Brain Advance Access originally published online on May 26, 2006
Brain 2006 129(7):1803-1821; doi:10.1093/brain/awl140
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Functional circuitry underlying visual neglect
1 Laboratory of Cerebral Dynamics, Plasticity and Rehabilitation Department of Anatomy and Neurobiology, Boston University School of Medicine Boston, MA 2 Centre for Brain and Mind, Departments of Physiology and Psychology, University of Western Ontario London, Ontario, Canada 3 School of Engineering and Science, International University Bremen Bremen, Germany
Correspondence to: R. Jarrett Rushmore, PhD, Laboratory of Cerebral Dynamics, Plasticity and Rehabilitation, Department of Anatomy and Neurobiology, Boston University School of Medicine, 700 Albany Street, W702, Boston, MA 02118, USA E-mail: rushmore{at}bu.edu
Visuospatial neglect is a common neurological syndrome caused by unilateral brain damage to the posterior and inferior parietal cerebral cortex, and is characterized by an inability to respond or orient to stimuli presented in the contralesional hemifield. Neglect has been elicited in experimental models of the rat, cat and monkey, and is thought to result in part from a pathological state of inhibition exerted on the damaged hemisphere by the hyperexcited intact hemisphere. We sought to test this theory by assessing neural activity levels in multiple brain structures during neglect using 2-deoxyglucose (2DG) as a metabolic marker of neural activity. Neglect was induced in two ways: (i) by cooling deactivation of posterior parietal cortex or (ii) in conjunction with broader cortical blindness produced by unilateral lesion of all contiguous visual cortical areas spanning occipital, parietal and temporal regions. The direction and magnitude of changes in 2DG uptake were measured in cerebral cortex and midbrain structures. Finally, the 2DG uptake was assessed in a group of cats in which the lesion-induced neglect component of blindness was cancelled by cooling of either the contralateral posterior parietal cortex or the contralateral superior colliculus (SC). Overall, we found that (i) both lesion- and cooling-induced neglect are associated with decreases in 2DG uptake in specific ipsilateral cortical and midbrain regions; (ii) levels of 2DG uptake in the intermediate and deep layers of the SC contralateral to both cooling and lesion deactivations are increased; (iii) changes in 2DG uptake were not identified in the contralateral cortex; and (iv) reversal of the lesion-induced neglect component of blindness is associated with a reduction of contralesional 2DG uptake to normal or subnormal levels. These data are in accord with theories of neglect that include mutually suppressive mechanisms between the two hemispheres, and we show that these mechanisms operate at the level of the SC, but are not apparent at the level of cortex. These results suggest that the most effective therapies for visual neglect will be those that act to decrease neural activity in the intermediate layers of the SC contralateral to the brain damage.
Key Words: visuospatial neglect; superior colliculus; animal models; parietal cortex; visual perception
Abbreviations: 2DG, 2-deoxyglucose; MSs, middle suprasylvian sulcus; pMS, posterior middle suprasylvian; SC, superior colliculus; SGI, stratum griseum intermediale; SGP, stratum griseum profundum; SGS, stratum griseum superficiale; SO, stratum opticum
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Received March 7, 2006. Revised April 24, 2006. Accepted April 26, 2006.
The death of Dr Bertram Payne occurred during the preparation of this manuscript.
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