570932
research-article2015
AORXXX10.1177/0003489415570932Annals of Otology, Rhinology & LaryngologyYang et al
Article
Value of Laryngeal Electromyography in Spasmodic Dysphonia Diagnosis and Therapy
Annals of Otology, Rhinology & Laryngology 2015, Vol. 124(7) 579–583 © The Author(s) 2015 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003489415570932 aor.sagepub.com
Qingwen Yang, MD1, Wen Xu, MD1, Yun Li, MD1, and Liyu Cheng, MD1
Abstract Objective: To investigate the role of laryngeal electromyography (LEMG) in the diagnosis and treatment of spasmodic dysphonia (SD). Methods: The clinical manifestations, characteristics of motor unit potentials (MUPs), recruitment potentials, and laryngeal nerve evoked potentials (EPs) in LEMG, as well as the changes after botulinum toxin (BTX) treatment, were analyzed in 39 patients with adductor SD. Results: The main clinical manifestations were a strained voice and phonation interruptions; in addition, the patients displayed hyper-adducted vocal folds during phonation. LEMG revealed significantly increased amplitudes of the thyroarytenoid muscle MUPs. The recruitment potentials were in a dense bunch, discharging full interference patterns with significantly increased amplitudes; the mean and maximum amplitude of recruitment potentials were 3090 μV and 5000 μV, respectively. The amplitude of EPs of thyroarytenoid muscle increased significantly; the mean and maximum amplitudes were 10.3 mV and 26.3 mV, respectively. After BTX was injected, the LEMG revealed denervation changes, and the EPs weakened or disappeared in the injected muscle. Conclusions: SD could be diagnosed, and the therapeutic efficacy of SD treatments could be evaluated based on clinical characteristics combined with LEMG characteristics. The increased amplitudes of the recruitment potentials and EPs of the thyroarytenoid muscle were the characteristic indexes. After BTX was injected, denervated potential characteristics appeared in the muscles. Keywords spasmodic dysphonia, laryngeal electromyography
Introduction Traube first described spasmodic dysphonia (SD) in 1871. SD is considered a primary, focal laryngeal dystonia, which causes the patient to suffer from strained phonation and voice break.1,2 However, the definite etiology, diagnostic characteristics, and treatment methods of SD remain the focus of debate to this day. In the present study, the clinical manifestations, laryngeal electromyograms, characteristics of the laryngeal nerve evoked potentials, and changes after the treatment of 39 patients with adductor SD were analyzed, and the role of laryngeal electromyography (LEMG) in diagnosing and treating SD is discussed.
Materials and Methods Thirty-nine patients with adductor SD originated from those who were diagnosed and treated in the Department of Otolaryngology-Head and Neck Surgery, Beijing Tongren hospital, China, from December 2003 to April 2014. There were 30 female patients and 9 male patients. The mean age
of the patients was 39.2 ± 10.5. The course of disease ranged from 2 months to 20 years. To eliminate the possibility of abnormal muscle tension caused by other reasons, patients underwent thorough head and neck examinations and received neurological and psychological consultations. The clinical characteristics and corresponding electromyographic changes of the laryngeal muscles of each patient were observed. The LEMG data were also collected from a healthy control group used in previous studies.3,4 The control group included 15 men and 21 women ranging in age from 20 to 74 years. All control subjects agreed to participate in this study. They were interviewed for confirmation that they had no history of voice disorders. 1
Department of Otorhinolaryngology-Head Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China Corresponding Author: Wen Xu, MD, Department of Otorhinolaryngology-Head Neck Surgery, Beijing Tongren, Hospital, 1 Dongjiaominxiang, Beijing 100730, China. Email: [email protected]
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Annals of Otology, Rhinology & Laryngology 124(7)
Table 1. Laryngeal Electromyography Parameters of Motor Unit Potential (Amplitude and Duration) and Maximum Amplitude in the Recruitment Phase of Adductor Patients With Spasmodic Dysphonia (SD).a Laryngeal Muscle Thyroarytenoid Cricothyroid Posterior cricoarytenoid
Group SD Normal subjects SD Normal subjects SD Normal subjects
Amplitude (μV)
Duration (ms)
Maximum Amplitude (μV)
346.9 ± 213.0* 283.9 ± 99.9 374.8 ± 297.8 382.6 ± 124.8 400.0 ± 302.1 459.9 ± 252.4
5.3 ± 1.2 6.3 ± 1.0 5.6 ± 1.6 6.8 ± 0.8 6.0 ± 1.6 6.8 ± 1.0
3089.74 ± 889.6** 1344.3 ± 657.1 2281.3 ± 811.0 1756.4 ± 774.1 1923.8 ± 758.2 1621.1 ± 846.1
*
P < .05. **P < .01, compared with normal subjects. Values are expressed as mean ± standard deviation.
a
The diagnosis and treatment schemes were determined based on the clinical manifestations and laryngeal electromyographic characteristics. Laryngostroboscopic signs were evaluated for the following characteristics: shape of the vocal folds, overall glottal closure, mucosal wave, movement of the vocal fold, and supraglottic involvement. A Nicolet Viking Quest electromyograph/evoked potential instrument (Nicolet Biomedical, Madison, Wisconsin, USA) was used. The electromyographic signals and audio sound signals were input simultaneously via 2 channels. All the EMG studies were performed by 2 trained physicians.
Laryngeal Electromyographic Examination The electromyographic characteristics (eg, spontaneous potential, motor unit potential, and recruitment potential) of the intrinsic laryngeal muscle (thyroarytenoid muscle, cricothyroid muscle, and posterior cricoarytenoid muscle) in different functional states (quiet, phonation, and respiration) were analyzed.
Analysis of the Laryngeal Nerve Evoked Potential A monopolar needle electrode with a current of 6.0 to 24.0 mA was used to simulate the recurrent laryngeal nerve and superior laryngeal nerve, and the latent periods, during time, amplitudes, and waveform changes of the evoked potentials of the corresponding intrinsic laryngeal muscles (thyroarytenoid muscle, cricothyroid muscle, and posterior cricoarytenoid muscle) were examined. Botulinum toxin type A injection was performed under electromyographic monitoring. Follow-ups were conducted 1 week, 2 weeks, 1 month, 2 months, and 3 months after the injection. All botulinum toxin injections were performed by the senior author. An analysis of variance was performed using SPSS version 8.0 software (SPSS Inc, Chicago, Illinois, USA).
Results The main clinical manifestations of the 39 patients with adductor SD were a strained voice and phonation interruptions;
these manifestations became more prominent when the patients spoke on the telephone or talked to strangers. The stroboscopic examination revealed that the patients had hyper-adducted vocal folds during phonation; compression was obvious in the interarytenoid region but was not obvious in the supraglottic region. Moreover, the SD was sometimes accompanied by laryngeal tremors; 2 patients also had tongue and soft palatal tremors during phonation. Laryngeal electromyographic characteristics are listed in Table 1. No abnormal spontaneous potential was observed in the intrinsic laryngeal muscles of any patient. No abnormal waveform, duration, or phase of the motor unit potential was detected. The wave amplitudes of the thyroarytenoid muscles of the patients increased significantly (mean, 346.9 µV; range, 101-1256 µV), which was significantly different from the wave amplitudes of the volunteers in the healthy control group (mean, 283.9 µV). The wave amplitudes of the cricothyroid muscle (mean, 374.8 µV; range, 332-2320 µV) and posterior cricoarytenoid muscle (mean, 400.0 µV; range, 125-2063 µV) in the patients did not differ significantly from those in the control group (Table 1). The recruitment activities of the thyroarytenoid, cricothyroid, and posterior cricoarytenoid muscle recruitment potentials of the patients were increased compared with the healthy control group and were in a dense bunch, discharging full interference patterns. The maximum potential amplitudes in the recruitment phase increased; the increase in the maximum potential amplitude of the thyroarytenoid muscle was the most significant (mean, 3090 µV; range, 1500-5000 µV) and significantly differed from that of the healthy control group (mean, 1344 µV) (P < .01). The maximum potential amplitude of the cricothyroid muscle (mean, 2281 µV; range, 1000-4000 µV) and posterior cricoarytenoid muscle (mean, 1923; µV, range 800-4500 µV) in the SD patients showed an increasing tendency without statistically significant differences (Table 1). The recruitment activity interval of the SD group was longer than that of the healthy control group. Laryngeal nerve evoked potential results are presented in Table 2. The evoked potential amplitudes of the patients increased to different degrees compared with the volunteers in the healthy control group. The increase in the amplitude of the evoked potential of thyroarytenoid muscle was
581
Yang et al Table 2. Evoked Laryngeal Electromyography Parameters of Adductor Patients With Spasmodic Dysphonia (SD).a Stimulated Laryngeal Nerve Recurrent laryngeal nerve
Laryngeal Muscle Thyroarytenoid Posterior cricoarytenoid
Superior laryngeal nerve
Cricothyroid
Group SD Normal subjects SD Normal subjects SD Normal subjects
Latent Period (ms)
Duration (ms)
Amplitude (μV)
1.7 ± 0.4 1.7 ± 0.3 1.7 ± 0.2 1.7 ± 0.3 1.8 ± 0.4 1.7 ± 0.4
5.0 ± 1.0 6.4 ± 1.5 5.3 ± 1.4 5.2 ± 1.1 5.7 ± 2.0 7.6 ± 2.7
10.3 ± 5.9* 7.6 ± 5.9 5.3 ± 2.7 4.4 ± 3.3 6.6 ± 4.0 4.9 ± 4.3
*
P < .05, compared with normal subjects. Values are expressed as mean ± standard deviation.
a
significant (P < .05), with a mean value of 10.3 mV and a range of 0.5 to 26.3 mV. No abnormal latent periods or durations were detected in the evoked potentials of the superior laryngeal nerve and recurrent laryngeal nerve. Of the 39 patients, 22 were performed botulinum toxin (BTX) injection (bilateral 10, unilateral 12). The dose of botulinum toxin ranged from 2.5 to 5 units, determined by the severity of symptoms and LEMG patterns. Eighteen patients completed EMG(s) reexamination at least once at 1 week, 2 weeks, 1 month, or 3 months post injection. Four patients dropped out after BTX injection. Twenty-four hours after the injection of botulinum toxin, the patients’ symptoms, such as a strained voice and phonation interruptions, improved or disappeared accompanied with hoarseness and breathy voice of different degrees. The laryngostroboscopic examination revealed that the vocal fold on the injection side was bowing, and the glottis was not closed completely. A follow-up was conducted 2 weeks after the injection treatment. The electromyographic reexamination demonstrated that fibrillation potentials (denervated changes) or electrical silence activity occurred, and the evoked potential of injected intrinsic laryngeal muscle could not be induced or weakened. Within 3 to 4 months of the injection treatment, the symptoms and electromyographic characteristics of the patients recovered to the pretreatment levels.
Discussion Spasmodic dysphonia manifests as a nonvoluntary spasm of 1 or multiple muscles during phonation, resulting in hyperadduction or hyper-abduction of the vocal folds, which leads to spasmodic phonation or phonation interruptions, which in turn affects the speech communication ability of the patient. Adductor SD is the most common and is mainly manifested as hyper-adduction (closure) of the vocal folds during phonation, resulting in voice breaks and a strained voice. Patients with adductor SD feel overexerted and easily fatigued during phonation.1,2,5 Currently, there is no generally accepted, specific criterion for SD diagnosis. The diagnosis of SD is still based on the clinical manifestations and is evaluated according to the
detailed medical history, phonatory characteristics, and endoscopic examination. All patients newly diagnosed with SD should also be evaluated by neurologists and psychologists to exclude all other neurogenic diseases and psychological obstacles. As an objective detection means, the application of LEMG for SD treatment has received increasing attention from professionals. The basic evaluation of LEMG includes characteristics of spontaneous activities, characteristics of the single motor unit potential, and characteristic variations in the recruitment potential when the contractile force of the laryngeal muscles increases. In the laryngeal electromyograms of the 39 patients with SD in the present study, no characteristics of nerve injury were detected. The waveform and phase of the single motor unit potential were normal, no abnormal spontaneous potential was detected, and the recruitment potential showed full interference patterns. However, the laryngeal electromyograms of the patients revealed that the myoelectricity was abnormally active, especially the thyroarytenoid muscle, which exhibited hypertensive electromyographic signals and a nonperiodic rhythm. Hillel et al6 used monopolar recordings with hook wire electrodes electromyography to analyze the electromyographic characteristics of normal subjects and patients with SD; they discovered that the latent periods, amplitudes, and frequencies of the thyroarytenoid muscles of the patients with SD increased, and the thyroarytenoid muscles of the patients with SD were continuously active during continuous phonation processes. Therefore, the continuously active, high-intensity, and high-frequency electromyographic activities of the thyroarytenoid muscle during phonation further explains why these patients were easily fatigued and experienced phonation interruptions. The variation range of the motor unit potential amplitude of the laryngeal muscles is relatively large; the potential amplitude of the posterior cricoarytenoid muscle is the largest, followed by the cricothyroid muscle and thyroarytenoid muscle. Our preliminary study and the present study both indicated that the motor unit potential amplitudes of patients with adductor SD increased significantly, which was significantly different from the volunteers in the healthy control group.7 With increasing laryngeal muscle activity, the
582 number of recruitment activity units increased, and the discharging frequency increased. When the laryngeal muscles contracted to the greatest extent, all the motor units were synchronized, myoelectricity was in a recruitment interference phase, and the potential amplitude of the maximum contraction increased by 80% to 200% compared with the potential amplitudes of mild contractions. We found that the recruitment potentials of the patients with adductor SD were in a dense bunch, discharging full interference patterns; the maximum potential amplitude in the recruitment phase increased significantly (mean, 3.090 µV; maximum, 5.000 µV), which was 2 to 4 times the corresponding value of the healthy control group; thus, the difference was significant. The increased potential amplitude of the myoelectric motor unit in the thyroarytenoid muscle and the increased maximum amplitude of the recruitment phase could be used as evaluation indexes for the abnormal increase in the muscle tension of patients; in particular, the increased maximum amplitude of the recruitment phase might reflect the abnormal active level of myoelectricity to a greater extent. The examination of the laryngeal nerve conduction function is a good supplement to the routine LEMG examination. Through examining nerve evoked potentials and stimulating motor nerves, the variations in the action potentials of compound muscles were observed. The latent periods of evoked potentials reflect the myelin sheath function (mean latent period, 1.7 ms). The amplitudes of nerve-evoked potentials reflect the number of the measured nerve fibers and the level of synchronized excitation; there are many influencing factors for the nerve evoked potential amplitude, which differ from individual to individual; the potential amplitude of the recurrent laryngeal nerve is generally greater than 1.0 µV. Our data demonstrated that the evoked potential amplitudes of thyroarytenoid muscle in patients with SD increased significantly (mean,10.3 µV; maximum, 26.3 µV). Therefore, the evoked potential might also be used to quantitatively determine the degree of the abnormal increase in the muscle tension of patients with SD. SD still cannot be completely cured. Currently, the local injection of botulinum toxin type A is the first choice of treatment method and involves the symptomatic treatment of SD through chemodenervation.5,8,9 The main injection method is using a special hollow-needle electroinjection electrode to inject botulinum toxin under electromyographic monitoring. For patients with adductor SD, botulinum toxin is injected into their thyroarytenoid muscles. It was also reported that injecting botulinum toxin into the lateral cricoarytenoid muscles of patients with adductor SD could yield good results. Moreover, our previous studies confirmed that the onset time was 6 hours to 2 days after the botulinum toxin injection; the peak effective time was 2 weeks, and the mean duration was 15.2 weeks.7 Two weeks
Annals of Otology, Rhinology & Laryngology 124(7) after the injection, the electromyographic examination showed that fibrillation potentials occurred or were in an electrically silent state, and the evoked potential could not be induced, indicating a complete drug effect. Fibrillary waves are a relatively sensitive parameter for evaluating early muscle denervation. Nerve evoked potentials can also provide additional information. The evoked potential of a patient with a completely injured recurrent laryngeal nerve disappears; the conduction function decreases in patients with a partially injured nerve, the latent period significantly increases, and the evoked potential amplitude significantly decreases. Three to 4 months after injection, the symptoms and electromyographic characteristics of the patients recovered to the pretreatment levels. Therefore, during the treatment, the therapeutic efficacy, dosage adjustment, and prognosis may be objectively determined based on the improvement in the patient’s symptoms after botulinum toxin injection combined with laryngeal electromyography, which may further provide a basis for the timing of the second injection. As we found, fibrillation potentials or electrical silence activity occurred and the evoked responses of the injected muscle could not be induced or weakened after BTX injection. The presence of denervation or unrecovered EPs may suggest sustained pharmacological effects of botulinum toxin. For avoiding irreversible muscular injury, we suggested that patients with those abnormal EMG patterns should not be considered to re-injection course at the beginning of their symptoms return, especially for the voice professionals and the young. The findings of the present study are in agreement with the reports of Klotz et al10 and Cyrus et al,11 namely, regardless of the spasm type, abnormal myoelectric activity is generally not restricted to 1 muscle—which is also the reason for treatment failure in certain patients. Therefore, it is necessary to also consider the interaction between different muscles in future studies. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Blitzer A, Brin MF, Fahn S, Lovelace RE. Clinical and laboratory characteristics of focal laryngeal dystonia: study of 110 cases. Laryngoscope. 1988;98(6 Pt 1):636-640. 2. Blitzer A, Brin MF, Stewart CF. Botulinum toxin management of spasmodic dysphonia (laryngeal dystonia): a 12-year experience in more than 900 patients. Laryngoscope. 1998;108(10):1435-1441.
Yang et al 3. Xu W, Han D, Hou L, Zhang L, Zhao G. Value of laryngeal electromyography in diagnosis of vocal fold immobility. Ann Otol Rhinol Laryngol. 2007;116(8):576-581. 4. Xu W, Han D, Hou L, Hu R, Wang L. Clinical and electrophysiological characteristics of larynx in myasthenia gravis. Ann Otol Rhinol Laryngol. 2009;118(9):656-661. 5. Blitzer A. Spasmodic dysphonia and botulinum toxin: experience from the largest treatment series. Eur J Neurol. 2010;17(suppl 1):28-30. 6. 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(4 Pt 2 suppl 97):1-47. 7. Xu W, Han DM, Hou LZ, et al. Patterns of spasmodic dysphonia and botulinum toxin injections. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2005;40(4):253-257.
583 8. Ludlow CL. Treatment for spasmodic dysphonia: limitations of current approaches. Curr Opin Otolaryngol Head Neck Surg. 2009;17(3):160-165. 9. Novakovic D, Waters HH, D’Elia JB, Blitzer A. Botulinum toxin treatment of adductor spasmodic dysphonia: longitudinal functional outcomes. Laryngoscope. 2011;121(3):606612. 10. Klotz DA, Maronian NC, Waugh PF, Shahinfar A, Robinson L, Hillel AD. Findings of multiple muscle involvement in a study of 214 patients with laryngeal dystonia using fine-wire electromyography. Ann Otol Rhinol Laryngol. 2004;113(8):602-612. 11. Cyrus CB, Bielamowicz S, Evans FJ, Ludlow CL. Adductor muscle activity abnormalities in abductor spasmodic dysphonia. Otolaryngol Head Neck Surg. 2001;124(1):23-30.
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research-article2015
AORXXX10.1177/0003489415570932Annals of Otology, Rhinology & LaryngologyYang et al
Article
Value of Laryngeal Electromyography in Spasmodic Dysphonia Diagnosis and Therapy
Annals of Otology, Rhinology & Laryngology 2015, Vol. 124(7) 579–583 © The Author(s) 2015 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003489415570932 aor.sagepub.com
Qingwen Yang, MD1, Wen Xu, MD1, Yun Li, MD1, and Liyu Cheng, MD1
Abstract Objective: To investigate the role of laryngeal electromyography (LEMG) in the diagnosis and treatment of spasmodic dysphonia (SD). Methods: The clinical manifestations, characteristics of motor unit potentials (MUPs), recruitment potentials, and laryngeal nerve evoked potentials (EPs) in LEMG, as well as the changes after botulinum toxin (BTX) treatment, were analyzed in 39 patients with adductor SD. Results: The main clinical manifestations were a strained voice and phonation interruptions; in addition, the patients displayed hyper-adducted vocal folds during phonation. LEMG revealed significantly increased amplitudes of the thyroarytenoid muscle MUPs. The recruitment potentials were in a dense bunch, discharging full interference patterns with significantly increased amplitudes; the mean and maximum amplitude of recruitment potentials were 3090 μV and 5000 μV, respectively. The amplitude of EPs of thyroarytenoid muscle increased significantly; the mean and maximum amplitudes were 10.3 mV and 26.3 mV, respectively. After BTX was injected, the LEMG revealed denervation changes, and the EPs weakened or disappeared in the injected muscle. Conclusions: SD could be diagnosed, and the therapeutic efficacy of SD treatments could be evaluated based on clinical characteristics combined with LEMG characteristics. The increased amplitudes of the recruitment potentials and EPs of the thyroarytenoid muscle were the characteristic indexes. After BTX was injected, denervated potential characteristics appeared in the muscles. Keywords spasmodic dysphonia, laryngeal electromyography
Introduction Traube first described spasmodic dysphonia (SD) in 1871. SD is considered a primary, focal laryngeal dystonia, which causes the patient to suffer from strained phonation and voice break.1,2 However, the definite etiology, diagnostic characteristics, and treatment methods of SD remain the focus of debate to this day. In the present study, the clinical manifestations, laryngeal electromyograms, characteristics of the laryngeal nerve evoked potentials, and changes after the treatment of 39 patients with adductor SD were analyzed, and the role of laryngeal electromyography (LEMG) in diagnosing and treating SD is discussed.
Materials and Methods Thirty-nine patients with adductor SD originated from those who were diagnosed and treated in the Department of Otolaryngology-Head and Neck Surgery, Beijing Tongren hospital, China, from December 2003 to April 2014. There were 30 female patients and 9 male patients. The mean age
of the patients was 39.2 ± 10.5. The course of disease ranged from 2 months to 20 years. To eliminate the possibility of abnormal muscle tension caused by other reasons, patients underwent thorough head and neck examinations and received neurological and psychological consultations. The clinical characteristics and corresponding electromyographic changes of the laryngeal muscles of each patient were observed. The LEMG data were also collected from a healthy control group used in previous studies.3,4 The control group included 15 men and 21 women ranging in age from 20 to 74 years. All control subjects agreed to participate in this study. They were interviewed for confirmation that they had no history of voice disorders. 1
Department of Otorhinolaryngology-Head Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China Corresponding Author: Wen Xu, MD, Department of Otorhinolaryngology-Head Neck Surgery, Beijing Tongren, Hospital, 1 Dongjiaominxiang, Beijing 100730, China. Email: [email protected]
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Annals of Otology, Rhinology & Laryngology 124(7)
Table 1. Laryngeal Electromyography Parameters of Motor Unit Potential (Amplitude and Duration) and Maximum Amplitude in the Recruitment Phase of Adductor Patients With Spasmodic Dysphonia (SD).a Laryngeal Muscle Thyroarytenoid Cricothyroid Posterior cricoarytenoid
Group SD Normal subjects SD Normal subjects SD Normal subjects
Amplitude (μV)
Duration (ms)
Maximum Amplitude (μV)
346.9 ± 213.0* 283.9 ± 99.9 374.8 ± 297.8 382.6 ± 124.8 400.0 ± 302.1 459.9 ± 252.4
5.3 ± 1.2 6.3 ± 1.0 5.6 ± 1.6 6.8 ± 0.8 6.0 ± 1.6 6.8 ± 1.0
3089.74 ± 889.6** 1344.3 ± 657.1 2281.3 ± 811.0 1756.4 ± 774.1 1923.8 ± 758.2 1621.1 ± 846.1
*
P < .05. **P < .01, compared with normal subjects. Values are expressed as mean ± standard deviation.
a
The diagnosis and treatment schemes were determined based on the clinical manifestations and laryngeal electromyographic characteristics. Laryngostroboscopic signs were evaluated for the following characteristics: shape of the vocal folds, overall glottal closure, mucosal wave, movement of the vocal fold, and supraglottic involvement. A Nicolet Viking Quest electromyograph/evoked potential instrument (Nicolet Biomedical, Madison, Wisconsin, USA) was used. The electromyographic signals and audio sound signals were input simultaneously via 2 channels. All the EMG studies were performed by 2 trained physicians.
Laryngeal Electromyographic Examination The electromyographic characteristics (eg, spontaneous potential, motor unit potential, and recruitment potential) of the intrinsic laryngeal muscle (thyroarytenoid muscle, cricothyroid muscle, and posterior cricoarytenoid muscle) in different functional states (quiet, phonation, and respiration) were analyzed.
Analysis of the Laryngeal Nerve Evoked Potential A monopolar needle electrode with a current of 6.0 to 24.0 mA was used to simulate the recurrent laryngeal nerve and superior laryngeal nerve, and the latent periods, during time, amplitudes, and waveform changes of the evoked potentials of the corresponding intrinsic laryngeal muscles (thyroarytenoid muscle, cricothyroid muscle, and posterior cricoarytenoid muscle) were examined. Botulinum toxin type A injection was performed under electromyographic monitoring. Follow-ups were conducted 1 week, 2 weeks, 1 month, 2 months, and 3 months after the injection. All botulinum toxin injections were performed by the senior author. An analysis of variance was performed using SPSS version 8.0 software (SPSS Inc, Chicago, Illinois, USA).
Results The main clinical manifestations of the 39 patients with adductor SD were a strained voice and phonation interruptions;
these manifestations became more prominent when the patients spoke on the telephone or talked to strangers. The stroboscopic examination revealed that the patients had hyper-adducted vocal folds during phonation; compression was obvious in the interarytenoid region but was not obvious in the supraglottic region. Moreover, the SD was sometimes accompanied by laryngeal tremors; 2 patients also had tongue and soft palatal tremors during phonation. Laryngeal electromyographic characteristics are listed in Table 1. No abnormal spontaneous potential was observed in the intrinsic laryngeal muscles of any patient. No abnormal waveform, duration, or phase of the motor unit potential was detected. The wave amplitudes of the thyroarytenoid muscles of the patients increased significantly (mean, 346.9 µV; range, 101-1256 µV), which was significantly different from the wave amplitudes of the volunteers in the healthy control group (mean, 283.9 µV). The wave amplitudes of the cricothyroid muscle (mean, 374.8 µV; range, 332-2320 µV) and posterior cricoarytenoid muscle (mean, 400.0 µV; range, 125-2063 µV) in the patients did not differ significantly from those in the control group (Table 1). The recruitment activities of the thyroarytenoid, cricothyroid, and posterior cricoarytenoid muscle recruitment potentials of the patients were increased compared with the healthy control group and were in a dense bunch, discharging full interference patterns. The maximum potential amplitudes in the recruitment phase increased; the increase in the maximum potential amplitude of the thyroarytenoid muscle was the most significant (mean, 3090 µV; range, 1500-5000 µV) and significantly differed from that of the healthy control group (mean, 1344 µV) (P < .01). The maximum potential amplitude of the cricothyroid muscle (mean, 2281 µV; range, 1000-4000 µV) and posterior cricoarytenoid muscle (mean, 1923; µV, range 800-4500 µV) in the SD patients showed an increasing tendency without statistically significant differences (Table 1). The recruitment activity interval of the SD group was longer than that of the healthy control group. Laryngeal nerve evoked potential results are presented in Table 2. The evoked potential amplitudes of the patients increased to different degrees compared with the volunteers in the healthy control group. The increase in the amplitude of the evoked potential of thyroarytenoid muscle was
581
Yang et al Table 2. Evoked Laryngeal Electromyography Parameters of Adductor Patients With Spasmodic Dysphonia (SD).a Stimulated Laryngeal Nerve Recurrent laryngeal nerve
Laryngeal Muscle Thyroarytenoid Posterior cricoarytenoid
Superior laryngeal nerve
Cricothyroid
Group SD Normal subjects SD Normal subjects SD Normal subjects
Latent Period (ms)
Duration (ms)
Amplitude (μV)
1.7 ± 0.4 1.7 ± 0.3 1.7 ± 0.2 1.7 ± 0.3 1.8 ± 0.4 1.7 ± 0.4
5.0 ± 1.0 6.4 ± 1.5 5.3 ± 1.4 5.2 ± 1.1 5.7 ± 2.0 7.6 ± 2.7
10.3 ± 5.9* 7.6 ± 5.9 5.3 ± 2.7 4.4 ± 3.3 6.6 ± 4.0 4.9 ± 4.3
*
P < .05, compared with normal subjects. Values are expressed as mean ± standard deviation.
a
significant (P < .05), with a mean value of 10.3 mV and a range of 0.5 to 26.3 mV. No abnormal latent periods or durations were detected in the evoked potentials of the superior laryngeal nerve and recurrent laryngeal nerve. Of the 39 patients, 22 were performed botulinum toxin (BTX) injection (bilateral 10, unilateral 12). The dose of botulinum toxin ranged from 2.5 to 5 units, determined by the severity of symptoms and LEMG patterns. Eighteen patients completed EMG(s) reexamination at least once at 1 week, 2 weeks, 1 month, or 3 months post injection. Four patients dropped out after BTX injection. Twenty-four hours after the injection of botulinum toxin, the patients’ symptoms, such as a strained voice and phonation interruptions, improved or disappeared accompanied with hoarseness and breathy voice of different degrees. The laryngostroboscopic examination revealed that the vocal fold on the injection side was bowing, and the glottis was not closed completely. A follow-up was conducted 2 weeks after the injection treatment. The electromyographic reexamination demonstrated that fibrillation potentials (denervated changes) or electrical silence activity occurred, and the evoked potential of injected intrinsic laryngeal muscle could not be induced or weakened. Within 3 to 4 months of the injection treatment, the symptoms and electromyographic characteristics of the patients recovered to the pretreatment levels.
Discussion Spasmodic dysphonia manifests as a nonvoluntary spasm of 1 or multiple muscles during phonation, resulting in hyperadduction or hyper-abduction of the vocal folds, which leads to spasmodic phonation or phonation interruptions, which in turn affects the speech communication ability of the patient. Adductor SD is the most common and is mainly manifested as hyper-adduction (closure) of the vocal folds during phonation, resulting in voice breaks and a strained voice. Patients with adductor SD feel overexerted and easily fatigued during phonation.1,2,5 Currently, there is no generally accepted, specific criterion for SD diagnosis. The diagnosis of SD is still based on the clinical manifestations and is evaluated according to the
detailed medical history, phonatory characteristics, and endoscopic examination. All patients newly diagnosed with SD should also be evaluated by neurologists and psychologists to exclude all other neurogenic diseases and psychological obstacles. As an objective detection means, the application of LEMG for SD treatment has received increasing attention from professionals. The basic evaluation of LEMG includes characteristics of spontaneous activities, characteristics of the single motor unit potential, and characteristic variations in the recruitment potential when the contractile force of the laryngeal muscles increases. In the laryngeal electromyograms of the 39 patients with SD in the present study, no characteristics of nerve injury were detected. The waveform and phase of the single motor unit potential were normal, no abnormal spontaneous potential was detected, and the recruitment potential showed full interference patterns. However, the laryngeal electromyograms of the patients revealed that the myoelectricity was abnormally active, especially the thyroarytenoid muscle, which exhibited hypertensive electromyographic signals and a nonperiodic rhythm. Hillel et al6 used monopolar recordings with hook wire electrodes electromyography to analyze the electromyographic characteristics of normal subjects and patients with SD; they discovered that the latent periods, amplitudes, and frequencies of the thyroarytenoid muscles of the patients with SD increased, and the thyroarytenoid muscles of the patients with SD were continuously active during continuous phonation processes. Therefore, the continuously active, high-intensity, and high-frequency electromyographic activities of the thyroarytenoid muscle during phonation further explains why these patients were easily fatigued and experienced phonation interruptions. The variation range of the motor unit potential amplitude of the laryngeal muscles is relatively large; the potential amplitude of the posterior cricoarytenoid muscle is the largest, followed by the cricothyroid muscle and thyroarytenoid muscle. Our preliminary study and the present study both indicated that the motor unit potential amplitudes of patients with adductor SD increased significantly, which was significantly different from the volunteers in the healthy control group.7 With increasing laryngeal muscle activity, the
582 number of recruitment activity units increased, and the discharging frequency increased. When the laryngeal muscles contracted to the greatest extent, all the motor units were synchronized, myoelectricity was in a recruitment interference phase, and the potential amplitude of the maximum contraction increased by 80% to 200% compared with the potential amplitudes of mild contractions. We found that the recruitment potentials of the patients with adductor SD were in a dense bunch, discharging full interference patterns; the maximum potential amplitude in the recruitment phase increased significantly (mean, 3.090 µV; maximum, 5.000 µV), which was 2 to 4 times the corresponding value of the healthy control group; thus, the difference was significant. The increased potential amplitude of the myoelectric motor unit in the thyroarytenoid muscle and the increased maximum amplitude of the recruitment phase could be used as evaluation indexes for the abnormal increase in the muscle tension of patients; in particular, the increased maximum amplitude of the recruitment phase might reflect the abnormal active level of myoelectricity to a greater extent. The examination of the laryngeal nerve conduction function is a good supplement to the routine LEMG examination. Through examining nerve evoked potentials and stimulating motor nerves, the variations in the action potentials of compound muscles were observed. The latent periods of evoked potentials reflect the myelin sheath function (mean latent period, 1.7 ms). The amplitudes of nerve-evoked potentials reflect the number of the measured nerve fibers and the level of synchronized excitation; there are many influencing factors for the nerve evoked potential amplitude, which differ from individual to individual; the potential amplitude of the recurrent laryngeal nerve is generally greater than 1.0 µV. Our data demonstrated that the evoked potential amplitudes of thyroarytenoid muscle in patients with SD increased significantly (mean,10.3 µV; maximum, 26.3 µV). Therefore, the evoked potential might also be used to quantitatively determine the degree of the abnormal increase in the muscle tension of patients with SD. SD still cannot be completely cured. Currently, the local injection of botulinum toxin type A is the first choice of treatment method and involves the symptomatic treatment of SD through chemodenervation.5,8,9 The main injection method is using a special hollow-needle electroinjection electrode to inject botulinum toxin under electromyographic monitoring. For patients with adductor SD, botulinum toxin is injected into their thyroarytenoid muscles. It was also reported that injecting botulinum toxin into the lateral cricoarytenoid muscles of patients with adductor SD could yield good results. Moreover, our previous studies confirmed that the onset time was 6 hours to 2 days after the botulinum toxin injection; the peak effective time was 2 weeks, and the mean duration was 15.2 weeks.7 Two weeks
Annals of Otology, Rhinology & Laryngology 124(7) after the injection, the electromyographic examination showed that fibrillation potentials occurred or were in an electrically silent state, and the evoked potential could not be induced, indicating a complete drug effect. Fibrillary waves are a relatively sensitive parameter for evaluating early muscle denervation. Nerve evoked potentials can also provide additional information. The evoked potential of a patient with a completely injured recurrent laryngeal nerve disappears; the conduction function decreases in patients with a partially injured nerve, the latent period significantly increases, and the evoked potential amplitude significantly decreases. Three to 4 months after injection, the symptoms and electromyographic characteristics of the patients recovered to the pretreatment levels. Therefore, during the treatment, the therapeutic efficacy, dosage adjustment, and prognosis may be objectively determined based on the improvement in the patient’s symptoms after botulinum toxin injection combined with laryngeal electromyography, which may further provide a basis for the timing of the second injection. As we found, fibrillation potentials or electrical silence activity occurred and the evoked responses of the injected muscle could not be induced or weakened after BTX injection. The presence of denervation or unrecovered EPs may suggest sustained pharmacological effects of botulinum toxin. For avoiding irreversible muscular injury, we suggested that patients with those abnormal EMG patterns should not be considered to re-injection course at the beginning of their symptoms return, especially for the voice professionals and the young. The findings of the present study are in agreement with the reports of Klotz et al10 and Cyrus et al,11 namely, regardless of the spasm type, abnormal myoelectric activity is generally not restricted to 1 muscle—which is also the reason for treatment failure in certain patients. Therefore, it is necessary to also consider the interaction between different muscles in future studies. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
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