Reviewing the author's 48year experiences of experimental as well as clinical investigation into voice disorders, he describes here their extracts that appear to have particular clinical implication. The topic of initial study was the control mechanism of vocal intensity and pitch. In the process of animal experiment, the author had been intrigued by the reflex that increased subglottal pressure induces glottal closure. This needs to be further studied in connection with mis-swallowing (dysphagia) for instance. The experiments with the excised larynx has later hinted and led to the development of arytenoid adduction technique for vocal fold paralysis, and the surgery for spasmodic dysphonia i.e. type 2 thyroplasty. The two main causes for hoarseness are imperfect closure of the glottis and stiff vocal fold or reduced mobility of the mucosa. In this connection the author emphasizes that any medialization procedure for imperfect closure of the glottis would not restore a good voice unless vocal fold mucosa is well mobile. Chordal injection of autologous tissue such as fat or fascia for augmentation or medialization also requires caution not to expand the overlying mucous membrane in excess or not to create wide scar adhesion between the mucosa and transplanted tissue. The tips of various thyroplasties and arytenoid adduction have briefly been described. As to the future tasks and prospect of voice research, the author stresses the need of biosyntheses or regeneration, using bioengineering technique, of the vocal folds such that covered with a well mobile mucosa. Clinically phonosurgery should steadily extend its indication, based on stable outcomes, not only to inveterate laryngeal diseases but also to aged voice or professional singers' problem for instance. The prospect of further development seems promising for the future.
One-hour discussion after the lecture was focussed on rather basic voice problems, a little apart from the clinical problems the author emphasized. They include 3 main topics. 1. The function of the vocal muscle According to recent reports, replacement of the vocal muscle with fat tissue, which was performed for spasmodic dysphonia, demonstrated that a fairly good voice could be obtained. Taking into account the clinical facts together with numerous experimental findings, the discussion tended to be settled at “the vocal muscle may not be essential for phonation but it is probably so for the control of voicing”. 2. Model for phonation Various models for phonation were discussed, including the Schoenhaerl, Hirano, Ishizaka, and Titze. The Hirano's “body and cover” model is essentially the same as the Schoenhaerl's concept emphasizing the mobility of the mucosa, the author thought. Since it is impossible to define the “body” discretely, whether it means the vocal muscle only or not, it may be misleading sometimes. In Titze's model, the figures for the body in terms of mass, location, and stiffness, is very difficult to assign on the anatomical basis. The only possible means to judge whether the model and hypothetical figures are correct or not would be to examine whether the model output curve matches well with the real vocal output under various physiological conditions. 3. Diplophonia This terminology is sometimes confusing. The voice of vocal fold paralysis is often referred to as diplophonia. But it should be realized that the two different musical tones are not being produced. It is a kind of irregular tone, or hoarseness. The two vocal folds with different tension do not produce twopitched tone. One vibrating vocal fold perse cannot be a source of sound in a practical sense. Possibility of producing a sound such as confusing with glottal sound in the articulatory organ was discussed.