The parietal cortex and episodic memory: an attentional account

The contribution of the parietal cortex to episodic memory is a fascinating scientific puzzle: although parietal lesions do not normally yield severe episodic-memory deficits, parietal activations are seen frequently in functional-neuroimaging studies of episodic-memory retrieval.Although parietal lesions do not impair standard cued recall and recognition tests, recent studies have demonstrated that when patients with parietal lesions try to remember complex events, the events' contextual details do not spring to mind automatically and do not trigger vivid remembering states.In some functional-neuroimaging studies, parietal activations have been associated with successful retrieval and vivid remembering, whereas in other studies they have been associated with 'old responses' or source-memory tasks, regardless of the accuracy with which the information was recalled. These activations have been attributed to working-memory maintenance of retrieved information, to the accumulation of an oldness signal, and to attention to internal representations, but none of these hypotheses accounts for all of the available evidence.A meta-analysis of event-related functional MRI studies shows that activations that are associated with familiarity and low-confidence recognition are more frequent in the dorsal parietal cortex (DPC; including the intraparietal sulcus, the superior parietal lobule and the precuneus (roughly, Brodmann area 7)). Recollection and high-confidence activations, on the other hand, are more frequent in the ventral parietal cortex (VPC; including the supramarginal and angular gyri (roughly, Brodmann areas 39 and 40).Extending to the episodic-memory domain a distinction that has been made in the attention literature, we propose that the DPC mediates attention that is guided by retrieval goals (top-down attention), whereas the VPC mediates attention that is captured by relevant memory cues and/or recovered memories (bottom-up attention). This attention to memory (AtoM) model provides a good account for functional-neuroimaging data and suggests that parietal lesions do not impair memory recovery, but rather the capacity of attending to recovered memories (memory neglect). This idea provides a potential solution to the aforementioned scientific puzzle.