Treatment of adductor spasmodic dysphonia with selective laryngeal adductor denervation and reinnervation surgery.
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Biomedical subjects
Publications and source records attributed to Gerald S Berke.
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OBJECTIVE: To examine the antigenic distribution of human leukocyte antigens (HLA) of the human larynx. STUDY DESIGN AND SETTING: Twelve human larynges were examined for Class I (HLA-A, -B, -C) and Class II (HLA-DR) histocompatibility antigens using mouse monoclonal antibodies in an indirect immunoperoxidase assay. Structures of the larynx and surrounding tissues were examined and given a semiquantitative score based on HLA Class I and II expression. RESULTS: The mucosal surface epithelium of the larynx stains 2+ or stronger for HLA Class I antigens and 1+ for Class II antigens. The deeper submucosal glands stain 1+ for Class I antigens and 2+ or stronger for Class II antigens. Thyroid cartilage showed 2+ or stronger staining of the chondrocytes for Class I antigens only. Thyroid follicular cells also stain only for Class I antigens. Perichondrium and Schwann cells of nerves stain stronger for Class I antigens than Class II antigens. Cartilage matrix, muscle cells, and axons of nerves do not stain for either class of antigens. Endothelium stains 3+ for both classes of antigens. CONCLUSIONS: The detailed distribution of major transplantation antigens in the human larynx is elucidated. Class II antigens implicated as initiators of organ transplant rejection were primarily found in 6 areas: mucosal surface epithelium, submucosal glands, ducts, vascular endothelium, perichondrium, and Schwann cells of nerves. The relevance of these findings to the initiation and detection of laryngeal allograft graft rejection is discussed.
OBJECTIVE: Eagle's syndrome (ES) or symptomatic elongated styloid process is an uncommon but important cause of chronic head and neck pain. This study reports our experience in the diagnosis and treatment of a series of patients with ES. STUDY DESIGN: Patient histories, radiographic tests, and operative reports of 3 patients over a 3-month period were prospectively collected. SETTING: Tertiary referral otolaryngology service. RESULTS: All patients had resolution of symptoms relating to their elongated styloid processes after surgical resection. CONCLUSION: Although sometimes clouded by coexisting symptoms, ES can be easily diagnosed based on good history taking and physical examination. If diagnosed appropriately, surgical treatment can be administered promptly. SIGNIFICANCE: Patients with ES commonly have a long history of chronic pain treated by multiple physicians. Appropriate diagnosis can lead to prompt treatment of this condition. EBM RATING: C-4.
Selective laryngeal adductor denervation-reinnervation surgery for the treatment of adductor spasmodic dysphonia was reported in 1999 in 21 patients with encouraging results. Here, we report long-term results of this procedure. Surgical outcome was evaluated using patient surveys and perceptual voice assessment. Measured outcomes included Voice Handicap Index (VHI)-10 scores, patient questionnaire, and perceptual evaluation for voice breaks and breathiness. Patient survey was obtained from 83 patients, and perceptual voice evaluation was performed in voice samples from 46 patients. Average follow-up interval was 49 months. Mean VHI-10 scores improved from a mean of 35.6 to 12.7. Eighty-three percent showed significantly improved VHI-10 scores, representing improved physical, social, and emotional well-being. There was a high degree of patient satisfaction, with 91% agreeing that their voice is more fluent after the surgery. Perceptual evaluation of postoperative voice samples revealed voice breaks in 26% (15% mild, 4% moderate, 7% severe) and breathiness in 30% (11% mild, 13% moderate, 6% severe). A majority of patients had stable, long-lasting resolution of spasmodic voice breaks.
OBJECTIVE: Knowledge of the location of the muscular process of the arytenoid cartilage and the recurrent laryngeal nerve is essential to performing a successful arytenoid adduction and laryngeal reinnervation surgery. We describe external landmarks useful in locating these structures. STUDY DESIGN: Cadaveric laryngeal dissection. METHODS: Posterior laryngeal dissection was performed in 16 human larynges. The position of the muscular process of the arytenoid was measured bilaterally relative to the inferior and superior borders of the thyroid lamina. The recurrent laryngeal nerve was followed distally from slightly below the level of the cricothyroid joint to its genu where its vertical course changes to an oblique intralaryngeal course. RESULTS: The muscular process of the arytenoid was usually found halfway between the roots of the superior and inferior cornu of the thyroid lamina. The recurrent laryngeal nerve was found just deep to the cricothyroid joint and lateral to the posterior cricoarytenoid muscle. There were no other nerves in this area. CONCLUSIONS: This study finds that the superior and inferior borders of the thyroid lamina are useful intraoperative landmarks to locate the muscular process of the arytenoid. The cricothyroid joint provides a good starting point to locate the recurrent laryngeal nerve, which can be identified slightly deeper between it and the posterior cricoarytenoid muscle.
OBJECTIVES/HYPOTHESIS: The purpose of this study was to measure the medial surface dynamics of a canine vocal fold during phonation. In particular, displacements, velocities, accelerations, and relative phase velocities of vocal fold fleshpoints were reported across the entire medial surface. Although the medial surface dynamics have a profound influence on voice production, such data are rare because of the inaccessibility of the vocal folds. STUDY DESIGN: Medial surface dynamics were investigated during both normal and fry-like phonation as a function of innervation to the recurrent laryngeal nerve for conditions of constant glottal airflow. METHODS: An in vivo canine model was used. The larynx was dissected similar to methods described in previous excised hemilarynx experiments. Phonation was induced with artificial airflow and innervation to the recurrent laryngeal nerve. The recordings were obtained using a high-speed digital imaging system. Three dimensional coordinates were computed for fleshpoints along the entire medial surface. The trajectories of the fleshpoints were preprocessed using the method of Empirical Eigenfunctions. RESULTS: Although considerable variability existed within the data, in general, the medial-lateral displacements and vertical displacements of the vocal fold fleshpoints were large compared with anterior-posterior displacements. For both normal and fry-like phonation, the largest displacements and velocities were concentrated in the upper medial portion. During normal phonation, the mucosal wave propagated primarily in a vertical direction. Above a certain threshold of subglottal pressure (or stimulation to the recurrent laryngeal nerve), an abrupt transition from chest-like to fry-like phonation was observed. CONCLUSIONS: The study reports unique, quantitative data regarding the medial surface dynamics of an in vivo canine vocal fold during phonation, capturing both chest-like and fry-like vibration patterns. These data quantify a complex set of dynamics. The mathematical modeling of such complexity is still in its infancy and requires quantitative data of this nature for development, validation, and testing.
Quantitative measurement of the medial surface dynamics of the vocal folds is important for understanding how sound is generated within the larynx. Building upon previous excised hemilarynx studies, the present study extended the hemilarynx methodology to the in vivo canine larynx. Through use of an in vivo model, the medial surface dynamics of the vocal fold were examined as a function of active thyroarytenoid muscle contraction. Data were collected using high-speed digital imaging at a sampling frequency of 2000 Hz, and a spatial resolution of 1024 x 1024 pixels. Chest-like and fry-like vibrations were observed, but could not be distinguished based on the input stimulation current to the recurrent laryngeal nerve. The subglottal pressure did distinguish the registers, as did an estimate of the thyroarytenoid muscle activity. Upon quantification of the three-dimensional motion, the method of Empirical Eigenfunctions was used to extract the underlying modes of vibration, and to investigate mechanisms of sustained oscillation. Results were compared with previous findings from excised larynx experiments and theoretical models.
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OBJECTIVES: To develop a canine model of vocal fold scar and to evaluate its treatment with lamina propria replacement therapy using autologous cultured fibroblasts. MATERIALS AND METHODS: Full thickness of the lamina propria layer in canine vocal folds was injured with a laser. Fibroblasts were cultured and expanded in the laboratory from a buccal mucosal biopsy. The scarred vocal folds were treated with 3 weekly injections of fourth, fifth, and sixth passage autologous fibroblasts. Mucosal waves and acoustic parameters were measured at baseline, after scarification, and several months after injection therapy. Histologic evaluation of the vocal folds for fibroblasts, collagen, elastin, reticulin, and hyaluronic acid was performed. RESULTS: Nine beagle dogs were used, and 1 animal served as control. Vocal fold scarring resulted in absent or severely limited mucosal waves and significantly worse acoustic parameters. Significant improvements in mucosal waves and acoustic parameters were obtained after lamina propria replacement therapy. After therapy, mucosal waves became normal in 4 animals and near normal in the other 4. No statistical difference was found in mucosal waves between baseline and post-therapy. All animals tolerated therapy without complications. The treated vocal folds demonstrated an increased density of fibroblasts, collagen, and reticulin, a decreased density of elastin, and no change in hyaluronic acid. CONCLUSIONS AND SIGNIFICANCE: Therapeutic options for vocal fold scars are limited. Lamina propria replacement therapy in the form of autologous cultured fibroblasts improves mucosal pliability and returns normal or near normal mucosal waves in experimentally scarred vocal folds. This novel therapeutic modality may hold new promise for treating vocal fold scars.
The ideal injectable agent for vocal fold medialization is biocompatible, durable, sized to prevent phagocytosis and migration, and formulated for easy injection and does not adversely affect the viscoelastic properties of the vocal fold. We tested a cohesive implant of calcium hydroxylapatite (CaHA) particles in a gel carrier in an in vivo canine model of phonation. Six dogs underwent unilateral recurrent laryngeal nerve section and injection laryngoplasty of the paralyzed vocal fold with a CaHA implant. The six follow-up examinations were performed at 1, 2, 3, 6, 9, and 12 months, and the larynx and bilateral neck lymphatic system were harvested for histologic analysis. The CaHA implant adequately medialized the vocal fold to regain glottal closure. The mucosal waves remained unaltered from baseline. The implant remained soft in the larynx and did not migrate to the neck lymphatic system. A localized foreign body giant cell reaction was present on histologic evaluation, but not acute or other chronic inflammation. A size analysis revealed no resorption of the CaHA particles. A decrease in medialization was noted at all follow-up intervals related to resorption of the aqueous-based gel carrier. The CaHA implant appears to be relatively safe and suitable for injection laryngoplasty.
OBJECTIVE: To compare the efficacy of vascularized bone grafts and bridging mandibular reconstruction plates for restoration of mandibular continuity in patients who undergo free flap reconstruction after segmental mandibulectomy. Study design and setting A total of 210 patients underwent microvascular flap reconstruction after segmental mandibulectomy. The rate of successful restoration of mandibular continuity in 151 patients with vascularized bone grafts was compared to 59 patients with soft tissue free flaps combined with bridging plates. RESULTS: Mandibular continuity was restored successfully for the duration of the follow-up period in 94% of patients who received bone grafts compared with 92% of patients with bridging mandibular reconstruction plates. This difference was not statistically significant. In patients who received bone grafts, most cases of reconstructive failure occurred during the perioperative period and were due to patient death or free flap thrombosis. In patients who received bridging plates, all instances of reconstructive failure were delayed for several months and were due to hardware extrusion or plate fracture. CONCLUSIONS: Vascularized bone-containing free flaps are preferred for reconstruction of most segmental mandibulectomy defects in patients undergoing microvascular flap reconstruction. However, use of a soft tissue flap with a bridging mandibular reconstruction plate is a reasonable alternative in patients with lateral oromandibular defects when the nature of the defect favors use of a soft tissue free flap. SIGNIFICANCE: Both bone grafts and bridging plates represent effective methods of restoring mandibular continuity following segmental mandibulectomy, with the former being the preferred technique for patients undergoing microvascular reconstruction.
OBJECTIVE: The safety of intralaryngeal injection of cidofovir remains a concern. Our goal was to evaluate local and systemic effects of intralaryngeal injection of cidofovir. STUDY DESIGN: Animal study using a canine model. METHODS: Two groups of three young beagle dogs (6 vocal folds in each group) were used. Subepithelial vocal fold injections were performed in each group biweekly for 6 months with 0, 2.5, 5, 10, 20, and 37.5 mg cidofovir in a 0.5 mL volume. Direct laryngoscopy was performed at each injection interval. Complete blood cell count and renal parameters were measured at baseline and monthly thereafter. Histopathologic examination of the vocal folds was performed after the 6-month injection period in one group of animals and after an additional 6-month observation period in the second group. RESULTS: Endomysial edema with muscle fiber separation and dose-dependent atrophy and scarring of the vocal folds was present. Onset of atrophy and scarring was observed after 3, 7, and 11 injections in the vocal folds injected with 37.5, 20, and 10 mg cidofovir, respectively. After the 6-month observation period, recovery of histologic abnormalities was complete in the low-dose (0, 2.5 mg) vocal folds, near complete in the intermediate-dose (5, 10 mg) vocal folds, and no apparent recovery was seen in the high-dose (20, 37.5 mg) vocal folds. Leukocyte count and renal parameters remained unchanged at up to 4.26 mg/kg body weight of systemic dose of cidofovir. CONCLUSIONS: Intralaryngeal cidofovir leads to dose-dependent scarification of the vocal folds that appears irreversible at higher doses. Lower concentrations of this drug should be used in intralesional intralaryngeal use.
PURPOSE OF REVIEW: Glottic insufficiency secondary to vocal fold scarring, atrophy, or paresis remains a clinically challenging problem for the laryngologist. Numerous methods have been described in the treatment of glottic insufficiency, belying the complexity of the problem. Type I thyroplasty and injection of fat, fascia, and gelatin powder have been the mainstay of treatment to date, but the ability to restore a normal mucosal waveform to a damaged vocal fold remains an elusive goal. RECENT FINDINGS: Advances in the material and biomedical sciences have allowed the introduction of newer substances and techniques not only to medialize the vocal fold but also to help restore its viscoelastic properties as well. These substances include expanded polytetrafluoroethylene (ePTFE), collagen, cross-linked hyaluronic acid, micronized acellular human dermis calcium hydroxyapatite, and polydimethylsiloxane. ePTFE can be introduced through a window in the thyroid ala or placed intracordally, and the others can be injected either transorally or transcutaneously, allowing in-office placement under simple topical anesthesia. SUMMARY: Although the ideal augmentation material and technique have yet to be devised, the laryngologist now has several options with which to address the problem of glottic insuffiency. Since the problem is complex and since it is possible that a customized solution may need to be devised on an individual basis, future laryngologists will need to be comfortable with the indications and applications that each material and technique will afford.
The source-filter theory of speech production describes a glottal energy source (volume velocity waveform) that is filtered by the vocal tract and radiates from the mouth as phonation. The characteristics of the volume velocity waveform, the source that drives phonation, have been estimated, but never directly measured at the glottis. To accomplish this measurement, constant temperature anemometer probes were used in an in vivo canine constant pressure model of phonation. A 3-probe array was positioned supraglottically, and an endoscopic camera was positioned subglottically. Simultaneous recordings of airflow velocity (using anemometry) and glottal area (using stroboscopy) were made in 3 animals. Glottal airflow velocities and areas were combined to produce direct measurements of glottal volume velocity waveforms. The anterior and middle parts of the glottis contributed significantly to the volume velocity waveform, with less contribution from the posterior part of the glottis. The measured volume velocity waveforms were successfully fitted to a well-known laryngeal airflow model. A noninvasive measured volume velocity waveform holds promise for future clinical use.
To elucidate the etiology and pathophysiology of spasmodic dysphonia, we examined the adductor branch of the recurrent laryngeal nerve and the lateral cricoarytenoid muscle from 9 consecutive patients with this disorder who were previously treated with botulinum toxin. Histologic examination revealed average muscle fiber diameters ranging from 21 to 57 microm. Botulinum toxin treatment-related muscle atrophy was observed up to 5 months after injection. Endomysial fibrosis was present in all samples. Histochemical analysis in 8 patients revealed type 2 fiber predominance in 7 patients and fiber type grouping in 2. Type-specific muscle fiber size changes were not present. Nerve samples were examined in plastic sections. In 8 patients the nerves contained homogeneous, large-diameter myelinated nerve fibers and sparse small fibers. One patient had a relatively increased proportion of small myelinated nerve fibers. Overall, the nerve fiber diameter was slightly larger in patients than in controls. These findings may implicate the central nervous system in the pathophysiology of adductor spasmodic dysphonia.
Functional laryngeal reinnervation depends upon the precise reinnervation of the laryngeal abductor and adductor muscle groups. While simple end-to-end anastomosis of the recurrent laryngeal nerve (RLN) main trunk results in synkinesis, functional reinnervation can be achieved by selective anastomosis of the abductor and adductor RLN divisions. Few previous studies have examined the intralaryngeal anatomy of the RLN to ascertain the characteristics that may lend themselves to laryngeal reinnervation. Ten human larynges without known laryngeal disorders were obtained from human cadavers for RLN microdissection. The bilateral intralaryngeal RLN branching patterns were determined, and the diameters and lengths of the abductor and adductor divisions were measured. The mean diameters of the abductor and adductor divisions were 0.8 and 0.7 mm, while their mean lengths were 5.7 and 6.1 mm, respectively. The abductor division usually consisted of one branch to the posterior cricoarytenoid muscle; however, in cases in which multiple branches were seen, at least one dominant branch could usually be identified. We conclude that the abductor and adductor divisions of the human RLN can be readily identified by an extralaryngeal approach. Several key landmarks aid in the identification of the branches to individual muscles. These data also indicate the feasibility of selective laryngeal reinnervation in patients who might be candidates for laryngeal transplantation after total laryngectomy.
A canine model for recurrent respiratory papillomatosis (RRP) was developed with canine oral papillomavirus (COPV) inoculated into the buccal mucosa and supraglottic larynx of 5 beagles. The animals received systemic immunosuppression with daily oral prednisone at doses of 0, 1, 2, 3, and 4 mg/kg. Buccal papillomata developed at 6 weeks in all animals and regressed by 10 weeks in the animals that received 0 and 1 mg/kg. The other animals had continuous growth of their buccal papillomata for 26 weeks. The animal that received 2 mg/kg developed papillomata on the lingual surface of the epiglottis that continued to grow through 26 weeks. Systemic oral prednisone successfully maintained COPV-induced oral and laryngeal papillomata in beagles. Thus, COPV-induced oral and laryngeal papillomata that are prednisone-maintained may have utility as a model for RRP.
OBJECTIVE: To review a case series of patients with systemic neurodegenerative disease presenting to a laryngologist for workup of dysphonia and found to have bilateral vocal fold paresis. DESIGN: Case series. SETTING: Tertiary care voice center. PATIENTS: Series of patients with neurodegenerative disorders examined for dysphonia. MAIN OUTCOME MEASURES: History and physical examination including fiberoptic laryngoscopy were performed on all patients. Some patients underwent polysomnography. RESULTS: Seven patients during a 2-year period were noted to have bilateral abductor vocal fold paresis. Five of 7 (71%) had the diagnosis of multiple system atrophy proposed by the laryngologist. All 7 patients described sleep-disordered breathing with stridor. CONCLUSIONS: Patients with systemic neurodegenerative disorders such as Parkinson disease should be examined for multiple system atrophy and for evidence of bilateral vocal fold paresis. Workup for stridor should include polysomnography. Treatment of glottic obstruction in these patients includes constant positive airway pressure at night or tracheotomy. The finding of bilateral vocal fold paresis can be life threatening.