Adductor Spasmodic Dysphonia

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Spasmodic dysphonia is a vocal disorder that is not well understood. It usually appears in adulthood in both males and females. What begins as a mild, strained hoarseness may develop over months or years into a more intensely strained voice. Severe, massive spasm of the true and false vocal folds can arrest phonation virtually completely. Sensitive to adverse listener reactions, these patients become withdrawn and depressed. Those who depend on their voices for a livelihood must find other work.

Spasmodic dysphonia can be classified into two types: 1) Adductor, which refers to hyperadduction of the true and false vocal folds with laryngeal elevation, and 2) Abductor, characterized by intermittent vocal cord abduction, resulting in moments of breathiness and unvoicing. Adductor spasmodic dysphonia is the focus of this review.

Spasmodic dysphonia was first described by Traube in 1871 who thought this was a form of nervous hoarseness. However, the pathophysiology of this condition remains elusive. Two theories of origin concerning spasmodic dysphonia exist: neurologic and psychiatric. The frequent association of neurologic disorders such as Meige's syndrome (craniofacial dystonias that are characterized by involuntary movements or uncontrolled spasms of the eyes, face, jaw palate, or neck) with adductor spasmodic dysphonia suggests a neurologic basis. Additionally, patients with essential tremor affecting the head, face, neck, tongue and soft palate also may have laryngeal tremor. The voice quavers during speech and tremor regularity can especially be observed when the patient sustains a vowel. Essential tremor of the larynx may produce spasmodic dysphonia because the adductor phase of the vocal fold tremor oscillation can occur with such great amplitude that the vocal cords hyperadduct against each other, momentarily arresting the exhaled air stream. When vocal fold oscillations are smaller, few, if any, voice arrests occur, and all that can be heard is voice tremor.

Classically, spasmodic dysphonia has been attributed to psychiatric illness: anxiety that produces heightened laryngeal musculoskeletal tension, depression, or as a type of conversion reaction. Proponents of a psychogenic basis point to 1) the bizarre sound and appearance of patients when they speak but not when they sing or laugh; 2) case histories of patients indicating a high incidence (40%) of emotionally stressful events surrounding onset; 3) the worsening of symptoms when the patient is subjected to additional stress, and 4) frequently negative laryngoscopic findings. However, Aronsen in 1973 pointed out that in contrast to vocal pathologies of psychogenic origin, in spasmodic dysphonia, one finds: 1) an equal sex ratio; 2) resistance to voice therapy; 3) frequent laryngospasm; and 4) a progressive rather than acute onset of symptoms.

Approximately 33% of cases of spasmodic dysphonia are idiopathic. The cardinal signs of adductor spasmodic dysphonia include effortful vocal straining, vocal harshness, quaver, and voice arrest due to laryngospasm in the midst of noneffortful phonatory periods. In order to achieve a freer, less effortful, flow of air through the glottis, the patient may resort to whispering, speaking on inhalations as well as exhalations, and laughing frequently. No satisfactory explanation has yet been brought forward for the finding that the voices of patients with spasmodic dysphonia are briefly normal when surprised or taken off guard; during and immediately following laughter, when singing, when shouting, when angry, when speaking in a higher-pitched voice or in falsetto register, when intoxicated, or when awakening from a general anesthetic. Examination of the larynx may reveal true and false vocal cord hyperadduction on speech.

Many treatment approaches have been attempted through the years with a significant improvement in vocal symptoms. Psychiatric treatment, voice therapy, hypnosis, biofeedback, acupuncture, drugs, and vitamins have all been attempted with limited, shortlasting improvements at best.

In 1976, Dedo proposed unilateral sectioning of the recurrent laryngeal nerve with the assumption that a unilateral vocal cord paralysis would facilitate a gentler approximation of the vocal folds and hence a slightly breathy but more easily produced voice. Though Dedo reported long-term improvement of voice in 92% of patients, other researchers have found recurrence rates of spasmodic dysphonia of up to 64% of patients. Dedo proposes that perhaps the poorer results of others are because only the severest cases of spasmodic dysphonia are offered recurrent laryngeal nerve section, and that these are the most likely to recur postop. For recurrence following recurrent laryngeal nerve section, Dedo recommends debulking of the paralyzed cord with a CO2 laser.

Recurrent laryngeal nerve crush has been tried for spasmodic dysphonia, but recurrence in up to 100% of patients is noted in some studies.

Botulinum toxin has been used successfully for a number of years in the treatment of a variety of orofacial dystonias. It is produced by the organism Clostridium Botulinum, whose ingestion is responsible for the disease entity botulism. There are at least eight immunologically distinct types. Type A is most frequently used in clinical settings. The mode of action of this toxin is at cholinergic nerve terminals where it inhibits the CaH dependent release of the neurotransmitter acetylcholine. It is injected into the thyroarytenoid muscle via a needle connected to a standard EMG machine. Correct positioning of the needle is confirmed by the presence of crisp action potentials on phonation. Botulinum toxin is then injected through the same needle. Unilateral injection of botulinum toxin in patients with adductor spasmodic dysphonia has been successfully performed at Baylor. The average length of maximal effect is ten weeks, and then the patient must be reinjected. The greatest improvements occur in those patients with focal laryngeal dystonia, without a tremor component or other craniofacial dystonias. Botulinum toxin injections can be performed in an outpatient setting, as patients tolerate it remarkably well.

Experimental therapies of spasmodic dysphonia include phonosurgery that posteriorly displaces the vocal ligaments to reduce tension, implants that stimulate the recurrent laryngeal nerve, and CO2 laser-assisted removal of the thyroarytenoid muscle.

Although spasmodic dysphonia is a disorder that has been recognized for over a century, we are still grappling with what it is, it's etiology, and it's most effective management.

A 32-year-old registered nurse noted, at the age of 28, progressive voice "tension", and spasms that worsened particularly during periods of excessive stress. She was quite bothered by the tension in her voice and the fact that people complained that they could not understand her. She began to avoid conversations and answering the telephone because of her speech problems. She saw a laryngologist in an other state who told her to reduce the stresses in her life. This did not work. She also underwent speech therapy to no avail. She was then referred to Houston. Physical examination revealed excess vocal fold tension upon adduction, yielding a voice that was strained, tense, and tight. Thirty units of botulinum toxin were injected into her left thyroarytenoid muscle under laryngeal electromyographic control. A remarkable improvement in her voice was noted.

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