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

Broca's aphasia is characterized by disorders on the phonemic, syntactic and lexical level of linguistic description. It is not only the patient's speech which is impaired; abilities to comprehend, read and write are likewise impaired. Articulatory disorders (dysarthria) which are due to an impaired innervation of the phonatory and articulatory musculature may exist. However these disorders do not account for all the linguistic deficits found in cases of Broca's aphasia. The characteristic feature enabling a differential diagnosis of Broca's aphasia is agrammatism.
 ...
PMID:[Broca's aphasia. The clinical picture and a consideration of the neurolinguistic structure (author's transl)]. 7 59

Language disturbances in cerebral palsy with mutism. The analysis of the afferent side of language in 18 cerebral palsy children with no oral expression shows that they form a very heterogeneous population. The semiological analysis concerning comprehension leads to their classification into four main groups akin to the classical dysphasia syndromes. Major agrammatism occurring in phonologico-syntactic dysphasia. Sensory dysphasias (or verbal deafness). Mixed (or global) dysphasias. Motor dysphasias: phonological programmation disturbances (anarthria) and motor production disturbances (dysarthria). The disclosure of these various dysphasias allows for specific rehabilitation and for education procedures suitable for each individual patient.
 ...
PMID:[Symptomatology of language disorders in cerebral palsy with mutism]. 821 52

We report three cases of effortful echolalia in patients with cerebral infarction. The clinical picture of speech disturbance is associated with Type 1 Transcortical Motor Aphasia (TCMA, Goldstein, 1915). The patients always spoke nonfluently with loss of speech initiative, dysarthria, dysprosody, agrammatism, and increased effort and were unable to repeat sentences longer than those containing four or six words. In conversation, they first repeated a few words spoken to them, and then produced self initiated speech. The initial repetition as well as the subsequent self initiated speech, which were realized equally laboriously, can be regarded as mitigated echolalia (Pick, 1924). They were always aware of their own echolalia and tried to control it without effect. These cases demonstrate that neither the ability to repeat nor fluent speech are always necessary for echolalia. The possibility that a lesion in the left medial frontal lobe, including the supplementary motor area, plays an important role in effortful echolalia is discussed.
 ...
PMID:Effortful echolalia. 953 94

Following a dramatic change of its reported incidence, it was only recently recognized that acquired crossed aphasia in dextral children represents a highly exceptional phenomenon. We describe in a three epoch time-frame model the aphasic and neurocognitive manifestations of an additional case and focus briefly on its anatomoclinical configurations. In our patient, a right parietal cortico-subcortical hemorrhagic lesion caused an initially severe aphasia. After remission of the global aphasic symptoms in the acute phase, an adynamic output disorder with relatively severe auditory-verbal comprehension disturbances developed. In addition to the adynamia of self-generated speech, formal language investigations performed 3 weeks postonset, revealed agrammatism, hypertonic dysarthria, and dysprosodia. A substantial improvement of the aphasic disorder was objectified 83 days postonset. Neuropsychological investigations disclosed both dominant and nondominant hemisphere dysfunctions. Reassessment of neurocognitive functions after a 10-year period evidenced discrete residual anomia, confined to visual confrontational naming and a discrete visuo-perceptual syndrome. Given the posterior localization of the lesion, the syndrome shift from global to predominantly adynamic aphasia represents a finding beyond the plausible anatomoclinical expectations holding in general for the uncrossed, classic types of childhood and adult aphasia. As the first representative of crossed aphasia in dextral children with an anomalous lesion-aphasia profile, our case provides evidence to enrich the discussion on lateralization and intrahemispherical organization of language functions in both childhood and adult aphasia.
 ...
PMID:Anomalous cerebral language organization: acquired crossed aphasia in a dextral child. 1125 55

Fourteen patients with nonfluent progressive aphasia (NFPA) performed a picture description task in both spoken- and written-output conditions, as well as tests of confrontation naming, spelling to dictation and reading aloud of single words and text. Relative to controls, the patients' spoken and written picture descriptions were reduced in length, speed and amount of information. Of particular interest, and accounting for the first part of the article's title, was a pervasive pattern of poorer spoken and written output associated with the requirement to produce more; this was true when 'more' meant either (a) longer vs. shorter single words or (b) connected language vs. single words. Deficits in spoken and written naming were largely parallel and modality-specific output impairments (such as dysarthria in speech or letter-formation problems in writing) seemed to account for the minority of cases who exhibited a discrepancy. Most patients showed no evidence of agrammatism or reduced verb production in their speech, which typically had normal proportions of content and function words as well as nouns and verbs. By contrast, some degree of telegraphic output was observed in the written narratives of a number of patients. Our results argue against several candidates for the main functional locus of impairment in NFPA, but it is likely that deficits in grammatical processing, working memory, planning/executive skills, speech motor abilities and phonological processing all play a role.
 ...
PMID:When more yields less: speaking and writing deficits in nonfluent progressive aphasia. 1578 53

This review summarizes clinical and imaging features associated with primary progressive aphasia (PPA). We investigate the hypothesis that these patients can be divided into subgroups of progressive non-fluent aphasia (PNFA) and semantic dementia (SD), based on their linguistic profiles and related imaging studies, and examine whether each of these major subgroups can be further subdivided. We focus on several critical features within each progressive aphasic subgroup. In PNFA, we examine agrammatism, phonologic disorder, and impaired verb processing to determine whether this syndrome is related to a modality-specific impairment in word formation and articulation, or a conceptual deficit that interferes with grammatical processing. In SD, we examine impaired semantic memory, limited remote memory, and anomia to assess whether this syndrome is due to a modality-neutral interruption of semantic memory, or the degradation of various material-specific representations of object features and words. We conclude that there is sufficiently consistent and converging evidence from clinical and imaging studies to support the claim that PNFA and SD are distinct subgroups of PPA. However, there does not appear to be sufficient evidence at this point to support further discrimination within these progressive aphasic subgroups. Testing hypotheses about finer-grained syndromes such as progressive dysarthria or progressive anomia has important consequences for improving our understanding of language organization and the neural basis for language.
 ...
PMID:Primary progressive aphasia: a review. 1584 55

A classical tenet of clinical neurology proposes that cerebellar disorders may give rise to speech motor disorders (ataxic dysarthria), but spare perceptual and cognitive aspects of verbal communication. During the past two decades, however, a variety of higher-order deficits of speech production, e.g., more or less exclusive agrammatism, amnesic or transcortical motor aphasia, have been noted in patients with vascular cerebellar lesions, and transient mutism following resection of posterior fossa tumors in children may develop into similar constellations. Perfusion studies provided evidence for cerebello-cerebral diaschisis as a possible pathomechanism in these instances. Tight functional connectivity between the language-dominant frontal lobe and the contralateral cerebellar hemisphere represents a prerequisite of such long-distance effects. Recent functional imaging data point at a contribution of the right cerebellar hemisphere, concomitant with language-dominant dorsolateral and medial frontal areas, to the temporal organization of a prearticulatory verbal code ('inner speech'), in terms of the sequencing of syllable strings at a speaker's habitual speech rate. Besides motor control, this network also appears to be engaged in executive functions, e.g., subvocal rehearsal mechanisms of verbal working memory, and seems to be recruited during distinct speech perception tasks. Taken together, thus, a prearticulatory verbal code bound to reciprocal right cerebellar/left frontal interactions might represent a common platform for a variety of cerebellar engagements in cognitive functions. The distinct computational operation provided by cerebellar structures within this framework appears to be the concatenation of syllable strings into coarticulated sequences.
 ...
PMID:The contribution of the cerebellum to speech production and speech perception: clinical and functional imaging data. 1778 16

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.
 ...
PMID:Progressive nonfluent aphasia and its characteristic motor speech deficits. 1809 Apr 19

Progressive nonfluent aphasia (PNFA) is one of the 3 clinical presentations of frontotemporal lobar degeneration (FTLD), the other 2 being frontotemporal dementia and semantic dementia (SD). PNFA and SD, both representing relentlessly progressive language impairment in the realm of FTLD, may share a large part with primary progressive aphasia (PPA). A salient distinction between PPA and PNFA or SD is that PPA includes another clinical type, namely, logopenic/phonemic aphasia (LPA), which is not represented in FTLD. This is primarily because LPA is usually caused by Alzheimer's disease (AD) and the brunt of the lesion is localized at the left temporo-parietal region of the brain. Further, PNFA/SD should be limited to the clinical consequencies of FTLD while PPA is more generous with regard to its causal pathology. By definition, PNFA is an expressive language impairment which is characterized by effortful speech, phonemic errors, grammatical impairment, and word-finding difficulties. Reading and writing may be comparatively impaired. Comprehension of single word meaning is normal, while comprehension of sentencies may sometimes be impaired. PNFA should be differentiated from SD, LPA, and pure progressive apraxia of speech (AOS or alternatively referred to as aphemia or anarthria). SD may be distinguished from PNFA by virtue of its fluency, characteristic loss of word meaning and absence of agrammatism. LPA is similar to PNFA, yet differs in that there is preservation of grammatical skills and speech motor function that is devoid of AOS and/or dysarthria. AOS is an impairment at the level of speech motor programming without language impairment. Thus, there may be a double dissociation between AOS and PNFA i. e., PNFA may or may not accompany AOS and vice versa. PNFA is associated with a localized lesion in the left frontotemporal area of the brain. Immunohistochemical investigations have revealed that ubiquitin/TAR DNA binding protein-43 (TDA-43) positive and tau negative pathology, mostly FTLD with ubiquitin-positive inclusions (FTLD-U) type 3, accounts for 90% of PNFA cases, while the remaining 10% may be caused by tauopathy. Therapeutic attempts for PNFA are currently unsuccessful.
 ...
PMID:[Clinical types of FTLD: progressive nonfluent aphasia; comparative discussions on the associated clinical presentations]. 1993 81

Classifying primary progressive aphasia (PPA) into variants that may predict the underlying pathology is important. However, some PPA patients cannot be classified. A 78-year-old woman had unclassifiable PPA characterized by anomia, dysarthria, and apraxia of speech without agrammatism. Magnetic resonance imaging revealed left mesial temporal atrophy and 18-flourodeoxy-glucose positron emission tomography showed left anterior temporal and posterior frontal (premotor) hypometabolism. Autopsy revealed a mixed tauopathy (argyrophilic grain disease) and transactive response-DNA-binding-protein-43 proteinopathy. Dual pathologies may explain the difficulty classifying some PPA patients and recognizing this will be important as new imaging techniques (particularly tau-positron emission tomography) are introduced and patients begin enrollment in clinical trials targeting the underlying proteinopathy.
...
PMID:Mixed tau and TDP-43 pathology in a patient with unclassifiable primary progressive aphasia. 2592 42


1 2 Next >>