Spasmodic dysphonia (SD), also referred to as laryngeal dystonia or spastic dysphonia, is a neurological condition, a focal dysphonia affecting vocal muscles of the larynx. The disorder is a result of involuntary, forceful separation of the vocal folds which interrupts the airstream. This movement of the vocal folds occurs when hyperactive motonuerons stimulate one or more laryngeal muscles (National Institutes of Health, 1992). The average age of onset is 45 to 50 years.
The full etiology of SD is not yet known. However, tremor and dystonia are closely related with SD which suggests SD is related to dysfunction of the extrapyramidal system, specifically dysfunction in the basal ganglia or cerebellar control circuits. There are three broad etiologic possibilities for the disorder. Spasmodic dysphonia can be neurogenic, psychogenic, or idiopathic.
Perceptual symptoms may include such characteristics as, continuous or intermittent strained-strangled effortful speech, and/or a tremulous, weak, or breathy voice, most obvious at the beginning of utterances or in voiceless consonant environments.
Physical symptoms may include, rhythmic or arrhythmic spasms
of true cords and arytenoids, and sometimes false cords and pharygeal constrictors,
during speech, as well as, jerky and arrhythmic thoracic/abdominal movements
and/or facial grimacing and neck/shoulder movements secondary to severe
Symptoms may worsen due to factors such as anxiety, stress, depression, physical exertion, or concentrating on speech. (Duffy, 1995)
The two basic types of SD are adductor and abductor:
Adductor spasmodic dysphonia (most common) is caused by involuntary excessive contraction of the muscles that bring the vocal cords together. This disorder may cause a stained-strangled, choked, effortful voice quality, often with abrupt initiation and termination of voicing, and a broken speech pattern.
Abductor spasmodic dysphonia is caused by an overcontraction of the muscles that separate the vocal folds. This disorder may cause a choppy and breathy whispering voice pattern or an irregular voice tremor.
The role of the speech-language pathologist (SLP) in the assessment process for SD is a collaborative process that begins after the client has had an evaluation from an otorhinolaryngologist (ENT-ear,nose,and throat physician). The SLP may be responsible for preparing an evaluation for the ENT, and may or may not perform a videostroboscopy. The ENT must authorize initiation of a therapy program performed by an SLP. The ENT and the SLP must collaborate in order to decide if therapy alone will be most beneficial for the patient, or if medications should be introduced into therapy. Finally, the SLP should inform the ENT of the therapeutic progress and discharge outcomes.
There are several treatment options for individuals with SD. The ENT decides the best treatment option according to the specific individual. The ENT may prescribe such treatments as voice rest without therapy, laryngeal surgery, or a referral to an SLP for therapy. A relatively new treatment option is injections of botulinum toxin.
Clinical studies have indicated that botulinum toxin (botox), a complex protein which causes paralysis by blocking the presynaptic release of acetylcholine, is an effective treatment for many conditions such as, spasmodic dysphonia. In 1984 Blitzer and Brin (1992) administered the first laryngeal injection of botulinum toxin. Since that time, they have treated over 450 patients with adductor spasmodic dysphonia and have found that botox is a safe and effective therapy for SD. However, because botox is a new treatment, there is still a great deal of debate over the indications, the nature of the long and short-term side effects, and the optimal method of use (National Institutes of Health, 1992).
Blitzer, A., & Brin, M.F. (1992). Treatment of spasmodic dysphonia (laryngeal dystonia) with local injections of botulinum toxin. Journal of Voice,6, 365-369.
Duffy, Joseph R. Motor Speech Disorders: Substrates, Differential Diagnosis, and Management.
1995 St.Louis:Mosby. 212-213.
National Institute of Health (1992). Consensus development panel on clinical use of botulinum toxin. Journal of Voice, 4, 394-400.