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The topography of metabolic deficits in posterior cortical atrophy (the visual variant of Alzheimer’s disease) with FDG-PET
  1. P J Nestor1,
  2. D Caine4,
  3. T D Fryer2,
  4. J Clarke3,
  5. J R Hodges1
  1. 1University of Cambridge, Neurology Unit, Addenbrooke’s Hospital, Cambridge, UK
  2. 2Wolfson Brain Imaging Centre, University of Cambridge, Addenbrooke’s Hospital
  3. 3Department of Orthoptics, Addenbrooke’s Hospital
  4. 4School of Psychology, University of Sydney, New South Wales, Australia
  1. Correspondence to:
 Professor John R Hodges, MRC Cognition and Brain Sciences Unit, 15 Chaucer Rd, Cambridge CB2 2EF, UK;


Background:The term “posterior cortical atrophy” (PCA) refers to a clinical syndrome in which higher order visual processing is disrupted owing to a neurodegenerative disorder, the most commonly associated pathology being Alzheimer’s disease.

Objective:To map the topography of hypometabolic brain regions in a group of subjects with PCA who had undergone detailed neuropsychological characterisation.

Methods:Resting cerebral metabolism was measured with (18F)fluorodeoxyglucose-positron emission tomography (FDG-PET) in patients with PCA (n = 6), typical Alzheimer’s disease (n = 10), and healthy controls (n = 10). The data were analysed using statistical parametric mapping (SPM99) and region of interest techniques.

Results:Clinically, the PCA subjects showed predominant visuospatial deficits (including features of Balint’s syndrome) consistent with damage to the dorsal stream of visual processing. Compared with the controls, the PCA group showed marked glucose hypometabolism primarily affecting the posterior cerebral hemispheres (right worse than left). In addition, the PCA group showed two symmetrical areas of hypometabolism in the region of the frontal eye fields. Compared with typical Alzheimer’s disease, the PCA group had selective hypometabolism in the occipito-parietal region (right much worse than left).

Conclusions:The neuropsychological and PET findings are consistent with damage predominantly to the dorsal stream of visual processing. Frontal eye field hypometabolism secondary to loss of input from the occipito-parietal region may be the mechanism for the ocular apraxia seen in Balint’s syndrome.

  • posterior cortical atrophy
  • Alzheimer’s disease, positron emission tomography
  • BA, Brodmann area
  • CMRglc, cerebral metabolic rate for glucose
  • FDG, (18F)fluorodeoxyglucose
  • MMSE, mini-mental state examination
  • MNI, Montreal Neurological Institute
  • nCMRglc, normalised cerebral metabolic rate for glucose
  • OMA, oculomotor area
  • PCA, posterior cortical atrophy
  • PET, positron emission tomography
  • ROI, region of interest
  • SPM, statistical parametric mapping
  • VOSP, visual object and space perception battery

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  • Competing interests: none declared