Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Spasmodic Dysphonia
Krista Olson, M.D.
November 4, 1999

Spasmodic dysphonia is classified as a dystonia. The vocal folds are normal at rest, but with an action-induced task specific movement, the muscle contracts inappropriately causing abnormal movement and spasms resulting in dysphonia during speaking.

In 1871, Troy coined the term spastic dysphonia when describing a patient with nervous hoarseness. In 1899, Gowers described functional laryngeal spasm where the cords were brought together forcefully while speaking. He contrasted this to phonic paralysis whereby the vocal cords could not be brought together during speaking. He also compared this state of functional laryngeal spasm to the onset of a writer's cramp.

In 1985, Dr. Blitzer linked spasmodic dysphonia to dystonia through a clinical and electromyographic evaluation of "spastic" dysphonic patients and patients with generalized dystonia. Dystonia is a neurologic disorder of central motor processing, characterized by abnormal, often action-induced involuntary movements or uncontrolled spasms, probably related to dysfunction of the basal ganglia. Symptoms usually begin as focal dystonias involving a single region of the body. Spread to other regions is commonly seen in childhood-onset dystonia, while adult onset dystonia tends to remain focal.

Other examples of focal dystonias include blepharospasm, torticollis and writer's cramps. Examples of generalized conditions associated with dystonias include Wilson's disease, Huntington's and Parkinson's disease.

In 1968, Aronson defined two main types of spasmodic dysphonia: the adductor and abductor forms. Difficulties with voice initiation, strain-strangled, effortful phonation with voice break, and glottal fry characterize adductor spasmodic dysphonia, which is the more common form. The abductor type is the less common form and affects less than 10% of patients with spasmodic dysphonia. It is characterized by intermittent hyperabduction of the vocal cords leading to a whispering voice, hypophonia and possible aphonic breaks. Both types of spasmodic dysphonia lead to decreased loudness and intelligibility of speech. Also, either type may be associated with an irregular tremor with phonation. In this talk, I will focus on the adductor form of spasmodic dysphonia.

Evaluation of the patient with symptoms of spasmodic dysphonia should begin with a thorough history and physical. One should search for symptoms of generalized dystonias and evaluate the patient for involuntary movements such as myoclonus and tremor.

Essential tremor, which is also known as familial tremor, can affect the larynx alone or in association with other motor systems and produces a tremor that is difficult to differentiate from spasmodic dysphonia. The tremor is an intention tremor and its frequency is between 4 and 12 Hz. Although the precise site of the lesion has not been identified, it is felt to be somewhere in the extrapyramidal system. Blitzer noted in electromyographic studies that 25% of spasmodic dysphonia patients have an irregular tremor, differing from the regular 4 to12 Hz tremor seen in patients with essential tremor. Functional disorders can also mimic spasmodic dysphonia making the diagnosis difficult.

Functional disorders are intermittent in nature and usually manifest during periods of stress. Although the symptoms of spasmodic dysphonia are usually worse during stress (which can include talking with strangers or talking on the telephone), patients will never be completely free of them. Patients with spasmodic dysphonia may note that they occasionally are able to complete one to two sentences without any breaks, but they will not be able to go for extended asymptomatic periods as do patients who have functional disorders.

A thorough family history is helpful in establishing the diagnosis of spasmodic dysphonia, as nearly 20% of patients with primary dystonia have a family history of dystonia. These patients have a genetic predisposition to the development of symptoms. In most cases of childhood-onset dystonia, familial studies show an autosomal dominant inheritance pattern with reduced penetrance. A marker for some cases of childhood-onset dystonia has been found on chromosome 9. Patients with a family history of dystonia usually develop symptoms at a younger age than patients without a family history.

Although some uniformity exists in the signs and symptoms of spasmodic dysphonia, it is clear that symptoms vary among patients. Stress has been found to amplify any underlying voice disorder and this sometimes confounds the diagnosis of spasmodic dysphonia.

There is a preponderance of spasmodic dysphonia among women. The mean age of presentation for laryngeal dystonias is 45 years of age.

The characteristic sign of adductor spasmodic dysphonia is the strained, strangled quality of the voice. The adductor form is characterized also by having a harsh voice, often associated with a tremor, inappropriate pitch breaks, breathiness, and glottal fry. The best way to evaluate the laryngeal function of a patient who has spasmodic dysphonia is with a flexible laryngoscope and stroboscopy looking for disruptions, spasms, breathy breaks, and tremors. It is important to observe the patient at rest to determine whether any spontaneous movements occur that are not associated with phonation. Although it is clear physiologically that the vocal folds will adduct tightly during phonation, this is often difficult to appreciate during laryngoscopy, except in the most severe cases in which patients have such tight adduction that virtually no sound is produced. Frequently, the patient will try to voluntarily abduct the cords to compensate for the hyperabduction.

Many patients will have a tremor that may involve not only the vocal folds but also the hypopharynx, tongue, and palate. Tremor of the palate is most easily detected during sustained phonation of vowel "I".

The subject of the case report is a 70-year-old woman who presented in 1995 when she complained of voice changes over the previous two to three years. She felt as though she had to strain to talk and she had constant hoarseness. She had used an inhaler and some cough syrup without relief for her voice. She had seen a speech therapist for her voice disturbance without any improvement. She had no other medical problems and she does not smoke. She denied symptoms of gastroesophageal reflux disease.

Although not necessary to diagnose spasmodic dysphonia, laryngeal electromyography (EMG) frequently demonstrates inappropriate laryngeal activity. The patient was diagnosed with spasmodic dysphonia and recovered following Botox injection into the thyroarytenoid muscle.

Spectrometry also provides a visual display of vocal harmonics and noise plotting time, intensity and frequency. It shows that the impact of resonance and articulation on the laryngeal buzz. Vocal spectrographic analysis is also of particular value in defining the tremor component of a vocal character in spasmodic dysphonia.

A detailed neurologic examination should also be performed. Patients should be examined while performing postures and tasks that might bring out signs of dystonia, tremor or other neurologic disorders. Neurologic conditions that can result in speech that sounds much like spasmodic dysphonia include Parkinsonism, myoclonus, tardive dyskinesia, cerebellar disorders, and multiple sclerosis. Although some of these patients may be candidates for botulinum toxin therapy, the underlying medical process should be identified to permit general medical treatment and patient counseling. Botox therapy has been shown to be of benefit in some patients who have myoclonus, Parkinsonism and cerebellar disorders, but only when the primary speech problem is adductor laryngeal spasm. It is not effective for hypokinetic Parkinsonism or for dysarthria.

Vocal function testing is important not only to diagnose the disorder, but also to quantify the severity, to aid in determining whether the BTX injection should be unilateral or bilateral and to establish the optimal dose. The primary parameters useful in documenting these effects are voice break factor, phonatory airflow and the rate of voice breaks. In adductor spasmodic dysphonia, mean airflow rates have been shown to range from normal to extremely low, and adductor spasms correlate with sudden drops in airflow, which correlates to voice breaks.

Voice testing and observation have allowed the development of criteria for classification of patients with spasmodic dysphonia. Ludlow and Connor developed the categories of constant symptom, intermittent symptom and tremor and applied them for both the abductor and adductor form. In the constant adductor type, the voice is constantly harsh and tight. The intermittent adductor has pitch and voice breaks in the middle of words. The adductor tremor has glottal stops with a 4-5 Hz tremor in the middle of words.

Kaufmann and Morrison proposed a staging system useful in describing the pretreatment phenomenology of the larynx in patients with adductor spasmodic dysphonia. Type 1 consists of hyperadduction or forceful contraction at the vocal fold level with tight compression of the vocal processes and arytenoid. Type 2 is forceful contraction including contact of the false cords. In Type 3, the thyroarytenoid muscle pulls the arytenoids anteriorly, narrowing the supraglottic airway. Type 4 is sphincteric closure, whereby the arytenoids are pulled so far anteriorly that they tightly close against the epiglottis.

Therapy for spasmodic dysphonia continues to evolve. Specific pharmacotherapy to treat the underlying identified defects is available only for a limited number of patients with dystonias, such as Wilson's disease. For other patients, the current treatment strategy is aimed at the management of symptom complexes. Patients with greater involvement than focal dystonia (segmental, multifocal, generalized) are usually treated with pharmacotherapy. Many more advanced patients, however, have benefited from Botox therapy directed towards the relief of spasm in one or many discrete regions of the body. Pharmacotherapy usually begins with an anticholinergic, benzodiazepine or baclofen. The choice of drug usually depends upon the age of the patient, prior exposure to medications, other concurrent medications, and other medical problems. In difficult cases, dopamine-depleting and receptor-blocking agents have also been added.

Voice therapy approaches spasmodic dysphonia by developing vocal techniques that reduce the degree of vocal tightness and the incidence of pitch breaks. If such techniques can be identified and mastered, the next problem is their incorporation into everyday speech. One technique that has been reported to be successful in some patients is the use of inverse phonation where patients learn to speak during inspiration. Some are able to use this as their mode of communication. Another method, referred to as direct voice rehabilitation, uses a battery of techniques to identify all dysfunctional vocal habits. The first step in this process is to identify and establish the use of natural or optimal pitch level and range. The second step is to relocate the tone focus away from the throat - where the spasms are occurring - to the nose and face. This not only diverts concentration from the spasms, but it also projects the voice more efficiently. Proper breath support is the third issue to be addressed.

Although some patients respond well to voice therapy alone, it is a long, arduous process that requires the dedicated input of the patient and therapist alike. Some patients who do well initially with voice therapy later develop recurrent problems, possibly because of progression of the disorder or the resumption of old habits. However, voice therapy is a very effective adjunct to botulinum toxin therapy. The duration of beneficial effect from botulinum toxin is significantly longer in patients who also receive voice therapy aimed at regulating breath support and avoiding excessive glottal adduction.

For many years, spasmodic dysphonia was considered a hopeless disorder. Psychotherapy and speech therapy were only rarely effective in substantially alleviating patients? symptoms. In the 1970s, Dr Dedo first reported the use of lidocaine blockade of one recurrent laryngeal nerve to temporarily improve speech in these patients. He theorized that if there were sustained contractions of the vocal cord preventing normal phonatory activity, impairing one would allow for normalized speech.

In 1976, he carried this theory over to the performance of recurrent laryngeal nerve section as permanent therapy for spasmodic dysphonia. In this procedure, a skin incision is made along the anterior border of the sternocleidomastoid muscle. The thyroid gland is then mobilized and reflected anteriorly. The recurrent laryngeal nerve is identified, as it lies in close proximity to the inferior thyroid artery in the tracheoesophageal groove. The nerve proceeds lateral and deep to the cricothyroid muscle as it penetrates the endolaryngeal musculature. The nerve then bifurcates into an anterior or adductor branch and a posterior or abductor branch. Once identified, the nerve is sectioned and a 2-cm segment of nerve is removed.

Selective section of the adductor branch can also be performed once the bifurcation is visualized. Carpenter and Snyder performed this procedure in 3 patients in 1981. The purpose of this selective nerve section was to create adductor weakness to offset the hyperadduction characteristic of patients with spasmodic dysphonia and to produce voice results similar to those seen immediately following complete recurrent laryngeal nerve section while still retaining some abductor function. They theorized that the maintenance of abductor function may offset the late failures after complete nerve section by preventing postsurgical vocal cord medialization. However, no follow up studies were done on these patients.

After a three-year follow up, Dedo reported a 10% to 15% recurrence rate of spasmodic dysphonia. The recurrences for the most part were less severe than the symptoms prior to nerve section. He stated that the failure is from a reduced glottic space and suggested postoperative voice therapy to avoid pushing or tensing the cords to increase volume.

Aronson and De Santo reported an initial success rate of 97% at six months for recurrent laryngeal nerve section, but at 3 years the success rate has dropped to 36%. Patients that failed nerve section have a strained, hoarse voice in addition to symptoms of iatrogenic vocal cord paralysis. Furthermor, Aronson and De Santo noted that failure is due to gradual overadduction of the intact vocal fold against the paralyzed vocal fold. They ultimately concluded that the effectiveness of unilateral recurrent laryngeal nerve section for the treatment of adductor spasmodic dysfunction decreases with time and results in permanent cord paralysis and treatment failure in a high number of patients.

Experimental results and clinical experience indicate that spasms experienced after recurrent laryngeal nerve section are due to regeneration of the nerve even when the cut ends have been securely ligated. To help solve the problem of nerve regeneration and subsequent spasm, Netterville proposed a procedure he termed "recurrent laryngeal nerve avulsion." This technique of neural avulsion involves removing the distal nerve up to its insertion into the laryngeal muscles. The short-term results for 12 patients were promising, but no long-term follow-up studies have been conducted.

A modification of an anterior laryngoplasty procedure has also been described to help decrease tension on the vocal cords. Anterior laryngoplasty is a procedure that involves relocating the anterior commissure at the point where the vocal folds insert on the thyroid cartilage. As originally described, the commissure was moved forward to produce increased vocal fold tension and better approximation in patients who have senile bowing of the glottis. Tucker modified this procedure by displacing the anterior commissure posteriorly to decrease the effects of thyroarytenoid contraction. He reported a 63% success rate in the first 16 patients treated with this procedure with a follow-up of 6 months to 2 years. Unfortunately, this technique fails in many cases owing to the way the muscle stretch receptors work, and leaves the patient with a very poor voice.

An implantable recurrent laryngeal nerve stimulator has been investigated as a possible treatment for spasmodic dysphonia. Initial experience with five patients was encouraging, but long-term outcome is not known and safety is not known.

Resection of a portion of thyroarytenoid muscle has also been proposed as a potential permanent alternative to the temporary chemodenervation achieved by botulinum toxin therapy in patients with adductor spasmodic dysphonia. Experiments in rabbits indicate that the muscle can be easily approached via a window in the thyroid cartilage and that the muscle does not regenerate. After 3 months, the defect is replaced by loose fibroareolar tissue, and no impairment of the vibratory edge of the vocal cord is seen. Currently, use in humans has not been studied.

Botulinum toxin therapy is currently considered by many to be the treatment of choice for spasmodic dysphonia. Scott first initiated the clinical use of Botox for the management of strabismus. He needed a method of blocking neuromuscular junctions in a particular muscle to weaken it and rebalance the extraocular muscles to achieve conjugate vision. He later used the toxin successfully for the management of blepharospasm, a focal dystonia of the orbicularis oculi muscle.

The first reported use of botulinum toxin to treat spasmodic dysphonia by injection came from Baylor in 1987 in an article by Drs. Miller, Woodson, and Jankovic.

The anaerobic bacterium Clostridium botulinum produces seven serologically distinct toxins that are potent neuroparalytic agents. These are designated A through G. Type A is the most lethal biologic toxin known and is the one that has been used clinically. Although the seven neurotoxins are antigenically distinct, they possess similar molecular weights and have a common subunit structure.

Botulinum toxin exerts its effect at the neuromuscular junction by inhibiting the release of acetylcholine at the presynaptic terminal causing a weakness or paralysis depending on the number of end plates affected.

The currently accepted notion about the mechanism of action in botulinum toxin is that the toxin is an enzyme acting as a zinc endopeptidase. The proteolysis of one or more neuronal proteins is probably the cause of the intercellular lesion that inhibits neurotransmitter release.

Studies on the long-term effects of exposure to botulinum toxin are emerging. In experimental models, long-term exposure causes denervation atrophy. In one study in humans, long-term exposure reportedly caused fibrosis and atrophy of the orbicularis oculi muscle. In another study, no necrosis or inflammatory changes were noted. There were detectable abnormalities, however, on single fiber EMG. It is not known how long these abnormalities persist or whether or not they have clinical significance.

Turning to the performance of the induction, the toxin is received as a frozen specimen and is reconstituted with normal saline to a final concentration of 2.5 units/0.1 cc. The toxin is injected via a monopolar, hollow-bored Teflon-coated EMG needle connected to an EMG recorder. The technique of injection as described by Blitzer involves placing the patient in the supine position with the neck extended. The needle is slightly curved to allow for a more anterior placement and is placed through the neck skin and cricothyroid muscle into the thyroarytenoid muscle under EMG guidance. The patient is asked to phonate and when the needle is in a very active area of the muscle, the toxin is injected. The patient is instructed not to cough or swallow when the needle is in the airway or in the muscle. The patient who has an uncontrollable cough with injection can be given 0.3 cc of 1% lidocaine injected through the cricoarytenoid membrane into the subglottic space. The recommended initial injection dose ranges from 5-15 units in one vocal fold to 2.5 to 5 units in each vocal fold for bilateral injection. All centers using Botox agree that regardless of the technique used for injection and the quantity injected, there is a dramatic improvement in symptoms, with 80%-90% reported improvement in speech function during therapy. Side effects include breathy hypophonia and clinically and significant aspiration. Both these side effects were transient and patients were free of side effects in approximately two weeks.

Blitzer theorized that unilateral vocal cord weakness may actually exacerbate the dystonic symptoms on the functional vocal fold and he began bilateral dosing in his patients. Some patients are sensitive to the toxin and do not have the best response to bilateral doses, picking up too much breathiness after the injection. They also can have side effects after larger unilateral doses and in these patients he staggers the larger doses and also performs a unilateral injection and gives the contralateral injection two weeks later. Some patients prefer more frequent smaller unilateral doses.

In 1998, Langeveld published the results of a prospective trial in which he assessed voice quality, duration of effect and side effects after unilateral and bilateral Botox injection. The first treatment consisted of the injection of 5 units in the left thyroarytenoid muscle. The second treatment took place once the effect of the first procedure had completely worn off, and consisted of 2.5 units injected into both thyroarytenoid muscles. By means of self-grading scales, effects and side effects were assessed for over at least three months. They found no difference between the procedures and either the duration of voice improvement or the occurrence of breathy dysphonia. After a bilateral injection, more patients reported swallowing problems.

Ford and colleagues reported an indirect laryngoscopic approach for injecting the toxin into the vocal folds. They reported that the technique has the advantage of being familiar to the otolaryngologist and requires no EMG equipment. In a 1996 study, Dr. Inagi analyzed in a retrospective fashion a total of 64 patients with spasmodic dysphonia who received Botox injections via the indirect laryngoscopic approach. He concluded that the injection to both the thyroarytenoid and the lateral cricoarytenoid simultaneously gave the best voice results. The overall improvement from baseline was longest and the period during which the voice was best was also longer lasting. Injections to the lateral cricoarytenoid and the thyroarytenoid muscle simultaneously also gave the shortest duration of undesirable side effects. Based on this data, the group recommends that initial Botox therapy for adductor spasmodic dysphonia should be a single, unilateral injection placed strategically at the posterior portion of the thyroarytenoid muscle and directed towards the lateral cricoarytenoid, so that both muscle groups are affected.

Regardless of the technique, Botox injections have several advantages over surgical therapy in the management of these patients. The patient is awake and there is no risk of anesthesia. Greater degrees of weakening can be achieved by varying the dose injected. Most adverse effects are transient.

Follow-up therapy is carefully individualized for each patient. The patient is counseled and different strategies may have to be tried to find the best long-term treatment program. Qualitative assessment of Botox results demonstrated that the adductor patients obtain nearly 95% of normal function for an average duration of 4.5 months. With repeated injections, the effective dose tends to decrease and the interval between injections tends to increase. Most patients settle into a schedule of a stable dose at regular intervals, often scheduling repeat injections before symptoms recur.

In conclusion, the major problem in evaluating the new treatment for spasmodic dysphonia is the lack of standardization in the diagnosis and documentation of the severity of the problem. A common way of expressing these parameters would greatly enhance research in this area. Presently, botulinum toxin holds great promise as an effective means of achieving consistent therapeutic success in treatment of these patients. Results from controlled trials of Botox undoubtedly will enhance our knowledge of the disorder and hopefully will lead to better treatment. The major limitation of Botox therapy is that it only mitigates the symptoms of spasmodic dysphonia and does not treat the underlying cause. Even when the voice is dramatically improved, normal function is never completely achieved. More research is also needed to delineate the role in the speech therapy and the management of patients who suffer from spasmodic dysphonia. Although results from speech therapy alone are disappointing, it seems clear that results from surgical or medical management may be enhanced by voice therapy. The key to improving the treatment of spasmodic dysphonia lies in determining its pathophysiology. Because an animal model is not feasible, the problem must be explored in humans. With carefully controlled studies, there are objective tools for the assessment of speech and neuromuscular function.

Case Presentation

A.M. is a 70-year-old woman who first presented in 1995 when she complained of voice changes over the previous 2-3 years. She felt as though she had to strain to talk and she had constant hoarseness. She had used an inhaler and some cough syrup without relief for her voice. She had seen a speech therapist for her voice disturbances without improvement. She has no airway distress, no stridor and no problems with sinusitis or GERD. She has no other medical problems and she does not smoke. She denied any neurologic disorders and had no family history of tremors or other dystonias.

On physical examination, she has normal tongue and palate mobility. On laryngeal examination, she has no mucosal lesions, although she does have some mild vocal fold edema. She has symmetric vocal fold mobility with adductor spasm and intermittent glottal stops and pitch breaks of mild to moderate severity. Stroboscopic exam was limited, as she cannot sustain constant pitch.

Her findings were consistent with Adductor Spasmodic Dysphonia and the patient was scheduled for botulinum toxin injections. She initially received 10 U of botulinum toxin injected into the left thyroarytenoid muscle under laryngeal EMG control. She tolerated the procedure well and noted significant improvement in voice quality that lasted approximately 4 months. She has subsequently received further botulinum toxin injections with good results.

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