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Cited by 473Posttraumatic Stress Disorder ResearchMemory and Neural MechanismsMemory Processes and Influences

Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)?

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Elzinga, B·2002·Journal of Affective Disorders
DOI 10.1016/s0165-0327(01)00351-2PMC PMC5580811
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Abstract

A model for the posttraumatic stress disorder (PTSD) as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD-patients is reviewed in relation to three brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, by way of its influence on these brain structures, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memory-functions in processing trauma-related information in PTSD. Implications of our model are reviewed.

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  • Smaller hippocampal volumes may be related to early life trauma because the hippocampus has a high density of glucocorticoid receptors and is highly sensitive to heightened release of cortisol, so chronic traumatic stress may lead to cell damage in this area.

    “Smaller hippocampal volumes may be related to early life trauma: the hippocampus has a high density of glucocorticoid receptors and is highly sensitive to a heightened release of the stress hormone cortisol—therefore, chronic traumatic stress may lead to cell damage in this area [31–34].”

    From Dissociation and Alterations in Brain Function and Structure: Implications for Borderline Personality Disorder (2017) · cites this paper as [33]

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  • The hippocampus and parahippocampal regions may be critical to the understanding of altered memory processing during dissociative states.

    “Furthermore, the hippocampus and parahippocampal regions may be critical to the understanding of altered memory processing during dissociative states [31–33, 61].”

    From Dissociation and Alterations in Brain Function and Structure: Implications for Borderline Personality Disorder (2017) · cites this paper as [33]

    Section 2.6 links dissociative reactions to impaired memory encoding, and section 4 proposes that hippocampal dysfunction may underlie trauma-related amnesia and fragmented memories. The paper does not identify parahippocampal regions as part of that explanation, so it supports only the hippocampal portion of the claim. (LLM, conf=0.85)

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Research works printed but not linked: 6

  1. American Psychiatric Association (APA) Diagnostic and statistical manual of mental disorders. 4. Washington DC: Author; 1994. [Google Scholar]
  2. Blanchard EB, Buckley TC. Psychophysiological assessment of posttraumatic stress disorder. In: Saigh P, Bremner JD, editors. Posttraumatic Stress Disorder: A Comprehensive Text. Allyn and Bacon; New York: 1999. pp. 248–266. [Google Scholar]
  3. Elzinga BM, Van Dyck R, van Spinhoven P. Three controversies about dissociative identity disorder. Clin. Psychol. Psychother. 1998;5:13–23. [Google Scholar]
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  5. Saigh PA, Bremner JD, editors. Posttraumatic Stress Disorder: A Comprehensive Text. Allyn and Bacon; New York: 1999. [Google Scholar]
  6. Uddo M, Vasterling JT, Brailey K, Sutker PB. Memory and attention in posttraumatic stress disorder. J. Psychopathol. Behav. Assessment. 1993;15:43–52. [Google Scholar]

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Authors
Elzinga, B.
Affiliations
Vrije Universiteit Amsterdam (NL)
Corresponding author
Elzinga, B
ORCID
Elzinga, B
Venue
Journal of Affective Disorders
Publisher
Elsevier BV
Published
2002-06
Volume
70
Issue
1
Pages
1-17
ISSN
0165-0327 (ISSN-L)
DOI
10.1016/s0165-0327(01)00351-2
PMC
PMC5580811
OpenAlex
W2168084483
Cited by
473
References
115
Citations by year
2026: 9 · 2025: 6 · 2024: 13 · 2023: 12 · 2022: 18 · 2021: 16 · 2020: 23 · 2019: 20 · 2018: 22 · 2017: 20 · 2016: 28 · 2015: 21 · 2014: 33 · 2013: 27 · 2012: 21
FWCI
18.10
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Affective Disorders (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Mental Health (R01MH056120)
Topics
  • Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
Keywords
post-traumatic stress disorder, memory disorders, intrusive memories, hippocampus, amygdala, medial prefrontal cortex, chronic stress, fear conditioning, memory retrieval, implicit memory
MeSH terms
Amygdala, Animals, Epilepsy, Post-Traumatic, Hippocampus, Humans, Hydrocortisone, Memory, Memory Disorders, Models, Neurological, Models, Psychological, Repression, Psychology, Stress, Psychological, Prefrontal Cortex

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