Speech is produced when air from the lungs is pushed between the vocal cords, causing them to vibrate (Luc & Zieve, 2012). Spasmodic dysphonia (SD) is a voice disorder characterized by involuntary movements or spasms that prevent the normal vibrations of the vocal cords and the production of a normal voice (see Figure 1). It is also referred to as laryngeal dystonia, which is a form of focal dystonia (National Institutes of Health [NIH], 2010a).
Dystonia is defined as involuntary muscle contractions that cause repeated movements generating tremors, twitches,or abnormal postures (National Institute of Neurological Disorders and Stroke [NINDS], 2011). Dystonias are classified according to the part of the body affected with generalized dystonia affecting most parts of the body.
* Focal dystonia is localized to one part of the body, such as the intrinsic laryngeal muscles in SD (Revelo et al., 2009).
* Multifocal dystonia occurs when two or more unrelated areas of the body are affected.
* Segmental dystonia involves two or more adjacent parts of the body.
* Hemidystonia affects the arm and leg on the same side of the body (NINDS, 2011).
Types of Spasmodic Dysphonia
There are three types of spasmodic dysphonia. In adductor spasmodic dysphonia, the vocal folds close together and stiffen with spasms, making vibration of the cords difficult. Patients with this condition find it difficult to start talking and words are often cut off with the spasms. In abductor spasmodic dysphonia, the vocal folds do not close properly due to muscle spasms that prevent the folds from vibrating to produce voice. In this situation, the voice will sound weak and breathy due to air escaping from the lungs during speech. In adductor and abductor spasmodic dysphonia conditions, the voice sounds normal while singing, shouting, laughing, and crying (NIH, 2010a). Mixed spasmodic dysphonia, which is rare, is characterized by spasms of the different muscles that open and close the vocal folds. As the name suggests, it has the characteristics of both adductor and abductor spasmodic dysphonia (NIH, 2010a).
The most common form of spasmodic dysphonia is the adductor type. The symptoms for adductor SD include a choked, strained voice with sudden breaks in speech in the middle of vowels. In the less common abductor type SD, the voice sounds breathy with whisper quality voice breaks. In mixed type SD, both types of symptoms are present (Revelo et al., 2009).
There are no known causes for spasmodic dysphonia because no long-term research data is available. SD was originally thought to be psychogenic in nature due to lack of readily available research information. However, current studies indicate that SD is a neurogenic voice disorder (Luc & Zieve, 2012). Some clinicians and genetic researchers believe SD may be hereditary because members of the same family often suffer from this disorder (NIH, 2010a).
Scientists and clinicians at the NIH facilities (as well as other medical centers), NINDS, and the National Institute on Deafness and Other Communication Disorders (NIDCD) are performing genetic research to identify causes of focal dystonias. These researchers believe that brainstem and basal ganglia lesions are contributing factors in such movement disorders. Patients with SD may also have spasms of other parts of the body such as the neck, jaw, arms and legs, eyelids, lips, or tongue (NIH, 2010a). The National Eye Institute (NEI) supports the study on Blepharospasm and other eye movement disorders, and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) supports research on dystonias and rehabilitation for such disorders (NINDS, 2011).
Spasmodic dysphonia is often undiagnosed in its early stages, because the symptoms are similar to other voice disorders. A detailed history must be obtained by an otolaryngologist who is specially trained in voice disorders, with special emphasis on the onset and progression of the voice dysfunction.
Deterioration of voice quality under stress and during telephone conversation is a typical feature of SD. Voice improvement is noted temporarily after the consumption of alcohol and sedatives (Revelo et al., 2009). Other conditions that may affect the voice such as amyotrophic lateral sclerosis (ALS), Wilson's, Huntington's, and Parkinson's diseases should be initially ruled out using past and present medical history, diagnostic tests, and referrals to other specialists (Revelo et al., 2009).
An otolaryngologist can diagnose SD as well as eliminate other speech pathologies such as voice tremors and vocal cord paralysis. The evaluation involves passing a flexible laryngoscope through the nose to the back of the throat to observe the movements of the vocal folds during phonation and cough. Electromyography, fiber optic laryngoscopy, videostroboscopy, aerodynamic testing, and vocal spectrographic analysis (see Table I) are other methods that aid in the diagnosis (Revelo et al., 2009).
No long-term research data is available for a definitive cure for spasmodic dysphonia. Symptomatic treatment to the larynx is the current treatment approach for SD. Speech therapy may be advised initially for mild symptoms of SD; however, if no improvement occurs after 8-10 therapy sessions, Botulinum Toxin A (Botox(r)) therapy is second line of treatment (Pitman, Kamat, Bliznikas, & Baredes, 2011).
Injections of very small amounts of Botox to the affected, hyperfunctional laryngeal muscles weaken them by blocking the nerve impulses (chemical denervation). The weakened muscles reduce spasms and improve voice quality for a few months (Revelo et al., 2009). Laryngeal electromyography is utilized to identify the muscles for the injection of the Botox. The voice may become breathy, and swallowing may be difficult for a few days after injection due to muscle weakening. The injections are repeated every 3-8 months per individual requirements for the maintenance of a normal voice (Revelo et al., 2009).
Clinicians and researchers are currently studying several surgical treatments; however, the results are conflicting. The types of possible surgeries include:
* Type 2 thyroplasty--This procedure changes the shape of the thyroid cartilage to relax and lateralize the vocal folds slightly to enable easier phonation (Isshiki, Yamamoto, & Fukagai, 2004). As of 2009, there were no long-term studies for this procedure according to Revelo and co-authors (2009).
* Recurrent laryngeal denervation and reinnervation--First attempted in 1999 by Dr. Gerald Berke at the University of California in Los Angeles, this intervention involves the resection and reanastomosis of bilateral adductor branches of the laryngeal nerve to the ansa cervicalis (Pitman et al" 2011).
* Bilateral transarytenoid and lateral cricoarytenoid myectomy--This surgery is usually performed one side at a time, at least six months apart. The myectomy weakens the vocal folds and prevents spasms (Pitman et al., 2011).
These surgical treatments need to be researched further and evaluated for long-term effects.
Hussain and Shakeel (2010) conducted a study in Scotland on selective lateral laser thyroarytenoid myotomy for adductor spasmodic dysphonia. Two women and two men who had been managed with Botox therapy for adductor spasmodic dysphonia for an average of 11 years underwent laser surgery. All four patients had improved voice quality and fluency and required no further Botox injections. At the time of publishing of the study, the subjects had been followed for 2.5 years. The weaknesses of the study are the small sample size and the short amount of time the subjects were studied. However, the results reveal promising innovations for SD management.
M.T., a 56-year-old Asian female, experienced worsening voice and speech problems for 10 years, and speech therapy provided no improvement. She remembers that stress worsened her vocal problems, and she reached a point where she was afraid to speak.
M.T.'s past history included occasional blepharospasms, as well as cervical, abdominal, upper, and lower extremity muscle spasms. Neurological evaluations of her spasms were reported as normal by her neurologist after a detailed physical assessment including reflex testing, blood tests for Myasthenia, and a brain MRI study. M.T. recalled having a maternal uncle who developed similar speaking difficulties in his fifties.
Prior to diagnosis and treatment, M.T. spoke with great effort in a strained voice and took frequent pauses to take deep breaths. No abnormal facial movements, ear, or nose problems were noted on initial examination. A fiber optic nasal endoscopy of her larynx revealed evidence of premature spasm with symmetric vocal cord movement. Her history and findings were consistent with adductor spasmodic dysphonia.
Treatment was initiated at the Grabscheid Voice Center in New York by an otolaryngologist who specializes in voice disorders. Her condition was treated with 2.5 units (0.1 mL) of Botulinum Toxin injections to the thyroarytenoid muscles (see Figure 2) using a transcricoid approach under electromyography guidance. Because this was M.T's first treatment, the otolaryngologist decided to inject only the right side to observe her response to the Botox. After one week of a breathy, weak voice, she began to speak without pausing.
After three months, M.T. returned to the Voice Center for a repeat injection because her speech was getting worse with spasms, and she had an increasing need to pause during conversation. At this appointment, she had both sides injected with 1.75 units of Botox, into the cricoarytenoid muscles, and she began speaking in a normal voice (which lasted about six months) after a breathy period of about three weeks.The next treatment was with 1.5 units of Botox (less than the previous dose) injection on each side. The breathy, weak voice lasted about two weeks, and she maintained her normal voice for almost ten months. M.T. returned for treatments whenever her voice problems would become evident again. The longest interval of normal voice for M.T was close to 19 months, after a unilateral (right side) injection of 2.0 units Botox.
Currently, M.T. continues to receive Botox injections to her vocal folds every 9-12 months. Her voice has returned to baseline, but she does notice a gradual return of symptoms as the injections wear off. M.T. states that the quality of her life has improved, as she is no longer afraid to speak.
People with spasmodic dysphonia may become anxious and introverted and avoid speaking in public to avoid embarrassment. They may encounter ridicule from those around them, and the stress and fear they experience may increase tension in the muscles, causing vocal cord spasms. Career advancement, as in the case of singers and public speakers, may be halted because voice use is a necessity in these vocations (NIH, 2010b). Quality of life may be affected because they are reluctant to speak and/or socialize.
Patients affected by voice disorders need understanding and support. Empathetic health care providers can decrease their anxiety and stress, thus decreasing tension of the laryngeal muscles (NIH, 2010b).
The National Spasmodic Dysphonia Association (NSDA) web site (http://www.dysphonia.org) has an online Bulletin Board with an interactive forum for people with SD, a video gallery with information on SD for review, and an online store. The online store offers free brochures on SD and books and videos for purchase. There are support groups, literature, and educational seminars which may be resourced from the website (NSDA, 2013). If there is no support group available in an area, one may be formed with the help of the NSDA.
Spasmodic dysphonia is a focal dystonia involving the laryngeal muscles and vocal cords. The current treatment of choice is Botulinum Toxin injections into the laryngeal muscles. More permanent, surgical treatments are still under research and review. The current treatments for SD are symptomatic. If the quest to find the underlying cause is successful, a cure for the disease may become an easier task for researchers.
Hussain, A., & Shakeel, M. (2010). Selective lateral laser thyroarytenoid myotomy for adductor spasmodic dysphonia. The Journal of Laryngology & Otology, 124(8), 886-891.
Isshiki, N" Yamamoto, I., & Fukagai, S. (2004). Type 2 thyroplasty for spasmodic dysphonia: Fixation using a titanium bridge. Acta Oto-laryngologica, 124(3), 309-312.
Luc, J., & Zieve, D. (2012). Spasmodic dysphonia. Retrieved from http://www.nlm.gov/ medlineplus/ency/article/000753.htm National Institute of Neurological Disorders and Stroke (NINDS). (2011). Dystonias fact sheet. Retrieved from http://www.nmds. nih.gov/disorders/dystonias/detail_ dystonias.htm
National Institutes of Health (NIH), National Institute on Deafness and Other Communication Disorders (NIDCD). (2010a). Spasmodic dysphonia. (NIH Publication No. 10-4214). Retrieved from http://www.nidcd.nih.gov/health/voice/ pages/spasdysp.aspx
National Institutes of Health (NIH), National Institute on Deafness and Other Communication Disorders (NIDCD). (2010b). Stuttering. (NIH Publication No. 10-4232). Retrieved from http:// www.nidcd.nih.gov/health/voice/ pages/stutter.aspx
National Spasmodic Dysphonia Association (NSDA). (2013). Spasmodic dysphonia. Retrieved from http://www.dysphonia .org/spasmodic-dysphonia.php
Pitman, M.J., Kamat, A., Bliznikas, D., & Baredes, S. (2011). Spasmodic dysphonia treatment & management. Retrieved from http:// emedicine.medscape.com/article/864079treatment
Revelo, O., Underbrink, M., & Quinn, F.B. Jr. (2009). Spasmodic dysphonia: Evaluation and management. Retrieved from http://www.researchgate.net/publication/ 239600703_TITLE_Spasmodic_ Dysphonia_Evaluation_and_Management _SOURCE_Grand_Rounds_Presentation _UTM B_Dept._of_Otolaryngology
Yeson Voice Center &Yeson Artceum. (2011). Clinical evaluation of voice. Retrieved from http://www.yesonvc.net/artceum/lx Function_06.asp
Elcy T. Mathew, BSN, RN, CNOR, is a Perioperative Nurse, Operating Room Clinical Manager, ENT, Neurology, Dental, Plastic, and Reconstructive Surgery Departments, Center for Ambulatory Surgery, Hackensack University Medical Center, Hackensack, NJ.
Table 1. Methods Used to Diagnose Spasmodic Dysphonia Electromyography: It is the recording of electrical activity of muscle with the use of an electromyograph machine to diagnose muscle and nerve disorders. Fiber optic laryngoscopy: A procedure done with a flexible lighted scope which is passed through the mouth or nose to view the larynx, vocal cords, and do biopsies if needed Phonatory aerodynamic test: This is a test done to check the air pressure and vibration during speech with the person speaking into a facial mask and tubing attached to machine. The test measures maximum phonation time, mean air flow rate, subglottic pressure, glottal efficiency, glottal resistance, and vital capacity. Videostroboscopy: This is a procedure done with a scope, camera, recording device and a strobe light to record slow motion images of the vocal cords at rest, as well as speech. A strobe light emits synchronized flashes of light to the moving vocal cords at a slower speed to create the image. Vocal Spectrography: This is a recording or picture of sound waves during speech. Source: Adapted from Yeson Voice Center & Yeson Artceum, 2011.
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|Author:||Mathew, Elcy T.|
|Article Type:||Disease/Disorder overview|
|Date:||May 1, 2014|
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