Disruption of Memory Consolidation May Explain Patterns of Memory Better Than Emotion-Induced Retrograde Amnesia in Study by Chen et al

To the Editor We read with interest the article by Chen et al,1 which focused on the significant number of patients who did not remember locations where they had been prior to midazolam administration. The authors suggest that one explanation for these memory deficits could be emotion-induced retrograde amnesia. However, we feel a more likely explanation of the presented memory deficits is γ-aminobutyric acid (GABA)-mediated disruption of memory consolidation. A major determinant of memory formation is memory consolidation, a series of neural processes that occur after memory encoding that strengthen and stabilize memory representations in the long term.2 Consolidation processes begin immediately after an event is encoded, but they continue over a longer time course. Consolidation is an especially vulnerable time for memory formation, and processes that interfere with consolidation can result in subsequent forgetting of those memories. Notably, previous work has shown that agonism of GABA receptors interferes with memory consolidation, resulting in impaired memory.3 In the current study, participants were given the GABA agonist midazolam, which may have interfered with the consolidation of memories of events in the preoperative holding area and operating room (OR) experienced before midazolam administration. The presented pattern of memory deficits is consistent with GABA-mediated disruption of memory consolidation because patients who had more time to consolidate memories of the locations where they were given midazolam were subsequently more likely to remember those locations. The authors show that 24.9% of patients remembered the preoperative holding area, where they may have spent hours awaiting surgery, at Washington University in St Louis and the University of Chicago (sites where midazolam was given in that location). However, only 15.4% of patients remembered the OR, where patients typically only spend minutes before the induction of anesthesia, at the University of Manitoba (where midazolam was only administered in the OR). The disruption of the consolidation process was more critical for information that was weakly encoded (ie, the operating room) than for information that had the chance to be more strongly encoded (ie, the preoperative holding area). We further support a mechanism of GABA-mediated disruption of memory consolidation over emotion-induced retrograde amnesia because previous research has shown that emotional events can actually enhance memory consolidation.2 Finally, and perhaps most important, because consolidation processes can vary depending on the content of memories (ie, the patients’ interactions with their anesthesiologists versus details of a location), it is unknown whether patients would have difficulty remembering their anesthesiologists simply because they did not remember the preoperative holding area. As suggested by Chen et al, more research regarding memory and the perioperative period is needed to appreciate the implications that retrograde amnesia may have on patient compliance and satisfaction. Stephen M. McHugh, MD[email protected]Department of AnesthesiologyUniversity of PittsburghPittsburgh, Pennsylvania James W. Ibinson, MD, PhDDepartment of AnesthesiologyUniversity of PittsburghPittsburgh, Pennsylvania Vishnu P. Murty, PhDDepartment of PsychiatryUniversity of PittsburghPittsburgh, Pennsylvania

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