Impaired delay eyeblink classical conditioning in individuals with anterograde amnesia resulting from anterior communicating artery aneurysm rupture

Catherine E. Myers, John DeLuca, Maria T. Schultheis, Geoffrey M. Schnirman, Brandon R. Ermita, Bruce Diamond, Stacey G. Warren, Mark A. Gluck

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Anterior communicating artery (ACoA) aneurysm rupture can lead to an anterograde amnesia syndrome similar to that observed after damage to the hippocampus and medial temporal lobes (MT). It is currently believed that ACoA amnesia results from basal forebrain damage that disrupts hippocampal processing without direct hippocampal damage. Converging evidence from animal studies and computational modeling suggests that qualitative differences may exist in the pattern of memory impairment after basal forebrain or MT damage. For example, animals with basal forebrain bur not hippocampal damage are impaired at delay eyeblink classical conditioning (EBCC). In this study, individuals with ACoA amnesia were shown to be impaired at delay EBCC compared with matched controls; this contrasts with the spared delay EBCC previously observed in MT amnesia. This finding suggests the beginning of a possible dissociation between the memory impairments in MT versus ACoA amnesia.

Original languageEnglish (US)
Pages (from-to)560-570
Number of pages11
JournalBehavioral Neuroscience
Volume115
Issue number3
DOIs
StatePublished - 2001

All Science Journal Classification (ASJC) codes

  • Behavioral Neuroscience

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