Hardy S C, Stein B E
Department of Physiology, Medical College of Virginia, Richmond 23298.
J Comp Neurol. 1988 Jul 22;273(4):527-42. doi: 10.1002/cne.902730408.
Previous experiments in cats have shown that complete contralateral visual neglect is produced by removing all known visual cortex on one side of the brain, which can then be reversed by damaging the opposite superior colliculus. Presumably, descending facilitatory influences from the visual cortex to the ipsilateral superior colliculus are counterbalanced by intercollicular inhibition (Sprague: Science 153:1544-1546, '66). However, not all of visual cortex or all of the superior colliculus needs to be involved in this circuit. It is the deep rather than the superficial laminae of the superior colliculus that are primarily involved in visual attentive and orientation behaviors, and these laminae are largely independent of primary visual cortex. However, they do depend on corticotectal influences from a comparatively small extraprimary visual area of the posterior region of the lateral suprasylvian cortex (PSSC-Ogasawara et al: J. Neurophysiol. 52:1226-1245, '84). The present experiments demonstrate that lesions only a few millimeters in diameter in this corticotectal zone of the PSSC can produce profound visual neglect. While damage to this area has little, if any, effect on superficial laminae visual activity, it produces a dramatic decrease in the visual activity of the deep laminae. These cats with PSSC lesions fail to orient to a visual stimulus that is introduced suddenly into the contralateral visual field, yet they respond on nearly 100% of the trials to this same stimulus when it is presented in the ipsilateral visual field. The lesion-induced visual neglect produced by PSSC lesions is long-lasting but can be abruptly ameliorated by a midbrain lesion that primarily involves, or undercuts, the deep laminae of the contralateral superior colliculus. Thus, 1) visual neglect can be produced by depriving the deep laminae of the superior colliculus of visual inputs from the cortex, even when the principal visual cortical regions (17, 18, and 19) and their target structures are intact, and 2) visually guided behavior can be restored by eliminating afferents originating in, or passing through, the deep laminae of the contralateral superior colliculus.
以往在猫身上进行的实验表明,通过切除大脑一侧所有已知的视觉皮层可导致完全对侧视觉忽视,随后通过损伤对侧上丘可使其逆转。据推测,从视觉皮层到同侧上丘的下行易化性影响被丘间抑制所抵消(斯普拉格:《科学》153:1544 - 1546,1966年)。然而,并非所有的视觉皮层或所有的上丘都需要参与这一回路。主要参与视觉注意力和定向行为的是上丘的深层而非浅层,并且这些层在很大程度上独立于初级视觉皮层。不过,它们确实依赖于来自外侧上薛氏回后部相对较小的额外初级视觉区域(PSSC - 小笠原等人:《神经生理学杂志》52:1226 - 1245,1984年)的皮质顶盖影响。目前的实验表明,在PSSC的这个皮质顶盖区中直径仅几毫米的损伤就能导致严重的视觉忽视。虽然对该区域的损伤对浅层视觉活动几乎没有影响(如果有影响的话),但它会使深层的视觉活动显著降低。这些患有PSSC损伤的猫不会对突然引入对侧视野的视觉刺激进行定向,但当相同刺激出现在同侧视野时,它们在几乎100%的试验中会做出反应。PSSC损伤所导致的损伤性视觉忽视是持久的,但可通过主要累及或切断对侧上丘深层的中脑损伤而突然改善。因此,1)即使主要视觉皮质区域(17、18和19区)及其目标结构完好,通过剥夺上丘深层来自皮层的视觉输入也可产生视觉忽视,并且2)通过消除起源于或经过对侧上丘深层的传入神经可恢复视觉引导行为。