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At least 19 recordsLinked to original sources

PubMed2001

Speech and language therapy for dysarthria due to non-progressive brain damage.

BACKGROUND: Dysarthria is a common sequel of non-progressive brain damage (typically stroke and traumatic brain damage). Impairment-based therapy and a wide variety of compensatory management strategies are undertaken by speech and language therapists with this patient population. OBJECTIVES: To determine the efficacy of speech and language therapy interventions for adults with dysarthria following non-progressive brain damage. SEARCH STRATEGY: This review has drawn on the search strategies developed for the following Cochrane Groups as a whole: Stroke, Injuries, and Infectious Diseases. Relevant trials were identified in the Specialised Registers of Controlled Trials (see Review Group Details for more information). We also searched the trials register of the Cochrane Rehabilitation and Related Therapies Field. The Cochrane Controlled Trials Register, MEDLINE, EMBASE, CINAHL, PsycLIT, and Linguistics and Language Behavior Abstracts were electronically searched. Hand-searching of The International Journal of Language and Communication Disorders and of reference lists from relevant articles and conference proceedings was also undertaken. Colleagues were approached to identify other possible published and unpublished studies. Date of most recent searches: May 2000. SELECTION CRITERIA: Unconfounded randomised controlled trials. DATA COLLECTION AND ANALYSIS: One reviewer assessed trial quality. Two co-reviewers were available to examine any potential trials for possible inclusion in the review. MAIN RESULTS: No trials of the required standard were identified. REVIEWER'S CONCLUSIONS: There is no evidence of the quality required by this review to support or refute the effectiveness of Speech and Language Therapy interventions for dysarthria following non-progressive brain damage. There is an urgent need for good quality research in this area.

Adult↗

PubMed1994

Pure dysarthria, isolated facial paresis, or dysarthria-facial paresis syndrome.

BACKGROUND AND PURPOSE: Pure dysarthria, isolated supranuclear facial paresis, and their combination without somatic motor dysfunction are rarely encountered clinical syndromes and have not yet been clearly characterized. METHODS: Thirteen patients (9 men, 4 women; aged 33 to 72 [mean, 56] years) with unilateral strokes who developed dysarthria with or without facial paresis but without somatic motor dysfunction were reviewed in addition to case reports from previous literature. RESULTS: Computed tomographic scan and/or magnetic resonance imaging showed infarcts on the corona radiata in 4 patients, basal ganglia abutting the internal capsule in 3, basal ganglia-corona radiata in 1, pontine base in 3, and cortical-subcortical bulbar motor area in 2. The dysarthria and facial paresis were usually mild and transient, and either one was likely to be unnoticed. CONCLUSIONS: It is suggested that pure dysarthria or isolated facial paresis syndrome be considered as an extreme continuum of dysarthria-facial paresis syndrome, which is likely to be a variant of dysarthria-clumsy hand syndrome.

Adult↗

PubMed1997

Variability in upper motor neurone-type dysarthria: an examination of five cases with dysarthria following cerebrovascular accident.

The degree of diversity in the nature and extent of the physiological deficits which occur in subjects with dysarthria with similar neurological damage is demonstrated through the individual assessment profiles of five subjects with dysarthria following upper motor neurone (UMN) damage. The perceptual profiles of each subject were compiled using perceptual ratings of deviant speech parameters, intelligibility ratings from the Assessment of Intelligibility of Dysarthric Speech (ASSIDS), and perceptual judgements of subsystem function determined from the Frenchay Dysarthria Assessment (FDA). For each individual, the perceptual profile of their speech impairments was compared and contrasted with the objective results of spirometric and kinematic assessments of respiratory function aerodynamic and electroglottographic evaluations of laryngeal function, pressure and strain gauge evaluations of articulatory function, and nasal accelerometric assessments of nasality. The outcomes of the individual perceptual and physiological profiles are discussed with respect to the presence of differential subsystem impairments both within each subject and between subjects with similar underlying pathophysiological deficits. The importance of interpreting the instrumental findings with respect to the interdependency of each of the motor speech subsystems, the limitations of perceptual assessments, and the advantages of utilising both perceptual and physiological analyses in the process of identifying treatment goals is discussed.

Aged↗

PubMed1998

The case of the lawyer's lugubrious language: dysarthria plus primary progressive aphasia or dysarthria plus dementia?

A productive, intelligent, 60-year-old practicing attorney slowly begins to notice that the language that he has commanded throughout his life is beginning to become more difficult to produce, exacting its toll on his mental energy and emotional stability. His search for answers to his diminished "memory for words" leads him through the fetid ranks of traditional medicine and into the search for a differential diagnosis involving clinical neurology, neuropsychology, and speech-language pathology. Consistencies and conflicts in the signs and symptoms between the competing diagnoses raise theoretical and clinical classification issues. A course of treatment for aphasia provides evidence to support the diagnosis of primary progressive aphasia, but the development of concommitant spastic dysarthria and dysphagia challenge current wisdom about the underlying neuropathology of aphasia and support a diagnosis of early dementia. A selective but steady and rapid decline of abilities over the course of 2 years leads to the patient's death and autopsy, from which a neuropathologic analysis was to provide the "final" and "ultimate" diagnosis. But it doesn't!

Aphasia↗

PubMed2003

The effect of pacing strategies on the variability of speech movement sequences in dysarthria.

There are many potential sources of variability in speech production, particularly in individuals with dysarthria. The degree and time course of stabilization of the speech production system during recovery from a neurological insult is not constant across individuals. Another source of variability in speech production is speaking rate. Although individuals with no neurological impairments typically show increased variability at reduced speaking rates, this phenomenon has not been explored extensively in individuals with dysarthria. Because rate control strategies are commonly used in dysarthria treatment, it is of clinical importance to know if individuals with dysarthria produce less variable speech with rate reduction. Six individuals with mild dysarthria, 6 with moderate-to-severe dysarthria, and 6 matched normal controls repeated an utterance in four speaking rate conditions: habitual, fast, breaks between words, and stretched. Data were analyzed using the spatiotemporal index (STI), a composite measure of spatial and temporal variability across token repetitions. The normal controls consistently demonstrated the least variability, regardless of rate condition. Both groups with dysarthria were the least variable in the stretched condition and the most variable in the fast condition. The STI values of the group with moderate-to-severe dysarthria were significantly different from both the individuals with mild dysarthria and the normal controls. There were no significant differences between the group with mild dysarthria and the normal controls. In general, slowing the speaking rate in individuals with dysarthria reduces spatiotemporal variability; however, the effect of reduced spatiotemporal variability on intelligibility requires further investigation.

Adult↗

PubMed2005

Impaired corticolingual pathways in patients with or without dysarthria after acute monohemispheric stroke.

The occurrence of dysarthria is not infrequent in stroke but little is known about its pathophysiology. The aims of the present study were to assess the central motor innervation of the tongue in normal adults using transcranial magnetic stimulation (TMS) and to compare this with that seen in stroke patients with or without dysarthria. The study included 46 patients with acute monohemispheric stroke due to occlusion of the territory of the middle cerebral artery as documented by CT brain scan (26 patients with dysarthria and 20 patients without dysarthria). Forty-five (age and sex matched) normal volunteers served as controls. Corticolingual pathways were assessed for each subject after TMS of each hemisphere. TMS over the motor cortex of healthy subjects elicited consistent ipsilateral and contralateral lingual responses. The ipsilateral response was usually smaller and approximately 73% of the amplitude of the contralateral response. The cross talk between the two halves of the tongue as estimated after unilateral electrical stimulation of hypoglossal nerve gave a contra/ipsi ratio of 36%, which was significantly smaller than the ratio seen after cortical stimulation (CL). For the patients, with or without dysarthria, motor evoked potential (MEP) latencies (ipsilateral and contralateral) were significantly prolonged after stimulation of affected hemisphere compared with the non-affected hemisphere or the control group (P< 0.001). MEP amplitudes were significantly smaller in hemiplegic patients with dysarthria compared to patients without dysarthria. In patients without dysarthria stimulation of the unaffected hemisphere tended to evoke responses that were of similar size on both sides. There were no significant associations between neurophysiological parameters and side of infarction. We conclude that interruption of the corticolingual pathways is frequent in stroke patients with or without dysarthria. The ability of unaffected hemisphere to evoke responses in the side contralateral to the lesion may relate to the absence or presence of dysarthria.

Adult↗

PubMed1995

[Dysarthria due to small cerebral infarction--the localization of lesion and clinical characteristics].

We compared locations of infarctions and clinical characteristics for patients with dysarthria and those without dysarthria. Subjects were 40 patients with a small infarction in the corona radiata or junctional zone to the capsule and 13 patients with infarctions in the internal capsule. Left corona radiata/junctional zone infarctions were significantly smaller than right sided lesions. Dysarthria was associated more frequently with the corona/junctional lesions on the left side than the right sided lesions. Asymptomatic infarctions on the contralateral side were seen in 41% of the patients with dysarthria. In these cases, dysarthria continued longer and dysphagia occurred more frequently than the cases without right sided lesions. Corona radiata/junctional zone infarctions with dysarthria were located significantly more anteriorly than those without dysarthria. The corona radiata/junctional zone infarctions presenting with dysarthria alone, upper limb dominant hemiparesis, and lower dominant hemiparesis were located in the anterior, middle, and posterior areas, respectively. In conclusion, dysarthria may occur with unilateral small cerebral infarctions, more frequently with left sided lesions than with right sided lesions. It is assumed that the left corona radiata/junctional zone infarction may interrupt simultaneously the corticobulbar pathway and callosal fibers to the right hemisphere which transmit motor information for speech to the right hemisphere. It is also possible that there are individual variations in the proportion of crossed and uncrossed corticobulbar innervation, which may explain dysarthria with unilateral cerebral lesions in some patients. It was suggested that there is an anterior-posterior somatotopy in the corona radiata/junctional zone as well as in the internal capsule.

Cerebral Infarction↗

PubMed2006

Left-hemispheric dominance for articulation: a prospective study on acute ischaemic dysarthria at different localizations.

Dysarthria is a frequent symptom in cerebral ischaemia. However, speech characteristics of these patients have not previously been investigated in relation to lesion site in a prospective study. We investigated the auditory perceptual features in 62 consecutive patients with dysarthria due to a single, non-space-occupying cerebral infarction confirmed by MRI. Standardized speech samples of all patients were stored within 72 h after stroke onset using a digital tape recorder. Speech samples were assessed independently by two experienced speech therapists, who were unaware of the clinical and neuroradiological findings, using an interval scale ranging from 0 to 6. Separately assessed were features of articulation, phonation, prosody, and the global severity for a total of 31 items. Extracerebellar infarctions (85.5%) were located in the lower motor cortex (14.5%), striatocapsular region (46.8%) and base of the pons (24.2%). Isolated cerebellar infarctions were present in 14.5% of patients. There was a strong correlation between the findings of both examiners, showing identical scores, or only minor differences (<1 on the assessment scale) for 80% of all items. The average severity of dysarthria was 2.9 +/- 1.3. Articulatory abnormalities were the predominant deviation characteristics, affecting in particular the production of consonants. However, phonatory and prosodic abnormalities were also frequently observed speech characteristics. As revealed by factor analysis of speech characteristics the total severity of dysarthria was mainly influenced by the impairment of articulation. Speech parameters describing characteristics of articulation and prosody showed significant side-to-side and area differences, while this effect was lacking for any voice parameter. Left cerebral lesions showed a more severe overall impairment of speech and articulation, independent of lesion topography. Thirty-eight of 62 patients were available for follow-up. Speech evaluation showed normal speech within weeks in 15 out of 38 patients (39.5%). In the other 23 patients overall severity of dysarthria was mild. This is the first prospective study which describes speech characteristics of dysarthria due to acute unilateral cerebral infarctions. We could demonstrate that dysarthria in extracerebellar infarctions was more frequently caused by left-sided lesions and that the severity of dysarthria was more pronounced in left-sided lesions independent from lesion topography. All extracerebellar lesions were located along the course of the cortico-bulbar tract fibres. Compatible with a common pathophysiological basis of dysarthria in these patients, none of the 31 speech items differed significantly between subcortical and brainstem lesions.

Acute Disease↗

PubMed1997

Acquired childhood dysarthria: review of its clinical presentation.

The adult classification of dysarthria correlating with the pathophysiology of the motor systems is usually applied to classify acquired childhood dysarthria. However, the validity of this adult model for children has not been studied systematically. All studies pertaining to analysis of speech features in acquired childhood dysarthria published since 1980 were reviewed. Studies were classified on the basis of neuroradiologic evidence of lesion site and associated motor disorder. This review demonstrates that knowledge of acquired childhood dysarthria is based on a limited number of single case studies, most of which pertain to dysarthria occurring after resection of cerebellar tumor. Definite similarities to adult dysarthria were not evident. Some similarity to acquired childhood dysarthria due to basal ganglia lesions was detected. We conclude that acquired childhood dysarthria requires its own classification.

Adolescent↗

PubMedDate not supplied

Prevalence and characteristics of dysarthria in a multiple-sclerosis incidence cohort: relation to neurological data.

Few attempts have been made to use degree and type of multiple sclerosis (MS) dysarthria in neurological evaluation. In the present study, 77 individuals drawn from an MS population were examined both by a speech pathologist and a neurologist, and data from three sources of information were subsequently combined: (1) a clinical dysarthria test procedure, (2) a perceptual analysis of speech characteristics in continuous speech, and (3) neurological deficit scoring. The speech of 15 age- and gender-matched healthy control subjects was also investigated. It was concluded that: (1) the prevalence of mild to severe dysarthria in this cohort was 51% and occurred in all components of speech production: respiration, phonation, prosody, articulation and nasality. (2) The clinical dysarthria test was sensitive in detecting subclinical speech signs. The prevalence of pathologic speech signs found on the basis of the test was found to be 62%. The prevalence of dysarthria based on the neurological evaluation alone was 20%. (3) The dysarthria of MS was a predominantly mixed dysarthria, with both ataxic and spastic speech signs frequently present in the speech of a given individual. (4) Furthermore, when a predominant type of dysarthria existed, it was not generally associated with a characteristic profile of neurological deficits. Rather, severity of speech deviation was positively correlated to overall severity of neurological involvement, type of disease course, and number of years in progression.

Adult↗

PubMed2001

Dysarthria in acute ischemic stroke: lesion topography, clinicoradiologic correlation, and etiology.

BACKGROUND AND PURPOSE: Although dysarthria is a frequent symptom in cerebral ischemia, there is little information on its anatomic specificity, spectrum of associated clinical characteristics, and etiologic mechanisms. METHODS: An investigation of 68 consecutive patients with sudden onset of dysarthria due to a single infarction confirmed by MRI or CT was conducted. RESULTS: Dysarthria was associated with a classic lacunar stroke syndrome in 52.9% of patients. Isolated dysarthria and dysarthria-central facial and lingual paresis occurred in 2.9% (n = 2) and 10.3% (n = 7), respectively. Dysarthria-clumsy hand syndrome was observed in 11.7% (n = 8) of patients and associated with pure motor hemiparesis and/or ataxic hemiparesis in 27.9% (n = 19). The lesions were due to small-vessel disease in 52.9% (n = 36), to cardioembolism in 11.8% (n = 8), and to large-vessel disease in only 4.4% (n = 3) of cases. Infarctions were located in the lower part of the primary motor cortex (5.9%; n = 4), middle part of the centrum semiovale (23.5%; n = 16), genu and ventral part of the dorsal segment of the internal capsule (8.8%; n = 6), cerebral peduncle (1.5%; n = 1), base of the pons (30.9%; n = 21), and ventral pontomedullary junction (1.5%; n = 1). Isolated cerebellar infarctions affected the rostral paravermal region in the superior cerebellar artery territory. CONCLUSIONS: Extracerebellar infarcts causing dysarthria were located in all patients along the course of the pyramidal tract. This finding correlates with the frequent occurrence of associated pyramidal tract signs in 90.7% (n = 62) of patients. Isolated cerebellar infarcts leading to dysarthria were in all cases located in the territory of the superior cerebellar artery.

Adult↗

PubMed1999

Cerebral blood flow in pure dysarthria: role of frontal cortical hypoperfusion.

BACKGROUND AND PURPOSE: Isolated dysarthria, termed pure dysarthria, develops rarely after stroke, and its pathophysiology remains unclear. To clarify the underlying mechanism of pure dysarthria, we investigated lesion sites and cerebral blood flow in patients with pure dysarthria. METHODS: We examined 12 patients with pure dysarthria who underwent MRI and cerebral blood flow study. To visualize cortical blood flow, a three-dimensional display was generated from single-photon emission computed tomography (SPECT). Regional cerebral blood flow of the patients was semiquantitatively measured with SPECT and N-isopropyl-p[123I]iodoamphetamine as a tracer and compared with that of 11 control subjects. RESULTS: On MRI, multiple lacunar infarctions were noted bilaterally in 11 patients, all of whom had lesions involving the internal capsule or corona radiata. The other patient had a unilateral internal capsule-corona radiata infarction. Three-dimensional display showed frontal cortical hypoperfusion in 8 patients. Since interhemispheric differences of blood flow were not significant in any region of the 12 patients, the mean of left and right cortical blood flow was analyzed. Compared with the control subjects, cortical perfusion was significantly reduced in the patients' frontal regions, sparing the sensorimotor, temporal, and parietal cortices and the cerebellum. Reductions of perfusion were rather pronounced in the anterior opercular, medial prefrontal and premotor, and anterior cingulate regions. CONCLUSIONS: Pure dysarthria results mainly from multiple lacunar infarctions, which induce frontal cortical hypoperfusion, probably due to interruption of corticosubcortical networks. We conclude that frontal cortical hypoperfusion, particularly in the anterior opercular and medial frontal regions, plays an important role in the development of pure dysarthria.

Aged↗

PubMed2003

Cerebellar speech representation: lesion topography in dysarthria as derived from cerebellar ischemia and functional magnetic resonance imaging.

BACKGROUND: Lesion topography and the pathophysiological background of dysarthria due to focal cerebellar lesions have not yet been fully clarified. OBJECTIVES: To investigate the lesion topography of dysarthria due to cerebellar ischemia and evaluate brainstem functions. DESIGN: Case studies. PATIENTS: Eighteen right-handed patients with sudden-onset dysarthria and cerebellar ischemia with and without brainstem involvement and 19 healthy, right-handed, monolingual, German-speaking volunteers. METHODS: In patients, we used multimodal electrophysiologic techniques to investigate brainstem functions. Functional magnetic resonance imaging (MRI) was performed in the 19 healthy volunteers. Activation tasks consisted of repetitive vertical silent movements of the tongue and lips at a self-paced rhythm. RESULTS: Cerebellar lesions and additional signs of brainstem involvement were observed in 11 patients with posterior inferior cerebellar artery, anterior inferior cerebellar artery, and superior cerebellar artery infarctions, respectively. In all other patients with isolated cerebellar infarction (n = 7), only the superior cerebellar artery territory (6 right-sided, 1 left-sided) was affected, and the common lesion site was the rostral paravermal region of the anterior lobe. Functional MRI in healthy volunteers indicated that the cerebellar representation of the tongue and orofacial muscles corresponds to that of the area involved in patients with cerebellar dysarthria. CONCLUSIONS: The results of this study demonstrate that articulatory movements of the tongue and orofacial muscles are involved in the activation of the rostral paravermal area of the anterior lobe. This location corresponds to the area involved in cerebellar ischemia in patients with dysarthria. Lesions in the upper paravermal area of the right cerebellar hemisphere, the site of coordination of articulatory movements of the tongue and orofacial muscles, may lead to the development of dysarthria that is unrelated to (often concomitant) brainstem infarctions.

Adult↗

PubMed2004

Effects of subthalamic nucleus stimulation on parkinsonian dysarthria and speech intelligibility.

Subthalamic stimulation is known to improve tremor, akinesia and rigidity in Parkinson's disease. However, other signs such as hypophonia and swallowing disorders can be relatively resistant to this technique. The effect on dysarthria remains unclear. The aim of this study was to investigate the effects of implantation of electrode and stimulation of the subthalamic nucleus (STN) on parkinsonian dysarthria. Seven patients were prospectively included. Electrodes (Medtronic) were implanted in both STN. The electrode contacts and stimulation parameters were adjusted to provide best relief of symptoms with fewest side effects. Assessment used global scales (Unified Parkinson Disease Rating Scale, UPDRS II and III), dyskinesia scale, exhaustive dysarthria assessment (bucco-facial movements, voice, articulation, intelligibility) and the 'dysarthria' item from the UPDRS III. Evaluations were performed in six conditions: before and three months after surgery (pre-op, post-op) stimulation turned off or on (off-stim, onstim), and without or with a suprathreshold levodopa dose (offdrug, on-drug). Performance level on the UPDRS III significantly improved following electrode implantation and stimulation. For dysarthria, modest beneficial effects were observed on several motor parameters, especially lip movements. Voice mildly improved, especially for the modulation in loudness and pitch. Articulation was not affected. Furthermore, intelligibility was slightly reduced in the on-stimulation condition, especially when patients received levodopa. At an individual level, negative effects on intelligibility were observed in two patients, and this was associated with a discrete increase in facial and trunk dyskinesias, but not with the electrode position or stimulation parameters. In conclusion, surgery had weak effects on dysarthria. Intelligibility can be worsened, especially in the on-drug condition. Thus, adaptation of the stimulation parameters can be difficult.

Aged↗

PubMed2004

Rate and loudness manipulations in dysarthria: acoustic and perceptual findings.

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.

Adult↗

PubMedDate not supplied

[The application of dysarthria profile tests in ALS patients for the detection of speech disturbances].

Dysarthria is an invalidating disability in ALS patients with motor neuron degeneration in the bulbar region. The methods to assess dysarthric disorders in ALS are seldom described in publications. This study was performed in 43 patients who had definite (n = 23) or probable (n = 20) ALS (of the bulbar group n = 15, of the limb group n = 28, mean age = 57.07 (range: 36-69 yr.)) according to WFN criteria. The method based on quantitative tests of dysarthria profile (by Robertson, 1986) was used and the results were compared with 37 age, sex-matched, healthy control subjects. Our study showed the existence of disturbances in all dysarthria profile tests which were of the statistic significance and more frequent as compared to the control subjects (p < 0.01). The analysis showed that quantitative assessment of some dysarthria profile tests (5 out of 8) might be useful in clinical practice to detect dysarthria in ALS patients. Using the dysarthria profile tests we also demonstrated that preclinical dysarthric processes occur among the limb ALS group.

Adult↗

PubMed1996

Characteristics of the dysarthria of multiple system atrophy.

OBJECTIVE: To characterize the dysarthria in patients with multiple system atrophy (MSA). DESIGN: Motor speech examinations, consisting of oral motor, oral agility, and perceptual speech analysis, were performed on 46 patients with MSA. SETTING: University department of neurology referral center. RESULTS: All patients had dysarthria with combinations of hypokinesia, ataxia, or spasticity. Thirty-two patients had all 3 components, 13 had 2 components, and 1 had only 1 component. In most patients the hypokinetic components were the most severe. Hypokinetic components predominated in 22 patients (48%), whereas ataxic components predominated in 16 (35%), and spastic components in 5 (11%). In 1 patient (2%) the hypokinetic and spastic components were equal and greater than the ataxic components, and in 1 patient (2%) the hypokinetic and ataxic components were equal and greater than the spastic components. One patient (2%) had only ataxic dysarthria. The predominant type of dysarthria corresponded well to the subtype of MSA. CONCLUSIONS: The finding of a mixed dysarthria with combinations of hypokinetic, ataxic, and spastic components is consistent with both the overall clinical and the neuropathologic changes in MSA. Motor speech examination can provide helpful information in evaluating patients who might have MSA.

Aged↗

PubMed2001

Progression of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders.

BACKGROUND: Dysarthria and dysphagia are known to occur in parkinsonian syndromes such as Parkinson disease (PD), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Differences in the evolution of these symptoms have not been studied systematically in postmortem-confirmed cases. OBJECTIVE: To study differences in the evolution of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders. PATIENTS AND METHODS: Eighty-three pathologically confirmed cases (PD, n = 17; MSA, n = 15; DLB, n = 14; PSP, n = 24; and CBD, n = 13) formed the basis for a multicenter clinicopathological study organized by the National Institute of Neurological Disorders and Stroke, Bethesda, Md. Cases with enough clinicopathological documentation for the purpose of the study were selected from research and neuropathological files of 7 medical centers in 4 countries (Austria, France, England, and the United States). RESULTS: Median dysarthria latencies were short in PSP and MSA (24 months each), intermediate in CBD and DLB (40 and 42 months), and long in PD (84 months). Median dysphagia latencies were intermediate in PSP (42 months), DLB (43 months), CBD (64 months), and MSA (67 months), and long in PD (130 months). Dysarthria or dysphagia within 1 year of disease onset was a distinguishing feature for atypical parkinsonian disorders (APDs) (specificity, 100%) but failed to further distinguish among the APDs. Survival time after onset of a complaint of dysphagia was similar in PD, MSA, and PSP (15 to 24 months, P =.7) and latency to a complaint of dysphagia was highly correlated with total survival time (rho = 0.88; P<.001) in all disorders. CONCLUSIONS: Latency to onset of dysarthria and dysphagia clearly differentiated PD from the APDs, but did not help distinguish different APDs. Survival after onset of dysphagia was similarly poor among all parkinsonian disorders. Evaluation and adequate treatment of patients with PD who complain of dysphagia might prevent or delay complications such as aspiration pneumonia, which in turn may improve quality of life and increase survival time.

Aged↗