Rushmore R Jarrett, Valero-Cabre Antoni, Lomber Stephen G, Hilgetag Claus C, Payne Bertram R
Laboratory of Cerebral Dynamics, Plasticity and Rehabilitation Department of Anatomy and Neurobiology, Boston University School of Medicine Boston, MA 02118, USA.
Brain. 2006 Jul;129(Pt 7):1803-21. doi: 10.1093/brain/awl140. Epub 2006 May 26.
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.
视觉空间忽视是一种常见的神经综合征，由大脑后下顶叶皮质的单侧损伤引起，其特征是无法对患侧半视野中呈现的刺激做出反应或定向。在大鼠、猫和猴子的实验模型中都诱发了忽视现象，人们认为这部分是由于兴奋过度的完整半球对受损半球施加抑制的病理状态所致。我们试图通过使用2-脱氧葡萄糖（2DG）作为神经活动的代谢标记物，在忽视期间评估多个脑结构中的神经活动水平来验证这一理论。通过两种方式诱发忽视：（i）通过冷却使后顶叶皮质失活，或（ii）与由跨越枕叶、顶叶和颞叶区域的所有相邻视觉皮质区域的单侧损伤产生的更广泛的皮质盲相结合。在大脑皮质和中脑结构中测量2DG摄取变化的方向和幅度。最后，在一组猫中评估2DG摄取情况，在这些猫中，通过冷却对侧后顶叶皮质或对侧上丘（SC）来消除由损伤引起的忽视性失明成分。总体而言，我们发现：（i）损伤和冷却诱发的忽视都与特定同侧皮质和中脑区域2DG摄取减少有关；（ii）冷却和损伤失活对侧的SC中间层和深层中的2DG摄取水平增加；（iii）在对侧皮质中未发现2DG摄取变化；（iv）损伤诱发的忽视性失明成分的逆转与患侧2DG摄取减少至正常或低于正常水平有关。这些数据与包括两个半球之间相互抑制机制的忽视理论一致，并且我们表明这些机制在SC水平起作用，但在皮质水平不明显。这些结果表明，治疗视觉忽视最有效的疗法将是那些能够降低脑损伤对侧SC中间层神经活动的疗法。
