Ten patients (aged 35 to 70 years) with neurologic adductor spastic dysphonia rated themselves on a 7-point scale of severity for degree of voice improvement and physical effort after a series of three injections of botulinum toxin. Symptoms were noticeably reduced 24 and 48 hours after injection; this improvement was followed by considerable fluctuations in voice quality and phonatory effort. With successive injections, patients differed in their post-injection experiences, the time required to reach optimal voice, and the total duration of benefit. The study shows that the course of voice change after botulinum toxin injection is not predictable, uniform, or equal among patients with spastic dysphonia.

In an attempt to clarify the origin and frequency characteristics of a rapid voice tremor, or “flutter,” in patients with amyotrophic lateral sclerosis (ALS), eight patients (four men and four women; ages 42 to 70 years) who had ALS and rapid voice tremor and an age-and sex-matched control group of eight subjects were asked to sustain the vowel /a/ and their voices were recorded for later analysis. Each segment of phonation was demodulated into amplitude and frequency components. From each subject's 8-second amplitude and frequency signals, a fast Fourier transform analysis was done on a 1-second segment previously identified perceptually as having the most apparent tremor or flutter. The results showed that patients with ALS had multiple combinations of levels and frequencies for amplitude and frequency modulations in comparison with control subjects, who had consistently low levels of modulations. In an attempt to quantify the tremor or flutter in ALS, amplitude and frequency modulations were not clearly or predominantly represented at one point along the spectrum. Nevertheless, these frequency and amplitude modulations are more prominent in patients with ALS than in normal subjects. The origins of these aberrant frequency and amplitude modulations in ALS patients remain obscure, although speculation is that they are of peripheral rather than central nervous system origin.

No AccessJournal of Speech, Language, and Hearing ResearchLetter to the Editor1 Aug 1991Neuroimaging Studies Do Not Prove the Existence of Brain Abnormalities in Spastic (Spasmodic) Dysphonia Arnold E. Aronson, Terrence D. Lagerlund, Section of Speech Pathology Mayo Clinic and Mayo Foundation Rochester, MNNeurophysiology Laboratory Mayo Clinic and Mayo Foundation Rochester, MN Arnold E. Aronson Requests for reprints should be sent to Arnold E. Aronson, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. Section of Speech Pathology Mayo Clinic and Mayo Foundation Rochester, MN Google Scholar More articles by this author , Terrence D. Lagerlund Neurophysiology Laboratory Mayo Clinic and Mayo Foundation Rochester, MN Google Scholar More articles by this author , Section of Speech Pathology Mayo Clinic and Mayo Foundation Rochester, MNNeurophysiology Laboratory Mayo Clinic and Mayo Foundation Rochester, MN https://doi.org/10.1044/jshr.3404.801 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationTrack Citations ShareFacebookTwitterLinked In References American Electroencephalographlc Society. (1987). Medical Instrumentation Committee (Nuwer, M. R., Chairman). Statement on the clinical use of quantitative EEG.Journal of Clinical Neurophysiology, 4, 197. Google Scholar Aminoff, M. J., Dedo, H. H., & Izdebski, K. (1978). Clinical aspects of spasmodic dysphonia.Journal of Neurology, Neurosurgery and Psychiatry, 41, 361–365. CrossrefMedlineGoogle Scholar Aronson, A. E., & Hartman, D. E. (1981). Adductor spastic dysphonia as a sign of essential (voice) tremor.Journal of Speech and Hearing Disorders, 46, 52–58. 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Sapienza Tanya K. Meyer, Scott M. Rickert, Lesley F. Childs and Andrew Blitzer (2012) Spasmodic dysphonia Handbook of Dystonia10.3109/9781841848525.0121 May 2012 Homeopathy98:1 (56-59)1 Jan 2009Treatment of spasmodic dysphonia with homeopathic medicine: a clinical case reportSteve An Xue, Luc de Schepper and Grace Jianping Hao Tanya K. Meyer and Andrew Blitzer (2006) Spasmodic Dysphonia Handbook of Dystonia10.3109/9781420019988.0121 Nov 2006 European Journal of Neurology13 (36-41)1 Feb 2006Botulinum toxin therapy of laryngeal muscle hyperactivity syndromes: comparing different botulinum toxin preparationsD. D. Truong and R. Bhidayasiri Annals of Otology, Rhinology & Laryngology109:8 (741-748)1 Aug 2000Perceptual Characteristics of Adductor Spasmodic DysphoniaTon P. M. Langeveld, Harm A. Drost, Aeilko H. Zwinderman, Johan H. M. Frijns and Robert J. Baatenburg De Jong Journal of Voice9:3 (270-281)1 Sep 1995Psychogenic spasmodic dysphonia: A case study with expert opinionsShimon Sapir Volume 34Issue 4August 1991Pages: 801-805 Get Permissions Add to your Mendeley library HistoryReceived: May 14, 1990Accepted: Aug 16, 1990 Published in issue: Aug 1, 1991 Metrics Topicsasha-article-typesCopyright & PermissionsCopyright © 1991 American Speech-Language-Hearing AssociationPDF downloadLoading ...

The treatment of adductor spasmodic dysphonia using botulinum toxin A was conducted in 13 patients as a double-blind, placebo-controlled study. Patients were diagnosed independently by an interdisciplinary team consisting of speech pathologists, an otolaryngologist, and a neurologist. The toxin or saline was injected into each thyroarytenoid muscle under electromyographic and laryngoscopic guidance. Botulinum toxin A markedly reduced perturbation, decreased fundamental frequency range, and improved the spectrographic characteristics of the voice. Fundamental frequency and phonation time remained unchanged. Patients injected with botulinum toxin A noticed significant improvement in their voices in comparison with the placebo-treated group. Excessive breathiness of the voice occurred in two patients, and mild bleeding in one patient in the botulinum toxin A-treated group. Injection with saline resulted in edema of the vocal cord in one patient. Botulinum toxin A proved to be an effective and safe treatment of adductor spasmodic dysphonia.

Depression, anxiety, and conversion reaction are common in neurologic patients. These disorders can produce neurologic-like symptoms that either mask or intensify those produced by the neurologic disease. This paper reviews clinical and research findings relating psychopathology to the formation and remediation of speech and language disorders in neurologic patients. The need to consider the psychosocial and psychopathological aspects of neurologic communicative disorders, and the link between emotional and communicative processes, are emphasized. Diagnostic criteria for the identification of psychogenic communicative disorders are outlined.

Four patients are described who had neurologic disease and accompanying dysphonia that proved to he partially or entirely psychogenic. The findings suggest that the association of a speech disorder with organic disease does not necessarily imply a causal relationship, even when the speech signs seem to arise from the site or organ system affected by disease. The potential for psychogenic factors to confuse the differential neurologic diagnosis of speech disorders is emphasised.

Four or more years after recurrent laryngeal nerve section for adductor spastic dysphonia, 25 patients assessed their voice quality and phonatory effort in relation to presurgical status, using categorical ratings (gradations of better or worse, and of easier and harder) and also numerical ratings. Quality was judged better by 88%, and effort easier by 84%; but many thought the improvement was only moderate or slight. Three speech pathologists, assessing presurgical and current recordings of the patient's voices numerically, rated the majority of the better and easier voices much closer to their presurgical status than to normal. Clinicians were highly consistent and reliable in their assessments. Patients were often in disagreement with clinician ratings and generally rated their dysphonia as less severe than the clinicians did. These discrepancies are discussed within the context of contradictory opinions regarding the efficacy of recurrent laryngeal nerve section for the treatment of adductor spastic dysphonia.

A recent study by Aronson and DeSanto (1983) showed that, although section of the recurrent laryngeal nerve to relieve adductor spastic dysphonia effected considerable improvement in nearly 100% of the voices immediately after surgery, within the next 3 years 64% had returned to their preoperative status or worse. These findings were based on ratings by one speech pathologist, and the study was not designed to measure the reliability of the rater's judgments.

ABSTRACT This report describes two patients with closed head injuries and post‐traumatic aphonia who regained their voices within one session of symptomatic voice therapy. Their abilities to cough and swallow were intact, and articulation was only mildly impaired. One patient had an ataxic dysarthria and the other had spastic (pseudobulbar) dysarthria. Neither patient had oral‐verbal apraxia. The findings argue against laryngeal paralysis or apraxia of phonation as the underlying cause of the aphonia. Neuropsychologic assessment revealed mild generalised intellectual impairment and frontal lobe signs but no aphasia. We postulate that the aphonia may have been due to a frontal lobe‐limbic system disturbance, which affected these patients' motivation, personality, and judgment. Diagnostic and therapeutic aspects of post‐traumatic aphonia are discussed.

Aphonia, originally due to laryngeal inflammation, became psychogenic and superimposed on the unstable pitch of adolescent voice change. We presumed that the aphonia was adopted as a means of dealing with peer pressure to maintain a high preadolescent pitch as well. Voice therapy was effective in alleviating both the aphonia and mutational falsetto. Clinicians should be alert to underlying mutational falsetto when confronted with an aphonic or dysphonic adolescent patient with no organic laryngeal pathologic condition.

Rate and regularity of diadochokinetic syllable repetitions of /p/, /t/, and /k/ in 30 normal subjects, 30 subjects with spastic dysarthria, and 30 subjects with ataxic dysarthria were measured by computer. Normal subjects had rates (syllables per second) of 6.4, 6.1, and 5.7; spastic dysarthric subjects, 4.6, 4.2, and 3.5; and ataxic dysarthric subjects, 3.8, 3.9, and 3.4 for /p/, /t/, and /k/, respectively. Spastic and ataxic subjects were significantly slower and more variable than normal subjects and ataxic subjects were significantly more variable than spastic subjects. The significantly slower than normal rate of repetition in the ataxic subjects and the significantly more variable than normal rhythm of repetition in the spastic subjects were unexpected findings and are in contrast with results from perceptually based investigations of dysarthria. The study demonstrates that slowness of syllable repetition is not restricted to spastic dysarthria and that dysrhythmia of syllable repetition is not restricted to ataxic dysarthria, thus suggesting the need for additional quantitative measurements of acoustic features on which certain notions about the dysarthrias are currently based.

Adductor spastic dysphonia may not be one disorder but a voice sign of several different neurologic and psychiatric syndromes. This study evaluates whether rhythmic voice arrests, often components of "spastic dysphonia," are signs of essential tremor, a neurologic disorder. Data on 22 patients originally diagnosed as having spastic dysphonia, who had tremor-like or rhythmic voice arrests, were compared with data on two groups of patients who had essential (voice) tremor. The frequency of voice arrest on vowel prolongation in the group labeled spastic dysphonia was compared with the frequency of voice tremor in the groups with essential tremor. The median frequencies of 5.7, 5.0, and 5.5 Hz were not significantly different among the three groups. Patients in all three groups had tremor in other parts of the body, other scattered neurologic signs, and histories of life stress associated with the onset of their voice disorders. Although the results do not prove conclusively that the patients diagnosed as having spastic dysphonia in this study actually had essential tremor, the similarities to that disorder strongly suggest a linkage.

After recurrent laryngeal nerve resection for adductor spastic dysphonia, the voices of 37 patients (ages 39 to 79 years) were assessed 24 hours, 1 month, 6 months, and 1 year after surgery, and those of 33 patients up to 1 1/2 years after surgery. By 24 hours after surgery, 97% of patients had improved and 3% had failed; by 1 month, 97% were still improved while 3% had failed; by 6 months, 92% had maintained improvement while 8% had failed; by 1 year, 68% were still improved but 32% had failed; and by a 1 1/2 years, 61% were still improved while 39% had failed. The patients whose voices improved varied from one another in both type and degree of residual dysphonia. The typical postsurgical voice was free of spasm, with some breathiness, hoarseness, and reduced volume being present. The voices of some patients approached normalcy. To most patients, relief from the physical effort to phonate was as important as the improved voice. Continued long-term follow-up studies and careful, collaborative selection of surgical candidates are needed.

Case history and voice data for 17 patients who presented with intermittent moments of breathy dysphonia (IBD) in contextual speech were analyzed. From recorded samples of vowel prolongation four variants of phonation were identified. Of 13 patients examined neurologically, 10 (77%) had positive neurologic signs. Psychiatric and physical illnesses were often associated with onset of the voice disorder. Sex ratio of the patients in this study was nearly the same as that for adductor spastic dysphonia. Age at onset was similar to that which has been described for "functional" voice disorders. Different therapies were generally ineffective in alleviating the disorder. Although not conclusive, patients presenting with IBD in connected speech may have an underlying neurologic or psychologic disorders.

Tongue force, rate of syllable repetition, and judgments of articulatory defectiveness were measures obtained on 19 dysarthric adults with amyotrophic lateral sclerosis and on 125 normal adults. Anterior and lateral tongue forces were measured by means of a pressure transducer clasped between the teeth; the tongue forces were recorded on a pen-writing ECG apparatus. Audio-recorded syllable repetitions of /p lambda/, /t lambda/, and /k lambda/ also were transcribed on ECG paper and counted. Three listeners rated articulatory precision on a 7-point scale of severity. The normal males had significantly higher tongue forces than normal females; normal subjects had significantly higher tongue forces than dysarthric patients; and anterior tongue forces were significantly greater than lateral in normal and dysarthric patients. There was a high negative correlation between tongue force and severity of articulatory defect. Syllable repetitions were significantly slower in the dysarthric patients than in the normal patients, and a high negative correlation was obtained between syllabic rate and severity of articulatory defect.

Spastic dysphonia is a disorder of phonation that is usually markedly improved by surgical resection of one recurrent laryngeal nerve (RLN). In this study, biopsies of the RLN were obtained at surgery from nine patients with spastic dysphonia (disease group) and eight patients with laryngeal cancer (control group). The RLN was found to be composed of several nerve regions having characteristic fiber compositions. For the various nerve regions and for the whole nerve, we evaluated morphology, median fiber diameter, density, and size distribution of fibers. The morphologies of teased fibers were also evaluated. We found no significant differences between the nerves of the disease and control groups. Therefore, we were unable to verify previous reports of neuropathic abnormality of the RLN in spastic dysphonia.