The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Asuka Nakajima - One of the best experts on this subject based on the ideXlab platform.
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Progressive Transcortical Sensory Aphasia and progressive ideational apraxia owing to temporoparietal cortical atrophy
BMC Neurology, 2015Co-Authors: Michitaka Funayama, Asuka NakajimaAbstract:Background In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive Aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive Aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive apraxia. However, not every patient clearly fits into one of these categories. Case presentation Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive Transcortical Sensory Aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Conclusions Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with Transcortical Sensory Aphasia, apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive Aphasia and posterior cortical atrophy.
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progressive Transcortical Sensory Aphasia and progressive ideational apraxia owing to temporoparietal cortical atrophy
BMC Neurology, 2015Co-Authors: Michitaka Funayama, Asuka NakajimaAbstract:In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive Aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive Aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive apraxia. However, not every patient clearly fits into one of these categories. Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive Transcortical Sensory Aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with Transcortical Sensory Aphasia, apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive Aphasia and posterior cortical atrophy.
Michitaka Funayama - One of the best experts on this subject based on the ideXlab platform.
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Progressive Transcortical Sensory Aphasia and progressive ideational apraxia owing to temporoparietal cortical atrophy
BMC Neurology, 2015Co-Authors: Michitaka Funayama, Asuka NakajimaAbstract:Background In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive Aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive Aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive apraxia. However, not every patient clearly fits into one of these categories. Case presentation Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive Transcortical Sensory Aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Conclusions Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with Transcortical Sensory Aphasia, apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive Aphasia and posterior cortical atrophy.
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progressive Transcortical Sensory Aphasia and progressive ideational apraxia owing to temporoparietal cortical atrophy
BMC Neurology, 2015Co-Authors: Michitaka Funayama, Asuka NakajimaAbstract:In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive Aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive Aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive apraxia. However, not every patient clearly fits into one of these categories. Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive Transcortical Sensory Aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with Transcortical Sensory Aphasia, apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive Aphasia and posterior cortical atrophy.
Shoji Tsuji - One of the best experts on this subject based on the ideXlab platform.
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difference between Transcortical Sensory Aphasia following the left frontal lesion and Transcortical Sensory Aphasia following the left posterior lesion
Nō to shinkei Brain and nerve, 1998Co-Authors: M Otsuki, Y Soma, Kenju Aoki, Osamu Iizuka, A Koyama, N Yoshimura, M Sahara, Hiroko Nagai, Ryoko Koike, Shoji TsujiAbstract:: We assessed the difference between Transcortical Sensory Aphasia (TCSA) following the left frontal lesions (F-TCSA) and TCSA following the left posterior lesions (P-TCSA). All the patients were right-handed and the 7 patients had the lesions in the only frontal lobe and the 10 patients had the lesions only in the left temporo-parieto-occipital regions. We administered pointing tasks, using 90 line drawings representing single nouns. We presented 6 line drawings a pointing board, and we used two kinds of pointing boards: one showed the line drawings each belonging to different categories (random categorized pointing task), the other showed the line drawings each belonging to only either two different categories (two categorized pointing task) and we presented 15 pointing boards each alternatively. The result was that regarding the patients of P-TCSA showed different number of correct answers between the random categorized pointing task and the two categorized pointing task with statistical significance. Regarding the patients of F-TCSA showed no difference between them. The results indicated that disturbance of P-TCSA on the pointing task was the disturbance of semantic process per se. And the disturbance of F-TCSA on the pointing task was that of not only semantic process but also the whole process including comprehending the presented words, searching the line drawings, comparing the line drawings with the presented word and final selection, which demanded persistent multiple memory process consistent with working memory.
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Transcortical Sensory Aphasia following left frontal infarction
Journal of Neurology, 1998Co-Authors: M Otsuki, Y Soma, A Koyama, N Yoshimura, Hiroko Furukawa, Shoji TsujiAbstract:Two right-handed patients who exhibited language disability after left frontal infarction are described. The patients spoke fluently and exhibited excellent repetition ability from the onset of infarction without exhibiting any oral apraxia, but had deficits in auditory comprehension, naming, reading and writing. In both patients, brain magnetic resonance imaging (MRI) revealed infarction in the left inferior frontal gyrus, the middle frontal gyrus and the anterior part of the lower precentral gyrus. Single photon emission computed tomography (SPECT) revealed decreased blood flow in the same regions as those shown to be infarcted by MRI. The MRI and SPECT findings and the symptoms of these patients suggest that left frontal lesions that encompass Broca’s area produce fluent Aphasia if the posterior part of the left precentral gyrus or motor cortex remains intact and that lesions anterior to Broca’s area and the middle frontal gyrus produce a deficit in auditory comprehension of single words as well as sentences.
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Posterior cortical atrophy with incomplete Bálint's syndrome
Nō to shinkei Brain and nerve, 1997Co-Authors: Iizuka O, Soma Y, Otsuki M, Endo K, Tanno Y, Shoji TsujiAbstract:We report a patient of posterior cortical atrophy (PCA) with progressive memory disturbance and incomplete Bálint's syndrome consisting of optic ataxie (ataxie optique type) and visual inattention without psychic paralysis of fixation of gaze. The patients is a 58-year-old woman who noticed memory disturbance at 53 years old. Neurological deficit at 54 years old was detected only in the domain of memory, and mild diffuse brain atrophy was revealed on MRI. Memory disturbance progressed gradually, and at the age of 58 she was noticed to have visual disorder. Neuropsychological examination revealed severe memory disorder, incomplete Bálint's syndrome, Transcortical Sensory Aphasia, mild ideational apraxia, and severe constructional apraxia. Visual inattention was too severe to evaluate visual acuity and visual field. MRI showed moderate dilatation of bilateral lateral ventricles, especially in their posterior horns, with atrophy of bilateral temporo-parieto-occipital lobes and hippocampus. IMP-SPECT revealed a diffuse decrease of cerebral blood flow in the bilateral temporo-parieto-occipital region, predominantly in the parietal regions. We believe that she is still in the early phase of PCA, and that psychic paralysis of fixation of gaze, visual agnosia will be noted in several years. Our patient represents an example of early stage PCA from neuropsychological and MRI findings.
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Familial posterior cortical atrophy with visual agnosia and Bálint's syndrome
Nō to shinkei Brain and nerve, 1995Co-Authors: Otsuki M, Soma Y, Tanno Y, Tanaka M, Keiko Tanaka, Uesugi Y, Shoji TsujiAbstract:We report a patient of posterior cortical atrophy with progressive visual agnosia, Balint's syndrome and dementia in which posterior cortical atrophy with similar characteristics on CT and progressive dementia were found in a sister. The patient was a 75-year-old woman who noted the onset of a progressive visual disorder at the age of 70, and whose family first noticed disoriented behavior at around the same period. Ophthalmologic examinations revealed mild cataract but no evidence of peripheral optic nerve or retinal lesions. Neuropsychological examination showed right homonymous hemianopia, visual agnosia, Balint's syndrome, mild Transcortical Sensory Aphasia, Gerstmann's syndrome, constructional apraxia, mild ideomotor apraxia and memory disorder. MRI showed marked dilatation of both lateral ventricles, especially the posterior horns, and severe atrophy of the occipital lobes, hippocampus, and the parahippocampal gyrus. Assessment of regional cerebral blood flow by IMP-SPECT revealed a generalized decrease in the temporo-parieto-occipital region bilaterally. The patient's sister began to show evidence of progressive dementia at 80 years of age and CT of the brain revealed marked atrophy, predominantly in the occipital lobes, similar to that of the patient. We believe this to be the first report of posterior cortical atrophy with a positive family history, suggesting the possibility of a hereditary syndrome.
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Transcortical Sensory Aphasia following a left frontal lesion case report
Nō to shinkei Brain and nerve, 1994Co-Authors: M Otsuki, Y Soma, A Koyama, Shoji TsujiAbstract:: We report a patient with Transcortical Sensory Aphasia (TCSA) following a left frontal lesion. The patient was a 63-year-old right handed Buddhist priest admitted to our hospital with a complaint of word-finding difficulty. Neurological examination failed to reveal any abnormal findings except Aphasia. The patients spontaneous speech was fluent, not agrammatic, and free of phonemic parAphasia but he sometimes exhibited semantic parAphasia. His ability to repeat sentences was excellent, but he had severe difficulty in word-finding, auditory comprehension and writing. He read aloud correctly, but his reading comprehension of kana (phonograms) was poor in contrast to excellent reading comprehension of kanji (morphonograms). His clinical picture was characterized by poor comprehension but excellent repetition, and a diagnosis of TCSA was made. CT and MRI revealed an infarction involving the pars opercularis and pars triangularis in the inferior frontal gyrus and the anterior portion of the lower prefrontal gyrus and the middle frontal gyrus. Regional cerebral blood flow was measured by single photon emission CT and was found to be decreased in the same region as indicated on CT and MRI. The clinical picture in this patient was comparable to that of TCSA due to a posterior parieto-occipital lesion, but the rapid improvement (within 1 to 2 months) of this patient was characteristic. Auditory comprehension, kana (phonograms) reading comprehension, and word recall, which were severely impaired in this patient, all demand interaction between phonological processes and semantic processes. Thus we conclude that this patient had impairment of the phonological-semantic interaction process.
Frederick Lenz - One of the best experts on this subject based on the ideXlab platform.
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Transcortical Sensory Aphasia revisited and revised
Brain, 2000Co-Authors: Dana F Boatman, Barry Gordon, John Hart, Ola A Selnes, Diana L Miglioretti, Frederick LenzAbstract:Transcortical Sensory Aphasia (TSA) is characterized by impaired auditory comprehension with intact repetition and fluent speech. We induced TSA transiently by electrical interference during routine cortical function mapping in six adult seizure patients. For each patient, TSA was associated with multiple posterior cortical sites, including the posterior superior and middle temporal gyri, in classical Wernicke's area. A number of TSA sites were immediately adjacent to sites where Wernicke's Aphasia was elicited in the same patients. Phonological decoding of speech sounds was assessed by auditory syllable discrimination and found to be intact at all sites where TSA was induced. At a subset of electrode sites where the pattern of language deficits otherwise resembled TSA, naming and word reading remained intact. Language lateralization testing by intracarotid amobarbital injection showed no evidence of independent right hemisphere language. These results suggest that TSA may result from a one-way disruption between left hemisphere phonology and lexical–semantic processing.
Dana F Boatman - One of the best experts on this subject based on the ideXlab platform.
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Transcortical Sensory Aphasia revisited and revised
Brain, 2000Co-Authors: Dana F Boatman, Barry Gordon, John Hart, Ola A Selnes, Diana L Miglioretti, Frederick LenzAbstract:Transcortical Sensory Aphasia (TSA) is characterized by impaired auditory comprehension with intact repetition and fluent speech. We induced TSA transiently by electrical interference during routine cortical function mapping in six adult seizure patients. For each patient, TSA was associated with multiple posterior cortical sites, including the posterior superior and middle temporal gyri, in classical Wernicke's area. A number of TSA sites were immediately adjacent to sites where Wernicke's Aphasia was elicited in the same patients. Phonological decoding of speech sounds was assessed by auditory syllable discrimination and found to be intact at all sites where TSA was induced. At a subset of electrode sites where the pattern of language deficits otherwise resembled TSA, naming and word reading remained intact. Language lateralization testing by intracarotid amobarbital injection showed no evidence of independent right hemisphere language. These results suggest that TSA may result from a one-way disruption between left hemisphere phonology and lexical–semantic processing.
