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BCM - Baylor College of Medicine

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Parkinson's Disease Center and Movement Disorders Clinic

Spasmodic Dysphonia (SD)

Spasmodic dysphonia is a neurological disorder caused by a dystonia (abnormal sustained muscle contraction) of the vocal cords. Depending on the vocal cord muscles that are affected, there are three types: adductor (involuntary vocal cord closing), abductor (involuntary vocal cord opening), or mixed. Adductor SD is more common and presents with a strained or strangled voice with irregular voice breaks. The severity of spasmodic dysphonia varies throughout the day and from day to day. Abductor dysphonia presents as excessive breathiness, pauses in the middle of the word, and difficulty in generating adequate volume of speech. Mixed dysphonia patients often have a chaotic combination of inappropriate adduction and abduction, resulting in halting speech and variable breathiness and tightness. Singing, shouting, and laughter may change the characteristics of all three types of dysphonia. In addition to their phonation difficulties, many patients with SD have an associated tremor of the voice, hands and head. This condition may be very debilitating especially for professionals such as teachers, trial attorneys or performers.

Causes

The cause of SD remains unknown, but the disorder is classified as a form of focal dystonia (syndrome of abnormal sustained muscle contractions) involving the vocal muscles. This neurologic disorder is probably caused by impairment in the normal motor control mechanisms within the basal ganglia (deep brain structures which help regulate movement). A few cases with single mutations in THAP1, a gene involved in transcription regulation, suggest that a weak genetic predisposition. SD may occur isolated or as part of a segmental dystonia, when it is associated with involuntary spasms of the face, jaw, and neck muscles (cranial or craniocervical dystonia). SD may also occur in patients with more generalized dystonia, also involving the trunk and limbs. This form of dystonia is often of genetic origin with several genes or gene markers already identified (see related information on dystonia).

Prevalence

Little is currently known about the incidence and prevalence of SD. There may be between 10,000 to 30,000 affected individuals in the United States as reported by the National Spasmodic Dysphonia Association, although this may grossly underestimate the true prevalence. Spasmodic dysphonia, like most focal dystonias, tends to emerge gradually in young adulthood or midlife and then reaches a plateau, when the severity of symptoms remains constant. Spontaneous remission occurs in a small percentage of patients, but it is usually transient and the symptoms may recur after a few weeks or months. Repetitive vocal cord strain and laryngeal trauma may precipitate SD

Treatments

Minor adductor overactivity may improve with speech therapy, relaxation techniques or alteration of vocal pitch. Oral medications (such as trihexyphenidyl or benzodiazepines) may be effective in mild cases, but botulinum toxin injections are clearly the treatment of choice for most patients. Techniques of injecting botulinum toxin into the vocal cords include percutaneously (through the skin) unilaterally or bilaterally, or through a transnasal fiberoptic approach. The effect may last up to three months and most patients are able to sustain a benefit with 2-4 injections per year. Voice therapy and voice rest following the injections of botulinum toxin may prolong the benefit of botulinum toxin. Treatment with botulinum toxin injections is proven to be effective in treating SD and it has markedly changed the prognosis of the disease.

Appendix

National Spasmodic Dysphonia Association
300 Park Blvd., Suite 335
Itasca, IL 60143
Toll free: (800) 795-6732
Fax: (630) 250-4505
Email: NSDA@dysphonia.org

©2011 Joseph Jankovic, M.D.

Selected References

Bielamowicz S, Squire S, Bidus K, Ludlow CL. Assessment of posterior cricoarytenoid botulinum toxin injections in patients with abductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2001;110:406-12.

Chang CY, Chabot P, Thomas JP. Relationship of botulinum dosage to duration of side effects and normal voice in adductor spasmodic dysphonia. Otolaryngol Head Neck Surg. 2007;136:894-9.

Chitkara A, Meyer T, Keidar A, Blitzer A. Singer's dystonia: first report of a variant of spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2006;115:89-92.

Djarmati A, Schneider SA, Lohmann K, et al. Mutations in THAP1 (DYT6) and generalised dystonia with prominent spasmodic dysphonia: a genetic screening study. Lancet Neurol. 2009;8:447-52.

Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders, Churchill Livingstone, Elsevier, Philadelphia, PA, 2011:1-548. (Includes on-line videos and references.)

Gündel H, Busch R, Ceballos-Baumann A, Seifert E. Psychiatric comorbidity in patients with spasmodic dysphonia: a controlled study. J Neurol Neurosurg Psychiatry. 2007;78(12):1398-400.

Jankovic J, Schwartz K, Donovan DT. Botulinum toxin treatment of cranial-cervical dystonia, spasmodic dysphonia, other focal dystonias, and hemifacial spasm. J Neurol Neurosurg Psychiatry. 1990;53:633-9.

Ludlow CL. Spasmodic dysphonia: a laryngeal control disorder specific to speech. J Neurosci. 2011;31:793-7.

Murry T, Woodson GE. Combined-modality treatment of adductor spasmodic dysphonia with botulinum toxin and voice therapy. J Voice. 1995;9:460-5.

Simpson DM, Blitzer A, Brashear A, Comella C, Dubinsky R, Hallett M, Jankovic J, Karp B, Ludlow CL, Miyasaki JM, Naumann M, So Y; Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Assessment: Botulinum neurotoxin for the treatment of movement disorders (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2008;70:1699-706.

Wong DL, Adams SG, Irish JC, Durkin LC, Hunt EJ, Charlton MP. Effect of neuromuscular activity on the response to botulinum toxin injections in spasmodic dysphonia. J Otolaryngol. 1995;24:209-16.

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