Elsevier

Neuropsychologia

Volume 46, Issue 7, June 2008, Pages 1813-1827
Neuropsychologia

Reviews and perspectives
Role of parietal regions in episodic memory retrieval: The dual attentional processes hypothesis

https://doi.org/10.1016/j.neuropsychologia.2008.03.019Get rights and content

Abstract

Although parietal cortex is frequently activated during episodic memory retrieval, damage to this region does not markedly impair episodic memory. To account for these and other findings, a new dual attentional processes (DAP) hypothesis is proposed. According to this hypothesis, dorsal parietal cortex (DPC) contributes top-down attentional processes guided by retrieval goals, whereas ventral parietal cortex (VPC) contributes bottom-up attentional processes captured by the retrieval output. Consistent with this hypothesis, DPC activity increases with retrieval effort whereas VPC activity increases with confidence in old and new responses. The DAP hypothesis can also account for the overlap of parietal activations across different cognitive domains and for opposing effects of parietal activity on encoding vs. retrieval. Finally, the DAP hypothesis explains why VPC lesions yield a memory neglect syndrome: a deficit in spontaneously reporting relevant memory details but not in accessing the same details when guided by specific questions.

Section snippets

Three hypotheses on the role of parietal cortex and episodic retrieval

The review by Wagner et al. (2005) considered three hypotheses on the role of parietal regions in episodic retrieval. First, the output buffer hypothesis postulates that parietal regions hold retrieved information in a form accessible to decision-making processes, similarly to one of Baddeley's working memory buffers. Second, the mnemonic accumulator hypothesis posits that parietal regions temporally integrate a memory-strength signal. Wagner et al. (2005) linked this idea to signal-detection

Functional neuroimaging evidence

As noted above, activations in lateral parietal cortex are among the most frequent findings in PET and fMRI studies of episodic retrieval (Cabeza & Nyberg, 2000; Rugg & Henson, 2002). Although summarizing the results of many of these studies can be very useful to identify basic patterns of parietal activity during episodic retrieval, as illustrated by the meta-analysis of Vilberg and Rugg (2008), these basic patterns can be accommodated by several competing hypotheses. For example, Vilberg and

Lesion evidence

Although functional neuroimaging evidence that parietal regions are frequently activated during episodic retrieval suggests that these regions play an important role in episodic retrieval, this idea is challenged by neuropsychological evidence that parietal lesions do not typically yield severe episodic memory deficits. Yet, if the contributions of parietal regions to episodic retrieval are related to their role in attention, then severe episodic memory deficits should not be expected. In

Open questions

Before concluding, it is important to consider several open questions regarding the DAP hypothesis. These include questions about (1) the overlap of activations in episodic retrieval and attention studies, (2) the domains of functional neuroimaging evidence accounted for by the DAP hypothesis, and (3) potential future extensions of the DAP hypothesis.

Conclusions

In sum, the present article introduced a new hypothesis regarding the contributions of parietal regions to episodic retrieval. According to this DAP hypothesis, DPC contributes top-down attentional processes guided by retrieval goals, whereas VPC contributes bottom-up attentional processes captured by the retrieval output. Although different, these processes interact very closely: goals determine the relevancy of incoming information and incoming targets may alter behavioral goals. The DAP

Acknowledgements

Special thanks to Marian Berryhill, Nancy Dennis, Scott Hayes, Morris Moscovitch, Lars Nyberg, Ingrid Olson, Michael Rugg, Kaia Vilberg, and three anonymous reviewers for insightful comments. This work was funded by NIH grants AG19731 and AG23770.

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