Recovered memory

Recovered memory is the description given to the apparent resurrection of the memory of events that had been forgotten or suppressed for a relatively long time. Retrograde amnesia secondary to physical or emotional trauma (i.e., traumatic amnesia), or the suppression of painful memories from any cause, is an accepted concept. The mechanisms that lead to such reports are not well understood, and the authenticity of recovered memories has often been challenged; in some cases, [recovered memories are fictitious, although in other cases they may be authentic. The term "recovered memory therapy" was created by members of the False Memory Syndrome Foundation to describe the process of recovering long-forgotten memories from people.

Authenticity

The issues surrounding recovered, or false memories have sparked "one of the greatest controversies in the mental health profession in the 20th century". Some therapists have suggested that memories of extreme trauma are buried in the subconscious by some special process, and are later reliably recovered, but others consider that the evidence to support this claim is flawed. Various manipulations can be used to implant false memories of traumatic events that can be quite compelling for those who develop them and can include details that make them seem credible to others. Brown et al. state that “the hypothesis that false memories can easily be implanted in psychotherapy...seriously overstates the available data. Since no studies have been conducted on suggested effects in psychotherapy per se, the idea of iatrogenic suggestion of false memories remains an untested hypothesis." The base rates for memory commission errors are quite low, at least in professional trauma treatment. The base rates in adult misinformation studies run between zero and 5 percent for adults and between 3 - 5 percent for children.

One of the most famous experiments in the field of memory research, conducted by Elizabeth Loftus, became widely known as "Lost in the Mall"; in this experiment subjects were given a booklet containing three accounts of real childhood events written by family members and a fourth account of a wholly fictitious event of being lost in a shopping mall. A quarter of the subjects reported remembering the fictitious event, and elaborated on it with extensive circumstantial detail. The lost in the mall study has been criticized as having "external misrepresentations" and "internal scientific methodological errors" as well as consultation and supervision issues. It has also been critiqued as being misapplied to trauma memories and psychotherapeutic situations.

Similar experiments were conducted by Porter et al., who found he could convince about half of his subjects that they had survived a vicious animal attack in childhood. Some of this research of possibly creating false memories has also been critiqued in terms of applicability to therapeutic situations. Another study has questioned the likelihood that a false memory of a traumatic memory can be created. One study has shown that chronic childhood abuse is related to the development of amnesia for abuse memories.

The growth in the USA of recovered memory therapy for past sexual abuse has caused great public and professional concern when memories are 'recovered' after long periods of amnesia, particularly when extraordinary means were used to secure the recovery of memory, there is a high probability that the memories are false, i.e. of incidents that had not occurred. The hypothesis that false memories can be created in therapy has been questioned. Chu's study suggests that psychotherapy is not usually connected to memory recovery and that the independent corroboration of these memories is often present. Cheit claims that the false memory movement has a "tendency to conceal or omit evidence of (the) corroboration" of recovered memories.

Both true and false memories can be recovered using memory work techniques, but there is no evidence that reliable discriminations can be made between them. Memories "recovered" under hypnotism are particularly likely to be false.

Some studies have concluded that recovered memories can occur in victims of trauma and that memories of child sexual abuse and other traumas can be forgotten. Herman writes about the existence of traumatic amnesia and the healing process from it. There is evidence that traumatic memories can be recovered spontaneously. and in some cases recovered memories of traumatic childhood abuse are said to have been corroborated. In one study 75% reported "confirmation of their childhood trauma." One study showed "the spontaneous return of (a) reportedly unrecallable memory during an interview," which was videotaped. Sheflin and Brown state that a total of 25 studies on amnesia for child sexual abuse (CSA) exist and that they demonstrate amnesia in their study subpopulations. In one study, 68% of those recovering memories of abuse in therapy got documentation of their abuse and 9% received information that demonstrated the inaccurateness of the recollection of their memory.

Betrayal Trauma Theory proposes that “that psychogenic amnesia is an adaptive response to childhood abuse” and that “victims may need to remain unaware of the trauma not to reduce suffering but rather to promote survival.”

Medico-Legal issues

Serious issues arise when recovered but false memories result in public allegations; false complaints carry serious consequences for the accused. Many of those who make false claims sincerely believe the truth of what they report. A special type of false allegation, the false memory syndrome, arises typically within therapy, when people report the 'recovery' of childhood memories of previously unknown abuse. The influence of practitioners' beliefs and practices in the eliciting of false 'memories' and of false complaints has come under particular criticism. Sometimes these memories are used as evidence in criminal prosecutions.

It is generally accepted that people sometimes are unable to recall traumatic experiences. The current version (DSM-IV) of the Diagnostic and Statistical Manual of Mental Disorders, published by the American Psychiatric Association, states in section 300.12: "Dissociative amnesia is characterized by an inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness." The term "recovered memory", however, is not listed in DSM-IV or used by any mainstream formal psychotherapy modality.

Alan Scheflin, a law professor, explains that this satisfies courts that recovered memories are admissible into evidence in court. "Both those who argue that repressed memories are always false and those who argue that repressed memories are always true [...] appear to be mistaken. Although the science is limited on this issue, the only three relevant studies conclude that repressed memories are no more and no less accurate than continuous memories....” A U.S. District Court accepted repressed memories as admissible evidence in a specific case. The apparent willingness of courts to credit the recovered memories of complainants but not the absence of memories by defendents has been commented on "It seems apparent that the courts need better guidelines around the issue of dissociative amnesia in both populations."

Neurological Basis of Memory

The neuroscientist Donald Hebb (1904 - 1985) was the first to distinguish between short-term memory and long-term memory. Things that we "notice" are stored in short-term memory for up to a few minutes. This memory is thought to depend on electrical activity in neuronal circuits, and is very easily destroyed by interruption or interference. Memories stored for longer than this are stored in long-term memory. Whether information is stored in long-term memory depends on its 'importance'; for any animal, memories of traumatic events are potentially important for the adaptive value that they have for future avoidance behaviour, and hormones that are released during stress are thought to have a role in determining what memories are preserved. In humans, traumatic stress is associated with acute secretion of epinephrine and norepinephrine (adrenaline and noradrenaline) from the adrenal medulla and cortisol from the adrenal cortex. Increases in these are thought to facilitate memory, but chronic stress associated with prolonged hypersecretion of cortisol may have the opposite effect. The limbic system, is critically involved in memory storage and retrieval as well as giving emotional significance to sensory inputs. Wihin the limbic system, the hippocampus is important for explicit memory, and for memory consolidation; it is also very sensitive to stress hormones, and has a role in recording the emotions of a stressful event. The amygdala is thought to assign emotional values to sensory inputs which are then elaborated upon by the neocortex and imbued with personal meaning.

Amnesia

Amnesia involves losses in explicit memory. It is shown by one’s inability to remember personal memories or discuss them verbally, or it may be shown by one’s inability to fully retain in conscious awareness temporarily retrieved memories. Amnesia is often considered to be a dissociative condition, such as dissociative amnesia. An individual may only remember parts of the event, or certain categories about the event (like feelings). Amnesia caused by deficits while encoding information may not be reversible, because the information was not encoded.

According to the defects in sequential processing theory, for a memory to become permanent, there needs to be a structural change in the brain. Amnesia is assumed to occur when the consolidation process is disrupted and either the memory trace doesn’t produce a structural change and gets lost or there is a structural change and access to the memory trace is lost. The multiple memory systems theories state that amnesia occurs due to a problem in one of the memory systems. These theories assume that the impairment of a psychological system may cause deficits in some kinds of memories but not others. However, none of these models can explain all aspects of amnesia.

Effects of trauma on memory

Brain imaging studies suggest that trauma is associated with limbic system abnormalities. When stress interferes with memory, it is possible that some of the memory is kept by a system that records emotional experience, but there is no symbolic placement of it in time or space. Traumatic memories are retrieved, at least at first, in the form of mental imprints that are dissociated. These imprints are of the affective and sensory elements of the traumatic experience. Clients have reported the slow emergence of a personal narrative that can be considered explicit (conscious) memory.

According to psychiatrist Bessel van der Kolk, memories of highly significant events are usually accurate and stable over time; aspects of traumatic experiences appear to get stuck in the mind, unaltered by time passing or experiences that may follow. The imprints of traumatic experiences appear to be different from those of nontraumatic events, perhaps because of alterations in attentional focusing or the fact that extreme emotional arousal interferes with the memory functions of the hippocampus.

Mechanisms of interference

Traumas can interfere with several memory functions. van der Kolk divided these functional disturbances into four sets

• traumatic amnesia
• global memory impairment
• dissociative processes
• traumatic memories’ sensorimotor organization.

Traumatic amnesia involves the loss of remembering traumatic experiences. The younger the subject and the longer the traumatic event is, the greater the chance of significant amnesia.

Global memory impairment makes it difficult for these subjects to construct an accurate account of their present and past history. Dissociation refers to memories being stored as fragments and not as unitary wholes. Not being able to integrate traumatic memories seems to be the main element which leads to PTSD. In the sensorimotor organization of traumatic memories, sensations are fragmented into different sensory components.

van der Kolk and Fisler’s study of 46 adults supports Jean Piaget’s notion that, when memories can’t be integrated linguistically or semantically, they are organized in a more primitive manner as somatic sensations or visual images. In a neuroimaging study, it was found that when subjects had flashbacks in the laboratory, there was increased activity in the right hemisphere in areas connected to the processing of emotional experiences and in the right visual association cortex. Broca’s areas in the left hemisphere showed significantly decreased activity. van der Kolk and Fisler’s hypothesis is that under extreme stress, the memory categorization system based in the hippocampus fails, allowing these memories to be kept as emotional and sensory states. Excessive arousal at the moment of trauma interferes with the clear memory processing of the event, leaving unaltered memory traces. When these traces are remembered and put into a personal narrative, they are subject to being condensed, contaminated and embellished upon. When traces are recalled, increased activity in the amygdala might cause the personal assignment of accuracy and individual significance.

In van der Kolk’s work on the psychobiology of PTSD, he states that trauma responses are bimodal. The response to trauma is hyperamnesia, over reaction to stimuli and reexperiencing the trauma, which exists with numbing, avoidance and amnesia. When compensating for chronic hyperarousal, behaviorally subjects with PTSD may shut down and avoid stimuli similar to the trauma. Psychobiologically, they may emotionally numb both to trauma and everyday experience. PTSD subjects may go directly from stimuli to response without an adequate appraisal of the situation, due to their overgeneralization of incoming stimuli, creating flight or fight reactions.

Physiological manifestations of stress disorder

Abnormal physiological responses in PTSD have been shown in two ways. One is due to reminders of the trauma. The second is due to intense, neutral stimuli, such as loud sounds. Individuals with PTSD show several autonomic responses to these stimuli, like blood pressure, skin conductance and heart rate. These highly elevated responses show the timelessness and intensity of how traumatic memories may affect one’s present experience. Lang proposed that emotional memories are stored as associative networks, which are activated when a person gets confronted by a sufficient number of elements that make up these networks. Kolb proposed that excessive stimulation of the CNS during trauma could cause permanent neuronal changes, with a detrimental effect on stimulus discrimination, habituation and learning.

Abnormal acoustic startle response (ASR) has been a main feature in trauma response for more than 50 years. Abnormalities in habituation are found in ASR with PTSD subjects. This failure of habituation for PTSD to loud sounds suggests problems with evaluating sensory input. The fact that PTSD subjects are unable to properly integrate trauma memories is shown physiologically by their misinterpretation of nonthreatening stimuli.

PTSD develops following intense stressors. Intense stress causes the release of stress hormones, like cortisol, norepinephrine, epinephrine, etc. Constant exposure to stress changes an organism’s adaptiveness and how it deals with its daily environment. Studies have shown neuroendocrine abnormalities in PTSD subjects. These studies have shown chronically increased activity of the sympathetic nervous system activity in PTSD. Putnam’s work shows large neuroendocrine changes in sexually abused girls when they are compared to normals.

Trauma victims do not respond to stress the way normals do. Pressure situations may cause a feeling of retraumatization. High states of arousal may promote the retrieval of trauma memories and associated phenomena such as sensory information or behaviors connected to prior trauma. Therefore, traumatic memories may be considered state dependent. Under stress, people secrete endogenous stress hormones that affect memory consolidation strength. Through studies on animal models, it is assumed that the large secretion of neurohormones during a traumatic event in part causes LTP and the over-consolidation of traumatic memories. This LTP may cause an organism to remember a trauma whenever aroused. Reliving the traumatic event may cause stress hormones to strength the memory trace causing a positive feedback loop.

Memory processing in trauma

van der Kolk theorizes that there is a difference between traumatic and nontraumatic memory storage and retrieval. The body’s need to respond in danger situations can be strong. There is a tremendous physiological and neurochemical cost to this type of response, due to the depletion of hormones and neurotransmitters. With adequate recovery time, the body can return to its own homeostasis. When there is inadequate recovery time between stressful situations, alterations may occur to the neurophysiological parts of one’s stress-response system. Some of these alterations may be irreversible. One’s body’s memory and learning systems may be altered affecting implicit and explicit memory. This may cause maladaptive or pathological responses. This damage may cause memory loss, learning deficits and other maladaptive symptoms. Children’s neurological and physiological systems are very vulnerable to the negative impact of trauma. Highly resilient people may have a better chance of experiencing a trauma without developing PTSD. But if a trauma is strong enough, no person is immune to the consequences of developing PTSD. Uncontrollable stress may have a similar impact biologically. It may be possible to look at an individual’s pre and post trauma neurochemistry and tell if they have experienced trauma, but it would not be possible to say what kind of trauma. Animal studies show that learned helplessness can develop from repeated exposure to inescapable trauma. In humans, physical paralysis is a main feature connected to a traumatic event. This paralysis is connected to hyperamnesia, amnesia and dissociation. Traumatic events may be unavailable to recall or may be recalled only in pieces.

Gaps in autobiographical memory are normal to PTSD sufferers, as are problems with nonstressful short-term memory tasks. The successful coding of memories entails alert focused awareness when the input is presented. Memory consolidation is most successful when the experience can be elaborated on in conscious thought. A lack of conscious awareness may hurt these processes. Extreme elevations of norepinephrine released in trauma situations are related to the strong implicit hyperamnesia memories and to the explicit deficits of memory of amnesia. Medium to high levels of norepinephrine cause the amygdala to promote LTP in the hippocampus, which may result in vivid memories. Very high levels of norepinephrine and heavy stimulation of the amygdala connected to extreme, prolonged or repeated stress appear to interfere with hippocampal functioning. This interference may hurt cognitive assessment and the encoding of the input.

Changes in the hippocampus’ functioning during uncontrollable stress may hurt and limit the consolidation of the input into the explicit memory system. Some mental representations of the input may remain in cortical emotional memory, which may cause phobias and anxiety. This explains how trauma sufferers may have amnesia for specific events, but not the emotions connected to them. Excessive levels of opioids released in the brain during trauma and the numbing response connected to them may also be a major factor for the impairment of memory. According to van der Kolk, in animal studies, memory is damaged when a situation can no longer be helped by the animal’s activity. Panic and freeze responses may be seen as defensive ways to allow an organism to not consciously experience overwhelming stress or to not remember an occurrence of overwhelming stress. The second is by changing one’s interpretation of detachment. These events are characteristic of dissociative responses. These influences may cause memories that are unrelated to or dissociated from the normal methods of explicit memory retrieval.

Chronic dopamine dysregulation may be a consequence of trauma. Dopamine’s relationship to working memory in the prefrontal cortex may also show its connection to problems of encoding and short term memory. High levels of cortisol (as mentioned previously by Kalat) may cause memory deficits because of its neurotoxic effects on the hippocampus. In animal studies, high levels of cortisol have been shown to cause hippocampal damage. In humans, MRI studies have shown reduced hippocampal volumes in combat veterans with PTSD, adults with posttraumatic symptoms and survivors of repeated childhood sexual or physical abuse. Hippocampal damage may cause short-term memory retention deficits. van der Kolk writes that PTSD’s essence is memory disturbances. Janet wrote that certain occurrences may leave intense memories in a person. With dissociative trauma survivors, trauma may also interfere with implicit memory, where periods of avoidance may be interrupted by intrusive emotional occurrences with no story to guide them.

Bremner cites several studies showing a connection between hippocampal volume and stress related disorders. Researchers have measured hippocampal volume with MRI; hippocampal volume was reduced in Vietnam combat veterans with PTSD, and in patients with PTSD related to early childhood sexual and physical abuse. Abuse and PTSD are related to a broad range of memory disturbances, and PTSD sufferers may be more susceptible to memory problems than normals. A difficult issue for Bremner is whether those presumably abused accurately recall their information.