Visuoperception test predicts pathologic diagnosis of Alzheimer disease in corticobasal syndrome

Boyd, Clara D.; Tierney, Michael; Wassermann, Eric M.; Spina, Salvatore; Oblak, Adrian L.; Ghetti, Bernardino; Grafman, Jordan; Huey, Edward D.

doi:10.1212/wnl.0000000000000667

Cited by 27 publications

(35 citation statements)

References 33 publications

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“…via consensus following a 1-week evaluation. Initial motor impairments in all of the patients with CBS consisted of an asymmetric progressive rigid syndrome resistant to therapeutic doses of levodopa evaluated in the months preceding the referral and confirmed at the clinical examination at the NINDS, associated with evidence of cortical deficits (as described by Boeve et al 12 ; the frequency of each cortical deficit for this cohort has been previously reported by our group 10 ). All patients underwent detailed clinical and neuropsychological examination and structural brain imaging (MRI in all but 4 patients who underwent CT scans).…”

Section: Participantssupporting

confidence: 66%

“…The findings in the CBS-AD group, moreover, confirm the observation of the posterior patterns of hypometabolism reported in patients with CBS presenting with positive in vivo biomarkers of amyloid deposition 9 and are in line with the more severe visuospatial impairment observed in patients with CBS-AD compared to patients with CBS without AD. 10 While a relative sparing of the deep gray structures is a common finding in AD and a feature that could help in the interpretation of FDG-PET scans, 35 moderate basal ganglia hypometabolism was observed in patients with CBS with positive in vivo markers of amyloid deposition. 9 That finding could also be due to the positivity of in vivo amyloid markers in non-AD conditions such as dementia with Lewy bodies, 36 which may show deep gray matter hypometabolism.…”

Section: Discussionmentioning

confidence: 99%

“…Patients were derived from a cohort of 98 patients with CBS who were enrolled at the National Institute of Neurological Disorders and Stroke (NINDS) from 2001 to 2009; 36 of those had a pathologic postmortem diagnosis, as previously described from the clinical point of view by our group. 10,11 The 69 patients with CBS not included did not fulfill the criteria above. Patients were recruited from across the United States via advertisement and had to have an established diagnosis of CBS before coming to our attention.…”

Section: Participantsmentioning

confidence: 99%

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FDG-PET patterns associated with underlying pathology in corticobasal syndrome

et al. 2019

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ObjectiveTo evaluate brain 18Fluorodeoxyglucose PET (FDG-PET) differences among patients with a clinical diagnosis of corticobasal syndrome (CBS) and distinct underling primary pathologies.MethodsWe studied 29 patients with a diagnosis of CBS who underwent FDG-PET scan and postmortem neuropathologic examination. Patients were divided into subgroups on the basis of primary pathologic diagnosis: CBS-corticobasal degeneration (CBS-CBD) (14 patients), CBS-Alzheimer disease (CBS-AD) (10 patients), and CBS–progressive supranuclear palsy (CBS-PSP) (5 patients). Thirteen age-matched healthy patients who underwent FDG-PET were the control group (HC). FDG-PET scans were compared between the subgroups and the HC using SPM-12, with a threshold of pFWE < 0.05.ResultsThere were no differences in Mattis Dementia Rating Scale or finger tapping scores between CBS groups. Compared to HC, the patients with CBS presented significant hypometabolism in frontoparietal regions, including the perirolandic area, basal ganglia, and thalamus of the clinically more affected hemisphere. Patients with CBS-CBD showed a similar pattern with a more marked, bilateral involvement of the basal ganglia. Patients with CBS-AD presented with posterior, asymmetric hypometabolism, including the lateral parietal and temporal lobes and the posterior cingulate. Finally, patients with CBS-PSP disclosed a more anterior hypometabolic pattern, including the medial frontal regions and the anterior cingulate. A conjunction analysis revealed that the primary motor cortex was the only common area of hypometabolism in all groups, irrespective of pathologic diagnosis.Discussion and conclusionsIn patients with CBS, different underling pathologies are associated with different patterns of hypometabolism. Our data suggest that FDG-PET scans could help in the etiologic diagnosis of CBS.

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Section: Participantssupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Participantsmentioning

confidence: 99%

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FDG-PET patterns associated with underlying pathology in corticobasal syndrome

et al. 2019

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“…For example, motor impairment (defined by asymmetrical left upper limb rigidity) has been found in 30% of a series of 44 patients all meeting the existing clinical criteria for PCA [ 60 ]. Visuospatial and visuoperceptual dysfunction in CBS patients has also been shown to predict AD pathology [ 30 , 61 , 62 ].…”

Section: Discussionmentioning

confidence: 99%

Consensus classification of posterior cortical atrophy

Crutch

Schott

Rabinovici

et al. 2017

Alzheimer's & Dementia

501

460

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IntroductionA classification framework for posterior cortical atrophy (PCA) is proposed to improve the uniformity of definition of the syndrome in a variety of research settings.MethodsConsensus statements about PCA were developed through a detailed literature review, the formation of an international multidisciplinary working party which convened on four occasions, and a Web-based quantitative survey regarding symptom frequency and the conceptualization of PCA.ResultsA three-level classification framework for PCA is described comprising both syndrome- and disease-level descriptions. Classification level 1 (PCA) defines the core clinical, cognitive, and neuroimaging features and exclusion criteria of the clinico-radiological syndrome. Classification level 2 (PCA-pure, PCA-plus) establishes whether, in addition to the core PCA syndrome, the core features of any other neurodegenerative syndromes are present. Classification level 3 (PCA attributable to AD [PCA-AD], Lewy body disease [PCA-LBD], corticobasal degeneration [PCA-CBD], prion disease [PCA-prion]) provides a more formal determination of the underlying cause of the PCA syndrome, based on available pathophysiological biomarker evidence. The issue of additional syndrome-level descriptors is discussed in relation to the challenges of defining stages of syndrome severity and characterizing phenotypic heterogeneity within the PCA spectrum.DiscussionThere was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. The framework and terminology may facilitate the interpretation of research data across studies, be applicable across a broad range of research scenarios (e.g., behavioral interventions, pharmacological trials), and provide a foundation for future collaborative work.

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“…fragmented letters) and space perception (Amsterdam UMC and UCSF: number location and dot counting) (Boyd et al, 2014). The visual test battery administered in the UCSF sample included more tests than in the Amsterdam UMC sample; two additional domains could be assessed within the UCSF cohort only: non-visual dominant parietal functions (calculations, spelling, and reading) and primary visual processing (point location, figure discrimination, shape discrimination, hue discrimination, visual acuity, size discrimination, letter cancellation, static circle detection and motion coherence (Kramer et al, 2003;Groot et al, 2018).…”

Section: Cognitionmentioning

confidence: 99%

Data-driven detection of latent atrophy factors related to phenotypical variants of posterior cortical atrophy

Groot

Yeo

Vogel

et al. 2019

Preprint

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Posterior cortical atrophy is a clinical-radiological syndrome characterized by visual processing deficits and atrophy in posterior parts of the brain, most often caused by Alzheimer's disease pathology. Recent consensus criteria describe four distinct phenotypical variants of posterior cortical atrophy defined by clinical and radiological features; i) object perception/occipitotemporal (ventral), ii) space perception/temporoparietal (dorsal), iii) nonvisual/dominant parietal and iv) primary visual (caudal). We employed a data-driven approach to identify atrophy factors related to these proposed variants in a multi-center cohort of 119 individuals with posterior cortical atrophy (age: 64 SD 7, 38% male, MMSE: 21 SD 5, 71% amyloid-β positive, 29% amyloid-β status unknown). A Bayesian modelling framework based on latent Dirichlet allocation was used to compute four latent atrophy factors in accordance with the four proposed variants. The model uses standardized gray matter density images as input (adjusted for age, sex, intracranial volume, field strength and whole-brain gray matter volume) and provides voxelwise probabilistic maps for all atrophy factors, allowing every individual to express each factor to a degree without a priori classification. The model revealed four distinct yet partially overlapping atrophy factors; right-dorsal, right-ventral, left-ventral, and limbic. Individual participant profiles revealed that the vast majority of participants expressed multiple factors, rather than predominantly expressing a single factor. To assess the relationship between atrophy factors and cognition, neuropsychological test scores covering four posterior cortical atrophy-specific cognitive domains were assessed (object perception, space perception, non-visual parietal functions and primary visual processing) and we used general linear models to examine the association between atrophy factor expression and cognition. We found that object perception and primary visual processing were associated with atrophy that predominantly reflects the rightventral factor. Furthermore, space perception was associated with atrophy that predominantly represents the right-ventral and right-dorsal factors. Similar to the atrophy factors, most participants had mixed clinical profiles with impairments across multiple domains. However, when selecting four participants with an isolated impairment, we observed atrophy patterns and factor expressions that were largely in accordance with the hypothesized variants. Taken together, our results indicate that variants of posterior cortical atrophy exist but these constitute phenotypical extremes and most individuals fall along a broad clinical-radiological spectrum, indicating that classification into four mutually exclusive variants is unlikely to be clinically useful.

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Visuoperception test predicts pathologic diagnosis of Alzheimer disease in corticobasal syndrome

Cited by 27 publications

References 33 publications

FDG-PET patterns associated with underlying pathology in corticobasal syndrome

FDG-PET patterns associated with underlying pathology in corticobasal syndrome

Consensus classification of posterior cortical atrophy

Data-driven detection of latent atrophy factors related to phenotypical variants of posterior cortical atrophy

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