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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasmodic dysphonia is a disturbance of phonation with laryngeal spasms. We report voice and neurologic examination findings in 45 subjects. Neurologic abnormalities were found in 32 subjects (71.1%). Rapid alternating movement abnormalities, weakness, and tremor were common. Incoordination and spasticity were rare. Lower extremity findings were frequent. Abnormalities were bilateral. Spasmodic dysphonia severity was related to age. Type, severity, and duration of vocal symptoms were not different for subjects with or without neurologic abnormalities. Vocal tremor was more frequent in neurologically abnormal subjects. Involvement of a pallidothalamic-supplementary motor area system could account for neurologic findings, brain imaging findings, and clinical heterogeneity. The view emerging is that spasmodic dysphonia is a manifestation of disordered motor control involving systems of neurons rather than single anatomical sites.
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PMID:Heterogeneity in spasmodic dysphonia. Neurologic and voice findings. 200 Nov 89

Spastic dysphonia is a central nervous system phenomenon of unknown etiology characterized by uncoordinated voice tremor with erratic patterns of laryngeal contraction. Standard treatments have not been entirely satisfactory. The authors propose to apply a concept of selective nerve activity blockage, which leaves normal contractions undisturbed, as the basis for suppression of laryngeal spasticity. Single pulses of constant duration and increasing amplitude were injected into specially designed blocking electrodes placed around six recurrent laryngeal nerves (three dogs). Vocal cord adduction was reduced or arrested within given "windows" of stimulation levels of the blocking electrodes, while it increased with higher amplitudes when the current was injected via standard bipolar electrodes (controls). Although this study demonstrates the feasibility of blocking action potentials passing along recurrent laryngeal nerves, it might eventually allow control of laryngeal spasm from information taken directly from the affected musculature.
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PMID:Electronic control of laryngeal spasm. I. Blockage of orthodromically induced action potentials in intact canine recurrent laryngeal nerves. 238 Dec 63

Spastic dysphonia is a syndrome often producing a strain-strangle voice. We have previously classified most of these patients as having focal laryngeal dystonia, a disorder of central motor processing. In a study of 1,280 cases of dystonia registered at the Dystonia Clinical Research Center at the Columbia-Presbyterian Medical Center, we found 110 patients who had vocal cord involvement. These patients had historical information evaluated for age of onset (mean 34.6 years), duration of symptoms (mean 13.8 years), sex (1.4:1 female to male) family history (positive in 23%), and primary (66%) and secondary (34%) etiology; neurological evaluation for other dystonic involvement (25% with segmental cranial involvement, 23% with generalized dystonia) or tremor (irregular 23%, regular 6% on EMG). Treatment options were evaluated and included speech therapy, psychotherapy, biofeedback (with limited success), systemic medication (limited success except in abductor cases), nerve section (with late failure rate), and the use of botulinum toxin (improvement in all 34 injected patients).
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PMID:Clinical and laboratory characteristics of focal laryngeal dystonia: study of 110 cases. 337 39

Spastic dysphonia is a clinical speech disorder characterized by spasms of the laryngeal muscles during phonation, producing a broken pattern of speech sometimes termed laryngeal stuttering. Fourteen patients with the diagnosis of spastic dysphonia based on voice quality were referred for evaluation; detailed clinical and electrophysiologic evaluations were performed. Laryngeal electromyographic (EMG) testing failed to demonstrate any spontaneous activity in the 14 patients tested. Seven patients (50%) had normal number and amplitude of motor unit potentials. Four of these had disparate amplitudes when compared with the other side, and two had complex motor unit potentials. The other seven patients (50%) had abnormal findings, including three patients with abnormally increased amplitude. Two patients had asynchronous activity characteristic of a tremor disorder. One patient had synchronous bursts of activity also affecting the diaphragm, later diagnosed as pyramidal and extrapyramidal disease. One patient had bursts of activity, and later presented with diffuse myoclonus. Laryngeal EMG therefore seemed to be a more precise way of evaluating patients presenting with a tremulous voice pattern termed spastic dysphonia. Clinical observation and EMG data demonstrated that spastic dysphonia is not a "spastic" disease. We identified patients with tremor (2), pyramidal and extrapyramidal disease (1), and myoclonic disorders (1). The remainder of the patients had clinical and EMG findings consistent with dystonia, a neurologic disorder characterized by abnormal, often action-induced, involuntary movements or uncontrolled spasms. We classify these patients as having "focal laryngeal dystonia" when the disorder occurs in isolation. It may also present as a component of a generalized dystonic syndrome.
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PMID:Electromyographic findings in focal laryngeal dystonia (spastic dysphonia). 407 37

Spasmodic dysphonia is a devastating voice disorder of unknown etiology, with a variable clinical presentation and response to treatment. Three independent evaluations of brain stem function were performed on spasmodic dysphonic patients, and age and sex-matched controls. Statistically significant (p less than 0.01 approximately 0.05) differences were noted between these groups, and the findings were consistent with impairment of somatic and visceral brain stem pathways. A significant correlation (p less than 0.05) was found between the severity of tested central nervous system impairment and vocal tremor, number of associated neurologic signs and duration of illness. Possible etiologies (viral or traumatic), age, and sex, did not correlate with the severity of brain stem impairment. Clinical signs and the brain stem findings appeared to stabilize 3 to 5 years after onset of dysphonia. The investigation of other spasmodic cranial nerve disorders afforded insight into the etiology and therapy for spasmodic dysphonia. Drawing upon previous observations and the results of the brain stem tests, two models are proposed for neuronal processing in spasmodic dysphonia, and future strategies are discussed. The evidence cited in this research project are consistent with spasmodic dysphonia being one of several spasmodic brain stem disorders with variable presentation which are known by the cranial nerve nuclei or pathways of major clinical involvement.
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PMID:Neuropathology of spasmodic dysphonia. 613 80

Spastic dysphonia is a severe vocal disability in which the patient speaks with hyperadducted vocal folds. The resulting abnormality is characterized by excessively low pitch, vocal tremor, laryngospasms, and strain-strangle voice quality. Until recently the disorder was regarded as psychogenic and treated unsuccessfully with speech therapy and psychotherapy. New evidence supports the theory that the etiology is neurologic, requiring management designed to alter neurophysiologic function. Section of the recurrent laryngeal nerve provides immediate results and a new voice virtually free of the previous unpleasant characteristics.
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PMID:Recurrent laryngeal nerve section in the treatment of spastic dysphonia. 728 Jul 51

Spasmodic dysphonia is a focal form of laryngeal dystonia that causes unintended contractions of vocal folds with speech interruptions and affecting the voice quality. There are adductor (82%), abductor (36%), mixed (1%) types and reported by Blitzer--respiratory adductor type with paradoxical vocal fold movement and stidor. As an example of diagnostic and therapeutic difficulties in spasmodic dysphonia and its multidisciplinary approach with needed cooperation of many specialists we presented patient with adductor spasmodic dysphonia. In stroboscopic evaluation there were observed glottic overclosure and hyperaduction in supraglotic stuctures (sphincteric). During diagnostic procedures there was made acoustic analysis by digital spectrograph (by KAY Elmetrics Company). IV degree of hoarsness and voice breaks were observed in sonogram. In multidimentional analysis there were deviations of the frequency, amplitude, noise, tremor and voice break parameters. Treatment included regular speech therapy, relaxation- and psychotherapy. The results of treatment were very instable because every stress-related problem released symptoms. Botulinum toxin injections into thyro-arytenoid muscle which had made before our hospitalisation were also not succeeding. Because of lack of etiologic factor and plenty diseases that can mimic spasmodic dysphonia, close communication between many specialists is needed.
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PMID:[Therapeutic difficulties in spasmodic dysphonia--case report]. 1687 62

Spasmodic dysphonia (SD) is a neurological disorder of the voice where a patient's ability to speak is compromised due to involuntary contractions of the intrinsic laryngeal muscles. Since the 1980s, SD has been treated with botulinum toxin A (BTX) injections into the throat. This therapy is limited by the delayed-onset of benefits, wearing-off effects, and repeated injections required every 3 months. In a patient with essential tremor (ET) and coincident SD, the authors set out to quantify the effects of thalamic deep brain stimulation (DBS) on vocal function while investigating the underlying motor thalamic circuitry. A 79-year-old right-handed woman with ET and coincident adductor SD was referred to our neurosurgical team. While primarily treating her limb tremor, the authors studied the effects of unilateral, thalamic DBS on vocal function using the Unified Spasmodic Dysphonia Rating Scale (USDRS) and voice-related quality of life (VRQOL). Since dystonia is increasingly being considered a multinodal network disorder, an anterior trajectory into the left thalamus was deliberately chosen such that the proximal contacts of the electrode were in the ventral oralis anterior (Voa) nucleus (pallidal outflow) and the distal contacts were in the ventral intermediate (Vim) nucleus (cerebellar outflow). In addition to assessing on/off unilateral thalamic Vim stimulation on voice, the authors experimentally assessed low-voltage unilateral Vim, Voa, or multitarget stimulation in a prospective, randomized, doubled-blinded manner. The evaluators were experienced at rating SD and were familiar with the vocal tremor of ET. A Wilcoxon signed-rank test was used to study the pre- and posttreatment effect of DBS on voice. Unilateral left thalamic Vim stimulation (DBS on) significantly improved SD vocal dysfunction compared with no stimulation (DBS off), as measured by the USDRS (p < 0.01) and VRQOL (p < 0.01). In the experimental interrogation, both low-voltage Vim (p < 0.01) and multitarget Vim + Voa (p < 0.01) stimulation were significantly superior to low-voltage Voa stimulation. For the first time, the effects of high-frequency stimulation of different neural circuits in SD have been quantified. Unexpectedly, focused Voa (pallidal outflow) stimulation was inferior to Vim (cerebellar outflow) stimulation despite the classification of SD as a dystonia. While only a single case, scattered reports exist on the positive effects of thalamic DBS on dysphonia. A Phase 1 pilot trial (DEBUSSY; clinical trial no. NCT02558634, clinicaltrials.gov) is underway at the authors' center to evaluate the safety and preliminary efficacy of DBS in SD. The authors hope that this current report stimulates neurosurgeons to investigate this new indication for DBS.
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PMID:The effect of unilateral thalamic deep brain stimulation on the vocal dysfunction in a patient with spasmodic dysphonia: interrogating cerebellar and pallidal neural circuits. 2830 88

Objective The purpose of this review is to describe the recent advances in identifying possible factors involved in the pathogenesis of spasmodic dysphonia. Spasmodic dysphonia is a task-specific focal laryngeal dystonia characterized by irregular and uncontrolled voice breaks. Pathogenesis of the disorder is poorly understood. Data Sources PubMed, Google Scholar, and Cochrane Library. Review Methods The data sources were searched using the following search terms: ( spasmodic dysphonia or laryngeal dystonia) and ( etiology, aetiology, diagnosis, pathogenesis, or pathophysiology). Conclusions Several potential etiological factors have been proposed by epidemiological, genetic, and neuropathological studies. Spasmodic dysphonia is a rare disorder primarily affecting females beginning in their 40s. Vocal tremor co-occurs in 30% to 60%. Large cohort studies identified risk factors such as a family history of neurological disorders including dystonia and tremor, recent viral illness, and heavy voice use. As none are rare events, a complex interactive process may contribute to pathogenesis in a small proportion of those at risk. Consequences to pathogenesis are neurological processes found in spasmodic dysphonia: loss of cortical inhibition, sensory processing disturbances, and neuroanatomical and physiological differences in the laryngeal motor control system. Implications for Practice Diagnosis of spasmodic dysphonia usually includes speech and laryngoscopic assessment. However, as diagnosis is sometimes problematic, measurement of neurophysiological abnormalities may contribute useful adjuncts for the diagnosis of spasmodic dysphonia in the future.
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PMID:Spasmodic Dysphonia: A Review. Part 1: Pathogenic Factors. 2885 Aug 1