A longitudinal investigation of the relationship between crowding and reading: A neurodegenerative approach

Yong, Keir X. X.; Rajdev, Kishan; Warrington, Elizabeth K.; Nicholas, Jennifer M.; Warren, Jason D.; Crutch, Sebastian J.

doi:10.1016/j.neuropsychologia.2016.02.022

Cited by 13 publications

(9 citation statements)

References 79 publications

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“…A small number of longitudinal case reports and case series have described the clinico-radiological progression of the condition (Ross et al , 1996; Goethals and Santens, 2001; Giovagnoli et al , 2009; Kennedy et al , 2012; Chang et al , 2015; Crutch et al , 2017) or the development of specific cognitive deficits [e.g. dyslexia and excessive visual crowding (Yong et al , 2016), dysgraphia (Primativo et al , 2017)]. The only previous longitudinal group study found comparable rates of widespread grey matter loss in patients with PCA and typical Alzheimer’s disease with a mean disease duration of 5 years, but participant numbers were small (17 PCA, 16 typical Alzheimer’s disease) and the time window limited (1-year interval) (Lehmann et al , 2012).…”

Section: Introductionmentioning

confidence: 99%

Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy

Firth

Primativo

Marinescu

et al. 2019

Brain

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Posterior cortical atrophy is a clinico-radiological syndrome characterized by progressive decline in visual processing and atrophy of posterior brain regions. With the majority of cases attributable to Alzheimer’s disease and recent evidence for genetic risk factors specifically related to posterior cortical atrophy, the syndrome can provide important insights into selective vulnerability and phenotypic diversity. The present study describes the first major longitudinal investigation of posterior cortical atrophy disease progression. Three hundred and sixty-one individuals (117 posterior cortical atrophy, 106 typical Alzheimer’s disease, 138 controls) fulfilling consensus criteria for posterior cortical atrophy-pure and typical Alzheimer’s disease were recruited from three centres in the UK, Spain and USA. Participants underwent up to six annual assessments involving MRI scans and neuropsychological testing. We constructed longitudinal trajectories of regional brain volumes within posterior cortical atrophy and typical Alzheimer’s disease using differential equation models. We compared and contrasted the order in which regional brain volumes become abnormal within posterior cortical atrophy and typical Alzheimer’s disease using event-based models. We also examined trajectories of cognitive decline and the order in which different cognitive tests show abnormality using the same models. Temporally aligned trajectories for eight regions of interest revealed distinct (P < 0.002) patterns of progression in posterior cortical atrophy and typical Alzheimer’s disease. Patients with posterior cortical atrophy showed early occipital and parietal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion leading to tissue loss of comparable extent later. Hippocampal, entorhinal and frontal regions underwent a lower rate of change and never approached the extent of posterior cortical involvement. Patients with typical Alzheimer’s disease showed early hippocampal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion. Cognitive models showed tests sensitive to visuospatial dysfunction declined earlier in posterior cortical atrophy than typical Alzheimer’s disease whilst tests sensitive to working memory impairment declined earlier in typical Alzheimer’s disease than posterior cortical atrophy. These findings indicate that posterior cortical atrophy and typical Alzheimer’s disease have distinct sites of onset and different profiles of spatial and temporal progression. The ordering of disease events both motivates investigation of biological factors underpinning phenotypic heterogeneity, and informs the selection of measures for clinical trials in posterior cortical atrophy.

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Section: Introductionmentioning

confidence: 99%

Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy

Firth

Primativo

Marinescu

et al. 2019

Brain

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“…newspaper headlines rather than smaller words); and letters appearing to move or merge [35,65,68]. Such loss is predominantly considered to reflect peripheral alexia, variously described as 'apperceptive' [68] or 'crowding dyslexia' [83,84]. Eye-tracking recordings emphasise inefficient fixations and saccades accompanying inaccurate reading [32], with patient reports of static text appearing to move possibly relating to fixation instability [41,78].…”

Section: Readingmentioning

confidence: 99%

Diagnosis and Management of Posterior Cortical Atrophy

Yong

Graff‐Radford

Ahmed

et al. 2023

Curr Treat Options Neurol

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Purpose of review The study aims to provide a summary of recent developments for diagnosing and managing posterior cortical atrophy (PCA). We present current efforts to improve PCA characterisation and recommendations regarding use of clinical, neuropsychological and biomarker methods in PCA diagnosis and management and highlight current knowledge gaps. Recent findings Recent multi-centre consensus recommendations provide PCA criteria with implications for different management strategies (e.g. targeting clinical features and/or disease). Studies emphasise the preponderance of primary or co-existing Alzheimer’s disease (AD) pathology underpinning PCA. Evidence of approaches to manage PCA symptoms is largely derived from small studies. Summary PCA diagnosis is frequently delayed, and people are likely to receive misdiagnoses of ocular or psychological conditions. Current treatment of PCA is symptomatic — pharmacological and non-pharmacological — and the use of most treatment options is based on small studies or expert opinion. Recommendations for non-pharmacological approaches include interdisciplinary management tailored to the PCA clinical profile — visual-spatial — rather than memory-led, predominantly young onset — and psychosocial implications. Whilst emerging disease-modifying treatments have not been tested in PCA, an accurate and timely diagnosis of PCA and determining underlying pathology is of increasing importance in the advent of disease-modifying therapies for AD and other albeit rare causes of PCA.

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“…Likewise, fMRI has revealed that activation within the ventral visual regions is related to facial and object recognition, while that in dorsal areas is related to motion and gestalt perception (29, 30). Visual word processing is a function of the ventral visual stream, and patients with PCA have been reported to exhibit functional deficits in word processing that are seen in reading disorders (31). Although weakened cortical peripheral visual field functions are similar to peripheral visual deficits seen in behavioral pathology, disruption of the dorsal stream has been suggested to result from impaired interconnectivity of feed-forward and -backward pathways.…”

Section: Pca Based On Posterior Cerebral Changesmentioning

confidence: 99%

Neural Mechanisms of Visual Dysfunction in Posterior Cortical Atrophy

et al. 2019

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Posterior cortical atrophy (PCA) is characterized predominantly by visual dysfunction that arises from bilateral impairments in occipital, parietal, and temporal regions of the brain. PCA is clinically identified based primarily on visual symptoms and neuroimaging findings. Region-specific gray and white matter deficits have been discussed in detail, and are associated with clinical manifestations that present with similar patterns of perfusion and metabolic findings. Here, we discuss both structural and functional changes in the ventral and dorsal visual streams along with their underlying relationships. We also discuss the most recent developments in neuroimaging characteristics and summarize correlations between distinct neuroimaging presentations.

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A longitudinal investigation of the relationship between crowding and reading: A neurodegenerative approach

Cited by 13 publications

References 79 publications

Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy

Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy

Diagnosis and Management of Posterior Cortical Atrophy

Neural Mechanisms of Visual Dysfunction in Posterior Cortical Atrophy

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