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)

Progressing stroke with neurological deterioration (PSND), i.e., neurological deterioration of patients during the first days following a stroke, although not an infrequent event, has hitherto been addressed only by few studies. This is the first investigation conducted in Israel with the aim to determine its prevalence and characteristics. Data regarding 140 patients with first ever stroke were collected prospectively between May 1999 and October 2000. All patients underwent a thorough daily neurological examination over the first 7 days, using the Canadian Neurological Scale. Most (90%), patients had hemiparesis, with dysarthria, aphasia and dysphagia being the most frequent associated neurological deficits. Thirty percent of the patients were on anti-aggregant therapy prior to the stroke. The prevalence of PSND was 23%. The 1-month in-hospital death rate of these PSND patients was 31%. Univariate analysis showed that previous anti-aggregant therapy, Parkinson's disease (PD), obesity, hyperlipidemia, and presence of aphasia were significantly more frequent in the PSND group. In addition, these patients arrived earlier to the emergency room. However, logistic regression analysis showed that only PD and obesity could possibly be considered as predictors for development of PSND. The prevalence as well as the death rate of PSND in this group of Israeli elderly is within the range reported in the literature. However, prior anti-aggregant treatment and PD, are here reported for the first time as associated conditions. Future research will possibly clarify the links between these entities and PSND.
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PMID:Progressing stroke with neurological deterioration in a group of Israeli elderly. 1591 Oct 42

Apraxia of speech (AOS) is a motor speech disorder that can occur in the absence of aphasia or dysarthria. AOS has been the subject of some controversy since the disorder was first named and described by Darley and his Mayo Clinic colleagues in the 1960s. A recent revival of interest in AOS is due in part to the fact that it is often the first symptom of neurodegenerative diseases, such as primary progressive aphasia and corticobasal degeneration. This article will provide a brief review of terminology associated with AOS, its clinical hallmarks and neuroanatomical correlates. Current models of motor programming will also be addressed as they relate to AOS and finally, typical treatment strategies used in rehabilitating the articulation and prosody deficits associated with AOS will be summarized.
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PMID:Apraxia of speech: an overview. 1639 56

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.
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PMID:Clinical study of 39 patients with atypical lacunar syndrome. 1648 49

Coincidental acute illness is common in patients with chronic progressive or stable neurological disability. Although the presentation of acute illness in these patients is often similar to that in people without pre-existing disability, sometimes it may be atypical. In addition, an adequate medical history is often difficult to obtain in patients with advanced neurological disease, for example because of the presence of aphasia, severe dysarthria, or cognitive impairment. In these circumstances early and accurate diagnosis of acute medical and surgical emergencies requires both clinical acumen and a high index of suspicion. The aim of this article is to describe the main atypical manifestations of acute illness in patients with chronic disabling neurological disorders.
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PMID:Recognition of acute illness in people with chronic neurological disability. 1659 14

This retrospective study determined whether specific neurological features were associated with initial and final swallowing outcomes in acute stroke patients. A chart review of 65 acute stroke patients suggested that certain clinical and neurocognitive behaviors were associated with swallowing outcomes. Hemispatial neglect was significantly associated with initial nonoral dietary intake, whereas aphasia was not associated with swallowing outcome. Results from the initial clinical swallowing evaluations suggested that the presence of at least four of six clinical features (cough after swallow, voice change after swallow, abnormal volitional cough, abnormal gag reflex, dysphonia, and dysarthria) were associated with poor initial and final swallowing outcomes. Whether specific lesion location, size, or a combination of clinical neurological deficits are associated with poor initial and final swallowing outcomes is unclear. Prospective studies are warranted for further investigation of these relationships.
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PMID:Clinical and cognitive predictors of swallowing recovery in stroke. 1704 16

Employing conversation analysis as a research technique, this study investigates the ways that unintelligibility is accounted for and overcome within a therapeutic encounter between an individual with aphasia and dysarthria and his clinician. The results emphasize the collaborative nature of intelligibility negotiation and demonstrate how both the individual with the impairment and his clinician employ various interactional strategies and knowledge resources to turn unintelligibility into intelligibility so that the therapeutic encounter may continue.
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PMID:The negotiation of intelligibility in an aphasic dyad. 1705 91

No clinical data have yet been presented to show that a lesion localized to the primary motor area (M1) can cause severe transient impairment of articulation, although a motor representation for articulation has been suggested to exist within M1. Here we describe three cases of patients who developed severe dysarthria, temporarily mimicking speech arrest or aphemia, due to a localized brain lesion near the left face representation of the human primary motor cortex (face-M1). Speech was slow, effortful, lacking normal prosody, and more affected than expected from the degree of facial or tongue palsy. There was a mild deficit in tongue movements in the sagittal plane that impaired palatolingual contact and rapid tongue movements. The speech disturbance was limited to verbal output, without aphasia or orofacial apraxia. Overlay of magnetic resonance images revealed a localized cortical region near face-M1, which displayed high intensity on diffusion weighted images, while the main portion of the corticobulbar fibers arising from the lower third of the motor cortex was preserved. The cases suggest the existence of a localized brain region specialized for articulation near face-M1. Cortico-cortical fibers connecting face-M1 with the lower premotor areas including Broca's area may also be important for articulatory control.
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PMID:Primary face motor area as the motor representation of articulation. 1738 Feb 43

Background. The purpose of this study was to characterize the speech and language disturbances seen in patients with traumatic brain injury aroused from long-term coma at the Rehabilitation Clinic of the Bydgoszcz Academy of Medicine. Material and methods. The research covered 94 patients (30 women, 64 men, average age 34.7). Speech and language disturbances were diagnosed with basic neuropsychological batteries and authorial methods, and classified as akinetic mutism, global aphasia, sensory aphasia, motor aphasia, dysarthria, or dysphonia. The patients were examined 3 times: at admission, after one month, and after two months. Results. The patients displayed various speech and language disturbances. In the first examination, 47 persons (50.0%) presented with dysarthria. Post-traumatic aphasia was seen in 28 persons (29.8%). Akinetic mutism was somewhat less common (12 persons, 12.8%) and dysphonia least common (6 persons, 6.3%). In the second examination there were numerous shifts between groups, and 15 persons no longer had any disturbances (16.0%). These trends continued in the third examination. Dysphonia was seen in 4 persons (4.3%), akinetic mutism in only 3 (3.2%). 23 persons (24.5%) did not show any speech and language disturbances. Conclusions. Patients aroused from long-term coma display various speech and language disturbances. A significant number have dysarthria and/or aphasia, somewhat fewer have akinetic mutism. Dysphonia is also seen. Mutism often resolves spontaneously, as does dysphonia, while the symptoms of aphasia and dysarthria are more persistent.
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PMID:Disturbances of speech and language in patients aroused from long-term coma subsequent to traumatic brain injury. 1767 75

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

A case of gliosarcoma composed of glioblastoma and liposarcoma is presented. A 70-year-old Japanese man was admitted to hospital because of dysarthria and aphasia. Magnetic resonance imaging indicated a brain tumor located in the temporal-parietal area of the left hemisphere. He rejected any therapy and died of respiratory failure. At autopsy the tumor was well-demarcated with firm consistency and myxoid appearance, accompanied by necrosis and hemorrhage. Microscopically the tumor consisted of both glial and sarcomatous components, compatible with a gliosarcoma. Lipoblast-like tumor cells were identified in the sarcomatous area. Glial component was observed in the periphery and was diffusely positive for CD56 and S100 protein and focally for glial fibrillary acidic protein. Only a small number of tumor cells in the sarcomatous area expressed neurogenic markers. Lipoblast-like tumor cells were positive for S100 protein but negative for any other neurogenic markers. A significant number of tumor cells were positive for retinoblastoma protein (pRB) in the glial area, whereas only a few of them were positive in the sarcomatous area, indicating alteration of pRB in sarcomatous component. The present tumor is a rare gliosarcoma with liposarcomatous differentiation; alteration of pRB may play a role in sarcomatous transformation of glial component.
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PMID:Immunohistochemistry of gliosarcoma with liposarcomatous differentiation. 1847 20


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