Combined-modality treatment of adductor spasmodic dysphonia with botulinum toxin and voice therapy

A combined-modality treatment program consisting of botulinum toxin injection (Botox) and voice therapy was used to treat 17 subjects diagnosed with adductor spasmodic dysphonia (ADD SD). Ten subjects with ADD SD served as the control and were given Botox only. Voice therapy after Botox injection was directed toward reducing the hyperfunctional vocal behaviors, primarily glottal overpressure at voice onset and anterior-posterior squeezing. The results indicated that subjects who underwent combined-modality treatment maintained significantly higher mean airflow rates for significantly longer periods. Moreover, there was a carryover effect in these patients when they received Botox only. Adductor spasmodic dysphonia is treated most effectively when intrinsic laryngeal muscle spasms are reduced or eliminated by Botox injection and extrinsic hyperfunctional vocal behaviors are treated with voice therapy     

Behavioral therapy for spasmodic dysphonia

This paper presents a general schema for classifying treatment approaches for both functional and organic voice disorders. It's use is illustrated by a review of treatments for Spasmodic Dysphonia. Most behavioral approaches have been found to be unsuccessful except for mild cases. Inhalation speech as a compensatory technique has been reported as somewhat successful for those mild/moderate cases for whom medical/surgical treatment has not been available. The fact that organic treatment levels have been more successful in the treatment of Spasmodic Dysphonia may lend support to an organic etiology     

Symptomatology of adductor spasmodic dysphonia: A physiologic model

Vocal symptomatology of adductor spasmodic dysphonia (SD) is reviewed critically from historical, epidemiologic, and clinical perspectives. A model of symptomatology of this disorder based on a large patient population, and clinical and physiologic observations is advanced. The model incorporates crucial symptomatic and asymptomatic phonatory and nonphonatory physiologic parameters of laryngeal behavior in these patients. These parameters include vocal fold contact area, vocal fold collision force, glottic compression, and subglottic air pressure. Inappropriate efferent discharges from brain-stem basal ganglia are hypothesized as causing overadduction of the vocal folds in phonation, generating the basic and fundamental vocal symptom of adductor SD—strained, strangled, overpressured voice quality. Cortical loops are implicated as accountable for compensatory vocal behavior, not as the primary site of the disorder. Symptom occurrence, variability, magnitude, effects, and failure of treatment approaches, as well as recurrence of symptoms after ablative or invasive procedures, are explained by this model. The model also predicts that symptomatology of adductor spasmodic dysphonia is unique to this disorder and that symptoms are phonotopically organized. The minimal diagnostic battery based on the model is presented, and it is shown how this battery aids in the differential diagnosis of adductor SD and other phonatory disorders that closely mimic the vocal symptoms of adductor spasmodic dysphonia, including tremor.     

Vocal stability in functional dysphonic versus healthy voices at different times of voice loading

Functional (nonorganic) dysphonia is often characterized by vocal instability. The purpose of the prospective study was to examine whether there is a difference in vocal instability of functional dysphonic voices compared with healthy ones, this means whether electroglottographic perturbation values differ (1) between healthy and dysphonic voices and (2) between two subgroups of the dysphponic voices (hpertonic and hypotonic dysphonic voices). Twenty-three patients with hypertonic functional dysphonia, 9 with hypotonic functional dysphonia and 31 healthy nonsmokers, were each examined electroglottographically before (Ex 1), immediately after (Ex 2), and 1 hour after (Ex 3) voice loading. Perturbations of frequency, amplitude, quasi-open-quotient, and contact-index were calculated from the EGG signal. At all three times of examination, hypertonic dysphonic voices showed higher perturbations than healthy voices, and they had higher perturbations than hypotonic dysphonic voices before and 1 hour after voice loading. Hypotonic dysphonic voices showed higher perturbations than healthy voices only 1 hour after voice loading. Voice loading induced different reactions in dysphonic voices: Some voices showed increased perturbations, and others exhibited normal or even decreased perturbation immediately after voice loading. Examination of electroglottographic-derived perturbations immediately after voice loading seems not to be useful. Differentiation of hypertonic and hypotonic dysphonic voices was possible with an estimated sensitivity of 88.9% and a specificity of 87.0% by using the sum of the amplitude-perturbation and the quasi-open-quotient-perturbation measured before voice loading.     

Functional assessment of patients with spasmodic dysphonia

Assessment of function in patients with spasmodic dysphonia is necessary to confirm diagnosis, plan therapy, predict response, and assess effectiveness of treatment. This task is difficult because symptom severity fluctuates, the test environment is artificial, and the objective parameters used to measure vocal function may not adequately reflect the handicap experienced by the patient. Available methods for assessing these patients are reviewed and the utility of each considered, particularly in managing patients with botulinum toxin therapy. Assessment should include a battery of tests, including subjective perceptual ratings and direct physical measurements.