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Memory and trauma

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Memory is described by psychology as the ability of an organism to store, retain, and subsequently retrieve information. When an individual experiences a traumatic event, whether physical or psychological, their memory can be affected in many ways. For example, trauma might affect their memory for that event, memory of previous or subsequent events, or thoughts in general. Additionally, It has been observed that memory records from traumatic events are more fragmented and disorganized than recall from non traumatic events.[1] Comparison between narrative of events directly after a traumatic event versus after treatment indicate memories can be processed and organized and that this change is associated with decrease in anxiety related symptoms.[2]

Physical trauma

When people experience physical trauma, such as a head injury in a car accident, this can have effects on their memory. The most common form of memory disturbance in cases of severe injuries or perceived physical distress due to a traumatic event is post-traumatic stress disorder,[3] discussed in depth later in the article.

Traumatic Brain Injury

Damage to different areas of the brain can have varied effects on memory. The temporal lobes, on the sides of the brain, contain the hippocampus and amygdala, and therefore have a lot to do with memory transition and formation. Patients who have had injury to this area have experienced problems creating new long-term memories. For example, the most studied individual in the history of brain research, HM, retained his previously stored long-term memory as well as functional short-term memory, but was unable to remember anything after it was out of his short-term memory.[4] A patient whose fornix was damaged bilaterally developed severe anterograde amnesia but no effect on any other forms of memory or cognition.[5]

Brain Trauma

In addition to physical damage to the brain as a result of mechanical injury, there are other changes in the brain that can be observed. Neuroimaging studies on PTSD repeatedly identify key structures associated with pathology development.[6] The structures observed to change are the amygdala, Anterior Cingulate Cortex (ACC),  Pre Frontal Cortex (PFC), insula, and hippocampus.[6] As a result of individual changes within different brain structures communication and regulation within structures is also impacted.[6]

Amygdala

The Amygdala is known as the "fear center of the brain," and is thought to be activated and regulated in response to stressful situations marked with perceived heightened stimulation. Specifically, the Amygdala is responsible for identifying threats of danger to self and safety.[7] Consistent exposure to trauma and or stress, may lead to over-perception and heighten responsibility and sensitivity to threat.[6] Increased activation in the fear center can impact communication with other circuits in the brain structure including connections between the PFC, amygdala, and hippocampus[6] which can in turn affect how memory are stored by the hippocampus. It is important to note that the amygdala does not fully develop until the late 20's and stress experienced prior to that age may have more extensive impact compared to stress experienced after amygdala is fully developed.[8]

Pre-Frontal Cortex

The PFC is a brain structure responsible for executive functioning skills. Included in executive function abilities are emotional regulation, impulse control, mental cognition, and working memory among many other abilities.The PFC is also in charge of modulating response from the Amygdala. However, during high-stress situations, the Amygdala can suppress higher thinking functions of the PFC.[7] Some PFC functions that may be impacted during traumatic stress include; failure of emotion reappraisal, heightened salience of emotional stimuli, failure to inhibit neuro-endocrine response to threat stimuli, inability to maintain or use extinction of conditioned fear.[6]). People who have experienced trauma, especially chronic and ongoing trauma, may be observed to have under-activation of multiple parts of the PFC.[7] Under activation of the PFC can lead to decreased modulation of the amygdala during a stress response.[6] The PFC in most vulnerable to the effects of stress during adolescent and a traumatic event during this time period would have more extensive changes than stress experience when the PFC is fully developed around the mid 20's.[8]

Hippocampus

The hippocampus is considered the memory center for the brain and is responsible for storing, encoding, retrieving, and reconsolidating memories.[7] ).Studies indicate that people who have PTSD may have a "shrunken" hippocampus, some estimates indicate that there may be up to a decrease in a range of 5-26%.[9] However, there are alternative explanations to account for the observed decreased hippocampus volume. One study by Gilbertson et al. (2002), suggests that perhaps decrease hippocampal volume may be a pre-existing factor that may predispose people for the development of PTSD.[10] There are conflicting interpretation in understanding if decreased hippocampal volumes are a consequence or a pre-existing vulnerability associated with PTSD.[10][9] While it is unclear if decreased hippocampal volume is evident as a consequence or prior to the traumatic event; there are numerous studies that indicate the hippocampus in under active during traumatic events and potentially also under-active after the event as well.[6][7][9][10] An underactive or dysregulated Hippocampus has many clinical implications including in areas of neurogenesis, disturbances to organization of memory, and ability to impact other endocrine functions such as a stress-response.[7][11][12]

The hippocampus is a major site of neurogenesis, it is where new neurons are born, impact to neurogenesis can have multiple implications. Some studies suggest that blocking of neurogenesis may have the ability to block the efficacy of anti-depressants which are used to treat symptoms of depression.[11] According to the DSM-5 there is comorbidity among depression and PTSD. In addition to comorbidity rates, the symptoms of PTSD and Major Depression Disorder (MDD) also have some overlap. Specifically, both list negative alteration in mood and cognitive disturbances as a symptom, underlying the idea of a "c" factor or a cognitive dysfunction that can be seen as a transdiagnostic dimension of psychopathology.[13] Trauma can impact the hippocampus and may have global implications in mood and symptom progression through the impacts on neurogenesis.[11]

Changes to the hippocampus also may have impact to a person's ability to recall the traumatic experience[7] and produce a trauma narrative .[1] There have been studies that further expand on how trauma can impact victims ability to recall traumatic events.[1][2] These memory difficulties in identifying, labeling, and completely processing the traumatic event can be targets for treatment through psychotherapy.[14] The age of a person when they experience a traumatic event can also modulate the effects of the hippocampus.[8] Particularly, the hippocampus is developing from birth to age 2 and is most vulnerable to the effects of stress during this time period.[8] During adolescence the hippocampus is fully organized and less vulnerable to the effects of stress.[8]

The Hippocampus also has connections with the body's stress response system.[9] The hippocampus is responsible for the negative feedback regulation of the Hypothalamic- pituitary-adrenal axis.[12] Failure to regulate stress response through the HPA axis can have long-term health effects through the experience of chronic stress.[12]

Psychological trauma

Relevant memory

Of the different aspects of memory – working, short-term, long-term, etc. – the one most commonly affected by psychological trauma is long-term memory.[15] Missing memories, changes to memory, intensified memories – all are cases of manipulations of long-term memory.

Physical aspect

Long-term memory is associated with many different areas of the brain including the hippocampus, amygdala, thalamus and hypothalamus, peripheral cortex and temporal cortex. The hippocampus and amygdala have been connected with transference of memory from short-term memory to long-term memory.[16] Thalamus and hypothalamus, located in the forebrain, are part of the limbic system; they are responsible for regulating different hormones and emotional and physical reactions to situations, including emotional stress or trauma. The thalamus is also related to reception of information and transferring the information, in the case of memories, to the cerebral cortex.

Physical effects

Psychological trauma has great effects on physical aspects of patients' brains, to the point that it can have detrimental effects akin to actual physical brain damage. The hippocampus, as mentioned above, is involved in the transference of short-term memories to long-term memories and it is especially sensitive to stress. Stress causes glucocorticoids (GCs), adrenal hormones, to be secreted and sustained exposure to these hormones can cause neural degeneration. The hippocampus is a principal target site for GCs and therefore experiences a severity of neuronal damage that other areas of the brain do not.[17] In severe trauma patients, especially those with post-traumatic stress disorder, the medial prefrontal cortex is volumetrically smaller in size than normal and is hyporesponsive when performing cognitive tasks, which could be a cause of involuntary recollection (intrusive thoughts).[18] The medial prefrontal cortex controls emotional responsiveness and conditioned fear responses to fear-inducing stimuli by interacting with the amygdala. In those cases, the metabolism in some parts of the medial prefrontal cortex didn't activate as they were supposed to when compared to those of a healthy subject.

Psychological effects

As with many areas of psychology, most of these effects are under constant review, trial, and dissent within the scientific world regarding the validity of each topic.

Repressed memory

Main article: Repressed memory

Perhaps one of the most controversial and well-known of the psychological effects trauma can have on patients is repressed memory. The theory/reality of repressed memory is the idea that an event is so traumatic, that the memory was not forgotten in the traditional sense, or kept secret in shame or fear, but removed from the conscious mind, still present in the long-term memory but hidden from the patient's knowledge.[19] Sigmund Freud originated the concept of repression and it has developed and changed since his original work.[20] In the eyes of critics of repressed memory, it is synonymous with false memory; however its proponents will argue that these people truly did have traumatic experiences.

Intrusive thoughts

Main article: Intrusive thoughts

Intrusive thoughts are defined as unwelcome, involuntary thoughts, images or unpleasant ideas that may become obsessions, are upsetting or distressing, and can be difficult to be free of and manage. In patients who have suffered from traumatic events, especially those with post-traumatic stress disorder, depression or obsessive-compulsive disorder, the thoughts are not as easy to ignore and can become troubling and severe. These thoughts are not typically acted on; the obsession of the thoughts usually comes from intense guilt, shame or anxiety relating to the fact that the patient is having the thoughts to begin with so they are unlikely to actually act on things they feel so badly about. In trauma patients, the intrusive thoughts are typically memories from traumatic experiences that come at unexpected and unwanted times. The primary difference from other intrusive thoughts for patients is that the memories are real rather than imagined.

Emotion

Emotion is a large part of trauma, especially near death experiences. The effect emotions have on memory in different instances is an integral part of the effect of trauma on memory. Emotional events tend to be recalled with more frequency and clarity than memories not associated with extreme emotions.[21] Typically traumatic events, such as physical attack or sexual abuse, are interrelated with strong negative emotions, causing these memories to be very strong and more easily recalled than memories not associated with similar emotions, or even those connected to positive emotions. Emotion's strong connection with memory also has to do with how much attention or focus an individual has on the event. If they are heavily emotionally involved in the event, a lot of their attention is directed at what's happening, rendering it a stronger memory. It is also the case with emotionally aroused situations that even if attention is limited, it is more likely that a memory associated with the strong emotion will remain as opposed to some neutral stimulus. Chemically, this is because the emotional and physical stress caused by traumatic events creates an almost identical stimulation in the brain to the physiological condition that heightens memory retention. It excites the neuron-chemical activity centers of the brain that affects memory encoding and recollection.[22] This reaction has been enforced by evolution as learning from high-stress environments is necessary in "fight or flight" decisions that characterize human survival.

Post-traumatic stress disorder

Main article: Posttraumatic stress disorder

Post-traumatic stress disorder is a psychological disorder (in the same category as: reactive attachment disorder, disinhibited social engagement disorder, acute stress disorder and adjustment disorders) caused by exposure to a terrifying event or ordeal involving the occurrence or threat of physical harm or where a person learns these terrible events happened to a close family member or someone whom they care about. It is one of the most severe and well-known of the different types of psychological trauma, mostly due to its prevalence in war veterans. It can manifest itself as early as after the first year of life.[23] Typically symptoms include avoidance of reminders of the traumatic event or mention thereof, irritability, trouble sleeping, emotional numbness and exaggerated reactions to surprises. One of the most common and powerful symptoms, is the recurrence of random intense memories from the event (intrusive thoughts). This can manifest itself in different ways such as flashbacks of the event and unwanted thoughts about the trauma (e.g. "why did this happen to me?").[24] PTSD patients who have gone through different traumatic experiences will have small variances in their symptoms, mostly insignificant. For example, PTSD patients who were rape victims will have aversion to words such as touch and dirty while patients who were in a fire or war experience will respond similarly to words like burn or fight.[24]

As mentioned above, the stress of PTSD can have an adverse effect on memory.[25] Specifically, this can have severe effects on the hippocampus,[26] including decrease in hippocampus volume,[27] causing problems with transferring short-term to long-term memory, and with the formation of short-term memories.[28][29] To expand on the relationship between PTSD and hippocampal volume, one meta-analysis found that individuals diagnosed with PTSD have significantly smaller hippocampi volumes compared to controls.[30] Another meta-analysis found that in adults who experienced childhood trauma, the hippocampi were smaller than control hippocampi.[31] In a broad overview, individuals with PTSD who have impairments to their memory generally have this impairment in their verbal memory,[32] more so than their visual memory.[33]

Though studies show that there is no singular way in which patients' memories are affected by PTSD.[34] North Korean refugees with PTSD were found to have generally lower scores on memory tests than control groups of refugees without PTSD. The early presentation of memory impairment compared to complications with other cognitive functions may be due to dysfunction in the hippocampus.[35]

See also

References

  1. ^ a b c Foa, E. B. (1993). "Posttraumatic stress disorder in rape victims". American Psychiatric Press Review of Psychiatry. 12: (pp. 273–303) – via Washington, D.C.: American Psychiatric Press.
  2. ^ a b Amir, Nader; Stafford, Jane; Freshman, Melinda S.; Foa, Edna B. (April 1998). "Relationship between trauma narratives and trauma pathology". Journal of Traumatic Stress. 11 (2): 385–392. doi:10.1023/a:1024415523495. ISSN 0894-9867. PMID 9565923. S2CID 42762378.
  3. ^ Davidson, J.R. (2000). Trauma: The impact of post-traumatic stress disorder. Journal of Psychopharmacology; 14(2 Suppl. 1):S5–S12.
  4. ^ Corkin, S. (2002). What's new with the amnesic patient H. M.? Nat. Rev. Neurosci. 3: 153-160.
  5. ^ Calabrese P, Markowitsch HJ, Harders AG, Scholz M, Gehlen W.(1995). Fornix damage and memory: A case report. (3):555-64. Physiological Psychology, University of Bielefeld
  6. ^ a b c d e f g h Liberzon, Israel; Sripada, Chandra Sekhar (2007), The functional neuroanatomy of PTSD: a critical review, Progress in Brain Research, vol. 167, Elsevier, pp. 151–169, doi:10.1016/s0079-6123(07)67011-3, ISBN 978-0-444-53140-7, PMID 18037013, retrieved 2021-11-17
  7. ^ a b c d e f g Sweeton, Jennifer (2019). Trauma treatment toolbox : 165 brain-changing tips, tools & handouts to move therapy forward. Eau Claire, WI. ISBN 978-1-68373-179-5. OCLC 1088900185.{{cite book}}: CS1 maint: location missing publisher (link)
  8. ^ a b c d e Lupien, Sonia J.; McEwen, Bruce S.; Gunnar, Megan R.; Heim, Christine (June 2009). "Effects of stress throughout the lifespan on the brain, behaviour and cognition". Nature Reviews Neuroscience. 10 (6): 434–445. doi:10.1038/nrn2639. ISSN 1471-003X. PMID 19401723. S2CID 205504945.
  9. ^ a b c d Garfinkel, Sarah N.; Liberzon, Israel (June 2009). "Neurobiology of PTSD: A Review of Neuroimaging Findings". Psychiatric Annals. 39 (6): 00485713–20090527–01. doi:10.3928/00485713-20090527-01. ISSN 0048-5713.
  10. ^ a b c Gilbertson, Mark W.; Shenton, Martha E.; Ciszewski, Aleksandra; Kasai, Kiyoto; Lasko, Natasha B.; Orr, Scott P.; Pitman, Roger K. (November 2002). "Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma". Nature Neuroscience. 5 (11): 1242–1247. doi:10.1038/nn958. ISSN 1097-6256. PMC 2819093. PMID 12379862.
  11. ^ a b c Warner-Schmidt, Jennifer L.; Duman, Ronald S. (2006). "Hippocampal neurogenesis: Opposing effects of stress and antidepressant treatment". Hippocampus. 16 (3): 239–249. doi:10.1002/hipo.20156. ISSN 1050-9631. PMID 16425236. S2CID 13852671.
  12. ^ a b c Young, Elizabeth A. (1991-08-01). "Loss of Glucocorticoid Fast Feedback in Depression". Archives of General Psychiatry. 48 (8): 693–699. doi:10.1001/archpsyc.1991.01810320017003. ISSN 0003-990X. PMID 1652926.
  13. ^ Abramovitch, Amitai; Short, Tatiana; Schweiger, Avraham (June 2021). "The C Factor: Cognitive dysfunction as a transdiagnostic dimension in psychopathology". Clinical Psychology Review. 86: 102007. doi:10.1016/j.cpr.2021.102007. PMID 33864968. S2CID 233291139.
  14. ^ Norrholm, Seth Davin; Jovanovic, Tanja (May 2018). "Fear Processing, Psychophysiology, and PTSD". Harvard Review of Psychiatry. 26 (3): 129–141. doi:10.1097/HRP.0000000000000189. ISSN 1465-7309. PMID 29734227. S2CID 13691655.
  15. ^ Squire, Larry S. (1987) Memory and Brain. New York, New York: Oxford University Press
  16. ^ Fuster, Joaquin M. (1995) Memory in the Cerebral Cortex: An Empirical Approach to Neural Networks in the Human and Nonhuman Primate. Cambridge, MA: The MIT Press.
  17. ^ Tarara, R., Else, J.G., Suleman, M.A., Sapolsky, R.M. (1989). Hippocampal damage associated with prolonged and fatal stress in primates. J Neurosci 9:1705-1711.
  18. ^ McNally, Richard J. (2006) Trends in Cognitive Sciences, Volume 10, Issue 6: Cognitive Abnormalities in Post Traumatic Stress Disorder. P271-277
  19. ^ Loftus, Elizabeth and Ketcham, Katherine. (1994) The Myth of Repressed Memory: False Memories and Allegations of Sexual Abuse. New York, New York: St. Martin's Press
  20. ^ Freud, Sigmund, and Breuer, Josef. (1895). Studies on hysteria
  21. ^ L. Cahill, B. Prins, M. Weber and J.L. McGaugh, (1999).4Beta-adrenergic activation and memory for emotional events. Nature 371, pp. 702–704
  22. ^ Christianson, S.A., & Loftus, E. (1990). Some characteristics of people's traumatic memories. Bulletin of the Psychonomic Society, 28, 195-198.
  23. ^ DSM-5 Task Force (2013). Diagnostic and statistical manual of mental disorders : DSM-5 (5th ed.). Arlington, VA: American Psychiatric Association. ISBN 978-0-8904-2554-1. OCLC 830807378.{{cite book}}: CS1 maint: numeric names: authors list (link)
  24. ^ a b Loftus, Elizabeth and Ketcham, Katherine. (1994) The Myth of Repressed Memory: False Memories and Allegations of Sexual Abuse. New York, New York: St. Martin's Press
  25. ^ Stricker, Nikki H.; Lippa, Sara M. (2017). "Elevated rates of memory impairment in military service-members and veterans with posttraumatic stress disorder". Journal of Clinical & Experimental Neuropsychology. 39 (8): 768–785. doi:10.1080/13803395.2016.1264575. PMID 27976973. S2CID 205804361.
  26. ^ Bremner, D. J. (2013). "The invisible epidemic: Post-Traumatic Stress Disorder, memory and the brain". The Doctor.
  27. ^ Emdad, R.; Sondergaard, H. P. (2005). "Impaired Memory and General Intelligence Related to Severity and Duration of Patients' Disease in Type A Posttraumatic Stress Disorder". Behavioral Medicine. 31 (2): 73–84. doi:10.3200/BMED.31.2.73-86. PMID 16130309. S2CID 40029018.
  28. ^ Emdad, R.; Sondergaard, H. P. (2006). "General intelligence and short-term memory impairments in Post Traumatic Stress Disorder patients". Journal of Mental Health. 15 (2): 205–216. doi:10.1080/09638230600608966. S2CID 144833060.
  29. ^ Emdad, R.; Sondergaard, H. P.; Theorell, Tores (2005). "Impairments in short-term memory, and figure logic, in PTSD patients compared to healthy controls with the same ethnic background". Journal of the International Society for the Investigation of Stress. 21: 33–44. doi:10.1002/smi.1034.
  30. ^ Smith, Michael E. (2005). "Bilateral hippocampal volume reduction in adults with post-traumatic stress disorder: A meta-analysis of structural MRI studies". Hippocampus. 15 (6): 798–807. doi:10.1002/hipo.20102. ISSN 1050-9631. PMID 15988763. S2CID 46206070.
  31. ^ Woon, Fu L.; Hedges, Dawson W. (2008). "Hippocampal and amygdala volumes in children and adults with childhood maltreatment-related posttraumatic stress disorder: A meta-analysis". Hippocampus. 18 (8): 729–736. doi:10.1002/hipo.20437. PMID 18446827. S2CID 31931903.
  32. ^ Johnsen, G. E.; Asbjornsen, A. E. (2008). "Consistent impaired verbal memory in PTSD: A meta-analysis". Journal of Affective Disorders. 111 (1): 74–82. doi:10.1016/j.jad.2008.02.007. PMID 18377999.
  33. ^ Bae, S. M.; Hyun, M. H.; Lee, S. H. (2014). "Comparison of Memory Function and MMPI-2 Profile between Post-traumatic Stress Disorder and Adjustment Disorder after a Traffic Accident". Clinical Psychopharmacology and Neuroscience. 12 (1): 41–47. doi:10.9758/cpn.2014.12.1.41. PMC 4022765. PMID 24851120.
  34. ^ Brewin, Chris R. (2003) Posttraumatic Stress Disorder: Malady or Myth?. New Haven and London: Yale University Press
  35. ^ Shin, J. E.; Choi, C. H.; Lee, J. M. (2017). "Association between memory impairment and brain metabolite concentrations in North Korean refugees with post traumatic stress disorder". PLOS ONE. 12 (12): e0188953. Bibcode:2017PLoSO..1288953S. doi:10.1371/journal.pone.0188953. PMC 5720673. PMID 29216235.
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