Traumatic memories

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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. [1] Traumatic memories are naturally stressful in nature and emotionally overwhelm people's existing coping mechanisms. [2]

Contents

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. [3] 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. [4] 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. [5]

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. [3]

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. [4] 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. [1] 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. [6]

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. [7]

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. [8] 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." [9] 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. [10] 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. [11]

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 [10] and it is by applying a pharmacological intervention at this plastic point whereby a traumatic memory can be erased.

The importance of the amygdala

Human brain in the coronal orientation. Amygdalae are shown in dark red. Constudoverbrain.png
Human brain in the coronal orientation. Amygdalae are shown in dark red.

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. [12] Research has also shown that the lateral nucleus of the amygdala is a crucial site of neural changes that occur during fear conditioning. [13]

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. [14] [15] [16] 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. [17]

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. [18] [19] 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. [20]

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. [20]

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 [21]

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. [22]

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. [12] 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. [23] 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. [24]

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. [25]

By repeatedly and carefully having a patient think about or encounter the stimuli and confront the emotions they are feeling, they will experience less and less distress. By systematically targeting distressing memories and stimuli, with exposure therapy, it has been shown levels of depression and symptoms of PTSD decrease significantly. [26] [27] Virtual reality can be used to simulate the original conditions of a traumatic event for use in exposure therapy. This is particularly useful when patients believe the memories of their experience are too strong for them to actively search for and retrieve. Virtual reality has been used to treat individuals with PTSD symptoms stemming from the terrorist attacks of 9/11. [28]

Cognitive behavioral therapies

Research has shown several cognitive behavioural therapies to be effective methods of reducing the emotional distress and negative thought patterns associated with traumatic memories in both those suffering from posttraumatic stress disorder and depression. [29] One such therapy is trauma-focused therapy. This therapy involves bringing the most disturbing elements of a traumatic memory to mind and using therapist-guided cognitive restructuring to change the way the memories are thought about. The change in evaluation usually involves highlighting that the feelings of certain death, extreme danger, hopelessness and helplessness within a traumatic memory do not apply to the person now, as they survived the event. The therapy also focuses on extending the memory so it is recalled beyond the most traumatic parts. Extending them to a point where the person felt safe again, so they remember the event in a more complete way with less focus on the negative aspects. As an example, a traumatic memory of wartime combat might be extended to after a battle, to when the person was no longer in immediate danger. In processing the memory in these ways it becomes less likely to intrude into their thoughts as an unwanted flashback. [30] The memory also becomes less vivid, less distressing and seems more distant to the person's present life.

Eye movement desensitization and reprocessing (EMDR)

Eye movement desensitization and reprocessing (EMDR) is a therapy for treating traumatic memories that involves elements of exposure therapy and cognitive behavioral therapy. [31] Despite controversy remaining in some quarters, EMDR is rated at the highest level of efficacy for PTSD by numerous organizations, most notably by the International Society for Traumatic Stress Studies in a comprehensive study of all effective treatments for PTSD. [32] There is an extensive theoretical model called adaptive information processing (AIP) underlying EMDR.[ citation needed ] The role and mechanism of eye movements, or more generally, bilateral, dual attention stimulation (BLS) is still unclear,[ citation needed ] and though early studies cast doubt on their necessity for EMDR's efficacy,[ citation needed ] BLS is still considered an integral part of the system by most practicing therapists.[ citation needed ]

EMDR begins by identifying troubling memories, cognitions and sensations a patient is struggling with. Then negative thoughts are found that the patient has associated with each memory. While both memory and thought are held in mind the patient follows a moving object with their eyes. After, a positive thought about the memory is discussed in an aim to replace the association the negative thought has to the memory with a preferable thought. [29] Experiments have shown that targeted negative memories are recalled less vividly and with less emotion after treatments with EMDR. [31] [33] Skin conductance responses, a measure of stress and arousal, have also shown lower levels when negative memories treated with EMDR were brought to mind. [31]

A possible mechanism for EMDR has been proposed. As memories are recalled they enter a labile state, where they become vulnerable to being forgotten again. Normally these memories would be reconsolidated, becoming stronger and more permanent again. Adding in eye movements creates extra demand on working memory (which keeps currently-used information available). This makes it difficult for all the details of the memory to be held at once. Once the memories are reconsolidated they are less emotional and vivid. [33]

Video gaming

Emily Holmes at the University of Oxford ran an experiment that showed the video game Tetris could be a potential method of reducing the strength of traumatic memories. [34] The experiment involved participants watching emotionally distressing video footage. Compared with a control group the participants who played Tetris experienced far less intrusive and upsetting thoughts about the footage over a week-long period. [34] The ability to recall details of the footage was not impaired by playing Tetris. [35] Another group of participants exposed to the same footage were given a different task as a distractor, a verbal "pub quiz" game. This involved answering trivia questions from a range of topics unrelated to the distressing video footage. Those in the pub quiz condition were more likely to experience flashbacks compared to both a no-task, waiting a comparable amount of time without an activity, and the Tetris conditions. Holmes and colleagues thus concluded that it was not merely that those playing Tetris were distracted but that they were distracted in a way that served to disrupt the formation of unwanted and intrusive memories. [35]

The explanation given for the success of administering Tetris as opposed to other interventions is that Tetris draws heavily on visuospatial processing power. Because the brain only has a limited supply of resources to process information, playing Tetris hinders the ability of the brain to focus on other visual information, such as traumatic images. [34] However, the details of the event can still be thought of and rehearsed verbally, as Tetris should not interfere with verbal processes of the brain. This explains why participants could remember the details of the footage they watched but why they still experienced fewer flashbacks.

Neuroscience has shown that memories are vulnerable to disruption for several hours after they form. [35] Holmes and colleagues proposed that because of this visuospatial distractors like Tetris, if administered within six hours of a traumatic event could help prevent symptoms of flashbacks. Also there is some evidence that memories can become vulnerable to disruption even at longer periods of time in a process known as reconsolidation. [34]

Ethical concerns

The prospect of memory erasure or alteration raises ethical issues. Some of these concern identity, as memory seems to play a role in how people perceive themselves. For example, if a traumatic memory were erased, a person might still remember related events in their lives, such as their emotional reactions to later experiences. Without the original memory to give them context, these remembered events might prompt the subjects to see themselves as emotional or irrational people. [36] In the United States, the President's Council on Bioethics devoted a chapter in its October 2003 report Beyond Therapy to the issue. [37] [38] The report discourages the use of drugs that blunt the effect of traumatic memories, warning against treating human emotional reactions to life events as a medical issue. [37]

Issues of self-deception arise when altering memories as well. Avoiding the pain and difficulty of dealing with a memory by taking a drug may not be an honest method of coping. Instead of dealing with the truth of the situation a new altered reality is created where the memory is dissociated from pain, or the memory is forgotten altogether. [36] [37] Another issue that arises is exposing patients to unnecessary risk. Traumatic experiences do not necessarily produce a long term traumatic memory, some individuals learn to cope and integrate their experience and it stops affecting their lives quite quickly. If drug treatments are administered when not needed, as when a person could learn to cope without drugs, they may be exposed to side effects and other risks without cause. [38] Loss of painful memories may actually end up causing more harm in some cases. Painful, frightening or even traumatic memories can serve to teach a person to avoid certain situations or experiences. By erasing those memories their adaptive function, to warn and protect individuals may be lost. [36] [37] Another possible result of this technology is a lack of tolerance. If the suffering induced by traumatic events were removable, people may become less sympathetic to that suffering, and put more social pressure on others to erase the memories. [36]

Despite potential risks and abuses, it can still be justifiable to erase traumatic memories when their presence is so disruptive to some and overcoming them can be a difficult process. [38]

Related Research Articles

<span class="mw-page-title-main">Phobia</span> Anxiety disorder classified by a persistent and excessive fear of an object or situation

A phobia is an anxiety disorder, defined by a persistent and excessive fear of an object or situation. Phobias typically result in a rapid onset of fear and are usually present for more than six months. Those affected go to great lengths to avoid the situation or object, to a degree greater than the actual danger posed. If the object or situation cannot be avoided, they experience significant distress. Other symptoms can include fainting, which may occur in blood or injury phobia, and panic attacks, often found in agoraphobia and emetophobia. Around 75% of those with phobias have multiple phobias.

Post-traumatic stress disorder (PTSD) is a mental and behavioral disorder that develops from experiencing a traumatic event, such as sexual assault, warfare, traffic collisions, child abuse, domestic violence, or other threats on a person's life or well-being. Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in the way a person thinks and feels, and an increase in the fight-or-flight response. These symptoms last for more than a month after the event. Young children are less likely to show distress, but instead may express their memories through play. A person with PTSD is at a higher risk of suicide and intentional self-harm.

<span class="mw-page-title-main">Amygdala</span> Each of two small structures deep within the temporal lobe of complex vertebrates

The amygdala is one of two almond-shaped clusters of nuclei located deep and medially within the temporal lobes of the brain's cerebrum in complex vertebrates, including humans. Shown to perform a primary role in the processing of memory, decision making, and emotional responses, the amygdalae are considered part of the limbic system. The term "amygdala" was first introduced by Karl Friedrich Burdach in 1822.

<span class="mw-page-title-main">Fear conditioning</span> Behavioral paradigm in which organisms learn to predict aversive events

Pavlovian fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events. It is a form of learning in which an aversive stimulus is associated with a particular neutral context or neutral stimulus, resulting in the expression of fear responses to the originally neutral stimulus or context. This can be done by pairing the neutral stimulus with an aversive stimulus. Eventually, the neutral stimulus alone can elicit the state of fear. In the vocabulary of classical conditioning, the neutral stimulus or context is the "conditional stimulus" (CS), the aversive stimulus is the "unconditional stimulus" (US), and the fear is the "conditional response" (CR).

<span class="mw-page-title-main">Nightmare disorder</span> Medical condition

Nightmare disorder is a sleep disorder characterized by repeated intense nightmares that most often center on threats to physical safety and security. The nightmares usually occur during the REM stage of sleep, and the person who experiences the nightmares typically remembers them well upon waking. More specifically, nightmare disorder is a type of parasomnia, a subset of sleep disorders categorized by abnormal movement or behavior or verbal actions during sleep or shortly before or after. Other parasomnias include sleepwalking, sleep terrors, bedwetting, and sleep paralysis.

Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy that is controversial within the psychological community. It was devised by Francine Shapiro in 1987 and originally designed to alleviate the distress associated with traumatic memories such as post-traumatic stress disorder (PTSD).

Acute stress reaction is a psychological response to a terrifying, traumatic or surprising experience. It may bring about delayed stress reactions if not correctly addressed. Acute stress may present in reactions which include but are not limited to: intrusive or dissociative symptoms, and reactivity symptoms such as avoidance or arousal. Reactions may be exhibited for days or weeks after the traumatic event.

A flashback, or involuntary recurrent memory, is a psychological phenomenon in which an individual has a sudden, usually powerful, re-experiencing of a past experience or elements of a past experience. These experiences can be frightful, happy, sad, exciting, or any number of other emotions. The term is used particularly when the memory is recalled involuntarily, especially when it is so intense that the person "relives" the experience, and is unable to fully recognize it as memory of a past experience and not something that is happening in "real time".

Complex post-traumatic stress disorder (CPTSD) is a stress-related mental disorder generally occurring in response to complex traumas, i.e., commonly prolonged or repetitive exposures to a series of traumatic events, within which individuals perceive little or no chance to escape.

Dominique de Quervain is a Swiss neuroscientist. He is professor of neuroscience and director of the Division of Cognitive Neuroscience at the University of Basel, Switzerland. He is known for his pioneering research into the use of glucocorticoids (cortisol) in the treatment of PTSD and phobias. He is understood to have found a link between cortisol and forgetting, specifically that cortisol can inhibit memory retrieval. Furthermore, he is known for his contributions to the field of genetics of human memory.

Memory and trauma is the deleterious effects that physical or psychological trauma has on memory.

Memory consolidation is a category of processes that stabilize a memory trace after its initial acquisition. A memory trace is a change in the nervous system caused by memorizing something. Consolidation is distinguished into two specific processes. The first, synaptic consolidation, which is thought to correspond to late-phase long-term potentiation, occurs on a small scale in the synaptic connections and neural circuits within the first few hours after learning. The second process is systems consolidation, occurring on a much larger scale in the brain, rendering hippocampus-dependent memories independent of the hippocampus over a period of weeks to years. Recently, a third process has become the focus of research, reconsolidation, in which previously consolidated memories can be made labile again through reactivation of the memory trace.

<span class="mw-page-title-main">Effects of stress on memory</span> Overview of the effects of stress on memory

The effects of stress on memory include interference with a person's capacity to encode memory and the ability to retrieve information. Stimuli, like stress, improved memory when it was related to learning the subject. During times of stress, the body reacts by secreting stress hormones into the bloodstream. Stress can cause acute and chronic changes in certain brain areas which can cause long-term damage. Over-secretion of stress hormones most frequently impairs long-term delayed recall memory, but can enhance short-term, immediate recall memory. This enhancement is particularly relative in emotional memory. In particular, the hippocampus, prefrontal cortex and the amygdala are affected. One class of stress hormone responsible for negatively affecting long-term, delayed recall memory is the glucocorticoids (GCs), the most notable of which is cortisol. Glucocorticoids facilitate and impair the actions of stress in the brain memory process. Cortisol is a known biomarker for stress. Under normal circumstances, the hippocampus regulates the production of cortisol through negative feedback because it has many receptors that are sensitive to these stress hormones. However, an excess of cortisol can impair the ability of the hippocampus to both encode and recall memories. These stress hormones are also hindering the hippocampus from receiving enough energy by diverting glucose levels to surrounding muscles.

PTSD or post-traumatic stress disorder, is a psychiatric disorder characterised by intrusive thoughts and memories, dreams or flashbacks of the event; avoidance of people, places and activities that remind the individual of the event; ongoing negative beliefs about oneself or the world, mood changes and persistent feelings of anger, guilt or fear; alterations in arousal such as increased irritability, angry outbursts, being hypervigilant, or having difficulty with concentration and sleep.

Many experiments have been done to find out how the brain interprets stimuli and how animals develop fear responses. The emotion, fear, has been hard-wired into almost every individual, due to its vital role in the survival of the individual. Researchers have found that fear is established unconsciously and that the amygdala is involved with fear conditioning.

Daniela Schiller is a neuroscientist who leads the Affective Neuroscience Lab at the Mount Sinai School of Medicine. She is best known for her work on memory reconsolidation, and on modification of emotional learning and memory.

Memory erasure is the selective artificial removal of memories or associations from the mind.

The hippocampus participates in the encoding, consolidation, and retrieval of memories. The hippocampus is located in the medial temporal lobe (subcortical), and is an infolding of the medial temporal cortex. The hippocampus plays an important role in the transfer of information from short-term memory to long-term memory during encoding and retrieval stages. These stages do not need to occur successively, but are, as studies seem to indicate, and they are broadly divided in the neuronal mechanisms that they require or even in the hippocampal areas that they seem to activate. According to Gazzaniga, "encoding is the processing of incoming information that creates memory traces to be stored." There are two steps to the encoding process: "acquisition" and "consolidation". During the acquisition process, stimuli are committed to short term memory. Then, consolidation is where the hippocampus along with other cortical structures stabilize an object within long term memory, which strengthens over time, and is a process for which a number of theories have arisen to explain the underlying mechanism. After encoding, the hippocampus is capable of going through the retrieval process. The retrieval process consists of accessing stored information; this allows learned behaviors to experience conscious depiction and execution. Encoding and retrieval are both affected by neurodegenerative and anxiety disorders and epilepsy.

Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These changes can lead to transgenerational stress inheritance.

<span class="mw-page-title-main">Dual representation theory</span>

Dual representation theory (DRT) is a psychological theory of post-traumatic stress disorder (PTSD) developed by Chris Brewin, Tim Dalgleish, and Stephen Joseph in 1996. This theory proposes that certain symptoms of PTSD - such as nightmares, flashbacks, and emotional disturbance - may be attributed to memory processes that occur after exposure to a traumatic event. DRT proposes the existence of two separate memory systems that run in parallel during memory formation: the verbally accessible memory system (VAM) and situationally accessible memory system (SAM). The VAM system contains information that was consciously processed and thus can be voluntarily recalled or described. In contrast, the SAM system contains unconsciously processed sensory information that cannot be voluntarily recalled. This theory suggests that the VAM system is impaired during a traumatic event because conscious attention is narrowly drawn to threat-related information. Therefore, memory of the trauma is heavily focused on fear, which affects information processing. This gives rise to PTSD symptoms such as trauma-related cognitions, appraisals, and emotions. The SAM system captures vivid sensory information during the traumatic event, which is automatically recalled through exposure to trauma-related triggers. This system is thought to be responsible for the presence of flashbacks and nightmares in PTSD symptomatology.

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