Visual System: How Does Blindsight Arise?
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Sakuno, T., and Watanabe, Y. (2009). 17. Hodges, C.A., Ilagan, A., Jennings, D., Keri, R., *E-mail: [email protected] Studies of meiosis disclose distinct roles Nilson, J., and Hunt, P.A. (2002). Experimental of cohesion in the core centromere and evidence that changes in oocyte growth pericentromeric regions. Chromosome Res. influence meiotic chromosome segregation. 17, 239–249. Hum. Reprod. 17, 1171–1180. DOI: 10.1016/j.cub.2010.08.011 Visual System: How Does Blindsight patients had been tested for decades. Patients were asked whether they saw Arise? anything in their field defects and with the exception of motion — and perhaps not even that — they said ‘‘No’’. But Some patients can discriminate unseen visual stimuli within a field defect monkeys were not asked this question. caused by damage to the primary visual cortex. The pathways for this Instead, and in order to get a reward, ‘blindsight’ have never been established, but recent studies implicate hitherto they had to choose between two overlooked cells in the thalamic LGN. visual stimuli — to make forced-choice decisions. This difference was Alan Cowey and pervades much of the research highlighted when several investigators on what is now called blindsight. [4,5], using forced-choice guessing, The primary visual cortex, or V1, is the Several investigators have studied demonstrated that patients were just as major cortical destination of the input the role of V1 in monkeys, the visual good as monkeys, and Cowey and from the eyes and contains a ‘map’ pathways of which closely resemble Stoerig [6] showed that monkeys of the image on the retina. Hardly our own. They have found an ever categorized visual stimuli that they surprising, then, that when it is partly increasing range of residual visual could detect as being not like a light, but destroyed, as often happens following sensitivity and discrimination within the invisible. In both cases the subjects stroke or traumatic injury to the back visual field defect caused by removing were showing ‘blindsight’, excellent of the brain, the patient has a visual part, or even all, of V1 (see [3] for forced choice performance in the face of field defect in which he is clinically review) — not just reflexes such as denial of consciously seeing anything. blind — part of the map has been the pupillary response to light, but Once the relevance of investigations deleted. Why the term ‘clinically blind’? also learned voluntary responses to on monkeys to human blindsight was Why not just blind? The answer lies in the orientation, shape, brightness, established the search was renewed in a controversy that began almost size and motion of visual stimuli. monkeys for the pathways that underlie a century ago between two eminent Unsurprisingly, monkeys, unlike human it. Did all the pathways shown in Figure 1 British neurologists. Gordon Holmes [1] patients, were considered to have contribute or only one or a few? Early concluded that, in the absence of part genuine residual vision and this was work [7] showed that monkeys with part of the striate cortex, the blindness is attributed to the many other pathways of V1 removed could still move their eyes complete, the field defect is absolute. from the eye into the brain, as shown to targets confined to the field defect but But George Riddoch [2], contemporary schematically in Figure 1. that this ability was destroyed if the and colleague, disagreed and argued But a huge puzzle remained: why corresponding part of the superior that such patients could perceive don’t patients have the same abilities colliculus, which also has a ‘map’ of the motion within their otherwise blind given that they too have these other retina, was subsequently extirpated. field. This controversy, like old pathways? The answer lies in the This still remains strong evidence that volcanoes, has rumbled on ever since different ways in which monkeys and the pathway from the eye to the superior Dispatch R703 colliculus [8], and perhaps onwards LGN LGN from there — which consists of more V1 than 104 fibres from each eye — is PARVO (P) responsible for blindsight, a conclusion V2 V2 that anatomical demonstrations of other MAGNO (M) pathways from eye to cortex that do not V3 V3 INTER (K) INTER (K) involve the superior colliculus have done little to modify. The recent paper by V4 V4 Schmid and colleagues [9] is bound to rekindle this debate. By combining behavioural, functional neuroimaging, V5 V5 and neuropharmacological methods, these authors provide the most compelling evidence yet that a direct TEO TEO pathway from the retina to the thalamic lateral geniculate nucleus (LGN), and from there to extrastriate visual cortex, TE TE is the key to understanding blindsight. The LGN has sometimes been likened IP to a jumbo club sandwich. It has six IP prominent layers of neurons, shown in Figure 2. The top 4, called ‘parvocellular’ because the neurons are small, receives input from the colour-opponent P SC SC ganglion cells of the eyes. The two bottom, ‘magnocellular’ layers receive PGN PGN their input from the retinal M ganglion ON ON cells, which are not colour opponent, or only slightly so. Almost every P and M NOT NOT cell in the LGN, about a million of them, degenerates within a few weeks of DTN DTN removing V1. It was previously assumed LTN LTN that all blindsight must therefore derive from the retinal ganglion cells that MTN MTN project to the midbrain, as shown in Figure 1. SCN SCN But what about the layers of the LGN between the P and M layers? In these interlaminar layers, the cells are Current Biology small and so pale in conventional Nissl stained sections that they Figure 1. The known pathways from the eye to the brain. were mistaken for interneurons or non-neuronal glial cells by many The right side of the diagram shows the normal arrangement; the left side shows the effect of removing V1. Thicker lines show the heavier projections. Dotted lines show numerically weaker investigators for many years. That this projections. The many onward cortical pathways from V2, V3, V4, etc. are omitted. On the left, lack- was incorrect became clear only ing V1, the major visual input to the temporal lobe processing stream is diminished but that from 10 years ago [10] with the discovery the K cells remains. The subcortical nuclei within the square outline at the bottom are chiefly con- that the K, or ‘konio’ retinal cells project cerned with reflexive responses to light. Labelling from bottom upwards: SCN, suprachiasmatic to these interlaminar layers, the cells nucleus; MTN, LTN and DTN, medial, lateral and dorsal terminal accessory optic nuclei; NOT, of which are as abundant as the large nucleus of the optic tract; ON, olivary nucleus; PGN, pregeniculate nucleus; SC, superior collicu- lus; IP, inferior pulvinar; LGN, lateral geniculate nucleus.