NORMAL PHYSIOLOGY, PATHOPHYSIOLOGY, AND TREATMENT OF VOICE DISORDERS

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Studies of neurotransmitters involved in the laryngeal sensori-motor pathways are being conducted. The regions in the medulla previously identified as functionally involved in the laryngeal glottic closure reflex were studied to determine which excitatory amino acid receptors play a role in this reflex. The distribution of AMPA-selective glutamate receptor subunits (GluR1-GluR4) and the NMDA receptor subunit NMDAR1 were also studied. Staining for all the antibodies were found in the nucleus tractus solitarius. However, the concentration of GluR1 was significantly greater than NMDAR1 or GluR4 in the interstitial subnucleus, a region previously found associated with laryngeal closure reflex responses. A study was also completed which examined the pattern of muscle activity in the thyroarytenoid muscle in patients with vocal fold paralysis either of idiopathic origin or following nerve injury. All patients had persistent paralysis with thyroarytenoid muscle reinnervation. To examine for evidence of synkinesis, bipolar electrode recordings were made of thyroarytenoid muscle activation during respiration and phonation. In all but one patient muscle activation was normal in amplitude and pattern of activation for respiration and phonation. These results suggest that the thyroarytenoid muscle was not affected by synkinesis. Other muscles and joint fixation need to be evaluated to determine the basis for the persistent paralysis despite reinnervation. To evaluate changes in pathophysiology following botulinum toxin injection in patients with adductor spasmodic dysphonia, thyroarytenoid and cricothyroid muscle bursting on both sides of the larynx were studied during sentence production in patients before, and several weeks after, unilateral thyroarytenoid botulinum toxin injection. The levels of muscle tone and muscle bursts were significantly reduced in both thyroarytenoid and cricothyroid muscles on both sides of the larynx indicating that the central mechanisms involved in symptom generation were altered following botulinum toxin injection.