Spasmodic Dysphonia is a disabling disorder of the voice characterized primarily by involuntary disruptions of phonation. It may also be accompanied by hoarseness, tremor, and pitch breaks. This disorder was originally thought to be psychological in origin. However, in recent years, spasmodic dysphonia has become classified as a movement disorder of the larynx. Thus, spasmodic dysphonia is a vocal dystonia. It is similar to such neurological disorders as writers cramp and blepharospasm, rapid eye-blinking movements. These disorders are all known as focal dysphonis. There are two general types of spasmodic dysphonia. Adductor spasmodic dysphonia (ADSD) is characterized by a squeezed, strained-strangled effortful phonation with voice stoppages and voice breaks. Abductor spasmodic dysphonia (ABSD) is characterized by an excess flow of air with intermittent lack of vocal fold closure. In some cases, patients have evidence of of both types. By far, the most common of these is the adductor type. In ADSD, irregular spasmodic movements of the vocal folds and hyperadduction of other structures in the larynx severely affect ones ability to communicate.

Previous treatment of spasmodic dysphonia has ranged from hypnosis to psychotherapy as well as voice therapy. In the mid 1970's, a surgical procedure was devised in which the nerve going to the vocal fold was severed. This procedure, called unilateral recurrent laryngeal nerve resection, resulted in a weakening of the vocal fold muscle similar to vocal fold paralysis and for some, there was improvement in voice use.. The voice, after recurrent laryngeal nerve resection, was generally softer, however, a number of these patients developed symptoms again.

The general consensus of using voice therapy alone has been that patients may achieve temporary improvement under limited speaking conditions, such as speaking at a whisper, speaking with a falsetto voice, or speaking while laughing. However, there was little lasting carryover. Although a few exceptions to the general findings have been noted, objective documentation is lacking to establish the efficacy of voice therapy as a single treatment in patients with a confirmed diagnosis of spasmodic dysphonia.

More recently, a new surgical technique has been advocated to treat the problem. However, this surgical treatment is still in the early stages and may not be reversable when a permanent treatment is found.

Approximately 15 years ago, a report on significant improvement in two patients was published. These patients were injected with Botulinum Toxin A (Botox) into the vocal fold muscle. Following that injection, there was a dramatic improvement in their ability to speak. Following these initial reports, botox became increasingly available and has since become the choice of treatment for patients with spasmodic dysphonia. For ADSD, botox is injected into the thyroarytenoid muscle by passing the needle between the cricoid and thyroid cartilages and into the vocal fold. For ABSD, the posterior cricoarytenoid muscle is usually injected. Although dosages and injection techniques vary, botox has become the choice of most patients and physicians for treating spasmodic dysphonia. Botox injection leads to symptom relief for up to six months and occasionally longer with few or no long term effects. Patients report less effort to vocalize one or two days after treatment. Although the treatment is temporary, the effects of botox are significant from a communication standpoint. That is, patients are able to engage in social conversation without the stigma of voice breaks and voice stoppages.

Treatment of spasmodic dysphonia begins with an accurate diagnosis. The diagnostic work up generally consists of a thorough case history, including neurological history. Although most patients have some difficulty in pinpointing the exact onset of the disorder, they generally describe a slow, progressing form of voice difficulty that consists of voice breaks, some degree of hoarseness, more difficulty speaking in noisy situations, and increased difficulty when attempting to use a loud voice. Acoustic and aerodynamic assessments of the voice are made to determine the severity as well as to objectively identify the presence of voice breaks. A flexible endoscopic examination of the larynx and vocal folds is also conducted. Videolaryngoscopic examination is necessary to rule out other diseases and conditions that may sound like spasmodic dysphonia. These include vocal fold atrophy, vocal fold paralysis, muscular tension disorders, and the presence of lesions on the vocal folds. If the patient does not have a current neurological examination, the patient is referred to a neurologist for comprehensive evaluation.

Following the evaluation, patients are given a thorough explanation of spasmodic dysphonia. Patients are advised that although other treatments are available, botox injection is the current choice of treatment at this point for this disorder. The patient returns for botox injection after he or she has had a chance to consider the alternatives, be examined by a neurologist, and discuss the treatment options with his or her family physician. Treatment consists of injections generally to both thyroarytenoid muscles. After applying a local anesthetic to the neck area and attaching electrodes to the patient to monitor needle placement, a small needle is inserted between the thyroid and cricoid cartilages and directed up to the vocal fold. In most cases of adductor spasmodic dysphonia, botox is injected into each thyroarytenoid muscle. In patients with severe ADSD, dosage may be greater, up to 2.5 units in each muscle. For those patients with ABSD, approximately 1.25 units of botox is injected into the posterior cricoarytenoid muscle on each side. This muscle has been found to be somewhat more difficult to reach. Thus, there has been less success with treating abductor spasmodic dysphonia in this way. In some cases, the dosage may be greater on one side if upon examination there was evidence of greater spasm activity on one side. The entire treatment process takes about 15 minutes and the patient is free to leave after the treatment.

Three to five days after treatment, the patients report back by telephone the changes in voice and other side effects such as possible swallowing difficulties in the ADSD group or breathing difficulty in the ABSD group. For patients with ADSD, the voice usually changes to a breathy quality 24 to 48 hours after injection; difficulty in swallowing liquids may occur because the vocal folds are weakened by the injection. For patients with ABSD, the side effects may be shortness of breath or difficulty breathing when doing exercise. If the conditions last longer than a week, a note of it is made and injection is slightly reduced in follow up treatments.

Approximately 10 days after injection, patients are invited to return for voice therapy. Voice therapy coupled with botox injections has been shown to extend the effects of injection as well as to give the patient a feeling of control over his or her voice. In our clinic, voice therapy begins approximately 10 days to two weeks after botox injection. Approximately six sessions of treatment are planned, and these are spread over a four to five week period. Voice therapy is an option, however, it is highly encouraged to treat the maladaptive compensatory strategies developed prior to botox treatment. The goal of voice therapy in the ADSD patient is to reduce hyperclosure of the vocal folds, to improve voice onset and to control breath flow over the length of a phrase. In patients with ABSD, easy onset followed by reduced explosion of sounds is the focus. By the final session, patients are encouraged to use the practice exercises they are given and to follow up with additional voice therapy. By monitoring the injection during the first four to five day we get a sense of the accuracy of the injection, the strength of response and the quality of the voice. From this information the dosage on the next treatment can be adjusted if necessary. With the addition of voice therapy after botox injection, the patients will extend the time between treatments by as much as 12 to 15 weeks. This is especially true in the ADSD subjects.

The treatment of spasmodic dysphonia continues to be investigated by numerous scientists studying movement disorders. New treatments are needed since botox is not a cure but a temporary relief. Surgical treatments that have been used in the past have also shown success as a treatment but not necessarily a cure. Current investigations include new surgical procedures to treat the disorder, other medications that may help to control movement disorders and improve management of the patient after botox injection. When one considers the significant debilitation caused by spasmodic dysphonia, whether it is ADSD or ABSD, treatments that provide relief are most welcome to all patients.

Please note that Dr. Murry has published extensively on the topic of Spasmodic Dysphonia. To view his publications, please click here.