Laryngopharyngeal reflux (LPR) disease and extraesophageal manifestations of gastroesophageal reflux have been recognized to have dramatic effects in the upper airways. Patient-reported symptoms alone underestimate the presence of LPR, making accurate clinical diagnosis difficult. Many previous studies examine populations with only standard dual-probe pH testing that does not include a test probe in the pharynx. Therefore, documentation of acid exposure at the laryngeal inlet is lacking. In adult patients with subglottic stenosis (SGS), whether due to granulomatous disease or presumed idiopathic causes, LPR is often a contributing or causative factor. A retrospective chart review from 1991 to 1999 identified 19 patients with SGS. Ten of the 19 patients had concomitant disease states, including sarcoidosis (3), Wegener's granulomatosis (3), laryngeal trauma (3), and a history of intubation (1). Fourteen patients underwent 24-hour ambulatory pH probe testing with 3- or 4-port probes. The proximal port in either catheter was positioned by manometric guidance directly behind the laryngeal inlet. Measurements of pH of less than 4 were recorded at the level of the larynx in 12 of the 14 patients tested (86%). This finding was noted in half of the patients despite empirical therapy with proton pump inhibitors at the time of the testing. Seven of 10 patients with underlying disease were studied, and all demonstrated acid reflux in the hypopharynx. In 9 patients, the stenosis was presumed to be idiopathic. Five of the 7 patients (71%) with idiopathic SGS tested had positive pH probe studies (pH below 4 in the pharyngeal probe). Our results demonstrate a strong association of LPR and SGS. In the idiopathic group, reflux is the probable cause of their stenosis. In the group of patients with underlying disease states, reflux was involved in all tested patients and likely acts as a synergistic factor that stimulates their granulomatous disease to react and subsequently result in the development of stenosis. Evaluation for LPR with pharyngeal pH testing should be performed in all patients with SGS.

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Abductor, adductor, and combined reinnervation procedures have been explored with variable success rates. We describe the experience of a tertiary care center with adductor reinnervation procedures, including preoperative and postoperative videostroboscopy and electromyography (EMG) findings. A retrospective chart review was performed from 1997 to 2001 that included 9 patients. Preoperative and postoperative voice comparison was performed by 3 blinded speech pathologists. Clinical comparisons of videostroboscopy findings for vocal fold bulk, tone, position, presence of gap, and movement are elucidated. The preoperative and postoperative EMG findings are described. In all patients, preoperative EMG revealed a dense, complete denervation of the affected recurrent laryngeal nerve. No movement was noted on videostroboscopy with persistent glottic gap. Reinnervation involved a nerve-muscle pedicle or a direct neurorrhaphy of the ansa cervicalis to the recurrent laryngeal nerve. Voice improvement was noted between 60 days and 3 months after reinnervation. Four postoperative EMG studies were performed. An early postoperative EMG study at 5 months revealed activation of the lateral cricoarytenoid muscle and thyroarytenoid muscle with head-lift. Videostroboscopy showed excellent near-midline static positioning of the vocal fold. Late EMG studies, performed 12 to 16 months after reinnervation, revealed "learning" of these muscles, with new activation on "eee" phonation. We conclude that recurrent laryngeal nerve reinnervation procedures belong in the armamentarium of the laryngologist for the treatment of vocal fold paralysis. The EMG findings reported in this study suggest that ongoing reinnervation allows for activation with phonation in matured neuronal anastomoses. Overall, this procedure results in excellent patient acceptance and near-normal vocal quality.

Laryngeal synkinesis involves the misdirected reinnervation of an injured recurrent laryngeal nerve to vocal fold abductor and adductor musculature. The resultant laryngeal dyscoordination can cause vocal fold immobility and airway compromise. Although this entity is sometimes considered in the differential diagnosis, it is only demonstrable with laryngeal electromyography (EMG). We propose a new EMG definition of synkinesis to assist in its identification during workup of vocal fold immobility. A retrospective chart review from 1992 to 1997 in the Voice Disorders Clinic identified 10 patients with laryngeal synkinesis. Five patients had bilateral immobility, and 5 had unilateral immobility. Monopolar EMG was performed on all patients. Fine-wire EMG was performed when monopolar EMG did not elucidate the cause of the immobility. The EMG studies revealed synkinetic reinnervation in all subjects. On the basis of the EMG results, 7 of the 10 patients were treated with botulinum toxin to weaken the undesired reinnervation. Three of the 7 patients had benefit from this therapy. Laryngeal synkinesis should be considered as part of the differential diagnosis of vocal fold immobility. Awake laryngeal EMG is the only method to demonstrate synkinesis of the larynx. The diagnosis of synkinesis is clinically significant in cases of immobility to identify patients who might benefit from botulinum toxin therapy. Additionally, the presence of synkinesis in cases of unilateral immobility may be a contraindication to laryngeal reinnervation procedures. The benefit of botulinum toxin therapy is likely greater in the treatment of bilateral as opposed to unilateral immobility.

Although perceptual and stroboscopic data help in diagnosing and classifying laryngeal dystonia, these measures do not aid the voice clinician in targeting which specific muscles to treat with botulinum toxin. Most patients achieve smoother, less effortful voicing with standard injection regimens. However, there is a notable failure rate. We performed fine-wire electromyography on 214 consecutive patients with laryngeal dystonia. We correlated voice ratings, stroboscopy data, and fine-wire electromyography data. Videostroboscopy was successful in visually demonstrating most of the audible findings in isolated vocal tremor, but it was much less successful in identifying breaks alone or a combination of breaks and tremor. Fine-wire electromyography revealed that the thyroarytenoid muscle was significantly more likely than the lateral cricoarytenoid muscle to be the predominant muscle associated with adductor spasmodic dysphonia, and that the thyroarytenoid and lateral cricoarytenoid muscles were equally likely to be predominantly involved in tremor spasmodic dysphonia. In addition, several patients in both the adductor spasmodic dysphonia and the tremor spasmodic dysphonia groups presented with interarytenoid muscle predominance. All of the intrinsic laryngeal muscles are capable of being the predominant muscle in laryngeal dystonia, and there are patterns of muscle abnormalities that differ between adductor spasmodic dysphonia and tremor spasmodic dysphonia. Some of the failures in treating adductor spasmodic dysphonia with botulinum toxin, and the greater difficulty with success in treating patients with tremor spasmodic dysphonia, are due to failure to deliver toxin to the appropriate muscles.