Projections from the lateral geniculate nucleus in the cat and monkey

684M. E. WILSON AND B. G. CRAGGlimited value because the posterior placement of the lesion caused the corticaldegeneration to occur in the posterior block. The surprising finding that the LGNappears to project to Visual II as well as to Visual I makes it desirable to determinewhether these degenerated projections could have arisen from structures borderingthe LGN. Examination of Nissl-stained sections of the thalamus did not reveal anyretrograde reaction in the nuclei medial to the LGN in any of these experiments.It nevertheless seemed desirable to place lesions in these more medial structures tosee whether the resultant pattern of degeneration would fit that seen after lesions ofthe LGN.Lesions of structures medial to the lateral geniculate nucleusOne cat (C 11) had a lesion that was centrally placed at the posterior end of theLGN, but that moved medially farther forwards to involve the medial interlaminarnucleus of the LGN. In the cortex degenerated fibres were distributed as an almostcontinuous band in the dorso-medial part of the lateral gyrus, as would be expectedof a lesion close to the representation of the vertical meridian. However, degeneratedfibres were also present in the lateral wall of the lateral gyrus, in a region that maybe either area 18 or 19. Some degeneration was again present in the lateral wall ofthe suprasylvian gyrus in the middle part of its antero-posterior extent. These resultsare similar to those obtained in C8 except for the added degeneration in the lateralwall of the lateral gyrus, and the added involvement of the medial interlaminarnucleus in the lesion.In cat C 12 a lesion was made within the posterior half of the pulvinar nucleus withinvolvement of the medial interlaminar nucleus of the LGN. No retrograde cellreaction was seen in the LGN in Nissl-stained preparations. No fibre degenerationoccurred in the dorsal or medial parts of the lateral gyrus (area 17), but degenerationin the lateral half of the lateral gyrus extended down into the depths of the lateralsulcus. In the suprasylvian gyrus, degeneration was moderate on the crown, butbecame dense in the lateral wall. There was also moderate degeneration in the medialwall of the ectosylvian gyrus, and a small patch at the bottom of the splenial sulcus.The last-named region had been free of degeneration in the brains described above,with the possible exception of C 11: no degeneration was seen in this brain, but themedial interlaminar nucleus was damaged anteriorly, and there was a gap in theseries of sections of this brain at an anterior level.In C 13 a small lesion damaged the medial interlaminar nucleus of the LGN andpart of the N. posterior and N. lateralis posterior. Cortical fibre degeneration wasfound in the lateral two-thirds of the lateral gyrus extending down the lateral wallof the gyrus, in the lateral half of the middle suprasylvian gyrus again extendingdown the wall, and in a small patch at the bottom of the splenial sulcus. Scantscattered degeneration occurred elsewhere in the medial wall of the hemisphere(area 17) and at the tip of the medial wall of the ectosylvian gyrus. The degenerationin area 17 was probably due to the passage of the needle track through the centralpart of the LGN. Degeneration found on the posterior ectosylvian gyrus is probablydue to track damage in the white matter.In C 14 the lesion penetrated the medial interlaminar nucleus and extended as farforwards as the N. ventralis anterior, causing also some damage in the pulvinar