The management of traumatic memories is important when treating mental health disorders such as post traumatic stress disorder. Traumatic memories can cause life problems even to individuals who do not meet the diagnostic criteria for a mental health disorder. They result from traumatic experiences, including natural disasters such as earthquakes and tsunamis; violent events such as kidnapping, terrorist attacks, war, domestic abuse and rape. Traumatic memories are naturally stressful in nature and emotionally overwhelm people's existing coping mechanisms.
When simple objects such as a photograph, or events such as a birthday party, bring traumatic memories to mind people often try to bar the unwanted experience from their minds so as to proceed with life, with varying degrees of success. The frequency of these reminders diminish over time for most people. There are strong individual differences in the rate at which the adjustment occurs. For some the number of intrusive memories diminish rapidly as the person adjusts to the situation, whereas for others intrusive memories may continue for decades with significant interference to their mental, physical and social well-being.
Several psychotherapies have been developed that change, weaken, or prevent the formation of traumatic memories. Pharmacological methods for erasing traumatic memories are currently the subject of active research. The ability to erase specific traumatic memories, even if possible, would create additional problems and so would not necessarily benefit the individual.
Effects
Biological impact Intense psychological stress caused by unwanted, troublesome memories can cause brain structures such as the amygdala, hippocampus and frontal cortex to become activated, as they process the memory. Related to this, there is some neuroimaging (fMRI) evidence that those who are susceptible to PTSD have a hippocampus with a reduced size. Research has also demonstrated the adrenal activity from intense stress dramatically increases activity in the amygdala and leads to changes in brain functioning as well as altering physiological indicators of stress; heart rate, blood pressure and an increase in salivary enzymes, all of which vary with individual responses to stress.
Children who have been exposed to traumatic events often display hippocampus-based learning and memory deficits. These children suffer academically and socially due to symptoms like fragmentation of memory, intrusive thoughts, dissociation and flashbacks, all of which may be related to hippocampal dysfunction.
Psycho-social impact People who are feeling distressed by unwanted traumatic memories, which they may constantly be "reliving" through nightmares or flashbacks may withdraw from family or their social circles in order to avoid exposing themselves to reminders of their traumatic memories. Physical aggression, conflicts and moodiness cause dysfunction in relationships with families, spouse, children and significant others. In order to cope with their memories they often resort to substance abuse, drugs or alcohol in order to deal with anxiety. Depression, severe anxiety and fear commonly stem from traumatic memories. If symptoms of apathy, feeling of inability to control impulsive behavior, sleeplessness or irritability persist the person can discuss this with their family doctor or a psychotherapist.
Consolidation Traumatic memories are formed after an experience that causes high levels of emotional arousal and the activation of stress hormones. These memories become consolidated, stable, and enduring long-term memories (LTMs) through the synthesis of proteins only a few hours after the initial experience. The release of the neurotransmitter Norepinephrine (Noradrenaline) plays a large role in consolidation of traumatic memory. Stimulation of beta-adrenergic receptors during arousal and stress strengthens memory consolidation. Increased release of Norepinephrine inhibits the prefrontal cortex, which plays a role in emotion control as well as extinction or suppression of memory. Additionally, the release also serves to stimulate the amygdala which plays a key role in generating fear behaviors.Dabiec, J. & Altemus, M., "Toward a New Treatment for Traumatic Memory" ,The Dana Foundation, September 01, 2006.
Reconsolidation Memory reconsolidation is a process of retrieving and altering a pre-existing long-term memory. Reconsolidation after retrieval can be used to strengthen existing memories and update or integrate new information. This allows a memory to be dynamic and plastic in nature. Just like in consolidation of memory, reconsolidation involves the synthesis of proteins. Inhibition of this protein synthesis directly before or after retrieval of a traumatic memory can disrupt expression of that memory. When a memory is reactivated it goes into a labile state, making it possible to treat patients with post-traumatic stress disorder or other similar anxiety based disorders. This is done by reactivating a memory so that it causes the process of reconsolidation to begin. One source described the process this way: "[O]ld information is called to mind, modified with the help of drugs or behavioral interventions, and then re-stored with new information incorporated." There are some serious ethical problems with this process as the reactivation of traumatic memories can be very harmful and in some cases cause anxiety attacks and extreme levels of stress. Inhibition of reconsolidation is possible through pharmacological means. The administration of several different types of protein synthesis antagonists can be used to block protein synthesis that occurs after a traumatic memory is reactivated. The inhibition of creation of new proteins will stop the reconsolidation process and make the memory imperfect.
Pharmacological interventions The use of chemical agents as a means to alter traumatic memories has a basis in Molecular Consolidation Theory. Molecular Consolidation theory says that memory is created and solidified (or consolidated) by specific chemical reactions in the brain. Initially, memories exist in a plastic, labile state before they are more solidly encoded. It has been argued that memory consolidation occurs more than once- each time a memory is recalled, it returns to a labile state. It states that things which cause memory loss after initial learning can also lead to memory loss after reactivation or retrieval and it is by applying a pharmacological intervention at this plastic point whereby a traumatic memory can be erased.
The importance of the amygdala
The amygdala is an important brain structure when it comes to learning fearful responses, in other words, it influences how people remember traumatic things. An increase in blood flow to this area has been shown when people look at scary faces, or remember traumatic events. Research has also shown that the lateral nucleus of the amygdala is a crucial site of neural changes that occur during fear conditioning.
In tests with rats, lesions to their basolateral amygdala were shown to reduce the memory enhancing effects of glucocorticoids. Likewise, post-training infusions of β-adrenoreceptor antagonists (beta-blocker) systemically or into the basolateral amygdala reduced fear acquisition, while infusions into other brain areas did not. Consistent with this, infusions of β-receptor agonists enhanced memory consolidation. Researchers conclude that the amygdala is an important mediator of the memory enhancing effects of glucocorticoids and epinephrine.
Anisomycin
The consolidation of memory requires the synthesis (creation) of certain proteins in the amygdala. Disruption of protein synthesis in the amygdala has been shown to prevent long-term memory for fear conditioning. Anisomycin inhibits the production of proteins. In tests where it is delivered to the lateral and basal nuclei in the amygdala of rats, the rats demonstrated that they had forgotten fear responses that they had been conditioned to display.
U0 126 U0126 is a MAPK inhibitor, it disrupts the synthesis of the proteins required to reconsolidate memory. Research has shown that administration of this drug in rats is correlated with a reduction in synaptic potentiation in the lateral amygdala. This means that the neurons in this area which are selective for a certain fear memory fire less easily in response to the memory when affected by the drug as compared to the ease with which they fire without the drug present.
Using U0 126, researchers were able to selectively knock out a fear memory for a specific audio tone and leave a fear memory for another audio tone in a group of rats. This was observed by recording brain activity in the amygdala of these rats when presented with tones they had been conditioned to fear.
Propranolol Propranolol is a blocker for the beta-adrenergic receptors in the amygdala which usually are bound to by stress hormones released by the adrenal gland- epinephrine and norepinephrine.
Research exploring the idea that blocking these receptors would disrupt the creation of proteins necessary for consolidating fearful memories in the amygdala. Propranolol is one such blocker, and in studies was shown to prevent the expression and return of fear in human subjects.
Another study showed that emotionally arousing stories generally predicted better memory recall than stories which were less so. Subjects who read or listened to these arousing stories were less able to remember the details in response to multiple choice questions or in free recall when they had been given a dose of propranolol prior to the story exposure.
D-Cycloserine It has been shown that the NMDA receptors in the amygdala play a pivotal role in extinction (forgetting) and acquisition (remembering)
The normal endogenous compounds which block the activation of NMDA receptors prevent forgetting. Knowing this, researchers hypothesized that hyper-activating these receptors (instead of blocking them) would enhance their activity, and increase forgetting. D-cycloserine is a chemical which enhances (agonist) the activity of the NMDA receptors. When used in rats, D-cycloserine was shown to produce results which reflected this idea. Rats which had been administered it had enhanced levels of forgetting than rats who had not been.
Neuropeptide Y Neuropeptide Y receptors have a great concentration in the amygdala, which is involved in the modulation of fear. Research where Neuropeptide Y was administered intracerebroventricularly showed that it was important in consolidation of memory because it increased immediate and long-term forgetting. The antagonizing of a subtype of receptor for Neuropeptide Y caused the opposite effects- it decreased the likelihood that a fearful memory would be forgotten.
Psychotherapeutic treatments
Exposure therapy
Exposure therapy involves gradually exposing individuals to a stimuli they find disturbing or fear inducing until it no longer provokes an emotional response. The stimuli can range from commonly feared situations and objects, such as heights or speaking publicly, to seemingly mundane objects and places that have become distressing through a traumatic experience. If someone is exposed to a traumatic experience it is common that being exposed to reminders, including memories, of the event will trigger anxiety attacks, emotional distress and flashbacks. A common mechanism to deal with these potential triggers is to avoid thinking about them and to avoid situations where they may be exposed to them. This can affect quality of life by limiting where someone feels they can go and what a person feels comfortable doing. Evidence has been found linking early traumatic experiences with agoraphobia, an anxiety disorder where individuals fear having panic attacks outdoors.