By Lyn Dee Harrelson
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.
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:
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. |
| AbSD | · Delay in voice onset time following production of
voiceless consonants · Episodes of voice interruption |
· Random variation of amplitude | · High air flows |
