Integrative Review and Framework of Suggested Mechanisms in Primary Muscle Tension Dysphonia

PURPOSE: Despite the high prevalence of primary muscle tension dysphonia (MTD-1), its underlying mechanisms and their interrelationships have yet to be fully identified. The objectives of this integrative review were (a) to describe and classify the suggested underlying mechanisms for MTD-1, (b) to appraise the empirical evidence supporting each of the proposed mechanisms, and (c) to summarize the information in an integrative model. METHOD: PubMed, Scopus, and CINAHL were searched for all publications pertaining to muscle tension dysphonia. Papers were retained if they included theoretical or empirical data pertaining to underlying mechanisms of MTD-1. A total of 921 papers initially qualified for screening, of which 100 remained for consideration in this review. Underlying mechanisms of MTD-1 were extracted using a consensus approach. RESULTS: Seven broad categories of putative mechanisms involved in MTD-1 were identified: psychosocial, autonomic, sensorimotor, respiratory, postural, inflammatory, and neuromuscular. These categories were further divided into 19 subcategories detailed in the body of this review article. Based on the reviewed evidence, our proposed integrative model presents MTD-1 as an idiosyncratic motor adaptation to physiological perturbation or perceived threat. Under this model, physiologically or psychologically aversive stimuli can instigate a series of motor adaptations at multiple levels of the nervous system, ultimately disturbing muscle activation patterns and their biomechanical outcomes. Importantly, these adaptations appear to have the potential to become chronic even after threatening stimuli are withdrawn. CONCLUSIONS: The proposed model highlights the importance of personalized rehabilitation in MTD-1 treatment. Limitations of the literature are discussed to provide guidance for future research aimed at improving our understanding of MTD-1. SUPPLEMENTAL MATERIAL: https://doi.org/10.23641/asha.19586065.