Progressive striatal atrophy has long been considered the pathological hallmark of Huntington's disease (HD), but is it now recognized that malfunction and degeneration of posterior-cortical territories are also prominent characteristics of the disease. The limited knowledge about the functional impact of these posterior-cortical changes could be partially attributed to the lack of sensitive measures to capture them. We hypothesized that early malfunction of specific territories of the ventral visual pathway in premanifest HD would lead to difficulties in the recognition of complex stimuli and to differences in their neurophysiological correlates.
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