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Slowly progressive aphasia without generalized dementia: studies with positron emission tomography.

Slowly progressive aphasia without generalized dementia is a degenerative syndrome selectively affecting dominant hemisphere language areas. We report changes in regional glucose metabolism measured by positron emission tomography in two patients with this condition. Striking abnormalities of glucose utilization in the left cerebral cortex were demonstrated in both patients. The findings of other neurodiagnostic studies were relatively unremarkable. The first patient had a 3-year history of progressive anomia and impaired auditory verbal recall. An electroencephalogram was normal, and computed tomography showed mild left perisylvian atrophy. Positron emission tomography revealed profound hypometabolism in the left temporal regions. The second patient also had a 3-year history of progressive anomia. Electroencephalography, computed tomography, and magnetic resonance imaging scans were normal. Positron emission tomography showed a major reduction in left parietal glucose utilization, with a lesser decrement in left temporal metabolism. Neither patient demonstrated significant contralateral or global abnormalities such as those reported in positron emission tomographic studies of Alzheimer's disease with or without focal clinical features. These observations support the concept of adult-onset progressive aphasia without dementia as a clinical syndrome distinct from Alzheimer's disease.

Aphasia↗

Progressive aphasia without dementia: two cases with focal spongiform degeneration.

Two patients with the syndrome of progressive aphasia without evidence of generalized dementia underwent postmortem neuropathological examinations. In both patients, characteristic changes of Alzheimer's disease, Pick's disease, or Creutzfeldt-Jakob disease were absent. Both patients showed a focal spongiform change involving primarily layer 2 of the left inferior frontal gyrus (and temporal cortex in Patient 1) and a mild astrocytosis in layer 2 and deeper cortical layers. This focal, spongiform cortical degeneration in patients with progressive aphasia does not appear to duplicate any known central nervous system degenerative disease.

Aphasia↗

Progressive aphasia without dementia: further documentation.

Two patients with progressive aphasia without dementia had magnetic resonance imaging findings of focal left temporal lobe abnormality. Unlike most of the other documented cases of progressive aphasia, onset was not presenile, occurring at ages 68 and 69.

Aged↗

Recovery from Wernicke's aphasia: a positron emission tomographic study.

Changes in the organization of the brain after recovery from aphasia were investigated by measuring increases in regional cerebral blood flow (rCBF) during repetition of pseudowords and during verb generation. Six right-handed patients who had recovered from Wernicke's aphasia caused by an infarction destroying the left posterior perisylvian language zone were compared with 6 healthy, right-handed volunteers. In the control subjects, strong rCBF increases were found in the left hemisphere in the posterior part of the superior and middle temporal gyrus (Wernicke's area), and during the generation task in lateral prefrontal cortex (LPFC) and in inferior frontal gyrus (Broca's area). There were some weak right hemisphere increases in superior temporal gyrus and inferior premotor cortex. In the patients, rCBF increases were preserved in the frontal areas. There was clear right hemisphere activation in superior temporal gyrus and inferior premotor and lateral prefrontal cortices, homotopic to the left hemisphere language zones. Increased left frontal and right perisylvian activity in patients with persisting destruction of Wernicke's area emphasizes redistribution of activity within the framework of a preexisting, parallel processing and bilateral network as the central mechanism in functional reorganization of the language system after stroke.

Aged↗

Clinical, neuroimaging, and pathologic features of progressive nonfluent aphasia.

We report the clinical, neuroimaging, and neuropathologic features of progressive nonfluent aphasia (PNFA), a rare neurodegenerative syndrome most notable for its distinct language disturbance. Longitudinal observations of 3 patients revealed progressively telegraphic speech and writing, followed by gradual deterioration of sentence comprehension, and finally, preterminal mutism and dementia. Magnetic resonance imaging revealed cortical atrophy most pronounced in anterior regions of the left hemisphere. Functional neuroimaging demonstrated reduced cerebral activity most prominently in left frontal and temporal regions. At necropsy, microscopic pathology of brain was most consistent with the diagnosis of "dementia lacking distinctive histology" (DLDH). A review of published primary progressive aphasia cases with adequate clinical and histopathological descriptions reveals that the most common pathology underlying PNFA is DLDH. PNFA is one example of a family of clinical syndromes with similar underlying histopathology that affects different regions of the frontal lobe.

Adult↗

A reappraisal of localization theory with reference to aphasia. Part 1: Historical considerations.

Aphasiology is deeply rooted in observations of human behavior, in classification systems for speech and language disturbances, and in language paradigms from outside neurology. A systematic examination of the behaviors that were historically incorporated into aphasia classifications, the changes over time in what behaviors were considered important enough to classify, and the context in which these observations took place can serve as the entry point for a critique of current aphasia studies. Part 1 of this three-part series therefore examines the historical roots of contemporary aphasiology with these issues in mind.

Aphasia↗

A reappraisal of localization theory with reference to aphasia. Part 2: Language theories from outside neurology.

Part 1 of this series explored various historical writings about aphasia in order to understand the current scope of the field and the prevailing neuroanatomical model. This paper will examine the contexts from which key aphasiologists mentioned in Part 1 wrote, with particular attention to influential language theories from outside neurology. Some biases of the Standard Average European languages used by these authors have shaped aphasia theories indirectly and will also be discussed. This analysis reveals an historical shift in the subject matter of aphasiology, from speech behaviors to "language," defined quite broadly. This shift in subject has serious implications for attempts to localize language in the brain.

Aphasia↗

Jean Martin Charcot and aphasia: treading the line between experimental physiology and pathological anatomy.

During his entire career Jean Martin Charcot published or lectured on aphasia and brain localization in man. He contributed case studies during the early 1860s, while in the 1870s he became the leading French promoter of localizationism. It was in 1883 and 1884 that he summarized his thoughts on aphasia in a series of 14 lectures he delivered at the Salpêtrière Hospice. His paramount ambition was to achieve didactic clarity. His proposed "bell diagram" was widely criticized for its simplicity, but nevertheless gained considerable popularity in France. His teaching borrowed extensively from the writings of contemporary researchers and was clearly associationist in nature. Charcot's major contribution in the history of aphasiology is that he introduced the works of "diagram-makers" to the French scientific community at large. Charcot's lecture series also played a key role in renewing interest in psychology. Charcot's dismissal of experimental physiology as a legitimate means of investigating central nervous functions in man allowed him to define a separate field of research for a new psychology, one, he believed, which should depart from introspection and turn to his clinicoanatomic method for guidance.

Anatomy↗

Hypothesis on the nature of comprehension deficit in a patient with transcortical mixed aphasia with preserved naming.

Patients with poor comprehension and preserved naming have been occasionally described. Such patients, who are affected by transcortical aphasia, have been taken as evidence of the possibility of naming an object while bypassing the semantic system. We describe a patient affected with mixed transcortical aphasia who presented a clear dissociation between ability in naming and difficulties in performing word-picture matching tasks. The pattern is explained by the existence of covert compulsory automatic naming that interferes with less automatic procedures involved in word-picture matching. In fact, when we tried to oppose automatic naming by using, in word-picture matching tasks, pictures difficult to name, the comprehension improved. This finding excludes a semantic deficit at the basis of poor comprehension of our patient. We suggest that the dissociation between naming and comprehension could be an expression of a computational limitation within the processes involved in word-picture matching, due to the competition for limited processing resources by automatically activated hyperactive naming.

Aphasia↗

Disconnected phonology: a linguistic analysis of phonemic jargon aphasia.

This paper reports on indications of the nature of the neurolinguistic connection between phonological and lexical components of language, based on a case of phonemic jargon aphasia. Following bihemispheric embolic infarcts, the subject presented with severe fluent aphasia, characterized by fluent strings of phonemes, with virtually no intelligible utterances. Despite nearly total jargonized output, the fundamental phonological processes of speech were largely intact. Specifically she demonstrated: (1) English phonotactics and English stress-timed rhythmic principles, (2) aspirated stops word-initially and glottalized stops word-finally, (3) utterance final declination of pitch, and (4) stressed syllable vowel lengthening. Additionally, regional-specific (Southern American English) phonological processes, including monophthongization, in-gliding, and front vowel backing, were also preserved. Overall, the investigation reveals an example of an intact phonological rule system operating on a grossly disturbed input (lexical representation).

Aphasia, Wernicke↗

Surface dyslexia in nonfluent progressive aphasia.

This article presents the case of a 59-year-old male, JH, with a 6-year history of primary progressive aphasia (PPA), a disorder characterized by isolated language deterioration with relative preservation of other cognitive abilities. JH also shows typical features of surface dyslexia, a reading disorder exemplified by the selective preservation of phonological reading. One recent theory is that surface dyslexia in individuals with PPA results from a loss of semantic knowledge. In this paper we consider an additional possibility and present data supporting the notion that surface dyslexia may also arise from the malfunction in the links between semantic representations and phonology. JH has remarkably preserved lexical semantic knowledge when assessed on tasks that do not require verbal output. Further, item-by-item comparisons of his oral reading and comprehension ability show no significant correspondence between his reading and semantic knowledge. These findings lead us to conclude that, in JH's case, the surface dyslexia is attributable not to a semantic deficit per se but rather to the inability to access phonological information from semantics. JH's language profile is considered in relation to potential sources of surface dyslexia and other cases of progressive aphasia.

Aphasia, Broca↗

Visible changes in lesion borders on CT scan after five years poststroke, and long-term recovery in aphasia.

This study examined 12 aphasia patients at approximately 1 year poststroke (Time 1) and again at 5-12 years poststroke (Time 2) with language testing and CT scan. Significant increases in naming scores, and phrase length in nonfluent speech were observed after 5 years poststroke. Significant expansion in visible lesion borders (lesion size) was observed after 5 years poststroke; an increase in lesion size of > 1% was present in 9/12 cases (75%). Not one case had a second stroke. Thus, it appears that even though lesion expansion may occur after 5 years poststroke, as long as this expansion is unilateral and gradual, it has no adverse effect on language, and in fact, continued recovery in naming and nonfluent speech may also occur. Long-term recovery patterns in aphasia which may be associated with brain reorganization deserve further study, especially with functional brain imaging techniques.

Aged↗

Brain plasticity in poststroke aphasia: what is the contribution of the right hemisphere?

The brain may use two strategies to recover from poststroke aphasia: the structural repair of primarily speech-relevant regions or the activation of compensatory areas. We studied the cortical metabolic recovery in aphasic stroke patients with positron emission tomography (PET) at rest and during word repetition. The left supplementary motor area (SMA) showed the most prominent compensatory activation in the subacute state of stroke. The restitution of the left superior temporal cortex determined the long-term prognosis of aphasia. The brain recruited right-hemispheric regions for speech processing, when the left-hemispheric centers were permanently impaired. This strategy, however, was significantly less effective than the repair of the original speech-relevant network.

Adult↗

Recruiting comparative crosslinguistic evidence to address competing accounts of agrammatic aphasia.

Several hypotheses have been advanced whose aim has been to provide a descriptive generalization of comprehension patterns in agrammatic aphasia in terms of current linguistic theory, most notably, the Trace-Deletion Hypothesis. The basic insight of these syntactic accounts of aphasia is that chains are disrupted. In this paper, we seek to confront the Trace-Deletion Hypothesis (TDH) and one of its variants, the Double-Dependency Hypothesis (DDH), with discriminating, crosslinguistic data. We adduce evidence that on raising constructions both hypotheses are able to derive Spanish agrammatic data correctly. However, neither the TDH nor the DDH are able to account for above-chance performance on SV or VS truncated passives. Finally, only the DDH explains the observed data on passive constructions in which a postverbal subject follows the by phrase (V-by phrase-S). The VS word order data are the critical cases because focusing simply on English would not allow these structures to be tested and, in the case of the V-by phrase-S passive, both hypotheses make different predictions. While the data on raising constructions extend the range of both the TDH and the DDH, the VS data suggest that modifications are required.

Aphasia, Broca↗

On processing lexical meanings in aphasia and Alzheimer's disease: some (re)considerations.

The time course of lexical inferences during language comprehension is discussed according to a Lexical Inference Model (LIM). It distinguishes among three types of lexical inferences, respectively generated from semantic, conceptual, and strategic representations. Following discussion of the model, data from lexical priming studies conducted with aphasic patients as well as with Alzheimer's Disease patients are (re)considered in light of the LIM. The view that "word-level priming" (WLP) is not a sufficient task to tap in the time course of lexical activation during online processing is favored. Since most lexical priming studies on aphasia and Alzheimer's Disease used the WLP paradigm with an interstimulus interval larger than 100 ms, initial claims regarding automatic or modularized lexical processing are shown to be premature. However, the deficient lexical access or integration processes found in aphasias of the Broca and Wernicke types and in the dementia of the Alzheimer type are predicted by the LIM.

Alzheimer Disease↗

Comprehension regularity in Broca's aphasia? There's more of it than you ever imagined.

We analyze the comprehension data in Broca's aphasia, pooled together by Berndt, Mitchum, and Haendinges (1996). We show that once analyzed properly, these data have statistical structure that is very similar to that revealed by the analysis in Grodzinsky, Pinango, Zurif, and Drai (1999). The suggestion that the latter authors doctored the data to obtain a desired outcome is as false as the claim that the data in Berndt et al. show no regularity. Comprehension scores in Broca's aphasia do have statistical structure, which correlates with syntactic structure. Thus, the role of Broca's area and its vicinity in language processing can be made more precise.

Aphasia, Broca↗

The effects of varying attentional demands on the word retrieval skills of adults with aphasia, right hemisphere brain damage, or no brain damage.

Adults with mild aphasia, right hemisphere brain damage (RBD), or no brain damage (NBD) provided one-word phrase completions under isolation, focused attention, and divided attention conditions and in response to relatively constrained or unconstrained phrase stems. Despite comparable word retrieval accuracy among groups during the isolation condition, aphasic and RBD groups performed less accurately than the NBD group during focused and divided attention conditions. Across conditions, there were no significant differences between aphasic and RBD groups. Only aphasic subjects demonstrated a significant effect of phrase type, responding more accurately when completing constrained versus unconstrained stimuli. For aphasic and RBD groups, error type analysis indicated that semantic and phonological aspects of word retrieval were influenced by increased attentional demands. These findings suggest that for adults with aphasia or RBD, there is a negative relation between attention impairments and word retrieval abilities.

Adult↗

The italian determiner system in normal acquisition, specific language impairment, and childhood aphasia.

The paper presents a comparison of the development of the Italian determiner system in three different populations: normally developing children, a child recovering from childhood aphasia from the age of 3 years, 9 months, and 11 specific language impairment (SLI) children. Data from Italian normal children provide evidence for the hypothesis (1) that no prefunctional stage exists as far as the determiner system is concerned and (2) that the syntactic properties of determiners play an essential triggering role early on. The analysis of the determiner system in the aphasic child has a double interest. On the one hand, it may help to shed light on some of the intriguing questions concerning this type of disorder; on the other, it may be relevant for the discussion of the notion of agrammatism. Results of the morphosyntactic analysis reveal that, apart from timing differences, recovery from childhood aphasia shares important features with normal development. Differently from mean length of utterance (MLU)-matched normal controls and the aphasic child, SLI children omit determiners significantly more often than almost any other functional category or free morpheme. We will argue that the reasons for the SLI children's atypical behavior have to be sought in the nonaccessibility to or in the misappreciation of one fundamental syntactic property of determiners: their role as elements that assign argumenthood to nominal expressions (Szabolcsi, 1987; Longobardi, 1994).

Aphasia↗