Encoding-related brain activity and accelerated forgetting in transient epileptic amnesia.


Journal

Cortex; a journal devoted to the study of the nervous system and behavior
ISSN: 1973-8102
Titre abrégé: Cortex
Pays: Italy
ID NLM: 0100725

Informations de publication

Date de publication:
01 2019
Historique:
received: 05 10 2017
revised: 06 04 2018
accepted: 30 04 2018
pubmed: 5 6 2018
medline: 23 2 2020
entrez: 5 6 2018
Statut: ppublish

Résumé

The accelerated forgetting of newly learned information is common amongst patients with epilepsy and, in particular, in the syndrome of transient epileptic amnesia (TEA). However, the neural mechanisms underlying accelerated forgetting are poorly understood. It has been hypothesised that interictal epileptiform activity during longer retention intervals disrupts normally established memory traces. Here, we tested a distinct hypothesis-that accelerated forgetting relates to the abnormal encoding of memories. We studied a group of 15 patients with TEA together with matched, healthy control subjects. Despite normal performance on standard anterograde memory tasks, patients showed accelerated forgetting of a word list over one week. We used a subsequent memory paradigm to compare encoding-related brain activity in patients and controls. Participants studied a series of visually presented scenes whilst undergoing functional MRI scanning. Recognition memory for these scenes was then probed outside the scanner after delays of 45 min and of 4 days. Patients showed poorer memory for the scenes compared with controls. In the patients but not the controls, subsequently forgotten stimuli were associated with reduced hippocampal activation at encoding. Furthermore, patients demonstrated reduced deactivation of posteromedial cortex regions upon viewing subsequently remembered stimuli as compared to subsequently forgotten ones. These data suggest that abnormal encoding-related activity in key memory areas of the brain contributes to accelerated forgetting in TEA. We propose that abnormally encoded memory traces may be particularly vulnerable to interference from subsequently encountered material and hence be forgotten more rapidly. Our results shed light on the mechanisms underlying memory impairment in epilepsy, and offer support to the proposal that accelerated forgetting may be a useful marker of subtle dysfunction in memory-related brain systems.

Identifiants

pubmed: 29861041
pii: S0010-9452(18)30147-3
doi: 10.1016/j.cortex.2018.04.015
pmc: PMC6335262
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

127-140

Subventions

Organisme : Medical Research Council
ID : MR/K010395/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 203139/Z/16/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 104571/Z/14/Z
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom

Informations de copyright

Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.

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Auteurs

Kathryn E Atherton (KE)

Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK; Department of Experimental Psychology and Oxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, UK.

Nicola Filippini (N)

Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK.

Adam Z J Zeman (AZJ)

Cognitive & Behavioural Neurology, University of Exeter Medical School, Exeter, UK.

Anna C Nobre (AC)

Department of Experimental Psychology and Oxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, UK.

Christopher R Butler (CR)

Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Electronic address: chris.butler@ndcn.ox.ac.uk.

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