Brain Advance Access published online on May 26, 2006
Brain, doi:10.1093/brain/awl140
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1 Laboratory of Cerebral Dynamics, Plasticity and Rehabilitation Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA, USA
* To whom correspondence should be addressed. 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.
Received March 7, 2006
Revised April 24, 2006
Accepted April 26, 2006
Article
Functional circuitry underlying visual neglect
R. Jarrett Rushmore 1 *,
Antoni Valero-Cabre 1,
Stephen G. Lomber 2,
Claus C. Hilgetag 3,
and
Bertram R. Payne 1 
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
R. Jarrett Rushmore, E-mail: rushmore{at}bu.edu
Abstract The death of Dr Bertram Payne occurred during the preparation of this manuscript.
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