James P Dworkin-Valenti*, Robert J Stachler, Noah Stern and Esmael H Amjad
Department of Otolaryngology, Head & Neck Surgery, Detroit Medical Center, Detroit, MI, USA
Received: 19 December, 2017; Accepted: 03 January, 2018; Published: 05 January, 2018
JP Valenti, Ph.D., 4160 John R., Ste. 1007, Department of Otolaryngology, Head & Neck Surgery, Detroit Medical Center, Detroit, MI 48201, USA, E-Mail:
Dworkin-Valenti JP, Stachler RJ, Stern N, Amjad EH (2018) Pathophysiologic Perspectives on Muscle Tension Dysphonia. Arch Otolaryngol Rhinol 4(1): 001-010. DOI: 10.17352/2455-1759.000065
© 2018 Dworkin-Valenti JP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
It is difficult to quantify the incidence of hyperfunctional muscle tension dysphonia (H-MTD). Although voice disorders in general have been noted to affect approximately 10% of the population in the United States, up to 40% of patient visits to voice specialists are for symptoms of H-MTD. Clearly this condition is a very common vocal pathology, yet its differential diagnosis is not always straightforward. The primary purpose of this tutorial is to present a comprehensive literature review on this condition, with particular focus on alternative etiologic theories and differential diagnostic and treatment techniques. The secondary purpose of this tutorial is to increase awareness that this disorder is a complex condition with highly variable causes, features, and treatment requirements. As a consequence of recent advances in the field of neurolaryngology, and for completeness, the neurological substrates of voice and speech production are also discussed in this review. This information is included to evoke a theoretical conversation about possible patho-neurologic correlates in some patients with H-MTD; especially those who do not respond favorably to standard behavioral therapy strategies. Whereas only a brief discussion of treatment options is rendered in this paper, more detailed information on this topic will be covered in a forthcoming companion tutorial.
It was more than 60 years ago that the concept of a physiologic linkage between the respiration, phonation, articulation, and resonation subsystems was proposed; that excess tension originating at any level of this unified speech production mechanism may result in referred hypertonicity and hyperfunction throughout this linear anatomical chain of musculoskeletal structures [1,2]. Since this seminal hypothesis, there have been countless investigations on the psychodynamic and pathophysiologic processes observed in individuals with hyperfunctional speech and voice disorders [3-17]. These inquiries have spawned numerous theoretical discussions about the most effective methods of differential diagnosis and treatment of these conditions.
Individuals who exhibit forceful or excessive contractions of muscles that drive voice and speech production often struggle with a broad spectrum of associated abnormal signs and symptoms, including 1) harsh-shrill vocal quality, 2) limited pitch and volume control, 3) falsetto pitch breaks, 4) episodic arrests of phonation, 5) reduced maximum phonation time, 6) vocal fatigue, and 7) extrinsic laryngeal, intrinsic laryngeal, mandibular, and tongue musculature hypertension. When these abnormalities are not caused by obvious signs of phonation subsystem pathology or tissue trauma, the diagnosis of primary or non-phonotraumatic H-MTD is descriptively appropriate. Figures 1, 2, and 3 illustrate videostroboscopy findings from a healthy 16 year old female who initially presented to our voice laboratory with perceptual features of primary H-MTD that persisted for 18 months, including pressed voice and intermittent outbursts of shrill vocalizations. She denied any history of voice abuse behaviors. Note the normal appearing vocal folds at rest in Figure 1. Figure 2 demonstrates the onset of abnormal bilateral ventricular vocal fold activity during phonation effort (ie., plica ventricularis). Figure 3 shows full approximation of theses merging folds in concert with the aforementioned abnormal voice characteristics. This patient is a classic example of non-phonotraumatic H-MTD. She exhibits significant voice difficulty, owing to suppressive supraglottal hyperfunctional activity, in the presence of normal true vocal fold anatomy.