Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the dysarthria of four children with bilateral supranuclear facial palsy and four with bilateral peripheral facial palsy. The children with peripheral lesions had only moderate dysarthria, characterized mainly by weakened vowels and consonants and by hypernasality. In contrast, children with supranuclear lesions were anarthric at first, followed by severe dysarthria with reduced stress and many pauses. Although there was a relation between severity of dysarthria and neurologic disorders, anarthria can be seen in children with bilateral supranuclear lesions and only slight neurologic disability. Damage to cortical or brainstem control mechanisms may be responsible.
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PMID:Acquired dysarthria in childhood: an analysis of dysarthric features in relation to neurologic deficits. 380 12

A rare case of acquired dysarthria caused by a brain-stem infarct in a six-year-old boy is reported. Applying the analysis of Darley et al. (1969, 1975), 14 'dimensions' of dysarthria were recognised. The course of this dysarthria is described, by comparing samples of spontaneous speech, repetition and singing. The dysarthria is mainly characterised by imprecise consonants, distorted vowels, hypernasality and a breathy voice.
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PMID:The analysis of acquired dysarthria in childhood. 683 1

A quantitative study was made of the effects of focal cerebellar stimulation on oral-motor control, duration of phonation, articulation and vocal characteristics in 10 patients with cerebral palsy. The patients were evaluated prior to surgery and again after approximately two and six months of cerebellar stimulation. One patient had normal speech, which was not affected by the stimulation; another case with moderate dysarthria due to severe hearing loss was not helped by the stimulation. Seven patients increased their duration of vowel phonation by about two seconds, a significant amount. Four of the patients with moderate dysarthria improved their articulation, particularly for the consonants S, Sh and Th, after two months of stimulation. Two patients had changes in oral-motor control, which included better tongue and lip movements, and two other cases had small alterations in hypernasality or breathiness. Most of the changes in sound production and speech intelligibility appear to be related to improved intra-oral breath control.
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PMID:Speech changes in cerebral-palsied patients after cerebellar stimulation. 696 96

This report of a case study of an unusual child aims to set the use of electropalatography (EPG) within the wider context of general communication therapy. It concerns a child of 12 years, diagnosed as having congenital suprabulbar paresis (Worster-Drought syndrome) who presents with severe developmental dysarthria; his speech is unintelligible, with hypernasality and glottalised articulation. His baseline EPG assessment patterns show minimal tongue-to-palate contact for all lingual obstruents, although he can demonstrate some tongue movement for non-speech skills, and has a slow but near normal swallow pattern. EPG therapy was used for tongue movements, but was adversely affected by his velopharyngeal insufficiency.
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PMID:EPG treatment of a child with the Worster-Drought syndrome. 749 56

We studied the clinical features and molecular genetics of a family, afflicted with a form of atypical parkinsonism, originating from the Madeira Islands of Portugal. We examined four affected individuals and reviewed clinical information on one other affected family member. Mean age at onset was 31 years. Parkinsonism (akinesia, rigidity, gait disturbance) was the most prominent feature in advanced disease. Levodopa responsiveness with peak-dose dyskinesia was present in one individual. Initial symptoms and other clinical features were variable and included other extrapyramidal signs (dystonia, action tremor of the limbs and bulbar muscles, synkinesis), ophthalmologic abnormalities (ptosis, slow saccades, progressive external ophthalmoplegia, hypometric saccades, saccadic pursuit movements), speech abnormalities (dysarthria, hypernasality), cortical impairment (dementia, frontal lobe dysfunction, palilalia, perseveration), minor cerebellar signs (dysmetria, gait ataxia), pyramidal abnormalities (spasticity, hyperreflexia), and peripheral nervous system abnormalities (propioceptive loss, areflexia, distal weakness, atrophy). The length of trinucleotide repeats in the MJD1 gene was in the normal range for all affected individuals.
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PMID:Atypical parkinsonism in a family of Portuguese ancestry: absence of CAG repeat expansion in the MJD1 gene. 915 59

Speech features were perceptually analyzed in two groups of children. The first group (n = 6) had undergone cerebellar tumor resection, and the second group (n = 6) included children with brainstem tumors. Children belonging to the first group became dysarthric after a postoperative mute phase. Slow speech rate was a specific feature, but scanning speech and irregular articulatory breakdown (i.e., prominent characteristics in adult ataxic dysarthria) were not observed. In the second group, hypernasality was a prominent characteristic and resembled flaccid dysarthria in adults. These findings suggest that acquired childhood dysarthria needs a proper classification.
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PMID:Dysarthria in children with cerebellar or brainstem tumors. 965 Jun 81

The aim of this study was to apply one-third-octave analysis for measuring an acoustic correlate of hypernasality in the speech of adults with a range of aetiologies (dysarthria, maxillectomy and cleft palate). Subjects included 12 speakers with hypernasality and 12 normal controls. The speech material was the vowel /i/ segmented from two Cantonese single words produced by each speaker. The results showed that speakers with hypernasality had significantly higher energy level for the one-third-octave bands centred at 630, 800 and 1000 Hz, and significantly lower amplitude for the band centred at 2500 Hz than speakers with normal resonance. These results are in general agreement with past findings about nasalization of vowels. This study showed that one-third-octave analysis has high intrajudge reliability and is applicable to the speech of adults with hypernasality due to different etiologies.
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PMID:Acoustic correlates of hypernasality. 1294

The bulbar symptoms of amyotrophic lateral sclerosis (ALS) include difficulty with the management of swallowing, saliva production, aspiration of secretion to the air ways and problems with spoken communication. These symptoms originate from the malfunction of the face muscles and pharynx sphincters. Patients with early symptoms of bulbar ALS are often referred to the otolaryngologist for the evaluation and management of dysphagia and dysarthria. The bulbar onset of ALS with hypernasality, articulation defects and voice harshness make the otolaryngologists the primary diagnostician for these signs. Careful examination of the speech quality and morphology as well as the function of vocal cords should be undertaken. Once the diagnosis of ALS is made, the otolaryngologist's involvement in medical treatment is necessary at different stages of the disease.
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PMID:[The importance of laryngological and phoniatric evaluation at the early stage of amyotrophic lateral sclerosis]. 1556 32

We investigated the evolution of the neurological and neuropsychological characteristics in a right-handed woman who was 53-years-old at the onset and who showed personality changes and behavioral disorders accompanied by progressive dysarthria. She had hypernasality and a slow rate of speech with distorted consonants and vowels, which progressed as motor disturbances affecting her speech apparatus increased; finally, she became mute two years post onset. Her dysarthria due to bilateral voluntary facio-velo-linguo-pharyngeal paralysis accompanied with automatic-voluntary dissociation fit the description of anterior opercular syndrome. She showed personality changes and behavioral abnormalities from the initial stage of the disease, as is generally observed in frontotemporal degeneration (FTD), and her magnetic resonance image showed progressive atrophy in the frontotemporal lobes; thus, she was clinically diagnosed with FTLD. This patient's symptoms suggest that FTLD, including bilateral anterior operculum degeneration, causes progressive pseudobulbar paretic dysarthria accompanied by clinical symptoms of FTD, which raises the possibility of a new clinical subtype in the FTLD spectrum.
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PMID:A case of frontotemporal lobar degeneration with progressive dysarthria. 1687 20

Progressive nonfluent aphasia (PNFA) is a clinical syndrome characterized by motor speech impairment and agrammatism, with relative sparing of single word comprehension and semantic memory. PNFA has been associated with the characteristic pattern of left anterior insular and posterior frontal atrophy, including the motor and premotor regions and Broca's area. Postmortem histopathologic evidence has shown that PNFA is usually associated with tau pathology, although focal Alzheimer disease pathology and tau-negative, ubiquitin-TDP-43 inclusions also have been reported in association with this clinical syndrome. We performed a detailed analysis of motor speech errors in 18 patients with PNFA and investigated their neural correlates using voxel-based morphometry on magnetic resonance imaging scans. Seven patients demonstrated only apraxia of speech (AOS) errors, whereas 11 showed AOS along with dysarthria. Slow rate of speech, effortful articulation with groping, and consonant distortions were the most common AOS errors. Hypernasality was the most represented dysarthric feature and dysarthria was most often classified as spastic, hypokinetic, or mixed spastic-hypokinetic. Neuroimaging results demonstrated that patients with AOS-only and AOS plus dysarthria showed atrophy in the left posterior frontal, anterior insular, and basal ganglia regions when compared with controls. Patients with AOS plus dysarthria showed greater damage than patients with AOS-only in the left face portion of primary motor cortex and left caudate. PNFA is a distinct frontotemporal lobar degeneration clinical syndrome associated with characteristic clinical, neuroimaging, and pathologic features. The clinical features are driven by the severity of left frontal and caudate damage.
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PMID:Progressive nonfluent aphasia and its characteristic motor speech deficits. 1809 Apr 19


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