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Prognostic Value of Laryngeal Electromyography in Vocal Fold Paralysis
Christian Sittel, MD;
Eberhard Stennert, MD;
Walter F. Thumfart, MD;
Ulrike Dapunt, MD;
Hans E. Eckel, MD
Arch Otolaryngol Head Neck Surg. 2001;127:155-160.
ABSTRACT
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Objective To analyze the value of electromyography in predicting recovery from
acute neurogenic vocal fold paralysis.
Study Design Prospective case series.
Setting University-based hospital of otorhinolaryngology–head and neck
surgery.
Patients Ninety-eight patients (56 women, with a mean age of 62.2 years; 42 men,
with a mean age of 39.8 years) with 111 paralyzed vocal folds. The causes
were varied, with thyroid surgery (53 cases) and idiopathic palsy (18 cases)
being the predominant factors.
Intervention Prognostication was based on electromyography performed no earlier than
14 days after onset of palsy. Findings were classified as neurapraxy, axonotmesis,
and neurotmesis. Prognosis is inherent in this classification, since neurapraxy
is presumed to resolve completely within 8 to 12 weeks, whereas axonotmesis
is most likely to be followed by impaired vocal fold mobility.
Main Outcome Measures Vocal fold mobility after 6 months.
Results In 102 vocal folds, some palsy of various degree persisted after 6 months.
Free mobility of the paralyzed vocal fold was restored in 9 cases. By means
of laryngeal electromyography, defective recovery, defined as absence of completely
free vocal fold mobility, was predicted correctly in 94.4% of cases (68/72).
For complete recovery, prognosis was accurate in only 12.8% of cases (5/39).
Conclusions The detection of neural degeneration by laryngeal electromyography allows
the prediction of poor functional outcome with sufficient reliability in an
early phase of the disease process. Conversely, the absence of signs of degeneration
does not imply that complete recovery is to be expected.
INTRODUCTION
UNILATERAL lower motoneuron-type palsy of the vagus or recurrent laryngeal
nerve with acute onset is a condition usually associated with immediate hoarseness
and breathiness of voice. Incomplete vocal fold adduction may cause formation
of a constant glottal gap, handicapping severely the ability to communicate
even in non–voice professionals. In contrast, simultaneous bilateral
recurrent nerve paralysis frequently leads to glottic stenosis with the vocal
folds in a fixed paramedian position. Inspiratory stridor and respiratory
distress, even without exertion, may be the result, requiring tracheostomy
in many cases.
The underlying cause of neurogenic vocal fold palsy may be trauma or
tumor erosion along the nerve's course from the skull base to the mediastinum
and back to the larynx. If no causative factor can be found despite complete
diagnostic workup, the paralysis is labeled idiopathic.
However, iatrogenic injury during surgery accounts for the majority of laryngeal
recurrent nerve lesions.1 Various procedures
endanger the integrity of the vagus and laryngeal recurrent nerves, including
thyroid surgery, cervical spine surgery via anterior approach, vascular surgery
of the carotid artery and the aortic arch, esophageal surgery, and surgery
of the skull base and of the neck.
Probably the questions most frequently asked by these patients are whether
their laryngeal function will return to normal and how long this is going
to take. In addition, an objective description of the extent of iatrogenic
nerve injury may become of medicolegal importance. The use of laryngeal electromyography
(LEMG) has been advocated to classify severity of neural damage,2
to establish a prognosis for nerve recovery, and to differentiate neurogenic
palsy from vocal fold immobility caused by arytenoid luxation.3
However, few data exist regarding validity, reliability, and reproducibility
of clinical electrophysiology of the recurrent laryngeal nerve. It is the
aim of this study to assess the prognostic significance of LEMG in patients
with vocal fold paralysis in a prospective design.
PATIENTS AND METHODS
LARYNGEAL ELECTROMYOGRAPHY
Basically, electromyography evaluates the integrity of the motor system
by recording action potentials generated in the muscle fibers. All 5 major
laryngeal muscles (thyroarytenoid [TA], lateral cricoarytenoid, posterior
cricoarytenoid, interarytenoid, and cricothyroid) lend themselves for electrophysiologic
examination. In this article, only electrophysiologic data obtained from the
TA muscle will be reviewed.
The TA muscle was approached in the awake patient either transcutaneously
or transorally. For the transcutaneous approach, which has been described
in detail elsewhere,4 bipolar concentric needle
electrodes 45 mm in length are inserted in the region of the cricothyroid
membrane after cleaning of the skin with alcohol. To evaluate the TA muscle,
the needle was inserted in the midline right above the cricothyroid notch,
a small depression immediately above the cricoid cartilage. After passing
through the cricothyroid membrane, the tip of the needle was angled to the
affected side laterally and superiorly 30° to 45°. If the patient
coughed, which indicated penetration of the airway space, the needle was withdrawn
and repositioned. An increase in LEMG activity while the patient was phonating
validated correct electrode position. In addition, standard verification gestures
to assist in localizing the position of needle electrodes were used, as described
elsewhere in detail.4 However, if no muscle
activity was detectable, electrode displacement could not be discriminated
from complete vocal fold paralysis by the transcutaneous technique.
For transoral LEMG, bipolar hooked-wire electrodes were used. The hooks
at the end of these thin flexible wires act as barbs, keeping the electrode
in place once positioned in the muscle. For endolaryngeal application, a specially
designed device was used: a curved metal cannula on a handpiece hiding a hollow
flexible needle that contains the hooked-wire electrode (Inomed Co, Teningen,
Germany). The device was inserted into the endolarynx under endoscopic guidance,
with the needle tip being secured in the applicator. Surface anesthesia of
the oropharynx and endolarynx was induced before the procedure. When the applicator
was positioned correctly above the mediodorsal aspect of the vocal fold, the
tip of the needle was pushed into the TA muscle. Because of the hooks at the
distal end of the wire, the electrode remained in position when the applicator
was withdrawn gently. This technique allowed better control over electrode
position than the transcutaneous approach but was more time consuming, significantly
more expensive, and technically more difficult. In addition, the majority
of patients feel transoral hooked-wire LEMG to be less tolerable. Therefore,
we used transoral LEMG only when a transcutaneous approach was not possible,
ie, in patients with tracheostomy or with a nonpalpable cricoid. In this series,
91 patients were studied transcutaneously vs 7 transorally.
Regardless of technique, electrophysiologic evaluation was performed
according to the following criteria. The use of LEMG allows for distinction
between normal silent resting potential, voluntary motor unit potential, spontaneous
fibrillation potential, and polyphasic reinnervation potential. The absence
of any electrical activity either on electrode insertion or on attempted voluntary
motion is called electrical silence. Normal voluntary
action potentials are diphasic or triphasic and are extremely variable in
amplitude (Figure 1 and Figure 2). Spontaneous
fibrillation activity is defined as involuntary potential generated
by a single muscle fiber, indicating axonal degeneration (Figure 3). However, this symptom of degeneration does not appear
earlier than 10 to 14 days after injury. Polyphasic motor units have 4 or
more phases and herald nerve regeneration (Figure 4).
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Figure 1. Extremely rarefied firing pattern
on phonation, but no spontaneous activity at rest (neurapraxy).
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Figure 2. Slightly reduced recruitment on
phonation, with no spontaneous activity at rest (neurapraxy).
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Figure 3. Spontaneus fibrillation activity
at rest, with minimal recruitment on voluntary action (axonotmesis).
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Figure 4. Polyphasic, prolonged action potentials
with giant amplitudes (reinnervation 4 months after nerve injury).
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Electrophysiologic findings were classified according to Seddon5 into neurapraxy, axonotmesis, or neurotmesis. For
neurapraxy, the diagnostic criteria on LEMG are detection of a rarefied recruitment
pattern or single action potentials on voluntary action without fibrillation
activity and without spontaneous positive sharp waves. Axonotmesis is suspected
when spontaneous activity, indicating neural degeneration, can be detected.
Usually, this is the case no earlier than 10 to 14 days after onset of paralysis.
Prognosis is inherent in this classification,2
since neurapraxy is most likely to resolve completely within 8 to 12 weeks,
while axonotmesis is thought to have only a poor chance of recovery to a functional
level. If reinnervation occurs after axonotmesis, usually it is associated
with sequelae such as synkinesis caused by neuronal misdirection.6, 7, 8 The result is simultaneous
activation of adducting and abducting intrinsic laryngeal muscles. For the
same situation in facial nerve disorders, the apposite term autoparalytic syndrome has been coined.9
Neurotmesis, representing complete destruction of the whole nerve structure
over its full diameter, apparently cannot be expected to resolve at all.
All LEMG examinations were performed with a computer-based electrodiagnostic
system (NeuroScreen Plus; Jaeger-Toennies Inc, Höchberg, Germany). Signals
were monitored by means of a speaker, bandpassed between 20 and 10 000
Hz, and stored in a database for later analysis.
PATIENT POPULATION
In the electrophysiologic unit at the Department of Otorhinolaryngology,
Head and Neck Surgery at University of Cologne, Cologne, Germany, 540 LEMG
studies were performed between May 1, 1995, and September 30, 1998. For the
98 patients analyzed in this study, follow-up was complete during at least
6 months. By means of videostroboscopy, final vocal fold mobility was classified
in 4 groups: free mobility when movement was normal
compared with the unaffected side, substantial mobility when the affected vocal cord was moving in a clearly reduced but functional
way, minimal mobility, when vocal folds moved in
a markedly reduced way without obvious functional effect, and no mobility when the affected vocal fold stood completely still or
showed only signs of passive movement. In 85 of these 98 cases, vocal fold
palsy was unilateral, and bilateral immobility was present in 13 patients,
for a total of 111 paralyzed vocal folds. The LEMG was performed on day 14
after onset of palsy at the earliest; the average delay was 27 days. For all
cases, reliable and exact information on the beginning of the disorder was
available. Fifty-six patients (57%) were women and 42 (43%) were men. Mean
age was 62.2 years for women and 39.8 years for men. Data regarding cause
of paralysis show that surgery involving the thyroid and neck contributed
the greatest to the overall number. In the female patients, thyroid surgery
was by far the single most important causative factor. In the male study population,
thyroid surgery, followed by cervical vascular surgery and idiopathic lesions,
accounted for the majority of vocal fold palsies. All 13 cases of bilateral
paralysis were caused by thyroid surgery. Table 1 gives a detailed overview of nerve injury causes, separated
for men and women.
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Table 1. Causes of Vocal Fold Paralysis by Sex
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RESULTS
At least 6 months after onset of palsy, completely free mobility of
the paralyzed cord was restored in 9 (8.1%) of 111 vocal folds. Twenty-two
vocal folds (19.8%) recovered substantial mobility, and 30 (27.0%), minimal
mobility, while 50 vocal folds (45.0%) remained immobile.
Phonatory function was normal or near normal again in 19 (19.4%) of
98 patients. Forty-five patients (45.9%) had fair voices and 14 (14.3%) had
usable voices, while severe dysphonia persisted in 20 (20.4%) of 98 patients.
The LEMG was used in all 98 patients on 111 paralyzed vocal folds. The
first examination took place an average of 27 days after onset of palsy. At
this point, all diagnostic criteria should have developed to allow a diagnosis
according to the Seddon classification, which implies a prognosis based on
the expected clinical course. Thirty-nine patients were diagnosed as having
neurapraxy, while 72 laryngeal palsies were characterized as axonotmesis.
Neurotmesis was found in no case. Table
2 gives a cross-tabulation of electrodiagnostic classification and
final facial function for this population. On the basis of these data, a positive
predictive value (PPV) and a negative predictive value (NPV) can be calculated
by the following formulas: PPV = [No. (defective recovery and positive test)]/[No.
(defective recovery and positive test) + No. (complete recovery and positive
test)]; and NPV = [No. (complete recovery and negative test)]/[No. (defective
recovery and negative test) + No. (complete recovery and negative test)].
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Table 2. Diagnosis at First Examination vs Actual Outcome
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In general, the concepts of PPV and NPV answer the question of what
the chances are that a positive test result actually reflects the presence
of a certain condition. In the context of this study, the PPV describes the
conditional probability that axonotmesis, defined as a positive test result,
leads to incomplete recovery of laryngeal nerve function with sequelae. The
opposite situation is highlighted in the NPV, showing how often neurapraxy,
defined as a negative test result, is actually followed by complete recovery
without sequelae. Calculated on this basis, the predictive value for poor
outcome was 94.4% (68/72). In sharp contrast, prediction of a favorable result
was accurate in only 12.8% (5/39).
COMMENT
There are at least 2 aspects to prognosis of vocal fold palsy: vocal
cord mobility and phonatory function. Imperfect function of the intrinsic
laryngeal muscles may be compensated for, with only minimal impact on vocal
ability. It is well known that phonation can be unaffected in patients who
have 1 or more vocal folds that abduct or adduct only weakly.10
In our study, free mobility of the paralyzed vocal fold was restored in only
8.1%, while 46.9% of all paralyzed vocal folds improved at least to a certain
extent. This is roughly consistent with a previously published large series
of recurrent laryngeal nerve palsies of different causes,11
in which complete and partial recovery was observed in 21.8% and 10.9%, respectively,
of 165 cases. In that study, spontaneous voice recovery to a good functional
level was observed in 76% of cases, which corresponds well with the 65.5%
found in our series. With vocal fold mobility restoration in 40% and voice
recovery in 90%, a similar report,12 focused
exclusively on outcome of recurrent laryngeal nerve injury caused by thyroid
surgery, found a comparable relationship. For idiopathic palsies, a rate of
less than 50% for partial and complete recovery was reported by Ward and Berci.13 Also in their study, the return of voice was satisfactory
in a significantly higher percentage (59%). Obviously, for the patient, outcome
in terms of vocal ability is of greatest importance. However, when the accuracy
of a prognostic test is investigated, the outcome variable should reflect
directly the system measured. Therefore, this analysis is focused on vocal
cord mobility as a key variable for outcome determination.
The clinical use of LEMG has been advocated for diagnosis and prognostication
of vocal fold palsy for more than 2 decades.10, 14, 15, 16
Surprisingly, there are few reports on the usefulness of this technique in
terms of reliability and prognostic accuracy. Min et al17
reported an impressive prognostic accuracy of 89% in patients with unilateral
vocal fold palsy. Their study is seriously flawed for at least 2 reasons:
first, the study population comprised 14 individuals only. Second, criteria
for prognostication were defined very generously: a positive prognosis for
laryngeal recovery was assumed when morphologic characteristics of the motor
unit waveform were normal and significant persistent overall electromyographic
activity as well as no electrical silence during voluntary tasks could be
found. Obviously, this combination of favorable findings should be considered
more an indication of a discrete lesion than an actual prognosis. Another
study investigating 18 patients18 was not truly
focused on the prognostic accuracy of LEMG. The authors of that study concluded
cautiously that LEMG may be of prognostic value.
Our data suggest that detection of neural degeneration in LEMG allows
for the prediction of poor functional outcome with high reliability in an
early phase of the disease process. This can be extremely valuable for the
timing of a definitive surgical intervention. In a study on patients with
bilateral vocal fold palsy conducted by Eckel et al,19
the routine use of LEMG was helpful to decide on partial cordectomy at a comparatively
early stage. As a consequence, tracheotomy was required in only 21% of the
study population. On the other hand, the absence of signs of degeneration
may not lead to the assumption that complete recovery is to be expected. This
interpretation needs to be considered under various aspects to determine its
validity.
STATISTICAL CONSIDERATIONS
To evaluate the validity of LEMG as a clinical test, the PPV and NPV,
representing statistical standard tests, were calculated. In the concepts
of PPV and NPV, the denominators are based on subjects with positive and negative
test results. The formula for the PPV is (subjects with positive test and
disease)/(all subjects with positive test). For the NPV, the general formula
is (subjects with negative test and no disease)/(all subjects with negative
test).
Thus in general, the prevalence of disease has a profound effect on
the usefulness of a test. If the prevalence is low, the PPV of the test is
low. Conversely, if the prevalence of disease is high, the PPV is high but
the NPV is low.20 This is the situation we
have with the data in this study. Most of the study population (102 of 111
vocal cords) had incomplete recovery of vocal fold mobility. An event occurring
so frequently is much easier to predict than the rare condition, at least
in our population, of complete recovery. Therefore, the PPV of 94.4% is not
as good and the NPV of 12.8% is not as bad as they might seem at first glance.
TECHNICAL CONSIDERATIONS
There are no generally accepted standardized guidelines for LEMG, nor
does a formal education exist for the laryngeal electromyographer.3 Even in centers with long experience in LEMG, the
first question before data interpretation should be whether data were sampled
in a technically appropriate and reliable manner. Since the ability and experience
of the investigator are crucial,21 only a critical
evaluation of the test routine can help to prevent systematic error.
Bipolar electrodes with both poles contained in the center core, as
used in this study, have been demonstrated to have the highest recording quality.22 In LEMG, electrode displacement is probably the most
critical point. When the transcutaneous technique is used, there are no clear-cut
criteria to separate true electrical silence from electrode displacement.
Transorally inserted hooked-wire electrodes allow better control of position
by visualization with indirect laryngoscopy. However, since depth of insertion
through the lamina propria of the vocal fold cannot be monitored, electrode
displacement still can occur. In addition to the fact that in our department
LEMG has been in clinical use in large numbers since 1986, we have another
reason to believe in the technical accuracy of our study: during LEMG, the
investigator is searching first for signs of neural degeneration, which is
the most important symptom to establish a diagnosis. Frequent electrode displacement
or wrong reading of the potentials recorded should lead to a great number
of false-negative results. However, in our population, individuals who had
been diagnosed as having neural degeneration actually had an unfavorable functional
outcome. It was in the group without signs of degeneration where a surprisingly
high number of vocal folds did not return to normal mobility. To blame undetected
neural degeneration for these results would suggest that laryngeal nerve palsy
is nearly always associated with neural degeneration. However, this is inconsistent
with the published literature.17, 18, 23, 24
PATHOPHYSIOLOGICAL CONSIDERATIONS
Laryngeal biomechanics and neural control are probably far more complex
than anticipated until recently.25 Even in
healthy subjects, considerable variation in firing patterns between motor
units within the same muscle as well as in vocal fold movements producing
the same speech sound could be demonstrated. Thus, our anatomic models serving
as a basis for interpretation of LEMG data may be much too simple. There is
increasing evidence of the existence of physiologically distinct compartments
within the laryngeal muscles. As a consequence, detection of neural degeneration
does not necessarily reflect a representative picture of the situation of
the whole functional unit.26 Thumfart14 hypothesized early that degenerative and nondegenerative
palsy may exist in parallel in the same vocal fold.
The outcome measure in this study was free vocal fold mobility, not
a normal LEMG. A case was coded as showing complete recovery only when there
was no sign of impaired mobility. Minor and minimal dysfunction of vocal fold
movement is not exclusively attributable to a neural disorder. The cricoarytenoid
joint, as a delicate counterpart in laryngeal movement, may also play an often
neglected role in the pathophysiology of vocal fold palsy. It may be speculated
that prolonged vocal fold immobility may lead to some kind of fibrosis of
the cricoarytenoid joint. In theory, this might cause a persistent deficit
in vocal fold mobility after neurogenic palsy even despite completely recovered
neural supply. This model might explain elegantly the gap between the high
PPV and low NPV calculated from our data. Patients with degenerative palsy
do not regain undisturbed vocal fold mobility, as predicted by LEMG. However,
for cases without signs of neural degeneration, there may still be a risk
of developing cricoarytenoid fibrosis because of immobilization over several
weeks. Although the clinical result is similar—the vocal fold cannot
move freely—the underlying mechanism would be different. Its delicate
anatomy,27 sophisticated physiologic characteristics28, 29 and similar susceptibility30, 31 to degenerative changes raise the
question why the cricoarytenoid joint should be less prone to malfunction
and fibrosis induced by prolonged immobilization than any other joint in the
human body. Friedrich32 formulated this hypothesis,
which may find strong support in our data.
CONCLUSIONS
In patients with vocal fold palsy of the lower motoneuron type, the
detection of well-defined signs of neural degeneration on LEMG allows for
the prediction of poor functional outcome with high reliability in an early
phase of the disease process.
In the presence of signs of neural degeneration detected by LEMG, the
decision for definitive surgical interventions such as thyroplasty or vocal
fold augmentation in unilateral or partial chordectomy in bilateral vocal
fold paralysis can be made safely at an earlier stage of the disease process.
Thus, LEMG can be helpful to significantly shorten the process of voice rehabilitation.
However, the absence of degenerative alterations in LEMG does not necessarily
indicate recovery to a normal or near-normal functional level. Hypothetically,
these findings may reflect secondary fibrosis of the cricoarytenoid joint
after prolonged vocal fold immobility of primarily neurogenic origin.
In summary, LEMG is a valuable tool in the workup of patients with vocal
fold palsy. Since prognostic accuracy for favorable results is comparatively
low, LEMG cannot replace clinical monitoring for at least 6 months or until
complete recovery has been reached.
AUTHOR INFORMATION
Accepted for publication July 13, 2000.
From the Department of Otorhinolaryngology, Head and Neck Surgery,
University of Cologne, Cologne, Germany (Drs Sittel, Stennert, Dapunt, and
Eckel); and Department of Otorhinolaryngology/Head and Neck Surgery, University
of Innsbruck, Innsbruck, Austria (Dr Thumfart).
Corresponding author: Christian Sittel, MD, Univ.-HNO-Klinik, J.-Stelzmann-Str.
9, 50924 Cologne, Germany (e-mail: christian.sittel{at}uni-koeln.de).
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