AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

Spasmodic dysphonia (SD) remains one of the most inveterate dysphonias despite various attempts to treat the disease. Because the cause of SD is still undetermined, management of this disorder continues to be directed at relief of symptomatic vocal spasm rather than cure.

History of the Procedure

• Traube, who believed the condition to be a form of nervous hoarseness, first described SD in 1871. For many years, the disorder was referred to as spastic dysphonia, but the term spasmodic dysphonia is more widely accepted today.
• Dedo first introduced a recurrent laryngeal nerve section for the treatment of SD in 1976. Other investigators modified this approach by introducing recurrent laryngeal nerve avulsion and selective section techniques; however, the use of these techniques gradually declined because of a high late recurrence rate and the inherent disability that occurred.
• In 1980, Isshiki et al introduced a laryngeal framework surgery (laryngoplasty) for patients with adductor SD. This technique permits adjustment of the position and tension in the vocal folds. This surgical approach is still experimental, and further investigation is required.
• Blitzer et al applied the botulinum toxin (BOTOX®) injection technique in 1984. This procedure has gained wide popularity in management of SD. Advantages of this technique include fewer surgical interventions and a higher success rate in restoring or improving the voice. However, BOTOX® injections provide only temporary symptomatic relief, and repeated intracordal injections are required.
• In 1987, Friedman et al proposed recurrent laryngeal nerve stimulation, although the implantation of a stimulator demonstrated a buildup of scar tissue around the nerve and no long-term follow-up data are available.
• Recent surgical advances include recurrent laryngeal nerve denervation and reinnervation, as well as thyroarytenoid (TA) and lateral cricoarytenoid myectomy.

Problem

SD is a chronic voice disorder of unknown origin that is characterized by excessive or inappropriate contraction of laryngeal muscles during speech. SD manifests as excessive glottic closure (adductor dysphonia) or incomplete, irregular vocal fold approximation (abductor dysphonia). Strained or strangled phonation and irregular voice stoppages (the form originally described and most commonly observed clinically) characterize adductor dysphonia. Abductor SD presents with a breathy or absent voice or brief vocal loss and is associated with abrupt widening of the glottis.

Frequency

Early textbooks reported that SD was a relatively rare voice disorder, although recent reports suggest that it is not rare but rather frequently goes undiagnosed. Most studies show that this disorder affects females more commonly than males, with a female-to-male ratio as high as 8:1.

Reports of the mean age of patients with SD typically indicate a range of 48-50 years; however, the condition may occur as early as the second decade of life in rare exceptions and as late as the ninth decade of life.

Although a genetic basis of SD has not been established, some patients (12%) report relatives with similar voice problems or other dystonias (Blitzer et al).

Etiology

The origin of SD is currently unknown. Primary generalized dystonia is clearly a genetic disorder and has been attributed to a defect on bands 9q32-34. The location of the genetic defect in patients with primary focal dystonias is unknown.

Pathophysiology

SD is currently understood to be a focal dystonia that affects laryngeal muscle control during speech. Dystonia refers to a syndrome of sustained muscle contractions. Focal dystonias involve abnormal activity in only a few muscles. Dystonic movements are aggravated or become manifest during voluntary movement and worsen with fatigue or physical and emotional stress. Dystonia may be generalized, regional, or focal. Although SD is considered a focal dystonia, it may present as regional dystonias such as Meigs syndrome, blepharospasm, or torticollis.

Focal SD, as with other neuromotor disorders, is frequently associated with tremor. Essential tremor causes 6- to 8-Hz shaking, primarily of the hands, head, and voice. In SD, the tremor may be isolated to the larynx or may involve the pharynx, head, or even hands.

Electromyography (EMG) reveals voluntary movement abnormalities of the vocal folds that are characteristic of focal dystonia. Patients with SD have abnormally high resting EMG activity levels in both the TA and cricothyroid (CT) muscles and an imbalance between TA and CT muscles that results in increased adduction and tension in the anteroposterior dimension during speech, swallowing, and quiet breathing.

SD may involve increased sensitivity of motoneuron pools in the brainstem. Electrophysiologic studies implicate dysfunction in the pyramidal tract and basal ganglia. A few biochemical studies of autopsied brains have demonstrated altered levels of neurotransmitters in various regions of the midbrain. A neurotransmitter defect is also suggested by the finding that some patients with dystonia significantly improve with L-dopa therapy. The preponderance of evidence suggests that idiopathic dystonias are due to an abnormality of neurotransmitters in the basal ganglia (putamen, head of caudate, and upper brainstem). Zweig et al suggested that the putamen and the striatopallidothalamocortical circuit are disrupted in patients with focal dystonias.

Clinical

Most patients with SD identify potential precipitating factors that are temporally related to the onset of the voice disorder. These factors can be summarized in 2 categories, as follows:

• Physical symptoms present at or near the time of diagnosis
  • Sore throat
  • Viral infection
  • Other focal dystonias
  • Traumatic head or neck injury or following laryngeal surgery
  • CNS disease
  • Tremor
• Emotional factors present near the time of onset or considered related to onset by the patient
  • Job stress
  • Family stress
  • Emotional traumatic events
  • Interpersonal conflicts
  • Suppression of aggression

Adductor and abductor SDs have different patterns of speech and voice symptoms.

Adductor spasmodic dysphonia

The voice is reduced in loudness and is monotone in patients with adductor SD. Patients report that symptoms are worse when they are under emotional stress, when they talk on the telephone, or when they give a presentation. The symptoms are often better upon awakening in the morning or after a drink of alcohol. Speech is characterized by strained or strangled phonation and intermittent voice offsets in the middle of vowels.

Voice is effortful, with strain and occasional hoarseness, but the essential symptom is voice breaks. These are heard in continually voiced sentences that contain mainly vowels (eg, liquids /r/, /l/, and /w/ and nasals /m/, /n/, and /ing/). The voice breaks are due to spasmodic hyperadductions of the folds that interrupt phonation. Upon fiberoptic laryngoscopy examination, the vocal folds of patients with adductor SC have intermittent rapid shortening and squeezing, which results in a quick glottic closure that shuts the glottis and interrupts airflow through the glottis. Patients are generally able to whisper or sing without strain or vocal breaks; this is often not the case with muscle tension dysphonia and helps to clinically distinguish between the 2 disorders.

Abductor spasmodic dysphonia

Abductor SD is rarer than the adductor type (13% of all patients with SD). Patients have prolonged voiceless consonants because of difficulties with voice onset following voiceless sounds such as /h/, /s/, /f/, /p/, /t/, and /k/. The voice is reduced in loudness. Additional symptoms in some patients with abductor SD include pitch changes, phonatory breaks during vowels, uncontrolled rises in vowels' fundamental frequency, or breathy voice quality. Upon fiberoptic laryngoscopy, patients with abductor SD have wide-ranging abduction movements for voiceless consonants that are prolonged and interfere with following vowels.

INDICATIONS

Section 3 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

A careful evaluation of the patient by a multidisciplinary team is needed before the best type of treatment for that patient can be selected. Counsel the patient about the advantages and disadvantages of each management approach and about the particular expected result with each.

The following treatment options are currently available:

• BOTOX® muscle injection
• Type II laryngoplasty
• Traditional voice therapy
• Recurrent laryngeal nerve denervation andreinnervation
• TA and lateral cricoarytenoid myectomy.

Note that voice therapy does not improve or treat the spasms caused by this neurologic disease. Therapy may help to relieve some of the tension and maladaptive behaviors that patients have developed while trying to speak with spasmodic dysphonia.

CONTRAINDICATIONS

Section 4 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

Contraindications and relative contraindications to BOTOX® therapy are as follows:

• Pregnancy: Use of BOTOX® by women who are pregnant or lactating is not recommended.
• Aminoglycosides: Recent use of aminoglycosides interferes with neuromuscular transmission and may increase the effect of the BOTOX® therapy. The authors recommend that patients receiving aminoglycoside treatment not receive concurrent BOTOX® injections.
• Gastroesophageal reflux: Administer antireflux therapy in patients with known or suspected reflux before considering BOTOX® injections. BOTOX® injections reduce the speed of vocal fold closure and may predispose the patient to aspiration.
• Preexisting neurologic disorders (eg, myasthenia gravis, Eaton-Lambert syndrome, motor neuron disease affecting the neuromuscular junction): Use caution when administering BOTOX® to patients with these disorders, especially when large doses are required. Although the amount of toxin that enters the systemic circulation after injection is minute, hyperkinetic symptoms could theoretically occur.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

Lab Studies

• The following tests are used to exclude other systemic disorders:
• • CBC count and chemistry panel
  • Erythrocyte sedimentation rate measurement
  • Thyroid function test

Imaging Studies

• CT scan with gadolinium or MRI: Reserve brain imaging for patients with focal findings upon neurologic examination that are beyond the distribution of spasmodic dysphonia (SD).

Other Tests

• Neurologic examination
• • The occurrence of other neurologic signs not associated with other dystonias or tremor suggests that SD is secondary to another disease process.
  • The neurologic examination may also reveal signs of other neurologic disorders that may be misconstrued as SD.
• Perceptual analysis
• • Grade, roughness, breathiness, atonicity, and strain (GRBAS) is the evaluation system currently used to evaluate perceptual judgment. GRBAS involves a scale of 0-3 (0 = normal or absence of deviance; 1 = slight deviance; 2 = moderate deviance; 3 = severe deviance).
  • Conversational speech or the reading of a passage is rated. The classic perceptual sign of SD is strained voice quality that is heard in contextual speech but not necessarily in singing, whispering, laughing, falsetto voice, or crying.
  • Sentences that elicit adductor breaks when spoken include the following:
    • "I eat apples and eggs."
    • "The dog dug a new bone."
    • "We mow our lawn all year."
    • "Early one morning, a man and a woman were ambling along a 1-mile lane, running near Rainy Island Avenue."
  • Sentences that elicit abductor breaks when spoken include the following:
    • "How high is Harry's hat?"
    • "Did he go to the right or to the left?"
    • "When he comes home, we'll feed him."
    • "He saw half a shape mystically cross a simple path, at least 50 or 60 steps in front of his sister Kathy's house."
• Acoustic analysis
• • Acoustic measures reflect the status of vocal function. Standard deviation of the fundamental frequency or jitter (measured in ms) and amplitude modulation or shimmer are significantly higher in patients with SD.
  • The signal-to-noise ratio is generally lower in patients with SD than in healthy control subjects.
• Aerodynamic analysis
• • Aerodynamic analysis of voice production includes the measurement of airflow and air pressure and their relationships during phonation.
  • In adductor SD, mean airflow rates range from normal to extremely low.
  • In abductor SD, mean phonatory airflow rate is generally above normal, with bursts of airflow occurring with the abductor spasm.
  • Subglottic pressure measures were estimated to be higher than normal in patients with adductor SD.
• Electromyographic analysis
• • In 2001, Hillel demonstrated that all the laryngeal muscles are involved in spasmodic dysphonia using examination with hooked wired electrodes.
  • Either abductor or adductor muscle spasms are believed to predominate, resulting in the corresponding symptoms.
  • Poor response to injection of one muscle with BOTOX® can often be improved with injection of multiple muscles within the affected group. For example, if suboptimal results occur after bilateral TA injections are performed, results may improve if the interarytenoid muscle is also injected. EMG can be used to identify which muscles are most affected, and these muscles can be targeted for therapy.
• Subjective evaluation by patient: The purpose of a subjective self-evaluation is to determine the deviance of voice quality and the severity of disability or handicap in daily professional and social life and to determine the possible emotional repercussions of the dysphonia.

Diagnostic Procedures

• Videolaryngostroboscopy
• • Videolaryngostroboscopy is the main clinical tool used in determining the origin of voice disorders. Abductor and adductor spasms can be visualized during voice breaks.
  • This procedure can also be used to assess the quality of vocal fold vibration to evaluate treatment effectiveness.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

Medical therapy

Voice Therapy

Clinicians have found that voice therapy in patients with spasmodic dysphonia (SD) generally has limited benefit, although it may help them gain greater insight into their voice production control difficulties and can be useful as adjunctive therapy to BOTOX® injection or thyroplasty.

At present, voice therapy is recommended for the following types of patients with SD:

• Patients with mild, intermittent symptoms of adductor SD
• Patients with a psychogenic dysphonia, psychogenic overlay, or symptom exaggeration
• Patients who request assistance with increasing benefit duration following BOTOX® injection
• Patients with abductor SD who are receiving limited benefit from BOTOX® injections
• Patients who develop significant muscle tension dysphonia while trying to compensate for muscle spasms

Voice therapy protocol

• Voice therapy usually lasts for 6-8 sessions over 8-10 weeks. The key element in this treatment is the reduction of excessive pressure; the maintenance of a nonspasmodic phonation gives patients a sense of control over their treatment.
• Focus on reducing the effort associated with voice onset by using gliding phonation with fricatives or vowels.
• The program includes replacing short shallow inspirations with slow smooth inspirations, first without phonation and then with phonation. Conscious awareness of lower thoracic breath control and the rhythm of breathing are initiated. Patients are taught to use only the amount of breath needed for a particular phrase. Emphasis is placed on coordinating the lower thoracic exhalation phase of breathing with the onset of phonation.
• Phrasing of 3-6 syllables is emphasized. Voiceless phonemes are added to the voiced phonemes to develop awareness in the patient that voicing is now produced more easily than in the past. Exercises to improve resonance are added after treatment for airflow control and breathing is established.

BOTOX® Therapy

The ideal treatment for SD has not been identified. Currently, the most widely accepted treatment is the injection of minute quantities of BOTOX® into laryngeal muscles. BOTOX® causes a chemical denervation of muscle fibers by blocking the release of acetylcholine at neuromuscular junctions. The clinical effect of toxin probably results from its peripheral effect.

BOTOX® injection is accomplished with a monopolar hollow polytetrafluoroethylene (Teflon)–coated EMG needle connected to an EMG recorder.

The patient is placed in either a nearly supine position with a pillow underneath the upper back and with the neck extended or a seated position in an examination chair with the neck extended. The thyroid and cricoid cartilages are palpated, and the midline of the CT membrane is identified.

Dosage

Percutaneous injection of BOTOX® into the TA muscle in adductor SD is usually performed with a starting dose of either 1.25 or 2.5 U into each TA muscle.

For patients with abductor SD, the dose is 5-7 U for unilateral posterior cricoarytenoid (PCA) injection. The patient returns 2 weeks later for a second contralateral injection. Prior to injection, flexible laryngoscopy is performed to confirm that weakened but adequate abduction of the injected vocal fold is present. If abduction is minimal, airway compromise due to contralateral injection is a significant risk. As a result, this injection is postponed. Alternatively, 1.25 U can be administered on one side, while 5-7 U are administered in the other side during the same visit. BOTOX® treatment in patients with abductor SD is more difficult and is associated with greater risk, including mild-to-severe stridor caused by PCA paralysis.

Procedure

In adductor SD, the needle is passed through the skin that lies over the superior edge of the cricoid, just lateral to midline. The needle is then advanced through the CT membrane and superiorly and laterally directed into the right or left vocal fold to reach the TA muscle (see Image 1).

By entering slightly off the midline, the injection can be accomplished totally submucosally, without entering the airway. The oscilloscope and auditory output of the EMG apparatus are monitored to detect muscle activity. When crisp action potentials are obtained with phonation, needle position in a TA muscle is confirmed. Once the position is confirmed, the toxin is slowly injected.

Injection of BOTOX® for abductor SD is more technically demanding. The larynx must be grasped and rotated away from the site of the planned injection. The needle is advanced through the inferior constrictor muscle at the posterior border of the thyroid cartilage at the junction of the lower third and upper two thirds of the cartilage. The needle is advanced to the cricoid cartilage and then slightly moved out (under EMG guidance) to the optimal position in the PCA muscle (see Image 2). The patient is asked to sniff—an action that yields maximal abduction of vocal folds. The EMG signal is observed for correct placement, and the toxin is injected in the area of brisk activity.

Evaluation and rating criteria

Patients are reevaluated in the second week after injection. Typically, the toxin's effect occurs within the first 48-72 hours. Patients' voices initially become hoarse or breathy. Some patients develop mild aspiration when drinking liquids. Accordingly, advise patients to sip through a straw, to avoid gulping liquids, or to use a supraglottic swallow technique.

Patients are given a diary so they can rate themselves before injection, then every day for 2 weeks after injection, and then weekly until the next injection. This rating aids assessment of BOTOX® treatment effectiveness and indicates the optimal timing for the next injection.

Blitzer et al use a standardized vocal rating scale validated in a multi-institutional study. Fifteen items are rated on a 1-7 scale from normal to very severe.

Treatment regimen

Because of differing sensitivity to BOTOX®, the injection protocol and dosage must be established for every patient on an individual basis. Each patient is started with a standard dose. This is then increased or decreased based on the patient's side effects, symptom response, and individual needs.

Some patients are very sensitive to toxin but do not have the best response to small bilateral doses and have too much breathiness at larger doses. For those patients, injections can be initiated with a larger dose unilaterally, with or without a contralateral injection 2 weeks later. A delay allows some recovery before the second dose is administered. Patients often do well with only a unilateral injection.

Another approach is more frequent administration of bilateral minidose injections (0.1-0.5 U). Although the duration of benefit in these patients is only 6-8 weeks, minidose injections are used to prevent breathiness in most patients.

Surgical therapy

In addition to BOTOX® injections, which have become the standard of care in the treatment of SD, several other treatment approaches are gaining interest.

Isshiki et al propose midline lateralization thyroplasty and thyroplasty type 2 techniques for adductor SD. These techniques were successful in 5 of 6 patients. The concept of these techniques is to change the thyroid cartilage shape to relax and slightly lateralize the vocal folds. The advantages of the surgery include (1) the ability to adjust optimal glottal closure for phonation, (2) unlikely recurrence, (3) no damage to the physiological function of phonation, (4) intraoperative reversibility if ineffective, and (5) the ability to perform readjustments when needed. A recent study by Chan et al did not replicate the success of Isshiki and colleagues.

Recurrent laryngeal nerve denervation and reinnervation was first described in 1999. The adductor branch of the recurrent laryngeal nerve is bilaterally denervated and the distal nerve is reanastomosed to the ansa cervicalis. In addition, a lateral cricoarytenoid myectomy is performed. The ansa cervicalis reinnervation results in toning of the TA muscle and prevents reinnervation in nerves affected by SD. A number of technical problems have been noted with the surgical outcome report from the long-term follow-up study (Koufman, 2006). However, 83% of patients would recommend or strongly recommend the surgery to others with SD, while 20% of patients had complications of moderate-to-severe breathiness.

A final surgical option for adductor spasmodic dysphonia is a bilateral TA and lateral cricoarytenoid myectomy staged a minimum of 6 months apart. This weakens the vocal folds bilaterally to prevent spasms. It is performed under local anesthesia and is titrated to breathiness to eliminate the risk of overresection. Short-term results in 5 patients revealed improved fluency in all patients. Long-term studies are needed, especially considering the history of blepharospasm treatment using a similar procedure. Many patients with blepharospasm treated with myectomy had either recurrence of symptoms or dysfunction due to muscular fibrosis or scarring.

These techniques require wider evaluation and long-term follow-up data before being considered as a standard treatment for SD.

Follow-up

For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article BOTOX® Injections.

COMPLICATIONS

Section 7 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

• Dysphagia is related to the toxin's partial diffusion into the inferior constrictor muscle when the target muscle is the PCA muscle. This adverse effect is transient and usually resolves in 1 week.
• Breathy hypophonia is usually a transient adverse effect of a BOTOX® injection into the TA muscle and usually resolves within 1-2 weeks.
• Clinically significant aspiration is a very rare complication that is related to the dose of BOTOX® injected into the TA muscle. Aspiration is transient and resolves in 1-2 weeks.
• Stridor is more serious in patients with abductor SD because of PCA paralysis. Paralysis is related to the BOTOX® dose, and men are at a higher risk for this complication.

OUTCOME AND PROGNOSIS

Section 8 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

Most patients experience toxin effect within the first 48-72 hours after injection, with a variable amount of breathy dysphonia and slight aspiration. These adverse effects disappear within the first week, but voice improvement persists for 10-24 weeks.

Results of BOTOX® injection may be best described by their effect on vocal output after injection. Investigators reported significant reductions in pitch and voice breaks in addition to phonatory periodicity and sentence duration in the 2 weeks after injection. They found that 4 acoustic measures—standard deviation of fundamental frequency, jitter, shimmer, and signal-to-noise ratio—were all improved within a week after injection.

Treatment of adductor spasmodic dysphonia (SD) with BOTOX® achieves good results, with an average benefit of 90% of normal voice function.

Treatment of abductor SD is more difficult; BOTOX® treatment achieves an average benefit of 66.7% of normal voice function. The abductor muscle (the PCA) is located between the larynx and pharynx and is more difficult to inject. Most patients require bilateral PCA injections and improve to an average of 70% normal function (less than the function for patients treated for adductor dysphonia). In general, abductor SD appears to be a more complex syndrome, with frequent involvement of respiratory muscles and intermittent or sustained failure of activation of adductor muscles during phonation.

FUTURE AND CONTROVERSIES

Section 9 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

See Surgical therapy. Although all current approaches for treatment of spasmodic dysphonia (SD) have enhanced our knowledge, the key to understanding this disorder is to understand its pathophysiology and that of other spasmodic movement disorders. Research in SD should include efforts to determine its etiology and efforts to search for associated defects that could improve function in these patients if corrected.

Current research, especially gene research, is progressing in the elucidation of the cause of focal dystonia. The authors hope that the cause of SD can soon be treated rather than its symptoms.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

Media file 1:  Thyroarytenoid injection for adductor spasmodic dysphonia. Needle is advanced through the cricothyroid membrane.
	View Full Size Image
Media type:  Image

Media file 2:  Posterior cricoarytenoid (PCA) injection for abductor spasmodic dysphonia. Needle is advanced through the inferior constrictor muscle to the PCA muscle.
	View Full Size Image
Media type:  Image

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Complications
• Outcome And Prognosis
• Future And Controversies
• Multimedia
• References

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• Berke GS, Blackwell KE, Gerratt BR, et al. Selective laryngeal adductor denervation-reinnervation: a new surgical treatment for adductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. Mar 1999;108(3):227-31. [Medline].
• Bidus KA, Thomas GR, Ludlow CL. Effects of adductor muscle stimulation on speech in abductor spasmodic dysphonia. Laryngoscope. Nov 2000;110(11):1943-9. [Medline].
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• Hillel AD. The study of laryngeal muscle activity in normal human subjects and in patients with laryngeal dystonia using multiple fine-wire electromyography. Laryngoscope. Apr 2001;111(4 Pt 2 Suppl 97):1-47. [Medline].
• Isshiki N, Haji T, Yamamoto Y. Thyroplasty for adductor spasmodic dysphonia: further experiences. Laryngoscope. Apr 2001;111(4 Pt 1):615-21. [Medline].
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• Koufman JA, Rees CJ, Halum SL, Blalock D. Treatment of adductor-type spasmodic dysphonia by surgical myectomy: a preliminary report. Ann Otol Rhinol Laryngol. Feb 2006;115(2):97-102. [Medline].
• Kramer PL, de Leon D, Ozelius L. Dystonia gene in Ashkenazi Jewish population is located on chromosome 9q32-34. Ann Neurol. Feb 1990;27(2):114-20. [Medline].
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• Schaefer SD. Neuropathology of spasmodic dysphonia. Laryngoscope. Sep 1983;93(9):1183-204. [Medline].
• Sellin LC. The action of batulinum toxin at the neuromuscular junction. Med Biol. Feb 1981;59(1):11-20. [Medline].
• Stong BC, DelGaudio JM, Hapner ER, Johns MM 3rd. Safety of simultaneous bilateral botulinum toxin injections for abductor spasmodic dysphonia. Arch Otolaryngol Head Neck Surg. Sep 2005;131(9):793-5. [Medline].
• Traube L. Spastishe form der nervosen helserkeit. Gesammelte beltrage zur pathologie und physiologie. 1871;2:677.
• Tucker HM. Laryngeal framework surgery in the management of spasmodic dysphonia. Preliminary report. Ann Otol Rhinol Laryngol. Jan 1989;98(1 Pt 1):52-4. [Medline].
• Zweig RM, Hedreen JC, Jankel WR. Pathology in brainstem regions of individuals with primary dystonia. Neurology. May 1988;38(5):702-6. [Medline].

Article Last Updated: Dec 29, 2006