Journal of Neuroscience, Vol 4, 1072-1085, Copyright © 1984 by Society for Neuroscience
Preserved learning in monkeys with medial temporal lesions: sparing of motor and cognitive skills
S Zola-Morgan and LR Squire
In an effort to bring into correspondence the findings from human amnesic
patients and the findings from monkeys with surgical lesions of those brain
regions thought to be affected in the human cases, we have addressed in
three experiments the implication of findings that human amnesia spares
motor and cognitive skills. In the first experiment, monkeys with conjoint
lesions of hippocampus and amygdala (H-A), which reproduced the surgical
removal sustained by the noted amnesic case H.M., were only mildly impaired
in learning relatively difficult pattern discrimination tasks. Monkeys with
lesions of temporal stem matter (TS) were severely impaired on the same
tasks, due to an apparent deficiency in visual information processing. In
the second experiment, monkeys with H-A lesions were severely impaired at
learning relatively easy discrimination tasks that could be acquired
rapidly by normal monkeys. Monkeys with TS lesions were not impaired. In
the third experiment, monkeys with H-A lesions exhibited normal acquisition
of two motor skill tasks. These data can be understood in the light of a
distinction between kinds of memory, founded in recent studies of the
neuropsychology of human amnesia. These studies have led to a distinction
between the learning of skills or procedures, which is spared in human
amnesia, and the learning of facts and episodes, which is impaired. Monkeys
with H-A lesions are normal at skill learning like human amnesic patients
with similar lesions. This conclusion depends in part on the argument
developed here that pattern discrimination learning, as accomplished by
monkeys, has a large skill-like component. These results bring into
correspondence the behavioral data from human amnesic patients and operated
monkeys and set the stage for identifying precisely what brain structures
must be damaged to produce amnesia.