Aggleton & Brown predict that recognition and episodic recall depend on different brain systems and can thus be dissociated from one another. However, intact recall with impaired recognition has not yet been demonstrated if the same type of information is used in both tests. Current evidence suggests that processes underlying familiarity-based recognition are redundant with processes underlying episodic memory.

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 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 hippocampalanterior thalamic and the perirhinal–medial dorsal thalamic systems are compromised, leading to severe deficits in both recall and recognition. (shrink)

Three comments are made. The proposal that recollection and familiarity-based recognition take different thalamic routes does not fit recent experimental evidence, suggesting that mediodorsal thalamus acts in an integrative role with respect to prefrontal cortex. Second, the role of frontal cortex in episodic memory has been understated. Third, the role of the hippocampal axis is likely to be the computation and storage of ideothetic information.