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. 2008 Nov 11;71(20):1628-33.
doi: 10.1212/01.wnl.0000334756.18558.92.

The anatomic correlate of prosopagnosia in semantic dementia

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The anatomic correlate of prosopagnosia in semantic dementia

K A Josephs et al. Neurology. .

Abstract

Objective: To determine the anatomic correlate of prosopagnosia in subjects with semantic dementia.

Methods: We identified all subjects who had been evaluated by an experienced behavioral neurologist, met criteria for semantic dementia, and had completed a volumetric head MRI scan. In all subjects, historical records were reviewed and subjects in which the presence (n = 15) or absence (n = 12) of prosopagnosia was specifically ascertained by the neurologist were identified. Voxel-based morphometry was used to assess patterns of gray matter atrophy in subjects with and without prosopagnosia compared to a group of age and gender-matched normal controls, and compared to each other.

Results: Compared to controls, both groups showed prominent temporal lobe volume loss. Those with prosopagnosia showed bilateral loss but with greater involvement of the right temporal lobe, while those without prosopagnosia showed predominantly left anterior temporal lobe loss. On direct comparison, subjects with prosopagnosia showed greater loss predominantly in the right amygdala, hippocampus, fusiform gyrus, and anterior temporal pole than those without prosopagnosia. No regions were involved to a greater degree in those without prosopagnosia, compared to those with prosopagnosia.

Conclusions: Prosopagnosia appears to be associated with volume loss of the right temporal lobe, particularly medial temporal lobe, fusiform gyrus, and anterior temporal pole, although in semantic dementia it is occurring in the context of bilateral temporal lobe volume loss.

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Figures

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Figure 1 Patterns of gray matter loss observed in subjects with semantic dementia and prosopagnosia compared to controls (A), and subjects with semantic dementia without prosopagnosia compared to controls (B) Results are shown on three-dimensional renders of the brain and representative coronal slices.
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Figure 2 Three-dimensional renders showing patterns of gray matter loss in subjects with semantic dementia and prosopagnosia compared to controls (A), and subjects with semantic dementia without prosopagnosia compared to controls (B), after global normalization
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Figure 3 Regions of greater gray matter loss in the semantic dementia subjects with prosopagnosia compared to the semantic dementia subjects without prosopagnosia Results are shown on representative coronal slices through the temporal lobe.

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