Cases reported "Aphasia"

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1/12. chorea and Broca aphasia induced by diabetic ketoacidosis in a type 1 diabetic patient diagnosed as moyamoya disease.

    We here report one case of hemichorea and Broca aphasia occurred with diabetic ketoacidosis. A 20-year-old woman with type 1 diabetes mellitus had experienced diabetic ketoacidosis fourth time after the onset of diabetes. At the third ketoacidotic episode, the patient was admitted to our hospital for the first time to show hemichorea of the left extremities. brain computed tomography (CT) demonstrated a high-density area in the right caudate head and low-density area in the right putamen. magnetic resonance angiography (MRA) demonstrated a stenosis at the root of the bilateral middle and anterior cerebral arteries. The hemichorea disappeared within 3 days. At the fourth ketoacidotic episode, not hemichorea but unconsciousness was there for 2 days even after ketoacidosis disappeared. After the unconscious state, Broca aphasia was demonstrated for 15 days. The cerebral angiography showed a finding compatible to moyamoya disease. These findings support that chorea and Broca aphasia induced by diabetic ketoacidosis was developed in addition to blood vessel abnormalities such as moyamoya disease. We suggest that poorly controlled diabetic patients with hemichorea should undergo cerebral angiography.
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2/12. ubiquitin-positive frontotemporal lobar degeneration presenting with progressive Gogi (word-meaning) aphasia. A neuropsychological, radiological and pathological evaluation of a Japanese semantic dementia patient.

    A patient with progressive anomia and alexia with agraphia for kanji (Japanese morphograms) is described. The patient showed a deficit in single-word comprehension and on-reading (a type of reading that conveys phonetic value) dominance in kanji reading, i.e. on-preceding (pronouncing first with on-reading, irrespective of its preferred reading) and kun-deletion (inability to recall and recognize kun-reading [another type of reading that conveys meaning]) when reading a single-character kanji. These features were due to loss of lexico-semantic information and thus the patient was regarded as having progressive Gogi (word-meaning) aphasia by Imura, a Japanese manifestation of semantic dementia. Macroscopically, neuropathological examination disclosed atrophy of the left frontotemporal lobe with accentuation in the anterior portion of the temporal lobe. Histologically, there was neuronal loss in the cerebral cortex, hippocampus, parahippocampal gyrus, amygdala, caudate nucleus, and putamen. ubiquitin-immunoreactive neuronal inclusions were present in the hippocampal dentate granular cells. This case demonstrates that progressive Gogi aphasia is semiologically identical to semantic dementia, and our patient clinicopathologically resembled those of Rossor et al. [Rossor, M.N., Revesz, T., Lantos, P.L., Warrington, E.K. Semantic dementia with ubiquitin-positive tau-negative inclusion bodies. brain 2000; 123: 267-76.] and Hodges et al. [Hodges, J.R., Davies, R.R., Xuereb, J.H., Casey, B., Broe, M., Bak, T.H., et al. Clinicopathological correlates in frontotemporal dementia. Ann Neurol 2004; 56: 399-406.].
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3/12. aphasia associated with verified subcortical lesions: three case reports.

    aphasia classically has been described as an acquired impairment of language behavior subsequent to cortical brain injury to the dominant hemisphere. Traditionally, lesions in the internal capsule have been described as resulting in pure motor deficits, which may be accompanied by dysarthria without aphasia. Only recently has the literature suggested that lesions in the putamen and internal capsule may result in aphasia. We describe three clinical cases in which aphasia resulted from left subcortical lesions. The lesions were demonstrated using computed tomographic (CT) scan; language deficits were measured objectively using the Porch Index of Communicative Ability (pica). Two of the three patients experienced excellent recovery of language skills, suggesting that subcortical lesions may have a more favorable prognosis in recovery from aphasia than do cortical lesions. The encouraging recovery may be related to fiber pathway disruption rather than cortical destruction.
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4/12. Left hemisphere intracerebral hemorrhages studied by ( (F-18)-fluorodeoxyglucose PET.

    We used PET to study patients with intracerebral hemorrhages in the left hemisphere. Three anatomic and physiologic patterns were observed. patients 1 and 2 had midputamen hemorrhages with diffuse left less than right hemispheric metabolic asymmetry most prominent in temporal and parietal regions. patients 3 and 4 had posterior putamen-insula-temporal hemorrhages with left less than right metabolic asymmetry in temporoparietal cortex and thalamus. patients 5, 6, and 7 had smaller posterior hemorrhages. Left cortical metabolism was little affected in these three cases. Persistent aphasia was associated with severe metabolic left less than right asymmetry in posterior middle temporal regions.
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5/12. Acalculia following a dominant-hemisphere subcortical infarct.

    A 60-year-old, right-handed woman experienced persistent impairment of calculating ability following a subcortical infarct involving the head of the left caudate nucleus, the anterior superior putamen, and the anterior limb of the internal capsule extending superiorly into the periventricular white matter. Acalculia resulted from defects of numerical syntax, the loss of ability to manipulate mathematical concepts, and impaired working memory.
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6/12. aphasia after left hemispheric intracerebral hemorrhage.

    The function of subcortical nuclear structures in language is uncertain, and language disorders after injury to these structures are described incompletely. We report 15 patients with left putaminal or thalamic hemorrhage, describe the range of language and behavioral disorders produced, and review the potential mechanisms of these disorders. Clinicoanatomic correlations revealed no definite differences between aphasia after hemorrhage in putamen or in thalamus.
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7/12. Acquired capsular/striatal aphasia in childhood.

    We studied a case of language loss caused by an acquired vascular lesion in the putamen, anterior limb of the internal capsule, and lateral aspect of the head of the caudate nucleus in a 7-year-old right-handed girl. Acute right-sided hemiplegia, mutism, oral apraxia, and disturbance in language comprehension but no dysarthria were present. During recovery, a nonfluent aphasia with anomia was evident. After six months, only mild hemiparesis and minor spelling difficulties persisted. We compared this patient with an 11-year-old right-handed girl with right-sided hemiparesis and dysarthria but no language loss following a lesion in the globus pallidus, a portion of the posterior limb of the internal capsule, and the body of the caudate. The presence of a language disturbance in the first but not the second patient was attributed to the difference in lesion location. The symptoms and lesions were similar to those in recent reports of adult patients. To our knowledge, this is the first report of these findings in a child with a left-hemisphere lesion.
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8/12. aphasia with nonhemorrhagic lesions in the basal ganglia and internal capsule.

    Atypical aphasia syndromes were associated with circumscribed nonhemorrhagic infarctions of the anterior limb of the internal capsule and of the striatum, in the dominant hemisphere. None of the several cases could be classified in terms of the classic cortical aphasia syndromes, nor did they correspond to the description of aphasia produced by hemorrhage in the thalamus or putamen. Control subjects without aphasia had lesions in the same structures of the nondominant hemisphere, or they had comparably circumscribed damage, which was located lateral or caudal to the previously indicated locus. The findings raise the question of participation of the dominant striatum, and of the connectional systems that course in the anterior limb of the internal capsule, in language processing.
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9/12. Acute basal ganglia infarction in propionic acidemia.

    An 8-year-old girl with propionic acidemia had acute and rapidly fatal symmetric necrosis of the caudate, globus pallidus, and putamen. Clinical presentation was with acute aphasia, generalized hypotonia, and muscle weakness. There was no evidence of metabolic decompensation, and analysis of the organic acids of the urine indicated good metabolic control. Organic acids in the cerebrospinal fluid were unremarkable. These observations indicate that the pathophysiology of "metabolic stroke" is more complicated than previously thought.
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10/12. Mechanism of reduction of cortical blood flow in striatocapsular infarction: studies using [123I]iomazenil SPECT.

    Single photon emission computed tomography (SPECT) using [123I]iomazenil (radioligand of central-type benzodiazepine receptors) was employed to examine two patients with striatocapsular infarction. Patient 1 was a 61-year-old female with motor aphasia and hemiplegia on the right side. magnetic resonance imaging (MRI) showed a lesion in the anterior limb of internal capsule and putamen on the left side. SPECT using 99mTc-HMPAO revealed a reduction of cerebral blood flow (CBF) in the frontoparietal region on the left side, but the delayed images in SPECT using [123I]iomazenil showed only a mild decrease of accumulation in the frontal lobe. Patient 2 was a 55-year-old male with hemiplegia on the left side. MRI showed a lesion localized in the basal ganglia and posterior limb of the internal capsule on the right side. SPECT using 99mTc-HMPAO revealed a reduction of CBF in the frontoparietal region on the right side and in the cerebellar hemisphere on the left side, but the delayed images in SPECT using [123I]iomazenil showed little decrease of accumulation in parietal lobe. The discrepancy between CBF and receptor images suggested that cortical hypoperfusion on striatocapsular infarction might reflect hypometabolism due to disconnection of the neuronal network between subcortical structure and cortex.
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