Vocal fold paralysis (VFP) refers to neurological causes of reduced or absent movement of one or both vocal folds. Bilateral VFP (BVFP) is characterized by inspiratory dyspnea due to narrowing of the airway at the glottic level with both vocal folds assuming a paramedian position. The primary objective of intervention for BVFP is to relieve patients’ dyspnea. Common clinical options for management include tracheostomy, arytenoidectomy and cordotomy. Other options that have been used with varying success include reinnervation techniques and botulinum toxin (Botox) injections into the vocal fold adductors. More recently, research has focused on neuromodulation, laryngeal pacing, gene therapy, and stem cell therapy. These newer approaches have the potential advantage of avoiding damage to the voicing mechanism of the larynx with an added goal of restoring some physiologic movement of the affected vocal folds. However, clinical data are scarce for these new treatment options (i.e., reinnervation and pacing), so more investigative work is needed. These areas of research are expected to provide dramatic improvements in the treatment of BVFP.

Electrical stimulation of the posterior cricoarytenoid (PCA) muscle, when paced with inspiration, offers a physiologic approach to restore ventilation in bilateral laryngeal paralysis without any of the disadvantages associated with conventional treatment. In an eighteen-month prospective study, six patients were successfully implanted with an Itrel ® II stimulator (Medtronic, Inc). In post-operative sessions, stimulated vocal fold abduction, patient ventilation, and voice were assessed and compared to pre-operative values. The optimum stimulus paradigm was a 1-2 second train of 1 millisecond pulses delivered at a frequency of 30-40 hertz and amplitude of 2-7 volts. PCA stimulation produced a large dynamic abduction (3.5 to 7 mm) in three patients and moderate abduction (3 mm) in a fourth patient. The fifth patient showed a large but delayed response of 4 mm to stimulation with some lateralization of the vocal fold. In the sixth patient, stimulated abduction was noted upon device implantation but lost postoperatively. All five patients with stimulated abduction postoperatively met the ventilatory criteria for decannulation, and three patients were subsequently decannulated. Chronic stimulation of the PCA muscle had no appreciable effect on voice quality. Electrical stimulation of the PCA muscle shows potential as an improved therapy for bilateral vocal fold paralysis.

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Objectives-An in-vivo rabbit model was used to study the effect of three hours of experimental induced phonation on messenger RNA expression of the normal vocal fold.Study Design-Prospective; animal model. Subjects and Methods-Ten rabbits received experimental phonation for three hours, followed by one hour of recovery. A separate group of five rabbits served as no-phonation controls. We measured messenger RNA expression of matrix metalloproteinase -1, -9, and interleukin-1β using real-time reverse transcribed polymerase chain reaction. Gene expression ratios from phonation and control animals were compared using the Mann Whitney U test.Results-Phonation (77 +/− 3 dB; 429 +/−141 Hz) resulted in increased matrix metalloproteinase -1 gene expression from rabbits receiving experimental phonation compared to controls, and a non-significant increase in matrix metalloproteinase -9 and interleukin-1β gene expression. Conclusion-Matrix metalloproteinases play a role in maintaining tissue homeostasis.Investigation of cellular responses to experimental phonation may provide insight into how matrix metalloproteinases and other extracellular matrices contribute to maintenance of the vocal fold and development of pathology.

Objectives/Hypothesis Our laboratory has developed an in vivo rabbit model to investigate the effects of phonation on expression and turnover of the vocal fold extracellular matrix. As a logical outgrowth of this research to include phonotrauma in the present study, we investigated the hypothesis that an increase in airflow rate delivered to the glottis produces a change in glottal configuration and an increase in mean phonation intensity. Study Design Prospective animal study. Methods Six New Zealand white breeder rabbits weighing 3 to 5 kg were used in this study. A rigid endoscope and camera were used to document glottal configuration. Acoustic signals of modal and raised phonation were recorded and digitized. Two separate one-way repeated measures analysis of variance (ANOVA) tests were used to investigate within subject differences in phonation intensity and fundamental frequency between modal and raised phonation. Results Phonation intensity was 54.19 dB SPL (6.21 standard deviations [SD]) during modal phonation, and 60.31 dB SPL (5.68 SD) during raised phonation. Endoscopic images revealed a convergent glottis, with greater separation of the vocal folds during raised phonation. Results of ANOVA revealed a significant within subjects effect for phonation intensity (P = .011). Pairwise comparisons revealed that phonation intensity increased significantly during raised phonation, compared to modal phonation (P = .008). No differences in mean fundamental frequency were observed between phonation conditions. Conclusions Improved understanding of factors that control phonation output in the in vivo rabbit model will result in improved capabilities to match phonation dose across animals and provide immediate direction to future biochemical studies.

Objectives We describe a method for eliciting phonation in an in vivo rabbit preparation using low-frequency, bipolar pulsed stimulation of the cricothyroid muscles with airflow delivered to the glottis. Methods Ten New Zealand White breeder rabbits weighing 3 to 5 kg were used in this study. The cricothyroid muscles were isolated bilaterally, and separate pairs of anode-cathode hooked-wire electrodes were inserted into each muscle. A Grass S-88 stimulator and 2 constant-current PSIU6 isolation units were used to deliver bipolar square wave pulses to each cricothyroid muscle, with airflow delivered to the glottis through a cuffed endotracheal tube. Results Phonation was evoked with a 50-Hz, 4-mA stimulus train of 1-ms pulses delivered to each cricothyroid muscle. The pulse trains were on for 2 seconds and were repeated every 5 seconds over a period of 180 minutes. Airflow was delivered at 143 cm3/s, producing phonation measuring 71 to 85 dB sound pressure level. Conclusions Evoked phonation is feasible in rabbits by use of bipolar stimulation of the cricothyroid muscles with airflow delivered to the glottis. The in vivo rabbit preparation described may provide a useful small animal option for studies of evoked phonation. From the level and consistency of the adduction observed, we hypothesize that current spreading to the underlying adductor muscles and nerves resulted in neural pathway involvement beyond discrete activation of the cricothyroid muscle, providing sufficient approximation of the vocal folds for phonation.

Inflammation of the facial nerve in Bell's palsy can be demonstrated on gadolinium-enhanced magnetic resonance imaging. We have studied a series of 17 Bell's palsy patients with gadolinium-enhanced magnetic resonance imaging, and the purpose of this paper is to report our findings and discuss their significance. Most acute Bell's palsy cases demonstrate facial nerve enhancement, usually in the distal internal auditory canal and labyrinthine/geniculate segments. Other segments demonstrate enhancement less often. Gadolinium enhancement occurs regardless of the severity of the paralysis and can persist after clinical improvement of the paralysis. The findings of this study corroborate other evidence that the segments of the facial nerve most often involved in Bell's palsy are the only segments that are most often enhanced with gadolinium-enhanced magnetic resonance imaging. The role of gadolinium-enhanced magnetic resonance imaging in the management of Bell's palsy patients is discussed.

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