Spasmodic Dysphonia: Evaluation and Management

TITLE: Spasmodic Dysphonia:<= span style=3D'mso-spacerun:yes'> Evaluation and Management
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: March 10, 2009
SENIOR MEDICAL STUDENT: Olvia Revelo
FACULTY PHYSICIAN: Michael Underbrink, MD
SERIES EDITORS: Francis B. Quinn, Jr., MD
ARCHIVIST: Melinda S. Quinn, MS(ICS)

"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head= and Neck Surgery and was not intended for clinical use in its present form. It = was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implie= d, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."

INTRODUCTION &= nbsp;

Spasmodic dysphonia = (SD) is a focal, adult-onset dystonia of the intrinsic laryngeal muscles. It is characterized by intermittent phonatory breaks during speech occurring secondary to laryngeal muscle spas= ms. Patients with SD typically manifest their symptoms when attempting voluntary speech. Individuals may be asymptomatic at= rest or during reflexive phonation such as coughing, crying, laughing, and yawning. Symptoms may fluctua= te during singing or whispering. Although the cause of SD is still unknown, it seems to be associated with certain triggers, illnesses, and environmental factors. Spasmo= dic dysphonia has been associated with other focal dystoni= as such as blepharospasm, tor= ticollis, and Writer’s Cramp. Neurological disorders such as Parkinson’s and amyotrophic lat= eral sclerosis have also been associated with SD. Finally, environmental factors suc= h as certain infections, trauma, stress or even medications have been suspected = to trigger SD.

Spasmodic dysphonia affects approximately 1:10,000 Americans with a = peak age of onset between 35-45 years of age.&n= bsp; It has a greater tendency to affect females, with the female to male ratio ranging from 3:1 up to 8:1. A positive family history exists in approximately 12 percent of affected population.

There are two main types of SD, adductor spasmodic dysphonia (ADSD) = and abductor spasmodic dysphonia (ABSD). In some rare instances both types of symptoms are present in which c= ase it is said to be mixed. Some authors believe both types are present in all patients with symptoms depend= ing on the predominance of either the adductor or abductor type.

There are nine cartilages that make up the larynx: thyroid, cricoid, epiglottic, = and paired arytenoids, corniculate and cuneiform. The thyroid cartila= ge is composed of two lamina that come together on the ant= erior side of the cartilage to form the laryngeal prominence. The posterior edge of each lamina articulates with the cricoid cartilage inferiorly at the cricothyroid joint. Movement of the cartilage at this joint produces a chan= ge in tension at the vocal folds, which in turn produces variation in pitch of= the voice. The longer the vocal fold, the higher the pitch (effect of length is offset by increase in tension). The entire superior edge of the thyroid cartilage is attached to the hyoid bone by the hyothyroid membrane. Another important landmark is a small prominence on the internal surface of the thy= roid cartilage midline which is the attachment point for the anterior commissure= of the vocal folds.

The cricoid cartilage is the only complete ring of cartilage around the trachea= . It attaches superiorly to the thyr= oid cartilage and inferiorly to the trachea. The function of the cricoid is to provide attachments for the various muscles, cartilages, and ligaments involved in opening and closing the airway and in speech production.

The pair of arytenoid cartilages rest upon and articulate at the base with the superior edge of the cricoid cartilage. They consist of two processes: the = vocal process to which the vocal ligament attaches to, and the muscular process w= hich serves as an insertion point for several laryngeal muscles.

The laryngeal muscles can be classified into two types: intrinsic and extrinsic. Intrinsic muscles act directly upo= n the arytenoids except for the cricothyroid muscle that acts indirectly, and the extrinsic or accessory muscles which are involved in the elevation and depression of the larynx. The= posterior cricoarytenoid muscles which attach inferiorly with the posterior surface of the cricoid cartilage and superiorly to the muscular process of the aryteno= id cartilage are the only abductors of the vocal cords. The lateral cricoarytenoid and tran= sverse arytenoid muscles are both involved in adducting the vocal folds. The thyroarytenoid muscle shortens= the vocal cords and consequently changes the frequency of vocal fold vibration. The c= ricothyroid muscle controls vocal fold lengthening and pitch.

There are two different neurologic pathways involved in voice production one being voluntary and the other involuntary. Corticobulbar fibers from the cerebral cortex descend through the internal capsule and synapse on the motor neurons in the nucleus ambiguus. = The nucleus ambiguus is the area within the brainstem (medulla) from which arise the fibers that will contribute to the vagus nerve. Lower motor neurons lea= ve the nucleus ambiguus and travel laterally, exiting the medulla between the olive and the pyramid as a series of eight to ten rootlets. These rootlets = coalesce into the vagus nerve, which then exits the skull base via the jugular foram= en. The vagus nerve descends in the carotid sheath, giving off three major branches: the pharyngeal branch, the superior laryngeal nerve (SLN), and the recurrent laryngeal nerve (RLN). The SLN supplies sensation to the glottic = and supraglottic larynx, as well as motor input to the cricothyroid muscle. The= RLN arises from the vagus nerve in the upper chest and loops under the aortic a= rch on the left and subclavian artery on the right and ascends back into the ne= ck traveling in the tracheoesophageal groove. The nerve enters the larynx posteriorly, adjacent to the cricothyroid joint. The RLN supplies all of the intrinsic laryngeal muscles with the exception of the cricothyroid muscle. = This pathway summarizes the voluntary pathway for voice production.

Etiology of SD remains unknown. Histor= ically this disorder has been considered psychogenic in nature but current theory involves a neurologic cause. Evidence supporting this theory include k= nowledge of basal ganglia involvement in other focal dystonias and the development o= f SD after head trauma.

D= iagnosis is based on history and careful examination of the glottis across a variety= of laryngeal tasks. Spasmodic dysphonia must be distinguished from other functional voice disorders such as voice tremor. An underlying neurologic disease mu= st also be ruled out especially Wilson’s, Huntington’s and Parkinson’s disease which may cause secondary SD.

Typical features on history include deterioration of voice quality u= nder stress or on telephone, and improvement with sedatives such as alcohol and benzodiazepines. Singing or laughing will sometimes result in greater fluen= cy, probably due to the task-specific nature of dystonia.

One author defined “idiopathic spastic dysphonia” by the following = criteria: 1. patient must exhibit the voice signs of SD, 2. there must be an absence = of vocal cord lesions or paralysis, 3. patient must exhibit normal remaining peripheral speech mechanisms, and 4. resistance of symptoms to voice therapy and psychotherapy.

Clinical features can help distinguish between the different types of SD. Adductor type SD (ADSD) is found in= about 85 percent of diagnosed cases in the United States. The most commo= n symptom associated with adductor type SD is a choked, strained-strangled voice with abrupt breaks in phonation in the middle of vowels. Breaks are due to hyper adduction of the vocal folds resulting in a quick glottic closure interrupt= ing airflow through the glottis and interrupting phonation. Patients may experi= ence difficulties with continually voiced sentences particularly when glottal st= ops mark word boundaries like “we_eat,”= or when two = voiced sounds occur in sequence within the word such as “ye_ar” or “d_og”. Examples = of sentences patients may have a difficulty with include “We eat eels ev= ery day”, “We mow our lawn all year” and “A dog dug a n= ew bone”.

Abductor type SD (ABSD) is less common, found in approximately 15 percent of patients with SD. = Patients usually exhibit a breathy, effortful voice with abrupt breaks resulting in = whispered elements of their speech characterized by excessive and prolonged abduction during voiceless consonants (/h/,/s/,/f/,/p/,/t/= ,/k/). Vocal fold abduction interferes with closure of the vowel sound that follow= s. To examine for symptoms of abductor= SD the patient’s speech should be compared during voiced sentences such = as “We mow our lawn all year,” which should contain few abnormalit= ies, with sentences containing a high proportion of voiceless consonants such as “The puppy bit the tape” and “When he comes home we’= ;ll feed him”. If severe enough, the patient may display complete aphonia= .

Mixed type SD is extremely rare.&nb= sp; Patients display symptoms of both adductor and abductor type SD. Dia= gnosis of a mixed disorder is important for predicting response to treatment. Diagnosis is similar to the diagnosis of either type of SD, with patients having difficulties with both types of tasks. Mixed patients are difficult = to treat as Botulinum toxin can produce unwanted side effects with no benefit.= Thyroarytenoid injection produces breathiness that exacerbates the disorder, while injecti= on to the posterior cricoarytenoid muscle may provide little benefit.

Diagnosis:

Diagnosis can be verified using electromyography, fiber optic laryngoscopy, videostroboscopy, aerodynamic testing, and vocal spectrograph= ic analysis. Examination during connected speech is most likely to reveal the involuntary laryngeal motion = that causes symptoms. That is why = the larynx is best examined with a flexible nasopharyngoscope. Insertion of laryngeal mirror or ri= gid endoscope combined with the necessary traction of the tongue may mask the features. Diagnosis is based = on speech symptoms and must be distinguished from functional voice disorder, a= nd an underlying neurologic disease must be ruled out.

Treatment:

Botox:<= /p>

There is no known cure for SD. Different types of therapy have been used to battle this debilitating condition including phar= macotherapy, voice therapy, and even surgery. The gold standard treatment for SD is Botulinum toxin (BTX). This toxin prevents presynaptic release of acetylcho= line (ACH) at the neuromuscular junction. It is important to note that different serotypes of botulinum toxin = exhibit specific proteolysis of proteins involved in transport and binding of Ach vesicles to presynaptic membranes. This reaction results in a temporary paralysis of the muscle involve= d. Historically, BTX injections have been used to successfully treat other focal dystonias including blepharospasms and torticollis.&= nbsp; This led researchers to develop protocols for the treatment of SD, a= nd in 1984 Blitzer et al applied it to SD. It is currently the gold standard treatment due to its mild side effects, easier technique, and cheap cost compared to the rest of the treatment modalities. Surgical interventions ar= e typically reserved for patients who do not respond to Botox treatment or develop resistance to it. There are 8 distinct subtypes of Botulinum toxin that exi= st (A, B,C1, C2, D, E, F, G). Types A and B are the onl= y subtypes manufa= ctured for clinical use: type A Botox (Dysport), and type B Myobloc (Neurobloc). Paralysis from botulinum toxin can be overcome in 2 ways: production of accessory axonal terminals, or by product= ion of new proteins by the cell.

In more detail, botulinum toxin binds to the neuronal cell membrane at the ner= ve terminus and enters the neuron by endocytosis. The light chain of botulinum toxin cleaves specific sites on the SNARE proteins, preventing complete assembly of the synaptic fusion complex and thereby blocking acetylcholine release. Botulinum toxins types B, D, F, and G cleave synaptobrevin; types = A, C, and E cleave SNAP-25; and type C cleaves syntaxin. Without acetylcholine= release, the muscle is unable to contract.

Treatment with BTX results in the reduction in voice breaks usually = by 48 hours post treatment. Trea= tment lasts an average of 3-4 months before recurrence of symptoms. The most common side effect is breathiness. Other side effec= ts include: dysphagia, prolonged voice loss, aspir= ation, hoarseness, pain at injection site and stridor (with PCA injection). Usually no overt changes are noted= for the first 48 to 72 hrs. The effects of toxin can continue to increase up to seven days after injection, probably because of diffusion of toxin through the muscle.&nbs= p; This may be why some patients with ADSD report that their voice is b= est three days after an injection in the thyroarytenoid muscle, followed by the= onset of breathiness and other side effects by day five. Breathiness can last 1-2 weeks and = may be more pronounced following bilateral injection. Dysphagia for liquids may oc= cur, with symptoms usually dissipating within 3-5 days. During the affected time period, p= atients should be advised to sip through a straw and to avoid attempting to swallow liquids quickly. Side effects can often be minimized with lower dosing, but= may be a trade off as the duration of effects may also be shortened. Dosage-side effect profile is very individual among patients. There are no absolute contraindications for the use of BTX injections and they may be used safely= in children. Since unknown potential for teratogenicity on neonates and infant= s, use in pregnant or lactating women is not advised. Aminoglycosides may potentiate effects of the toxin.

Patients with known reflux should be treated with anti-reflux medications because, theoretically, the slowed vocal fold closure after injection may predispose them to aspiration. Unfortunately, 3 – 5% of patients undergoing BTX injection have developed resistance to the toxin. This is believed to occur= by development of antibodies. Risk factors for developing immunogenicity inclu= de use of higher doses, shorter intervals between injections (<3 months), booster doses, and young age. There is no assay to test for presence of antibodies. Some centers conf= irm resistance by injecting 15 U of BTX into one side of the frontalis muscle w= ith retained symmetry indicating resistance. Resistant patients can sometimes be treated with other toxin serotypes. BTX is supplied in crystallized powder = form which should be diluted in preservative free saline before use.

There are several techniques used to inject BTX into the vocal cord muscles for treatment of ADSD. In one method, a percutaneous injection is g= uided by EMG signals obtained through use of a teflon-coated hollow needle. The n= eedle is inserted through the thyrocricoid membrane (located through palpation) a= nd directed upward toward the contralateral thyroarytenoid muscle (TA). By hav= ing the patient phonate and observing and hearing the resultant EMG interference pattern when the needle comes in contact with the desired muscle, we can en= sure correct positioning. During t= he procedure the patient is asked not to cough or swallow to prevent movement = of the needle once in the TA.

Alternate injection techniques for ADSD include the transoral laryngoscopic approach,= transnasal laryngoscopic approach, and transcartilaginous “point touch” injection technique. Techniques which allow for other means of locat= ing the injection site were developed in an effort to increase the accuracy with which toxin could be administered while eliminating the need for EMG monito= ring for injection. The transoral approach involved indirect visualization of the vocal folds via standard laryngoscopic procedure. The vocal folds are anesthetized t= hrough the application of a topical cocaine solution. BTX is then injected along t= he superior margin of the vocal folds.

The transnasal technique uses a flexible nasolaryngoscope with a working channel that is equipped with a flexible catheter needle. Topical phenylephrine and lidocaine are sprayed transnasally, then the sco= pe is introduced. Once in place, lidocaine solution drip is applied to the surfac= e of the vocal folds via the working channel while the patient phonates to preve= nt airway penetration or aspiration. The needle is inserted through the surface of the thyroid cartilage halfway bet= ween the thyroid notch and inferior edge. Following insertion the needle is passed through the cartilage and i= nto TA muscle where BTX is injected. All methods yield comparable results. Tech= nique chosen is very patient and physician dependent.

The injection technique for abductor type SD requires access to the posterior cricoarytenoid muscles. In th= is approach, the larynx is rotated manually away from the injection site. The needle is passed posterior to = the posterior edge of the thyroid and then advanced toward the posterior plate = of the cricoid cartilage and positioned in the PCA under EMG guidance. The pat= ient is asked to sniff to contract the posterior cricoarytenoid muscles and veri= fy correct position. There is usually sufficient response by weakeni= ng just one posterior cricoarytenoid muscle.

Blitzer et al. (1999) reported their 12 year experience with BTX with more than 900 patients with SD. Ninety percent of patients with ADSD and 66.7% with ABSD achieved a normal voice after injection. Injection after nerve section fail= ure showed up to 81% improvement. However these patients never did as well as t= hose who have never undergone surgery and their perception of improvement was lo= wer on average. Patients with combined abnormalities only had 30% improvement.<= /p>

Advantages of using BTX include: a less invasive procedure than surgery, no permanent damage to nerve or laryngeal structures, temporary nature allows for dosage adjustments, and wide availability. Some disadvantages of BTX are the need = for repeated injections, the unpredictable relationship between dosage and resp= onse, risk for resistance to treatment, and the adverse side effects associated w= ith treatment.

Pharmacological Treatment:

No controlled studies have demonstrated effective symptom control using neuropharmacology. Examples of agents used include beta blockers such as propranolol, the anticholinergic trihexyphenidylHCl (Artane), and benzodiaz= epines like diazepam and alprazolam. The role of this pharmacology has been to provide relief without any demonstrable symptom reduction. However, clinicians often have individual patients who have reported significant sym= ptom relief. At present the role of these medications in the management of SD is only as an adjunct to other approaches.

Voice Therapy

Voice therapy is another approach to treatment which has unfortunate= ly not had any demonstrated effectiveness in treating SD. It may help rule out a psychogenic disorder and may be used to provide support for those who do not benefit fr= om Botox (mild symptoms). Some patients use it in adjunct to Botox to prolong symptom free periods. Traditional voice therapy approache= s for ADSD employ techniques for avoiding overpressure. Breathy voice onsets, red= uced speech force, using a head focus, and laryngeal manipulation are all techni= ques aimed at reducing laryngeal tension. Therapy can also use relaxation and respiration training to help gain insight and control of laryngeal tension during speech.

Surgical Treatment:

The first surgical technique used to try and correct SD was recurrent laryngeal nerve section described by Dedo in 1976. His fir= st publication was a case series in which he described the outcomes of 34 pati= ents who underwent RLN section. They observed that RLN paralysis retracts the involved vocal cord from midline (in the paramedian position) so the normal fold fails to reach as firmly as usual, causing a breathy but often phonato= ry soft voice. Dedo first tried lidocaine injections on one of his patients wh= o was relieved of the spasms and agreed to undergo RLN s= ection for a more permanent relief. He then sectioned the RLN in 34 patients after temporary paralysis with Xylocaine showed significant improvement in vocal quality. They treated patients with unilateral RLN section thinking that the creation of unilateral vocal cord paralysis could prevent hyper adduction a= nd loss of speech fluency at the cost of the dysphonia associated with paralys= is.

In his 1991 publication, a retrospective review of pre and post operative recordings of 300 patients who underwent RLN section. Patients answered questionnaires regarding voice production and voice recordings were analyzed by perceptual voice evaluation and acoustic analysis of voice spectra. Fifteen percent of the patients we= re reported to have developed recurrence of mild to moderate spasticity 6 to 2= 4 months after RLN section. Eighty-two percent had little or no voice spasticity 5 t= o 14 years after RLN section. Since then, this approach has been abandoned by most laryngologists in favor of t= he reliability of BTX injections.

Aronson and DeSanto (1983) followed 33 patients for 3 years post RLN section. Thirty-six percent of patients main= tained improved voices on follow up. Of the 64% failed voices, 48% were worse than before surgery. They concluded that the effectiven= ess of unilateral RLN section for severe ADSD decreases with time and results in voice failure in= a sizeable percentage of patients. They postulated that return of symptoms was not due to reactivation = of the vocal cords, but rather hyper adduction of the normal vocal folds alone= or along with other muscles of the supraglottis and extrinsic musculature. Since = this study RLN section was widely abandoned for the simpler BTX injection method= for temporary relief of SD symptoms.

In 1991 Netterville et al reported on a modification of the RLN surgery after a patient who developed recurring adductor spasm 1 year after section was reexplored with identification of neural regrowth into the distal segment of the RLN. In this modification= the RLN was followed distally toward the intrinsic laryngeal muscles and then avulsed. They theorized that = with this technique, neural re-growth would be diminished and recurrence of SD symptoms would be reduced. He published a retrospective review= of 12 patients with no recurrence at 1.5 years after surgery. A follow up report in 1996 o= f 18 patients followed for 3-7 years post RLN avulsion showed 16 of 18 patients = were without spasm. The most commo= n side effect reported was breathy voice. <= /span>The remaining patients had minimal spasm and six underwent medialization laryngoplasty to improve voicing. The RLN avulsion procedure hold promise in management of SD patients not responsive or tolerant to BTS injections, but still at the cost of the breathy dysphonia associated with unilateral vocal cord paralysis. Further resea= rch still needs to take place before recommending this on a regular basis.

Currently there are several surgical techniques being explored for the treatment of SD but are still considered experimental.&nbs= p; These procedures include recurrent laryngeal nerve denervation and <= span class=3DGramE>reinnervation , type II thyroplasty , and posterior cricoarytenoid myoplasty with medialization thyroplasty.

In 1999 Berke was the first to describe a technique for selective bilateral RLN denervation followed by reinnervation with the ansa cervicalis. The procedu= re specifically denervates the laryngeal adductors and spares the abductors. This allows treatment of both side= s of the larynx without compromising the patient’s airway function. In this procedure, a modified thyroplasty type window is created bilaterally. This window is situated more poste= riorly and inferiorly than for a thyroplasty.&nbs= p; The intrinsic RLN is visualized as it courses toward its terminus in= the TA muscle. Verification of th= e anatomy is made by intraoperative evoked EMG performed with nerve stimulation and custom made endotracheal tube that places surface electrodes on the vocal c= ord mucosa. The PCA branch is protected behind a strut of the inferior cornu of= the thyroid cartilage. This branc= h is not disturbed. The nerve is then dissected under magnification, and branche= s to the TA and LCA are isolated. = The TA and LCA branches are lysed, and then using microneurosurgical technique, the sternohyoid branch of the ansa cervicalis is sutured to the distal TA branc= h of the RLN. In this fashion reinnervation of the TA can occur with a nerve that is uninvolved by SD. This reinnervation preserves= the tone of the TA muscle and gives the patient improved voicing when the muscle reinnervates. This controlled reinnervation prevents aberrant reinnervation= by the severed RLN stump, an unwanted result observed in the original Dedo treated patients. The proximal RLN stump is sutured outside the thyroid cartilage and = the cartilage window is closed to prevent aberrant reinnervation. In his initial report in 1999 Berke presented preliminary results of 21 patients who had been followed up= a median of 36 months. At that = time 19 of 21 patients had absent to mild dysphonia, and only 1 underwent post o= perative BTX treatment.

In his 2006 paper, Berke gives long term follow up results for the procedure.<= span style=3D'mso-spacerun:yes'> The study is a retrospective analysis of surgical outcome with average follow up interval of 49 months. Surgical outcome was evaluated using patient surveys and perceptual voice analysis. Out of 136 patients, 83 returned surveys with 91% satisfied with fluency of voice. Forty-six patients provided voice recordings for perceptual evaluation, results showed 26% had voice breaks, and 30% breathiness.= Limitations for the study include a high dropout rate (61%), small sample size, and lack of long term prospective studies. Attributable advantages of the pro= cedure include the permanence of treatment effect and less breathiness due to maintenance of vocal fold tone from ansa cervicalis innervation. Disadvanta= ges to consider are the technical difficulty of the surgery, recurrence of symptom= s, and lack of reproducibility. A prospective study is underway.

M= idline lateralization thyroplasty, otherwise known as thyroplasty type II, was proposed by Isshiki et al for treatment of SD. In their 2001 retrospective review of 6 SD patients, 5 out of 6 patients obtained near normal voices. The concept is to decrease adducto= ry forces by changing the anatomy of the larynx. Since there is an excess glot= tal closure during spasms leading to dysphonia the procedure makes an effort to control the degree of glottal closure to obtain a predictable voice result.= Isshiki performs a midline incision= in the thyroid cartilage dividing the thyroid ala. Each ala is then lateralized and t= his position is maintained by either a silicone shim placed over a muscle space= r, or they have recently created a titanium bridge. To achieve additional vocal cord lateralization, the anterior commissure is divided with a needle to create a tiny defect and a composite cartilage graft is placed to prevent granuloma formation.

A big advantage of the procedure is that it does not deprive the patient of n= erve or muscle function. Failures were attributed to difficulty in lateralization and concurrent focal neck dystonia. Limitations include small sample size, no current long term prospect= ive studies, and no objective measurements were described.

Midline lateralization thyroplasty was proposed by Chan in 2004. He published a prospective case se= ries with 13 subjects. He used the same method described by Isshiki, but his res= ults showed that 9 of 13 patients failed and 2 had their surgery reversed. Reasons for failure were unclear, e= specially when they had good early results after surgery. They presume that with time vocal = fold hyper adduction is able to overcome the initial lateralization created by the shi= ms because the underlying neuropathology has not been resolved. Limitations of= the study include the small study sample, the use of self-rating assessments an= d no objective measures. Advantage= s of this type of surgery are that an optimal glottal closure can be adjusted and readjusted, there is no damage of physiologic function, and it is reversibl= e. Some disadvantages described include the technical difficulty of the surgery and= shim displacement, the fact that it does not relieve the cause of SD, and lack o= f reproducibility.

Posterior cricoarytenoid myoplasty with medialization thyroplasty was proposed by Sha= w in his 2003 case report of 3 patients with ABSD. Three patients refractory to = BTX were treated with the surgery one unilaterally, and the other two bilateral= ly. The patient’s voices were analyzed both with subjective surveys and perce= ptual voice analyzed in different intervals up to a year. Their voices were recorded and a b= linded speech pathologist listened for prolonged voiceless consonants. These patie= nts were treated with surgery and followed up to a year post surgery. The procedure consists of approachi= ng the PCA insertion in the muscular process of the arytenoid through a window in = the posterior part of the thyroid ala. Then disinsertion of the muscle is done = and a plastic sheet is placed and secured between the elevated muscle and aryte= noid cartilage to prevent reinsertion. Once the sheet is adequately positioned a= nd secured, a medialization thyroplasty is performed. All patients reported improved subjective symptoms and showed objective reduction in phonatory breaks. The unilaterally treated patient h= ad to undergo the procedure on the opposite sides due to recurrence of symptoms a= fter 6 months. There was no airway compromise or other post operative complications. Obviously larger sample a= nd follow up needed. Medialization thyroplasties have been tried in the past to treat ABSD with only short lived improvement. As stated earlier, there is less s= uccess with BTX treatment for patients with ABSD.= This procedure is proposed for these refractory patients.

Summary

Sp= asmodic dysphonia is an idiopathic disorder of the larynx. The mainstay of treatment continue= s to be BTX injections into the laryngeal muscles. BTX treatment is not perfect; ther= e is an onset time characterized by a breathy voice and dysphagia and an offset = time characterized by recurrence of symptoms.&n= bsp; Occasionally patients can develop antibodies and resistance. Some patients do not like to recei= ve multiple injections a year. B= ecause of these shortcomings, alternative, more permanent treatments have been sou= ght. Surgery for ASDS was initially developed in the 1970s but has been abandoned because of poor long term results. A RLN denervation and reinnervation and laryngoplastic techniques may hold promise for long term treatment. All current therapies for SD are dire= cted toward the symptoms of the disorder. There is still work toward understanding the underlying cause so we = can then possibly develop a cure for the disease.

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