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

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

Patients with spastic dysphonia were studied to identify the characteristics of patients benefiting from recurrent laryngeal nerve (RLN) surgery. Studies included laryngeal video recordings made during speech, measures of frequency and amplitude variations during extended phonation, the effects of altered auditory feedback on dysfluencies, and temporary unilateral RLN block. Two patients had vocal fold adductor spasms during connected speech, had increased acoustic phonatory tremor in frequency, were not benefited by altered auditory feedback, and responded favorably to nerve block. Subsequent RLN section improved the speech of both patients. Other patients had speech blocks, repetitions and prolongations, vocal fold tremors during phonation, reduced dysfluencies during altered auditory feedback, and were not benefited by temporary nerve block. Two subtypes of spastic dysphonic patients are proposed.
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PMID:Procedures for the selection of spastic dysphonia patients for recurrent laryngeal nerve section. 642 12

Primidone has been reported to be effective in reducing tremor in patients with benign essential tremor. There is at least one report that suggests that the medication may reduce voice tremor, a frequent component of the essential tremor syndrome. Three patients with spastic dysphonia of essential (voice) tremor and one with more typical essential (voice) tremor were treated with primidone and experienced no alleviation in the voice signs. The side effects experienced by all patients were consistent with those noted in previous reports. Primidone does not seem to be effective in treating essential voice tremor or spastic dysphonia of essential voice tremor.
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PMID:Spastic dysphonia and essential (voice) tremor treated with primidone. 672 82

The voices of 33 patients, ages 44 to 79 years, were assessed after recurrent laryngeal nerve resection for adductor spastic dysphonia. Voice improvement was noted in all patients 24 hours after surgery: in 97% at 1 month, 97% at 6 months, 82% at 1 year, 70% at 1 1/2 years, 58% at 2 years, 52% at 2 1/2 years, and 36% at 3 years. Of the 64% with failed voices by 3 years, 48% were worse than before surgery. Of the 36% whose voices remained improved, 58% were worse than at any previous period and 42% were better. Failures among women (77%) were considerably higher than among men (36%). Except for one patient, none of the patients with improvement achieved a normal voice. Patients with improvement had varied types and degrees of dysphonia: breathiness, hoarseness, diplophonia, and falsetto pitch breaks. The voices of some patients approached normalcy. A high percent of patients had voice tremor and regular voice arrests on vowel prolongation, signaling that the spastic dysphonia may have been related to essential (voice) tremor and that the spastic dysphonia returned because of increased severity of the neurologic tremor. We conclude that recurrent laryngeal nerve surgery for adductor spastic dysphonia has long-term limitations and that the differential diagnosis between neurologic and psychogenic types is imperative prior to therapeutic decision making.
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PMID:Adductor spastic dysphonia: three years after recurrent laryngeal nerve resection. 682 65

We evaluated prospectively 100 patients, the largest reported series, with blepharospasm and orofacial-cervical dystonia, or Meige syndrome. The mean age at onset was 51.7 years, and 81% presented between the ages of 40 and 70. Women outnumbered men three to two. Blepharospasm was the initial symptom in 58 patients, but only 23 had involuntary movements localized to the orbicularis oculi. Sixty-one patients had the complete syndrome, blepharospasm and oromandibular dystonia, and 60 had neck or generalized dystonia in addition to the orofacial movements. Twenty-one patients with spasmodic dysphonia were included; in 12 of these patients, spasmodic dysphonia was part of the complete (Meige) syndrome, and 16 of these patients had neck or generalized dystonia or essential tremor. An organic cause of Meige syndrome is supported by a high correlation with essential tremor and other movement disorders and by positive family history in some patients. Response to medication was inconsistent, but 69% of patient trials resulted in some improvement; in 22% the benefit was marked and persistent. Tetrabenazine, lithium, and trihexyphenidyl were most useful for the treatment of oromandibular dystonia, and clonazepam was useful in some patients with blepharospasm.
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PMID:Blepharospasm and orofacial-cervical dystonia: clinical and pharmacological findings in 100 patients. 683 74

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.
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PMID:Adductor spastic dysphonia as a sign of essential (voice) tremor. 720 78

Two familial cases of late onset spasmodic dysphonia and low Arylsulphatase A (ASA) are reported. In one case spasmodic dysphonia was associated with negative head tremor and orthostatic tremor, both displayed postural tremor of the upper extremities. A familial predisposition for both focal dystonia and metabolic lysosomal impairment is suggested by similar observations.
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PMID:Familial spasmodic dysphonia with low arylsulphatase A (ASA) level. 883 12

Local injections of botulinum toxin is a well-accepted treatment for focal dystonias, hemifacial spasms and strabismus. Its use by skilled neurologists has been reported to be safe and effective. We report our experience with botulinum toxin injections in 108 patients with various central nervous system disorders. Botox was effective in upper face dystonia (86% improvement), spastic dysphonia (92% improvement), platysma muscle spasms and spasmodic torticollis (range of movement 61%, pain and tension 90%). It was also very effective in a few patients with apraxia of eyelid opening, parkinsonian jaw tremor, teeth clenching, palatal myoclonus and adductor leg spasticity. No serious side effects were recorded. Botulinum toxin is a useful symptomatic treatment for many neurological disorders, and one of the leading mode of treatments in the new subspecialty in neurology called "Interventional neurology."
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PMID:Interventional neurology: botulinum toxin as a potent symptomatic treatment in neurology. 798 70

Clinical, neurological, endoscopic, psychological findings, questionnaire data on vegetative sphere, diaphragm x-ray, articulation test and Viene test system evidence obtained on 25 patients with phonic spasm confirm organic neurological nature of spastic dysphonia as focal muscular dystonia. This condition can be accompanied with tremor, rotatory, winking and writers' spasms, oromandibular dystonia. As indicated by positive treatment outcomes, combined treatment of phonic spasm with GABA-ergic drugs of clonazepam (antelepsin) and baclofen, orthophonic voice correction, physiotherapy is pathogenetically justified.
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PMID:[Clinical features of spastic dysphonia]. 855 15


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