Botulinum toxin therapy of laryngeal muscle hyperactivity syndromes: comparing different botulinum toxin preparations D. D. Truong a and R. Bhidayasiri a,b,c a The Parkinson’s and Movement Disorder Institute, Fountain Valley, CA, USA; b Movement Disorders Group, Division of Neurology, Chulalongkorn University Hospital, Bangkok, Thailand; and c Department of Neurology, UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA Keywords: abductor spasmodic dys- phonia, adductor spas- modic dysphonia, botulinum toxin, laryngeal spasmodic dyspnea, voice tremor, voice tremors Spasmodic dysphonia (SD) is a focal dystonia characterized by a strained, strangled voice. Botulinum toxin is a symptomatic treatment for SD and has become the mainstay of therapy over the last two decades. In this manuscript, we briefly review different laryngeal muscle hyperactivity syndromes, their injection techniques and toxins currently available. Adductor SD is the most common indication for botulinum toxin treatment in the larynx. All studies report similar results with regard to improvement, patient satisfaction and side effects. We describe different injection techniques to treat this disorder such as the percutaneous, transoral, transnasal, point- touch techniques. In abductor SD, a subtype of SD, the treatment is aimed at the posterior cricoarytenoid muscle. Other applications of botulinum toxin in the larynx include spasmodic laryngeal dyspnea and voice tremors. We also review injection techniques, the different toxin types used, and toxin doses. Introduction Spasmodic dysphonia (SD) is a focal dystonia charac- terized by task-specific, action-induced spasm of the vocal cords. It adversely affects the patient’s ability to communicate. It was first described by Traube in 1871 as a Ônervous hoarsenessÕ and assigned the label of spastic dysphonia (source: National Spasmodic Dys- ponia Association). It can occur independently, as part of Meige’s syndrome, or in other disorders such as in tardive dyskinesia. Historically, SD was thought to be psychogenic or traumatic in origin [1]. Dedo’s recurrent nerve surgeries were a bold solution at a time when his contemporaries still advocated psychotherapy as the mainstay of treat- ment. Such surgery offered a solution to the problem of inappropriate glottic function, but disappointing long- term results limited its usefulness. It was soon replaced by chemical denervation with botulinum toxin, which offers a temporary but repeatable benefit over the long term. Clinical features There are three types of SD: the adductor type, the abductor type and the mixed type. Adductor spasmodic dysphonia (ADSD) is characterized by a strained- strangled voice quality and intermittent voice stoppage or breaks due to overadduction of the vocal folds, resulting in a staccato-like voice [2,3]. Abductor spas- modic dysphonia (ABSD) is characterized by intermit- tent breathy breaks, associated with prolonged abduction folds during voiceless consonants in speech [2–4]. Patients with the mixed type have presentations of both. Symptoms of SD develop gradually over several months to years. The condition typically affects patients in their mid-forties and is more common in women [5,6]. A high incidence of childhood viral illness has been found in patients with SD [6]. A significantly higher incidence of essential tremor and writer’s cramps were also observed [6]. Fourteen percent of patients with SD showed spreading of dystonia beyond the larynx [7]. The body parts that are most commonly involved are the lower face, jaw, tongue and neck. For these patients, the mean duration before spreading was 7.3 years, with a median of 4 years [7]. SD may coexist with vocal tremor [8]. Patients with ADSD show evidence of phonatory breaks during vocalization [9]. The vocal breaks typic- ally occur during phonation associated with voiced speech sounds [10,11]. Stress commonly exacerbates speech symptoms, whilst they are absent during laughing, throat clearing, coughing, whispering, hum- ming and falsetto speech productions [2,8,10]. The voice tends to improve when the patient is emotional. Speech studies have shown that SD is a movement- control disorder affecting vocal fold for phonation onset, with no laryngeal movement difficulty [10]. Magnetic resonance imaging of patients with SD has Correspondence: Daniel D. Truong, MD, The Parkinson’s and Movement Disorder Institute, 9940 Talbert Ave, Fountain Valley, CA 92708, USA (tel.: +1 714 378 5062; fax: +1 714 378 5061; e-mail: dtruong@pmdi.org). 36 Ó 2006 EFNS European Journal of Neurology 2006, 13 (Suppl. 1): 36–41