Botulinum Toxin for Laryngeal Dystonia
- Author: Jayita Poduval, MS, MBBS, DNB(ENT), DORL; Chief Editor: Arlen D Meyers, MD, MBA more...
Laryngeal dystonia (LD) is a muscle-contraction disorder of the larynx and laryngeal musculature. It was once referred to as spasmodic dysphonia (SD), which refers to a group of dystonias, or muscle-contraction disorders, in which involuntary muscle movements in a particular organ or region of the body interfere with normal function. However, the term spasmodic dysphonia is an inaccurate description of laryngeal dystonia, since no lesion in the pyramidal or extrapyramidal tract has yet been identified to account for the spasticity.
Other synonyms of historical significance for laryngeal dystonia have included spastic aphonia, spastic dysphonia, phonic laryngeal spasm, coordinated laryngeal spasm, mogiphonia, laryngeal stuttering, and nervous hoarseness.
Although Traube is believed to have coined the term “spasmodic dysphonia” in 1871, further extensive studies using electromyography and, subsequently, the use of botulinum toxin to treat laryngeal dystonia in 1986 are credited to Blitzer and his colleagues.
Laryngeal dystonias are classified according to the specific muscle(s) involved, into 4 distinct types, as follows:
Adductor type: This type accounts for most cases of laryngeal dystonia, around 80%. In this condition, the true vocal cords close intermittently and irregularly during connected speech, resulting in voice breaks and a strained, strangled voice quality and effortful speech.
Abductor type: This type is rare and causes a soft, whispery voice due to increased breathiness and vocal air escape. Complete aphonia can occur in severe cases.
Mixed type: This has features of both adductor and abductor types.
Adductor laryngeal breathing dysphonia (ALBD): In this condition, the voice is normal, but there is an inspiratory stridor, which may persist and complicate swallowing, leading to paroxysmal cough and dysphagia.
Laryngeal dystonia is characterized by the severe impairment of connected speech without associated problems with singing, humming, or laughing or related activities such as yawning, yelling, or sneezing.
Laryngeal dystonia is usually precipitated by stress and may be temporarily controlled with alcohol, tranquilizers, and/or sedatives. It must be distinguished from essential voice tremor, functional aphonia, malingering, and neurological diseases. Associated focal dystonias in other areas may be seen, such as torticollis, blepharospasm, hemifacial spasm, strabismus, and writer’s cramp.
Laryngeal dystonia is significantly more common in female than in males, and its peak age of onset is 35-45 years. Familial clustering has been reported.
A detailed history and thorough physical examination are essential to diagnose the condition and to rule out other neurological lesions. Investigations of choice in laryngeal dystonia are fiberoptic laryngoscopy and laryngeal videostroboscopy. Other tests include aerodynamic, acoustic, perceptual, and spectral voice analysis.
Laryngeal dystonias result from poorly coordinated muscle movement; therefore, treatment involves weakening one side of the agonist and antagonist groups of muscle. Although laryngeal dystonias have no known cure, various pharmacological, surgical, and physiotherapeutic options may be used for treatment. Injection of botulinum toxin (BT) is now the criterion standard of treatment.
Indications for botulinum toxin treatment of laryngeal dystonias include the following:
Contraindications to botulinum toxin treatment of laryngeal dystonia are as follows:
Very young age (neonates, infants)
Motor neuron disease, neuromuscular disorders
Concomitant aminoglycoside use
Untreated gastroesophageal reflux disease
The response of botulinum toxin treatment of laryngeal dystonias is typically better in younger patients.
The success rate approaches 85%-90% and is higher in adductor laryngeal dystonia than in abductor laryngeal dystonia. Essential voice tremor is associated with the poorest success rate.
Injections into the posterior cricoarytenoid (PCA) muscle are technically more difficult than into the thyroarytenoid and lateral cricoarytenoid (TA/LCA) and may be less satisfactory in patients with abductor laryngeal dystonia, since the PCA muscle is more difficult to access and/or some patients believed to have abductor laryngeal dystonia actually have the mixed type (ie, a combination of adductor and abductor laryngeal dystonia).
Large or repeated doses may cause resistance by formation of antibodies; this may occur in about 3%-10% of patients and is also related to younger age and booster doses. It may be treated by using another serotype (eg botulinum toxin B).
Otolaryngologic Clinics Of North America. Laryngeal Dystonia. Phonosurgery. February 2006. Number 1. 39.:
Blitzer A, Brin MF, Fahn S, Lange D, Lovelace RE. Botulinum toxin (BOTOX) for the treatment of "spastic dysphonia" as part of a trial of toxin injections for the treatment of other cranial dystonias. Laryngoscope. 1986 Nov. 96(11):1300-1. [Medline].
Brin MF,Fahn S,Blitzer A et al. Movement disorders of the larynx. In: Neurological disorders of the larynx. New York: Thieme Medical Publishers; 1992:240-8.
Office-based laryngeal procedures. Operative Otolaryngology. In: Eugene N. Myers. Volume 1. Chapter 36.
Scott AB, Suzuki D. Systemic toxicity of botulinum toxin by intramuscular injection in the monkey. Mov Disor. 1988;3:333-5.
Upile T, Elmiyeh B, Jerjes W, Prasad V, Kafas P, Abiola J. Unilateral versus bilateral thyroarytenoid Botulinum toxin injections in adductor spasmodic dysphonia: a prospective study. Head Face Med. 2009. 5:20. [Medline].