Hi! I'm a second year Speech-Language Pathology Student at McGill University![1]

What else is known about "whispering dysphonia"? I'd like to look into this further. Additionally, I'd like to research more information pertaining to epidemiology, and perhaps introduce a quality of life section for individuals with SD. Finally, I'm curious about what else is known regarding pathophysiology of SD, and potential structural changes in the brain. Feedback is always welcome! ~~~~

Spasmodic dysphonia is a disorder characterized by a change in function of the muscles of the larynx, contributing to changes in voice during speech^[1].

Find citation: It is commonly reported by people with spasmodic dysphonia that symptoms almost only occur on vocal/speech sounds that require phonation.

Find citation: However, a recent study that examined the mutation of these three genes in 86 SD patients found that only 2.3% of the patients had novel/rare variants in THAP1 but none in TUBB4A and TOR1A.^[2]

Find citation: 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 person's mind rather than from a physical cause. This was especially true in the 19th and 20th centuries.^[3] No medical organizations or groups take this position.

Find citation: "As a result, the voices of these individuals often sound weak, quiet, and breathy or whispery." -->speech can also be effortful; less is known about ABSD than ADSD

Recent studies are looking into the effects of basal ganglia function on vocal folds.^[4]

Edit: The three types of spasmodic dysphonia (SD) are adductor spasmodic dysphonia, abductor spasmodic dysphonia, and mixed spasmodic dysphonia. A fourth type, whispering dysphonia, has also been proposed.

Adductor spasmodic dysphonia (ADSD) is the most common type, affecting around 87% of individuals with SD.^[3] As the name suggests, these spasms occur in the adductor muscles of the vocal folds, specifically the thyroarytenoid and the lateral cricoarytenoid.^[5]

ABSD - second most common affecting about 13% of cases.^[3] As the name suggests, these spasms occur in the single abductor muscle of the vocal folds, called the posterior cricoarytenoid.

Mixed is the most rare^[3]. Some researchers believe that a subset of cases classified as mixed Spasmodic Dysphonia are actually AD or AB subtype with compensatory behaviours that make it appear mixed.^[3] This further adds to the difficulty in accurate diagnosis.

aerodynamic measures may be used to differentiate subtypes.^[6]

It has been suggested that significant performance differences on sustained tasks and connected speech tasks in SD and MTD may help to differentiate these disorders.^[7]

One way to help differentiate between SD and MTD is to assess the contexts in which the symptoms, such as voice breaks, occur; SD symptoms are typically seen during specific speech tasks, whereas MTD symptoms are noticed more generally across all contexts.^[3]

Botulinum toxin (Botox) is often used to improve some symptoms of spasmodic dysphonia through weakening or paralyzing the vocal folds, thus preventing muscle spasms.^[5]

Botox injections are best used for treatment of ADSD compared to other types of SD.^[8] This is because it can target adductor muscles, which draw the vocal folds together, thus weakening them and preventing spasms. Targeting abductor muscles, which draw vocal folds apart, can be more dangerous as it can cause airway blockage if the muscles weaken and do not open the airway sufficiently.

Is this treatment method still "unknown effectiveness"? - find review

Mixed AB-AD can be difficult to manage as it has features of both types of SD.^[6]

If other measures are not effective, surgery may be considered; however, evidence to support surgery as a treatment for SD is limited. Like with Botox, treatment outcomes are generally positive, though more research is required to determine its effectiveness. Surgical approaches include recurrent laryngeal nerve resection, selective laryngeal adductor denervation-reinnervation (SLAD-R), thyroplasty, thyroarytenoid myectomy, and laryngeal nerve crush.^[5] As of 2011, surgery was rarely used as a treatment approach for SD.

This involves removing a section of the recurrent laryngeal nerve.^[9] Recurrent laryngeal nerve avulsion is a more drastic removal of sections of the nerve,^[9] and has positive outcomes of 80% at three years.

SLAD-R is effective specifically for adductor spasmodic dysphonia, and has shown good outcomes in about 80% of people at 8 years

This approach ultimately changes the position or length of the vocal folds. After thyroplasty there is an increase in both objective and subjective measures of speech

One operation that may be done is known as recurrent laryngeal nerve resection. Another is "selective laryngeal adductor denervation-rennervation (SLAD-R)" is effective specifically for adductor spasmodic dysphonia which has shown good outcomes in about 80% of people at 8 years. Post-surgery voices can be imperfect and about 15% of people have significant difficulties. If symptoms do recur this is typically in the first 12 months. Another operation called "recurrent laryngeal nerve avulsion" has positive outcomes of 80% at three years.

Another surgical option is a thyroplasty, which ultimately changes the position or length of the vocal folds. After thyroplasty there is an increase in both objective and subjective measures of speech.

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