Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00306932607174,00302841026182,alsfakia@gmail.com
Treatments for spasmodic dysphonia
Symptom reduction occurs when the kinetic output of the laryngeal muscles is reduced either by unilateral recurrent laryngeal nerve section (Dedo, 1976), or by botulinum injections into the adductor muscles for adductor SD or the abductor muscle for abductor SD (Blitzer et al., 1998). Following nerve section, benefits occur until reinnervation takes place and symptoms return (Dedo, 1976; Aronson and DeSanto, 1981; Fritzell et al., 1982). Further approaches were to avulse a long section of the recurrent nerve to prevent reinnervation (Netterville et al., 1991; Weed et al., 1996) or bilaterally section and reinnervate the nerve branch going to the thyroarytenoid muscle to the ansa cervicalis to prevent reinnervation by the recurrent laryngeal nerve (Berke et al., 1999; Chhetri et al., 2006). In these treatments, a balance must be achieved between adequately reducing vocal fold hyperadduction while not producing aspiration during swallowing or aphonic speech (Salassa et al., 1982).
These treatment approaches interfere with muscle action rather than blocking abnormal interneuron firing patterns in the laryngeal efferent pathway. As mentioned earlier, symptom reduction might be due to alterations in sensory feedback to the CNS (Bielamowicz and Ludlow, 2000) or retrograde transmission of botulinum toxin to modulate interneurons in the CNS affecting motor neuron firing (Moreno-López et al., 1997; Antonucci et al., 2008). Clinically, after unilateral injections of botulinum toxin into the thyroarytenoid muscle in adductor SD, the numbers of spasms in the untreated muscles on the opposite side of the larynx were reduced (Bielamowicz and Ludlow, 2000). Reduced muscle force in the larynx may reduce sensory feedback to the central pattern generators in the brainstem or the sensorimotor cortex. One study of SD patients before and after successful treatment with botulinum toxin injection found increased activity in the sensorimotor cortex in untreated SD patients, which normalized after treatment with botulinum toxin muscle injection (Ali et al., 2006).
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