Projections from the lateral geniculate nucleus in the cat and monkey

682M. E. WILSON AND B. G. CRAGGLGN lesionsThree cats (C 8-C 10) had thalamic damage entirely confined to the LGN, while inothers there was additional involvement of medially placed structures. The threelesions to be described were small enough to produce an interesting topographicaldistribution of degeneration in the visual cortex. To understand this it is necessaryto remember that the vertical meridian of the visual field is represented on the medialedge of the LGN (Bishop, Kozak, Levick & Vakkur, 1962; Seneviratne & Whitteridge,1962). On the cortex, the vertical meridian is represented at the boundary between theareas designated as Visual I and Visual II (Talbot & Marshall, 1941 ; Bilge, Seneviratne& Whitteridge, 1963). Hubel & Weisel (1965) and Whitteridge (1966) showed thatthis boundary coincided with that between the area striata (17) and the area occipitalis(18) as defined by Otsuka & Hassler (1962). Furthermore, the anterior part ofthe LGN projects to the anterior visual cortex, and the posterior part of the LGNposteriorly (Minkowski, 1913).In the first cat (C 8), the lesion extends from postero-lateral to antero-medial LGN(Fig. 3), and thus affects the representation of the peripheral visual field at the posteriorend of the LGN, and the field near the vertical meridian at the anterior end ofthe LGN. Since the lesion extends to the antero-medial tip of the LGN, the mostanterior degeneration seen on the cortex (Fig. 3) corresponds to the anterior limitof the visual area. In the cortex, two areas of degeneration are found, one on themedial wall of the hemisphere in area 17 or Visual I, and the other on the top of thelateral gyrus in area 18 or Visual II. In the posterior part of the middle block, adegeneration-free zone intervenes between these two areas of degeneration whichare widely separated, as are the representations of the peripheral field (away fromthe vertical meridian) in Visual I and Visual II. Anteriorly, the two areas of degenerationcome together at the representation of the vertical meridian on the lateral side ofVisual I and the adjoining medial side of Visual II (see Fig. 3). It will be argued belowthat this topographical correspondence between the distribution of the cortical-fibredegeneration and the position of the lesion in the LGN is a strong reason for thinkingthat the cells of the LGN project to the two areas Visual I and Visual II, and that theresult is not due to damage to fibres of other origin which happen to be passing nearthe lesion in the LGN.In C8 no degeneration was found on the medial lip of the lateral sulcus correspondingto area praeoccipitalis (19), the Visual III of the electrophysiologists.However, a sparse but definite projection was found to the lateral wall of the middlesuprasylvian gyrus, a region that was clear of degeneration in all the control brains.In the three areas of degeneration described above, the broken fibres were of similarmedium calibre, and were dense in the deeper layers of the cortex, but scarcelyextended above layer 4.In the second cat, C9, the lesion was on the lateral edge of the LGN, and passedforwards to the anterior extremity of the nucleus, with some possibility of damageto the reticular nucleus just beyond, and to one small bundle of fibres from thenucleus lateralis posterior. This then was a lesion in the representation of the farperipheral visual field. In the striate cortex the fibre degeneration was ventro-medialnear the splenial sulcus (Fig. 4). A second patch of degeneration appeared on the