Cases reported "aphasia, wernicke"

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1/130. Plasticity of language-related brain function during recovery from stroke.

    BACKGROUND AND PURPOSE: This study was undertaken to correlate functional recovery from aphasia after acute stroke with the temporal evolution of the anatomic, physiological, and functional changes as measured by MRI. methods: blood oxygenation level-dependent contrast and echo-planar MRI were used to map language comprehension in 6 normal adults and in 2 adult patients during recovery from acute stroke presenting with aphasia. perfusion, diffusion, sodium, and conventional anatomic MRI were used to follow physiological and structural changes. RESULTS: The normal activation pattern for language comprehension showed activation predominately in left-sided Wernicke's and Broca's areas, with laterality ratios of 0.8 and 0.3, respectively. Recovery of the patient confirmed as having a completed stroke affecting Broca's area occurred rapidly with a shift of activation to the homologous region in the right hemisphere within 3 days, with continued rightward lateralization over 6 months. In the second patient, in whom mapping was performed fortuitously before stroke, recovery of a Wernicke's aphasia showed a similar increasing rightward shift in activation recruitment over 9 months after the event. CONCLUSIONS: Recovery of aphasia in adults can occur rapidly and is concomitant with an activation pattern that changes from left to a homologous right hemispheric pattern. Such recovery occurs even when the stroke evolves to completion. Such plasticity must be considered when evaluating stroke interventions based on behavioral and neurological measurements. ( info)

2/130. 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. ( info)

3/130. Transcortical sensory aphasia in a right-handed patient following watershed infarcts in the right cerebral hemisphere: a 15-month evaluation of another case of crossed aphasia.

    Well-documented cases of crossed (transcortical sensory) aphasia, especially those with longitudinal evaluation, are rare. We report a case of crossed transcortical sensory aphasia following watershed infarcts in the right hemisphere, from the moment of the accident until 15 months afterward. The aphasia type, and the course of recovery, is a "mirror" representation of that seen in cases of uncrossed aphasia. Unfortunately, the data do not permit strong conclusions regarding the lateralization of language in association with praxis and visuospatial abilities. This underlines the need for more well-documented (case) studies to come to a better understanding of the mechanisms through which lateralization occurs. ( info)

4/130. Transcortical sensory aphasia due to a left frontal subcortical haemorrhage.

    A case of transcortical sensory aphasia caused by a cerebral haemorrhage in the left frontal lobe is presented. A 72-year-old right-handed woman was admitted to the hospital, with a history of acute onset of speech disturbance and headache. On initial assessment, her spontaneous speech was fluent. She had no difficulty initiating speech, articulated normally, and did not exhibit logorrhea. Her ability to repeat phonemes and short sentences (5-6 words) was fully preserved, however she had severe difficulty with visual recognition of words, and with aural comprehension at the word level, although she was able to read words aloud. Computed tomography and magnetic resonance imaging showed cerebral haemorrhage in the left frontal lobe, involving the superior and middle frontal gyrus. Single photon emission CT revealed a wider area of low perfusion over the entire left frontal lobe, including the superior, middle and inferior frontal gyrus. The aphasia symptoms, mainly poor comprehension, disappeared quickly several weeks after the event. This may have been due to a reduction in the size of the haematoma and a resolution of the oedema around the haematoma. Clinically, the transcortical sensory aphasia in this case was indistinguishable from that caused by damage to the posterior language areas. Further case reports of transcortical sensory aphasia associated with frontal lobe lesions would help to confirm whether a relatively rapid recovery is characteristic in cases such as this. ( info)

5/130. The role of speech production in auditory-verbal short-term memory: evidence from progressive fluent aphasia.

    We report investigations of auditory-verbal short-term memory (AVSTM) in a patient with progressive fluent anomic aphasia. Despite having apparently normal AVSTM as measured by digital span, FM was significantly impaired in immediate serial recall of short sequences of familiar words, and even in reproducing a single word after a filled delay of just a few seconds. In both tasks, unlike normal subjects, she produced numerous phonological errors, often consisting of phonological segments from the intended target word concatenated with segments from other words in the stimulus sequence. Her success in these tasks was modulated (i) consistently by word frequency (high > low), (ii) inconsistently by word imageability (high > low), and (iii) most dramatically by 'nameability': that is, FM was much more likely to reproduce a word correctly in AVSTM if it was a word that she could also produce successfully in picture-naming tasks. On the basis of these and additional experiments designed to exclude other interpretations, we conclude that AVSTM may be crucially supported by activation of the lexical phonological representations responsible for production of content words in speech. ( info)

6/130. Chronological progression of a language deficit appearing to be postictally reversible in a patient with symptomatic localization-related epilepsy.

    A language deficit occurring interictally, with chronological progression, and postictally in a patient with symptomatic localization-related epilepsy, which began at 1.6 years of age, is reported. The patient was a 30-year-old right-handed man whose seizures seemed to originate from the left frontal lobe and to involve the left temporal lobe. The deficit in oral language consisted mainly of features of motor aphasia, including delayed initiation of speech with great effort, echolalic and palilalic tendencies, and word-finding difficulty, but he also showed features of sensory aphasia. Written language had agraphia observed in sensory aphasia, including well-formed letters, paraphasias, neologisms, and paragrammatism. Postictally, the language deficit appeared to be superficially reversible, and evolved from mutism through non-fluent jargon to the interictal level of language. Analysis of the patient's diaries from 10 to 26 years of age disclosed chronologically progressive deterioration of language with paragrammatism, showing an increase of grammatical errors, neologismus, literal and verbal paraphasias and misconstruction of sentences. The results suggest that localization-related epilepsy of presumably left frontal lobe origin causes not only a postictal language deficit but also a slowly progressive deficit of language function. ( info)

7/130. diffusion- and perfusion-weighted MRI in a patient with a prolonged reversible ischaemic neurological deficit.

    We report acute and follow-up diffusion- and perfusion-weighted MRI (DWI, PWI) findings in a patient with a prolonged reversible ischaemic neurological deficit. PWI 12 h after the patient was last seen to be without symptoms revealed a large perfusion deficit in the left posterior MCA territory with a relatively inconspicuous and much smaller abnormality on DWI. Follow-up showed resolution of abnormalities on both DWI and PWI, and conventional MRI was normal, apart from a very slight abnormality, visible only on FLAIR images, at the centre of the initially DWI-positive region. These findings demonstrate the utility of PWI when be used in combination with DWI to investigate the pathophysiology of transient ischemic syndromes. ( info)

8/130. The experience of Wernicke's aphasia.

    The authors induced a transient Wernicke's aphasia in a patient with left frontal arteriovenous malformation by superselective Wada injection exclusively into the lower division of the left middle cerebral artery. The patient was then asked to recall his experience, which the authors matched against his language during anesthesia. The patient's account showed that there was a more systematic attempt to respond appropriately than the authors could infer from his overt behavior. His narrative suggests that a thought process not measured by aphasia examinations may exist independent of language. ( info)

9/130. The selective impairment of phonological processing in speech production.

    We report the naming performance of a patient (DM) with a fluent progressive aphasia who made phonological errors in all language production tasks. The pattern of errors in naming was strikingly clear: DM made very many phonological errors that resulted almost always in nonword responses. The complete absence of semantic errors and the very low ratio of formal errors relative to nonword errors (1.6:30.3) in DM's performance are discussed in the context of recent claims about the nature of naming deficits in fluent aphasics. We argue that DM's performance makes highly improbable the claim that fluent aphasia results from global lesions affecting all levels of the lexical access system equally. ( info)

10/130. Dissociation of semantic and phonological errors in naming.

    We report the naming performance of a fluent aphasic, DP, who shows a striking dissociation between semantic and phonological (nonword) errors: he produced numerous semantic errors but virtually no phonological errors. DP's pattern of performance is the reverse of that reported for patient DM (Caramazza, Papagno, & Ruml, 2000), who only made phonological errors in a naming task. These patterns of performance are inconsistent with the proposal by Dell, Schwartz, Martin, Saffran, and Gagnon (1997) that the naming deficit in fluent aphasia is the result of global damage to all levels of the lexical access system and support instead the hypothesis that brain damage can selectively disrupt distinct subcomponents of the lexical processing system. ( info)
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