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| CASE REPORT |
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| Year : 2014 | Volume
: 4
| Issue : 1 | Page : 28-31 |
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Laryngeal framework surgery for adductor spasmodic dysphonia
Akshat Malik, Satish Nair, Ajith Nilakantan
Department of Ear, Nose and Throat Head and Neck Surgery, Army Hospital (R & R), Delhi Cantt, New Delhi, India
| Date of Web Publication | 22-Sep-2014 |
Correspondence Address:
Akshat Malik
A1/61, Third Floor, Freedom Fighter Enclave, Neb Sarai, New Delhi - 110 068
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2230-9748.141464
 Abstract | | |
Adductor spasmodic dysphonia is difficult to diagnose and treat. Botulinum toxin is considered to be treatment of choice for adductor spasmodic dysphonia. We present a case here, who had become refractory to the effects of botulinium toxin. He subsequently underwent type II thyroplasty and had satisfactory improvement in voice with it.
Keywords: Adductor spasmodic dysphonia, botulinum toxin, laryngeal framework surgery, spasmodic dysphonia, thyroplasty type II
How to cite this article:
Malik A, Nair S, Nilakantan A. Laryngeal framework surgery for adductor spasmodic dysphonia
. J Laryngol Voice 2014;4:28-31 |
| Introduction | |  |
Spasmodic dysphonia is a specific type of dystonia affecting the laryngeal muscles. About 90% of the cases of spasmodic dysphonia are those of adductor spasmodic dysphonia (AdSD). The diagnosis and treatment of AdSD is a challenging task. Botulinum toxin injection is considered to be the gold standard treatment. We present a case of AdSD. This patient had an initial improvement in voice with injection Botulinum toxin but subsequently he became refractory to it. The patient was thereafter managed by laryngeal framework surgery (type II thyroplasty) with satisfactory voice outcome.
| Case report | | |
A 58-year-old male presented with complaints of difficulty in speaking of 1-year duration. On detailed history, he complained of lack of fluency of speech due to voice breaks and strangulations during speech which were insidious in onset and gradually increasing in severity. He was having difficulty in day-to-day communication with his family members especially on telephone. A complete ENT evaluation followed by meticulous videolaryngoscopy, stroboscopy and analysis of voice parameters was done. On videolaryngoscopy the true, false vocal folds were found to go into a spasm at the time of phonation especially during adduction [Figure 1]a. Flexible laryngoscopic assisted recording of vocal cord motion was done at the time of speaking which revealed the spasmodic contraction of the vocal folds occurring at the time of adduction. A thorough neurological assessment was carried out which revealed absence of any other muscular dystonia or neuromuscular disorder. The patient was thus diagnosed to have adductor spasmodic dysphonia. | Figure 1: Hopkins Telescopic examination (a) Pre-op – showing vocal cords going into spasm during adduction (b) Post-op – showing relaxed vocal cords during adduction
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He received speech therapy for 3 months with no improvement in voice. He was then planned to be injected with Injection Botulinum toxin into the thyroarytenoid muscle. Toxin was injected under EMG guidance. 1.5 U was injected in the thyroarytenoid muscles. Post-injection patient showed marked improvement with reduction in voice breaks and improved fluency. His symptoms recurred after 5 months. Subsequently he received 6 more cycles of Botulinum toxin injection over the next 2 years. With subsequent injections the asymptomatic period kept reducing and after fourth injection there was no improvement in speech breaks and strangulations. Jitter, shimmer increased and maximum phonation time was shortened. Dose was increased to 3 U in the last two injections but no improvement in outcome was seen.
As the patient was having no effect with Botulinum toxin alternate surgical options were explored. He was then planned for laryngeal framework surgery. Pre-operatively patient's speech was assessed by GRBAS; subjective assessment was by Voice handicap index (VHI), self-assessment scale and acoustic analysis was done using Dr Speech software (Tiger Inc). The patient then underwent Thyroplasty type II with insertion of a silastic bridge between the cut edges of thyroid cartilage in midline [Figure 2], [Figure 3], [Figure 4]. With the help of the bridge the vocal folds were held further apart. Sternothyroid muscle was then covered over it. | Figure 4: Silastic block placed in midline separating the two ends of the thyroid cartilage
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Initially the patient had hoarse voice for first 2 weeks. By 4-6 weeks his fluency improved, there were less voice breaks and strangulations. By 3-6 months, minimal hoarseness was present and his speech became fluent. Patient's voice was assessed 6 months post-operatively by VHI, self assessment scale, GRBAS and acoustic analysis. A comparison of pre and post-operative data is made in [Table 1]. Improvement was seen in all the domains except that breathiness increased. The patient's speech was found to have less number of voice breaks, tremors and he could speak more fluently. He has been on follow-up for 1 year presently with no further deterioration in voice and flexible laryngoscopic examination also showed no spasms [Figure 1]b.
| Discussion | | |
Spasmodic dysphonia is a class of disorders of central motor processing that causes involuntary movements affecting the laryngeal muscles during speech. It is also called Laryngeal dystonia and is of two type's adductor and abductor spasmodic dysphonia. Adductor spasmodic dysphonia (AdSD) (90%) is a common disorder compared to Abductor spasmodic dysphonia. [1] It is characterized by strained, strangled breaks in vowels during speech due to intermittent hyper adduction of the vocal folds. There are also prolonged voiceless consonants before initiation of the following vowels. The precise etiology is not known though it is thought to be a central motor disorder with tonic contractions of the laryngeal muscles.
Diagnosis and evaluation of AdSD is challenging as there are no specific tests to diagnose it. Various tests mentioned in literature are perceptual, acoustic analysis, and subjective self-assessment tests. These can be used to help in diagnosis and also to evaluate voice post-procedure. [2] Perceptual tests include rating on GRBAS scale, phonatory break analysis. Post intervention, acoustic analysis may show improvement in jitter, shimmer and maximum phonation time. Subjective tests like VHI can also be used to assess the improvements in voice. Aerodynamic measurements or electromyography may also be used.
Diagnosis can be confused with muscle tension dysphonia. [3] The patient may present in a similar manner and laryngoscopic imaging may be confusing. AdSD can be differentiated by evidence of voice breaks during vocalization, greater variation in speech; also spasms in muscle tension dysphonia are sustained throughout, whereas in adductor spasmodic dysphonia they are irregularly placed at the time of adduction.
Various treatment modalities have been described. Unilateral sectioning of RLN was the first treatment introduced for spasmodic dysphonia; it acted by paralyzing all the muscles on one side of larynx. [4] Botulinum toxin injection is presently the gold standard treatment modality. Under EMG guidance 0.25-2.5 U of Botulinum toxin can be injected into the thyroarytenoid muscle bilaterally. 1.5 U of toxin has been found to be adequate without causing any side effects. [5],[6] These injections need to be repeated every 6 monthly though a lower dose may be required after initial sittings because of long-term effects of Botulinum toxin. [6] It acts by blocking the release of acetylcholine at the motor endplates; a central action is also suggested. Patient can have breathiness, swallowing difficulty following the injection which resolves over time. The dose of Botulinum toxin used should be such that benefit of improvement in voice should be matched with risk of producing aphonia, breathiness, and swallowing difficulties. After a few weeks of injection, innervation of new fibers is started by the nerve endings resulting in re-appearance of symptoms by 4-6 months. After one to five injections results have been found to be consistent. [5] Surgical options available for intractable cases of AdSD not responding to medical management are bilateral thyroarytenoid muscle myectomy, neurectomy, combined neurectomy and myomectomy, and laryngoplasties. Trans-oral laser assisted partial thyroarytenoid myectomy has also been described. [7] Functional reinnervation of vocal folds after selective laryngeal adductor denervation has also been tried recently. Laryngoplasties/Laryngeal framework surgeries involve changing the shape of the laryngeal cartilage. In AdSD this can be done by pushing the anterior commisure back to relax the vocal cords. Isshiki described the type II thyroplasty which comprised widening of the thyroid cartilage. [8],[9] It involved incising the thyroid cartilage and placing a piece of silastic between the two edges, as the vocal cords will be held apart thus reducing the effect of hyper adduction on the vocal cords. Improvements in symptoms such as hyper function, tremor of voice have been reported. Surgeries for AdSD invariably result in a breathy voice. [8] Long-term effects of the type II thyroplasty were questioned earlier but a few recent studies have established the improvement in voice with the surgery. [10]
Our patient, a case of AdSD who had good improvement initially with injection Botulinum toxin failed to show improvement with subsequent injections. As he was an intractable case of AdSD and his quality of life was affected, he was taken up for thyroplasty after appropriate counseling about the hoarseness of voice expected after surgery. Thyroplasty type II was preferred because it does not demand high expertise or technicality and is a completely reversible, low cost procedure which can be done under local anesthesia with gratifying results.
| Conclusions | | |
The message of this article is to highlight that Botulinum toxin is the gold standard for treatment of AdSD and in intractable cases with deterioration of quality of life surgical techniques like thyroplasty type II may be utilized.
| References | | |
| 1. | Edgar JD, Sapienza CM, Bidus K, Ludlow CL. Acoustic measures of symptoms in abductor spasmodic dysphonia. J Voice 2001;15:362-72. 
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| 2. | Langeveld TP, van Rossum M, Houtman EH, Zwinderman AH, Briaire JJ, Baatenburg de Jong RJ. Evaluation of voice quality in adductor spasmodic dysphonia before and after botulinum toxin treatment. Ann Otol Rhinol Laryngol 2001;110:627-34.
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| 3. | Sapienza CM, Walton S, Murry T. Adductor spasmodic dysphonia and muscular tension dysphonia: Acoustic analysis of sustained phonation and reading. J Voice 2000;14:502-20.
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| 4. | Fritzell B, Hammarberg B, Schiratzki H, Haglund S, Knutsson E, Mårtensson A. Long-term results of recurrent laryngeal nerve resection for adductor spasmodic dysphonia. J Voice 1993;7:172-8.
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| 5. | Ludlow CL. Treatment of spasmodic dysphonia: Limitation of current approaches. Curr Opin Otolaryngol Head Neck Surg 2009;17:160-5.
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| 6. | Birkent H, Maronian N, Waugh P, Merati AL, Perkel D, Hillel AD. Dosage changes in patients with long term botulinium toxin for use of laryngeal dystonia. Otolaryngol Head Neck Surg 2009;140:43-7.
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| 7. | Tsuji DH, Chrispim FS, Imamura R, Sennes LU, Hachiya A. Impact in vocal quality in partial myectomy and neurectomy endoscopic of thyroarytenoid muscle in patients with adductor spasmodic dysphonia. Braz J Otorhinolaryngol 2006;72:261-6.
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| 8. | Chhetri DK, Mendelsohn AH, Blumin JH, Berke GS. Long-term follow up results of selective laryngeal adductor denervation-reinnervation surgery for adductor spasmodic dysphonia. Laryngoscope 2006;116:635-42.
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| 9. | Isshiki N, Sanuki T. Surgical tips for type II thyroplasty for adductor spasmodic dysphonia: Modified technique after reviewing unsatisfactory cases. Acta Otolaryngol 2010;130:275-80.
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| 10. | Sanuki T, Isshiki N. Overall evaluation of effectiveness of type II thyroplasty for adductor spasmodic dysphonia. Laryngoscope 2007;117:2255-9.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1]
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