Cases reported "Aphasia, Conduction"

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1/11. Primary progressive aphasia presenting as conduction aphasia.

    We report a case of a woman with primary progressive aphasia (PPA) who presented with conduction aphasia. A 60-year-old, right-handed, Japanese female suffering from progressive aphasia had difficulty in repeating words and phrases. She displayed phonemic paraphasias but had preserved comprehension and had no cognitive or behavior disorder for more than 6 years after the onset of the condition. She was able to continue to work successfully and to perform all her normal daily activities. T1-weighted magnetic resonance imaging revealed minute dilatation of the left inferior horn and sulci in the left hemisphere, and positron emission tomography revealed mild hypometabolism in the left supramarginal gyrus and its surrounding areas. Therefore, she was diagnosed as suffering from PPA presenting as conduction aphasia. We believe that the progressive conduction aphasia of the patient belongs to one of the fluent forms of PPA, and the ability to continue normal work along with the clinical portrayal of preserved memory and cognition skills may be features of a form of PPA presenting as conduction aphasia.
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2/11. Conduction aphasia and the arcuate fasciculus: A reexamination of the Wernicke-Geschwind model.

    Wernicke, and later Geschwind, posited that the critical lesion in conduction aphasia is in the dominant hemisphere's arcuate fasciculus. This white matter pathway was thought to connect the anterior language production areas with the posterior language areas that contain auditory memories of words (a phonological lexicon). Alternatively, conduction aphasia might be induced by cortical dysfunction, which impairs the phonological output lexicon. We observed an epileptic patient who, during cortical stimulation of her posterior superior temporal gyrus, demonstrated frequent phonemic paraphasias, decreased repetition of words, and yet had intact semantic knowledge, a pattern consistent with conduction aphasia. These findings suggest that cortical dysfunction alone may induce conduction aphasia.
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3/11. Acute conduction aphasia: an analysis of 20 cases.

    In this study, the linguistic performance of 20 patients with acute conduction aphasia (CA) is described. CA presented as a relatively homogeneous aphasic syndrome characterized by a severe impairment of repetition and fluent expressive language functions with frequent phonemic paraphasias, repetitive self-corrections, word-finding difficulties, and paraphrasing. language comprehension as assessed by tests of auditory and reading comprehension was only mildly impaired, whereas most patients performed poorly on the Token Test. Verbal-auditory short-term memory was reduced in all patients except one and seems to play a role in associated cognitive deficits, such as impaired syntactic comprehension or reduced mental arithmetics. A follow-up examination of 12 patients showed that CA often resulted in a chronic language deficit. Lesion locations were the posterior temporal and inferior parietal lobe.
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4/11. Demonstrating a wordlikeness effect on nonword repetition performance in a conduction aphasic patient.

    The purpose of this study was to identify the nature of the deficit for a conduction aphasic patient in order to evaluate two different theories of conduction aphasia. First, a conduction aphasic patient FS was tested on auditory word-pair discrimination, word-repetition, and picture-naming. The results of these tasks indicated that her deficit was likely to be post-lexical rather than perceptual or lexical. Next, we examined her repetition performance for two types of nonwords (high-wordlike and low-wordlike nonwords) to distinguish the two theories. FS exhibited a wordlikeness effect: she produced more correct moras and more correct combinations of moras for high-wordlike nonwords than low-wordlike nonwords. We conclude that she had difficulty in maintaining stable phonological representations of verbal materials in the output buffer.
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5/11. Functional MRI follow-up study of language processes in healthy subjects and during recovery in a case of aphasia.

    BACKGROUND AND PURPOSE: The goal of this study was to develop a functional MRI (fMRI) paradigm robust and reproducible enough in healthy subjects to be adapted for a follow-up study aiming at evaluating the anatomical substratum of recovery in poststroke aphasia. methods: Ten right-handed subjects were studied longitudinally using fMRI (7 of them being scanned twice) and compared with a patient with conduction aphasia during the first year of stroke recovery. RESULTS: Controls exhibited reproducible activation patterns between subjects and between sessions during language tasks. In contrast, the patient exhibited dynamic changes in brain activation pattern, particularly in the phonological task, during the 2 fMRI sessions. At 1 month after stroke, language homotopic right areas were recruited, whereas large perilesional left involvement occurred later (12 months). CONCLUSIONS: We first demonstrate intersubject robustness and intrasubject reproducibility of our paradigm in 10 healthy subjects and thus its validity in a patient follow-up study over a stroke recovery time course. Indeed, results suggest a spatiotemporal poststroke brain reorganization involving both hemispheres during the recovery course, with an early implication of a new contralateral functional neural network and a later implication of an ipsilateral one.
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6/11. Dysgraphia in two forms of conduction aphasia.

    Recent clinical observations, in the absence of experimental data, appear to suggest that written expression in conduction aphasics parallels their speech (Goodglass, 1992). The current study undertakes an analysis of word level writing in two conduction aphasics, and attempts to explore the posited 'parallel' relationship between speech production deficits and deficits in written expression. JL, a 66-year-old female with left posterior parietal lobe lesion and PP, a 65-year-old female with a left posterior temporo-parietal lobe lesion served as subjects of this study. Their response patterns on boston Naming Test (BNT) and written naming task (John Hopkins Dysgraphia Battery) were utilized to verify the parallel hypothesis. Although both cases have exhibited phonological and semantic paraphasias on BNT, PP's overall performance was far superior to that of JL. JL produced numerous multiple responses to stimuli compared to PP's occasional multiple responses. PP's performance on the written naming task was far inferior to that of JL. JL's predominant error pattern in writing was the production of phonologically similar words to the target words. This paper argues that such seemingly contradictory, unpredicted patterns can be parsimoniously better explained, not by the parallel hypothesis but by current cognitive-neuropsychological models of writing.
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7/11. Conduction aphasia as a function of the dominant posterior perisylvian cortex. Report of two cases.

    Assessment of eloquent functions during brain mapping usually relies on testing reading, speech, and comprehension to uncover transient deficits during electrical stimulation. These tests stem from findings predicted by the Geschwind-Wernicke hypothesis of receptive and expressive cortices connected by white matter tracts. Later work, however, has emphasized cortical mechanisms of language function. The authors report two cases that demonstrate that conduction aphasia is cortically mediated and can be inadequately assessed if not specifically evaluated during brain mapping. To determine the distribution of language on the dominant cortex, electrical cortical stimulation was performed in two cases by using implanted subdural electrodes during brain mapping before epilepsy surgery. A transient isolated deficit in repetition of language was reported during stimulation of the posterior portion of the dominant superior temporal gyrus in one patient and during stimulation of the supramarginal gyrus in the other patient. These cases demonstrate a localization of language repetition to the posterior perisylvian cortex. brain mapping of this region should include assessment of verbal repetition to avoid potential deficits resembling conduction aphasia.
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8/11. MRI of white matter changes in the sjogren-larsson syndrome.

    We report a case of sjogren-larsson syndrome with spastic diplegia and conduction aphasia. MRI demonstrated the white matter changes deep in the cerebral hemispheres. We analyse the MRI findings and compare the results with neuropsychological signs.
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9/11. "Semantic" conduction aphasia from a posterior insular cortex infarction.

    A unique infarction limited to the posterior insula and intrasylvian parietal opercular cortex produced a subtype of conduction aphasia, characterized by a predominance of semantic paraphasias. temporal lobe hypoperfusion seen on hexamethylpropyleneamineoxime single-photon emission computed tomography in the absence of any signs of ischemia suggested that cortical diaschisis played a role in the emergence of this syndrome.
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10/11. Mechanism of short-term memory and repetition in conduction aphasia and related cognitive disorders: a neuropsychological, audiological and neuroimaging study.

    To evaluate the role of the sub-cortical white matter and cortical areas of the supramarginal gyrus in short-term memory impairment (shortened digit or letter span) and repetition difficulty, four patients with conduction aphasia and impaired short-term memory and two patients with only short-term memory impairment were given digit span, letter span, speech audiometry and dichotic listening tests. The results showed that in most of the patients letter span was inferior to digit span and that bilateral ear suppression in the dichotic listening test was observed in two patients with a lesion in the inferior part of the supramarginal gyrus, suggesting that what was affected was phonological information and that the supramarginal gyrus was the storage site. The overlapped lesion of conduction aphasia patients with short-term memory impairment was the periventricular white matter at the upper to middle part of the trigone, while patients with only short-term memory impairment had a lesion in the inferior supramarginal gyrus in common. Thus, damage to the periventricular white matter at the trigone may yield the phonemic paraphasia characteristic of conduction aphasia, while damage to the inferior part of the supramarginal gyrus may result in the impairment of short-term memory. We believe that as a part of the mechanisms of short-term memory and repetition, phonological information is processed in the primary auditory cortex and goes through the periventricular white matter to the inferior part of the supramarginal gyrus and is temporarily stored there.
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