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The goal of the experiment was to study whether an inflammatory response can cause changes in central nervous system (CNS) vocal fold control to provide insight on the onset of spasmodic dysphonia. Spasmodic dysphonia is an idiopathic voice disorder that affects motor-control of laryngeal muscles during speech[1]. Onset of the disorder occurs gradually during midlife, and approximately one third of patients associate its manifestation with an upper respiratory tract infection[2]. Adductor spasmodic dysphonia (ADSD) is the most common form of spasmodic dysphonia, identified by hyperadduction of the vocal folds that cause phonatory breaks during vowels[1]. These movements are attributed to involuntary thyroarytenoid (TA) muscle bursts[3].

Electrical stimulation of the internal branch of the superior laryngeal nerve (ISLN) can elicit the laryngeal adductor reflex, characterized by an ipsilateral R1 response and a bilateral R2 response[4]. When stimuli are presented in pairs, the second responses are generally reduced in amplitude. This conditioning effect is a result of inhibitory mechanisms in the neural pathway that controls the reflex[5]. It is thought that, normally, suppression of adductor responses to multiple stimuli prevents reflexive spasms from disrupting speech. This is supported by the finding that patients with ADSD have reduced or no suppression after a second stimuli[5].

For the experiment, we sought to reproduce the conditions of an upper respiratory tract infection in a rat model. The experimental group received an injection of lipopolysaccharide (LPS) to the thyroarytenoid (TA) muscle of the larynx, an agent known to elicit an inflammatory response. The control groups received either pre-treatment with IL-1 receptor antagonist before the LPS injection, a saline injection, or no treatment. Pre-treatment with an IL-1b receptor antagonist was designed to block the CNS responses to the LPS and test the influence of only local inflammation on the adductor reflex. Similarly, the saline injection control examined the effect of tissue damage caused by the injection on the laryngeal reflexes. Electrical stimulation of the ISLN was used to test the laryngeal reflex. Stimuli were presented in pairs of equal intensity with varying inter-stimulus intervals (ISI) and the muscle responses were recorded by electromyography. For this project, I marked R2 responses on the EMG recordings of TA muscle activity and ran a statistical analysis to compare responses across groups. I looked for differences in response amplitude, latency and duration which would indicate a change in muscle enervation.

1. Rubin, J.S., R.T. Sataloff, and G.S. Korovin, Diagnosis and treatment of voice disorders. 3rd ed. 2006, San Diego: Plural Pub. xviii, 815 p.

2. Aronson, A.E., Clinical voice disorders, an interdisciplinary approach. 1980, New York: B. C. Decker. ix, 261 p.

3. Shipp, T., et al., Intrinsic laryngeal muscle activity in a spastic dysphonia patient. J Speech Hear Disord, 1985. 50(1): p. 54-9.

4. Ludlow, C.L., F. Van Pelt, and J. Koda, Characteristics of late responses to superior laryngeal nerve stimulation in humans. Ann Otol Rhinol Laryngol, 1992. 101(2 Pt 1): p. 127-34.

5. Ludlow, C.L., et al., Abnormalities in long latency responses to superior laryngeal nerve stimulation in adductor spasmodic dysphonia. Ann Otol Rhinol Laryngol, 1995. 104(12): p. 928-35.

Last updated November 16, 2007