Alzheimer's disease presenting as slowly progressive aphasia

Pogacar, S.

doi:10.1093/neucas/1.1.39-u

Cited by 23 publications

(35 citation statements)

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“…The basal ganglia were spared in the index cases of CBD as described by Rebeiz et al [31,32]. There are reports of similar extrapyramidal findings despite relatively normal basal ganglia and substantia nigra in patients diagnosed pathologically with Alzheimer's disease [33][34][35] and Pick's disease [36,37]. Therefore, detectable degeneration of these subcortical gray and pigmented structures is not necessary to produce extrapyramidal symptomatology, but rather may reflect dysfunction of the somatosensory, motor and/or premotor cortices and their afferent/efferent projections.…”

Section: Discussionmentioning

confidence: 61%

Corticobasal Degeneration and Frontotemporal Dementia Presentations in a Kindred with Nonspecific Histopathology

Boeve

Maraganore

Parisi

et al. 2002

Dement Geriatr Cogn Disord

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We report the clinical, neuropsychological, electroencephalographic and radiologic findings in a kindred with varying clinical presentations of a neurodegenerative disorder. Postmortem examination of one member with clinically suspected corticobasal degeneration (CBD) revealed nonspecific histopathology maximally involving the frontoparietal cortex with negligible degenerative changes in the basal ganglia and substantia nigra. The findings in this and other kindreds demonstrate that (1) similar findings on ancillary testing can occur in relatives presumably suffering from the same pathophysiologic process despite dissimilar clinical presentations, (2) the ‘CBD syndrome’ is not specific for CBD, (3) extrapyramidal dysfunction can exist in the absence of appreciable basal ganglia and nigral degeneration, (4) nonspecific histopathology can underlie familial focal/asymmetric cortical degeneration syndromes and (5) many of the findings in CBD are comparable to those reported in frontotemporal dementia.

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Section: Discussionmentioning

confidence: 61%

Corticobasal Degeneration and Frontotemporal Dementia Presentations in a Kindred with Nonspecific Histopathology

Boeve

Maraganore

Parisi

et al. 2002

Dement Geriatr Cogn Disord

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“…According to some authors, PPX is not a clinical entity in and of itself, but a precursor to a more generalized dementia of the Pick-Alzheimer spectrum (among others, Mingazzini 1914, K'echsler 1977, Kirshner et al 1984, Pogacar and Williams 1984, Poeck and Luzzatti 1988, Craenhals e t a/. 1990, Scholten 1990).…”

Section: The Primary Progressive Aphasia Syndromementioning

confidence: 99%

Principled syllabic dissolution in a primary progressive aphasia case

Beland

Paradis

1997

Aphasiology

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In this longitudinal study, the syllabic paraphasias (here defined as insertions or deletions of a phoneme) produced by a Primary Progressive Aphasia case to syllabic adaptations of loanwords were compared. It is shown that paraphasias are phonologically principled and thus highly predictable. More specifically, it it shown that the repair strategies applied by the patient are very similar to those applied by normal speakers when they adapt borrowings. The rate of segment preservation as opposed to segment deletion is very high in borrowings and in the syllabic errors produced by the patient. However, the type of repair strategy applied by the patient changes with the progression of the phonological deficit, segment deletions being more frequent than segment insertions in the late stages of the illness. The evolution of the syllabic error pattern is accounted for by the effect of two principles: the Preservation and the Threshold Principles. The combined effects of these two principles entail that segment preservation has the edge over segment deletion except when the preservation of a segment requires too many phonological operations. It is suggested in this study that the Preservation Principle remains effective even in the late stages but its effect is reduced with the progression of the deficit because the patient's tolerance threshold to complex (multi-step) repair is lowered.

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“…As many as one third of patients diagnosed clinically as either progressive non-Xuent aphasia (PNFA) or semantic dementia showed this pattern [36]. Some reports have remarked the relative sparing of medial temporal lobe structures (hippocampus and entorhinal cortex) [16,17,56]. Galton et al [10] have reported a large series of atypical presentations of pathologically conWrmed AD, which included six cases of PPA.…”

Section: Introductionmentioning

confidence: 99%

Argyrophilic thorny astrocyte clusters in association with Alzheimer’s disease pathology in possible primary progressive aphasia

2007

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Although most cases of primary progressive aphasia (PPA) have one of the varieties of frontotemporal lobar degeneration (FTLD) as their pathological substrate, a subset shows Alzheimer's disease (AD) pathology. We report that all eight cases in our clinic diagnosed as possible PPA, on account of the presence of episodic memory diYculties in addition to severe language impairment at the onset of disease, showed AD pathology. Neither focal accentuation of AD pathology nor vascular lesions in language-related areas was observed. Seven of these eight patients showed large argyrophilic thorny astrocyte clusters (ATAC) in the fronto-temporo-parietal cortex and subcortical white matter. The intensely tau immunoreactive astrocytes in ATAC were morphologically similar to the perivascular, subpial, and subependymal astrocytes in elderly brains, but ATAC diVer from the latter by the cortical and subcortical location, widespread distribution outside the medial temporal lobe, and intense argyrophilia. The location of ATAC was related to neither local variations in the load of AD pathology, nor the myelin density of white matter. ATAC were not seen in a comparison group of six cases of AD without a prominent aphasia syndrome. Because of the similarity of astrocytes in ATAC to those seen independently of AD pathology in several subtypes of FTLD and two reported cases of PPA we hypothesize that they are a marker of a pathological process concurrent with AD, and related to the focality of the clinical presentation.

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Alzheimer's disease presenting as slowly progressive aphasia

Cited by 23 publications

References 0 publications

Corticobasal Degeneration and Frontotemporal Dementia Presentations in a Kindred with Nonspecific Histopathology

Corticobasal Degeneration and Frontotemporal Dementia Presentations in a Kindred with Nonspecific Histopathology

Principled syllabic dissolution in a primary progressive aphasia case

Argyrophilic thorny astrocyte clusters in association with Alzheimer’s disease pathology in possible primary progressive aphasia

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