PubMed · 13085184
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M D SCHECHTER. 1953. Visual agnosia for animate objects.. https://doi.org/10.1097/00005053-195304000-00007
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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.
Two patients with slowly progressive visuospatial impairment demonstrated a peculiar type of visuoconstructive deficit. The most prominent manifestation appeared when handling kanji (logogram) characters and other figurative patterns. The patients showed pure agraphia for complex kanji but not for kana (syllabogram) or Arabic numerals. Their abilities to read and understand kanji characters and to orally describe the structure of a kanji character were preserved. They could not draw or copy figures or symbols except for single lines or simple symbols, although they could identify and name the targets easily. They also performed poorly in such visuoconstructive tasks as the block design subtest and matching to sample tests that require the ability to simultaneously attend to multiple saliencies. When asked to copy multiple kana characters scattered on a sheet of paper, they could correctly describe the location of a particular character in relation to the others, but actually wrote each character in grossly mislocated positions. These findings suggest that when the patients start particular tasks, which require detailed visual analysis, their range of visual attention becomes extremely narrow. This task-dependent narrowing and fixation of visual attention might explain some of the visuoconstructive symptoms described in patients with slowly progressive visuospatial impairment.
In recent years, research on unilateral spatial neglect has focused on dissociations between different aspects of the clinical syndrome, which is now considered by many students as a multi-componential disorder. Notwithstanding this leading view, there is at least one empirical argument which supports a unitary interpretation of the disorder. This is based on the observation, now replicated many times, that a variety of sensory stimulations (vestibular, optokinetic, transcutaneous mechanical vibration and nervous electrical, visual prism adaptation) involving a lateral change (left-right asymmetry) in the input pattern, affect in a very similar fashion virtually all manifestations of the syndrome, including: visuo-spatial neglect; hemianaesthesia (somatosensory hemi-inattention); extinction, hemiparesis, hemiplegia, and anosognosia for these motor disorders; somatoparaphrenia. These effects may be accounted for with reference to a spatial medium, articulated in a number of specific components, which is modulated by sensory input in a fundamentally similar fashion. Recent investigations concerning the neural bases of some of these stimulations support this view. In this chapter the case of the co-variation of the effects of vestibular stimulation on motor deficits and on anosognosia for hemiplegia is considered. The suggestion is made that one mechanism underlying anosognosia for hemiplegia is unawareness of a deficit of intention, or movement planning component, rather than, or in addition to, unawareness of a primary motor deficit. Temporary remission of anosognosia after vestibular stimulation may represent recovery from this neglect-related component, of which, as of other manifestations of the syndrome, patients are typically unaware. The recovered intention to move may allow the detection by the patient of the presence of a residual primary motor deficit, through a feedback mechanism.