By utilizing new information from both clinical and
experimental (lesion, electrophysiological, and gene-activation)
studies with animals, the anatomy underlying anterograde amnesia
has been reformulated. The distinction between temporal lobe and
diencephalic amnesia is of limited value in that a common feature
of anterograde amnesia is damage to part of an “extended
hippocampal system” comprising the hippocampus, the fornix,
the mamillary bodies, and the anterior thalamic nuclei. This view,
which can be traced back to Delay and Brion (1969), differs from
other recent models in placing critical importance on the efferents
from the hippocampus via the fornix to the diencephalon. These
are necessary for the encoding and, hence, the effective subsequent
recall of episodic memory. An additional feature of this
hippocampal–anterior thalamic axis is the presence
of projections back from the diencephalon to the temporal
cortex and hippocampus that also support episodic memory.
In contrast, this hippocampal system is not required for tests
of item recognition that primarily tax familiarity judgements.
Familiarity judgements reflect an independent process that depends
on a distinct system involving the perirhinal cortex of the temporal
lobe and the medial dorsal nucleus of the thalamus. In the large
majority of amnesic cases both the hippocampal–anterior
thalamic and the perirhinal–medial dorsal thalamic systems
are compromised, leading to severe deficits in both recall and
recognition.