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 describe herein the case of a 57 year old man who, over the last five years, has presented ataxic and spastic gait on the right side, a reduction in fine motor movement of the fingers mainly on the right side, superficial right side brachiocrural hypoesthesia and a marked dysarthria associated with internuclear ophthalmoplegia. The neurological picture, after an initial progressive worsening which lasted some months, remained relatively stable over the years. Repeated magnetic resonance imaging (MRI) of the brain and spinal cord documented the presence of demyelinating plaques spread in the white matter of the periventricular region and the semioval centres, and a right side paramedian plaque at the C4-C5 level, none of which were in the active phase. Oligoclonal bands were revealed in the cerebrospinal fluid (CSF). Monoclonal IgM/lambda gammopathy with anti-myelin and anti-nucleo reactivity, found with serum immunofixation, were confirmed several times in successive annual controls, not associated to myeloproliferative pathology. The lack of progression in the clinical picture would seem to contradict the diagnosis of late Multiple Sclerosis. The presence of antibody activity against the myelin might support the hypothesis of a pathogenetic role of the immunoglobulins at the onset of the demyelinating disease in this patient. However, in the end, there is the possibility of casual association with a poorly functioning immune system connected to age.
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PMID:Demyelinating disease in monoclonal gammopathy of undetermined significance. 1286 87

Diadochokinesis (DDK) for speakers with dysarthria has been described using a variety of acoustic measures. A clinical protocol for the objective assessment of DDK requires a unified approach, however, to facilitate implementation across clinics and laboratories. A protocol for the acoustic analysis of DDK that incorporates temporal and energy measures has been used to describe DDK characteristics for dysarthria secondary to stroke as well as ataxic dysarthria. The current study sought to validate and extend the protocol to a new set of etiological groups, including dysarthria secondary to multiple sclerosis (MS) and Parkinson's disease (PD). The results suggest that temporal measures are more useful than energy measures for distinguishing among dysarthria secondary to MS, dysarthria secondary to PD, and healthy controls. The results also highlight the value of including both alternating and sequential motion rate tasks in the assessment of DDK and of supplementing quantitative measures with qualitative spectrographic observations.
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PMID:Characteristics of diadochokinesis in multiple sclerosis and Parkinson's disease. 1293 Oct 58

Research investigating coarticulatory patterns in dysarthria has the potential to provide insight regarding deficits in the organizational coherence of phonetic events that may underlie deviant perceptual characteristics. The current study investigated anticipatory coarticulation for 17 speakers with multiple sclerosis (MS), 12 speakers with Parkinson's disease (PD), and 29 healthy control speakers. V1-C-V2 sequences were used to investigate intersyllabic vowel to vowel effects (V2 to V1 effects), intersyllabic consonant to vowel effects (C to V1 effects), and intrasyllabic vowel to consonant effects (V2 to C effects). Second formant frequencies and first moment coefficients were used to infer coarticulation. In general, patterns of intersyllabic and intrasyllabic coarticulation were similar for speakers with MS, speakers with PD, and healthy control speakers. It therefore appears unlikely that coarticulatory patterns for speakers diagnosed with MS or PD strongly contribute to deviant perceptual characteristics, at least for the current group of speakers, most of whom were mildly to moderately impaired. Anticipatory vowel effects in /k/+vowel sequences, however, tended to be reduced for speakers with MS and speakers with PD when data for these 2 speaker groups were pooled and compared to control speakers. These results were not attributable to group differences in speech rate or articulatory scaling, defined as the extent of articulatory movements, and further suggest that coarticulatory deficits are not unique to particular neurological diagnoses or dysarthrias. Potential explanations for the /k/+vowel results include difficulties with anterior-posterior tongue positioning and the competing influences of minimizing articulatory effort and maintaining sufficient perceptual contrast. Despite this subtle difference in coarticulation between disordered speakers and healthy control speakers, the overall results suggest that anticipatory coarticulation for speakers with MS and speakers with PD is preserved.
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PMID:Anticipatory coarticulation in multiple sclerosis and Parkinson's disease. 1295 75

Both rate reduction and increased loudness reportedly are associated with an increase in the size of the articulatory-acoustic working space and improved acoustic distinctiveness for speakers with dysarthria. Improved intelligibility also has been reported. Few studies have directly compared rate and loudness effects for speakers with dysarthria, however, although rate reduction and increasing vocal loudness are common treatment techniques. In the current study, 15 speakers with dysarthria secondary to multiple sclerosis, 12 speakers with dysarthria secondary to Parkinson's disease (PD), and 15 healthy controls read a passage in habitual, loud, and slow conditions. Rate and loudness variations were elicited using magnitude production. Acoustic measures included articulatory rate, sound pressure level, vowel space area, first moment difference measures, and F2 trajectory characteristics for diphthongs. Ten listeners scaled intelligibility for reading passages produced by the speakers with dysarthria. Relationships between intelligibility estimates and acoustic measures were determined by regression analysis. All speaker groups reduced articulatory rate for the slow condition and increased vocal intensity for the loud condition, relative to the habitual condition. Vowel acoustic distinctiveness, as indexed by vowel space area, was maximized in the slow condition, but stop consonant acoustic distinctiveness, as indexed by first moment difference measures, was maximized in the loud condition. F2 slope measures for diphthongs were not consistently affected by rate or loudness. Scaled intelligibility for speakers with PD also improved in the loud condition relative to both the habitual and slow conditions. Intelligibility estimates for speakers with dysarthria, however, were not strongly related to acoustic measures of supraglottal behavior. Findings are compared with previous studies, and hypotheses for future treatment studies are discussed.
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PMID:Rate and loudness manipulations in dysarthria: acoustic and perceptual findings. 1532 85

October 2004. A 49-year-old right-handed man developed progressive cognitive difficulties over a 4-month period. There was impairment in recent memory, calculations and language. He also developed fatigue, weight loss, gait imbalance and urinary incontinence. Past history included transfusion-associated Hepatitis C. Neurologic exam showed mild dysarthria, dysnomia, left sided neglect, bilateral Babinski signs, and a prominent grasp reflex. Laboratory testing provided no positive etiologic data. An EEG showed generalized intermittent slowing suggestive of a diffuse encephalopathy and decreased background in the right hemisphere, suggestive of a structural lesion. MRI showed multiple areas of high signal on FLAIR imaging and patchy enhancement. FDG-PET showed multi-focal areas of increased uptake, correlating with the abnormal areas on MRI, on a background of decreased uptake. A 4-vessel cerebral angiogram showed no abnormalities. A brain biopsy showed diffuse infiltrates of large malignant cells that were immunoreactive with antibodies to CD20, diagnostic of diffuse large B cell lymphoma. In summary, the clinical presentation suggested bilateral hemispheric involvement, which was supported by physical examination, EEG, MRI, and PET scans. The differential diagnosis for this presentation is limited to demyelinating disease such as multiple sclerosis, vascular dementia, and infiltrating neoplasm such as glioblastoma multiforme or lymphoma. Diagnosis was made by morphologic and immunohistochemical analysis of brain tissue.
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PMID:October 2004: a 49-year-old man with progressive dementia. 1591 74

The present study compared patterns of anticipatory coarticulation for utterances produced in habitual, loud, and slow conditions by 17 individuals with multiple sclerosis (MS), 12 individuals with Parkinson's disease (PD), and 15 healthy controls. Coarticulation was inferred from vowel F2 frequencies and consonant first-moment coefficients. Rate-related changes in coarticulation differed depending on the particular phonetic events in an utterance. In some instances, the slow condition was associated with stronger anticipatory effects, but in other instances the slow condition was associated with weaker anticipatory effects, relative to other speaking conditions. In contrast, coarticulatory patterns for the loud and habitual conditions typically did not differ. Coarticulatory patterns also tended to be similar among speaker groups within each condition. Finally, when acoustic measures of coarticulation differed among speaking conditions, the direction and magnitude of the effect generally were similar for healthy controls, speakers with MS, and speakers with PD. These results are consistent with studies suggesting mostly preserved patterns of coarticulation for speakers with mild to moderate dysarthria, as well as research indicating only subtle coordination deficits for individuals with dysarthria. The finding that increased loudness had a negligible effect on coarticulation also appears to be at odds with the suggestion that increased loudness stimulates orofacial coordination for speakers with dysarthria, although studies including speakers exhibiting coordination impairments at habitual speaking rates would provide a stronger test of this suggestion. Lastly, the fact that speaking condition similarly affected acoustic measures of anticipatory coarticulation for all speaker groups suggests the feasibility of applying theories and models of speech production for neurologically normal talkers to the study of dysarthria.
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PMID:Effect of rate reduction and increased loudness on acoustic measures of anticipatory coarticulation in multiple sclerosis and Parkinson's disease. 1598 91

Most movement disorders, reflecting degenerative disorders, develop in a slowly progressive fashion. Some movement disorders, however, manifest with an acute onset. We wish to give an overview of the management and therapy of those acute-onset movement disorders.Drug-induced movement disorders are mainly caused by dopamine-receptor blockers (DRB) as used as antipsychotics (neuroleptics) and antiemetics. Acute dystonic reactions usually occur within the first four days of treatment. Typically, cranial pharyngeal and cervical muscles are affected. Anticholinergics produce a prompt relief. Akathisia is characterized by an often exceedingly bothersome feeling of restlessness and the inability to remain still. It is a common side effect of DRB and occurs within few days after their initiation. It subsides when DRB are ceased. Neuroleptic Malignant Syndrome is a rare, but life-threatening adverse reaction to DRB which may occur at any time during DRB application. It is characterised by hyperthermia, rigidity, reduced consciousness and autonomic failure. Therapeutically immediate DRB withdrawal is crucial. Additional dantrolene or bromocriptine application together with symptomatic treatment may be necessary. Paroxysmal dyskinesias are childhood onset disorders characterised by dystonic postures, chorea, athetosis and ballism occurring at irregular intervals. In Paroxysmal Kinesigenic Dyskinesia they are triggered by rapid movements, startle reactions or hyperventilation. They last up to 5 minutes, occur up to 100 times per day and are highly sensitive to anticonvulsants. In Paroxysmal Non-Kinesiogenic Dyskinesia they cannot be triggered, occur less frequently and last longer. Other paroxysmal dyskinesias include hypnogenic paroxysmal dyskinesias, paroxysmal exertional dyskinesia, infantile paroxysmal dystonias, Sandifer's syndrome and symptomatic paroxysmal dyskinesias. In Hereditary Episodic Ataxia Type 1 attacks of ataxia last for up to two minutes, may be accompanied by dysarthria and dystonia and usually respond to phenytoin. In Type 2 they can last for several hours, may be accompanied by vertigo, headache and malaise and usually respond to acetazolamide. Symptomatic episodic ataxias can occur in a number of metabolic disorders, but also in multiple sclerosis and Behcet's disease.
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PMID:Diagnosis and management of acute movement disorders. 1620 29

Multiple sclerosis (MS) is almost always diagnosed in current medical practice on the basis of clinical, biologic and imaging criteria without need for tissue diagnosis. There are, however, rare pseudo tumoral cases of MS with atypical clinical and imaging features that suggest initially a neoplastic or an infectious processes and in which a stereotactic brain biopsy becomes needed for the diagnosis. We report the case of a 28-year-old man who presented with a right hemiparesis of rapid onset. Magnetic resonance imaging (MRI) of the brain showed a left contrast enhancing fronto-parietal mass lesion with important peripheral edema and displacement of the lateral ventricle. The patient underwent stereotactic biopsy of the mass. The pathologic examination revealed gross architectural disorganization of the white matter with massive infiltration by numerous foamy macrophages and a few lymphocytes consistent with a demyelinating disease. Despite a standard corticoid therapy regimen with initial clinical improvement, the patient was readmitted to the hospital three weeks later for relapse of right hemiparesis. Two months later, he recovered almost entirely except for a slight residual weakness in his right arm and a mild dysarthria. The MRI at that time showed a marked decrease in size of the brain lesion. The stereotactic brain biopsy remains to date the most dependable means for diagnosing the rare pseudotumoral forms of MS and differentiating them from their neoplastic and infectious mimickers.
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PMID:[Multiple sclerosis mimicking brain tumor: an unusual presentation]. 1639 12

Although diversity of symptoms and urgency of needs pose many challenges, management of the degenerative dysarthrias is a crucial aspect of clinical practice. The purpose of this article is to review current research literature on selected degenerative dysarthrias including those associated with Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis. These dysarthrias are prevalent yet represent distinct patterns of underlying neuropathology, symptoms, age of onset, and rate of progression. Literature searches including the period 1997-2006 yielded 148 different studies reporting data on communication issues related to dysarthria. By far the largest category of studies was that which provided a basic description of speech production including the neurophysiologic, acoustic, or perceptual properties of dysarthria. Other categories included management (assessment and treatment) and the psychosocial consequences of dysarthria. While the topic of management of degenerative dysarthria is a focused one, it provides a window into many issues critical to the field of communication disorders including fundamental properties of speech production, development of evidence-based treatment techniques, the staging of these techniques into an effective management sequence, and the psychosocial consequences of communication disorders along with techniques to maintain communicative participation in the face of degenerative conditions.
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PMID:The degenerative dysarthrias: a window into critical clinical and research issues. 1755 54

Disabling tremor is common in multiple sclerosis and up to 75% of patients experience tremor at some point during their disease. The treatment of this tremor, however, remains challenging. Pharmacotherapy in general has been disappointing and stereotactic neurosurgery is becoming increasingly popular. However, the results of stereotactic treatments reported are variable and no systematic review has been performed. The aim of this study was to assess the role of thalamotomy and deep brain stimulation in the treatment of tremor in multiple sclerosis, and to compare the differences in efficacy and safety between the two techniques. We identified the relevant published studies and cases by searching the MEDLINE, EMBASS and the references lists of related articles, and performed a systematic review and assessment of the full texts of all articles selected. Initial tremor suppression was seen in 93.8% of patients who had thalamotomy and 96% in those who had deep brain stimulation. A total of 63.5% of patients had persistent tremor suppression at 12 months or more after thalamotomy. Twelve results for deep brain stimulation were not available in the reviewed literature. Functional improvement was seen only in 47.8% of those who underwent thalamotomy as opposed to 85.2% of those who had deep brain stimulation. While three of the four reported deaths were in patients who underwent thalamotomy, three of the four procedure-related haemorrhages followed DBS. Other common adverse effects like hemiparesis, dysarthria, swallowing difficulties, balance disorder, etc., was reported in both procedures. Numerous studies have attempted to assess the efficacy and safety of thalamotomy and DBS in the treatment of MS tremor, but no standardized outcome measures were used. Nonetheless, the data suggest that both thalamotomy and thalamic DBS are comparable procedures for tremor suppression and that adverse effects can occur with both procedures.
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PMID:Stereotactic neurosurgery for disabling tremor in multiple sclerosis: thalamotomy or deep brain stimulation? 1767 53


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