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Notes: Abstract The contribution of the lateral suprasylvian cortex to pattern recognition was studied by behavioural detection experiments in combination with bilateral lesions of different parts of the lateral suprasylvian areas (LSA) and area 7 in seven cats. In a two-alternatives forced choice task the cats had to discriminate simple outline patterns which were additively superimposed on a structured visual background made up of broadband Gaussian noise. For various stimulus conditions (moving or stationary patterns and/or background) the detection probability (P D) of the cats was measured as a function of the signal to noise ratio (S/N). Each cat was tested before and after the lesion. Four different types of lesion could be distinguished depending on their extent: (1) lesion of parts of the (LSA); (2) lesion of parts of the LSA with undercutting of areas 17, 18 and 19; (3) lesion of area 7; (4) lesion of area 7 and parts of the LSA. 1. We found that a large bilateral lesion of the LSA led to significant deficits in all test situations which were dependent on the existence of relative velocity of moving patterns against a structured background. The ability of the cats to discriminate simple outline patterns which were kept stationary was not reduced. On the contrary, when they were tested with stationary and moving patterns on unfocused (empty) backgrounds, we found, to our great surprise, that the performance of the lesioned cats was significantly improved compared with intact animals. As these lesioned cats had no deficits with moving patterns on a uniformly grey background, we conclude that the deficits with the moving patterns must have been caused by interactions between patterns and background, and not by movement of a pattern per se. 2. As soon as the lesion of the LSA was extended by a bilateral undercutting of areas 17, 18 and 19 we found very severe deficits in all test situations, regardless of whether the patterns were moving or kept stationary, or whether they were superimposed on a background or not. The most substantial deficits occurred when the patterns were moving on a stationary background. In these situations the cats were no longer able to reach the 84% correct criterion. Again, the cats were able to reach criterion with moving patterns on a uniformly grey background indicating that this deficit is probably caused by the interaction of patterns and background and not by motion of the patterns per se. 3. A large lesion of area 7 led to modest but significant deficits of more or less the same degree in all test situations with the exception of quickly moving patterns on a structured background. In contrast, a much smaller lesion of area 7 yielded significant deficits only when the background was moved and there was a low relative velocity between the patterns and the background. 4. In brief, the combination of a lesion of area 7 with that of the LSA roughly provoked a combination of the effects of the two lesions (1 and 3) alone. We found significant deficits in all test situations. We did not find evidence for any type of functional recovery in any of the lesions described. All deficits were permanent. Our results support the idea of a functional segregation between the LSA and area 7. They confirm that the LSA are involved in pattern recognition whenever it is associated with motion in combination with object-background interactions. This suggests an involvement of the LSA in the analysis of object- and self-induced motion. An interpretation of the results of lesioning area 7 is based on the conjecture that the mechanism of vergence movements or of binocular fusion of both retina images might be impaired. Under this condition it seems conceivable to expect double images or a reduced visual acuity because the images are out of focus. This would have a similar effect on the detection performance in each stimulus configuration. In addition, the results of lesion 4 provide evidence that both functional subunits (LSA and area 7) are not able to compensate for one another. Finally, we conclude from the results after lesion 2 that the LSA is part of a system which is based on the cooperation with striate cortex and requires intact primary cortex for its full function.