Neurological Concomitants in Spasmodic Dysphonia
By Lyn Dee Harrelson

spasmodic dysphonia

To first understand the basis for the research behind the neurological concomitants in spasmodic dysphonia, it is important to understand what is known about the etiology, effects, and characteristics of spasmodic dysphonia.


What is spasmodic dysphonia (SD)?

Spasmodic dysphonia (SD) is a voice disorder that impacts the function of the musculature associated with the larynx. Usually, there is no atrophy of the muscles involved, however, the muscles tend to be uncontrollably tense. SD can manifest as either adduction (opened), abduction (closed), or mixed adduction-abduction of the vocal folds. Research has proven that SD involves not only the intrinsic laryngeal muscles, but also the involvement of the ventricular folds and extrinsic laryngeal muscles. The etiology behind SD is controversial. Research supports the SD as having a neurological substrate with additional components (i.e., psychologic). SD is classified as a dystonia, meaning the manifestations of SD originate in the basal ganglia and/or extrapyramidal tract (indirect activation pathways) of the brain. The basal ganglia serves as a control station. With SD, there is a breakdown in the input processing system causing either hyper or hypo function of the laryngeal muscles. SD is referred to as a focal dystonia. This is because of the acute localization of spastic symptoms located in the laryngeal muscles due to malfunction in neurological processing.

Adductor Spasmodic Dysphonia

Simply put, adductor spasmodic dysphonia (AdSD) is when the vocal folds are closed and do not allow the release of air pressure to create normal voicing.

Abductor Spasmodic Dysphonia

Abductor spasmodic dysphonia (AbSD) is characterized as breathy dysphonia. The uncontrollable spastic reactions of the vocal folds tend to cause the vocal folds to remain open during voicing.

What causes SD?

The etiology is unknown. The more common consensus suggests that SD has a neurological base and manifests in combination with other factors to manifest the characteristics of SD. Some of the reported triggering incidences are physical illness, stress, and emotional trauma. These inscidences usually are not the cause of this organic problem associated with the malfunction of the basal ganglia, but these inscidences tend to exacerbate the symptoms of SD.

Other resources:

UNC ENT - Spasmodic Dysphonia

What are the perceptual characteristics of SD?

In 1871, Traube first described SD as "a spastic form of nervous hoarseness". The perceptual characteristics of SD continue to manifest in the same manner, but Colton and Casper (1996) have incorporated other perceptual signs that are characteristic of either AbSD and/or AdSD.

  Perceptual Acoustic Physical
AdSD · Strain/struggle
· Sudden interruption of voicing
· Tension
· Loudness and pitch variations
· Pitch breaks
· Stoppages of phonation (primarily with vowels)

· Greater variation in fundamental frequency
· Increased subglottal air pressures.
·Low air flows

· Hyperadduction of the vocal folds, and/or quick or slow movements of the true vocal folds.
· Normal looking structure
· Function can vary from patient to patient.

AbSD · Delay in voice onset time following production of voiceless consonants
· Episodes of voice interruption
· Random variation of amplitude · High air flows

Spasmodic Dysphonia Neurological Concomitants Differential Diagnosis Treatment Links