This further adds to the difficulty in achieving accurate diagnosis. Whispering dysphonia
A fourth type has also been described. This appears to be caused by mutations in the TUBB4 gene on the short arm of chromosome 19 (19p13.2-p13.3). This gene encodes a tubulin gene. The pathophysiology of this condition has yet to be determined. Treatment
There are a number of potential treatments for spasmodic dysphonia, including Botox, voice therapy, and surgery. A number of medications have also been tried including anticholinergics (such as benztropine) which have been found to be effective in 40-50% of people, but which are associated with a number of side effects. Botulinum toxin
Botulinum toxin (Botox) is often used to improve some symptoms of spasmodic dysphonia through weakening or paralyzing the vocal folds, thus preventing muscle spasms. The level of evidence for its use is currently limited; little is known about optimal dosage, frequency of injections, or exact location of injection. However, it remains a choice for many people due to the predictability and low chance of long term side effects. It results in periods of some improvement, with the duration of benefit lasting for 10–12 weeks on average before symptoms return to baseline. Repeat injection is required to sustain good vocal production, as results are only temporary. Some transient side effects observed in adductor spasmodic dysphonia include reduced speaking volume, difficulty swallowing, and a breathy and hoarse voice quality. While treatment outcomes are generally positive, it is presently unclear whether this treatment approach is more or less effective than others.
The pathophysiology underlying dystonia is becoming better understood as a result of discoveries about genetically based forms of the disorder, and this approach is the most promising avenue to a long-term solution.SD is classified as a neurological disorder. However, because the voice can sound normal or near normal at times, some practitioners believe it to be psychogenic; that is, originating in the affected persons mind rather than from a physical cause. This was especially true in the 19th and 20th centuries. No medical organizations or groups take this position. A comparison of SD patients compared with vocal fold paralysis (VFP) patients found that 41.7% of the SD patients met the DSM-IV criteria for psychiatric comorbidity compared with 19.5% of the VFP group. However, another study found the opposite, with SD patients having significantly less psychiatric comorbidity compared to VFP patients: "The prevalence of major psychiatric cases varied considerably among the groups, from a low of seven percent (1/14) for spasmodic dysphonia, to 29.4 percent (5/17) for functional dysphonia, to a high of 63.6 percent (7/11) for vocal cord paralysis." A review in the journal Swiss Medicine Weekly states that "Psychogenic causes, a psychological disequilibrium, and an increased tension of the laryngeal muscles are presumed to be one end of the spectrum of possible factors leading to the development of the disorder".