Kinaesthetic Loss as a Marker for Spasmodic Dysphonia

University Of Minnesota, Minneapolis MN

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Abstract

DESCRIPTION (provided by applicant): Spasmodic dysphonia (SD) is a voice disorder characterized by involuntary movement of laryngeal muscles that leads to voice breaks and a strained or strangled voice quality, and which can severely impair communication. SD is believed neurogenic in origin and shares some symptoms with focal dystonia (FD) of the head and neck. The diagnosis of SD has been proven to be difficult, because it often presents with symptoms similar to muscle-tension dysphonia (MTD). MTD is caused by abnormal phonation believed to be in response to swelling of vocal fold tissue. Misdiagnosis is not uncommon and can lead to inappropriate treatment. SD is treated primarily with botulinum toxin injections while MTD is treated with behavioral therapy. The current gold standard of diagnosis uses an elaborate, time-intensive, and costly 3-step approach involving questionnaire, a clinical-perceptual evaluation, and a nasoendoscopic evaluation. Recent research documented that patients with focal dystonia affecting head and neck musculature, such as blepharospasm and torticollis, reveal kinaesthetic deficits in the non-dystonic musculature of their upper limbs suggesting a central origin of these disorders. Thus, the central idea behind this proposal is to examine, if SD also presents with kinaesthetic deficits in non-dystonic limb systems that are clinically symptom-free. This link has never been established, but is suggested by our pilot data. If, in contrast, MTD patients have normal limb kinaesthesia, then kinaesthetic loss would be a potential marker for SD that could help to differentiate between SD and MTD. Our approach would be to examine kinaesthetic acuity by determining precise psychophysical thresholds for detecting arm motion or for discriminating between arm motion stimuli - a procedure that has never been applied to SD patients. The scientific impact of linking SD to a general kinaesthetic deficit would be increased evidence that FD and SD share a similar pathomechanism that alters the central process of integrating peripheral proprioceptive information with volitional motor commands. The health significance of showing that SD but not MTD is associated with a general kinaesthetic loss is that it opens the avenue to develop easy-to-administer, standardized, time-efficient clinical tests for the diagnosis of SD (and FD) that complements the current diagnostic arsenal and reduces the risk of a misdiagnosis.