Neural correlates of cognitive impairment in posterior cortical atrophy
Brain. 2011-04-07; 134(5): 1464-1478
DOI: 10.1093/brain/awr055
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1. Brain. 2011 May;134(Pt 5):1464-78. doi: 10.1093/brain/awr055. Epub 2011 Apr 7.
Neural correlates of cognitive impairment in posterior cortical atrophy.
Kas A(1), de Souza LC, Samri D, Bartolomeo P, Lacomblez L, Kalafat M, Migliaccio
R, Thiebaut de Schotten M, Cohen L, Dubois B, Habert MO, Sarazin M.
Author information:
(1)Service de Médecine Nucléaire, GH Pitié-Salpêtrière, 47-83, boulevard de
l’Hôpital, 75651 Paris Cedex 13, France.
With the prospect of disease-modifying drugs that will target the
physiopathological process of Alzheimer’s disease, it is now crucial to increase
the understanding of the atypical focal presentations of Alzheimer’s disease,
such as posterior cortical atrophy. This study aimed to (i) characterize the
brain perfusion profile in posterior cortical atrophy using regions of interest
and a voxel-based approach; (ii) study the influence of the disease duration on
the clinical and imaging profiles; and (iii) explore the correlations between
brain perfusion and cognitive deficits. Thirty-nine patients with posterior
cortical atrophy underwent a specific battery of neuropsychological tests, mainly
targeting visuospatial functions, and a brain perfusion scintigraphy with
99mTc-ethyl cysteinate dimer. The imaging analysis included a comparison with a
group of 24 patients with Alzheimer’s disease, matched for age, disease duration
and Mini-Mental State Examination, and 24 healthy controls. The single-photon
emission computed tomography profile in patients with posterior cortical atrophy
was characterized by extensive and severe hypoperfusion in the occipital,
parietal, posterior temporal cortices and in a smaller cortical area
corresponding to the frontal eye fields (Brodmann areas 6/8). Compared with
patients with Alzheimer’s disease, the group with posterior cortical atrophy
showed more severe occipitoparietal hypoperfusion and higher perfusion in the
frontal, anterior cingulate and mesiotemporal regions. When considering the
disease duration, the functional changes began and remained centred on the
posterior lobes, even in the late stage. Correlation analyses of brain perfusion
and neuropsychological scores in posterior cortical atrophy highlighted the
prominent role of left inferior parietal damage in acalculia, Gerstmann’s
syndrome, left-right indistinction and limb apraxia, whereas damage to the
bilateral dorsal occipitoparietal regions appeared to be involved in Bálint’s
syndrome. Our findings provide new insight into the natural history of functional
changes according to disease duration and highlight the role of parietal and
occipital cortices in the cognitive syndromes that characterize the posterior
cortical atrophy.
DOI: 10.1093/brain/awr055
PMID: 21478188 [Indexed for MEDLINE]