Spasmodic Dysphonia: Let’s Look at That Again

Thomas Murry, New York, New York

Summary: G. Paul Moore influenced the study of spasmodic dysphonia (SD) with his 1960 publication that examined

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the neurological, medical, and vocal fold behavior in a group of patients with adductor spasmodic dysphonia (ADSD).This review of advances in the diagnosis and treatment of SD follows a time line of research that can be traced in part tothe early work ofMoore et al. This article reviews the research in ADSD over the past 50 plus years. The capstone eventsthat brought SD to its present day level of management by laryngologists and speech-language pathologists are high-lighted. A look to the future to understand more of the disorder is offered for this debilitating disorder.Key Words: G. Paul Moore–Adductor spasmodic dysphonia–Botulinum toxin.

INTRODUCTION

Spasmodic dysphonia (SD) is a disorder of speech and voice inwhich irregular and uncontrolled vocal spasms interrupt thenormal speech flow. Irregular voice breaks, effortful phonation,and breathiness are thought to start out gradually and then prog-ress slowly before becoming chronic.1–3 Using high-speed mo-tion pictures, Moore4 described SD as an intermittent squeezingof the vocal folds disrupting the flow of speech. Early reports ofthis disorder (also called spastic dysphonia [SD]) were thoughtto be psychosomatic.5 For almost 100 years, the literature per-sisted on categorizing this disorder as a personality disordermanaged by counseling and voice therapy. However, there isnow sufficient evidence to show that SD is a task-specific focaldystonia of the larynx consisting of disruptions in the speechand voice.6,7 Since the early work of Moore and others, twomajor types of SD have emerged. Adductor spasmodicdysphonia (ADSD) is characterized by interruptions in theclosure of voice during speech. Abductor spasmodicdysphonia (ABSD) is characterized by breathy interruptionsof ongoing phonation. A small percentage of patients havesigns of both ADSD and ABSD. This discussion will focusprimarily on ADSD and the research and treatments that haveevolved over the last 55 years to manage this disorder.

EARLY YEARS OF ADSD

The history relating SD to G. Paul Moore dates back to the early1960s and reflects the character of Moore’s clinical and scienti-fic acumen. He was often found in the voice laboratory to say‘‘Let’s look at that again.’’ His interest in ‘‘spastic’’ dysphoniaderived from his continuing approach to understanding thebiomechanics and neurological functions of the larynx, specif-ically the vocal folds, and to find evidence that would guidethe treatment of patients. He indicated that early experimentalwork suggested that the cause may be neurological. Mooredeveloped a strong interest in SD based on the early work of Be-rendes8 who described many of the characteristics of the speech

ted for publication March 17, 2014.. Paul Moore Lecture, 42nd Annual Symposium: Care of the Professional Voice,hia, PA, June 1, 2013.he Department of Otolaryngology—Head and Neck Surgery, Weill Cornell Med-ege, New York, New York.ss correspondence and reprint requests to Thomas Murry, Department of Otolar-—Head and Neck Surgery, Weill Cornell Medical College, 1305 York Avenue,, New York, NY 10021. E-mail: tm2103@msn.coml of Voice, Vol. -, No. -, pp. 1-6997/$36.004 The Voice Foundationx.doi.org/10.1016/j.jvoice.2014.03.007

of individuals that now have been documented to be associatedwith SD. Another early investigator of SD, Arnold,9 originallyfelt that SD was because of primitive subcortical centers actingwithout inhibition in patients with known personality problems.9

Nonetheless, in 1959, despite these early suggestions that theremay be a neurological basis for the disorder, there was still apersistent belief that disruptions in personality had a strong rela-tionship to the disorder. In 1960, Robe et al10 reported on 10 pa-tients diagnosed with SD ranging from 6 months to 15 years.The subjects completed questionnaires, had thorough ear,nose, and throat examinations as well as neurological examina-tions, and they also underwent electroencephalograms. All thesepatients had signs of central nervous system abnormalities.Their signs included irregular discharges in the right temporal-parietal region in nine of the 10 subjects, four subjects with fa-milial neurological diseases, eight with transient leg or armweakness, and other conditions such as parasthesias in thehands, arms, or legs. Several of the subjects reported the onsetassociated with a sickness such as an upper respiratory diseaseor with stressful events leading up to the onset of the condition.Robe et al10 concluded that SD was a phonatory disorder result-ing from a disturbance in neural function and possible neuralstructure. This was the first study to present clinical neurologicalevidence that SD was linked to a neurological disorder. Thiswork of Moore et al opened up new avenues of study with thehope that treatment options would follow.

Soon after the classic work of Moore et al, Aronson et al11

identified two types of the disorders, adductor consisting ofstrained and strangled speech production and abductor, an inter-mittent breathiness. They suggested that these disordersdemonstrated a somewhat different movement pattern in thelarynx than the rigidity of spastic muscles, hence the term spas-modic dysphonia (either adductor spasmodic dysphonia, ADSDor abductor spasmodic dysphonia, ABSD). These terms havebeen used consistently since 1968.

In the 1960s, several studies reported on various behavioraltreatment attempts despite the trend at that time toward a neuro-logical basis. Rethi12 suggested inspiratory and expiratoryphonation exercises similar to those used to treat stuttering.Bloch13 examined the neuropsychological aspects of the disor-der in an attempt to identify patterns of behavior that maycontribute to the disorder and therefore be amenable to medicaltreatment and counseling. Their results did not show long-termpositive outcomes.

Although the evidence for a neurological basis of SD beganto mount in the 1960s, it was not until 1976 that direct evidence

TABLE 1.

A Summary of the Acoustic and Physiological Findings

From Studies That Reported Pre- and Post-BTX Results

Parameter Findings

Vowels

Fo Unchanged pre vs post BTX

Jitter Lower post BTX

Shimmer Lower post BTX

Harmonic/noise ratio Lower post BTX

Subglottic pressure Lower post BTX

Airflow rate Higher post BTX

Near normal 2 wk post BTX

Voice breaks Fewer post BTX

Tremor Improved post BTX

Speech

Journal of Voice, Vol. -, No. -, 20142

was presented to show that SD was a neurological disorder.Dedo temporarily paralyzed the recurrent laryngeal nerve(RLN), and a significant improvement in voice quality resulted.Dedo14 reported the sectioning of the RLN in 34 patients withADSD. Izdebski et al15 reported that with postoperative voicetherapy, all subjects exhibited some improvement and approx-imately one-half of the group returned to a near normal voicebut with less overall volume. Dedo et al16 subsequently foundthat through histological analysis of the RLN, patients withADSD had significantly more abnormalities compared withage-matched controls. The finding of a change in the speechand voice after resection of the RLN led others to try it. How-ever, sectioning of the RLN was not universally accepted, andlater Aronson17 reported that in some subjects the long-term re-sults were poor.

Mean Fo Unchanged pre vs post BTX

Speech rate Faster post BTX

Airflow rate Higher post BTX

Voice breaks Fewer post BTX

THE BOTULINUM TOXIN ERA

The findings by Dedo14,16 and Robe et al10 encouraged other in-vestigators to look more closely at the disorder. Electromyo-graphic results of Kiml,18 Tluchowski,19 as well as Caraceniand Zibordi20 identified abnormalities in the peripheral nerveor in the corticonuclear tracts suggesting that a neurological ab-normality exists in patients with spastic speech. These findingswere later supported with studies by Sellin et al,21 Rosenfieldet al,22 Jankovic,23 and Dolly et al24 that paved the way forthe treatment of the dystonic movement of the larynx with bot-ulinum toxin (BTX), a neurotoxin of which the most potent typeis type A. Jankovic23 demonstrated the usefulness of BTX in thetreatment of Meige symptoms, which are associated withADSD in a percentage of cases. Early patients’ reports of treat-ment with BTX were encouraging.25 Blitzer et al26 reported onthe first large case series treated with BTX. Initially, BTX wasused primarily for ADSD, but later reports of treatment forABSD followed.26 BTX has since been reported to be safe forthe treatment of ADSD and ABSD and has been used to manageSD for the past 30 years.

The speech and voice abnormalities of SD achieved greaterrecognition in the 1980s and 1990s; thanks to the success gener-ated by the work of Dedo14,15 and successful use of BTX as atreatment. However, descriptions and assessments of ADSDremained primarily subjective with perceptual terms such as‘‘strained-strangled’’ and ‘‘effortful phonation’’ predominantin the literature. Numerous studies of functional outcomes inthe voice and speech of patients with SD before and afterBTX treatments followed as its use became accepted.

Investigators have examined the pre- to post-BTX findings ofacoustic, aerodynamic, and perceptual studies in demonstratingthe positive voice changes after BTX injections. Treatment ofADSD with BTX over the past 30 years has demonstrated im-provements in the acoustic, aerodynamic, and perceptual char-acteristics of the voice. The results are based on numerousmethods of treatment (bilateral injection vs unilateral injection)and various measures obtained from sustained and spokenspeech samples. Table 1 summarizes the acoustic and physio-logical findings. Investigators have found that after BTX injec-tion, there was no significant change in fundamental frequency,

jitter, shimmer, signal-to-noise ratio (SNR), and maximumphonation time.27–36

Data from connected speech by Cannito et al35 demonstratedthat although overall fundamental frequency did not change af-ter BTX treatment, the number of low frequency events and theSNR were significantly different after treatment compared withpretreatment. Moreover, the variation in fundamental frequencyand the SNRwere related to listener judgments of voice quality.Investigators did find significant post-BTX changes in the

prosodic aspects of speech, namely, the number of voice breaks,time to read a sentence or paragraph, and control of speech in-tensity.2,28–30,32 Despite the lack of statistical evidence in someof the forgoing studies, the general conclusions from the post-BTX data imply an improvement in communication and acloser relationship to normal speech and voice acousticparameters.Fewer investigators studied the physiological measures asso-

ciated with treatment using BTX. Airflowmeasures obtained byZwirner et al29 and also by Murry and Woodson37 before BTXinjection in patients with ADSD were found to be lower thanage-matched normal subjects. However, Adams et al36,38 intwo different groups found airflow rates to be within normalrange before BTX injections. After BTX injection, airflowrate changes increased significantly for the first few weeksand then stabilized to near normal flow rates after the initialperiod.29,36–38

Physiological measures based on electromyography (EMG)have been studied by Ludlow39 as well as Davidson and Lu-dlow.40 Based on their EMG findings, Davidson and Ludlow40

suggest that motor unit reorganization may continue long afterthe effects of the BTX injection dissipate.As might be expected, perceptual studies of ADSD show sig-

nificant changes after BTX injection. However, it is unsure ifthe perceptual changes after BTX treatment are related to tem-poral aspects of the speech or specific acoustic and physiolog-ical properties of the voice signal or some combination of the

Thomas Murry Spasmodic Dysphonia 3

changes. Cannito et al41 found a weak positive relationship be-tween voice quality and the combination of frequency variationand SNR measures. Silverman et al42 found that the perceivedseverity of the dysphonia in ADSD was related primarily tothe amount of aperiodicity and the number of voice breaks.Similar to that found by Cannito et al, the perceptual relation-ships identified by Silverman, and also by Dejonkere et al,43 ac-counted for only a portion of the variance of the perceptual data.Thus, there remains a need to understand the effects of BTXchanges in ADSD on listeners’ perception of voice quality aftertreatment.

SURGICAL APPROACHES TO THE TREATMENT OF

ADSD

At the same time, although the use of BTX gained wide accep-tance by some, others were not completely satisfied with thistreatment method as BTX required frequent injections, rela-tionships between dose and response were unpredictable, andoccasional transient swallowing problems occurred. In addi-tion, there was a postinjection period of up to 2 weeks in whichthe voice was breathy and thus limited communication. As aresult, others took a look at the treatment of ADSD and consid-ered surgical procedures that might be useful. In 1980, Isshiki44

reported on a thyroplasty procedure, identified as type II thyro-plasty, which divided and widened the thyroid cartilage at themidline thus reducing the squeeze effect of the vocal folds inADSD. Although this procedure did not gain enthusiasm forthe treatment of ADSD in the United States because of themore accessible use of BTX, it nonetheless stimulated interestamong surgeons to look for other avenues of treatment forADSD. Chan et al45 reported on 13 patients with the diagnosisof ADSD who were previously treated successfully with BTXand then were recruited for type II thyroplasty as describedby Isshiki. Self-rating assessment of the degree of severityand vocal effort were recorded and compared with the BTXtreatment. Patients’ self-assessments and long-term follow-ups were not supportive of the procedure; only five patients re-ported some degree of satisfaction with the procedure.

As knowledge of neural function of the larynx and specif-ically the vocal folds increased and the growing acceptance ofADSD as a neurological voice disorder evolved, other surgicaltreatments were explored. Although BTX was successful inreducing laryngeal spasms and patients were generally satisfiedwith the injections, speech was not normal after BTX injectionand more importantly, the speech and voice fluctuated as theBTX wore off. An early animal study reported by Genacket al46 showed that thyroarytenoid (TA) myectomy resulted inreduced vocal fold closure but with vocalization remaining.Other investigations followed this work on patients withADSD. Although the results by various investigators demon-strated the elimination of severe constrictions and in some casesimproved scores on the Voice Handicap Index and other assess-ment tools, patients remained with a weak voice for protractedperiods.47

Weeds et al48 reported on the long-term results of RLN avul-sion in 18 patients. Although the patients’ voices remained

weak in volume, 16 of the 18 had no recurrence of spasms after3 years. In patients who were followed longer, they also foundthat several of those who were offered medialization thyro-plasty for their weak voices had a recurrence of spasms despiteprevious absence of spasms for more than 3 years.48

Following the early surgical options previously mentioned,investigators began to look at ways to reduce the closing forceof the vocal folds to reduce the spasm effect in patients withADSD. Iwamura49,50 reported that the EMG findings ofpatients with SD showed that the percentage of thin motorfibers in the TA muscle is greater in patients with ADSD thanin control subjects. By removing part of the TA muscle andthus reducing the number of thin motor fibers, they found areduction or elimination in the spasms.

The work of Iwamura was followed by Berke et al51 who re-ported on selective adductor denervation surgery (SLAD-R).Earlier, Green and Berke52 studied the effects of hyperadduc-tion in canines and the effects of denervation. The SLAD-R pro-cedure reduces the force of the closing phase of vibrationbecause of weakening of the TA muscle. Long-term results ofthe procedure reported by Chhetri et al53 showed that patientshad reduced or eliminated the spasms, had lower Voice Hand-icap Index scores, and were generally satisfied with the resultscompared with previous treatments with BTX. They reportedthat patients achieved long-term spasm-free voice with breath-iness lasting the first 3–6 months after the surgery. Mendelsohnand Berke54 found that as long as 14 years after the SLAD-Rprocedure, patients were more satisfied with their voices thanwhen they were previously treated with BTX. Although theSLAD-R procedure is generally no longer used nowadays, thelong-term data of Chhetri et al53 as well as Mendelsohn andBerke54 suggest that it is a viable treatment for ADSD, and itrepresents an alternative to the regular treatments of BTXwith its accompanying voice changes as the BTX wears off.

THE CURRENT ERA

The pathogenesis of ADSD remains unknown at this time, but aneurological basis including endogenous and exogenous factorsis now supported by the literature.55 That is not to say that pa-tients with ADSD do not have psychological issues. It is wellknown that when patients with ADSD speak under stress, theirvoice disorders are judged to be more severe than when theyhum a tune. Moreover, any significant illness is usually associ-ated with psychological or psychosocial factors. Murry et al56

obtained self-ratings of depression, state anxiety (a temporaryanxiety associated with a task such as speaking), and trait anx-iety from patients before and after BTX injection. Before BTXtreatment, patients exhibited mildly elevated scores of depres-sion and state anxiety but no trait anxiety compared with sub-jects with other voice disorders. In addition, the BTXpretreatment scores were similar to those in patients with otherneuropsychological disorders. The findings were interpreted tosuggest that the state of speaking in patients with ADSD beforeBTX treatment was the basis for anxiety in the 16 of 32 patientswho reported elevated state but not trait anxiety. Improvementin speech after BTX resulted in lower scores on all measures.

TABLE 2.

Summary of Risk Factors Identified in Patients With

Diagnosis of ADSD by Investigators Who Studied Large

Groups

Characteristic Reference

Middle decades of life 15,55,58

Female 5,15,55,61

Stress event in life 15,55,58,61

Injury outside the vocal tract 15

Childhood measles and mumps 15,55,58

Upper respiratory infection 55,61

Family history of essential tremor 15,55

Family history of other neurological disease 15,55,58

Cervical dystonia 55

Sinus and throat illnesses 15,55

Family history of meningitis 55

Pregnancy and parturition 61

Journal of Voice, Vol. -, No. -, 20144

White et al57 recently found that patients with ADSD had nogreater scores on depression and anxiety scales than patientswith other voice disorders.

The current era has increased the understanding of changesthat occur in ADSD as a result of chemical and surgical treat-ments. Currently, there is also an increasing understanding offactors that contribute to the risk and onset of the disorder.Thus, although chemical and surgical procedures offer alterna-tives to managing ADSD, a better model for managementmight include an understanding of the factors leading to thedisorder. Furthermore, there remains a need to explore thesefactors for ADSD and ABSD. Perceptual studies have shownthat ADSD is characterized by hyperadduction and hypoad-duction. High subglottic pressures associated with suddenadduction followed by high airflow associated with voicebreaks are the prominent aerodynamic findings correlatedwith perceptual judgments of ADSD. BTX helps to reduceboth these characteristics. After surgical or BTX treatment,episodic high subglottic pressures decrease, airflow rates re-turn to near normal values, and listeners perceive the voiceas more normal than before BTX.29,45

Epidemiological studies have recently contributed to a betterunderstanding of factors that are prominently related to ADSD.Izdebski et al15 were the first to explore factors that were asso-ciated with ADSD in a group of 200 patients. They found pa-tients with ADSD had extensive histories of voice use andvoice use under stress. Schweinfurth et al58 used a question-naire to evaluate demographics, educational level, work history,and life events in 168 patients and compared their findings torelatives of the patients. They found a 65% history of measlesand mumps in the ADSD group compared with the relativesof patients with ADSD.

Recently, Tanner55 used an extensive questionnaire with 150ADSD patients and 136 patients with other structural, neurolog-ical, or functional voice disorders. Several factors were signif-icant in the ADSD group. Those included a personal history ofcervical dystonia, sinus, and throat illnesses, mumps, dust expo-sure, rubella, and extensive voice use. They also found a familyor extended family history of voice disorders, vocal tremor,ocular disease, and meningitis. Table 2 summarizes the risk fac-tors identified by the works from five different groups reportingon large numbers of subjects. These multifactorial findings ofrisks and environmental factors are supported by studies ofother focal dystonias.59,60

Although clinical observations have suggested that morewomen than men develop ADSD, the implications for thisfinding are not clear. Moreover, although some patients asso-ciate their onset with a particular event, others do not. Childset al61 reviewed the records of 350 patients treated in twodifferent centers. Her group found that 80% were females and2% of them had a history of other focal dystonias. In a subsetof those 350 patients who were able to identify the onset ofADSD, 92 of the patients identified a gradual onset of the prob-lem, whereas 77 patients characterized their onset as sudden(developing within 1 week). Fifty-nine of those patients witha sudden onset identified the onset trigger. The most commontrigger in all patients was stress. Other frequently identified

triggers were upper respiratory infection, pregnancy and partu-rition, and postintubation for surgery. The findings of Childset al and others (Table 2) suggest that stress may be a relevantpsychological factor that requires further investigation (or asMoore would say ‘‘Let’s look at that again’’).One of the sudden onset factors that Childs et al61 identified

was pregnancy and parturition. Ankola et al62 examined fivesubjects in this group in more detail. They found that this groupthat was significantly younger than others in the sudden onsetgroup of Childs et al had significantly increased avocationalvoice use during their pregnancy (they were full-time used)and had other risk factors such as a history of viral infectionor sinus infection at the time of ADSD onset compared with anonpregnant age-matched group. The authors concluded thathoarseness or dysphonia during or shortly after pregnancymay be a risk factor for ADSD, especially in thosewho continueto work or who are using their voice extensively. Cliniciansshould be aware of these issues to appropriately counsel andtreat hoarseness during pregnancy.

SUMMARY

The management of ADSD has evolved from a diagnosticframework of psychological factors to a neurological basis.The pioneering work of G. Paul Moore played a significantrole in that evolution. His early work identified neurologicalfactors present in patients with SD. After Moore’s initialwork, clinicians and investigators in a variety of disciplineshave spent the past 55 years trying to understand the epidemi-ology, pathogenesis, and treatment methods that improve thevoice and speech of patients with ADSD. Studies of the anat-omy, physiology, and histology of patients with ADSD haveled to an understanding that this disorder is not a psychologicaldisorder but a movement disorder of the larynx, a focal dysto-nia. Surgical approaches that emanated from early histologicalstudies have provided patients with alternative treatments. Sur-gical results from TAmyectomy to RLN avulsion and to SLAD-R have shown improvement for extended periods. Although

Thomas Murry Spasmodic Dysphonia 5

most surgical treatments have the drawbacks of the need forgeneral anesthesia, depend on the skills of the surgeon, andthe acceptance by the patients, they offer a long-term approachto voice improvement compared with BTX, which is generallyrequired every 3–4 months.

Acoustic and aerodynamic studies predominantly during the1980s and 1990s provided information about the changes inADSD after treatment with BTX. The 2007 National Institutesof Health multidisciplinary panel reported in 2008 on theresearch priorities in ADSD and found that, among other areas,the identification of risk factors that contribute to the onset ofthe disorders was highly needed. The study of risk factorsthat has gone on and been refined over the past 30 years nowprovides today’s clinicians with useful information in coun-seling patients with ADSD.

The use of BTX has been the main treatment approach for thepast 35 years. The procedure is done in the office without gen-eral anesthesia, requires no preparation on the part of the pa-tient, and has been shown to improve speech and voicesignificantly from the patient’s point of view and that of the lis-teners. The combined treatment of voice therapy and BTX hasproduced mixed results, and additional prospective studies ofcombined BTX-voice therapy are needed to determine the valueof post-BTX therapy.

The need to understand central processes in ADSD remains.ADSD is likely multifactorial in etiology and pathophysiology.Tremors exist with ADSD in some patients and not in others.Some patients experience both ADSD and ABSD symptoms;extensive voice use under stress appears to help identifyADSD in some patients. Future studies of ADSD are requiredto examine the epidemiological and pathophysiological factorsin ADSD and the intersection of those factors with other exog-enous and endogenous risks for the disorder. Genetic studies offamilies with various focal dystonias including ADSD shouldbe directed to add further information to improve the manage-ment of this debilitating disorder.

REFERENCES1. Blitzer A, Brin MF, Fahn S, Lovelace RE. Clinical and laboratory charac-

teristics of focal laryngeal dystonia: study of 110 cases. Laryngoscope.

1988;98:636–640.

2. Ludlow CL, Naunton RF, Sedory SE, Schulz GM, Hallett M. Effects of bot-

ulinum toxin injections on speech in adductor spasmodic dysphonia.

Neurology. 1988;38:1220–1225.

3. Ludlow CL, Adler CH, Berke GS, et al. Research priorities in spasmodic

dysphonia. Otolaryngol Head Neck Surg. 2008;139:495–505.

4. Moore GP. Organic Voice Disorders. Englewood Cliffs, NJ: Prentice Hall,

Inc; 1971:9–10.

5. Traube L. Gesammelte Beitr€age zur Pathologie und Physiologie. I, II. Ber-lin, Germany: August Hirschwald; 1871.

6. Schaefer SD. Neuropathology of spasmodic dysphonia. Laryngoscope.

1983;93:1183–1204.

7. Simonyan K, Tovar-Moll F, Ostuni J, et al. Focal white matter changes in

spasmodic dysphonia: a combined diffusion tensor imaging and neuropath-

ological study. Brain. 2008;131:447–459.

8. Berendes J. Zur Entstehung und Behandlung der Dysphonia spastica.

Zeitschr F Hals Heilk. 1938;44:78.

9. Arnold GE. Spastic dysphonia: changing interpretations of a persistent

affliction. Logos. 1959;2:3.

10. Robe E, Brumlick J, Moore GP. A study of spastic dysphonia. Neurologic

and electroencephalographic abnormalities. Laryngoscope. 1960;70:

219–245.

11. Aronson AE, Brown JR, Litin EM, Pearson JS. Spastic dysphonia. I. Voice,

neurologic, and psychiatric aspects. J Speech Hear Disord. 1968;33:

203–218.

12. Rethi A. On the treatment of stuttering and of spastic dysphonia with inspi-

ratory and expiratory phonation. Monatsschr Ohrenheilkd Laryngorhinol.

1965;99:240–246.

13. Bloch P. Neuro-psychiatric aspects of spastic dysphonia. Folia Phoniatr

(Basel). 1965;17:301–364.

14. Dedo HH. Recurrent laryngeal nerve section for spastic dysphonia. Ann

Otol Rhinol Laryngol. 1976;85:451–459.

15. Izdebski K, Dedo HH, Boles L. Spastic dysphonia: a patient profile of 200

cases. Am J Otolaryngol. 1984;5:7–14.

16. Dedo HH, Izdebski K, Townsend JJ. Current evidence for the organic etiol-

ogy of spastic dysphonia. Otolaryngology. 1978;86:875–880.

17. Aronson AE, DeSanto LW, Salassa JR. Adductor spastic dysphonia: three

years after recurrent laryngeal nerve resection. Laryngoscope. 1983;93:

1–8.

18. Kiml J. Experimental research on spastic dysphonia. Folia Phoniatr

(Basel). 1965;17:241–300.

19. Tluchowski W. Electromyographic studies of the cricothyroid and sterno-

thyroid muscles in functional dysphonia. Folia Phoniatr (Basel). 1965;

17:179–184.

20. Caraceni T, Zibordi F. Electromyography in neural pathology of the larynx.

Rev Otoneuroophtalmol. 1965;37:65–91.

21. Sellin LC, Polak RL, Thesleff S. Acetylcholine content and release in

denervated or botulinum poisoned rat skeletal muscle. J Physiol. 1981;

319:253–259.

22. Rosenfield DB, Miller RH, Jankovic J. Spasmodic dysphonia: a neurolog-

ical movement disorder. Neurology. 1984;34(suppl 1):148.

23. Jankovic J. Cranial-cervical cystonia. In: Appel SH, ed. Current

Neurology6. Chicago, IL: Year Book Medical Publishers, Inc.; 1986:

153–176.

24. Dolly JO, Black JD, Williams RS. Acceptors for botulinum neurotoxin

reside on motor nerve terminals and mediate its internalization. Nature.

1984;307:457–460.

25. Miller RH,WoodsonGE, Jankovic J. Botulinum toxin injection of the vocal

fold for spasmodic dysphonia: a preliminary report.ArchOtolaryngol Head

Neck Surg. 1987;113:603–605.

26. Blizter A, Brin MF, Stewart C, et al. Laryngeal botulinum toxin injections

for disabling stuttering in adults. Neurology. 1994;44:2262–2266.

27. Woodson GE, Zwirner P, Murry T, Swenson MR. Functional assessment of

patient with spasmodic dysphonia. J Voice. 1992;6:338–343.

28. Zwirner P, Murry T, Swenson M, Woodson GE. Acoustic changes in spas-

modic dysphonia after botulinum toxin injection. J Voice. 1991;5:78–84.

29. Zwirner P, Murry T, Swenson M, Woodson GE. Effects of botulinum

toxin therapy in patients with adductor spasmodic dysphonia: acoustic,

aerodynamic, and videoendoscopic findings. Laryngoscope. 1992;102:

400–406.

30. Ford CN, Bless DM, Patel NY. Botulinum toxin treatment of spasmodic

dysphonia: techniques, indications, efficacy. J Voice. 1992;6:370–376.

31. Rhew K, Fiedler DA, Ludlow CL. Technique for injection of botulinum

toxin through the flexible nasolaryngoscope. Otolaryngol Head Neck

Surg. 1994;111:787–794.

32. Wong DL, Adams SG, Irish JC, et al. Effect of neuromuscular activity on

the response to botulinum toxin injections in spasmodic dysphonia. J Oto-

laryngol. 1995;24:209–216.

33. Adams SG, Hunt EJ, Charles DA, Lang AE. Unilateral versus bilateral bot-

ulinum toxin injections in spasmodic dysphonia: acoustic and perceptual

results. J Otolaryngol. 1993;22:171–175.

34. Shonweiler R, Wohlfarth K, Dengler R, Ptok M. Supraglottal injection of

botulinum toxin type A in adductor type spasmodic dysphonia with both

intrinsic and extrinsic hyperfunction. Laryngoscope. 1998;108:55–63.

35. CannitoMP,Woodson GE,Murry T, Bender B. Perceptual analysis of spas-

modic dysphonia before and after treatment. Arch Otolaryngol Head Neck

Surg. 2004;130:1393–1399.

Journal of Voice, Vol. -, No. -, 20146

36. Adams SG, Hunt EJ, Durkin LC, et al. Comparison of botulinum toxin in-

jection procedures in adductor spasmodic dysphonia. J Otolaryngol. 1995;

24:345–351.

37. Murry T, Woodson GE. Combined-modality treatment of adductor spas-

modic dysphonia with botulinum toxin and voice therapy. J Voice. 1995;

9:460–465.

38. Adams SG, Durkin LC, Irish JC, Wong DL, Hunt EJ. Effects of botulinum

toxin type A injections on aerodynamic measures of spasmodic dysphonia.

Laryngoscope. 1996;106:296–300.

39. Ludlow CL. Treatment of speech and voice disorders with botulinum toxin.

JAMA. 1990;264:2671–2675.

40. Davidson BJ, LudlowCL. Long-term effects of botulinum toxin injection in

spasmodic dysphonia. Ann Otol Rhinol Laryngol. 1996;105:33–42.

41. Cannito MP, Doiuchi M, Murry T, Woodson GE. Perceptual structure of

adductor spasmodic dysphonia and its acoustic correlates. J Voice. 2012;

26:818.e5–818.e13.

42. Silverman EP, Garvan C, Rahul S, Sapienza CM. Combined modality treat-

ment of adductor spasmodic dysphonia. J Voice. 2012;26:77–86.

43. Dejonkere P, Martens JP, MoermanM, et al. Spasmodic dysphonia, percep-

tual, and acoustic analysis: presenting new diagnostic tools. Eur Arch Oto-

rhinolaryngol. 2009;266:1915–1922.

44. Isshiki N. Recent advances in phonosurgery. Folia Phoniatr (Basel). 1980;

32:119–154.

45. Chan SW, Baxter M, Oates J, Yorston A. Long-term results of type II thy-

roplasty for adductor spasmodic dysphonia. Laryngoscope. 2004;114:

1604–1608.

46. Genack SH, Woo P, Colton RH, Goyette D. Partial thyroarytenoid myec-

tomy: an animal study investigating a proposed new treatment for adductor

spasmodic dysphonia. Otolaryngol Head Neck Surg. 1993;108:256–264.

47. Nakamura K, Muta H, Watanabe Y, Mochizuki R, Yoshida T, Suzuki M.

Surgical treatment for adductor spasmodic dysphonia—efficacy of bilateral

thyroarytenoid myectomy under microlaryngoscopy. Acta Otolaryngol.

2008;128:1348–1353.

48. Weeds DT, Netterville JL, Jewett BS, et al. Long-term follow-up of recur-

rent laryngeal nerve avulsion for the treatment of spastic dysphonia. Ann

Otol Rhinol Laryngol. 1996;105:592–601.

49. Iwamura S. Spasmodic dysphonia. Otolaryngol Head Neck Surg. 1986;2:

497–500.

50. Iwamura S. An EMG study of spastic dysphonia; spastic or spasmodic. J

Otolaryngol Jpn. 1991;94:1495–1496.

51. Berke GS, Blackwell KE, Gerratt RR, et al. Selective laryngeal adductor

denervation-reinnervation: a new surgical treatment for adductor spas-

modic dysphonia. Ann Otol Rhinol Laryngol. 1999;108:227–231.

52. GreenDC, Berke GS. An in vivo caninemodel for testing treatment effects in

laryngeal hyperadduction disorders. Laryngoscope. 1990;100:1229–1235.

53. Chhetri DK, Berke GS, Mendelsohn AH, Blumin JH. Long-term follow-up

results of selective laryngeal adductor denervation-reinnervation surgery

for adductor spasmodic dysphonia. Laryngoscope. 2006;116:635–642.

54. Mendelsohn AH, Berke GS. Surgery or botulinum toxin for adductor spas-

modic dysphonia: comparative study. Ann Otol Rhinol Laryngol. 2012;121:

231–238.

55. Tanner K. Epidemiologic advances in spasmodic dysphonia. Am Speech

Lang Hear Assoc. 2012;22:104–111.

56. Murry T, Cannito MP, Woodson GE. Spasmodic dysphonia: emotional

states and botulinum toxin treatment. Arch Otolaryngol Head Neck Surg.

1994;120:310–316.

57. White LJ, Hapner ER, Klein AM. Coprevalence of anxiety and depression

with spasmodic dysphonia: a case-control study. J Voice. 2012;26:667.

e1–667.e6.

58. Schweinfurth JM, Billante M, Courey MS. Risk factors and demographics

in patients with spasmodic dysphonia. Laryngoscope. 2002;112:220–223.

59. Frucht SJ. Focal task-specific dystonia in musicians. Adv Neurol. 2004;94:

225–230.

60. Leube B, Kessler KR, Goecke T, Auburger G, Benecke R. Frequency of fa-

milial inheritance among 488 index patients with idiopathic focal dystonia

and clinical variability in a large family.Mov Disord. 1997;12:1000–1006.

61. Childs L, Rickert S,Murry T, Blitzer A, Sulica L. Patient perceptions of fac-

tors leading to spasmodic dysphonia: a combined clinical experience of 350

patients. Laryngoscope. 2011;121:2195–2198.

62. Ankola A, Sulica L,Murry T. Laryngeal dystonia gravidarum: sudden onset

of adductor spasmodic dysphonia in pregnancy. Laryngoscope. 2013;123:

3127–3130.