher
values of jitter and shimmer have been correlated with rough- or harsh-sounding
voices.13 Patients with SD clearly have significantly
higher jitter and shimmer values compared with controls. This observation
has been corroborated in previous studies.5
Although there is a trend toward decreased jitter and shimmer values after
BT therapy, these measurements remain higher than normal.
Signal-to-noise ratio represents the ratio of the energy in the acoustic
signal to the noise components in the vocal symptoms and serves as an objective
assessment of voice loudness. Typically, a value of 15 or greater is considered
normal for SNR. Patients with SD develop an increase in the amount of noise
in the acoustic spectrum and thus typically have lower SNR values. No significant
change in SNR was noted in this study after BT therapy, although SNR values
did trend up at the T2 and T4 postinjection evaluations compared with the
T1 and T3 preinjection values. Previous studies5, 14
have also shown modest increases in SNR values after BT therapy.
Maximum phonation time is a function of airflow across the glottis during
phonation. With disorders such as SD that result in low airflow rates, the
MPT is expected to be lower than normal. Our pretreatment data are consistent
with this expectation. Normative data for MPT obtained in this study agree
with those obtained from the literature: 22.2 seconds for men and 18.4 seconds
for women.15 A previous study by Truong et
al11 showed that phonation times did not improve
in patients with adductor SD treated with BT. This was believed to be because
BT treatment results in chemodenervation of the adductor muscles of the vocal
folds, which can cause decreased vocal fold approximation and thus no improvement
or even a decrease in phonation time. In the present study, average MPT decreased
significantly in the 3 posttreatment groups compared with the 3 pretreatment
groups. These results are consistent with the hypothesis of Truong et al and
likely reflect increased air escape due to decreased laryngeal resistance
after BT therapy.
In addition to quantitative acoustic and aerodynamic data, we qualitatively
looked at EMG signals to gauge whether any change resulted with repeated BT
injections into the laryngeal muscles. Our observations of lower-amplitude
EMG signals with repeated BT injections suggest that the reinnervation process
after treatment takes a long time. In addition, because patients are likely
to return for additional injections before their symptoms are at their worst,
there is likely to be a small chemodenervation effect remaining from the previous
injection. This residual effect manifests itself in lower-amplitude EMG signals.
Davidson and Ludlow16 noted that although the
physiological effects of BT are reversible, the reinnervation process continues
past 12 months after injection.
CONCLUSIONS
This study demonstrates that BT is not only a safe and effective therapy
for SD but that its benefit is maintained even with repeated use over the
long term. We objectively documented that BT treatment results in an increase
in translaryngeal airflow and that this increase is not compromised even with
prolonged use. In addition, BT use results in improvements in vocal perturbation
measures such as jitter and shimmer, which correlate with perceptual improvements
in voice as being less harsh and strangled.
In addition to the objective measures discussed herein, the quality
of life, economic impact, and perceptual analysis of voice recordings from
this group of patients with SD treated with BT are presented in separate reports
(unpublished data, submitted for publication) but parallel the improvements
described herein. Treatment with BT continues to provide effective relief
of symptoms and voice perturbations in patients who undergo long-term cumulative
therapy and might even have a positive and permanent effect on the overall
severity of the disorder.
AUTHOR INFORMATION
Accepted for publication September 5, 2000.
From the Division of Otolaryngology, University of California, San
Diego, School of Medicine.
Corresponding author and reprints: Lisa A. Orloff, MD, Division of
Otolaryngology, University of California, San Diego School of Medicine, 200
W Arbor Dr, San Diego, CA 92103-8891 (e-mail: lorloff{at}ucsd.edu).
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