Acta Oto-Laryngologica

ISSN: 0001-6489 (Print) 1651-2251 (Online) Journal homepage: http://www.tandfonline.com/loi/ioto20

Vocal Fold Fixation in Laryngeal Carcinomas Minoru Hirano, Shigejiro Kurita, Hidetaka Matsuoka & Morio Tateishi To cite this article: Minoru Hirano, Shigejiro Kurita, Hidetaka Matsuoka & Morio Tateishi (1991) Vocal Fold Fixation in Laryngeal Carcinomas, Acta Oto-Laryngologica, 111:2, 449-454, DOI: 10.3109/00016489109137418 To link to this article: http://dx.doi.org/10.3109/00016489109137418

Published online: 08 Jul 2009.

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Date: 23 March 2016, At: 14:43

Acta Otolaryngol (Stockh) 1991; 111: 449-454

Vocal Fold Fixation in Laryngeal Carcinomas MINORU HIRANO, SHIGEJIRO KURITA, HIDETAKA MATSUOKA and MORIO TATEISHI

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From the Department of Otolaryngology-Head and Neck Surgery, Kurume Uniuersity, Kurume, Japan

Hirano M, Kurita S, Matsuoka H, Tateishi M. Vocal fold fixation in laryngeal carcinomas. Acta Otolaryngol (Stockh) 1991; 11 1 : 449-454. The mechanisms of vocal fold fixation were determined by means of a whole-organ serial section study. A total of 80 laryngectomy specimens, 36 supraglottic and 44 glottic carcinomas, was investigated. In the supraglottic carcinomas, the most frequent cause of fixation of the ipsilateral vocal fold was a deep massive tumor invasion in the arytenoid eminence and the second most frequent cause was an extensive involvement of the thyroarytenoid (TA) muscle. Fixation of the contralateral vocal fold resulted from a deep tumor invasion in the contralateral arytenoid eminence. In the glottic carcinomas, fvtation of the ipsilateral vocal fold resulted from an extensive invasion into the TA muscle. Fixation of the contralateral vocal fold was caused chiefly by an invasion into the contralateral TA muscle through the anterior commissure region. It resulted occasionally from an invasion into the interarytenoid muscle and contralateral arytenoid cartilage and cricoarytenoid joint via the posterior part of the larynx. Key words: laryngeal carcinoma, supraglottic carcinoma, glottic carcinoma, vocal fold fiation, histological study.

INTRODUCTION

Vocal fold fixation in glottic carcinomas has been attributed chiefly to deep tumor invasion into the thyroarytenoid (TA) muscle (14) In. supraglottic carcinomas, clear descriptions about the mechanism of vocal fold fixation have been few (1,4). The purpose of this study was to investigate mechanisms that could cause fixation of the ipsiiateral and contralateral vocal folds in cases with laryngeal carcinoma.

METHODS A total of 80 laryngectomy specimens with laryngeal carcinoma was subjected to a wholeorgan serial section study. Parafin preparations and hematoxylin-eosin stain were employed. Of the 80 specimens, 36 were supraglottic (15:T2, 16:T3, 5:T4 in 1987 UICC classification) and 44 glottic carcinomas (3:Tlb, 9T2, 20:T3, 12:T4). “Ti-ansglottic” carcinomas which have been defined as a growth crossing the ventricle in a vertical direction and invading the paraglottic space (2, 3) were forcedly classified into either supraglottic or glottic carcinoma depending o n the major site of the lesion. The UICC classification (5) does not have a category of “transglottic”. In the histopathological study, we focused on tumor invasion chiefly into the TA muscle, the arytenoid cartilage (AC) and the cncoarytenoid (CA) joint. In addition, involvements of the arytenoid eminence were investigated for supraglottic carcinoma. The mobility of the vocal fold was classified into three categories: mobile, impaired and fixed. RESULTS Supraglottic carcinoma. Table I shows the results for the supraglottic carcinomas. The ipsilateral vocal fold was mobile in 14, of impaired mobility in 8 and fixed in 14 cases. The most frequent finding to which the vocal fold fixation was attributed was a deep massive tumor invasion in the arytenoid eminence (Fig. 1 a). This was found for 1 I of the 14 fixed vocal folds. The second most frequent finding for the fixed vocal folds was an involvement

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Acta Otolaryngol (Stockh) 111

of more than three fourths of the TA muscle (5 of the 14). The TA muscle of these cases was totaily or near totally replaced by carcinoma. There were 3 “transglottic” carcinomas in the 5 cases with a fixed vocal fold accompanied by an extensive TA muscle involvement. In all of the 3, the TA muscle was totally replaced by tumor. One of them also had a deep massive invasion of the arytenoid

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Table I. Mobility of the wcal fold versus tumor invasion of laryngeal structures. Supraglottic carcinomas (n=36) Ipsilateral Mobile (n=14) TA muscle Negative

Contralateral Impaired (n=8)

Fixed (n=14)

Mobile (n=33)

Impaired (n=2)

Fixed (n=l)

-114 114-214 2l4-314 314-

13 1 0 0 0

33 0 0 0

AC Negative Positive

14 0

8 0

12 2

33 0

2 0

1 0

CA joint Negative Positive

14 0

8 0

13 1

33 0

2 0

1 0

Arytenoid eminence Negative Superficial Moderate Deep

12 2 0 0

2 0 1

33 0 0 0

0

11

Table 11. Mobiliry of the vocal fold versus tumor invasion of laryngeal structures. Glottic carcinoma (n=44) Ipsilateral Mobile (n=4)

Contralateral Impaired (n=8)

TA muscle Negative -114 114-214 2/4-314 314AC Negative Positive

4 0

8 0

CA joint Negative Positive

4 0

Fixed (n=32)

0

0 0 0 32

Mobile (n=28)

Impaired (n=10)

Fixed (n=6)

4 2

26 2 0 0 0

13 19

28

10

0

0

8

14

28

0

18

0

10 0

5

1

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Vocal fold furation in laryngeal carcinomas 451

Fig. I . Histological pictures demonstrating carcinomatous invasions causing fixation and imapired mobility of the vocal fold in cases with supraglottic carcinoma. ( a ) Deep massive invasion in the arytenoid eminence (arrow); ( b ) large tumor (arrows)involving the vocal fold (double arrows);(c) multiple lesions (arrours) involving the vocal fold (doublearrows); (d)moderate invasion of the arytenoid eminence (arrow);(e) multiple lesions (arrows) involving the ventricle (double arrows); v) large tumor of the ventricular fold (arrow) impairing vocal fold mobility.

eminence, another had a moderate degree of invasion and the third had no invasion of the arytenoid eminence. The other 2 of the 5 cases with extensive TA muscle involvement were not of the “transglottic” type. One of them had a large tumor involving the epiglottis, the bilateral arytenoid eminences, the bilateral ventricular folds, the ipsilateral vocal fold and the anterior portion of the contralateral vocal fold (Fig. 1 b). The other case presented with involvements of the epiglottis, bilateral ventricular folds and the ipsilateral vocal fold, suggesting a possibility of multiple origins (Fig. 1 c). Thus, the vocal fold fixation was accounted for by a deep massive invasion of the arytenoid eminence in 9, by an extensive TA muscle involvement in 3 and by both in 2 cases.

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Acfa Ofolaryngol (Stockh) I 1 1

Fig. 2. Histological pictures demonstrating carcinomatous invasions causing fixation and impaired mobility of the vocal fold in cases with glottic carcinoma. ( a ) Extensive invasion in the TA muscle (arrow); ( b ) “transglottic” carcinoma (arrow); (c) moderate invasion in the TA muscles (arrows); (d)invasion in the 1A muscle (arrow); ( e ) invasion in the 1A muscle and contralateral CA joint (arrows); (f) invasion in the 1A muscle (double arrows) causing

impaired mobility of the contralateral vocal fold. The cricoid cartilage is markedly involved on the affected side (arrow).

One patient with vocal fold fixation presented with an invasion of the AC in addition to an extensive TA muscle involvement. Another patient had invasions of the AC and the CA joint in addition to those of the arytenoid eminence and TA muscle. The involvement of the AC and the CA joints were not the primary cause of vocal fold fixation in these cases. The mobility of the ipsilateral vocal fold was impaired in 8 cases. Of the 8, 6 had superficial or moderate tumor invasion of the arytenoid eminence (Fig. 1 d). Two of them also had involvement of one to two fourths of the TA muscle. The 7th case had multifocal lesions in the epiglottis, left ventricular fold, bilateral vocal folds and the lateral aspect of the bilateral ventricle. The lesion of the right ventricle seemed to be an early-stage “transglottic” carcinoma (Fig. 1 e) causing impaired vocal fold mobility. The 8th case had

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Vocal fold faation in laryngeal carcinomas 453

tumor invasion neither in the arytenoid eminence nor in the TA muscle, but presented with a large tumor of the left ventricular fold which sat on the vocal fold and invaded the lateral upper portion of the vocal fold (fig. 18. The contralateral vocal fold was mobile in 33, of impaired mobility in 2 and fixed in 1 case. The fixation was caused by a deep tumor invasion of the arytenoid eminence and the impaired mobility resulted from a moderate invasion of the arytenoid eminence. Glottic carcinoma. Table I1 shows the results for the cases with glottic carcinoma. The ipsilateral vocal fold was mobile in 4, of impaired mobility in 8 and fixed in 32 cases. All the 32 cases with a fixed vocal fold had tumor invasion of more than three fourths of the TA muscle. The TA muscles of these cases were totally or near totally replaced with carcinomatous tissue (Fig. 2a). The AC was invaded in 19 and the CA joint was involved in 18 of the 32 cases. There were 10 cases of “transglottis type” all of whom presented with vocal fold fixation (Fig. 2 b). Of the 8 cases with impaired mobility, 7 had a tumor invasion of one to three fourths of the TA muscle (Fig. 2c). In the 8th case, the major lesion was located on the right side of the posterior glottis and invaded the interarytenoid (IA) muscle (Fig. 2 4 . A separate small superficial lesion was found at the anterior portion of the right membranous vocal fold. The impaired mobility appeared to have been caused by IA muscle involvement. The contralateral vocal fold was mobile in 28, of impaired mobility in 10 and fixed in 6 cases. Of the 6 cases with a fixed vocal fold, 5 had extensive tumor invasion into the TA muscle via the anterior commissure region. The 6th case had no TA muscle involvement on the contralateral side but presented with a tumor extending along the posterior portion of the larynx into the IA muscle and the contralateral AC and CA joints (Fig. 2 e). Of the 10 cases with an impaired mobility, 9 had tumor invasion of one to three fourths of the contralateral TA muscle. The invasion into the contralateral TA muscle appeared to have taken place through the anterior commissure region in all 9 cases. In the 10th case with impaired vocal fold mobility, the contralateral TA muscle was not affected. The impaired mobility appeared to have resulted from involvement of and around the IA muscle (Fig. 2jj.

DISCUSSION The results of this study indicate that there are different mechanisms of vocal fold fixation. In supraglottic carcinoma, the most frequent cause of fixation of the ipsilateral vocal fold was a deep massive tumor invasion of the arytenoid eminence and the second most frequent cause was an extensive invasion into the TA-muscle. Ogura (1) stated that, in carcinomas of the epiglottis, aryepiglottic fold, arytenoid eminence or piriform sinus, fixation of the vocal fold was due to a tumor about the perichondnum of the AC and secondary invasion of the intrinsic muscle. Kurita et al. (4) described that vocal fold fixation in cases with supraglottic carcinoma was caused by a massive invasion in the upper aspect of the arytenoid cartilage. The results of these two papers appear to agree basically with those of the present study. Fixation of the contralateral vocal fold in supraglottic carcinomas has not been clearly described previously in the literature. In the present study, fixation and impaired mobility of the contralateral vocal fold resulted from involvement of the contralateral arytenoid eminence. It has been well described that vocal fold fixation is caused by extensive TA muscle involvement in cases with glottic carcinoma ( 1 4 ) . The results of the present study basically agree with these previous reports. In the present study, the relationship between the degree of TA muscle involvement and the mobility of the vocal fold was determined:

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Invasions of less than one fourth of the TA muscle do not produce disturbance of mobility, those of one to three fourths of the TA muscle result in impaired mobility and those of more than three fourths of the TA muscle cause fixation. Fixation and impaired mobility of the contralateral vocal fold in cases of glottic carcinoma have not been clearly discussed in the literature. The results of the present study indicate that the most frequent cause of mobility disturbance is an invasion into the contralateral TA muscle through the anterior commissure region. Occasionally, a tumor extension to the contralateral side takes place through the posterior portion of the larynx, invading the IA muscle, and the contralateral AC and CA joints. This is another mechanism of fixation of the contralateral vocal folds. “Transglottic” carcinoma is a well documented category (3, 4), although it is not employed in the UICC categorization (5). Kirchner (3) used the term “transglottic” for those growths that crossed the ventricle in a vertical direction and was associated with vocal fold fixation. He also stated that the site of origin of the transglottic type remained uncertain but some of the smaller transglottic growths appeared to involve mainly the depth of the ventricle. The finding of Fig. 1e in the present paper confirms this.

ACKNOWLEDGEMENT This investigation was supported in part by a Grant-in-Aid for Scientific Research (No.02454399) from the Japanese Ministry of Education, Science and Culture.

REFERENCES 1. Ogura JH. Surgical pathology of cancer of the larynx. Laryngoscope 1955; 65: 867-926. 2. Kirchner JA. One hundred laryngeal cancers studied by serial section. Ann Otol Rhino1 Laryngol 1969; 78: 689-709. 3. Kirchner JA. Two hundred laryngeal cancers: Patterns of growth and spread as seen in serial section. Laryngoscope 1977; 87: 474-82. 4. Kurita S, Hirano M,Matsuoka H, Tateishi M, Sat0 K. A histopathological study of carcinoma of the larynx. Auris-Nasus-Larynx (Tokyo) 1985; 12: S172-77. 5. Hermanek P, Sobin LH, eds. TNM classification of malignant tumours. Heidelberg: SpringerVerlag, 1987.

Address for correspondence: Minoru Hirano, Department of Otolaryngology-Head and Neck Surgery, Kurume University, 67 Asahi-machi, Kururne, Japan

Vocal fold fixation in laryngeal carcinomas.

The mechanisms of vocal fold fixation were determined by means of a whole-organ serial section study. A total of 80 laryngectomy specimens, 36 supragl...
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