Damage to the default mode network disrupts autobiographical memory retrieval
Carissa L. Philippi, Daniel Tranel, Melissa Duff, David Rudrauf
Social Cognitive and Affective Neuroscience May 2, 2014 DOI: 10.1093/scan/nsu070 via OpenAlex
Summary
AI-generated from the abstractDamage to parts of the brain's default mode network (DMN) impairs autobiographical memory. In 92 patients with focal brain lesions, damage to the medial prefrontal cortex, posterior cingulate cortex, inferior parietal lobule, or medial temporal lobe led to memory deficits. Semantic and episodic autobiographical memories rely on largely distinct neural regions: semantic deficits followed left medial prefrontal and medial temporal damage, while episodic deficits followed right-sided damage, with overlap only in the right inferior parietal lobule. These results provide neuropsychological evidence that the DMN is necessary for autobiographical memory and clarify its role in self-referential processing.
Study at a glance
| Characteristics | Voxelwise lesion-deficit study Peer reviewed |
|---|---|
| Sample size | 92 |
| Population | Patients with focal, stable brain lesions |
| Citations | 152 |
| Key finding | Damage to regions within the default mode network impairs autobiographical memory, with semantic and episodic memory relying on largely distinct neural correlates. |
Abstract
Functional neuroimaging studies have implicated the default mode network (DMN) in autobiographical memory (AM). Convergent evidence from a lesion approach would help clarify the role of the DMN in AM. In this study, we used a voxelwise lesion-deficit approach to test the hypothesis that regions of the DMN are necessary for AM. We also explored whether the neural correlates of semantic AM (SAM) and episodic AM (EAM) were overlapping or distinct. Using the Iowa Autobiographical Memory Questionnaire, we tested AM retrieval in 92 patients with focal, stable brain lesions. In support of our hypothesis, damage to regions within the DMN (medial prefrontal cortex, mPFC; posterior cingulate cortex, PCC; inferior parietal lobule, IPL; medial temporal lobe, MTL) was associated with AM impairments. Within areas of effective lesion coverage, the neural correlates of SAM and EAM were largely distinct, with limited areas of overlap in right IPL. Whereas SAM deficits were associated with left mPFC and MTL damage, EAM deficits were associated with right mPFC and MTL damage. These results provide novel neuropsychological evidence for the necessary role of parts of the DMN in AM. More broadly, the findings shed new light on how the DMN participates in self-referential processing.