Psychoanatomical substrates of Bálint's syndrome.
OBJECTIVE
From a series of glimpses, we perceive a seamless and richly detailed visual world. Cerebral damage, however, can destroy this illusion. In the case of Bálint's syndrome, the visual world is perceived erratically, as a series of single objects. The goal of this review is to explore a range of psychological and anatomical explanations for this striking visual disorder and to propose new directions for interpreting the findings in Bálint's syndrome and related cerebral disorders of visual processing.


METHODS
Bálint's syndrome is reviewed in the light of current concepts and methodologies of vision research.


RESULTS
The syndrome affects visual perception (causing simultanagnosia/visual disorientation) and visual control of eye and hand movement (causing ocular apraxia and optic ataxia). Although it has been generally construed as a biparietal syndrome causing an inability to see more than one object at a time, other lesions and mechanisms are also possible. Key syndrome components are dissociable and comprise a range of disturbances that overlap the hemineglect syndrome. Inouye's observations in similar cases, beginning in 1900, antedated Bálint's initial report. Because Bálint's syndrome is not common and is difficult to assess with standard clinical tools, the literature is dominated by case reports and confounded by case selection bias, non-uniform application of operational definitions, inadequate study of basic vision, poor lesion localisation, and failure to distinguish between deficits in the acute and chronic phases of recovery.


CONCLUSIONS
Studies of Bálint's syndrome have provided unique evidence on neural substrates for attention, perception, and visuomotor control. Future studies should address possible underlying psychoanatomical mechanisms at "bottom up" and "top down" levels, and should specifically consider visual working memory and attention (including object based attention) as well as systems for identification of object structure and depth from binocular stereopsis, kinetic depth, motion parallax, eye movement signals, and other cues.
Rizzo
M
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University of Iowa College of Medicine, Department of Neurology, 200 Hawkins Drive, Iowa City, IA 52242-1053, USA. matthew-rizzo@uiowa.edu
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D000377:Agnosia / Q000473:pathology* / Q000503:physiopathology; D001288:Attention / Q000502:physiology*; D001931:Brain Mapping; D002561:Cerebrovascular Disorders / Q000473:pathology / Q000503:physiopathology; D004292:Dominance, Cerebral / Q000502:physiology*; D006801:Humans; D009778:Occipital Lobe / Q000473:pathology / Q000503:physiopathology; D010468:Perceptual Disorders / Q000473:pathology* / Q000503:physiopathology; D011596:Psychomotor Disorders / Q000473:pathology / Q000503:physiopathology; D014793:Visual Cortex / Q000473:pathology / Q000503:physiopathology; D014796:Visual Perception / Q000502:physiology*