Memory integration in humans with hippocampal lesions

Adaptive behavior frequently depends on inference from past experience. Recent studies suggest that the underlying process of integrating related memories may depend on interaction between hippocampus and prefrontal cortex. Here, we investigated how hippocampal damage affects memory integration. Sub...

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Bibliographic Details
Published in:Hippocampus 2017-12, Vol.27 (12), p.1230-1238
Main Authors: Pajkert, Anna, Finke, Carsten, Shing, Yee Lee, Hoffmann, Martina, Sommer, Werner, Heekeren, Hauke R., Ploner, Christoph J.
Format: Article
Language:English
Subjects:
Adult
Association Learning
Brain Neoplasms - psychology
Brain Neoplasms - surgery
Clinical trials
decision making
encoding
Female
Hippocampus
Hippocampus - injuries
Hippocampus - surgery
Humans
Integration
Learning
Male
Memory
Memory Disorders
memory integration
Middle Aged
Neuropsychological Tests
Patients
Pattern Recognition, Visual
Prefrontal cortex
relational inference
Young Adult
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Summary:Adaptive behavior frequently depends on inference from past experience. Recent studies suggest that the underlying process of integrating related memories may depend on interaction between hippocampus and prefrontal cortex. Here, we investigated how hippocampal damage affects memory integration. Subjects with mediotemporal lesions and healthy controls learned a set of overlapping AB‐ and BC‐associations (object‐face‐ and face‐object pairs) and were then tested for memory of these associations (“direct” trials) and of inferential AC‐associations (“indirect” trials). The experiment consisted of four encoding/retrieval cycles. In direct trials, performance of patients and controls was similar and stable across cycles. By contrast, in indirect trials, patients and controls showed distinct patterns of behavior. Whereas patients and controls initially showed only minor differences, controls increased performance across subsequent cycles, while patient performance decreased to chance level. Further analysis suggested that this deficit was not merely a consequence of impaired associative memory but rather resulted from an additional hippocampal contribution to memory integration. Our findings further suggest that contextual factors modulate this contribution. Patient deficits in more complex memory‐guided behavior may depend on the flexible interaction of hippocampus‐dependent and ‐independent mechanisms of memory integration.
ISSN:1050-9631
1098-1063
DOI:10.1002/hipo.22766