Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When parents are concerned about the development of stuttering in their child they often consult their pediatrician or family physician. Theories on the development of stuttering are briefly examined in this article, and guidelines are provided to help the physician determine if the child's dysfluencies are within the normal range. Referral to a speech therapist should be considered when any of the following are noted: excessive repetition of the first syllable of words; tremor of the muscles of mouth or jaw, increase in pitch or loudness, or evidence of fear or emotion as the child struggles with a word; evidence that the child avoids certain words or situations; and excessive concern of parents, teachers or the dysfluent individual. Two approaches to therapy, traditional and behavioural, are described. The latter has resulted in significant gains in fluency among stutterers.
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PMID:Stuttering: recent developments in theory and in therapy. 68 28

We report palilalia and acquired stuttering in a 60-year-old Japanese male with Parkinson's disease. At the age of 54, he presented with resting tremor in the hand and foot on the left, and gradual slowness in voluntary movements. Two years later, resting tremor involved the right foot, and an expressionless face and frozen gait occurred. A diagnosis of Parkinson's disease was made and treatment with L-dopa and carbidopa resulted in conspicuous improvement. At the age of 57, he developed compulsive repetitions of syllables, words and phrases, and sentences infrequently when he spoke. They have been persisting for four years. Repetitions increased in spontaneous speech while they decreased in oral reading and repetition of sentences. These repetitions in speech were symptomatologically diagnosed as palilalia and acquired stuttering. Brain CT showed slight brain atrophy, and brain MRI disclosed a few lesions indicating lacunae in the left substantia nigra, left putamen, and right internal capsule. SPECT showed a slight decrease in blood flow in the frontal lobes and basal ganglia bilaterally. Full IQ on WAIS was 105, and neither agnosia nor apraxia was detected. Palilalia and acquired stuttering, though the pathomechanism has not been clarified, have been reported to occur usually secondary to cerebral vascucular lesions and very rarely in Parkinson's disease. In the present case, they may have been produced by the parkinsonian nigro-striatal lesions. Alternatively, they may have been induced by the small vascular lesions demonstrated by MRI.
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PMID:[Palilalia and acquired stuttering in a case of Parkinson's disease]. 149 Mar 13

A study of 71 patients with idiopathic torsion dystonia (ITD) and 71 matched controls was performed to investigate the range of possible clinical expression of ITD and the role of environmental factors in the development of the disease. A family history of tremor and stuttering were the only factors significantly associated with ITD. No associated environmental factor was identified.
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PMID:A case-control study of idiopathic torsion dystonia. 148 41

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

The purpose of this study was to describe the temporal patterns and spectral characteristics of antagonist lip muscle EMG and lip displacement during bilabial disfluencies in adult stutterers. Selective EMG recordings were obtained in five adult stutterers of mentalis and depressor labii inferior motor units (MENT and DLI) that were activated in a reciprocal manner during fluent speech. During disfluencies (N = 91) these same motor units were activated primarily in a reciprocal manner or DLI was not activated. These findings are not consistent with previous reports that stutterers' disfluencies involve cocontraction and overall increases in the activation levels of antagonist muscles. Spectral analysis of bilabial disfluencies revealed peaks at 5-9 Hz in the MENT EMG spectra of the five subjects and at 5-6 Hz in the displacement spectra of two subjects. A refinement in the classification of stutterers' disfluencies is suggested on the basis of individual differences in lip EMG and displacement spectra, and the mechanisms of stuttering tremor are discussed.
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PMID:Lower-lip EMG and displacement during bilabial disfluencies in adult stutterers. 648 3

Stuttering onset in adulthood is rare. With no prior history of stuttering or demonstrable neurological insult, diagnosis is often that of a conversion reaction. Stuttering as the first sign of a parkinsonian-like syndrome in extrapyramidal disease has only been reported once in the previous 30 years (Koller, 1983). The present case study differs from and builds upon the case reports in the literature, and describes a 29-year-old white male who began stuttering purportedly secondary to psychological stress. The fluency evaluation revealed severe stuttering characterized by multiple repetitions and/or blocks, with 20 or more repetitions per word routinely noted during both conversational speech and oral reading. No starters or secondary stuttering characteristics, no specific word fears or avoidances, and no situational fears were exhibited. The subsequent neurological examination found resting tremor in hands and legs, lingual fasciculations, gait imbalance, and numbness and tingling of the hands and feet, all of which were progressive in nature. Rehabilitation initially focused on fluency therapy, but then included psychiatric therapy, and finally medical intervention. Fluency and psychiatric therapies were unsuccessful in eliminating stuttering. Following a diagnosis of parkinsonian-like syndrome, medical intervention with carbidopa-levodopa resulted in dramatic improvement of motor, sensory, and fluency symptoms. It is important to consider extrapyramidal disease as an etiological factor in patients with adult onset of stuttering.
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PMID:Adult onset of stuttering as a presenting sign in a parkinsonian-like syndrome: a case report. 895 3

A 30-year-old woman hit her head during an automobile accident and was admitted to the hospital. One week later magnetic resonance imaging (MRI) showed a right frontal/parietal lesion. Among the behavioral sequelae were mild ataxia with trunkal instability and dysfluent speech accompanied by prominent shaking of the right leg, face and neck tension, and facial twitching. The speech-language pathologist thought the patient was not aphasic but rather was stuttering and treated her for about a month with pacing and "easy onset" techniques to which she showed fair response. The diagnostic question in this case is whether the stuttering was the result of the brain damage (neurogenic) or of the stressful events she had experienced (psychogenic). In this article we review her case and the process we used in arriving at an "expert" opinion.
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PMID:Sudden onset of "stuttering" in an adult: neurogenic or psychogenic? 951 89

Adduction spastic dystonia (SD) is currently considered a focal dystonia involving laryngeal muscles. SD is one of the most poorly known focal dystonias. We reviewed our experience with twentynine patients with adduction SD and compared the clinical and epidemiologic variables with the other focal dystonias studied at our institution in the last five years (132 patients). Mean age of patients (47.2 +/- 13 years), sex, clinical course in years (5.7 +/- 5) and presence of circadian fluctuations did not differ significantly from those observed in patients with other focal dystonias. Likewise, there were no significant differences regarding the presence of a family history of dystonia, essential tremor, or stuttering. Our results confirm the similarity of the clinical and epidemiologic data of SD with the other focal dystonias. All patients with SD were treated with a local injection of botulinum toxin. A total of 108 treatments were performed, 41 with a visually guided transoral technique and 67 with a percutaneous technique. The transoral technique was effective in all cases (41/41) but not all treatments with the percutaneous technique were effective (53/67). Three patients required the shift to the transoral procedure to achieve enough symptomatic alleviation.
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PMID:[Adduction spastic dysphonia: clinical and treatment]. 958 38

We reported a 73-year-old man with pure akinesia syndrome who showed severe acquired stuttering and paradoxical kinesia on speech. He was evaluated in another hospital for bradykinesia and frozen gait at age of 67 when his cranial MRI disclosed ischemic changes in bilateral basal ganglia and periventricular deep white matter. The treatment with L-dopa and L-threo DOPS was not effective. His symptoms were slowly progressive and got worse gradually. At age of 72, he began to have difficulty in speech due to severe acquired stuttering, and one year later, he visited our hospital. The diagnosis of pure akinesia syndrome was made because of akinesia, micrographia, marked frozen gait with paradoxical kinesia and disturbance of postural reflex without tremor and rigidity. His speech showed severe acquired stuttering with marked blocking and repetition of initial phonemes at the beginning of speech. But intelligible speech recurred with pointing the characters by his finger or with writing an initial letter of word, although his speech was small and monotonous. Surface EMG findings of muscles participating speech in acquired stuttering showed the similar tonic discharge to those of muscles of lower extremity in frozen gait. These results implied that freezing phenomenon and festination of muscles participating speech in our patient may result in acquired stuttering.
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PMID:[A management for severe acquired stuttering in a case of pure akinesia syndrome]. 959 12

The efficacy of botulinum toxin (BTX) without systemic effects has led to the rapid development of applications in neuromuscular disorders, hyperactivity of sudomotor cholinergic-mediated glandular function, and pain syndromes. The successful use of BTX in conditions with muscle overactivity, such as dystonia and spasticity, has been established and new areas in the field of movement disorders such as tics, tremor, myoclonic jerks, and stuttering has been explored with satisfactory results. Strategies to temporarily inactivate muscle function after orthopaedic or neurosurgery have also been developed. BTX treatment of hyperhidrosis was followed by its application in other hypersecretory conditions (hyperlacrimation and nasal hypersecretion) and in excessive drooling. Studies are in progress, aimed at optimising the technique and protocol of administration. Other applications for BTX have been proposed in gastroenterological and urogenital practice; it appears to be effective in replacing standard surgical procedures. Trials of BTX in painful conditions are ongoing mainly on refractory tension headache, migraine, and backache as well as dystonia-complex regional pain syndrome and myofascial pain with promising results. Recently, the fastest growing use for BTX toxin has been in the cosmetic applications. Clearly, the indications for the use of BTX are expanding, but further clinical trials will be needed in many different areas.
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PMID:New therapeutic indications for botulinum toxins. 1502 69


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