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Craig H. Zalvan, Phillip C. Song,
Nwanmegha Young, and Andrew Blitzer

For almost 20 years, botulinum neurotoxin (BoNT) has been the gold-standard treatment for spasmodic dysphonia. Since it was first publicized in mainstream society, the use of BoNT has grown at a staggering rate, with toxin being utilized in almost every field of medicine. Within the field of laryngology, the use of BoNT has also found a multitude of uses other than for spasmodic dysphonia. Almost any type of hyperkinetic or compensatory behavior found can be treated with the use of this toxin with a high degree of success, a low side-effect profile, and significant patient satisfaction. Toxin has been injected into the laryngopharynx for vocal tics, stuttering, vocal tremor, ventricular dysphonia, bilateral vocal fold paralysis, tracheoesophageal speech failure, as well as many other applications. By using toxin, many of these symptoms are controlled more easily, often requiring less systemic medication. Also, toxin is used as an adjunct to other types of traditional therapy, such as voice therapy and swallowing therapy, and even to surgical interventions. Additionally, because of the physiologic effects of weakening muscle, the toxin can be used to “rebalance” the larynx. In cases of bilateral vocal fold paresis, selectively weakening the adductor muscles can provide for an adequate airway and help avoid a surgical intervention. Patients with vocal fold granulomas can benefit from toxin injection to help decrease the traumatic forces of the posterior glottis, thus decreasing the recurrence of granuloma and helping with resolution of persistent granulomas. In almost every situation of hyperfunction of the laryngeal and extralaryngeal musculature, BoNT can be used to help ameliorate symptoms and provide significant, reproducible relief for patients.

Bilateral vocal fold paralysis can be a devastating consequence of neck surgery, brainstem disease, or systemic disease that often leaves a patient with severe debilitation including shortness of breath and stridor with airway compromise. Patients often require airway intervention ranging from tracheotomy to simple posterior vocal fold cordectomy. Most laryngologists advocate waiting at least 1 year from the onset of the bilateral paralysis before performing a laryngeal destructive procedure to create an adequate airway to allow for laryngeal patency and removal of a tracheotomy tube. The problem arises when patients have bilateral vocal paresis with probable return of function. In these cases, patients are newly diagnosed with airway compromise and may be stable at rest or moderately symptomatic without distress. In this situation, a tracheotomy can possibly be avoided, removed early, or capped, by using BoNT injection into either a unilateral or bilateral thyroarytenoid and lateral cricoarytenoid (TA/LCA) muscle complex. By inhibiting the adductory function during reinnervation, the abductor muscles can contract unopposed, often leading to a larger airway caliber that allows for better airflow. In a recent study, 10 of 11 patients obtained substantial relief from airway obstruction after either bilateral or unilateral followed by bilateral BoNT injection into the TA/LCA complex.1

Another group injected into the thyroarytenoid and interarytenoid muscles, yielding similar results of increased airway patency at rest and with activity. “Rebalancing” of the paralyzed vocal folds allowed for more abduction and hence a larger airway.² There has also been animal based research demonstrating the value of BoNT injection for bilateral vocal fold paralysis.³

Another use of BoNT in patients with bilateral vocal fold paralysis pertains to those with implantable laryngeal stimulators within the posterior cricoarytenoid muscle. By weakening the opposing adductory forces with chemical denervation, the airway patency was increased, alleviating the symptoms of dyspnea. Thus by using electrical stimulation and chemical denervation, this group was able to decannulate patients with longstanding bilateral vocal fold paralysis.4

Typical treatment utilizing BoNT involves bilateral injections of the thyroarytenoid muscles utilizing the standard EMG-guided anterior neck approach; 2.5 units (U) of toxin is injected bilaterally as the initial dose. A second dose of 0.5 to 1 U can be injected 2 to 3 weeks after the initial dose if there has been little or no response. Typical side effects can range from no ill effects to severe breathiness and occasional coughing while drinking liquids. Gross aspiration is possible but has not occurred in our experience. Patients with severe airway compromise or progressive compromise despite BoNT injection are not good candidates for this type of medical intervention, and airway security is the primary concern.

Tracheoesophageal Speech Failure

Loss of voice after total laryngectomy is an unavoidable morbidity. However, with the widespread use of a tracheoesophageal puncture (TEP) and voice prosthesis, patients can develop and maintain the ability to communicate. A major disappointment occurs when that ability is lost again because of dysfunction of the prosthesis from fungal infection, dislodgement, and hyperfunction of the cricopharyngeus or pharyngoesophageal segment, preventing normal airflow through the TEP. In addition, some laryngectomy patients initially fail an insufflation test of the pharyngoesophageal segment, demonstrating hyperfunction of this segment and likely poor TEP function.

The use of BoNT had repeatedly been shown to be an excellent adjunct in the treatment of these hyperfunctional disorders of the pharyngoesophageal segment. In cases where the diagnosis of failure of the TEP is uncertain, BoNT injection into the inferior constrictor and cricopharyngeal fibers can provide diagnostic information by either its success or failure. In addition, this can provide long-term treatment as well. By paralyzing the hyperfunctional muscle fibers, airflow through that segment is possible, allowing for diversion through the TEP and thus normal function. Typically the toxin is administered using EMG guidance and injecting transcutaneously through the neck; 50 U is the typical starting dose delivered bilaterally in equal doses. If there is no response, up to another 50 U can then be administered. The cricopharyngeus muscle is identified by finding baseline activity at rest, which diminishes with a swallow with prompt return of function after the swallow.^5,6 Side effects are rare and may include some dysphagia from weakened constrictor muscles from toxin diffusion. Because of the alaryngeal state, there is no risk of aspiration or airway compromise.

Benign Vocal Fold Disease

Benign vocal fold disease such as vocal fold nodules, polyps, cysts, granulomas, and hemorrhages all share a common etiologic factor: trauma. Chronic overuse of the voice, vocal abuse, acute phonatory trauma from coughing and yelling, and excessive Valsalva maneuver can all lead to thickening of the epithelium of the vocal folds, subepithelial fibrosis, and vocal hemorrhage. In many of these cases, voice therapy is the gold standard of treatment. Other cases require microsurgical intervention using a microflap technique of removal to optimize vocal outcome. However, often patients are reluctant to undergo surgery, and surgery does entail some inherent risk to long-term outcome. In certain circumstances, in patients with recurrent vocal fold benign disease, or dysphonia that persists despite voice therapy and surgery, BoNT can be used as an adjunct to temporarily weaken the adductory forces of the glottis to allow for healing or resolution of the benign vocal fold disease. By using this technique, there is no risk to the superficial lamina propria from surgical trauma. In addition, patients can continue undergoing voice therapy to help prevent recurrent lesions. Some patients can develop a temporary breathiness inherent in injecting the adductor muscles with BoNT. This tends to be short lived and is lessened by a decreased quantity of injected toxin if subsequent injections are deemed necessary.7 The typical starting dose is 1 U of toxin delivered by EMG-guided injection into the thyroarytenoid muscle. Side effects are typical for BoNT injection and include breathiness and possible aspiration. Mild breathiness for a few weeks is ideal, as this gives time for the mucosal pathology to resolve. With ongoing voice therapy, these lesions can actually regress and often do not recur once behavioral changes have been made.

Although BoNT may be very successful for a variety of hyperkinetic laryngeal disorders, care must be taken to evaluate the larynx in a systematic and critical manner. We have used selective chemodenervation for a variety of conditions such as muscle tension dysphonia, laryngeal tremor, vocal cord dysfunction or paradoxical vocal fold motion, spastic dysarthria, arytenoids rebalancing, idiopathic chronic cough, and contact granulomas, and results can be variable. The following potential problems may occur with selective laryngeal chemodenervation using BoNT:

1. The specificity of injections may be inadequate due to inherent difficulties with site localization and diffusion of BoNT to adjacent muscles.

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