aphasia/infarction

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Aphasia owing to subcortical brain infarcts in childhood.

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The aim of this study was to further define the clinical features of subcortical aphasia in children with deep brain infarcts and to define the sequelae associated with childhood strokes. We retrospectively studied nine children with left subcortical brain infarcts who presented with acquired

Left medial parietal lobe and receptive language functions: mixed transcortical aphasia after left anterior cerebral artery infarction.

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Three aphasic patients with infarctions involving the left anterior cerebral artery have been studied. Two had trancortical motor aphasia, and one had mixed transcortical (or isolation) aphasia. Based on computerized tomography in two patients and whole-brain sections in one, the patient with mixed

Neurophysiological predictors of aphasia recovery in patients with large left-hemispheric infarction: a mismatch negativity study.

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Although the rehabilitation of aphasia has been extensively studied, the prediction of language outcome still has not received sufficient attention. The aim of this study was to predict the language outcome using mismatch negativity (MMN) in patients with large left-hemispheric

Transcortical sensory aphasia following a left frontal lobe infarction probably due to anomalously represented language areas.

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A 57-year-old right-handed man presented with speech disturbance 1 day prior to his admission. The standardized aphasia test batteries showed transcortical sensory aphasia. MRI revealed a left frontal and insular infarct. Positron emission tomography scans also revealed a glucose hypometabolism in

Akinetic mutism and mixed transcortical aphasia following left thalamo-mesencephalic infarction.

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A 54-year-old man developed somnolent akinetic mutism and acute mixed transcortical aphasia following a left thalamo-mesencephalic infarction. He also exhibited behavioural changes, namely apathy, slowness, lack of spontaneity, disinhibition, perseveration, gait apraxia and incontinence consistent

Aphasia in border-zone infarcts has a specific initial pattern and good long-term prognosis.

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BACKGROUND While border-zone infarcts (BZI) account for about 10% of strokes, studies on related aphasia are infrequent. The aim of this work was to redefine specifically their early clinical pattern and evolution. METHODS We prospectively studied consecutive patients referred to our stroke unit

Correlation of aphasia and/or neglect with cortical infarction in a subpopulation of RANTTAS.

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Classically in neurology, aphasia and neglect were accepted as reliable markers of cortical lesions. The actual prognostic values of aphasia and neglect have yet to be formally tested. This analysis sought to determine the predictive accuracy of aphasia and/or neglect in acute stroke for cortical

Acute transcortical mixed aphasia. A carotid occlusion syndrome with pial and watershed infarcts.

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Four of 1,200 consecutive patients with their first stroke showed acute transcortical mixed aphasia (TMA) characterized by nonfluent speech with impaired naming, semantic paraphasias, echolalia, impaired comprehension, good repetition, reading, and writing on dictation. All 4 had left internal

Aphasia with infarction in the territory of the anterior cerebral artery.

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Two right-handed patients with clinical evidence of major infarction in the territory of the left anterior cerebral artery developed a profound but transient aphasia characterized by (1) a striking dissociation between intact repetition and grossly disturbed spontaneous conversational speech, (2) an

On the occurrence and prognosis of aphasia in patients with cerebral infarction.

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Of 338 consecutive patients with cerebral infarction, aphasia in the acute phase was found in 96. Of these, 18 had totally recovered from aphasic speech disturbances when leaving the hospital. The patients were examined 2-8, in average 6 years after the onset of the illness. 39% of them had died,

Study of two cases of aphasia by infarction of the left thalamus, without cortical lesion.

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Two patients suffering from a left thalamus infarct were studied over a long period. The precise location of the lesion has been demonstrated by the C.T. scan. In spite of the absence of any cortical lesion, both presented with aphasia and other neuropsychological disorders (left-right confusion,

[Assessment of regional cerebral blood flow in subcortical infarction with aphasia].

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We assessed the regional cerebral blood flow (rCBF) in 8 patients with subcortical aphasia and 8 patients with subcortical infarction without aphasia using the N-isopropyl-P-[123I]-iodoamphetamine autoradiography (123I-IMP ARG) method. In this study, we evaluated vermis to left cortex ratio of CBF.

Aphasia due to isolated infarction of the corpus callosum.

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A 63-year-old man with an isolated infarction of the corpus callosum developed expressive aphasia in addition to the deficits traditionally associated with a disconnection syndrome.

[Sensory syndrome and aphasia after left insular infarct].

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BACKGROUND Sensorial impairment without hemiplegia is usually caused by a thalamic lesion. METHODS A 28-year-old woman presented with hemianesthesia associated with aphasia following a left insular lesion, subsequent to subarachnoid hemorrhage. Brain MRI Flair sequence revealed a high intensity

Persistent Broca's aphasia after right cerebral infarction in a right-hander.

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A strongly right-handed man developed sudden mutism and left hemiplegia 2 days after a myocardial infarct. Evaluation 6 1/2 years later revealed persistent Broca's aphasia. There was no clinical, CT, or EEG evidence of left brain injury or disease. This case is another example of dissociation of

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