Posterior cortical atrophy: variant of Alzheimer?s disease?

Schmidtke, Klaus; Hüll, Michael; Talazko, Jochen

doi:10.1007/s00415-005-0594-5

Cited by 73 publications

(43 citation statements)

References 31 publications

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“…Selective deficits in dorsal pathways have previously been demonstrated using volume measurements [8], PET [47] and SPECT [48]. Since the BOLD fMRI signal is known to be influenced by cortical atrophy, metabolism and blood flow, our data support and add to the existing literature.…”

Section: Discussionsupporting

confidence: 87%

Functional neural substrates of posterior cortical atrophy patients

2015

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Posterior cortical atrophy (PCA) is a neurodegenerative syndrome in which the most pronounced pathologic involvement is in the occipito-parietal visual regions. Herein, we aimed to better define the cortical reflection of this unique syndrome using a thorough battery of behavioral and functional MRI (fMRI) tests. Eight PCA patients underwent extensive testing to map their visual deficits. Assessments included visual functions associated with lower and higher components of the cortical hierarchy, as well as dorsal- and ventral-related cortical functions. fMRI was performed on five patients to examine the neuronal substrate of their visual functions. The PCA patient cohort exhibited stereopsis, saccadic eye movements and higher dorsal stream-related functional impairments, including simultant perception, image orientation, figure-from-ground segregation, closure and spatial orientation. In accordance with the behavioral findings, fMRI revealed intact activation in the ventral visual regions of face and object perception while more dorsal aspects of perception, including motion and gestalt perception, revealed impaired patterns of activity. In most of the patients, there was a lack of activity in the word form area, which is known to be linked to reading disorders. Finally, there was evidence of reduced cortical representation of the peripheral visual field, corresponding to the behaviorally assessed peripheral visual deficit. The findings are discussed in the context of networks extending from parietal regions, which mediate navigationally related processing, visually guided actions, eye movement control and working memory, suggesting that damage to these networks might explain the wide range of deficits in PCA patients.

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Section: Discussionsupporting

confidence: 87%

Functional neural substrates of posterior cortical atrophy patients

2015

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“…Homonymous hemianopia may also be present [5]. Magnetic resonance imaging (MRI) usually shows cortical atrophy in the parietal, occipital and posterior temporal regions [6], while [ 18 F]fluorodeoxyglucose positron emission tomography (FDG-PET) may reveal hypometabolism in the posterior cerebral hemispheres, even in the absence of concomitant atrophy [7,8]. This syndrome almost universally progresses to more diffuse cognitive impairment and dementia.…”

Section: Introductionmentioning

confidence: 99%

In vivo demonstration of amyloid burden in posterior cortical atrophy: a case series with PET and CSF findings

et al. 2011

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Our objective was to evaluate amyloid deposition in posterior cortical atrophy (PCA), using both cerebrospinal fluid (CSF) biomarker analysis and amyloid imaging. Five PCA patients, selected based on their neuropsychological profile and atrophic changes in posterior regions on MRI, underwent CSF analysis. CSF amyloidbeta 1-42, total tau, and phosphorylated tau at threonine 181 levels were determined. They also had positron emission tomography (PET) with Pittsburgh Compound B ([ 11 C]PIB). [ 11 C]PIB ratio images were assessed with visual, regional and voxel-based analyses and compared to eight typical Alzheimer's disease (AD) patients and eight controls. The biological profile in the five PCA patients, resulting from CSF and [ 11 C]PIB images analysis, was consistent with AD. Individual comparisons of PCA patients' [ 11 C]PIB images with the AD group with Statistical Parametric Mapping (SPM) revealed a distinctive posterior uptake in four out of the five patients showing increased amyloid deposition in occipital, temporal, and/or parietal regions. ROI group analysis showed a tendency for higher amyloid deposition in occipital and temporal regions. However, this pattern was not found with SPM group analysis when the global level of [ 11 C]PIB uptake was used as a covariate. Our results indicate that amyloid burden can be demonstrated in vivo in PCA suggesting a diagnosis of AD. PCA patients may present a higher global amyloid load than AD that was not related to age at onset, disease severity, disease duration, or educational level in our study. Combined CSF and PET biomarkers seem helpful for in vivo diagnosis of this focal syndrome with underlying AD pathology.

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“…Consistent with their clinical presentation, patients with PCA show gray matter (GM) loss in parieto-occipital and posterior temporal cortices, which is often more prominent in the right hemisphere (Galton et al, 2000; Whitwell et al, 2007). Positron emission topography (PET) studies have reported a prominent hypometabolism in the same posterior brain areas (Nestor et al, 2003; Schmidtke et al, 2005; Bokde et al, 2005). Although PCA patients do not meet clinical criteria for Alzheimer’s disease (AD), because of the lack of memory impairment as core of the syndrome, pathological series have found that the majority of PCA patients have senile plaques and neurofibrillary tangles, both hallmarks of AD, at autopsy (von Gunten et al, 2006; Renner et al, 2004; Tang-Wai et al, 2004; Alladi et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Brain networks in posterior cortical atrophy: A single case tractography study and literature review

Migliaccio

Agosta

Toba

et al. 2012

Cortex

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Posterior cortical atrophy (PCA) is rare neurodegenerative dementia, clinically characterized by a progressive decline in higher-visual object and space processing. After a brief review of the literature on the neuroimaging in PCA, here we present a study of the brain structural connectivity in a patient with PCA and progressive isolated visual and visuo-motor signs. Clinical and cognitive data were acquired in a 58-years-old patient (woman, right-handed, disease duration 18 months). Brain structural and diffusion tensor (DT) Magnetic Resonance Imaging (MRI) were obtained. A voxel-based morphometry (VBM) study was performed to explore the pattern of gray matter (GM) atrophy, and a fully automatic segmentation was assessed to obtain the hippocampal volumes. DT MRI-based tractography was used to assess the integrity of long-range white matter (WM) pathways in the patient and in six sex- and age-matched healthy subjects. This PCA patient had a clinical syndrome characterized by left visual neglect, optic ataxia, and left limb apraxia, as well as mild visuo-spatial episodic memory impairment. VBM study showed bilateral posterior GM atrophy with right predominance; DT MRI tractography demonstrated WM damage to the right hemisphere only, including the superior and inferior longitudinal fasciculi and the inferior fronto-occipital fasciculus, as compared to age-matched controls. The homologous left-hemisphere tracts were spared. No difference was found between left and right hippocampal volumes. These data suggest that selective visuo-spatial deficits typical of PCA might not result from cortical damage alone, but by a right-lateralized network-level dysfunction including WM damage along the major visual pathways.

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Posterior cortical atrophy: variant of Alzheimer?s disease?

Cited by 73 publications

References 31 publications

Functional neural substrates of posterior cortical atrophy patients

Functional neural substrates of posterior cortical atrophy patients

In vivo demonstration of amyloid burden in posterior cortical atrophy: a case series with PET and CSF findings

Brain networks in posterior cortical atrophy: A single case tractography study and literature review

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