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May 24, 2011; 76 (21) Editorials

Looking into posterior cortical atrophy

Providing insight into Alzheimer disease

David F. Tang-Wai, Neill R. Graff-Radford
First published April 27, 2011, DOI: https://doi.org/10.1212/WNL.0b013e31821ccd4f
David F. Tang-Wai
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Neill R. Graff-Radford
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Looking into posterior cortical atrophy
Providing insight into Alzheimer disease
David F. Tang-Wai, Neill R. Graff-Radford
Neurology May 2011, 76 (21) 1778-1779; DOI: 10.1212/WNL.0b013e31821ccd4f

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Posterior cortical atrophy (PCA) is a dementing syndrome that presents with signs and symptoms of cortical visual dysfunction.1 The clinical features of PCA reflect dysfunction mainly of the dorsal/occipito-parietal pathway causing Balint syndrome (simultanagnosia, optic ataxia, and ocular apraxia), transcortical sensory aphasia, apraxia, and some or all elements of Gerstmann syndrome (agraphia, acalculia, finger agnosia, right-left disorientation).1,2 Formal neuropsychological testing has confirmed a relative greater impairment of dorsal visual stream function while frontal lobe functions and memory are relatively preserved until later in the course of the disease.2 Structural and functional neuroimaging has consistently revealed atrophy or metabolic changes in the posterior regions of the brain.3 Although PCA is a clinically homogeneous syndrome, there is pathologic heterogeneity. Corticobasal degeneration, dementia with Lewy bodies, subcortical gliosis, fatal familial insomnia, and Creutzfeldt-Jacob disease have all been described as causing PCA.1,4 However, the most common reported pathologic cause is Alzheimer disease (AD) with increased density of neurofibrillary …

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