Behavioral and neuroanatomical consequences of a thiamine-deficient diet, combined with the application of a thiamine-antagonist (pyrithiamine) were investigated in the cat. Eight cats (the experimental group) were subjected to a vitamin-B1-poor diet until they developed neurological symptoms (epileptic attacks, ataxia, gait disturbances), while 24 cats were fed normally and served as control group. Immediately following the appearance of neurological signs, a high dose of thiamine was given to the cats of the experimental group; they were then allowed to recover for ten days. Thereafter the performance in learning an alternation task in a T-maze was tested and compared with that of the control group. Behaviorally, the cats of the experimental group manifested drastically retarded acquisition rates in the learning task compared to the cats of the control group. Neuroanatomically, damage was found in the brains of each of the cats in the experimental group; this damage consisted mainly of enlarged ventricles, hemorrhages, neuronal loss and gliosis. Those regions most consistently affected were the periaqueductal gray, the inferior colliculi and the mamillary nuclei. The thalamic mediodorsal nucleus was affected to a minor degree in three cats only. Four cats manifested damage in the hippocampal formation. No damage was found in the cerebellum. Most of the damaged neuroanatomical loci resemble those found in patients with a Wernicke-Korsakoff syndrome.