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The Neuroscientist Comments

Blindsight is a curious phenomenon, previously reviewed in The Neuroscientist (Ptito and Leh 2007), in which patients who have sustained injury to the primary visual cortex (V1) report that they are blind but, on careful clinical testing, are found to have retained a subset of visually guided behaviors in the absence of visual awareness. Despite substantial study, the neuroanatomical structures responsible for the retained visual behaviors remain controversial. Schmid and others (2010) provide new data that may shed some light on this question in a report presenting evidence that the lateral geniculate nucleus, a visual processing nucleus within the thalamus, plays an important role in the processing of visual information, independent of the primary visual cortex. Studying adult macaque monkeys with chronic lesions of the primary visual cortex, they first used fMRI to show that high-contrast stimuli, presented to the lesion-affected visual field (i.e., within the scotoma), evoked significant activation of the extrastriate cortical areas, V2, V3, V4, V5/middle temporal, fundus of the superior temporal sulcus, and lateral intraparietal area, independent of the primary visual cortex. In behavioral tests, they demonstrated that the animals were able to correctly locate these stimuli. They next inactivated the lateral geniculate nucleus within the lesioned hemisphere via local injection of the gaBaa receptor agonist THIP and found that both these fMRI responses and behavioral detections were abolished. In an effort to quantitatively assess the information transmitted via the lateral geniculate nucleus, they also compared the sizes of fMRI responses under normal visual stimulation conditions with responses obtained with stimulation inside the scotoma, with and without inactivation of the lateral geniculate. This analysis revealed that, on average, stimulation within the scotoma with the lateral geniculate intact evoked fMRI activation levels of approximately 20% of those seen under normal conditions, consistent with earlier reports of fMRI activation patterns in primate models and humans with blindsight. The authors argue that the almost complete loss of extrastriate activation and behavioral performance after inactivation of the lateral geniculate nucleus implicates this thalamic structure as a critical hub for blindsight and further contend that these results argue against the existence of alternative pathways that do not involve the lateral geniculate. In this regard, it is interesting that a subset of neurons within the lateral geniculate projects directly to the extrastriate cortex, and these neurons tend to receive input from the superior colliculus, a midbrain structure that has previously been implicated in blindsight. Building on their demonstration that the lateral geniculate has a causal role in visual function independent of the primary visual cortex, the authors suggest that by providing a pathway for transmission of short-latency visual signals to high-level extrastriate regions of the visual cortex, this thalamic nucleus may provide a short cut that can facilitate rapid behavioral responses to visual stimuli.