Abstract

Neuroanatomical, neurophysiological, and computational constraints are used to motivate a set of hypotheses about the functional organization of high-level vision. A set of processing subsystems is posited that underlies the later stages of visual object recognition and identification; these subsystems have been implemented in a running computer simulation model. The model is damaged in a variety of ways, and its performance on a set of tasks is observed. Dysfunctions arise from disruptions of the subsystems, disruptions of their interconnections, compensations by intact subsystems, and diminished activational capacity. The most common dysfunctions of high-level vision following brain damage are then reviewed, and accounts are offered by reference to the stimulation model. According to the theory and model, each type of dysfunction can arise from numerous underlying causes, all of which are potentially distinguishable by empirical methods.