Lr. Squire et Sm. Zola, AMNESIA, MEMORY AND BRAIN SYSTEMS, Philosophical transactions-Royal Society of London. Biological sciences, 352(1362), 1997, pp. 1663-1673
Bilateral damage to either the medial temporal lobe or the diencephali
c midline causes an amnesic syndrome, i.e. a global impairment in the
ability to acquire new memories regardless of sensory modality, and a
loss of some memories, especially recent ones, from the period before
amnesia began. The memory deficit can occur against a background of in
tact intellectual and perceptual functions. Two themes have been promi
nent in recent work. First, the amnesic syndrome is narrower than once
believed in the sense that a number of learning and memory abilities
are preserved (e.g. skill and habit learning, simple forms of conditio
ning and the phenomenon of priming). Second, the brain system damaged
in amnesia has only a temporary role in memory. As time passes after l
earning, memory is reorganized and consolidated within neocortex, such
that eventually medial temporal lobe and diencephalic structures are
not needed for storage or retrieval.