Cases reported "Aphasia, Wernicke"

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1/4. A case of progressive aphasia without dementia: "temporal" Pick's disease?

    We report a patient who suffered from progressive aphasia for nine years, before developing mild behavioural disturbances. Sequential computed tomography (CT) scanning and magnetic resonance (MRI) imaging showed progressive bilateral temporal atrophy. The case is thought to be a temporal form of Pick's disease, in which isolated progressive aphasia was the only symptom over many years.
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ranking = 1
keywords = behaviour
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2/4. Deep left parietal lobe syndrome: conduction aphasia and other neurobehavioural disorders due to a small subcortical lesion.

    A patient with sudden onset of conduction aphasia in the context of an ischaemic stroke is reported. Other neurological and neuropsychological findings included bilateral ideomotor apraxia, right hemisensory defect and paradoxical left ear extinction on a dichotic listening test. Lesion location, as inferred from magnetic resonance imaging, involved a restricted subcortical area in the left parietal lobe, near the lateral wall of the cerebral ventricle. The anatomical correlate for each of the clinical findings is discussed in the light of classical anatomo-clinical correlations. It is concluded that this tetrad constitutes a specific syndrome which may be easily recognised and ascribed to a single lesion in the deep white matter of the left parietal lobe.
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ranking = 4
keywords = behaviour
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3/4. Quantification of cortical atrophy in a case of progressive fluent aphasia.

    A patient with a rapidly developing fluent progressive aphasia was tested prospectively up to the time of death and examined neuropathologically. Severe impairment in accessing semantic skills with substantially intact phonological, syntactic and discourse skills was found. Some social behavioural difficulties were also noted. This case presented a unique opportunity to relate this significant language impairment to the pattern of neurodegeneration, a difficult task in most neuropathological studies of severe end-stage dementia. A detailed neuropathological examination revealed focal atrophy with neuronal loss without neuronal inclusions (Pick bodies, lewy bodies, neurofibrillary tangles or senile plaques) or neuronal changes (shrinkage or swelling). In addition, spongiform degeneration (confined to layer two of the cortex) and gliosis were detected at atrophic sites. To establish the amount of tissue loss and pathology associated with the focal language deficit, volume analyses were performed and compared with two age- and sex-matched, neurologically normal controls. Both the left and right angular gyri and Brodmann's area 37 showed marked volume reduction compared with controls. The predominant language impairment seen in this case is likely to reflect these marked changes in the posterior parieto-temporal areas. The milder unilateral atrophy was concentrated in the right temporal lobe as well as the right hemisphere homologue of Broca's area. Recent work suggests a relationship between such unilateral changes and the social behavioural difficulties which were noted in this case. The hippocampus and other gyri such as the supramarginal gyrus showed no volume loss compared with controls correlating with the relative preservation of other language skills.
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ranking = 2
keywords = behaviour
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4/4. Competition between past and present. Assessment and interpretation of verbal perseverations.

    Perseveration consists of the inappropriate repetition of a preceding behaviour when a new adapted response is expected. We have developed statistical tools that make it possible to reveal such perseverations, assess their significance and study their finer characteristics, such as their temporal course and impaired processing level. This approach is illustrated and evaluated through analyses of naming errors produced by three patients with impairments affecting different stages of the processing chain leading from visual perception to speech production. These examples of perseverations include the intrusion not only of whole words (patient R.A.V.) but also of isolated phonemes (patient D.U.M.) or of visual features (patient Y.M.) from previous trials. In all cases, the probability that an error is a perseveration from a previous trial is an exponentially decreasing function of the lag between the two trials considered. This suggests that perseverations reflect a decaying internal variable, such as an internal level of activation of previous utterances. Based on these empirical results, we put forward a tentative mechanism for the generation of perseverations: whenever a given processing level is deprived of its normal input, persistent activity inherited from previous trials is no longer overcome by current input, and is revealed in the form of perseverations.
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ranking = 1
keywords = behaviour
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