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Research Papers

Interaction Between the Thyroarytenoid and Lateral Cricoarytenoid Muscles in the Control of Vocal Fold Adduction and Eigenfrequencies

[+] Author and Article Information
Jun Yin

Speech Production Laboratory,
Department of Head and Neck Surgery,
University of California, Los Angeles,
31-24 Rehabilitation Center,
1000 Veteran Avenue,
Los Angeles, CA 90095-1794

Zhaoyan Zhang

Speech Production Laboratory,
Department of Head and Neck Surgery,
University of California, Los Angeles,
31-24 Rehabilitation Center,
1000 Veteran Avenue,
Los Angeles, CA 90095-1794
e-mail: zyzhang@ucla.edu

1Present address: Department of Mechanics and Engineering Science, Fudan University, Shanghai, China.

2Corresponding author.

Manuscript received March 24, 2014; final manuscript received August 5, 2014; accepted manuscript posted August 28, 2014; published online September 11, 2014. Assoc. Editor: Jonathan Vande Geest.

J Biomech Eng 136(11), 111006 (Sep 11, 2014) (10 pages) Paper No: BIO-14-1132; doi: 10.1115/1.4028428 History: Received March 24, 2014; Revised August 05, 2014; Accepted August 28, 2014

Although it is known vocal fold adduction is achieved through laryngeal muscle activation, it is still unclear how interaction between individual laryngeal muscle activations affects vocal fold adduction and vocal fold stiffness, both of which are important factors determining vocal fold vibration and the resulting voice quality. In this study, a three-dimensional (3D) finite element model was developed to investigate vocal fold adduction and changes in vocal fold eigenfrequencies due to the interaction between the lateral cricoarytenoid (LCA) and thyroarytenoid (TA) muscles. The results showed that LCA contraction led to a medial and downward rocking motion of the arytenoid cartilage in the coronal plane about the long axis of the cricoid cartilage facet, which adducted the posterior portion of the glottis but had little influence on vocal fold eigenfrequencies. In contrast, TA activation caused a medial rotation of the vocal folds toward the glottal midline, resulting in adduction of the anterior portion of the glottis and significant increase in vocal fold eigenfrequencies. This vocal fold-stiffening effect of TA activation also reduced the posterior adductory effect of LCA activation. The implications of the results for phonation control are discussed.

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Figures

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Fig. 1

(a) A sketch of the laryngeal framework including the vocal fold, the thyroid, cricoid, and arytenoid cartilages, and the LCA and IA muscles from a superior view. (b) Superior view of a canine larynx at resting (respiratory) position. (c) LCA activation adducts the glottis but leaves a gap in the middle-membranous glottis. (d) TA activation completely closes the anterior glottis but leaves a large gap at the posterior glottis. Figures (b)–(d) are images obtained from in vivo canine larynx experiments in Choi et al. (1993).

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Fig. 2

A sketch of the computational model from (a) a top view and (b) a side view, and (c) the cross section of the vocal fold model. Note that the curves on the surface of the cartilages represent the curved surface of the cartilages, not the actual meshes used in the simulations. Figure 2(a) also defines a point A located at the medial posterior corner of the superior surface, a line located at the posterior edge on the superior surface of the vocal fold, and three coronal cross sections, the results on which are shown in Figs. 4, 5, and 7.

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Fig. 3

The glottal shape (a,e) and the deformed model in a top view (b,f), side view (c,g), and frontal view (d,h) under the condition of full LCA activation alone (top) and full TA activation alone (bottom). The thin lines indicate the original glottal shape or geometry. Note that the curves on the surface of the cartilages represent the curved surface of the cartilages, not the actual meshes used in the simulations.

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Fig. 4

(a) The three components of the displacement of point A as a function of the LCA activation level. (b) The rotation angles of the posterior edge in the coronal plane and the horizontal plane as a function of the LCA activation level. The point A and the posterior edge were defined in Fig. 2(a).

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Fig. 5

The deformed geometry of the anterior (left), middle (middle), and posterior (right) cross sections of the vocal fold at the condition of full LCA activation alone (top) and full TA activation alone (bottom). The solid lines indicate the undeformed geometry of the body and cover layer. The three cross sections are defined in Fig. 2(a). The color within the cross sections represents the AP Strain εxx.

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Fig. 6

Model deformation in a top view (a), side view (b), and frontal view (c) under full LCA activation but without considering the passive forces of PCA and IA muscles

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Fig. 7

Contours of the glottal width at locations of (a) cross section 1, (b) cross section 2, (c) cross section 3, and (d) the posterior edge of the superior surface of the vocal fold as a function of the LCA and TA activation levels

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Fig. 8

Contour plot of the first vocal fold eigenfrequency as a function of the LCA and TA activation levels

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Fig. 9

The first ten eigenfrequencies of the vocal fold as a function of the LCA activation level for three levels of TA activation ((a): αTA = 0; (b): αTA = 0.5; and (c): αTA = 1) and as a function of the TA activation level for three levels of LCA activation ((d): αLCA = 0; (e): αLCA = 0.5; (f): αLCA = 1)

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