aphasia/atrophy

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Atrophy and microglial distribution in primary progressive aphasia with transactive response DNA-binding protein-43 kDa.

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OBJECTIVE To quantitatively determine the density and distribution of activated microglia across cortical regions and hemispheres in the brains of primary progressive aphasia (PPA) participants with pathological diagnoses of frontotemporal lobar degeneration with transactive response DNA-binding

Longitudinal assessment of short-term memory deterioration in a logopenic variant primary progressive aphasia with post-mortem confirmed Alzheimer's Disease pathology.

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In the field of dementia research, there are reports of neurodegenerative cases with a focal loss of language, termed primary progressive aphasia (PPA). Currently, this condition has been further sub-classified, with the most recent sub-type dubbed logopenic variant (PPA-LV). As yet, there remains

Primary progressive aphasia, left anterior atrophy, and neurofibrillary hippocampal pathology: observations in an unusual case.

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A 71-year-old, right-handed woman experienced onset of a slowly progressive, nonfluent language disorder. She maintained normal cognitive abilities until age 80 and developed a mild spastic right hemiparesis the following year. By age 82, she had become severely demented, mute, and akinetic.

Clinical and pathological overlap between frontotemporal dementia, primary progressive aphasia and corticobasal degeneration: the Pick complex.

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A substantive overlap between the clinical syndromes of frontal lobe dementia (FLD), frontotemporal dementia (FTD), or primary progressive aphasia (PPA), and corticobasal degeneration syndrome (CBDS) has been demonstrated in a population of 55 patients followed for more than 3 years in a cognitive

Disruption of large-scale neural networks in non-fluent/agrammatic variant primary progressive aphasia associated with frontotemporal degeneration pathology.

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Non-fluent/agrammatic primary progressive aphasia (naPPA) is a progressive neurodegenerative condition most prominently associated with slowed, effortful speech. A clinical imaging marker of naPPA is disease centered in the left inferior frontal lobe. We used multimodal imaging to assess large-scale

Brain atrophy in primary progressive aphasia involves the cholinergic basal forebrain and Ayala's nucleus.

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Primary progressive aphasia (PPA) is characterized by left hemispheric frontotemporal cortical atrophy. Evidence from anatomical studies suggests that the nucleus subputaminalis (NSP), a subnucleus of the cholinergic basal forebrain, may be involved in the pathological process of PPA. Therefore, we

[Progressive primary aphasia associated with corticobasal degeneration].

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BACKGROUND Progressive primary aphasia generally progresses to global cognitive deterioration of Alzheimer type, although occasionally it remains unchanged. The neuropathological findings are varied: Alzheimer, spongiform etc. The case we describe followed a very unusual course. Initially there was

Familial progressive aphasia: its relationship to other forms of lobar atrophy.

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Two brothers presented with slowly progressive aphasia. One brother, who became behaviourally disturbed only at the end of his illness, was found at necropsy to have predominant left frontotemporal atrophy. The other brother developed severe behavioural disturbances shortly after the onset of

A clinical profile of corticobasal degeneration presenting as primary progressive aphasia.

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We report a patient with primary progressive aphasia who first presented with amnesic aphasia that developed over the course of 3 years into nonfluent aphasia with buccofacial apraxia, followed in the next year by cognitive impairment and parkinsonism. Pathological findings were typical for

Primary progressive aphasia as the initial manifestation of corticobasal degeneration. A "three in one " syndrome?

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In 1994, the term "Pick complex" was proposed to indicate significant clinical and pathological overlapping between primary progressive aphasia, frontal lobe dementia and corticobasal degeneration. We report the case of a 60-year-old man, who initially presented progressive non-fluent aphasia with

[A case of corticobasal degeneration presenting with primary progressive aphasia].

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We report a 64-year-old right-handed woman whose initial symptom was slowly progressive aphasia without generalized dementia and who was subsequently diagnosed as having corticobasal degeneration (CBD). Neurological examination revealed disturbed vertical gaze, dysarthria, rigidity of the right

Pick Complex: an integrative approach to frontotemporal dementia: primary progressive aphasia, corticobasal degeneration, and progressive supranuclear palsy.

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BACKGROUND Frontotemporal dementia (FTD) is a new label for clinical Pick's disease (PiD) because the eponymic term is increasingly restricted to the pathologic finding of Pick bodies. This restriction created the impression that PiD is rare and that is it difficult to diagnose. FTD is also a term

Progressive neuropsychological and extrapyramidal deterioration resembling progressive supranuclear palsy: is aphasia relevant for correct diagnosis?

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We describe the case of a woman presenting with a clinical syndrome closely resembling progressive supranuclear palsy, who also showed some progressive neuropsychological defects (aphasia and apraxia) not consistent with a simple loss of timing and activation as is generally postulated in this

Rapidly progressive aphasia and motor neuron disease: a clinical, radiological, and pathological study of an autopsy case with circumscribed lobar atrophy.

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This report concerns an autopsy case of rapidly progressive aphasia and motor neuron disease. The patient was a Japanese woman who was 75 years old at the time of death. The family history did not reveal hereditary burden. She developed language disturbances and difficulty in swallowing at age 74.

Corticobasal degeneration with primary progressive aphasia and accentuated cortical lesion in superior temporal gyrus: case report and review.

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A 57-year-old woman showed progressive sensory aphasia as an initial symptom, and then developed total aphasia within 6 years and, finally, severe dementia. Neuropathologically, the cerebral cortex was most severely affected in the superior and transverse temporal gyri, and subsequently in the

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