PubMed · 13618100
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F M FORSTER, C D SHIELDS. 1959. Cortical sensory defects causing disability.. https://pubmed.ncbi.nlm.nih.gov/13618100/
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D.F., a patient with severe visual form agnosia, has been the subject of extensive research during the past decade. The fact that she could process visual input accurately for the purposes of guiding action despite being unable to perform visual discriminations on the same visual input inspired a novel interpretation of the functions of the two main cortical visual pathways or 'streams'. Within this theoretical context, the authors proposed that D.F. had suffered severe bilateral damage to her occipitotemporal visual system (the 'ventral stream'), while retaining the use of her occipitoparietal visual system (the 'dorsal stream'). The present paper reports a direct test of this idea, which was initially derived from purely behavioural data, before the advent of modern functional neuroimaging. We used functional MRI to examine activation in her ventral and dorsal streams during object recognition and object-directed grasping tasks. We found that D.F. showed no difference in activation when presented with line drawings of common objects compared with scrambled line drawings in the lateral occipital cortex (LO) of the ventral stream, an area that responded differentially to these stimuli in healthy individuals. Moreover, high-resolution anatomical MRI showed that her lesion corresponded bilaterally with the location of LO in healthy participants. The lack of activation with line drawings in D.F. mirrors her poor performance in identifying the objects depicted in the drawings. With coloured and greyscale pictures, stimuli that she can identify more often, D.F. did show some ventral-stream activation. These activations were, however, more widely distributed than those seen in control participants and did not include LO. In contrast to the absent or abnormal activation observed during these perceptual tasks, D.F. showed robust activation in the expected dorsal stream regions during object grasping, despite considerable atrophy in some regions of the parietal lobes. In particular, an area in the anterior intraparietal sulcus was activated more for grasping an object than for just reaching to that object, for both D.F. and controls. In conclusion, we have been able to confirm directly that D.F.'s visual form agnosia is associated with extensive damage to the ventral stream, and that her spared visuomotor skills are associated with visual processing in the dorsal stream.
Optic ataxia and visual agnosia have been proposed to constitute a double dissociation which provides the main argument for the assimilation of the anatomical distinction between a dorsal and a ventral visual stream to the functional distinction between perception and action. In the present review, we argue that insufficient evidence has been collected to argue for this double dissociation. Several criteria are reviewed: (1) exploration of the visuomotor behavior in central versus peripheral vision has not been matched for the two types of patients; (2) the temporal constraints of visual processes that are impaired in the two neurological conditions appear to play a crucial role in the apparent dissociation; (3) the necessary reductionism of experimental conditions used to study action has led to an overconsideration of optic ataxia as a global deficit for action. Altogether optic ataxia appears to result from a specific impairment of immediate visuomotor control rather than of visually guided action as a whole. These results are discussed in the light of recent research on optic ataxia and on motor control, and directions for future research are proposed.
The visual agnosias are an intriguing class of clinical phenomena that have important implications for current theories of high-level vision. Visual agnosia is defined as impaired object recognition that cannot be attributed to visual loss, language impairment, or a general mental decline. At least in some instances, agnostic patients generate an adequate internal representation of the stimulus but fail to recognize it. In this review, we begin by describing the classic works related to the visual agnosias, followed by a description of the major clinical variants and their occurrence in degenerative disorders. In keeping with the theme of this issue, we then discuss recent contributions to this domain. Finally, we present evidence from functional imaging studies to support the clinical distinction between the various types of visual agnosias.