When we try to forget something unpleasant, whether a bad argument or a traumatic event, we may be unintentionally inducing amnesia of unrelated memories. According to a new study, this temporary state of amnesia mimics organic amnesia, disrupting the processes in the hippocampus that lead to long-term memory creation.
The work, says senior author Michael Anderson of the University of Cambridge, “suggests that the functional state of the hippocampus can be dynamically disrupted by cognitive control, creating ‘virtual lesions’ that impede memory functioning.” The researchers were inspired by the desire to understand the memory impairments individuals commonly report after a trauma.
In the experiment, after studying word pairs such as “leap-ballet,” participants had to either retrieve (“think” trials) or suppress retrieval (“no-think” trials) of the second word in each pair, given the first word as a reminder. Researchers have used this think/no-think paradigm extensively in the past to study how suppressing an unwanted memory can make it harder to retrieve the suppressed memory later on.
For the new study, Justin Hulbert (now at Bard College), Richard Henson, and Anderson inserted novel (“bystander”) pictures in between think and no-think trials. Each of these pictures presented an object in a location, such as a peacock in a parking lot or a soccer ball on a table, and participants had to imagine how the object came to its location.
The researchers wanted to understand if surrounding the bystander pictures with no-think trials reduced later memory for the pictures, creating an “amnesic shadow.” In a final memory test, participants had to recall the object that had appeared in each bystander scene. As reported in Nature Communications this month, the researchers found that, compared with being surrounded by think trials, participants accurately recalled the object’s identity about 45% less frequently if the scene was presented shortly before or after the no-think – memory suppression – trials. These amnesic shadows were still present after 24 hours.
CNS spoke to Hulbert about this study, widely reported in the press, and its broader implications for trying to suppress memories, particularly following a traumatic event.
CNS: How does the induced amnesia you studied differ from other forms of amnesia?
Hulbert: By amnesia, we mean a loss of episodic memory for personal experiences arising as a result of disruption to hippocampal functions needed to encode and consolidate those memories. With organic amnesia, a person suffers permanent damage to key memory structures, like the hippocampus, leading to permanent disruption to the ability to store new episodic memories.
In our study, we showed that, in the natural course of events, people can engage in mental activities that temporarily disrupt hippocampal function – in reversible fashion – so that, for brief windows of time, the ability to encode or consolidate memories is temporarily disabled, leading to memory loss much like organic amnesia. In our particular procedure, this hippocampal disruption was achieved by asking people to suppress memory retrieval – i.e., to stop themselves from retrieving a memory given a reminder to it – a process known to reduce hippocampal activity. We showed that this process induced a short-term disruption in hippocampal function that created windows of amnesia in people. Thus, people induced amnesia in themselves, by engaging in a cognitive activity that disrupts hippocampal function.
CNS: In what circumstances might this occur?
Hulbert: Well, for one, when people consistently are confronted with reminders to intrusive memories, they often make an effort to exclude these unpleasant memories from mind, simply to cope. People do this because the more one pushes such unwanted memories out of mind, the harder it becomes to later remember those specific instances – something we have shown in past work. In this sense, the ability forget might be beneficial to daily functioning.
But this new research indicates that attempts to push unwanted memories out of mind also have the unintended side effect of leaving the brain in a temporary state of general amnesia, handicapping the ability to form detailed new memories about life events. So one might have trouble remembering whether they were supposed to pick up the kids at 3 or 5 in the afternoon simply because that arrangement was discussed near in time to a person suppressing thoughts about an earlier argument they had with someone.
CNS: How did you become personally interested in this research area?
Hulbert: This work was partly inspired by the experience of a student in one of our introductory psychology lectures about organic amnesia, a condition in which people are rendered unable to form new episodic memories due to brain damage. This student raised her hand to tell the class that she experienced a time in her life when she had many of the same symptoms. She went on to explain that she was an innocent bystander in a widely reported, tragic high school shooting.** In the weeks following the trauma, students were encouraged to return to classes at the school, to achieve “normalcy” again. It was during this period, and the months that followed, that she suffered what she now recognized (having heard the lecture) as a condition strikingly similar to organic amnesia. During this period, her episodic memory was severely impaired. She could understand classroom lectures, only to forget the material the next day, along with other details about daily events.
There are many reasons why the student might have had difficulty learning after such an event. But we began to ask ourselves whether there was any evidence to suggest that the very act of suppressing unwanted memories in response to continual, inescapable reminders, could alter hippocampal functioning in such a way that it produces a condition akin to organic amnesia. And we realized that we had been sitting on neuroimaging data consistent with just such a mechanism. It was this student’s report, combined with our knowledge of how suppression affects hippocampal activity, that led to the insight behind this work. Our key mission was to robustly examine whether this astonishing side effect, which we call the “amnesic shadow,” is something that truly affects people, and, if so, whether it follows theoretically expected characteristics of hippocampal amnesia.
CNS: Have these “windows” or “shadows” of amnesia been previously reported?
Hulbert: In clinical psychology, generalized memory deficits that arise in the aftermath of trauma have been widely documented and are considered an important clinical feature to resolve. Although a number of theories for this pattern have been proposed, this clinical phenomenon has never before been interpreted as the result of a cognitively induced amnesia arising from efforts to voluntarily control the retrieval of unwanted memories. Indeed, the idea that a state very much like organic amnesia might be naturally created by our own mental activities and their effects on the state of the hippocampus – i.e., the “window of amnesia” – has not been widely discussed.
In basic cognitive psychology and cognitive neuroscience, the windows of amnesia identified here – the forgetting caused by hippocampal modulation – have never been identified as a core process of forgetting. Indeed, the “amnesic shadow” does not fit traditional explanations of forgetting. Based on the new evidence, it’s as if hippocampal down-regulation creates a “lesion” in the hippocampus, which is a known cause of amnesia like that which we report. But unlike actual brain damage, the “virtual” lesioning could, in principle, be a daily occurrence in the face of reminders of unwanted thoughts—and one that, fortunately, is reversible.
Interestingly, work out of Trinity College Dublin by Mullally and O’Mara independently noted that a working memory task known to modulate activity in the hippocampus yields a similar behavioral side effect. This study provides some converging evidence for the notion of cognitively induced amnesia. So while a number of cognitive processes may modulate activity in the hippocampus, the common result may be cognitively induced fluctuations in the ability of the hippocampus to perform its normal encoding and consolidation functions, resulting in disruptions to episodic memory.
CNS: What were you most excited or surprised to find?
Hulbert: We were shocked – really just as much as the participants were after the fact – that their memory for novel events (like seeing a photo of a peacock standing in a parking lot) could be reduced by nearly half, simply because they had engaged in an unrelated word-suppression task shortly before or after the image of the peacock appeared. If you think about it, it is really quite stunning. Who would have guessed that suppressing the fact that you studied “ballet” when cued with “leap” would make a person less likely to recall that they saw a picture of a peacock in a parking lot? Most people would not find that intuitive.
Indeed, it is for precisely this reason – the utter unrelatedness of what is being suppressed to the memories that later suffer side effects – that memory deficits associated with trauma seem so puzzling; people might not generally connect the fact that suppressing intrusive memories of an unpleasant event could generally impede memory function. Yet, that is precisely what our data suggest.
Interestingly, when we tested people’s ability to recognize bystander stimuli (instead of having to recall them), they often judged them as familiar, but could not remember details of the context in which they had seen the item. This particular set of findings nicely accords with other research indicating that the hippocampus is especially critical for this type of strong, context-bound memory.
We also have evidence that people are able to pay attention to the bystander experiences between periods of memory suppression, so it’s not simply lack of attention that is driving the amnesia effect. And it’s not simply that memory suppression is especially difficult. Other difficult tasks we tested don’t induce amnesia. Instead, it seems as though reducing activation in the hippocampal memory system to limit reflexive memory retrieval creates a temporary functional lesion linked to episodic memory problems.
CNS: What are the implications of the work for people undergoing therapy to deal with difficult memories?
Hulbert: The first main benefit comes from simply understanding the origins of memory deficits in the aftermath of trauma. Although there are likely to be several sources of these deficits, we believe that people’s own coping strategy – i.e., suppressing retrieval of intruding memories – may play an important and previously underappreciated role in such deficits. So, difficulties with memory in general can be understood as a side effect of trying to control memory via retrieval stopping, something that comes naturally to people. This side effect can be viewed as a tradeoff for the benefit provided by suppression in reducing the intrusiveness of their memories—one that might need to be endured until intrusions abate.
However, it could also be that there are other ways of reducing the intrusiveness of unwanted memories that don’t have an amnesic shadow as a side effect. For example, we found that generating distracting thoughts in response to reminders (an activity designed to engage the hippocampus instead of suppressing it) eliminated the amnesic shadow for bystander events. This discovery enables us to better isolate ways in which people can control intrusive memories without inducing an amnesic shadow.
CNS: What’s next for this line of work?
Hulbert: There is much still to discover about this new form of amnesia. Exactly how long does this side effect last? Could suppressing now affect our ability to remember unrelated experiences from minutes, hours, or days before or after? Moreover, it will be important to pinpoint the cellular changes that correspond to the systemic hippocampal modulations we report as a result of memory suppression. More broadly, is retrieval suppression simply one form of a broader class of mechanisms that reduce hippocampal activity? Does any cognitive process that modulates hippocampal activity – whether it involves retrieval suppression or not – cause an amnesic shadow and, if so, might this dynamic contribute significantly to everyday forgetting? Dynamic modulation of hippocampal state by control processes may be a fundamental mechanism of forgetting that has not previously been identified.
-Lisa M.P. Munoz
**For privacy for the student, the researchers asked that we not name the shooting event.
