Recovered memory

Recovered memory is the description given to the apparent memory of event(s) that, if they occurred at all, was previously apparently forgotten for a relatively lomg time. People sometimes report recovering long-forgotten memories of, for example, childhood sexual abuse. 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 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.

Neurological Basis of Memory

The neuropsychologist and theoretical neuroscientist Donald Hebb (1904 - 1985) was the first to distinguish between short-term memory and long-term memory. When the brain receives a sensory input, for example, visual and auditory stimuli, a sensory memory retains an exact copy of what is seen or heard, but this memory lasts for at most only a few seconds. What is retained longer than this depends on selective attention - things that we "notice" may be 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. Short term memory includes iconic memory, to hold visual images; acoustic memory, to hold sounds; and working memory, an active process to keep a memory until it is put to use.

Memories stored for longer than this are stored in long-term memory. Hebb's main contribution to neuroscience was his theory that the basis of long-term memory was a form of synaptic plasticity - a long term alteration in the strength of connections between neurons now thought to involve a phenomenon called "long-term potentiation" (LTP). This is relatively permanent storage, and it requires the synthesis of new proteins.

Whether information is stored in long-term memory depends on its 'importance'; for any animal, memories associated with stress or trauma are potentially important for the adaptive value that such memories have for future avoidance behaviour, and the hormones that are released during stress are thought to have an important role in determining what memories are preserved. In humans, acute traumatic stress is associated with acute secretion of epinephrine and norepinephrine (adrenaline and noradrenaline) from the adrenal medulla and more prolonged secretion of cortisol from the adrenal cortex. Acute increases in these hormones are thought to facilitate memory while chronic stress associated with prolonged hypersecretion of cortisol may have the opposite effect. The limbic system, including the hippocampus and amygdala in particular, is critically involved in memory storage and retrieval as well as giving emotional significance to sensory inputs.The hippocampus is important for explicit memory, and for memory consolidation; it is also very sensitive to stress and has a role in recording the emotions of a stressful event. The hippocampus receives input from many different parts of the neocortex and sends its output out to different parts of the brain. The amygdala, may assign emotional values to sensory inputs which are then elaborated upon by the neocortex and imbued with personal meaning. It may also integrate internal representations of the external world in memory image form associating emotional experiences with these memories. The septo-hippocampal system is thought to record memory in temporal and spatial dimensions, and plays an important role in storing and categorizing incoming stimuli in memory.

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.

Kolb and Whishaw describe two groups of theories about amnesia. The defects in sequential processing theory states that to get 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. Kolb and Whishaw claim that none of these models can explain all aspects of amnesia.

Effects of trauma on memory

Patients with amygdalar damage are no more likely to remember emotionally charged words than nonemotionally charged ones. Hippocampal damage

Brain imaging studies suggest that trauma is associated with limbic system abnormalities. Hippocampal damage is connected to over responsiveness to external stimuli. When stress interferes with the hippocampus’ mediation of 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. In animals, high stimulation of the amygdala interferes with hippocampal processing. Strong affect may disallow proper evaluating and categorizing of an experience.

van der Kolk and Fisler’s research shows that 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. The level of emotional significance of a memory correlates directly with the memory’s veracity. Studies of subjective reports of memory show that memories of highly significant events are unusually accurate and stable over time. There are a variety of memory systems which usually operate outside of conscious awareness. These systems operate with some independence from the other memory systems. While people appear to easily assimilate expected and known experiences, 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 qualitatively different from those of nontraumatic events. Explicit memories of personal facts or events are affected by lesions of the front lobe and hippocampus. These parts of the brain are also involved in PTSD neurobiology. Traumatic memories may be coded differently than ordinary event memories, possibly because of alterations in attentional focusing or the fact that extreme emotional arousal interferes with the memory functions of the hippocampus.

Traumas can interfere with several memory functions. van der Kolk divided these functional disturbances into four sets, traumatic amnesia, global memory impairment, dissociative processes and 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 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.

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.

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 us that learned helplessness can develop from repeated exposure to inescapable trauma. In humans, physical paralysis has been shown to be a main feature connected to a traumatic event. This paralysis has been shown to be 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.

Bremner’s work states that changes in the neurotransmitter GABA in response to uncontrolled stress have been connected to losses in memory and learning. 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.