How i do it: Head and neck and plastic surgery: A targeted problem and its solution a method for the treatment of abductor spasmodic dysphonia with botulinum toxin injections: A preliminary report

Rontal, Michael; Rontal, Eugene; Rolnick, Michael I.; Merson, Richard M.; Silverman, Bruce; Truong, Daniel

doi:10.1288/00005537-199108000-00019

Cited by 22 publications

(1 citation statement)

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“…This type affects at least 80% of persons with SD and disrupts sentences like, “we e at e ggs e very d a y” (Erickson, 2003). The abductor type is rarer with uncontrolled spasms in the vocal fold opening (abductor) muscle resulting in breathy bursts when attempting to start voice after voiceless consonants such as /s/, /f/, /h/, /p/, /t/, and /k/ (Rodriquez et al, 1994) and disrupts sentences such as, “ h e h ad h alf a h ead of h air” (Rontal et al, 1991). Rarely, both types occur in one person.…”

Section: Introductionmentioning

confidence: 99%

Spasmodic Dysphonia: a Laryngeal Control Disorder Specific to Speech: Figure 1.

Ludlow¹

2011

J. Neurosci.

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Spasmodic dysphonia (SD) is a rare neurological disorder that emerges in middle age, is usually sporadic, and affects intrinsic laryngeal muscle control only during speech. Spasmodic bursts in particular laryngeal muscles disrupt voluntary control during vowel sounds in adductor SD and interfere with voice onset after voiceless consonants in abductor SD. Little is known about its origins; it is classified as a focal dystonia secondary to an unknown neurobiological mechanism that produces a chronic abnormality of laryngeal motor neuron regulation during speech. It develops primarily in females and does not interfere with breathing, crying, laughter, and shouting. Recent postmortem studies have implicated the accumulation of clusters in the parenchyma and perivascular regions with inflammatory changes in the brainstem in one to two cases. A few cases with single mutations in THAP1, a gene involved in transcription regulation, suggest that a weak genetic predisposition may contribute to mechanisms causing a nonprogressive abnormality in laryngeal motor neuron control for speech but not for vocal emotional expression. Research is needed to address the basic cellular and proteomic mechanisms that produce this disorder to provide intervention that could target the pathogenesis of the disorder rather than only providing temporary symptom relief.

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Section: Introductionmentioning

confidence: 99%