This chapter critically reviews arguments supporting the role of the frontal cortex in light-sensitive epilepsy of the baboon Papio papio in the light of the most recent neurophysiological research. In particular, it is known that spontaneous or ILS-induced paroxysmal discharges, as well as generalized seizures, originate in the frontorolandic cortical region. In this region during ILS, neurons behave in the same manner as hyperexcitable neurons in focal epileptogenic lesions of animals and man. Aso, section of the corpus callosum causes deterioration or even destruction of the synchronization that exists naturally between the two frontorolandic areas. Lastly experimental focal irritative lesions enhance light sensitivity if they are located in the frontorolandic region and inhibit it if they are located in the occipital cortex. Opposing these arguments are those that support the important role the occipital cortex plays, since its ablation makes excessive light sensitivity in the baboon disappear. Studies of the primary and nonprimary visual messages and pathways have also contributed evidence. In particular, demonstration of the existence of large numbers of direct occipitofrontal connections may help reconcile the two opposing arguments. Other evidence favoring the role of the frontal cortex is furnished by the still fragmentary studies on activation of the motor pathways and by studies in neuropharmacology. The significance and value of this type of epilepsy as an animal model of the generalized reflex epilepsies of man are discussed.