Features of Vocal Fold Adductor Paralysis and the Management of Posterior Muscle in Thyroplasty *Ujimoto Konomi, *,†Ryoji Tokashiki, *,‡Hiroyuki Hiramatsu, *Ray Motohashi, *Eriko Sakurai, *Fumimasa Toyomura, *Masaki Nomoto, *Yuri Kawada, and *Mamoru Suzuki, *yzTokyo, Japan Summary: Objective. To present the pathologic characteristics of unilateral recurrent nerve adductor branch paralysis (AdBP), and to investigate the management of posterior cricoarytenoid (PCA) muscle on the basis of our experience of surgical treatment for AdBP. Study Design. This is a retrospective review of clinical records Methods. Four cases of AdBP, in which surgical treatment was performed, are presented. AdBP shows disorders of vocal fold adduction because of paralysis of the thyroarytenoid and lateral cricoarytenoid muscles. The PCA muscle, dominated by the recurrent nerve PCA muscle branch, does not show paralysis. Thus, this type of partial recurrent nerve paresis retains the abductive function and is difficult to distinguish from arytenoid cartilage dislocation because of their similar endoscopic findings. The features include acute onset, and all cases were idiopathic etiology. Thyroarytenoid muscle paralysis was determined by electromyography and stroboscopic findings. The adduction and abduction of paralytic arytenoids were evaluated from 3 dimensional computed tomography (3DCT). Results. In all cases, surgical treatments were arytenoid adduction combined with thyroplasty. When we adducted the arytenoid cartilage during inspiration, strong resistance was observed. In the two cases where we could cut the PCA muscle sufficiently, the maximum phonation time was improved to 30 seconds after surgery, from 2 to 3 seconds preoperatively, providing good postoperative voices. In contrast, in the two cases of insufficient resection, the surgical outcomes were poorer. Conclusions. Because the preoperative voice in AdBP patients is typically very coarse, surgical treatment is needed, as well as ordinary recurrent nerve paralysis. In our experience, adequate PCA muscle resection might be helpful in surgical treatment of AdBP. Key Words: Recurrent nerve paresis–Adductor branch paralysis–Posterior cricoarytenoid muscle–Arytenoid adduction–Thyroplasty–3DCT. INTRODUCTION The purpose of this report was to present four cases of unilateral vocal fold paresis, originating in recurrent nerve adductor branch paralysis (AdBP), who underwent operative treatment in the Department of Otolaryngology, Tokyo Medical University, and to assess the pathologic characteristics of AdBP, and also to discuss the meaning of posterior cricoarytenoid (PCA) muscle resection in the operative procedure in ABP. Phonatory function in the vocal folds is mainly controlled by the inner laryngeal muscles, which are dominated by the recurrent nerve, and the cricothyroid (CT) muscles, which are dominated by the superior laryngeal nerve outer branch. If vocal fold movement is fairly limited, namely it is fixed without passive movement in general endoscopic finding, vocal fold paralysis is almost evident. However, if some mobility of vocal folds persists, it may seem ambiguous. Paralysis versus paresis can sometimes be demonstrated by laryngeal electromyography (LEMG). Accepted for publication April 29, 2015. The language (English) in this document has been checked by at least two professional editors, both native speakers of English. For a certificate, please see http://www.textcheck. com/certificate/Ocl4kr. The results in this article were presented at the 58th Annual Meeting of The Japan Society of Logopedics and Phoniatrics, Kochi, Japan, October 17, 2013. From the *Department of Otolaryngology, School of Medicine, Tokyo Medical University, Tokyo, Japan; yShinjuku Voice Clinic, Tokyo, Japan; and the zHiramatsu ENT Clinic, Tokyo, Japan. Address correspondence and reprint requests to Ujimoto Konomi, Department of Otolaryngology, School of Medicine, Tokyo Medical University, 6-7-1, Nishi-Shinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. E-mail: [email protected] Journal of Voice, Vol. -, No. -, pp. 1-8 0892-1997/$36.00 Ó 2015 The Voice Foundation http://dx.doi.org/10.1016/j.jvoice.2015.04.019

However, the complete confirmation of palsy for all inner laryngeal muscles, such as the thyroarytenoid (TA) muscle, the lateral cricoarytenoid (LCA) muscle, the PCA muscle, and the intraarytenoid (IA) muscle, is difficult to distinguish by LEMG alone in general practice.1,2 This is due to both technical and evaluative difficulties with LEMG. Thus, information from LEMG does not always lead to a conclusive diagnosis of palsy. Presently, paresis and paralysis of inner laryngeal muscles are diagnosed by a synthetic judgment based on endoscopic findings, clinical examinations, including LEMG, and a history of palsy.3 Currently, distinguishing which of the TA, LCA, PCA, and CT muscles shows paralysis or paresis is challenging.4 Clinically, there are patients with partial interior laryngeal muscle paralysis who are considered as an only adductor impairment case. Such AdBP patients show high-grade breathy hoarseness, because of the highly impaired vocal fold adduction, whereas abductor function is almost normal. In previous studies, we reported the efficacy of 3 dimensional computed tomography (3DCT) in the evaluation of phonatory function.5–7 In 3DCT, the adductor and abductor mobility of the paralytic vocal fold can be assessed by the position of the arytenoid cartilage during inspiration and phonation, which is compared with the normal side in unilateral vocal fold paralysis (UVFP) patients. With 3DCT, it is possible to clarify the movement of the vocal fold and, further, laryngeal muscle function. In patients with suspicious idiopathic UVFP, we performed 3DCT to assess the degree of vocal fold palsy from the mobility

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of the arytenoid cartilage, in addition to endoscopic findings, and used LEMG together with the other techniques to diagnose partial laryngeal muscle paralysis or paresis. In the present study, four cases of AdBP patients with paralysis of TA and LCA muscles and with no impairment of PCA muscle are presented. In addition, the diagnosis of and treatment procedures for AdBP are described. All AdBP cases underwent phonosurgery, and the meaning of PCA muscle resection in the operative procedure is discussed.

Endoscopic Findings. The laryngeal endoscopic impression of AdBP was that the bilateral vocal folds were moving, but laterality was confirmed (Figure 1A). During phonation, the paralytic vocal fold was not adducted, staying in an intermediate position, and the passive movement of the arytenoids was also confirmed,7 whereas in inspiration, abductive movement of paralytic vocal fold was equal to the normal side; atrophic slackness of the vocal fold was observed. Because these endoscopic findings in AdBP are similar to some in arytenoid cartilage dislocation, it is difficult to distinguish between AdBP and dislocation by endoscopy only. TA muscle palsy can be determined by the phase difference and the flaccid vocal fold of the affected side in stroboscopic findings. Regarding the grade of TA muscle palsy, LEMG provides more objective information (mentioned in the section ‘‘LEMG findings’’).

MATERIALS AND METHODS Subjects Four cases of unilateral AdBP patients are presented. Those patients visited to the voice clinic at the Department of Otolaryngology, Tokyo Medical University, from 2007 to 2013 with hoarseness as a chief complaint and further received surgical treatment. Their mean age was 54.8 years and all were men. The causes were all idiopathic etiology; one (25%) case had a preceding common cold history. In all cases, in neck and chest computed tomography scans, there were no findings related to vocal fold palsy, and patients had no family histories, no previous diseases, such as neuropathy or cerebral infarction, and to date, no history of general anesthesia or surgical treatment for other diseases related to hoarseness. All cases had visited other otolaryngology clinics and/or university hospitals, and most of them had been diagnosed with idiopathic vocal fold palsy or paresis. They were observed while not receiving any treatment. Almost 1 year passed until the first visit to our outpatient clinic after onset, and in case 2, 6 years passed before his first visit (Table 1).

Evaluating Arytenoid Movement by 3DCT. Evaluations of arytenoid adductive and abductive movement by 3DCT showed that the paralytic arytenoids were located within the cricoarytenoid joint, clearly distinguishing an arytenoid dislocation (Figures 2 and 3). In addition, 3DCT results showed that the abductive positions of the arytenoid cartilage during inspiration were normal on both sides. In the phonation state, the paralytic side of the arytenoid cartilage was not adducted and remained in an intermediate position and also moved to cranial side as a passive movement. This type of arytenoid movement in 3DCT can be explained in that the PCA muscle has preserved, almost normal, function, whereas the LCA muscle showed high-grade palsy. The 3DCT findings were similar in all four cases.

Methods Diagnostic procedures for AdBP. Diagnosis of AdBP was made mainly by endoscopy and 3DCT findings. LEMG was used as a subsidiary measure. AdBP shows normal function of the PCA muscle and dysfunction in the TA and LCA muscles.

LEMG Findings. LEMGs were performed preoperatively for TA, LCA, and CT muscles. Regarding the CT muscle, the normal interference waves were observed. For TA and LCA muscles, the interference waves had disappeared, and a giant spike and positive sharp wave, indicating neurogenic muscle paralysis, were confirmed. In one of the four patients, LEMG

TABLE 1. Background of ABP Patients Case No. Age (y) Paralysis side Term from onset to first visit (mo) Timing of postoperative measurement (months after operation) Inducement Type of physician before first visit Diagnosis before first visit Family history Past history

1

2

3

4

47 Right 14

65 Left 74

46 Right 13

61 Left 10

12

4

15

3

— ENT department of University Hospital Vocal fold paresis

— ENT clinic

Cold ENT department of University Hospital Normal

— ENT department of University Hospital Idiopathic vocal fold paralysis — Acute cardiac infarction

— —

Idiopathic vocal fold paralysis — —

— —

Ujimoto Konomi, et al

Features of vocal fold adductor paralysis

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FIGURE 1. Endoscopic findings of ABP (case 4). (A) Preoperative findings. During inspiration, the right paralytic vocal fold showed atrophy and the arytenoid abducted similarly to the normal side. During phonation, the paralytic arytenoid was not adducted from the middle position and showed passive movement. (B) Postoperative findings. During inspiration, the paralytic vocal fold stayed at the center position with the surgical treatment. During phonation, the preoperative slit of the vocal fold had been closed. was carried out during a surgical operation facing the PCA and IA muscles on the paralytic side. Normal contraction findings were seen in IA muscle because the IA muscle dominated bilaterally. In addition, a normal pattern of LEMG was seen in the

PCA muscle. The interference wave of the PCA muscle during inspiration was confirmed with quite strong contractions, and the interference wave disappeared in phonation of speech fundamental frequencies.

FIGURE 2. 3DCT endolaryngeal image of ABP. As in the endoscopic findings, the vocal folds were normally abducted during inspiration. During phonation, vocal fold disclosure was seen because the paralytic arytenoid cartilage was not adducted.

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FIGURE 3. Movement of the arytenoid cartilage in 3DCT (dorsal view). The arytenoid cartilages abducted normally without laterality during inspiration. During phonation, the paralytic arytenoid cartilage was not adducted from the middle position and moved to the head side, reflecting passive movement. This finding suggested that only the adductive muscles were impaired. Surgical procedures. Surgical treatment is proposed to AdBP patients who hope to restore their vocal function 1 year after onset with conservative observation with no recovery from their phonatory dysfunction and endoscopic findings. The surgical procedure was based on arytenoid adduction (AA),8 combined with thyroplasty type 1 (TP1). The PCA muscle was cut in three patients and not in one patient (Figure 4). Regarding the AA, we reported previously the ‘‘fenestration approach’’ and achieved good outcomes in terms of postoperative voice quality.9 In the four cases, however, Maragos’ procedure was performed, in which the posterior edge of the thyroid cartilage was opened widely to confirm and allow cutting the PCA muscle.10 For TP1, GORE-TEX (W. L. Gore and

Associates. Inc., Newark, DE) was used to reconstruct the paralytic vocal fold atrophy. The surgery was performed under local anesthesia, and the voice condition could be monitored during operation. In the operations on these AdBP patients, when we adducted their arytenoid cartilage by pulling a thread knotted on the muscular process, we detected strong resistance caused by PCA muscle contraction during inspiration. Thus, first, the PCA muscle was cut off, and then after confirming the disappearance of vocal fold abductive movement, the thread of AA was fixed. Measurement of voice parameters. Maximum phonation time (MPT), mean flow rate (MFR), pitch range (PR),

FIGURE 4. PCA muscle resection in the arytenoid adduction combined with type 1 thyroplasty. Strong contraction of the PCA muscle was confirmed during inspiration when we adducted the arytenoid cartilage by pulling a thread sutured on muscular process. After resection of PCA muscle, the abductive movement disappeared.

Ujimoto Konomi, et al

31 113 20 0.44 2.1 0.14 8 501 14 4.18 10.42 0.28 AA + TP1 + Abbreviations: AA, arytenoid adduction; TP1, thyroplasty type 1; TP4, thyroplasty type 4; PCA, posterior cricoarytenoid.

2 1202 8 12.85 13.72 0.35 5 8 875 605 — 25 — 4.43 — 7.31 — 0.15 AA + TP1 + TP4 — 2 1550 — 7.07 19.33 0.37

MPT (s) MFR (mL/s) Pitch range (semitone) Jitter% Shimmer% NHR Operation procedure PCA muscle resection

AA + TP1 + (incomplete?)

Postoperative No.

Preoperative

1

8 415 23 1.22 2.77 0.14

Preoperative

2

Postoperative

Preoperative

3

Postoperative

39 117 16 0.35 2.59 0.14

4 Successful Unsuccessful

TABLE 2. Preoperative and Postoperative Voice Parameters and Operative Procedure in Each Case

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perceptual voice quality, jitter%, shimmer%, and noise-toharmonic ratio (NHR) were measured and evaluated. MFR was measured with a phonatory function analyzer (PS-77E; Nagashima Medical Instruments Co., Ltd., Tokyo, Japan). Jitter%, shimmer%, and NHR were assessed with a CSL model 4500 (Rion Co., Ltd., Tokyo, Japan). PR was measured semiobjectively with a keyboard and pitch meter, without using a mouth piece. MPT and PR measurements were performed with phonation of the vowel /a/. Preoperative evaluations were performed within 2 months before the operation. Postoperative measurements were assessed at 3–15 months after the operation (Table 1).

AA +

Postoperative Preoperative

Features of vocal fold adductor paralysis

RESULTS The preoperative and postoperative voice parameters are indicated in Table 2. Before operation, high-grade breathy voices were observed in all four AdBP patients, and preoperative MPT (pre-MPT) was 2–8 seconds, and pre-MFR was 501–1550 mL/ s. In three patients, excluding case 4, their pre-MPT values were 800 mL/s, and the preoperative voice of the ABP patients was considered to be similar to the breathy voice of typical severe UVFP patients. Postoperative voice qualities of cases 3 and 4, the successful cases, where the PCA muscles were fully cut off, showed excellent recovery and were almost within normal function range (Figure 1B). In case 3, MPT improved from preoperative 2 seconds to postoperative 39 seconds, MFR went from 1202 mL/s to 117 mL/s. In case 4, MPT recovered from 8 to 31 seconds, and MFR went from 501 to 113 mL/s. Postoperative PRs were 16 semitone in case 3 and 20 semitone in case 4. Jitter%, shimmer%, and NHR in the acoustic analysis also improved, to within normal ranges. Patients were satisfied with their postoperative voice qualities. In case 1, although the PCA muscle was cut off and phonation was markedly improved by the operation, abductive movement of the affected arytenoid appeared on day 5 postoperatively. At 2 weeks after the operation, the abductive movement disappeared again and the vocal fold was fixed; however, the improvement in voice parameters was limited, from 2 to 8 seconds in MPT, and 1550 to 415 mL/s in MFR. In case 2, the operation was finished without cutting the PCA muscle because it was relatively easy to adjust AA and restore phonatory function. Consequently, abductive movement of arytenoid continued in the postoperative days and also fixation of the adductive arytenoid cartilage became more incomplete. Nevertheless, postoperative voice parameters improved (MPT from 5 to 8 seconds and MFR from 875 to 605 mL/s of MFR), and although the voice improvement was incomplete, the patient was relatively satisfied with his postoperative voice, and reoperation was not requested by the patient. DISCUSSION Partial recurrent nerve paralysis and AdBP The recurrent nerve branches off the PCA muscle branch and adductor branch in the larynx. The PCA muscle branch

6 dominates the PCA muscle, and the adductor branch further diverges nerve branches to the IA, TA, and LCA muscles (Figure 5). Recurrent nerve paresis is considered to involve various types of paresis and paralysis in each branch. Regarding partial recurrent nerve palsy, independent TA muscle palsy caused by pressed injury of the recurrent nerve TA muscle branch after endotracheal intubation11 has been reported. In addition, bilateral PCA muscle palsy resulting from neuropathies and neurodegenerative diseases has been reported.12 The AdBP cases in this report were considered cases of such partial recurrent nerve paralysis, and all cases were of idiopathic etiology. The key features of AdBP are adductive impairment of the vocal fold caused by TA and LCA muscles palsy, and almost normal function of the PCA muscle branch. Origin of AdBP The origin of partial recurrent nerve paralysis was considered to be difficult to explain theoretically if whole nervous injury of axonotmesis or neurotmesis occurred at the recurrent nerve trunk level.13 However, the occurrence of vocal fold paresis that is caused by a partial nervous injury included neuropraxia is possible to be a partial branch paralysis. In case of a recurrent nerve palsy caused by some surgical resection, the state of paralysis might be explained by a result of synkinesis with reinnervation.14 However, the pathology of recurrent nerve paresis or partial recurrent nerve paralysis might be presumed more complicated reinnervation process because affected nervous fibers might be contained various degree of injury. After viral neuropathy, causing facial nerve palsy, we often come across patients recovering to a different degree in each branch. Because there is a complex process of nervous reinnervation from the trunk to the branches in high-grade injury, it seems reasonable that the recurrent nerve paresis also has such a process of nervous recovery in especially idiopathic cases. AdBP was considered as unilateral TA and LCA muscle paralysis resulting from sudden recurrent nerve neuropathy, and paralyses in the four cases in this report remained even after long-term observation. In fact, it has been reported that the origin of idiopathic UVFP was a supposed herpes virus infection; however, the pathogenesis of idiopathic UVFP remains poorly understood.15 In a previous review,16 complete recovery of vocal fold motion in idiopathic UVFP was observed in 36 ± 22%, and complete recovery of the voice was observed in 52 ± 17%. Most (>99%) recovered in 22 seconds) without PCA muscle resection when we performed AA during the operation. However, without PCA muscle resection, abductive movement relapsed postoperatively, similar to the preoperative vocal fold movement. In this case, we believe that the thread of the AA became loose because of strong PCA muscle contraction. We considered that once arytenoid cartilage was fixed by the thread, AA suture could overcome PCA muscle activity. However, postoperative arytenoid movement in case 1 and 2 made the operative efficacy unstable. On the other hand, if PCA muscle is cut off, it is possible to be predicted that any subsequent activity of TA or LCA muscle, and/or the tension from the AA suture, would pull the arytenoid

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anteriorly and be unopposed in long-term observation. In case 3, however, during 15-month observation period, vocal condition was not getting worse. At a point of 2 and 5 months after operation, postoperative voice parameters in case 3 were as follows: MPT was 30 and 34 seconds, MFR was 260 and 153 mL/s, PR was 16 and 15 semitones, respectively. One review of LEMG reported that contraction of the PCA muscle disappeared in phonation,2 whereas another stated that the PCA muscle was effective only in high-pitched phonation.24 This possible postoperative disadvantage should be considered further. Postoperative voice quality In cases 3 and 4, the operations were successful and the postoperative voice function was restored to similar to normal, with completely cutting off the PCA muscle. In contrast, in cases 1 and 2, postoperative phonation was limited, and fixed arytenoids moved after the operation because of possibly remaining PCA muscle contraction. Thus, we conclude that PCA muscle resection in the thyroplastic surgery of AdBP patients might lead to better stable postoperative phonation in present. Furthermore, long-term follow-up is needed to determine whether this is significant concern. CONCLUSIONS Because the preoperative phonation state of AdBP patients was quite poor, the operative treatment performed should be similar to that in typical UVFP. Postoperative voice outcome was possible to reach for almost normal range. The systematic diagnosis and treatment of partial UVFP including AdBP has not been established. Obtaining particularized endoscopic findings depends on which laryngeal muscles were paralyzed. It is possible to diagnose partial UVFP using LEMG and 3DCT together. Because an optimal diagnosis and operation can possibly lead to restoration of a normal range of phonation in AdBP, the concept of partial UVFP must be better established. Acknowledgments The authors thank Masanobu Kumada, MD, of the Kumada Clinic in Tokyo for support in LEM data collection and clinical assessments. There are no financial disclosures and conflicts of interest.

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Features of Vocal Fold Adductor Paralysis and the Management of Posterior Muscle in Thyroplasty.

To present the pathologic characteristics of unilateral recurrent nerve adductor branch paralysis (AdBP), and to investigate the management of posteri...
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