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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
 
Otolaryngol Head Neck Surg. Author manuscript; available in PMC 2010 June 1.
Published in final edited form as:
PMCID: PMC2758662
NIHMSID: NIHMS90741

Invited Article: Recommendations of the Neurolaryngology Study Group on Laryngeal Electromyography

Abstract

The Neurolaryngology Study Group convened a multidisciplinary panel of experts in neuromuscular physiology, electromyography, physical medicine and rehabilitation, neurology, and laryngology to meet with interested members from the American Academy of Otolaryngology Head and Neck Surgery, the Neurolaryngology Subcommittee and the Neurolaryngology Study Group to address the use of laryngeal electromyography (LEMG) for electrodiagnosis of laryngeal disorders. The panel addressed the use of LEMG for: 1) diagnosis of vocal fold paresis, 2) best practice application of equipment and techniques for LEMG, 3) estimation of time of injury and prediction of recovery of neural injuries, 4) diagnosis of neuromuscular diseases of the laryngeal muscles, and, 5) differentiation between central nervous system and behaviorally based laryngeal disorders. The panel also addressed establishing standardized techniques and methods for future assessment of LEMG sensitivity, specificity and reliability for identification, assessment and prognosis of neurolaryngeal disorders. Previously an evidence-based review of the clinical utility of LEMG published in 2004 only found evidence supported that LEMG was possibly useful for guiding injections of botulinum toxin into the laryngeal muscles. An updated traditional/narrative literature review and expert opinions were used to direct discussion and format conclusions. In current clinical practice, LEMG is a qualitative and not a quantitative examination. Specific recommendations were made to standardize electrode types, muscles to be sampled, sampling techniques, and reporting requirements. Prospective studies are needed to determine the clinical utility of LEMG. Use of the standardized methods and reporting will support future studies correlating electro-diagnostic findings with voice and upper airway function.

Introduction

The Neurolaryngology Study Group, a long standing discussion group addressing both basic sciences and clinical aspects of neurolaryngology, convened a workshop focusing on the use of laryngeal electromyography (LEMG). A multidisciplinary panel of experts included scientists in neuromuscular physiology, electromyography, physical medicine and rehabilitation, neurology, and laryngology, who met with interested members from the American Academy of Otolaryngology Head and Neck Surgery Neurolaryngology Subcommittee and the Neurolaryngology Study Group to address the use of LEMG for electrodiagnosis of laryngeal disorders.

While LEMG is considered an essential component in laryngeal assessment by some, others have expressed reservations. A lack of agreement exists on methodology, interpretation, validity, and clinical application of LEMG. Some practitioners claim that LEMG is an invaluable component of dysphonia assessment. Others point to the lack of scientific evidence supporting its use; most published reports are class IV retrospective non-blinded case series1. In their 2004 evidence-based review of 584 articles, Sataloff, Mandel, Mann, and Ludlow2 concluded that LEMG was “possibly useful for the injection of botulinum toxin” but that evidence to support other uses was lacking. This contrasts with the clinical use of LEMG by some in the community3.

The charge was to examine the basic science and advance relevant points of consensus4. The examination was to include the current status of LEMG technology, and the clinical experience of leaders in the field. Five reviewers addressed a particular question regarding the use of LEMG by refining the question into a testable hypothesis. Next, they examined provisional support for the applicability, methodology, and validity of LEMG for the hypothesized purpose beyond the review in 20042. A conclusion could only be reached if there was a body of knowledge available to either reject or confirm a hypothesis. Finally, after identifying voids and key remaining questions, the reviewers were asked to describe what additional studies are needed, and feasible designs that could be executed.

The process was constrained by the available data, which are likely to change and self-correct over time. With the cumulative growth of knowledge over time, some concepts will be retained and others abandoned. Medical practice is constrained by the incomplete mastery of available knowledge; the limitations in current medical knowledge; and the difficulty in distinguishing between the first two5. The goal of this report was to reduce the level of uncertainty by clarifying the limitations of knowledge about LEMG and identify what needs to be learned.

The purpose of this review was not to conduct an evidence-based review regarding the specificity and sensitivity and reliability of LEMG as this was previously addressed in the extensive evidence-based review published in 20042. Rather the need was to move the field to the next step by identifying what parameters must be considered in attempting to develop standardized methods for LEMG for use in prospective controlled blinded assessments of LEMG sensitivity, specificity and reliability for identification, assessment and prognosis for neurolaryngological disorders.

Definitions

Peripheral versus Central Nervous System Disorders

LEMG is considered of use in diagnosis and assessment of peripheral and central neurological disorders affecting laryngeal function and to differentiate neurolaryngological disorders from other disorders causing changes in laryngeal function such as cricoarytenoid joint fixation. Peripheral neurolaryngological disorders may affect either efferent lower motor neurons and/or afferent/sensory neurons, neuromuscular junctions and/or muscles (in myopathies), while central neurological disorders (CNS) affect the firing rates of motor neurons, upper motor neurons, or central sensory pathways in the spinal cord, brainstem, or brain (Figure 1). Vocal fold paralysis can be caused either by traumatic peripheral nerve injuries, neuropathies affecting axons6 or central disorders such as laryngeal motor neuron death7,8 or brain stem stroke9. LEMG has potential for distinguishing between peripheral and CNS disorders and to differentiate vocal fold paresis/paralysis from other factors producing vocal fold immobility such as joint fixation.

Figure 1
Peripheral innervation of the laryngeal muscles and sensory feedback to the brain stem are identified on the lower left side of the figure and upper motor neuron input pathways to the laryngeal motor neurons are identified on the upper right side of the ...

Qualitative Electromyography (EMG)

Qualitative EMG samples the discharge patterns of muscle fiber action potentials (MFAP) and motor unit action potentials (MUAP), the waveform emitted by simultaneous activation of all the muscle fibers innervated by the axon of a single motor neuron. Motor units in large muscles may include many muscle fibers (1000 fibers/axon). In contrast, given the small number of human laryngeal muscle fibers10 and the numbers of mammalian laryngeal motorneurons 11, the laryngeal motor neurons likely innervate only a small number of fibers. Given these differences, experience recording the typical MUAPs of laryngeal muscles is needed to interpret whether or not the MUAP patterns are abnormal to identify denervation, reinnervation or muscle disease. The electromyographer must be familiar with the typical MUAP shape and hearing the sound of MUAPs from a particular muscle to identify MUAP abnormalities in that muscle.

Several aspects of LEMG can be identified. Insertional activity is the burst of activity that occurs when the electrode is first inserted or moved in a muscle. This normally lasts no more than 300 ms after needle movement and can be described as normal, reduced, or increased/prolonged with a description of the waveform and its discharge rate (as presented on p. 1478 in 12). Activity prolonged beyond needle insertion is termed spontaneous activity, which may include fibrillation potentials, i.e. spontaneously discharging muscle fibers seen as short duration MFAPs (less than 5 ms in duration). However, the identification of fibrillation potentials depends upon the normal durations of MUAP in a particular muscle. Normal laryngeal muscle MUAPs which contain few muscle fibers per motor unit, are often less than 5 ms in duration with peak to peak amplitudes of 200 microvolts13,14. Positive sharp waves are also spontaneous short duration MFAPs always in the positive (downwards) direction. Both have a regular pattern of discharge and are associated with denervation. Complex repetitive discharges (CRD) occur in chronic myopathies and neuropathies due to ephatic transmission between muscle fibers where one muscle fiber serves as a pacer cell for others. CRDs start and end abruptly, and have a harsh, machinery-like sound. Fasciculations are spontaneous discharges of entire motor units originating either from the motor neuron or distally along the axon, in an irregular pattern sounding like raindrops on a tin roof. Fasciculations occur in neuropathy or motor neuron diseases such as amyotrophic lateral sclerosis.

When an axon is first damaged and the muscle fibers are denervated, spontaneous discharges usually only occur when the muscle fibers are stimulated directly by needle movement. Spontaneous activity begins to develop after about a week, with positive waves and fibrillations. Over weeks to months, intact neighboring axons may sprout to reinnervate adjacent denervated muscle fibers. Because the axonal sprouts are thin and poorly myelinated, their conduction is slower than the original axonal branches resulting in asynchronous activation of muscle fibers with increased MUAP durations and more complex waveforms. These MUAPs are polyphasic potentials with multiple baseline (zero) crossings (at least four zero crossings producing five phases)12. Only if the same complex waveform reappears many times can a polyphasic MUAP be distinguished from chance simultaneous firing of multiple MUAPs.

Motor Unit Recruitment Patterns

With increased force of muscle contraction, MUAPs firing rates increase and additional MUAPs are recruited. The recruitment pattern should change from a few slowly firing MUAPs that can be individually distinguished, to a larger number of MUAPs firing at faster rates, producing a full "interference pattern" when MUAPs overlap interfering with the detection of individual MUAPs. Motor neurons are typically recruited in an order from the smallest to largest, referred to as the Henneman size principal15. During soft phonation small slowly firing thyroarytenoid motor units should be recruited in contrast with valsalva. By using graded tasks, the electromyographer can judge whether the person can recruit their muscles normally. Qualitative judgments can estimate whether or not the patient has “no, poor, moderate or slightly reduced” voluntary recruitment of laryngeal motor unit firing.

The qualitative examination screens several muscles to identify prolonged insertional spontaneous activity and screen for fibrillation potentials, positive sharp waves, complex repetitive discharges and fasciculations. An ordinal rating scale from 0 to +4 is usually used with 0 representing no discharges and 4+ filling the entire baseline with discharges and being most abnormal16.

Qualitative EMG is highly dependent upon the experience of the individual with the particular muscles being tested. Even experienced electromyographers familiar with sampling MUAPs in larger muscles may erroneously identify laryngeal muscle MUAPs to be fibrillation potentials because of smaller amplitudes and of shorter durations in laryngeal MUAPs than other muscles13.

Synkinesis

Abnormal muscle activation patterning occurs when the axon from an intact motor neuron for a different muscle has reinnervated a muscle that was previously denervated17,18. For example, if fibers in a posterior cricoarytenoid muscle are reinnervated by axons that normally innervate the thyroarytenoid muscle, then MUAPs within the posterior cricoarytenoid muscle may be more active for vocal fold closure rather than for vocal fold opening producing an abnormal synkinetic pattern of activity. Synkinesis may be difficult to define; the adductor muscles and the cricothyroid are normally active during both phases of respiration19 and during both vocal fold closing and opening for speech and non-speech gestures20. In addition, the posterior cricoarytenoid muscle is normally active during high pitched phonation21. Although different types of patterns have been proposed as indicative of abnormal reinnervation22,23, the accuracy of detection of synkinesis in prospective blinded controlled studies needs to be determined.

Quantitative Electromyography

Quantitative electromyography (QEMG) developed in an effort to objectively differentiate weakness caused by muscle disease from that caused by diseases of the peripheral nerve. Normative data on MUAP characteristics for each muscle across different age groups was gathered for objectively determining if a MUAP within a particular muscle was abnormal13,24. Some studies have gathered quantitative data on the MUAPs of each of the laryngeal muscles 2528. Generally, myopathies and neuromuscular junction diseases will produce short duration small amplitude MUAPs, while neuropathic conditions produce long duration, large amplitude MUAPs.

MUAP Quantification

Initially QEMG was done manually and was labor intensive. Now, commercially available machines support automatic detection of MUAPs with normative values stored for lookup of expected MUAP amplitudes and durations for different muscles. None of these machines currently have normative values for laryngeal muscle MUAPs. This would aid standardized testing of the thyroarytenoid muscle to assess the integrity of the recurrent laryngeal nerve (RLN) and the cricothyroid muscle to assess the external branch of the superior laryngeal nerve (eSLN).

For QEMG on laryngeal muscles, changing the depth and rate of breathing and easy phonation are useful for isolating individual units14,19,29. Commercially available EMG machines have automatic programs for detecting repeated firings of the same MUAP. The operator can identify a unit and store parameters from other firings of the same MUAP. The amplitude and duration can be compared with the norms for that muscle in a person of the same age range when the same EMG electrode is used. These computerized systems make QEMG much less time consuming and cumbersome than previous manual methods and need to incorporate normative data for laryngeal muscles.

Turns Analysis

A quantitative approach to measuring the fullness of an interference pattern includes “turns” analysis that estimates the number of motor units being fired in the muscle using measures of the number of turns/second and mean amplitude/turn when the patient recruits the muscle at a specific force30,31. Lindestad and colleagues used voice pitch and loudness changes to control muscle recruitment and examined whether or not a “turns “ analysis could quantify interference patterns across individuals. The approach was partially successful and should be examined further32,33.

Quantification of EMG signals

Quantitative MUAP measures used in QEMG (Table 1) include the amplitude from the positive to the negative peak, duration from the initial deflection from baseline to the terminal return to baseline, and the phase number. The mean duration of 20 MUAPs from each muscle distinguished between myopathy and neurogenic disorders using manual methods34. More automated methods such as the “Multi-MUP” method35 allow for decomposition of an EMG pattern into individual MUAPs during contraction between 5–30% force. Between 20–30 MUAPs can be defined in a few minutes for detecting abnormalities36. Multichannel electrodes are also useful for identifying different MUAPs within the same territory37. Although used in laryngeal muscles28 the accuracy for detecting laryngeal neuropathy is unknown.

Table 1
Clinically Used Quantification for EMG signals

Normal Laryngeal MUAP Characteristics

Faaborg-Andersen used a concentric needle electrode manually documenting the short durations (3–7 ms) and small amplitudes (100– 800 microvolts) of normal laryngeal MUAPs. Similar values were obtained using computerized quantification of manually detected units26,38. Using the Multi-MUP method, reference values obtained from 40 healthy volunteers with a concentric electrode in the cricothyroid and thyroarytenoid muscles, had mean MUAP durations of 4.5 ms and mean amplitudes of 350 microvolts in the thyroarytenoid and 280 in the cricothyroid27. On the other hand, normative values obtained from normal adults between 20 and 75 years using a concentric bipolar electrode in the thyroarytenoid muscles found MUAP mean durations of 1.70 ms that increased with age; doubling after 60 years14. These differences in normative values illustrate the need for standardizing electrodes and techniques before developing norms for detecting pathology using laryngeal QEMG.

EMG Electrodes

To quantify MUAPs, the same electrode type must be used as was used in obtaining reference values because of differences in recording areas between electrode types (Table 2). Filter settings must also be consistent. The monopolar electrode picks up from a large circular region with an uptake region 1.5 times that of the concentric electrode12. Dedo compared the specificity of concentric and bipolar concentric needle electrodes in denervated thyroarytenoid muscles39,40 adjacent to intact cricothyroid muscles. The concentric electrode in a denervated thyroarytenoid picked up potentials from the intact cricothyroid while no potentials were recorded with the bipolar concentric electrode in the denervated thyroarytenoid along side an intact cricothyroid. Unfortunately the bipolar concentric electrode is no longer commercially available. Most reports on MUAP characteristics in the thyroarytenoid and cricothyroid muscles have used the concentric electrode and therefore this electrode is preferred despite its lesser selectivity. One study employed commercially available single fiber EMG (SFEMG) electrodes and provided normative data on 10 adults in their 30’s. Measures of fiber density and jitter may have clinical utility41. SFEMG is preferred for the diagnosis of neuromuscular junction abnormalities42,43.

Table 2
Characteristics of various electrode types, adapted from12

Operators

Recording from the laryngeal muscles is technically difficult although methods are well described in the literature44. Otolaryngologists who regularly inject botulinum toxin into thyroarytenoid muscles for treatment of spasmodic dysphonia are skilled in performing LEMG; however, few have had training in reading MUAP signals. An otolaryngologist and an experienced electromyographer with clinical neurophysiology training (either a neurologist or physiatrist) should work as a team to develop experience with the specific attributes of normal laryngeal muscles.

Equipment

Commercially available EMG machines have a range of features. Some simply have 1–2 channel EMG amplifier inputs to a laptop with a speaker and display the EMG trace(s). More specialized EMG machines allowing for automatic MUAP detection and analyses and are essential for QEMG.

Proposed Uses for LEMG

1. Injection for Botulinum Toxin

The 2004 evidence –based review 2 concluded that LEMG was "possibly useful for the injection of botulinum toxin." However, other approaches are available for the injection of botulinum toxin into the thyroarytenoid and/or the lateral cricoarytenoid muscles in adductor spasmodic dysphonia such as: a peroral approach that allows visual confirmation of placement45 or use of the point-touch approach using anatomical landmarks46. For injection of the posterior cricoarytenoid muscle in abductor spasmodic dysphonia, there are also other approaches besides LEMG such as using a channeled nasolaryngoscope47. When the endoscopic technique was compared with percutaneous injection with LEMG neither approach reduced symptoms and no difference in outcome was found between the two approaches48. To date, no comparisons have been conducted between the use of LEMG and peroral or point-touch approach for injection of adductor spasmodic dysphonia49.

2. Diagnosis of Vocal Fold Paresis

Vocal fold paralysis refers to a loss or impairment of motor function due to a lesion of the neural or muscular mechanism while paresis is a partial movement impairment also of neural or muscular origin. Partial or total vocal fold immobility should be used when the basis for the impairment is unknown or results from mechanical limitations such as a bulk effect of cancer or joint pathology (fixation or dislocation).

Laryngeal/voice dysfunction may result from vocal fold paralysis/paresis, however, some patients with vocal fold paralysis are asymptomatic, possibly due to adequate compensation. The prevalence of vocal fold paralysis/paresis and its significance for producing laryngeal/voice dysfunction, therefore, is unknown.

Laryngeal physiology may be impacted by vocal fold paralysis/paresis. Aerodynamic measures correlated with qualitative unblinded EMG findings in symptomatic patients with vocal fold paresis/ paralysis; those with fewer normal motor units on LEMG had higher mean translaryngeal air flows”16. and poor recruitment was associated with reduced maximum phonation times and higher mean flows. Symptomatic paresis was reported to result in hyperfunction 50or abnormal vibration, the theoretical basis of the “paresis podule”51. The impact of partial movement reductions due to neurological impairments (paresis) on airway and swallowing functions has not been well studied.

To examine whether LEMG can identify vocal fold paresis, 22 symptomatic patients had unblinded qualitative LEMG studies and laryngeal examinations and 19/22 cases were judged to have neuropathy on LEMG52. In another report, 13 patients underwent qualitative LEMG and 12/13 patients with clinically suspected vocal fold paresis were judged to have abnormalities on unblinded LEMG53. The only patient with a normal EMG had a prior history of intubation following head injury and a stiff cricoarytenoid joint on direct laryngoscopy. These findings suggest that in symptomatic patients with suspected vocal fold paresis, motion abnormalities likely reflect some degree of neurological impairment that correlate with findings on unblinded qualitative LEMG52,53. The EMG findings in suspected paresis cases may be similar to paralysis as there are no different criteria54. In a retrospective study of 50 vocal fold paresis symptomatic patients55, unblinded qualitative LEMG indicated unilateral neuropathic findings in 60%, bilateral findings in 40% and contralateral neuropathy in 26%. Isolated eSLN involvement was indicated in 16%; isolated RLN neuropathy in 44%; and combined eSLN and RLN neuropathy in 40%, although all were unblinded qualitative exams.

Blinded studies are needed to determine if LEMG can distinguish between neurological and mechanical vocal fold impairments55,56. However, the clinical utility of this information, particularly considering the disagreement regarding the prevalence of arytenoid dislocation/subluxation, is unknown.

To address the accuracy of LEMG in vocal fold paresis for detecting neurological abnormalities, prospective studies are needed to identify what LEMG findings would be expected in vocal fold paresis on qualitative and/or quantitative LEMG.

3. Predicting Recovery from Acute Unilateral Vocal Fold Paralysis/Paresis Following Recurrent Laryngeal Nerve Injury

Although LEMG has been advocated as providing prognostic information in cases of vocal fold paresis, the data are limited. If the purpose of the “prognosis” is for early management decisions, caution should be applied. Koufman and colleagues reported that LEMG altered their management 63% of the time56. Of these, 12% were useful in differentiating paralysis from fixation, although the criteria were not provided and the change in patient care was not detailed. With regard to the 11% for whom the imaging choices were driven by EMG, no imaging modality was shown superior to the other (magnetic resonance imaging (MRI) vs. computed tomography, CT). The importance of the LEMG prognosis on surgical decision is dependent on knowing how LEMG-driven surgical outcomes are superior to other management approaches for vocal fold paralysis.

Serial LEMG examinations in the same patient over time may be helpful. A retrospective review of 31 cases of vocal fold paralysis examined between 21 days and 6 months post onset, assessed the value of qualitative LEMG in predicting persistent vocal fold paralysis57. A poor prognosis was defined as reduced motor unit recruitment (a decreased interference pattern) with acute or chronic spontaneous activity. An excellent prognosis included a normal motor unit recruitment pattern with only a slightly decreased interference pattern and no fibrillation potentials or positive sharp waves. Fair prognosis was “moderately decreased motor unit recruitment”, a diminished interference pattern and spontaneous discharge but no complex repetitive discharges. The outcome measure was the resolution of vocal fold with substantial return of movement by 6 months post onset. The sensitivity, the percentage of cases with persistent vocal fold paralysis with fair to poor LEMG, was 91%. The specificity, the percentage of patients with good recovery who had an excellent prognosis on LEMG, was 44% (4/9 cases). A stepwise regression showed that the LEMG findings predicted 44.4% of the resolved cases. Judgment of motor unit recruitment on LEMG was most useful for prediction, but was unblinded.

These results are not based on prospective blinded LEMG examination. Judgments made by one electromyographer need to be replicated by others.

3. Accuracy of LEMG for Diagnosis of Neuromuscular Diseases of the Larynx

Diagnosis of myasthenia gravis (MG), the most common disorder affecting the neuromuscular junction, depends upon repetitive nerve stimulation (RNS) to affected muscles58,59. Antibody production against acetylcholine in MG blocks neurotransmission to muscle fibers causing fatigue and decreased muscle response during RNS after exercise. If the response to RNS is normal and there is still a high suspicion of a neuromuscular junction disorder, then SFEMG of at least one symptomatic muscle is recommended. The study should be considered abnormal if 10% of fiber potential pairs exceed normal jitter or have impulse blockade, and/or jitter exceeds normal limits58,59.

The accuracy of these guidelines has not been examined in the laryngeal muscles. One of the major obstacles is poor accessibility of the RLN for repetitive stimulation; it lies in the tracheo-esophageal groove, making reliable stimulation over many minutes extremely difficult. Moreover, needle recording is not ideal for obtaining stable motor amplitudes. Alternatively transcranial magnetic stimulation might be used although the reliability of the muscle responses with repeated placements needs to be asessed60. At least one study has shown that SFEMG can be applied in the larynx; these standards could be evaluated for diagnostic validity for LEMG in MG. Although MG rarely affects the laryngeal muscles61, the rarity of such cases can lead to misdiagnosis6266.

4. Use of LEMG for Identification of Movement Disorders

Disorders affecting upper motor neuron firing can alter the rate and pattern of firing of motor neurons in the nucleus ambiguus in the medulla controlling the laryngeal muscles. Examples are Parkinson disease with neuronal death in the substantia nigra altering basal ganglia feedback to the cortex67(Figure 1), multiple systems atrophy (or Shy Drager syndrome)68,69, supranuclear palsy70 and pseudobulbar palsy71. In other disorders, such as spasmodic dysphonia72, patients have symptoms during speech but have normal voice during laughter and cry73. Voice tremor also involves laryngeal motor neuron firing abnormalities.

Often patients with laryngeal motor control disorders are taking medications, affecting LEMG. Others can imitate the symptoms of some laryngeal motor control disorders leading to difficulties in differentiating behaviorally and neurologically based movement disorders. Such disorders include muscular tension dysphonia (MTD)—a habitual misuse of the laryngeal muscles during voicing74, psychogenic voice disorders, and malingering where the patient is imitating a voice disorder for some gain. Although MTD is thought to be due to increased muscle tone interfering with voice production75, no quantitative/objective study has demonstrated the physiological basis for the disorder. LEMG measures proposed for laryngeal motor control disorders include: motor unit firing rate28, cross-correlation of recruitment across muscles28,76,77, resting levels of motor unit firing78, recruitment on the right and left sides26,79 spectral analysis of frequency components in the LEMG80; muscle bursts during phonation26,81; relating muscle tone to speech symptoms82; recruitment patterns across tasks69; relationship between resting activity and task recruitment83; co-contraction of antagonistic muscles84; the percent increase for speech over rest85,86; and turns/amplitude analyses of motor unit firing3133. Although some have proposed using qualitative judgments of muscle activity patterns during voice production to detect which muscles produce voice breaks26,87,88, the accuracy of such judgments for differentiating motor control disorders from normal when subject identity is masked is unknown. Further, intra- and inter-rater reliability for making such judgments is unknown.

To determine if any new studies had been appeared in the literature since the publication of the evidence-based review in 20042 that pertained to the application of laryngeal electromyography in movement disorders, several searches were conducted. A PubMed search, “laryngeal + electromyography + diagnosis + dysphonia” was conducted along with and searches for “psychogenic + voice + electromyography”, “tension + dysphonia + electromyography”, and “tremor + dysphonia + electromyography”. Only 5 studies that were published since the previous review were identified (Table 3). None of these studies nor previous studies reviewed prior to 2004 (available in Supplementary Materials Online) demonstrated that LEMG was valid for diagnosis of: upper motor neuron disorders, spasmodic dysphonia, vocal tremor, malingering or psychogenic dysphonia. The searches on “muscle tension dysphonia” and laryngeal electromyography did not identify any new studies since 2004 and “medication + laryngeal + electromyography” and “drug + laryngeal + electromyography”, did not identify any new human studies examining neuropharmacological effects on LEMG since 2004.

Table 3
A review of Studies Published Since 2004 Relevant to the Role of Laryngeal Electromyography for the Diagnosis of Laryngeal Movement Disorders and Injection of Botulinum Toxin in Spasmodic Dysphonia.

The diagnostic validity of LEMG is unknown for upper motor neuron disorders involving the larynx, laryngeal dystonia and vocal tremor, muscular tension dysphonia, malingering and psychogenic dysphonia. The ability of LEMG to determine neuropharmacological effects on laryngeal musculature is unknown.

Several un-blinded studies compared patients and controls on measures of LEMG that could be used in future evaluations of the validity of LEMG as a diagnostic tool for laryngeal motor control disorders29,76,78,82,89,90. Small prospective Class II studies should initially determine the validity and reliability of particular LEMG measures in a blinded study for differentiating between cases and controls.

Final Recommendations

The Panel concluded that there is a role for LEMG in the diagnosis of disorders of laryngeal (vocal fold) movement, for guiding injections of botulinum toxin in laryngeal muscles and as a useful tool for laryngeal research. Although other uses are ongoing in clinical practice, no consensus was reached about their utility and evaluation is needed.

Several recommendations were made to reduce the variability in the results of LEMG:

  1. To standardize electrodes used for different purposes:
    1. Concentric needles provide a uniform field for MUAP waveform analysis.
    2. Monopolar needles are useful for guiding botulinum toxin injection in laryngeal muscles.
    3. Bipolar hooked wires are useful for multiple muscle recordings and/or repetitive tasks.
  2. A team of an otolaryngologist and an electromyographer is useful in diagnostic LEMG.
  3. A basic examination will depend upon the intervention decisions that are required for a particular patient. It may include:
    1. Recording from the thyroarytenoid/lateral cricoarytenoid complex bilaterally to compare the “affected” side with the “unaffected” side.
    2. Recording from the cricothyroid bilaterally to compare the “affected” side with the “unaffected” side.
    3. Additional muscles as clinically indicated.
    4. Adequate sampling of insertional activity.
    5. Recruitment measures including numbers of units, amplitudes and firing rates.
    6. Recordings of MUAPs (durations, amplitudes, and percent polyphasic units with identical firings).
  4. Evaluation for neuropathy should consider that:
    1. Multiple criteria must be used and abnormalities must be concordant across several aspects.
    2. Commonly available diagnostic equipment does not usually provide accurate quantitative assessment for the laryngeal muscles.
    3. Multiple samples in 2 or 3 different locations per muscle are needed to evaluate recruitment, spontaneous activity and fibrillation potentials.
  5. A LEMG report should include:
    1. The reason for the study
    2. What procedures were performed including anesthetic agents, electrodes, muscles sampled, and adequacy of the examination
    3. Data Tables with normative values if available
    4. Findings
    5. Interpretation
    6. Clinical Comments

Future Directions for Laryngeal Electromyography

LEMG is in its early developmental stages. Future research in this area should concentrate on standardization, determining optimum utility of the technique in conjunction with videostroboscopy, and determining the value of this tool as a prognostic indicator. Evidence based studies are needed to assess the value of LEMG, and to define clinical parameters. LEMG is potentially a valuable diagnostic tool that clinicians may use to aid understanding of laryngeal abnormalities, and in many cases, may offer information helpful for deciding on recommendations for intervention. The large degree of normal variation in human laryngeal muscle activation for speech and respiratory tasks needs to be more fully examined 19,20.

Currently, LEMG is a qualitative examination. Further work is needed to validate qualitative examination results across centers and physicians. Reliability may be improved with quantitative methods. Prospective studies are needed to determine the clinical utility of LEMG and correlate electro-diagnostic findings with voice and upper airway functions to determine the significance of LEMG. Future studies should compare different techniques for electrode placement, employ blinded (masked) assessment and assess inter-rater and intra-rater reliability. The following measurement parameters should be evaluated for validity: MUAP duration and amplitude, serial LEMGs for the prediction of recovery and tasks to identify and measure synkinesis.

Supplementary Material

Supplementary

Acknowledgment

Preparation of the manuscript was supported in part by the Intramural Research Program of the National Institute of Neurological Disorders and Stroke, National Institutes of health, Bethesda, MD

Contributor Information

Andrew Blitzer, M.D., DDS, Head and Neck Surgical Group, New York, NY.

Roger L. Crumley, M.D., MBA, Department of Otolaryngology-Head and neck Surgery, University of California-Irvine, CA.

Seth H. Dailey, M.D., Division of Otolaryngology-Head and Neck Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI.

Charles N. Ford, M.D., Division of Otolaryngology-Head and Neck Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI.

Mary Kay Floeter, M..D., Ph.D., National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.

Allen D. Hillel, M.D., Department of Otolaryngology – Head and Neck Surgery, University of Washington School of Medicine, Seattle, WA.

Henry T. Hoffman, MD, Department of Otolaryngology-Head and Neck Surgery, University of Iowa, Iowa City, IA.

Christy L. Ludlow, Ph.D., National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.

Albert Merati, M.D., Department of Otolaryngology – Head and Neck Surgery, University of Washington School of Medicine, Seattle, WA.

Michael C. Munin, M.D., Department of Physical Medicine and Rehabilitation, University of Pittsburgh School of Medicine, University of Pittsburgh, Pittsburgh, PA.

Lawrence R. Robinson, M.D., Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle, WA.

Clark Rosen, M.D., Department of Otolaryngology, University of Pittsburgh School of Medicine, University of Pittsburgh, Pittsburgh, PA.

Keith G. Saxon, M.D., Department of Surgery, Division of Otolaryngology, Harvard Medical School, Boston MA.

Lucian Sulica, MD, Department of Otorhinolaryngology, Weill Medical College of Cornell University, NYC, NY.

Susan L. Thibeault, Ph.D., Division of Otolaryngology-Head and Neck Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI.

Ingo Titze, Ph.D., University of Iowa, Iowa City, IA.

Peak Woo, M.D., Department of Otolaryngology, Mt Sinai School of Medicine, New York, NY.

Gayle E. Woodson, M.D., Department of Otolaryngology-Head and Neck Surgery, Southern Illinois University, Springfield, IL.

References

1. Goodin D, Edlund W. Process for developing trechnology assessment. St. Paul, MN: American Academy of Neurology; 1999.
2. Sataloff RT, Mandel S, Mann E, et al. Laryngeal electromyography: an evidence-based review. Muscle Nerve. 2003;28:767–772. [PubMed]
3. Halum SL, Patel N, Smith TL, et al. Laryngeal electromyography for adult unilateral vocal fold immobility: a survey of the American Broncho-Esophagological Association. Ann Otol Rhinol Laryngol. 2005;114:425–428. [PubMed]
4. Shermer M. The most precious thing we have: the difference between science and pseudoscience. In: Shermer M, editor. Why people believe weird things. New York, NY: Henry Holt and Co; 2002.
5. Groopman J. The uncertainty of the expert. In: Groopman J, editor. How doctors think. New York, NY: Houghton Mifflin; 2007.
6. Dyck PJ, Litchy WJ, Minnerath S, et al. Hereditary motor and sensory neuropathy with diaphragm and vocal cord paresis. Annals of Neurology. 1994;35:608–615. [PubMed]
7. Puls I, Jonnakuty C, LaMonte BH, et al. Mutant dynactin in motor neuron disease. Nat Genet. 2003;33:455–456. [PubMed]
8. Puls I, Oh SJ, Sumner CJ, et al. Distal spinal and bulbar muscular atrophy caused by dynactin mutation. Ann Neurol. 2005;57:687–694. [PMC free article] [PubMed]
9. Aydogdu I, Ertekin C, Tarlaci S, et al. Dysphagia in lateral medullary infarction (Wallenberg's syndrome): an acute disconnection syndrome in premotor neurons related to swallowing activity? Stroke. 2001;32:2081–2087. [PubMed]
10. Perie S, Guily JL, Callard P, et al. Innervation of adult human laryngeal muscle fibers. Neurol Sci. 1997;149:81–86. [PubMed]
11. Davis PJ, Nail BS. On the location and size of laryngeal motoneurons in the cat and rabbit. JCompNeurol. 1984;230:13–32. [PubMed]
12. Dumitru D, Amato AA, Zwarts M. 2nd ed. Philadelphia, PA: Hanley & Belfus, Inc; 2002. Electrodiagnostic Medicine.
13. Buchthal F, Pinelli P, Rosenfalck P. Action potentials parameters in normal human muscles and their physiological determinants. Acta Physiol Scand. 1954;32:219–229. [PubMed]
14. Takeda N, Thomas GR, Ludlow CL. Aging effects on motor units in the human thyroarytenoid muscle. Laryngoscope. 2000;110:1018–1025. [PubMed]
15. Henneman E, Somjen G, Carpenter D. Excitability and inhibitability of motorneurons of different sizes. J Neurobiol. 1965;28:599–620. [PubMed]
16. Bielamowicz S, Stager SV. Diagnosis of unilateral recurrent laryngeal nerve paralysis: laryngeal electromyography, subjective rating scales, acoustic and aerodynamic measures. Laryngoscope. 2006;116:359–364. [PubMed]
17. Crumley RL. Laryngeal synkinesis: its significance to the laryngologist. Ann Otol Rhinol Laryngol. 1989;98(2):87–92. [PubMed]
18. Crumley RL. Mechanism of synkinesis. Laryngoscope. 1979;89:1847–1854. [PubMed]
19. Chanaud CM, Ludlow CL. Single motor unit activity of human intrinsic laryngeal muscles during respiration. Ann Otol Rhinol Laryngol. 1992;101:832–840. [PubMed]
20. Poletto CJ, Verdun LP, Strominger R, et al. Correspondence between laryngeal vocal fold movement and muscle activity during speech and nonspeech gestures. J Appl Physiol. 2004;97:858–866. [PMC free article] [PubMed]
21. Fujita M, Ludlow CL, Woodson GE, et al. A new surface electrode for recording from the posterior cricoarytenoid muscle. Laryngoscope. 1989;99:316–320. [PubMed]
22. Crumley RL. Laryngeal synkinesis revisited. Ann Otol Rhinol Laryngol. 2000;109:365–371. [PubMed]
23. Maronian NC, Robinson L, Waugh P, et al. A new electromyographic definition of laryngeal synkinesis. Ann Otol Rhinol Laryngol. 2004;113:877–886. [PubMed]
24. Sacco G, Buchthal P, Rosenfalck P. Motor unit potentials at different ages. Arch Neurol. 1962;6:44–51. [PubMed]
25. Faaborg-Andersen K. Electromyographic investigation of intrinsic laryngeal muscles in humans. Acta Physiologica Scandinavica. 1957;41(140):1–149. [PubMed]
26. Kimaid PA, Quagliato EM, Crespo AN, et al. Laryngeal electromyography in movement disorders: preliminary data. Arq Neuropsiquiatr. 2004;62:741–744. [PubMed]
27. Koivu MK, Jaaskelainen SK, Falck BB. Multi-MUP analysis of laryngeal muscles. Clin Neurophysiol. 2002;113:1077–1081. [PubMed]
28. Roark RM, Li JC, Schaefer SD, et al. Multiple motor unit recordings of laryngeal muscles: the technique of vector laryngeal electromyography. Laryngoscope. 2002;112:2196–2203. [PubMed]
29. Luschei ES, Ramig LO, Baker KL, et al. Discharge characteristics of laryngeal single motor units during phonation in young and older adults and in persons with parkinson disease. J Neurophysiol. 1999;81:2131–2139. [PubMed]
30. Buchman AS, Comella CL, Stebbins GT, et al. Quantitative electromyographic analysis of changes in muscle- activity following botulinum toxin therapy for cervical dystonia. Clinical Neuropharmacology. 1993;16:205–210. [PubMed]
31. Fuglsang-Frederiksen A. The utility of interference pattern analysis. Muscle Nerve. 2000;23:18–36. [PubMed]
32. Lindestad PA, Fritzell B, Persson A. Evaluation of laryngeal muscle function by quantitative analysis of the emg interference pattern. Acta Otolaryngol (Stockh) 1990;109:467–472. [PubMed]
33. Lindestad PA, Fritzell B, Persson A. Quantitative analysis of laryngeal EMG in normal subjects. Acta Otolaryngol (Stockh) 1991;111:1146–1152. [PubMed]
34. Buchthal F, Clemmesen S. On differentiation of muscle atrophy by electromyography. Acta Psychiatr Neurol Scand. 1941;16:143–181.
35. Stalberg E, Falck B, Sonoo M, et al. Multi-MUP EMG analysis--a two year experience in daily clinical work. Electroencephalogr Clin Neurophysiol. 1995;97:145–154. [PubMed]
36. Stalberg E, Erdem H. Quantitative motor unit potential analysis in routine. Electromyogr Clin Neurophysiol. 2002;42:433–442. [PubMed]
37. DeLuca CJ. Precision decomposition of EMG signals. Methods in Clinical Neurophsyiology. 1993;4
38. Crespo AN, Kimaid PA, Quagliato EM, et al. Laryngeal electromyography: technical features. Electromyogr Clin Neurophysiol. 2004;44:237–241. [PubMed]
39. Dedo HH. The paralyzed larynx: an electromyographic study in dogs and humans. Laryngoscope. 1970;80:1445–1517. [PubMed]
40. Dedo HH, Hall WN. Electrodes in laryngeal electromyography: reliability comparison. Annals of Otology, Rhinology and Laryngology. 1969;78:172–180. [PubMed]
41. Schweizer V, Woodson GE, Bertorini TE. Single-fiber electromyography of the laryngeal muscles. Muscle Nerve. 1999;22:111–114. [PubMed]
42. Sanders DB, Stalberg EV. AAEM minimonograph #25: single-fiber electromyography. Muscle Nerve. 1996;19:1069–1083. [PubMed]
43. Trontelj JV, Stalberg EV. Single fiber EMG and spectral analysis of surface EMG in myotonia congenita with or without transient weakness. Muscle Nerve. 1995;18:252–254. [PubMed]
44. Hirano M, Ohala J. Use of hooked-wire electrodes for electromyography of the intrinsic laryngeal muscles. J Speech Hear Res. 1969;12:362–373. [PubMed]
45. Ford CN, Bless DM, Lowery JD. Indirect laryngoscopic approach for injection of botulinum toxin in spasmodic dysphonia. Otolaryngology-Head and Neck Surgery. 1990;103:752–758. [PubMed]
46. Green DC, Berke GS, Ward PH, et al. Point-touch technique of botulinum toxin injection for the treatment of spasmodic dysphonia. Annals of Otology, Rhinology and Laryngology. 1992;101:883–887. [PubMed]
47. Rhew k, Fiedler D, Ludlow CL. Endoscopic technique for injection of botulinum toxin through the flexible nasolaryngoscope. Otolaryngology-Head and Neck Surgery. 1994 in press. [PubMed]
48. Bielamowicz S, Squire S, Bidus K, et al. Assessment of posterior cricoarytenoid botulinum toxin injections in patients with abductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2001;110:406–412. [PubMed]
49. Watts CR, Truong DD, Nye C. Evidence for the effectiveness of botulinum toxin for spasmodic dysphonia from high-quality research designs. J Neural Transm. 2008;115:625–630. [PubMed]
50. Belafsky PC, Postma GN, Reulbach TR, et al. Muscle tension dysphonia as a sign of underlying glottal insufficiency. Otolaryngol Head Neck Surg. 2002;127:448–451. [PubMed]
51. Koufman JA, Belafsky PC. Unilateral or localized Reinke's edema (pseudocyst) as a manifestation of vocal fold paresis: the paresis podule. Laryngoscope. 2001;111:576–580. [PubMed]
52. Heman-Ackah YD, Barr A. Mild vocal fold paresis: understanding clinical presentation and electromyographic findings. J Voice. 2006;20:269–281. [PubMed]
53. Merati AL, Shemirani N, Smith TL, et al. Changing trends in the nature of vocal fold motion impairment. Am J Otolaryngol. 2006;27:106–108. [PubMed]
54. Sulica L, Blitzer A. Vocal fold paresis: evidence and controversies. Curr Opin Otolaryngol Head Neck Surg. 2007;15:159–162. [PubMed]
55. Koufman JA, Postma GN, Cummins MM, et al. Vocal fold paresis. Otolaryngol Head Neck Surg. 2000;122:537–541. [PubMed]
56. Koufman JA, Postma GN, Whang CS, et al. Diagnostic laryngeal electromyography: The Wake Forest experience 1995–1999. Otolaryngol Head Neck Surg. 2001;124:603–606. [PubMed]
57. Munin MC, Rosen CA, Zullo T. Utility of laryngeal electromyography in predicting recovery after vocal fold paralysis. Arch Phys Med Rehabil. 2003;84:1150–1153. [PubMed]
58. Literature review of the usefulness of repetitive nerve stimulation and single fiber EMG in the electrodiagnostic evaluation of patients with suspected myasthenia gravis or Lambert-Eaton myasthenic syndrome. Muscle Nerve. 2001;24:1239–1247. [PubMed]
59. Practice parameter for repetitive nerve stimulation and single fiber EMG evaluation of adults with suspected myasthenia gravis or Lambert-Eaton myasthenic syndrome: summary statement. Muscle Nerve. 2001;24:1236–1238. [PubMed]
60. Sims S, Yamashita T, Rhew k, et al. An evaluation of the use of magnetic stimulation to measure laryngeal muscle response latencies in normal subjects Otolaryngology-Head and Neck Surgery. 1996;114:761–767.
61. Liu WB, Xia Q, Men LN, et al. Dysphonia as a primary manifestation in myasthenia gravis (MG): a retrospective review of 7 cases among 1520 MG patients. J Neurol Sci. 2007;260:16–22. [PubMed]
62. Hara K, Mashima T, Matsuda A, et al. Vocal cord paralysis in myasthenia gravis with anti-MuSK antibodies. Neurology. 2007;68:621–622. [PubMed]
63. Hartl DM, Leboulleux S, Klap P, et al. Myasthenia gravis mimicking unilateral vocal fold paralysis at presentation. J Laryngol Otol. 2007;121:174–178. [PubMed]
64. Mao VH, Abaza M, Spiegel JR, et al. Laryngeal myasthenia gravis: report of 40 cases. J Voice. 2001;15:122–130. [PubMed]
65. Colton-Hudson A, Koopman WJ, Moosa T, et al. A prospective assessment of the characteristics of dysphagia in myasthenia gravis. Dysphagia. 2002;17:147–151. [PubMed]
66. Ertekin C, Yuceyar N, Aydogdu I. Clinical and electrophysiological evaluation of dysphagia in myasthenia gravis. J Neurol Neurosurg Psychiatry. 1998;65:848–856. [PMC free article] [PubMed]
67. Jellinger KA. Pathology of Parkinson's disease. Changes other than the nigrostriatal pathway. Mol Chem Neuropathol. 1991;14:153–197. [PubMed]
68. Wenning GK, Tison F, Ben Shlomo Y, et al. Multiple system atrophy: a review of 203 pathologically proven cases. Mov Disord. 1997;12:133–147. [PubMed]
69. Vetrugno R, Liguori R, Cortelli P, et al. Sleep-related stridor due to dystonic vocal cord motion and neurogenic tachypnea/tachycardia in multiple system atrophy. Mov Disord. 2007;22:673–678. [PubMed]
70. Kluin KJ, Foster NL, Berent S, et al. Perceptual analysis of speech disorders in progressive supranuclear palsy. Neurology. 1993;43:563–566. [PubMed]
71. Jurgens U. Neural pathways underlying vocal control. Neurosci Biobehav Rev. 2002;26:235–258. [PubMed]
72. Perlmutter JS, Mink JW. Dysfunction of dopaminergic pathways in dystonia. Adv Neurol. 2004;94:163–170. [PubMed]
73. Bloch CS, Hirano M, Gould WJ. Symptom improvement of spastic dysphonia in response to phonatory tasks. Annals of Otology, Rhinology and Laryngology. 1985;94:51–54. [PubMed]
74. Morrison MD, Nichol H, Rammage RA. Diagnostic criteria in functional dysphonia. Laryngoscope. 1986;96:1–8. [PubMed]
75. Belisle GM, Morrison MD. Anatomic correlation for muscle tension dysphonia. J Otolaryngol. 1983;12:319–321. [PubMed]
76. Koda J, Ludlow CL. An evaluation of laryngeal muscle activation in patients with voice tremor. Otolaryngol Head Neck Surg. 1992;107:684–696. [PubMed]
77. Finnegan EM, Luschei ES, Barkmeier JM, et al. Synchrony of laryngeal muscle activity in persons with vocal tremor. Arch Otolaryngol Head Neck Surg. 2003;129:313–318. [PubMed]
78. Zarzur AP, Duprat AC, Shinzato G, et al. Laryngeal electromyography in adults with Parkinson's disease and voice complaints. Laryngoscope. 2007;117:831–834. [PubMed]
79. Cyrus CB, Bielamowicz S, Evans FJ, et al. Adductor muscle activity abnormalities in abductor spasmodic dysphonia. Otolaryngol Head Neck Surg. 2001;124:23–30. [PubMed]
80. Boucher VJ, Ahmarani C, Ayad T. Physiologic features of vocal fatigue: electromyographic spectral-compression in laryngeal muscles. Laryngoscope. 2006;116:959–965. [PubMed]
81. Bielamowicz S, Ludlow CL. Effects of botulinum toxin on pathophysiology in spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2000;109:194–203. [PubMed]
82. Nash EA, Ludlow CL. Laryngeal muscle activity during speech breaks in adductor spasmodic dysphonia. Laryngoscope. 1996;106:484–489. [PubMed]
83. Gallena S, Smith PJ, Zeffiro T, et al. Effects of levodopa on laryngeal muscle activity for voice onset and offset in Parkinson disease. J Speech Lang Hear Res. 2001;44:1284–1299. [PubMed]
84. Hartl DM, Leboulleux S, Klap P, et al. Myasthenia gravis mimicking unilateral vocal fold paralysis at presentation. J Laryngol Otol. 2006:1–5. [PubMed]
85. Ludlow CL, Schulz G, Naunton RF. The effects of diazepam on intrinsic laryngeal muscle activation during respiration and speech. Journal of Voice. 1988;2:70–77.
86. Van Pelt F, Ludlow CL, Smith PJ. Comparison of muscle activation patterns in adductor and abductor spasmodic dysphonia. Ann Otol RhinolLaryngol. 1994;103:192–200. [PubMed]
87. Klotz DA, Maronian NC, Waugh PF, et al. Findings of multiple muscle involvement in a study of 214 patients with laryngeal dystonia using fine-wire electromyography. Ann Otol Rhinol Laryngol. 2004;113:602–612. [PubMed]
88. Hillel AD, Maronian NC, Waugh PF, et al. Treatment of the interarytenoid muscle with botulinum toxin for laryngeal dystonia. Ann Otol Rhinol Laryngol. 2004;113:341–348. [PubMed]
89. Hillel AD. The study of laryngeal muscle activity in normal human subjects and in patients with laryngeal dystonia using multiple fine-wire electromyography. Laryngoscope. 2001;111:1–47. [PubMed]
90. Hocevar-Boltezar I, Janko M, Zargi M. Role of surface EMG in diagnostics and treatment of muscle tension dysphonia. Acta Otolaryngol. 1998;118:739–743. [PubMed]
91. Adler CH, Bansberg SF, Krein-Jones K, et al. Safety and efficacy of botulinum toxin type B (Myobloc) in adductor spasmodic dysphonia. Mov Disord. 2004;19:1075–1079. [PubMed]