阿尔茨海默病
医学
疾病
心理学
神经科学
听力学
病理
出处
期刊:Neurology
[Ovid Technologies (Wolters Kluwer)]
日期:1999-01-01
卷期号:52 (1): 10-10
被引量:39
摘要
In this issue of Neurology, Giannakopoulos et al.1 useneuropsychologic testing to characterize visual losses in AD. They find that associative visual agnosias— failures to recognize something by seeing it—reflect the density of neurofibrillary tangles (NFTs), but not senile plaques (SPs), in visual association cortex. Their neuropsychologic tests may have also uncovered a continuum from the sensory processes of perception to the interpretive processes of cognition, from seeing to knowing.2 Thus, their work has implications about the pathophysiology of AD and about the brain mechanisms of mental life.
Giannakopoulos et al.1 use the classic framework of Lissauer,3 who first asserted that there are two types of visual agnosias: 1) apperceptive visual agnosias, which affect the perception of elementary properties, such as color and motion, to support the recognition of an object’s shape or of the spatial arrangement of objects; and 2) associative visual agnosias, which affect the integration of such characteristics for the recognition of specific categories of images such as faces and words.
The boundaries of the visual agnosias have always been obscured by the fact that a failure to recognize something by seeing it might actually reflect a failure to see it. Thus, the loss of color vision in cerebral achromatopsia or the loss of movement perception in cerebral akinetopsia might create apperceptive agnosia when the shape of an object is indicated by its color or movement. Likewise, memory …
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