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Spasmodic dysphonia (SD) is considered a rare focal laryngeal dystonia characterized by task-specific voice dysfluency resulting from selective intrinsic laryngeal musculature hyperfunction. Symptoms may be attenuated by a sensory trick. Although SD can be seen at times in generalized dystonia syndrome, it is typically a sporadic phenomenon, and the involvement of the laryngeal adductor muscles is more common than that of the abductor muscles. This research reviews the literature for the pathogenesis, clinical characteristics, treatment options, and current management methods of SD. Technological advances have enabled clinicians to better understand the connection between laryngeal function and dysfunction. Refinements in imaging and genetic investigation techniques have helped better understand the underlying mechanisms of this neurolaryngology disorder. Currently, the standard of care for SD is the symptomatic management of botulinum toxin (BT) chemodenervation. This is supported by a large body of literature attesting to its efficacy in many different research studies, particularly in the uncomplicated adductor form of the disorder. Efforts towards surgical treatment predate the development of BT treatment by a decade, but the long-term efficacy has not been proven and, further research is expected. Symptom relief in patients with abductor SD and dystonia with tremors after surgical and BT treatments and those in patients remains suboptimal.

OBJECTIVE Titanium bridges are used to separate the thyroid ala during type 2 thyroplasty for adductor spasmodic dysphonia. Revision surgeries have adventitiously indicated that bridge wing failure occurs in the area of the medial hole in some cases. This study investigated the rate and cause of device malfunctions and developed an improved device. METHODS We conducted a questionnaire survey to determine the number of surgeries performed in Japan up to the end of 2014, and to obtain information about revision cases. In addition, damage analyses were performed on the fracture surfaces of recovered titanium bridges through use of scanning electron microscopy (SEM). RESULTS Between 2002 and 2014, titanium bridges were used in 385 patients. Revision surgery was performed in 19 cases. Revision surgeries revealed that in 11 cases breakage occurred in the wings of the device in the region of the medial hole. However, such fractures were not associated with any signs of recurrence or any adverse events. SEM analyses of fracture surfaces confirmed that fatigue fractures were caused by repeated bending stress in the area of the medial hole. Based on these results, the shape of the hole was changed from round to oval and the wing thickness was increased to prevent breakage. CONCLUSIONS The wings of titanium bridges may break without any associated signs, symptoms or tissue damage. Based on the malfunctions detected and analyses of the devices recovered following malfunction, changes to the specification were made for commercial development of the titanium bridge.

Endoscopic endonasal skull base surgery has become popular due to its minimally invasive nature to the patient and the development of various medical devices. The reason why it is considered less invasive is that it is possible to reach the anterior skull base lesion using the corridor of the nasal cavity and paranasal sinuses. The roles of the nasal sinuses include acting as breathing pathways, warming, humidifying, and filtering of inhaled air, olfaction, and being a resonant cavity, all of which are important for a comfortable life, and the loss of these functions reduces the quality of life. Therefore, to perform endoscopic endonasal skull base surgery in a minimally invasive and safe manner, it is necessary to understand the anatomy of the nasal sinuses to reach anterior skull base lesions while preserving nasal structures as much as possible. This article describes the normal local anatomy of the nasal cavity and the paranasal sinuses, as well as the surgical techniques, especially the anterior skull base approach and the pterygopalatine fossa approach, for endoscopic endonasal skull base surgery.

To evaluate whether vocal function exercises (VFE) could be an adjunct treatment for patients with unilateral vocal fold paralysis (UVFP) who were not satisfied with their postoperative voices after reinnervation surgeries.Retrospective.Medical records of the patients with UVFP who underwent laryngeal reinnervation between October 2011 and October 2014 were reviewed. Patients were classified into two groups: one received VFE according to patients' desire (VFE group) and the other did not have voice therapy (control group). Effects of VFE were assessed by vocal fold vibration (regularity, amplitude and glottal gap), aerodynamic measurements (maximum phonation time (MPT) and mean airflow rate (MFR)), GRBAS scale, acoustic parameters (pitch range, pitch perturbation and amplitude perturbation quotients (PPQ, APQ), and noise-to-harmonics ratio (NHR)) and subjective evaluation by patients (Voice Handicap Index-10 (VHI-10)). Phonatory function was also compared between the two groups at three time points: before reinnervation surgery, before VFE, and after VFE.Thirty patients were enrolled (11 men, 19 women). The VFE group included eight patients, and 22 patients served as controls. In the VFE group, several parameters (amplitude, MPT, MFR, pitch range, APQ, and NHR) did not improve significantly after surgery, while all parameters examined improved significantly in the control group. After VFE, amplitude, glottal gap, MFR, B score, pitch range, and PPQ showed significant improvement, while the control group did not show a significant improvement except in VHI-10, during the corresponding period. Significant differences in G and B scores and VHI-10 between the two groups were observed at the third time point.VFE may be used as an adjunct treatment for patients with UVFP who are not satisfied with their voices after reinnervation surgery. However, phonatory function after VFE may not reach the same level as for those who are satisfied with their voices after reinnervation surgery.

Adductor spasmodic dysphonia (AdSD) is caused by hyperadduction of the vocal folds during phonation, resulting in a strained voice. Animal models are not yet used to elucidate this intractable disease because AdSD has a difficult pathology without a definitive origin. For the first step, we established an animal model with vocal fold hyperadduction and evaluated its validity by assessing laryngeal function.In this experimental animal study, three adult Japanese 20-week-old rabbits were used. The models were created using a combination of cricothyroid approximation, forced airflow, and electrical stimulation of the recurrent laryngeal nerves (RLNs). Cricothyroid approximation was added to produce a glottal slit. Thereafter, both RLNs were electrically stimulated to induce vocal fold hyperadduction. Finally, the left RLN was transected to relieve hyperadduction. The sound, endoscopic images, and subglottal pressure were recorded, and acoustic analysis was performed.Subglottal pressure increased significantly, and the strained sound was produced after the electrical stimulation of the RLNs. After transecting the left RLN, the subglottal pressure decreased significantly, and the strained sound decreased. Acoustic analysis revealed an elevation of the standard deviation of F0 (SDF0) and degree of voice breaks (DVB) through stimulation of the RLNs, and degradation of SDF0 and DVB through RLN transection. Formant bands in the sound spectrogram were interrupted by the stimulation and appeared again after the RLN section.This study developed a rabbit model with vocal fold hyperadduction . The subglottal pressure and acoustic analysis of this model resembled the characteristics of patients with AdSD. This model could be helpful to elucidate the pathology of the larynx caused by hyperadduction, and evaluate and compare the treatments for strained phonation.