Mild Vocal Fold Paresis: Understanding Clinical Presentation and Electromyographic Findings

Mild Vocal Fold Paresis: Understanding Clinical Presentation and Electromyographic Findings *Yolanda D. Heman-Ackah and †Arlene Barr *Philadelphia, Pennsylvania and †Chicago, Illinois

Summary: The implications of mild vocal fold hypomobility are incompletely understood. This study describes the clinical, electromyographic, and probable etiologic findings in patients who presented with complaints of dysphonia and whose physical examination revealed vocal fold paresis as a factor possibly contributing to their voice complaints. A retrospective chart review of all patients who presented to a tertiary laryngology referral center over a 13month period, who had a clinical diagnosis of mild vocal fold hypomobility and who underwent laryngeal electromyography, were included in the study. A total of 22 patients completed the medical evaluation of their voice complaint. Of these patients, 19 (86.4%) were found to have evidence of neuropathy on laryngeal electromyography. The clinical picture indicated the following probable origins for the vocal fold paresis: goiter/thyroiditis (7/22 or 31.8%), idiopathic (4/22 or 18.2%), viral neuritis (4/22 or 18.2%), trauma (3/22 or 13.6%), and Lyme’s disease (1/22 or 4.5%). This article describes the clinical entity of mild vocal fold hypomobility and associated flexible laryngoscopic, rigid strobovideolaryngoscopic, and laryngeal electromyographic findings. Key Words: Vocal fold paresis—Vocal fold hypomobility—Laryngeal electromyography—EMG—Larynx.

BACKGROUND AND SIGNIFICANCE Mild vocal fold hypomobility is a common finding whose clinical significance is incompletely understood. The term “vocal fold hypomobility” describes a mobile vocal fold that exhibits mild sluggishness in adduction, abduction, and/or longitudinal tension that is observed with repetitive phonatory maneuvers and that is not immediately apparent with the assessment of the vocal folds at rest or with an assessment of vocal fold mobility during sustained phonation alone. Previous studies have reported a prevalence of mild vocal fold hypomobility of 46% among patients with vocal complaints, 71% among singing teachers with complaints of technical difficulties, and 23% among singing teachers with no vocal complaints.1,2 In these studies, the diagnosis of mild vocal fold hypomobility was based on clinical

Accepted for publication March 8, 2005. Presented at the American Laryngological Association Meeting at COSM, April 30–May 1, 2004. From the *American Institute for Voice and Ear Research and the Departments of Otolaryngology-Head and Neck Surgery, Thomas Jefferson University and Graduate Hospital, Philadelphia, Pennsylvania; and the †Department of Neurology, University of Illinois at Chicago, Chicago, Illinois. Supported by the Institutional Review Board at Graduate Hospital, Philadelphia, Pennsylvania. Address correspondence and reprint requests to Yolanda D. Heman-Ackah, American Institute for Voice and Ear Research, 1721 Pine Street, Philadelphia, PA 19103. E-mail: [email protected] Journal of Voice, Vol. 20, No. 2, pp. 269–281 0892-1997/$32.00 쑕 2006 The Voice Foundation doi:10.1016/j.jvoice.2005.03.010

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observation only; laryngeal electromyography was not performed to confirm or refute the presence of neuropathy as the cause of the hypomobile vocal folds. Interest in mild vocal fold paresis as a contributor to the pathophysiology of dysphonia is increasing; however, some controversy exists regarding the spectrum of normality in assessing vocal fold mobility as well as in the interpretation of laryngeal electromyographic findings.3–5 Most studies that have described electromyographic findings in the larynx have been performed in immobile vocal folds.6–12 Few studies have investigated the relationship between electromyography and mild vocal fold hypomobility.13–18 Abnormalities in the electrical signal have been found with electromyography in cases in which vocal fold paresis was suspected.13–16,18 The purpose of this study is to describe our experience with laryngeal electromyography in the evaluation of mild hypomobility of the vocal fold. METHODS A retrospective chart review of all patients who presented to a university-based tertiary laryngology referral center for evaluation of dysphonia over the course of the 13-month period from March 2002 through April 2003 was performed. All patients had given consent to have their medical records used for research purposes at the time of their initial evaluation according to HIPAA regulations, and this study was approved by the Institutional Review Board at Graduate Hospital, Philadelphia, PA. All patients with a laryngeal examination that revealed evidence of mild hypomobility of one or both vocal folds in adduction, abduction, and/or longitudinal stretch and who underwent laryngeal electromyography were included in the study. Our technique for assessing mobility of the vocal folds involves assessment of vocal fold mobility, coordination, and use of accessory muscles of phonation.17,19,20 The neurolaryngeal evaluation is performed with a flexible laryngoscope to prevent distortion of the larynx and muscle forces in the larynx that can result from holding the tongue forward for indirect and rigid stroboscopic examinations. The purpose of the neurolaryngeal examination is to assess the mobility of the vocal folds, elicit Journal of Voice, Vol. 20, No. 2, 2006

movement disorders, detect paresis or paralysis, differentiate paresis and/or paralysis from joint hypomobility, diagnose hyperfunctional or hypofunctional vocal behaviors, and evaluate muscle tone and agility. Our examination consists of two major components: observation of the larynx at rest and while performing phonatory maneuvers. Observation of the larynx at rest allows one to assess the normal resting tone and position of the vocal folds. Under normal circumstances, the vocal folds sit in a predominantly abducted position at rest, adducting slightly with expiration and abducting during inspiration. A median position of one or both vocal folds usually implies vocal fold fixation either from paralysis, scar, or joint immobility. A paramedian position is usually associated with moderate-to-severe vocal fold paresis, scar, or joint hypomobility. Paradoxical vocal fold movement, which is characterized by adduction during inspiration and abduction during expiration, is usually associated with reflux-induced or asthma-induced laryngospasm and anxiety. Spontaneous activity at rest is usually caused by tremor or myoclonic activity. Tremor in the larynx is characteristically observed as involuntary, rhythmic, periodic spasms of the glottic, supraglottic, or pharyngeal muscles. The reliable periodicity of the spasms, which is similar to the ticking of a clock, is the key feature of a tremor. Tremors can occur at rest or with intention, which in the larynx is observed during sustained phonation. Myoclonus is differentiated from tremor in that the spasms observed during myoclonic activity are jerky and arrhythmic.21 Endoscopic evaluation of the larynx during running speech and during singing allows one to assess the use of accessory muscles of phonation and to assess the presence of dystonic activity during phonation. The ideal position of the supraglottic and pharyngeal muscles during phonation is in a relaxed position, with all adductory and tensor actions being observed in the vocal folds only. Muscle tension dysphonia (also commonly referred to as supraglottic hyperfunction) occurs when the glottic, supraglottic, pharyngeal, and strap muscles are overly recruited during phonation. On examination, this dysphonia has the appearance of an anterior-toposterior or lateral-to-medial squeezing of the false vocal folds and the pharyngeal muscles. Typically,

VOCAL FOLD PARESIS AND LARYNGEAL EMG this behavior is present consistently throughout an entire sample of running speech and singing. Laryngeal dystonias produce spastic activity of the involved muscles. With an adductor dystonia, spastic adduction of the vocal folds is usually accompanied by spastic closure of the false vocal folds during phonation. Unlike supraglottic hyperfunction, this activity occurs intermittently during speech, at unpredictable intervals. With abductor dystonias, spastic abduction of the vocal folds occurs during running speech. Mixed dystonias have features of both adductor and abductor spasmodic dysphonia. In a patient with a pure dystonia, spasms typically do not occur during singing or caricature speech (for example, talking in a “Minnie Mouse-like” voice).22 The last components of our neurolaryngeal examination include isolation, repetition, and opposition testing. Phonatory tasks that allow one to isolate the abductor, adductor, and tensor muscle groups of the larynx while eliminating supraglottic hyperfunction allow the examiner to detect mild vocal fold hypomobility and differentiate paresis and/or paralysis form cricoarytenoid joint dysfunction. These tasks include repetition to allow one to assess not only for paralysis but also for fatigability and agility, which are more specific for diagnosing mild paresis and neuromuscular junction abnormalities. Isolation of the abductor muscles is best achieved by having the patient sniff repetitively. Evaluation of the adductor muscles can be performed by having the patient alternate between a sniff and the sound /i/ repeatedly. The cricothyroid muscles of the larynx and their ability to stretch the vocal folds longitudinally are evaluated by having the patient perform the glissando maneuver, that is, having the patient slide from his/her lowest pitch to his/her highest pitch while phonating the sound /i/ and then sliding down from high to low. Agility and fatigability of the vocal folds is assessed by having the patient alternate the sounds /i/ and /hi/ repetitively, past the point at which the patient is out of breath. During the examination, one is assessing not only the mobility of the vocal folds, but also the symmetry of motion, the dexterity, and the evidence of fatigue with repetition. Such testing accentuates mild hypomobility of the vocal folds that would otherwise be overlooked with assessment of the vocal folds in static positions or

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with having the patient say a prolonged “/i/” as the only assessment of vocal fold mobility. Coordination and flexibility are assessed with opposition testing. In this instance, the patient is asked to repeat a phonatory task that involves alternating between adduction and abduction, such as repeating the phrase /pɑ/ - /tɑ/ - /kɑ/. Like assessing rapid alternating movements elsewhere in the body, such tasks should demonstrate fluidity of movement in the larynx. Uncoordinated efforts represent dysdiadokinesis. The presence of cogwheeling as the patient transitions from abduction to adduction is a sign of rigidity.19,20 All patients were evaluated with this same diagnostic protocol. For the purposes of this study, superior laryngeal nerve paresis was suspected if there was hypomobility or asymmetry in vocal fold longitudinal stretch, with or without hypomobility in vocal fold adduction. A recurrent laryngeal nerve paresis was suspected if there was hypomobility in vocal fold adduction and/or abduction. A mixed superior and recurrent laryngeal nerve paresis was suspected if there was hypomobility in vocal fold adduction, abduction, and longitudinal stretch.13,14,23 All patients also underwent rigid strobovideolaryngoscopic evaluation of the vocal folds to evaluate for mucosal wave abnormalities. Rigid videostroboscopic findings of decreased vocal fold tone, glottic gap, asymmetric mucosal wave, and asymmetrical longitudinal stretch of the vocal folds in the presence of the flexible laryngoscopic findings listed above helped to support the clinical suspicion of vocal fold paresis (Table 1).19,20 Patients who were found to have unilateral or bilateral vocal fold immobility were excluded for purposes of this study, as were patients with diagnoses of spasmodic dysphonia/laryngeal dystonia, dystonic tremor, myoclonus, Parkinsonism, stroke, or other central neurologic processes. Twenty-two patients met the criteria for inclusion into this study. Of these patients, 7 were men and 15 were women. The mean age was 40.4 years (range, 13–74 years). All patients underwent diagnostic evaluation with imaging and laboratory testing as dictated by the clinical presentation to determine the origin of the vocal fold paresis. All patients completed the recommended diagnostic tests. A detailed review of the findings on clinical examination, the findings on Journal of Voice, Vol. 20, No. 2, 2006

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Direction of Duration Supraglottic Patient of Symptoms Hyperfunction

Flexible Fiberoptic–Right Vocal Fold

1

AP and lateral

↓ adduction

Normal

↓ ↓ ↓ ↓ ↓

3 years

abduction stretch adduction abduction stretch

2

7 years

AP and lateral

3

8 months

Lateral

↓ adduction ↓ stretch

4

2 months

Lateral

5

10 years

Lateral

↓ adduction ↓ abduction ↓ stretch var adduction ↓ abduction ↓ stretch

6

2 months

Lateral

7

3–6 months

Lateral

8

6 months

AP and lateral

9

4 years, worse in last year

AP and lateral

↓ ↓ ↓ ↓ ↓

adduction abduction stretch adduction stretch

↓ ↓ ↓ ↓

adduction abduction stretch adduction

Flexible Fiberoptic–Left Vocal Fold

Phase of Mucosal Wave

Glottic Closure

Mucosal Lesions

Pre-EMG Suspicion

Unable to assess (anxiety)

Incomplete

None

R SLN

R RLN

Variable adduction Asymmetric

Intermittently incomplete

None

↓ adduction ↓ abduction ↓ stretch Normal

Asymmetric

Hour-glass

Bilateral cysts

Asymmetric

Hour-glass

Bilateral polyps

R SLN R RLN L RLN L SLN R SLN L SLN L RLN R SLN R RLN

R SLN R RLN L RLN L SLN Subacute R SLN L RLN Subacute R RLN

Variable adduction Symmetric ↓ stretch

Incomplete

Bilateral bowing and atrophy

Normal

Normal

Asymmetric

Incomplete

None

R RLN R SLN L RLN L SLN R SLN R RLN

↓ adduction ↓ abduction ↓ stretch

Symmetric

Intermittently incomplete

None

R SLN L SLN L RLN

Normal

Symmetric

Complete

Bilateral Reinke’s edema

R SLN R RLN

R SLN R RLN L RLN R SLN L SLN Subacute L RLN R SLN R RLN

Normal

Asymmetric

Intermittently incomplete

Bilateral Reinke’s edema

R SLN

R SLN

R SLN L RLN

Subacute R RLN R SLN Tremor

↓ stretch 10

1 year

AP and lateral

var adduction ↓ stretch

Variable adduction Asymmetric ↓ abduction

Hour-glass

Bilateral cysts

Post-EMG Diagnosis

(Continued)

YOLANDA D. HEMAN-ACKAH AND ARLENE BARR

Journal of Voice, Vol. 20, No. 2, 2006

TABLE 1. Findings on Physical Examination in Suspected Laryngeal Paresis

TABLE 1. Continued Flexible Fiberoptic–Right Vocal Fold

11

↓ adduction ↓ abduction ↓ stretch ↓ adduction ↓ stretch ↓ adduction ↓ stretch Normal

1 year

AP and lateral

12

5 years

AP and lateral

13

8 months

Lateral

14

6 months

Lateral

15

1 year

AP and lateral

Normal

16

6 weeks

AP and lateral

17

15 years

Lateral

↓ ↓ ↓ ↓

18

5–6 years

19

1 year 2 years

Lateral Lateral

↓ adduction ↓ abduction ↓ stretch ↓ adduction ↓ abduction Variable adduction ↓ abduction

Normal

Phase of Mucosal Wave

Asymmetric

Variable adduction Symmetric ↓ abduction Normal Asymmetric

Glottic Closure

Hour-glass

Mucosal Lesions

Bilateral polyps

Pre-EMG Suspicion

R RLN R SLN

Hour-glass

Bilateral polyps

Incomplete

None

R SLN L RLN R SLN

Incomplete

Bilateral Reinke’s edema

L SLN

22

1 year

6–12 months

Lateral

AP and lateral

↓ adduction ↓ abduction

L SLN Normal

↓ adduction ↓ stretch

Asymmetric

↓ adduction ↓ abduction ↓ stretch

Symmetric

Complete

Right cyst

L RLN

R RLN L RLN R SLN R RLN L SLN L RLN Normal

Unable to assess

Incomplete

None

R SLN R RLN

Subacute R RLN

↓ adduction

Asymmetric

Hour-glass

Bilateral polyps

↓ adduction

Asymmetric

Intermittently incomplete

None

Normal

Asymmetric

Incomplete

Bilateral Reinke’s

R RLN L RLN R SLN R RLN L RLN R RLN

↓ adduction ↓ stretch

Symmetric

Intermittently incomplete

None

R RLN L SLN

21

Post-EMG Diagnosis

↓ adduction ↓ abduction ↓ stretch

Symmetric

Variable adduction ↓ adduction ↓ stretch ↓ abduction

Symmetric

Intermittently incomplete

Bilateral Reinke’s edema

Intermittently incomplete

Bilateral Reinke’s edema

R RLN L SLN L RLN R SLN L RLN

Abbreviations: AP, anterior to posterior; R, right; L, left; RLN, recurrent laryngeal nerve; SLN, superior laryngeal nerve; ↓, decreased.

R SLN R RLN L RLN LSLN LRLN

L RLN R SLN R RLN L SLN L RLN tremor R SLN R RLN L SLN L RLN R SLN Subacute L SLN

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20

AP and lateral

adduction abduction stretch abduction

Flexible Fiberoptic–Left Vocal Fold

VOCAL FOLD PARESIS AND LARYNGEAL EMG

Direction of Duration Supraglottic Patient of Symptoms Hyperfunction

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laryngeal electromyography, the etiologic diagnoses, and the presenting complaints was performed. All diagnostic evaluations were performed by the first author (Y.D.H.), and both authors performed all laryngeal electromyographic procedures. Our technique for laryngeal electromyography involved placement of the needle electrodes by the laryngologist (Y.D.H.), operation of the electromyography machine by the neurologist (A.B.), and interpretation of the signal by both the laryngologist and the neurologist. The neurologist was blinded to the clinical suspicion of hypomobility in all cases. The only clinical information available to the neurologist at the time of interpretation was suspicion for a neurolaryngeal abnormality. Laryngeal electromyography is not routinely recommended by the first author (Y.D.H.) unless clinical examination reveals abnormal vocal fold mobility. Thus, there are no available controls for this retrospective study. We use a Teca (Oxford, U.K.) Sapphire Premiere M570 electromyography machine with 25 mm × 0.30 mm (30 G) concentric Medtronic (Minneapolis, MN) needle electrodes. Both cricothyroid and thyroarytenoid muscles are tested routinely. Testing of the posterior cricoarytenoid muscles is performed when synkinesis, isolated abductor paresis, or another isolated pathology of the posterior cricoarytenoid muscle is suspected. Needle placement and position are confirmed with standard percutaneous laryngeal electromyographic techniques.18,24,25 Placement into the thyroarytenoid muscles was confirmed by the presence of recruitment during phonation and silence during passive and active inspiration. Thyroarytenoid muscle activity was evaluated both during speech and during sustained phonation of the sound /i/. If placement into the thyroarytenoid muscle revealed recruitment in that muscle during inspiration, synkinesis was suspected. In these instances, evaluation of the posterior cricoarytenoid muscle was performed as well. Placement into the posterior cricoarytenoid muscle was confirmed by the presence of recruitment during active inspiration and silence during sustained phonation. If both phonation and inspiration produced recruitment in both the thyroarytenoid and posterior cricoarytenoid muscles, then these findings were interpreted as evidence of synkinesis. Placement into the cricothyroid muscle was confirmed by the Journal of Voice, Vol. 20, No. 2, 2006

demonstration of increased recruitment during a high-pitched /i/ and less recruitment during a lowpitched /i/. All muscles were tested during moderate effort, which was defined as modal volume. Three to five different sites were tested within each muscle, with placement near individual motor units confirmed by the characteristic crisp sound and fine biphasic motor unit potentials (Figure 1). We routinely assess six different parameters: insertional activity, amplitude of the motor unit action potential (MUAP), MUAP duration, MUAP morphology, recruitment pattern, and evidence of synkinesis. A normal MUAP in the larynx is biphasic, has a duration of 5–10 ms, and has an amplitude of 200–700 µV. A normal laryngeal recruitment pattern includes 30–40 MUAPs per second (Figure 1).18,25 The lowfrequency filter is set at 20 Hz, and the highfrequency filter is set at 10,000 Hz. Insertional activity is recorded at sweep speeds of 100–200 ms and at a gain of 50 µV. At phonation, which is tested at moderate intensity (normal speaking level), MUAP morphology, amplitude, duration, and recruitment patterns are assessed at sweep speeds of 100–200 ms and at gains of 200–500 µV. Abnormalities that are observed in more than one site within the muscle being tested are considered significant. Neuropathy was defined as an abnormality in MUAP amplitude, MUAP duration, recruitment pattern, and/or insertional activity with the above-mentioned, predefined normative parameters and in accordance with existing literature regarding electromyographic findings in vocal fold paralysis (Figures 1–3).6–15,18,25 Increased MUAP duration was defined as a MUAP duration greater than 20 ms. Increased amplitude was defined as a MUAP amplitude that was greater than 1 mV. Decreased recruitment was defined as less than 20 MUAPs per second with moderate effort. Neuropathies meeting these criteria were defined as involving the superior laryngeal nerve if the muscle being tested was the cricothyroid muscle and as involving the recurrent laryngeal nerve if the muscle being tested was either the thyroarytenoid or the posterior cricoarytenoid muscle. As noted by Koufman et al,26 decreased muscle tone in the larynx does not always affect vocal fold position in a predictable manner in cases of laryngeal nerve paralysis. One could argue that even less of a decrease in muscle tone, as is observed

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275

FIGURE 1. Normal motor unit action potential waveform and recruitment pattern on laryngeal electromyography (patient 19, left cricothyroid muscle).

with a mild paresis, could potentially produce similar observations. Thus, findings on laryngeal electromyography were considered the “gold standard” in defining the presence of, and the site of, neuropathy for the purposes of this study. Criteria for the diagnosis of movement disorders in the larynx have been described elsewhere, and we used common criteria for diagnosis as is described in both the laryngology and the neurology literature.22,25,27–36 The diagnosis of neuropathy (ie, paresis and/or paralysis) was made if there was decreased recruitment, increased MUAP amplitude, and/or the presence of polyphasic MUAPs. A subacute process was diagnosed if there was evidence of ongoing denervation. Ongoing denervation was diagnosed if there was evidence of fibrillation potentials, positive sharp waves, complex repetitive discharges, or polyphasic nascent MUAPs. The absence of subacute findings in the presence of signs of neuropathy was interpreted as a chronic neuropathic process. RESULTS Twenty-two patients were suspected of having vocal fold paresis on clinical examination (Table 1).

All patients underwent laryngeal electromyographic testing of both recurrent laryngeal and superior laryngeal nerves, which totaled 88 nerves sampled. All patients completed the remainder of the diagnostic evaluation, including either computed tomography (CT) scan with contrast or magnetic resonance imaging (MRI) with gadolinium of the skull base through mediastinum and laboratory testing of fasting glucose, fasting cholesterol, fasting triglycerides, free thyroxine, thyroid stimulating hormone, antithyroidperoxidase antibodies, antithyroglobulin antibodies, antinuclear antibodies, rheumatoid factor, erythrocyte sedimentation rate, Lyme titre, and fluorescent Treponemal antibody absorption levels. In cases in which imaging or laboratory testing suggested a thyroid abnormality, thyroid ultrasound was obtained as well. Of these 22 patients with signs of vocal fold hypomobility on laryngeal examination, laryngeal electromyography revealed evidence of neuropathy in one or more laryngeal nerves in 19 patients (86.4%). The electromyographic and probable etiologic findings are presented in Table 2. Of the 42 paretic nerves, 23 (54.7%) were recurrent laryngeal nerves Journal of Voice, Vol. 20, No. 2, 2006

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YOLANDA D. HEMAN-ACKAH AND ARLENE BARR

FIGURE 2. Polyphasic and high-amplitude motor unit action potentials and decreased recruitment on laryngeal electromyography (patient 19, left thyroarytenoid muscle). Note also the decreased recruitment in comparison with Figure 1, also from the same patient.

and 19 (45.2%) were superior laryngeal nerves. The paresis was bilateral in 10 (52.6%) patients and unilateral in 9 (47.3%). Six (31.5%) patients had a mononeuropathy. Physical examination (ie, the combination of the flexible laryngoscopic and rigid strobovideolaryngoscopic evaluations) correctly identified the paretic laryngeal nerve in 27 of 42 (64.3%) nerves found to have electrical evidence of dysfunction on laryngeal electromyography. Physical examination correctly identified the normally functioning laryngeal nerves in 27 of 46 (58.7%) nerves found to have normal electrical activity on laryngeal electromyography. The finding of neuropathy in this patient population was statistically significant (chi-square ⫽ 545.3, df ⫽ 3, P ⬍ 0.001). There was no statistically significant difference in the ability to correctly identify a recurrent versus a superior laryngeal nerve paresis on physical examination (P ⬎ 0.05). There was electrical evidence of ongoing axonal loss as well as reinnervation in 6 (27.2%) patients who underwent laryngeal electromyography. The diagnoses are presented in Table 2. The patient who was found to have a viral neuritis (patient 3) was examined initially 4 months after an upper respiratory infection that resulted in the progressively worsening dysphonia. She was treated initially with voice therapy but continued to complain of vocal fatigue and voice breaks. She underwent laryngeal Journal of Voice, Vol. 20, No. 2, 2006

electromyography after 4 months of voice therapy. After the laryngeal electromyography, and placement on antiinflammatory medications, her voice improved and remained stable over the course of the next 6 months. The three patients with Hashimoto’s thyroiditis (patients 4, 7, and 9) were found to have the thyroid abnormality as a result of the diagnostic evaluation of their laryngeal paresis and were treated subsequently with thyroid suppressive medication, antiinflammatory medications, and voice therapy. Two patients (patients 4 and 7) had improvement in their pareses and complete resolution of their dysphonia within 3 months of treatment that remained stable after 12 months of treatment. The other patient (patient 9) had improvement but incomplete resolution of her dysphonia within 3 months of treatment. She continued to complain of some vocal fatigue and stopped taking the antiinflammatory medications after 3 months. She had persistent but stable symptoms at 12-month follow-up. The patient with neck trauma (patient 6) was evaluated for persistent dysphonia 6 weeks after having been hit with a soccer ball in the neck. He was treated successfully with nonsteroidal antiinflammatory medication and showed improvement in his voice within 6 weeks of treatment that remained stable at his 6-month follow-up examination. The patient with idiopathic vocal fold paresis (patient 22) did not

VOCAL FOLD PARESIS AND LARYNGEAL EMG

277

FIGURE 3. Low-amplitude polyphasic motor unit action potentials and decreased recruitment on laryngeal electromyography (patient 14, left cricothyroid muscle).

wish to pursue treatment with nonsteroidal antiinflammatory medications. His voice improved with voice therapy, but he continued to complain of vocal fatigue and had persistent signs of paresis even at his 1-year follow-up examination. Of the 42 nerves with electrical abnormalities, 39 (92.8%) were found to have decreased recruitment as one sign of paresis; 29 (69.0%) were found to have abnormalities in MUAP amplitude; 28 (66.7%) were found to have increased duration of the waveform; and 29 (69.0%) were found to have polyphasic motor unit potentials as one sign of paresis. In seven (16.6%) paretic nerves, decreased recruitment was the only electrical abnormality; this was possibly secondary to a demyelinating neuropathy. However, because of anatomical limitations, laryngeal nerve conduction studies to confirm abnormal conduction velocity were not feasible, and currently, no normative data exist to support the routine clinical use of magnetic stimulation to measure response latencies in the larynx.37 In each of these instances, other nerves within the tested larynx had other signs of paresis other than decreased recruitment and all patients had at least one other nerve within the tested larynx that did not have any electrical signs of neuropathy. In each of these instances, the decreased

recruitment observed was significantly less than that observed in the nerves with a full recruitment pattern. Three nerves with electrical signs of neuropathy did not show signs of decreased recruitment. In two of these nerves, increased MUAP amplitude was the only abnormality found, and in the other, increased MUAP amplitude, increased MUAP duration, and evidence of polyphasic motor unit potentials were found. These findings can be subtle and do not always result in major abnormalities in recruitment. DISCUSSION The results of this study indicate that when mild hypomobility of a vocal fold is observed on physical examination, in at least 86.3% of the cases, evidence of a laryngeal neuropathy can be found on laryngeal electromyography. Interestingly, no muscle pattern of hypomobility can identify the paretic nerve or nerves accurately. When abnormalities in mobility of the vocal folds in the direction of action of the suspected paretic nerve are observed on laryngeal examination, an exact correlation with the suspected nerve is not always found on laryngeal electromyography. In fact, although laryngeal examination correctly identified larynges that had an abnormal Journal of Voice, Vol. 20, No. 2, 2006

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YOLANDA D. HEMAN-ACKAH AND ARLENE BARR TABLE 2. Findings on Laryngeal EMG and Diagnostic Evaluation of Suspected Laryngeal Paresis

Pre-EMG Post-EMG Patient Suspicion Diagnosis Recruitment Amplitude Duration Waveform 1

R SLN

R RLN

2

R SLN R RLN L RLN L SLN R SLN L SLN L RLN R SLN R RLN R RLN R SLN L RLN L SLN R SLN R RLN

R SLN R RLN L RLN L SLN Subacute R SLN L RLN Subacute R RLN Normal

3

4 5

6

7

R SLN L SLN L RLN

8

R SLN R RLN R SLN

9

10 11 12 13

R SLN L RLN R RLN R SLN R SLN L RLN R SLN

14 L SLN

15

L RLN

16

R SLN R SLN

17

18

R RLN L RLN R SLN R RLN L RLN

R SLN R RLN L RLN R SLN L SLN Subacute L RLN R SLN R RLN R SLN Subacute R RLN R SLN Tremor L SLN Normal R RLN L RLN R SLN RRLN L SLN L RLN Normal Subacute R RLN R SLN R RLN L RLN LSLN LRLN

Spontaneous/ Synkinesis

n No n poly Right synkinesis poly

Etiology

n ↓ ↓ ↓ ↓

n n ↓ ↓ ↓

n ↓ ↑ ↑ ↑

n n ↑ ↑ ↑

n ↑ ↑ ↑

n n ↑ ↑

n poly poly poly

↓ n

n n

↑ n

n ↑

↑ n

n ↑

poly n Positive sharp n poly waves (R CT)

Viral neuritis

n ↓ n n

n n n n

n ↑ n n

n n n n

n ↑ n n

n n n n

n n n n

Hashimoto’s thyroiditis/ multinodular goiter Normal (MTD)

↓ ↓

n ↓

n ↑

n n

n ↑

n ↑

n n No poly poly

Viral neuritis

↓ n

↓ ↓

n n

↓ ↓

n n

↑ ↑

n n

poly Fibrillation poly potentials (L TA)

Hashimoto’s thyroiditis/ multinodular goiter

↓ ↓ ↓ ↓

n n n n

n ↑ ↑ ↑

n n n n

n ↑ ↑ ↑

n n n n

n poly poly poly

n n n n

No

Goiter

Complex repetitive discharges (R TA)

Hashimoto’s thyroiditis/goiter

↓ n n n n n n ↓ ↓ ↓

n n n n n n n ↓ ↓ ↓

↑ n n n n n n ↓ n ↑

n n ↑ n n n n ↑ ↓ ↑

↑ n n n n n n n n ↑

n n n n n n n n ↑ ↑

poly n n n n n n poly n poly

n n n n n n n poly poly poly

No, tremor

Idiopathic

No

Left goiter/cyst near nerve

No

Normal (MTD)

No

Viral neuritis

n n n ↓ ↓ ↓

n n n n n ↓

n n n ↑ n ↑

n n n n n n

n n n n n ↑

n n n n n ↑

n n n n n poly

n No n n Fibrillation n potentials (R TA) n No poly

n n

↓ ↓

n n

n n

n n

↑ ↑

n n

poly No poly

n n n n

Complex repetitive discharges (R TA) No

Neck and chest trauma Goiter with cysts

Decreased insertional Postherpetic activity (R and L CT) viral neuritis

Normal (MTD) Neck trauma Idiopathic

Idiopathic

(Continued)

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TABLE 2. Continued Pre-EMG Post-EMG Patient Suspicion Diagnosis Recruitment Amplitude Duration Waveform 19

R RLN L RLN

20

R RLN

R RLN L SLN L RLN R SLN

R SLN R RLN L SLN L RLN tremor R SLN R RLN L SLN L RLN R SLN

L RLN

Subacute L SLN

L SLN

21

22

Spontaneous/ Synkinesis

n n n ↓ ↓

n ↓ n ↓ ↓

n n n ↑ ↑

n ↑ n ↑ ↑

n n n n ↑

n ↑ n n ↑

n n n n poly

n No poly n n No, tremor poly

↓ ↓

↓ n

n n

n ↑

n n

n n

n n

n n

↓

↓

↑

↑

↑

↑

n

n

n

n

n

n

poly poly Complex Repetitive Discharges (L CT) n n

Etiology Neck trauma

Lyme’s disease

No

Goiter

Idiopathic

Notes: In each cell under Recruitment, Amplitude, Duration, and Waveform, the muscles tested are as follows: R CT L CT R TA L TA For patients 2 and 19, the third line in the boxes represent right and left posterior cricoarytenoid muscles. Abbreviations: R, right; L, left; RLN, recurrent laryngeal nerve; SLN, superior laryngeal nerve; n, normal; ↓, decreased; ↑, increased; poly, polyphasic waveform; TA, thyroarytenoid muscle; CT, cricothyroid muscle; Rx, therapy.

laryngeal nerve, identification of which nerve in particular was responsible for the asymmetric movements of the vocal folds was correct in 64.3% (27 of 42) of the cases. This result implies that paresis of the laryngeal nerves results in asymmetrical muscle forces in the larynx, and depending on the relative compensation from the unaffected muscles and the degree of pull from the affected muscle, the pattern of hypomobility observed may not necessarily coincide with the expected mobility pattern. One rationale for these observations may be that in patients with mild vocal fold paresis, the normally functioning muscles may compensate for the relative weakness of the paretic nerves. With hyperfunctional, compensatory vocal behaviors, these muscles are likely to fatigue easily. During an examination that is designed to produce fatigue, it may be first noted in the “overworked” normal muscles and secondarily or to a lesser extent in those that truly have paresis and, thus, cannot recruit as strongly to produce hyperfunction initially. Of all parameters that commonly assess neurologic integrity, a decrease in recruitment pattern seems to be the one variable that is present most

reliably when there are other electrical signs of neuropathy. In this study, a finding of decreased recruitment was present in 92.8% of the paretic laryngeal nerves. When decreased recruitment was found, it accompanied other electrical findings of neuropathy in the same nerve being tested 82.0% (32/39) of the time. In all but one instance in which decreased recruitment was an isolated finding in the muscle being tested, there was at least one muscle within that larynx that demonstrated a normal recruitment pattern for comparison. Recruitment is an indicator of the ability to activate more motor units with effort. Recruitment can be increased when a significant degree of effort contracts the muscle of interest. Similarly, recruitment can be decreased when less effort is exerted during recording. In all of our electromyographic studies, an attempt was made to have the patient as relaxed as possible during the recording of the signals and to have the patient exert a similar degree of effort with each muscle tested. Thus, in this instance, the finding of decreased recruitment is less likely to be related to effort, and more probably related to neuropathy. The implication of this observation is that for the Journal of Voice, Vol. 20, No. 2, 2006

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YOLANDA D. HEMAN-ACKAH AND ARLENE BARR

otolaryngologist who is unfamiliar with the nuances of identifying abnormalities in waveform, duration, or amplitude, assessment of recruitment pattern seems to be a reliable indicator of paresis. An interesting finding in this study was the number of cases in which ongoing axonal loss and reinnervation were diagnosed and the etiologic factors associated with these. The finding of ongoing axonal loss is observed when looking at insertional activity and is termed abnormal spontaneous activity at rest, which may include fibrillation potentials, positive sharp waves, and/or complex repetitive discharges. Each of these entities has a characteristic waveform that is identifiable at rest. Findings of axonal regeneration include high-amplitude MUAPs and prolonged and/or polyphasic MUAPs with consequent decreased recruitment patterns. There were three patients with diagnoses of Hashimoto’s thyroiditis, one patient with a diagnosis of viral neuritis, one with a recent history of neck trauma, and one with idiopathic paresis who demonstrated signs of ongoing axonal loss as well as reinnervation in the larynx. All patients had symptoms of dysphonia that had been ongoing and progressively worsening for the 1.5–12 months before presentation and treatment. In the patients who were treated with antiinflammatory medications and in the patients with thyroiditis who were also treated with thyroid suppressive medications, the paresis either stabilized or improved within the first 3 months of treatment, and that effect was still apparent at the 6- and 12-month follow-up examinations. The finding of an acute or ongoing neuropathic process is important diagnostically, and it affords the clinician the opportunity to intervene and prevent progression of the neuropathy. Although the number of patients in this study are too few to determine statistical significance of the observed improvement with antiinflammatory medications, the trend with these six patients was that those with a subacute process that was treated with antiinflammatory medications improved significantly within 3 months of treatment and remained asymptomatic, whereas those who chose not to purse antiinflammatory medications or that stopped taking the medications improved somewhat but continued to complain of vocal fatigue, even after 1 year of voice therapy. That 27.2% (6 of 22) of the patients who presented with hypomobility of the vocal folds and Journal of Voice, Vol. 20, No. 2, 2006

dysphonia were found to have an active neuropathic process supports the notion that laryngeal electromyography may be a helpful diagnostic tool that can aid the evaluation and management of dysphonic patients with vocal fold hypomobility. CONCLUSION The results of this study indicate that mild vocal fold hypomobility is a clinical entity that usually is associated with findings of neuropathy on laryngeal electromyography. The clinical laryngeal examination can identify abnormalities in vocal fold mobility; however, the dynamics of asymmetrical muscle forces in the larynx do not allow one to accurately predict the dysfunctioning nerve based on physical examination findings alone. The most common electrical finding is abnormal motor unit action potential morphology with decreased recruitment. A finding of decreased recruitment can be a screening tool to help identify those persons who may have true vocal fold paresis. Findings of ongoing degenerative and/ or regenerative processes can occur in patients with vocal fold hypomobility, and the origin of the vocal fold paresis should be sought and treated appropriately. Laryngeal electromyography is a useful adjunct to the physical examination, and it can clinically help guide the evaluation and management of mild vocal fold hypomobility. REFERENCES 1. Heman-Ackah YD, Batory M. Determining the cause of mild vocal fold hypomobility. J Voice. 2003;17:579–588. 2. Heman-Ackah YD, Dean C, Sataloff RT. Strobovideolaryngoscopic findings in singing teachers. J Voice. 2002;16: 81–86. 3. Woo P. Laryngeal electromyography is a cost-effective clinically useful tool in the evaluation of vocal fold function. Arch Otolaryngol Head Neck Surg. 1998;124:472–475. 4. Woodson GE. Clinical value of laryngeal EMG is dependent on experience of the clinician. Arch Otolaryngol Head Neck Surg. 1998;124:476. 5. Ford CN. Laryngeal EMG in clinical neurolaryngology. Arch Otolaryngol Head Neck Surg. 1998;124:476–477. 6. Hiroto I, Hirano M, Tomita H. Electromyographic investigation of human vocal cord paralysis. Ann Otol Rhinol Laryngol. 1968;77:296–304. 7. Kotby MN, Haugen LK. Clinical application of electromyography in vocal fold mobility disorders. Acta Otolaryngol. 1970;70:428–437.

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