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Spasmodic Dysphonia Evaluation and Management

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1 Spasmodic Dysphonia Evaluation and Management
UTMB Department of Otolaryngology Olvia Revelo, MSIV Faculty Advisor:Michael Underbrink, MD Grand Rounds Presentation March 10, 2009

2 Overview Introduction Anatomy of the larynx Etiology Diagnosis
Clinical features Therapy Pharmacologic Surgical Conclusion

3 Introduction Spasmodic dysphonia (SD)
Focal, adult-onset dystonia of laryngeal muscles Intermittent phonatory breaks during speech secondary to spasms Usually task specific - symptomatic when attempting voluntary speech May be asymptomatic during reflexive phonation (coughing, laughing, crying, yawning) Symptoms reduced/absent during singing or whisper

4 Associations May be associated with: Other focal dystonias
Blepharospasms, Torticollis, Writer’s Cramp Underlying neurological Parkinson’s, ALS Environmental Infection, trauma, meds Psychogenic stimulus Stress

5 Demographics Affects approximately 1:10,000 Americans
Female to male ratio 3:1 up to 8:1 Peak age of onset 35-45 Positive family history in 12% of affected pt’s

6 Types of Laryngeal Dystonias
Adductor – irregular hyperadduction of vocal folds with excessive glottic closure Abductor – incomplete, irregular vocal fold approximation Mixed – both elements are present

7 Anatomy: Laryngeal Cartilage

8 Anatomy: Laryngeal Cartilage

9 Anatomy: Laryngeal Muscles

10 Anatomy: Laryngeal Muscles

11 Anatomy: Laryngeal Motion
Abduction of vocal ligament Netter

12 Anatomy: Laryngeal Motion
Adduction of vocal ligament Netter

13 Anatomy: Laryngeal Motion
Tension of vocal ligament Netter


15 Anatomy: Laryngeal Innervation

16 Etiology Currently unknown Historically psychogenic disorder
Traube 1871 “nervous hoarseness” Current theory involves neurologic cause Basal ganglia involved in other focal dystonias Some patients have developed SD post head trauma

17 Diagnosis Diagnosis is based on history and examination of the glottis during various laryngeal tasks. Aronson defined “idiopathic spastic dysphonia”: The voice signs of SD Absence of VC lesions/paralysis Normal peripheral speech mechanisms Resistance of symptoms to voice therapy and psychotherapy

18 Clinical Features: Adductor Type
Most common ~85% of diagnosed cases Choked, strained-strangled voice, with abrupt breaks in phonation in the middle of vowels Breaks are due to hyper-adduction of the folds Difficulty with “We eat eels every day” and “We mow our lawn all year”

19 Clinical features: Abductor Type
Rare ~15% of patients with SD Breathy, effortful voice with abrupt breaks resulting in whispered elements of their speech. Excessive and prolonged abduction during voiceless consonants (/h/,/s/,/f/,/p/,/t/,/k/) Difficulty with “The puppy bit the tape” and “When he comes home we’ll feed him”

20 Mixed Type Extremely rare, with symptoms of both adductor and abductor type Diagnosis important for predicting treatment response

21 Diagnosis Electromyography Fiberoptic laryngoscopy Videostroboscopy
Aerodynamic testing Vocal spectrographic analysis

22 Therapy Pharmacotherapy Voice Therapy Surgical Botox
Neuropharmacologic Voice Therapy Surgical Recurrent laryngeal nerve section Recurrent laryngeal nerve avulsion

23 Therapy Surgical - Experimental
Recurrent laryngeal nerve denervation and reinnervation Type II thyroplasty Posterior cricoarytenoid myoplasty with medialization thyroplasty

24 Botulinum Toxin Goldstandard treatment for SD
Prevents presynaptic release of acetylcholine (Ach) at neuromuscular junction. Different serotypes of botulinum toxin exhibit specific proteolysis of proteins involved in transport and binding of Ach vesicles to presynaptic membrane. Result in temporary paralysis

25 Botox mechanism of action
Release of acetylcholine at the neuromuscular junction is mediated by the assembly of a synaptic fusion complex that allows the membrane of the synaptic vesicle containing acetylcholine to fuse with the neuronal cell membrane. The synaptic fusion complex is a set of SNARE proteins, which include synaptobrevin, SNAP-25, and syntaxin. After membrane fusion, acetylcholine is released into the synaptic cleft and then bound by receptors on the muscle cell. JAMA. 2001;285:

26 Botox mechanism of action
Botulinum toxin binds to the neuronal cell membrane at the nerve 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.

27 Botulinum Toxin Effects and Side Effects:
Reduction in voice breaks reported by 48 hrs Treatment lasts an average of 3-4 months before recurrence of symptoms Most common side effect is breathiness Other side effects include: dysphagia, prologued voice loss, aspiration, hoarseness, pain at injection site and stridor (with PCA injection)

28 Botulinum Toxin No absolute contraindications Used safely in children
Give antireflux medication to patients with reflux 3 – 5% of patients have developed resistance to the toxin Resistant patients can sometimes be treated with other toxin serotypes

29 Botulinum Toxin Injection technique for adductor SD (AdSD)
Percutaneous injection guided by electromyographic (EMG) signals. Needle inserted through thyrocricoid membrane and directed upward toward contralateral thyroarytenoid m. Phonation and observation of interference pattern on EMG verifies position

30 Thyroarytenoid injection for adductor spasmodic dysphonia
Thyroarytenoid injection for adductor spasmodic dysphonia. Needle is advanced through the cricothyroid membrane. Pitman MJ

31 Botulinum Toxin Alternate injection techniques for AdSD All methods yield comparable results. Very patient and physician dependent. Transoral laryngoscopic injections The transoral approach involved indirect visualization of the VF via standard laryngoscopicprecedure. VF anesthetized through application of topical cocaine sol’n. BTX is then injected along the superior margin of the VF Transnasal laryngoscopic injections 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 scope is introduced. Once in place, lidocainesol’n drip is applied to the surface of the VF via the working channel while the pt phonates to prevent airway penetration or aspiration. Then inject just lateral to the true VF (to avoid damage to VF mucosa) Transcartilaginous “point touch” injections Insertion of the needle through the surface of the thyroid cartilage halfway b/w thyroid notch and inferior edge. Following insertion the needle is passed through the cartilage and into TA muscle where BTX is injected

32 Botulinum Toxin Injection technique for abductor SD (AbSD)
Requires access to posterior cricoarytenoids Larynx is rotated manually away from injection site. Needle passed posterior to the posterior edge of thyroid at cricoid level into the PCA. Patient is asked to sniff to contract PCA and verify correct position

33 Posterior cricoarytenoid (PCA) injection for abductor spasmodic dysphonia. Needle is advanced through the inferior constrictor muscle to the PCA muscle. Pitman MJ

34 Botulinum Toxin Blitzer et al. 1999
Reported their 12 yr experience with more than 900 patients with SD 90% of patients with AdSD and 66.7% with AbSD achieved a normal voice after injection Injection after nerve section failure showed up to 81% improvement Patients with combined abnormalities only had 30% improvement -Level of evidence (LOE): A

35 Botulinum Toxin Advantages Disadvantages Less invasive than surgery
No permanent damage to nerve or laryngeal structures Temporary nature allows for dosage adjustments Readily available Disadvantages Need for repeated injections Unpredictable relationship between dosage and response Resistance to treatment Adverse side effects

36 Pre-Botox Treatment

37 Post-Botox Treatment

38 Pre-Botox Treatment

39 Post-Botox Treatment

40 Neuropharmacology No controlled studies demonstrate effective symptom control Beta blockers – propranolol Anticholinergics – trihexyphenidylHCl (Artane) Benzodiazepines – diazepam, alprazolam Role has been to provide relief without any demonstrable symptom reduction

41 Voice Therapy No demonstrated effectiveness in treating SD May help:
Rule out psychogenic disorder Provide support for those who do not benefit from Botox (mild symptoms) Some patients use it in adjunct to Botox to prolong symptom free period Traditional voice therapy approaches for ADSD employ techniques for avoiding overpressure. Breathy voice onsets, reduced speech force, using a head focus, and laryngeal manipulation are aimed at reducing laryngeal tension. Can also use relaxation and respiration training to help gain insight and control of laryngeal tension during speech.

42 Recurrent laryngeal nerve section
Dedo 1976 Case series of 34 patients that had RLN section “All experienced symptom improvement” No objective measurement of outcome -LOE:C Dedo 1991 Retrospective review of 300 patients after RLN section 82% had little or no symptoms after 5-14 years No prospective comparative data available -LOE:B (add pics and make it 2 slides if necessary) Dedo first recognized that ADSD could be surgically treated d/o. His first publication was a case series in which he describes the outcomes of 34 pts who underwent RLN. They observed that RLN paralysis retract the involved VC from midline (in paramedian position) so the nml fails to reach as firmly as usual, causing a breathy but often phonatory soft voice. Tried lidocaine injections on one of his pts who was relieved of the spasms and agreed to indogoe RLN section for a more permanent relief. He then sectioned the RLN in 34 pts after they showed improvement after Xylocaine temporary paralysis showed significant improvement in vocal quality. They treated pts w unilateral RLN section. Thinking that the Creation of unilateral VC paralysis could prevent hypperadduction and loss of speech fluency at the cost of the dysphonia associated with paralysis. In his 1991 publication, which was a retrospective review of pre and post operative I recordings, of 300 pts who underwent RLN section. Pts answered questionaires regarding voice production and voice recordings analyzed by perceptual voice eval and acoustic analysis of voice spectra. 15% developed recurrence of mild to moderate spasticity 6-24mo after RLN section. – curable w laser cord thinning via DL. 82% had little or no voice spasticity 5-14yr after RLN section Aronson and DeSanto Since then, this approach has been abandoned by most laryngologists in favor of the reliability of BTX injections.

43 Recurrent laryngeal nerve section
Aronson and DeSanto 1983 Followed 33 patients for 3 years post RLN section 36% maintained improved voices Of the 64% failed voices, 48% were worse than before surgery Effectiveness of unilateral RLN section for severe ADSD decreases with time Limitations: small sample study -LOE:C (Pics from article – scan) They concluded that the effectiveness of unilat RLN section for severe ADSD decreases with time and results in voice failure in a sizeable percentage of patients. Return of sxs not due to reactivation of VC, but hyper adduction of normal VF alone or along with other m of supra glottis and extrinsic laryngeal m. Since this study RLN section was widely abandoned for the simpler BTX injection method for temporary relief of SD sxs.

44 Recurrent laryngeal nerve avulsion
Netterville 1991 Retrospective review of 12 patients No recurrence at 1.5 years LOE:C Follow up report 1996 18 patients followed for 3-7 yrs post RLN avulsion 16/18 patients were without spasm Most common side effect was breathy voice – Six underwent medialization laryngoplasty LOE:C

45 Therapy Surgical Experimental
Recurrent laryngeal nerve denervation and reinnervation Type II thyroplasty Posterior cricoarytenoidmyoplasty with medializationthyroplasty

46 Recurrent laryngeal nerve denervation and reinnervation
Berke and Blumin 2006 Retrospective study analyzing satisfaction surveys and perceptual evaluation of post operative voice 83 of 136 patients returned surveys with 91% satisfied with fluency of voice 46 patients provided voice recordings for perceptual evaluation: 26% had voice breaks, and 30% breathiness -LOE:B

47 Recurrent laryngeal nerve denervation and reinnervation
Limitations: high drop out rate (61%), small sample size, no long term prospective studies Disadvantages Technical difficulty Recurrence of symptoms Does not prevent unwanted reinnervations Advantages Permanent effect Less breathiness due to maintenance of VF tone from ansa cervicalis innervation

48 Midline lateralization thyroplasty
Isshiki et al. 2001 Retrospective review of 6 SD patients 5/6 patients obtained near normal voices Failure attributed to difficulty in lateralization and concurrent focal neck dystonia Limitations: small samples, no long term prospective studies, no objective measures described -LOE:C

49 Atlas of Head & Neck Surgery—otolaryngology By Byron J. Bailey, Karen H. Calhoun, Norman

50 Modified Type II Thyroplasty
Midline lateralization thyroplasty (type 2 thyroplasty) after completion of the procedure. “A” type using a composite graft for the closure of a tiny perforation at or slightly above the anterior commissure. A muscle flap is used to cover the graft. G = A composite graft. Isshiki: Laryngoscope, Volume 111(4).April

51 Modified Type II Thyroplasty
B” type without using a graft. (A) The incised edges are pulled apart to test the lateralization effect on voice. (B) The incised edges are separated at a desired distance (usually 3–4 mm) and fixed with silicone shims. Isshiki: Laryngoscope, Volume 111(4).April

52 Midline lateralization thyroplasty
Chan 2004 Prospective case series with 13 subjects Used method described by Isshiki 9/13 patients failed; 2 had their surgery reversed Reason for failure unclear Limitations: small sample, only used self-rating assessments and no objective measures LOE:C Unclear why some pts deteriorate over time, especially when they had good early results p sx. Presume that with time the VF hyperadduction is able to overcome the initial lateralization created by the shims because the underlying neuropathology has not been resolved. Continue to recommend BTX as gold standard.

53 Midline lateralization thyroplasty
Advantages: Optimal glottal closure can be adjusted and readjusted No damage of physiologic function Reversible Disadvantages: Technically difficult Shim displacement Does not relieve cause of SD Require careful patient selection Lacks reproducibility Limitations of a retrospective study

54 Posterior cricoarytenoid myoplasty with medialization thyroplasty
Shaw 2003 Case report of 3 patients with AbSD refractory to BTX treated with surgery and followed up to a year post surgery All reported improved subjective symptoms and showed objective reduction in phonatory breaks Limitations: Small sample and no long term prospective outcomes -LOE:D

55 Posterior cricoarytenoid myoplasty with medialization thyroplasty
Shaw , Ann OtolRhynolLaryngol (2003) 112:

56 Summary Treatment Advantage Disadvantage Botulinum Toxin
Type A (Botox) Current “gold standard”; Readily available; less invasive Not permanent cure; risk of immunoresistance; “breathy” voice Type B (Myobloc) Alternative for resistant patients Limited availability and use in SD Voice Therapy Inexpensive; No side effects; non-invasive; no contraindications; adjunct to BTX Not effective alone; requires high patient compliance; takes time to learn RLN Section / Avulsion “permanent” treatment Invasive; symptom recurrence Laryngeal adductor denervation-reinnervation “permanent” treatment; option for patients resistant to BTX Invasive; limited availability and long term outcome data Laryngeal framework approach “permanent” treatment; does not target nerve function, reversible PCA myoplasty with medializationthyroplasty “permanent” treatment; does not target nerve function

57 Summary SD is an idiopathic d/o of the larynx. The mainstay of treatment continues to be BTX injections into the laryngeal muscles. BTX txt is not perfect -- there is an onset time characterized by a breathy voice and dusphagia and an offset time characterized by a recurrence of sxs. Occasionally pts can develop antibodies and resistance. Some pts don’t like to receive multiple injections a year. Because of these shortcomings alternative, more permanent treatments have been sought. Surgery for ASDS was initially developed in the 1970s but has been abandoned because of poor long term results. A RLN denervation and reinervation and laryngoplastic techniques may hold promise for long term treatment. All current therapies for SD are directed toward the symptoms of the d/o. There is still work toward understanding the underlying cause so we can then possibly develop a cure to the disease.

58 References Pearson EJ and Sapienzam CM. Historical approaches to the treatment of Adductor-Type Spasmodic Dysphonia: Review and tutorial. NeuroRehabilitation (2003) 18: Sulica L. Contemporary management of spasmodic dysphonia. CurrOpinOtolaryngol Head Neck Surg (2004) 12: Berke GS and Blumin JH. Spasmodic dysphonia: therapeutic options. CurrOpinOtolaryngol Head Neck Surg (2000) 8: Grillone GA and Chan T. Laryngeal Dystonia. OtolaryngolClin N Am (2006) 39:87-100 Blitzer A, Brin MF, Stewart C. Botulinum toxin management of Spasmodic Dysphonia: 12-year experience in more than 900 patients. Laryngoscope (1998) 108(10): Mehta RP et al. Long-term therapy for spasmodic dysphonia-acoustic and aerodynamic outcomes. Arch Otolaryngol Head Neck Surg (2001) 127: Aronson AE and DeSanto LW. Adductor spastic dysphonia: three years after recurrent laryngeal nerve resection. Laryngoscope (1983) 93:1-8 Dedo HH and Behlau MS. Reccurent laryngeal nerve section for spastic dysphonia: 5 to 14 year preliminary results in the first 300 patients. Ann OtolRhinolLaryngol (1991) 100: Dedo HH. Recurrent laryngeal nerve section for spastic dysphonia. Ann Otol (1976) 85:451459 Weed DT et al. Long term follow up of recurrent laryngeal nerve avulsion for the treatment of spastic dysphonia. Ann OtolRhinolLaryngol (1996) 105:

59 References Netterville JL et al. Recurrent laryngeal nerve avulsion for traemtent of spasmodic dysphonia. Ann OtolRhinolLaryngol (1991) 100:10-14 Chhetri DK, Mendelsohn AH, Blumin JH, Berke GS. Long term follow up results of selective laryngeal adductor dennervation-reinnervation surgery for adductor spasmodic dysphonia. Laryngoscope ( 2006) 116: Berke GS et al. Selective laryngeal adductor denervation-reinnervation: a new surgical treatment for adductor spasmodic dysphonia. Ann OtolRhinolLaryngol (1999) 108: Isshiki N et al. Midline lateralization thyroplasty for adductor spasmodic dysphonia. Ann OtolRhinolLaryngol (2000) 109: Isshiki N, Yamamoto I, Fukagai S Type 2 thyroplasty for spasmodic dysphonia fixation using a titanium bridge. ActaOtolaryngol (2004) 124: Isshiki N et al. Thyroplasty for adductor spasmodic dysphonia: further experience. Laryngoscope (2001) 111: Shaw GY, Sechtem PR, Rideout B. Posterior cricoarytenoidmyoplsty with medializationthyroplasty in the management of refractory abductor spasmodic dysphonia. Ann OtolRhynolLaryngol (2003) 112: Simonyan K et al. Focal white matter changes in spasmodic dysphonia: a combined diffusion tensor imaging and neuropathological study. Brain (2008) 131: Jurgens U. Neural pathways underlying vocal control. Neuroscience and Biobehavioral Reviews (2002) 26:

60 References Stemple JC. Clinical Voice Pathology 3rd ed. Singular publishing grp(2000) SataloffRT. Treatment of Voice Disorders. (2005) Plural Publishing Inc. San Diego StempleJC. Voice Therapy: Clinical Studies. Mosby-Year Book, Inc. (1993) Fried MP. The Larynx: A Muiltidisciplinary Approach. 2nd Ed. (1996) Mosby-Year Book, Inc Cummings Shaefer SD. Neuropathology of spasmodic dysphonia. Laryngoscope (1983) 93: Rubin J, Satalof R, Korovin G. Diagnosis and Treatment of Voice Disorders. 3rd Ed. Plural Publishing Inc (2006) San Diego, CA Add all of the articles

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