Recovered memory

From Citizendium
Revision as of 10:05, 18 March 2009 by imported>Chris Day (I)
Jump to navigation Jump to search
This article is developing and not approved.
 Main Article
 Discussion
Related Articles  [?]
Bibliography  [?]
External Links  [?]
Citable Version  [?]
 
https://en.citizendium.org/wiki/index.php?title=Recovered_memory&printable=yes
This editable Main Article is under development and subject to a disclaimer.

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, although some dispute that recovered memories are either reliable or factual. The term "recovered memory therapy" was created by members of the False Memory Syndrome Foundation[1] to describe the process of recovering long-forgotten memories from people, an example of such memories is childhood sexual abuse.[2] 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.[3] [4] [5]

Authenticity

The issues surrounding recovered, or false memories have sparked "one of the greatest controversies in the mental health profession in the 20th century".[6] 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.[7][8] Brown, Scheflin and Hammond 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."[9] 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.[9]

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. [10] The lost in the mall study has been critiqued as having having "external misrepresentations" and "internal scientific methodological errors" as well as consultation and supervision issues.[11] It has also been critiqued as being misapplied to trauma memories and psychotherapeutic situations.[12].

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 .[13] Some of this research of possibly creating false memories has also been critiqued in terms of applicability to therapeutic situations.[11] Another study has questioned the likelihood that a false memory of a traumatic memory can be created. [14]

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.[15] The hypothesis that false memories can be created in therapy has been questioned[16].

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. [17] [18] Memories 'recovered' under hypnotism are particularly likely to be false.[19]

Some studies have concluded that recovered memories can occur in victims of trauma[20][21][22][23] and that memories of child sexual abuse and other traumas can be forgotten[24] [25][26][27]. There is evidence that traumatic memories can be recovered spontaneously[28] [29][30] and in some cases recovered memories of traumatic childhood abuse have been corroborated.[31].

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.” [32][33]

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. [34]. 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."[35] (The term 'recovered memory' is not listed in DSM-IV or used by any mainstream formal psychotherapy modality.)[1]

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....”[36] A decision in U.S. District Court accepted repressed memories as valid. [37]. 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."[38]

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 is thought to assign emotional values to sensory inputs which are then elaborated upon by the neocortex and imbued with personal meaning; thus patients with amygdalar damage are no more likely to remember emotionally charged words than nonemotionally charged ones. The amygdala 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.

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. [39]

Effects of trauma on memory

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.[40] 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 emotional significance of a memory correlates with its veracity; memories of highly significant events are usually accurate and stable over time. 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.[41]

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.[41]

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.[41]

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.[40]

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.[40]

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.[40]

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.[40]

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.[40]

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.[42]

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.[42]

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.[42]

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.[42]

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. [43]

References

  1. ↑ 1.0 1.1 Whitfield, Charles L.; Joyanna L. Silberg, Paul Jay Fink (2001). Misinformation Concerning Child Sexual Abuse and Adult Survivors. Haworth Press, 56. ISBN 0789019019. 
  2. ↑ Corwin, D (1997). "Videotaped discovery of a reportedly unrecallable memory of child sexual abuse: comparison with a childhood interview videotaped 11 Years before". Child Maltreatment 2: 91–112. DOI:10.1177/1077559597002002001. Research Blogging.
  3. ↑ Geraerts E et al. (2009) Cognitive mechanisms underlying recovered-memory experiences of childhood sexual abuse. Psychol Sci 20:92-8. PMID 19037903
  4. ↑ Geraerts E, McNally RJ (2008) Forgetting unwanted memories: directed forgetting and thought suppression methods. Acta Psychol (Amst) 127:614-22. PMID 18164273
  5. ↑ Brewin CR, Andrews B (1998) Recovered memories of trauma: phenomenology and cognitive mechanisms. Clin Psychol Rev 18:949-70. PMID 9885769
  6. ↑ Loftus EF, Davis D (2006) Recovered memories. Annu Rev Clin Psychol 2:469-98. PMID 17716079
  7. ↑ Laney C, Loftus EF (2005) Traumatic memories are not necessarily accurate memories. Can J Psychiatry 50:823-8. PMID 16483115
  8. ↑ Pezdek K, Lam S (2007) What research paradigms have cognitive psychologists used to study "false memory," and what are the implications of these choices? Conscious Cogn 16:2-17. PMID 16157490
  9. ↑ 9.0 9.1 Brown, Scheflin and Hammond (1998). Memory, Trauma Treatment, And the Law. New York, NY: W. W. Norton. ISBN 0-393-70254-5. 
  10. ↑ See Loftus E (1997) Creating false memories Scientific American 227 no 3 for a popular account
  11. ↑ 11.0 11.1 Crook, L (1999). "Lost in a Shopping Mall--A Breach of Professional Ethics.". Ethics & Behavior. 9: 39–50. DOI:10.1207/s15327019eb0901_3. Research Blogging.
  12. ↑ Pope, K. (1996). "Memory, abuse, and science: questioning claims about the false memory syndrome epidemic". American Psychologist 51: 957. DOI:10.1037/0003-066X.51.9.957. Research Blogging.
  13. ↑ Porter S et al.(1999) The nature of real, implanted, and fabricated memories for emotional childhood events: implications for the recovered memory debate. Law Hum Behav 23:517-37. PMID 10487147
  14. ↑ Pezdek, K; Hodge D (1999), "Planting false childhood memories in children: the role of event plausibility", Child Development: 887–95
  15. ↑ Brandon S et al. (1998) Recovered memories of childhood sexual abuse. Implications for clinical practice. Br J Psychiatry 172:296-307. PMID 9722329
  16. ↑ Hammond, D. Corydon; Brown, Daniel P.; Scheflin, Alan W. (1998). Memory, trauma treatment, and the law. New York: W.W. Norton. ISBN 0-393-70254-5. 
  17. ↑ Stocks JT (1998) Recovered memory therapy: a dubious practice technique. Soc Work 43:423-36 PMID 9739631
  18. ↑ Gutheil TG, Simon RI (1997) Clinically based risk management principles for recovered memory cases. Psychiatr Serv 48:1403-7 PMID 9355166 ("Controversy over cases involving so-called recovered memories of sexual abuse has threatened to divide the mental health field, ... The authors review issues in this controversy, including the role of misdirected advocacy for recovered memory by some practitioners, the distinction between the actual events and patient's narrative truth as a factor in the therapeutic alliance, and the contrast between therapeutic and legal remedies.")
  19. ↑ Kihlstrom JF (1997) Hypnosis, memory and amnesia. Philos Trans R Soc Lond B Biol Sci 29:3521727-32. PMID 9415925 ("Hypnotized subjects respond to suggestions from the hypnotist for imaginative experiences involving alterations in perception and memory. ... Hypnotic hypermnesia refers to improved memory for past events. However, such improvements are illusory: hypermnesia suggestions increase false recollection, as well as subjects' confidence in both true and false memories. Hypnotic age regression can be subjectively compelling, but does not involve the ablation of adult memory, or the reinstatement of childlike modes of mental functioning, or the revivification of memory. The clinical and forensic use of hypermnesia and age regression to enhance memory in patients, victims and witnesses (e.g. recovered memory therapy for child sexual abuse) should be discouraged.")
  20. ↑ Widom, Cathy Spatz; Shepard, Robin L. (December 1996). "Accuracy of adult recollections of childhood victimization : Part 1. Childhood physical abuse". Psychological Assessment 8: 412–21. DOI:10.1037/1040-3590.8.4.412. ISSN 1040-3590. EJ542113. Research Blogging.
  21. ↑ Widom, SC; Morris S (1997). "Accuracy of Adult Recollections of Childhood Victimization: Part 2. Childhood Sexual Abuse". Psychological Assessment 9: 34–46. DOI:10.1037/1040-3590.9.1.34. ISSN 1040-3590. EJ545434. Research Blogging.
  22. ↑ Sheflin, AW; Brown, Daniel (1996). "Repressed Memory or Dissociative Amnesia: What the Science Says". J Psychiat Law 24: 143–88. ISSN 0093-1853.
  23. ↑ Herman, Judith Lewis (1997). Trauma and recovery: The aftermath of violence from domestic abuse to political terror. Basic Books, 119–122. ISBN 0465087302. 
  24. ↑ Williams LM (1994). "Recall of childhood trauma: a prospective study of women's memories of child sexual abuse". J Consult Clin Psychol 62: 1167–76. PMID 7860814. [e]
  25. ↑ Research on the Effect of Trauma on Memory. The Leadership Council (2005). Retrieved on 2008-02-07.
  26. ↑ Bowman ES (1996). "Delayed memories of child abuse: Part I: An overview of research findings on forgetting, remembering, and corroborating trauma". Dissociation 9: 221–31.
  27. ↑ Corroboration of child abuse memories. About.com (2006-02-20).
  28. ↑ Chu, J; et al. (1999). "Memories of childhood abuse: dissociation, amnesia, and corroboration". Am J Psychiatry 156: 749–55. PMID 10327909.
  29. ↑ Duggal, S; Sroufe LA (1998). "Recovered memory of childhood sexual trauma: A documented case from a longitudinal study". J Traumatic Stress 11: 301–21. DOI:10.1023/A:1024403220769. Research Blogging.
  30. ↑ Freyd, Jennifer J. (1996). Betrayal Trauma - The Logic of Forgetting Childhood Abuse. Cambridge, MA: Harvard University Press. ISBN 0-674-06805-x. 
  31. ↑ Cheit, Ross E (1998). "Consider This, Skeptics of Recovered Memory". Ethics & Behavior 8: 141–60. DOI:10.1207/s15327019eb0802_4. Research Blogging.
  32. ↑ Freyd, J. (1994). "Betrayal trauma: Traumatic amnesia as an adaptive response to childhood abuse". Ethics & Behavior 4 (4): 307–329.
  33. ↑ Freyd, J.J (1996). Betrayal trauma: the logic of forgetting childhood abuse. Cambridge, MA: Harvard University Press. 
  34. ↑ Boakes J (1999) False complaints of sexual assault: recovered memories of childhood sexual abuse. Med Sci Law 39:112-20. PMID 10332158 '
  35. ↑ DSM-IV Diagnostic and Statistical Manual, American Psychiatric Association
  36. ↑ Scheflin, A (1999), "Ground Lost: the False Memory/Recovered Memory Therapy Debate", Psychiatric Times 16
  37. ↑ “The Validity of Recovered Memory: Decision of a US District Court” Judge Edward F. Harrington, Presentation by Jim Hopper, Ph.D. The legal documentation citation is: 923 Federal Supplement 286 (D. Mass. 1996), United States District Court - District of Massachusetts Ann Shahzade, plaintiff Civil Action No.: V. 92-12139-EFH George Gregory, Defendant. http://www.jimhopper.com/memory-decision/
  38. ↑ Porter S et al.(2001) Memory for murder. A psychological perspective on dissociative amnesia in legal contexts. Int J Law Psychiatry 24:23-42. PMID 11346990 '
  39. ↑ Kolb, B; Whishaw I (1995). Fundamentals of human neuropsychology (4th ed.).. New York: W.H. Freeman. 
  40. ↑ 40.0 40.1 40.2 40.3 40.4 40.5 van der Kolk, Bessel (1994), "The Body Keeps the Score: Memory and the Evolving Psychobiology of Posttraumatic Stress", Harvard Rev Psychiat 1 (5): 253–65, DOI:10.3109/10673229409017088
  41. ↑ 41.0 41.1 41.2 van der Kolk, BA & R Fisler (1995), "Dissociation and the fragmentary nature of traumatic memories: Overview and exploratory study", J Traumatic Stress 8: 505–25
  42. ↑ 42.0 42.1 42.2 42.3 Knopp, Fay Honey (1996). A Primer on the Complexities of Traumatic Memory of Childhood Sexual Abuse - A Psychobiological Approach. Brandon, VT: Safer Society Press. ISBN 1-884444-20-2. 
  43. ↑ Bremner, JD (2002). Does Stress Damage the Brain? Understanding Trauma-Related Disorders from a Neurological Perspective. New York: W.W. Norton and Company. 
Retrieved from "https://citizendium.org/wiki/index.php?title=Recovered_memory&oldid=581082"