When an individual suffers from a traumatic injury, their ability to form short-term and long-term memories may be negatively impacted. People suffering from post-traumatic stress disorder have reported memory loss after the event that brought about the condition, as well as uncontrollable thoughts and nightmares. As research expands into the mutability of long-term memory formation, treatments for patients with post-traumatic stress disorder may soon be at hand.
Since the late 19th century, clinicians, biologists, and psychologists have undertaken research to gain insight into the mechanisms of memory formation, storage, and recall. A recent breakthrough in this study of memories has revealed that for a short period of time after a memory is recalled, it becomes vulnerable to disruption (Nader, Schafe, & Ledoux, 2000; Alberini, 2005). The implications of this study suggest that it may be possible to ameliorate memories of bad experiences. For people suffering from post-traumatic stress disorder whose bad memories intrude upon their quality of life, the memories of traumatic events may even be erased. This possibility has attracted the attention of physicians and psychiatrists, who are interested in the application of memory erasure to patients crippled by painful memories.
The potential to change or erase memories gives rise to many ethical concerns. Despite continuous advances in the field, much remains unknown about the nature of memory recall or how the recollection of memories changes the memories themselves. Although studies of memory disruption in healthy humans has yielded verifiable information, data from the study of individuals with mental illnesses such as post-traumatic stress disorder have been less conclusive. More research is required to bring about a greater understanding of how memories are strengthened with the passing of time, how memories are able to withstand disruption, and which specific aspects of memory are most vulnerable to being disrupted.
It is a fact of neuroscience that people tend to remember tasks and events that are important to their lives, and to forget experiences that are insignificant. The majority of our day-to-day experiences do not get stored away as long-lasting memories. Rather, for most people information is retained for only a few minutes or hours before it is discarded.
Long term memory is created through repetition or emotional state. When a significant or traumatic event occurs, such as the death of a loved one or birth of a daughter or son, a different sort of memory is formed than when an event happens repeatedly, such as a drive to work or school. The first kind of memory is known as declarative memory, while the second kind is known as procedural memory. It is the former kind of memories that are typically consolidated and stored for the long term, to be able to be recalled years after their formation. Events that take an emotional toll tend to be remembered much more so than events that are commonplace and unremarkable, and the stronger the emotion that is felt, the more “durable” the memory (Pittenger & Duman, 2008).
The biological context of a memory is what makes the memory useful. For example, we remember events that cause pain in order that we can learn to avoid the painful situation in the future. We remember events that cause joy because they represent a time when we achieved our greatest biological fitness, be it in terms of food, sex, or ability to adapt to changes in our surroundings (Alberini, 2009).
More is known about the formation of painful memories than the formation of pleasant and happy memories, because painful memories are easier to study. In addition, traumatic memories contribute to the development of psychiatric disorders such as depression, anxiety, post-traumatic stress, substance abuse, and borderline personality. Therefore, the study of these diseases goes hand-in-hand with the study of stressful memories (Pittenger & Duman, 2008). Typically, a person's response to the recall of a traumatic experience scales with the degree of the averseness of the memory. For example, a memory of an unpleasant encounter with a high school bully will invoke a different type of response as the memory of a near-death experience.
The last century of research into the subject of memory consolidation has demonstrated that newly created memories will exist in a prolonged state of of fragility. During this time, the creation of long-term memory may be disrupted by functional interferences, such as the kind brought about by physical trauma. As an example, a person's ability to recall a car accident can be impaired by the physical injury experienced during the accident. Right after the event occurs, memory is at its most fragile. However, after a period of time passes, the memory becomes more resilient to disruption (McGaugh, 2000).
The temporal, or time-dependent, stabilization of memory is known as memory consolidation (McGaugh, 2000). Sudies of individuals who have experienced a stroke, seizure, or even the partial removal of brain tissue have shown that the process of memory consolidation takes place in the medial temporal lobe over a period of weeks to years. Once the memory has been consolidated, its storage is spread out to other brain regions, especially the cortical areas.
The consolidation of memory requires the activation of cellular pathways and the synthesis of proteins. Cristina Alberini (2005) writes:
“Studies based on the use of inhibitors showed that memory consolidation requires RNA and protein synthesisOver the past 15 years, signalling pathways involving Ca2+, cAMP, mitogen-activated protein (MAP) kinases and tyrosine kinases have been shown to be required for the consolidation of various kinds of memories, and numerous genes have been identified as essential for memory formation (p. 51).”
These pathways are involved in cell survival, stress response, and the release of several different neurotransmitters. The activation of these pathways at the time of learning will lead to the modification of synapses, which are the points of contact between neural cells. If the process of synaptic modification is interfered with through pharmacological or functional disruptions, memory consolidation is prevented. However, the period of memory fragility in response to biological interferences is thought to last only about 24 hours (Alberini, 2009).
Reconsolidation of Memories
In an experiment conducted ten years ago, researchers studying the consolidation of memories discovered that memories that were over a day old became vulnerable to biochemical interferences again if they were remembered. This means that recalling a memory makes the memory labile, or mutable (Alberini, 2005). During this new period of fragility, the memory will restabilize and consolidate in a way similar to the initial phase of memory consolidation. Thus, we create a new memory from the recall of old memories. After another day has passed, the new memory is again resistant to disruption.
It has been postulated that the purpose of memory reconsolidation may be to reinforce memories (Tronel, Milekic, & Alberini, 2005). If something is important to remember, then memory reconsolidation will help us not to forget it. Tronel, Milekic, and Alberini (2005) write:
“The overall process of memory consolidation is therefore a process of time and number of reactivation events and eventually leads to a memory that is increasingly strengthened, as suggested by findings that recent, but not old, memories are sensitive to protein synthesis inhibitors administered after reactivation (p. 1630).”
Two separate processes happen when a memory is recalled. First, the original memory is reconsolidated, leading to the strengthening of memory. Second, new associations are formed to link the memory to current experiences. Therefore, by recalling a past memory, we not only retain the old information, we also process the information in the context of our present experiences, which presents us with the opportunity to make behavioral choices (Tronel et al., 2005).
Reconsolidation in Individuals with Post-Traumatic Stress Disorder
The reinforcement of memories through the process of reconsolidation is of great clinical interest to doctors involved in the treatment of patients who struggle with post-traumatc stress disorder. In theory, if a memory can be disrupted and changed after recollection, then it may also be weakened or erased. Even intensely painful memories such as the kind experienced by those with PTSD or addiction may be able to be mitigated by disrupting the reconsolidation process.
According to a recent survey, approximately 8 percent of Americans suffer from post-traumatic stress disorder, and 15 percent of all combat veterans experience symptoms of PTSD after returning from combat (Brady, Pearlstein, Asnis, Baker, Rothbaum, Sikes, & Farfel, 2000). According to Brady et al.,
“The clinical presentation of PTSD is characterized by moderate-to-severe symptoms in 3 separate domains: reexperiencing (intrusive thoughts, nightmares, flashbacks, images, or memories), emotional numbing and avoidance (flattened affect or detachment, loss of interest and motivation, and avoidance of any activity, place, person, or topic associated with the trauma); and increased arousal (p. 1837).”
The symptoms of PTSD may be able to be treated in a clinical setting by the disruption of the reconsolidation of fearful memories. Some clinical trials have utilized Propanolol, a beta blocker that inhibits the receptor of the stress hormone noradrenaline, as a source of pharmacological interference in reconsolidation (Debiec & Ledoux, 2004). Propanolol, which is normally used for hypertension, was chosen for treatment because only the fear associated with the memory, and not the content of the memory itself, would be disrupted. This would allow patients to remember the traumatic experience without re-experiencing the pain of the event.
Alberini, C. (2005). Mechanisms of Memory Stabilization: Are Consolidation and Reconsolidation Similar or Distinct Processes? Trends in Neurosciences 28 (1): 51-56.
Alberini, C. M. (2009). Transcription factors in long-term memory and synaptic plasticity. Physiological reviews, 89(1), 121-145.
Brady, K., Pearlstein, T., Asnis, G. M., Baker, D., Rothbaum, B., Sikes, C. R., & Farfel, G. M. (2000). Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial. Jama, 283(14), 1837-1844.
Dębiec, J., & Ledoux, J. E. (2004). Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala. Neuroscience, 129(2), 267-272.
Pittenger, C., & Duman, R. S. (2008). Stress, depression, and neuroplasticity: a convergence of mechanisms. Neuropsychopharmacology, 33(1), 88-109.
Tronel, S., Milekic, M. H., & Alberini, C. M. (2005). Linking new information to a reactivated memory requires consolidation and not reconsolidation mechanisms. PLoS biology, 3(9), 1630.