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Running head: NEUROSCIENCE, DISSOCIATIVE AMNESIA, AND REPRESSSED
MEMORY 1
The Neuroscience of Dissociative Amnesia and Repressed Memory:
Premature Conclusions and Unanswered Questions
Henry Otgaar1,2, Mark L. Howe3, Lawrence Patihis4, Ivan Mangiulli5, Olivier Dodier6, Rafaële
Huntjens7, Elisa Krackow8, Marko Jelicic1 & Steven Jay Lynn9
1Maastricht University, the Netherlands
2KU Leuven, Belgium
3City, University of London, UK
4University of Portsmouth, UK
5Universiti of Bari “Aldo Moro”, Italy
6University of Nîmes, France
7University of Groningen, the Netherlands
8West Virgiana University, US
9Binghamton University, US
In Press, Legal and Criminological Psychology
Correspondence should be sent to Henry.Otgaar@maastrichtuniversity.nl
Data can be found on: https://osf.io/wkph9/
The current version might deviate from the published version
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
2
Abstract
Purpose: A heated debate exists on whether traumatic memories can be dissociated or repressed.
One way in which researchers have attempted to prove the existence of dissociative amnesia or
repressed memory is to examine whether claims of amnesia for traumatic events are associated
with specific neural markers.
Methods: Here, we will argue that such neuroscientific examinations do not tell us whether
traumatic memories can be unconsciously repressed or dissociated from consciousness,
respectively.
Results: We discuss neuroscientific studies on dissociative amnesia and repressed memory and
show that there are no reliable biological markers for dissociative amnesia and that the alleged
involved brain areas are heterogenous among studies. Furthermore, we will demonstrate that it is
unclear whether these studies truly involved patients with dissociative amnesia and that
alternative explanations of dissociative amnesia were often not ruled out (e.g., malingering,
organic amnesia). Moreover, we will make the case that the discussed patients in the studies do
not meet the DSM-5 criteria for dissociative amnesia.
Conclusions: Taken together, neuroscientific research into dissociative amnesia does not present
a convincing case for a biological basis of the purported memory loss.
Keywords: Dissociative Amnesia; Repressed Memory; Memory Wars; Neuroscience
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
3
The Neuroscience of Dissociative Amnesia and Repressed Memory:
Premature Conclusions and Unanswered Questions
There is widespread interest in how traumatic experiences are remembered. Knowledge
on this topic is relevant for the clinical field as an aid in the diagnosis and treatment of those who
have developed psychological complaints as a result of experiencing traumatic events (Phelps &
Hofmann, 2019). In legal systems, victims, witnesses, and defendants oftentimes provide
testimony about traumatic events that they allegedly experienced (Otgaar et al., 2022). In
therapy, knowing whether traumatic memories are accurate and refer to experienced events is not
actually treated as a priority or considered necessary—but accuracy is crucially important in
legal contexts. That is, truth seeking is the cornerstone of the legal arena and hence, it is pivotal
to know how (accurate) traumatic experiences are recollected.
For many years, there has been a debate about whether traumatic memories can be
repressed or dissociated from consciousness and accurately recovered many years later (Loftus,
1994; Otgaar et al., 2019). Some clinicians assert that traumatic memories can be unconsciously
repressed or dissociated from consciousness1 and lie dormant for many years, to be exhumed in
therapy in their original unaltered form (e.g., van der Kolk & Fisler, 1995). However, other
clinicians and memory scientists have argued that therapeutic interventions used to ostensibly
unlock memories can be suggestive and may lead to the creation of false autobiographical
memories (Loftus & Ketcham, 1996; Piper et al., 2008). Also, empirical memory research has
1 1 We use the term repressed to refer to traumatic memories being stored in the unconscious and
not accessible to the conscious mind, whereas we refer to dissociated as similar to the concept of
repression in which trauma is stored, but temporarily not retrievable, yet (because it is stored) retrievable
at a later time.
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
4
shown that plausible alternative explanations exist for claims of repressed memory loss (e.g.,
ordinary forgetting including childhood amnesia) and that memories recovered spontaneously are
likely to be the result of ordinary memory mechanisms (e.g., ordinary forgetting). This
contentious debate regarding whether or not traumatic memories can be repressed or dissociated
or not has also been termed the memory wars (Crews, 1995; Loftus, 1994; Lynn et al., in press).
In past years, some authors have claimed that there is neuroscientific evidence in favor of
the idea that traumatic experiences can be unconsciously repressed or dissociated from
consciousness. Specifically, some researchers have investigated the neural correlates of claims of
dissociative amnesia which is a disorder analogous to repressed memory, but is also used as a
diagnostic criterion of posttraumatic stress disorder (PTSD) or dissociative identity disorder
(DID; e.g., Staniloiu & Markowitsch, 2012). As we will explain, the diagnostic criteria of the
disorder dissociative amnesia are strikingly similar to the tenets of the concept of repressed
memory in which the core idea is that traumatic memories can be completely abolished from
consciousness and retrieved in original form (Otgaar et al., 2021; Pope et al., 2022).
In the current article, we will provide a critical discussion of what such neuroscientific
studies can and cannot tell us about whether traumatic memories can be unconsciously repressed
or dissociated. Specifically, we provide a critical discussion of neuroscientific studies on
dissociative amnesia. We will first provide a general overview of these neuroscientific studies
and critically review the observed key findings. That is, we will present a literature search on
these neuroscientific studies and first examine which brain regions are allegedly associated with
the claimed traumatic memory loss. Second, we will provide several critical comments on
whether neuroscientific research on dissociative amnesia and repressed memory actually
included participants with dissociative amnesia. Third, we will discuss methodological and
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
5
conceptual problems and argue that the key claims of neuroscientific research on dissociative
amnesia and repressed memory are seemingly in contrast with the tenets of dissociative amnesia.
Finally, we will provide recommendations for this relatively young field with a strong focus on
advocating open science practices.
The Neuroscience of Repressed Memory and Dissociative Amnesia
The kernel of the concepts of repressed memory and dissociative amnesia is that when
people experience severe traumatic events such as childhood sexual abuse, defense mechanisms
need to be applied to deal with the overwhelming nature of the psychological trauma. Purported
underlying mechanisms are, for example: 1) repression whereby automatically and
unconsciously traumatic memories are processed, or 2) dissociation which is regarded as an
"unconscious, automatic, defensive coping response to highly aversive events” (Lynn et al.,
2022, p. 22.3; but see also Ross et al., 2022 for a discussion on the conceptualization of
repression and dissociation). For example, instead of the term repressed memory, the term
dissociative amnesia is often used to designate traumatic memory loss (Mangiulli et al., 2022;
McNally, 2023). When examining the criteria of dissociative amnesia in the DSM–5 (American
Psychiatric Association, 2013), they are strikingly similar to the tenets of repressed memory (see
Otgaar et al., 2019; McNally, 2023). Both conceptualizations include the idea that memory loss
is due to a coping response needed to deal with the trauma, that the memory becomes
inaccessible to retrieval, and that it can be accurately recalled in its original form at a later point
in time.
For several years, studies have examined the neural markers of dissociative amnesia that
might provide clues regarding the mechanisms underlying the memory loss for trauma. For
example, Kikuchi and colleagues (2009) had two patients with purported dissociative amnesia
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
6
and control participants undergo fMRI and concluded that “memory repression in dissociative
amnesia is associated with an altered pattern of neural activity” (p. 620). Such a statement
strongly implies that dissociative amnesia can be readily identified using brain imaging tools.
Which Memory Systems and Brain Areas are Involved?
We conducted a literature search to identify relevant papers examining the different brain
areas that scholars have claimed to be involved in cases of dissociative amnesia and repressed
memory. The search was conducted on September 22 and October 12 and 26, 2022. We
attempted to find all relevant papers published prior to 2022. We inspected the Web of Science
database using several search terms (see https://osf.io/zkwhj). Our search identified 207 hits.
After removing duplicates, screening (i.e., looking at the title and abstract), and assessing papers
for eligibility, 29 papers remained. Four extra papers were identified from Mangiulli et al.’s
(2022) critical review on case studies of dissociative amnesia leading to a final set of 33 papers
(see Figure 1; see also https://osf.io/wkph9/). Specifically, we only included papers in which
researchers used brain imaging tools to examine the neural correlates of repressed memory and
dissociative amnesia and review papers in which researchers proposed brain regions involved in
dissociative amnesia and repressed memory.
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
7
Figure 1. PRISMA Flowchart of included papers
What becomes clear from this body of evidence is that different brain imaging tools have
been used to examine potential brain regions involved in dissociative amnesia and repressed
memory. Such methods include structural methods (e.g., MRI [13 papers; 39%] and functional
methods (fMRI [5 papers; 15%], EEG [4 papers; 12%], PET [8 papers; 28%]; Table 1). Seven
papers (21%) examined the neuroscience of dissociative amnesia or repressed memory using a
functional method called single-photon emission computerized tomography (SPECT; e.g., Efrati
et al., 2018). Structural methods are used to quantify volume of the brain structure whereas
functional methods are used to study the functions of brain regions.
A key result from our search was the great variability of brain regions found to be
involved in reports of dissociative amnesia. Specifically, across papers, a bit over half of them (n
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
8
= 21; 64%) noted that the (pre)frontal cortex was associated with the dissociative memory loss.
However, which specific area of the prefrontal cortex (e.g., dorsolateral, orbitofrontal) was
involved varied as well across studies. There was also much variation in other involved brain
areas with papers mentioning areas such as left fusiform gyrus (1 paper; 3%), hippocampus (7
papers; 21%), temporal cortex (14 papers; 42%), parietal cortex (4 papers; 12%), and the
precuneus (2 papers; 6%). Many of these brain areas are involved in the function of memory
(e.g., Lundstrom et al., 2005), but it is remarkable that no clear and consistent pattern emerged in
terms of which brain areas are associated with dissociative amnesia. Of course, this outcome
might also be due to the use of different tasks that subjects performed during functional imaging
(see Table 1) and the use of structural versus functional methods.
Another result from our search is that in most functional imaging studies, the tasks used
or the instructions to participants during imaging were not specified or did not tap into
dissociative amnesia for autobiographical events, but rather other memory systems or no
memory systems at all. For example, in a study by Brand et al. (2009), participants were only
instructed to be relaxed and to not think about specific issues (i.e., resting state). Other studies
have included tasks as varied as classifying words as real words versus nonwords, listening to
rare tones and sentences. Unless in the context of DID, where patients may report deficits in
other memory systems, these tasks and instructions are not related to the dissociative amnesia for
autobiographical life events as defined in the DSM-5 dissociative amnesia criteria.
However, even within and among the use of these methods, there was large variation. To
give some examples, Chechko et al. (2008) used fMRI in a patient with dissociative amnesia.
They found that although the patient could not recognize the faces of friends and relatives, there
was increased activity in the hippocampus. This finding is in stark contrast to Kikuchi and
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
9
colleagues (2009) who also used fMRI and reported reduced activity in the hippocampus. To
further complicate matters, Glisky et al. (2004) noted that there were not many differences in
brain activations between patients and control participants. These inconsistencies also emerged
when structural imaging methods (MRI) were used. For example, whereas MacDonald and
MacDonald (2009) and Reinhold and Markowitsch (2009) found no brain structure abnormalities
in their patients with dissociative amnesia, Tramoni et al. (2009) found structural changes in the
prefrontal cortex.
This latter finding is interesting as it is reminiscent of discussions regarding whether
traumatic stress can cause smaller hippocampal volumes in people with PTSD (e.g., Bremner,
1999; 2002). However, Jelicic and Merckelbach (2004) argued that most of these studies
contained several methodological flaws (e.g., use of cross-sectional studies), and therefore any
causal relation between traumatic stress and reduced hippocampus could not be established. In
fact, longitudinal MRI research on hippocampal volumes in trauma survivors showed that
survivors who developed PTSD 6 months after exposure to a traumatic event did not have
smaller hippocampal volume than survivors who did not develop PTSD (Bonne et al., 2001).
Also, there is research suggesting that smaller hippocampal volumes are not a consequence, but a
risk factor for developing PTSD that questions the direction of the causal relation, if any (see for
a review Szeszko et al., 2018).
Taken together, the papers examining the brain areas associated with reported
dissociative amnesia provide a far from consistent picture concerning its neural underpinnings.
Although myriad reasons might be related to this heterogeneity, we now draw attention to what
we believe is especially imperative in discussions of dissociative amnesia. That is, did the
included papers really involve people with dissociative amnesia?
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
10
Did These Cases Really Assess Dissociative Amnesia?
A central issue when examining the neural correlates of dissociative amnesia (and
repressed memory) is to know with a degree of certainty that patients who were tested did indeed
suffer from dissociative amnesia. Mangiulli and colleagues (2022) reviewed 128 case studies on
apparent dissociative amnesia that were published over the past 20 years (2000–2020). Their
analysis showed that although all cases involved reported autobiographical memory loss, none
was fully in line with the DSM–5 criteria for dissociative amnesia. For example, in a quarter of
cases, no psychological trauma was reported to explain the claimed memory loss. Also, most
case studies did not rule out alternative, but plausible explanations for the purported memory loss
such as malingering or ordinary forgetting. In addition, in some cases it was not established that
the traumatic events were actually inaccessible for a time, or in others whether the traumatic
events were encoded initially and therefore available (i.e., recoverable) (see DSM-5 criteria for
dissociative amnesia).
In the selected papers in Table 1, 45% (n = 15) were also included in the critical review
conducted by Mangiulli et al. (2022). Arguably, the authors of these 15 papers did not truly
examine patients with dissociative amnesia that met DSM-5 criteria, but perhaps something
different such as malingering, amnesia with an organic cause, and so on. Hence, any detected
brain region might have nothing to do with dissociative amnesia but could be related to other
reasons such as faking memory loss, organic amnesia, or the co-occurrence of another
psychological disorder.
A case in point on whether dissociative amnesia was truly involved in the tested patients
is the study by Dimitrova et al. (2021). In that study, possible neurostructural markers of
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
11
dissociative amnesia were examined using MRI. One problem with this study is that dissociative
amnesia was measured using a subjective index of dissociative amnesia comprised of self-report
scores on the dissociative amnesia scale of the Dissociative Experiences Scale (DES; self-report
instrument). The DES amnesic subscale does not measure dissociative amnesia as defined in the
DSM-5 but instead measures individual’s self-reported experience of gaps in memory—and
centrally problematic to this is both the subjective nature of the measure and the fact that all
people experience gaps in memory through normal memory mechanisms. Hence, what they
measured was subjective amnesia and not objective amnesia (i.e., the inability to retrieve
information). This distinction is crucial, as the latter can only be measured by including a task
that objectively indexes memory functioning rather than the DES. In the context of DID, a whole
series of studies has indicated that once objective tasks are included to test subjective amnesia,
the results indicate there is actually transfer of information between identities in DID, both on
explicit and implicit memory tasks, neutral and trauma-related as well as autobiographical and
other self-relevant material (e.g., as an example see Huntjens et al., 2012 and Marsh et al., 2018).
Subjective reports of dissociative amnesia may be explained by specific dissociation-
related dysfunctional metamemory beliefs (i.e., metacognitive beliefs about one’s own memory
functioning). These include positive beliefs about amnesia (e.g. “I believe it is better to forget the
painful events that I experienced in life”), fear of losing control (e.g., “I believe I would lose
control of my life if I allowed myself to remember painful things that happened to me “), beliefs
about fragmentation (e.g., “I believe I can remember distressing events in parts, but not as a
whole”), and lack of self-reference (e.g., “I believe the bad things that I sometimes remember
happening in my life actually didn’t happen”). A recent study has indicated that patients with
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
12
DID score high on a scale developed to index these dysfunctional beliefs and in the general
population, these beliefs correlate strongly with scores on the DES (Huntjens et al., 2022).
Other examples similarly illustrate the possible misdiagnosis of dissociative amnesia.
Fukuzako and colleagues (1999) examined the P300 amplitude with participants they labelled as
having dissociative amnesia. Although the authors stated that they also examined malingering in
their patients, it is unclear what they exactly did and which tests were used to detect feigning
behavior. Also, Fukuzako et al. reported which events might have caused the traumatic loss.
Interestingly, at first sight, some of these events do not appear to meet the DSM-5 criterion for
traumatic stress (i.e., actual or threatened death, serious injury, or sexual violence) and are more
related to “ordinary” stress such as experiencing “trouble in love affairs.” Also, some of the
patients might have tried to forget these distressing events which is not the same as dissociative
amnesia. Finally, Mitsui and colleagues (2019) describe a man who was diagnosed with
dissociative amnesia, but they do not mention the specific psychological traumatic event that
purportedly precipitated the alleged memory loss.
To obtain a more precise assessment of whether the cases in Table 1 reflected
dissociative amnesia, we adopted the coding scheme as was used in Mangiulli et al. (2022) to
code the studies in our table that were not mentioned in Mangiulli et al.’s review. Specifically,
the case studies were coded on the following features: 1) was the person given a diagnosis of
amnesia, 2) differential diagnosis (did the case descriptions differentiate between dissociative
amnesia and other related conditions), 3) malingering, 4) alternative mechanisms, and 5)
diagnostic features (for a more detailed explanation, see https://osf.io/8hp2t; to view the coding,
see https://osf.io/n87qa and https://osf.io/srpuk). The first and fourth author coded the features
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
13
with interrater reliability agreements (Krippendorff’s alpha) ranging from .70 to 1 (see
https://osf.io/kch8n).
Following this coding, we examined all case studies (n = 51; including the ones included
in Mangiulli et al. (2022; see Table 1) and found the following. First, although in 38 cases (75%;
for similar results see Taïb et al., 2023), the authors mentioned the presence of trauma, 10 cases
(26%) were related to organic trauma. This is noteworthy as to qualify for a diagnosis of
dissociative amnesia, memory non-reporting must not be the result of an organic cause. Second,
we examined whether the case studies met the diagnostic features of the DSM-5. Only two cases
(3.9%) met all diagnostic features of dissociative amnesia (i.e., mentioning of trauma, not due to
substances, mentioning of type of dissociative amnesia, mentioning of duration of amnesic
period, and mentioning of impairment in functioning). However, even these two case studies
were not convincing examples of dissociative amnesia because in one a car accident was
mentioned as trauma indicating that an organic cause cannot be ruled out. In the other case,
losing a job was regarded as the traumatic cause and it was unclear whether malingering could be
fully ruled out. Equally interesting, in 13 cases (26%), no mention was even made of a possible
traumatic cause (see Figure 1; https://osf.io/wkph9/).
Collectively, case studies of dissociative amnesia are frequently hampered by the fact that
it is not certain whether the diagnostic criteria for dissociative amnesia are met. Therefore, it is
imperative that alternative explanations for amnesia be ruled out before the label of dissociative
amnesia is warranted (Mangiulli et al., 2022).
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
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Figure 1. Frequencies of type of alleged traumatic cause
0
2
4
6
8
10
12
14
Stress Confict with
relatives/parents
Trauma during
adulthood
Trauma during
childhood
Organic trauma Legal issues Unknown No trauma
reported
Frequency
Running head: NEUROSCIENCE, DISSOCIATIVE AMNESIA, AND REPRESSSED MEMORY 15
Table 1. Overview of papers on the neuroscience of dissociative amnesia and repressed memory
Study
Brain Areas involved in alleged memory loss
Main Used Imaging
Tool
In
Mangiulli
et al.,
(2022)
review
Sample
Task
instructions
Type of
Amnesia/Di
agnosis
How was
the
diagnosis
established?
Arzy et al.
(2011)
Functional changes in left posterior parietal
cortex (normal MRI)
fMRI/PET/EEG/MRI
No
1 patient,
12
compariso
ns
Subject had
to indicate
whether
certain
events
happened or
would
happen
(fMRI)
Psychogenic
amnesia
Psychiatric
evaluation
Back et al.
(1998)
CT and MRI showed lesions in temporal lobe,
no focal changes (SPECT)
CT/MRI/SPECT
No
1 patient
Psychogenic
amnesia
Confirmed
by detection
of
psychologic
al conflict
Botzung et al.
(2008)
Functional changes in medial temporal,
dorsolateral prefrontal cortex, tempero-parieto-
occipital loci
fMRI
Yes
1 patient
Retrieve
autobiograp
hical
memories
Psychogenic
amnesia
No
information
Brand et al.
(2009)
Decreased glucose utilization in right
inferolateral prefrontal cortex
PET
Yes
14
patients,
19
compariso
ns
Subjects had
to be relaxed
and not
think about
specific
issues.
Dissociative
amnesia
Dissociative
amnesia
based on
Structural
Clinical
Interview for
DSM-IV
Chechko et al.
(2018)
Stronger involvement of the left fusiform gyrus,
the bilateral hippocampus/amygdala region, the
orbitofrontal cortex, the middle temporal
fMRI
Yes
1 patient
Subject had
to learn
names or
Dissociative
amnesia
No formal
diagnosis
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
16
regions, and the precuneus, weaker involvement
of the hippocampus
look at
newly
presented
faces
Dimitrova et
al. (2021)
Reduced bilateral hippocampal CA1 subfield
volumes
MRI
No
32 DID
and 43
compariso
ns
Dissociative
amnesia/Dis
sociative
identity
disorder
Structural
Clinical
Interview for
DSM-IV
Dissociative
disorders
Efrati et al.
(2018)
Prefrontal cortex appeared suppressed
SPECT
Yes
3 case
studies
Repressed
memory
No
information
Fukuzako et
al. (1999)
Lower P300 amplitudes (not latencies)
P300
No
6 patients
versus 12
compariso
ns
Subjects had
to press a
button when
hearing rare
tones
Dissociative
amnesia
Patients
fulfilled
criteria for
DSM-IV
(but unclear
how this was
done)
Glisky et al.
(2004)
Much overlap in areas between patient and
control. No striatal activation in patient. Greater
parietal activation relative to frontal activation
fMRI
Yes
1 patient
versus 15
compariso
ns
Classify
words as
real words
or non-
words
Dissociative
amnesia
No formal
diagnosis
Kikuchi et al.
(2009)
Increased activity prefrontal cortex and
decreased left hippocampus, MRI, EEG, and
SPECT were normal
fMRI (MRI, EEG,
SPECT)
Yes
2 patients
Judge
whether a
face was
familiar and
recall
relation with
the familiar
face
Dissociative
amnesia
Based on
neuropsycho
logical
assessment
and DSM-5
criteria
Kitamura et al.
(2014)
High 5-HT1A receptor bindings in the right
superior and middle frontal cortex,left inferior
frontal and orbito frontal cortex and bilateral
inferior temporal cortex
PET/MRI
Yes
1 patient
versus 14
compariso
ns
No
information
Dissociative
amnesia
Based on
DSM-IV-TR
criteria
Kunii et al.
(2012)
Increase frontal cortex after retrieval
SPECT
Yes
1 patient
Psychogenic
amnesia
Psychiatric
evaluation
Kuo et al.
(2013)
Normal findings in EEG and CT
EEG/CT
Yes
1 patient
Dissociative
amnesia
No
information
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
17
Li et al. (2021)
Change in prefrontal cortex
CT
No
1 patient
Dissociative
amnesia
No formal
diagnosis
MacDonald &
MacDonald
(2009)
Normal EEG and MRI
EEG/MRI
Yes
1 patient
Dissociative
amnesia
No
information
Markowitsch
et al. (1997)
Normal CT/MRI, reduced perfusion in temporal
and frontal areas (SPECT), neural activity in
precuneus, parietal and prefrontal cortex
CT/MRI/SPECT/PE
T
No
1 patient
Listen to
sentences
Psychogenic
amnesia
No
information
Mitsui et al.
(2019)
Hypoperfusion in the right medial temporal
area.
SPECT
No
1 patient
No
information
Dissociative
amnesia
Based on
DSM-IV-TR
criteria
Reinhold &
Markowitsch
(2009)
No structural or functional brain pathology
detectable activation of frontal brain regions.
CT/MRI/PET
Yes
2 patients
(1 patient
underwent
imaging)
Dissociative
amnesia
No
information
Serra et al.
(2007)
Hyperintense signal in frontal lobes, atropic
changes in hippocampus
MRI/SPECT
Yes
2 patients
Psychogenic
amnesia
No
information
Smith et al.
(2010)
Normal MRI findings
MRI
No
1 patient
Functional/
psychogenic
amnesia
Neuropsych
ological and
psychiatric
evaluation
Thomas-
Anterion et al.
(2014)
Absence of structural lesion. Voxel-based
group analysis highlighted a metabolic
impairment of the right posterior middle
temporal gyrus
PET
Yes
3 patients
versus 15
compariso
ns
No
information
Dissociative
amnesia
No
information
Tramoni et al.
(2009)
Metabolic and structural changes in white
matter of right prefrontal cortex
MRI
No
1 patient
versus 25
compariso
ns
Functional
amnesia
No
information
Yasuno et al.
(2000)
Right anterior medial temporal region was
activated (PET), differences in activation levels
in anterior cingulate cortex and prefrontal
cortex (PET), CT and MRI were normal
PET/CT/MRI
No
1 patient
versus 12
compariso
ns
Indicate
whether
faces are
famous
politicians
Psychogenic
amnesia
In line with
DSM-IV
criteria
Weniger et al.
(2008)
Normal amygdala and
hippocampal size
MRI
No
23
patients
versus 25
compariso
ns
Dissociative
amnesia
Clinical
interview
and DSM-IV
criteria
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
18
Allesandro et
al. (2020)
Prefrontal dysfunction, hypometabolism in
right fronto-temporal area, mainly inferolateral
and anterior temporal prefrontal cortex
Review
No
Dissociative
amnesia
Bidzan (2017)
Prefrontal cortex, hippocampus, amygdala
Review
No
Dissociative
amnesia
Harrison et al.
(2017)
History of past head injury was more common
than relevant neurological symptoms
Review
No
53
patients
versus 21
patients
and 14
compariso
ns
Dissociative
amnesia
Joseph (1999)
High levels of arousal and traumatic stress exert
deleterious effects on the functional integrity of
the brain and the hippocampus.
Review
No
Dissociative
amnesia
Markowitsch
& Staniloiu
(2013)
Reductions in the temporo-frontal regions of
the right hemisphere. Subtle structural changes
in the white matter of the (right) frontal cortex
Review
Yes
5 patients
Dissociative
amnesia
Staniloiu &
Markowitsch
(2012a)
Synchronization abnormality between a frontal
lobe system, important for autonoetic
consciousness, and a temporo-amygdalar
system,
Review
Yes
Dissociative
amnesia
Staniloiu &
Markowitsch
(2014)
Disruption of prefrontal–temporal connectivity
Review
No
Dissociative
amnesia
Staniloiu &
Markowitsch
(2012b)
Right temporo-frontal hypometabolism
Review/PET
No
Dissociative
amnesia
Thomas-
Anterion
(2017)
Functional alterations in the bilateral
hippocampus, right temporal areas, and
inferolateral prefrontal cortex
Review
No
Dissociative
amnesia
Note. The Efrati et al. (2018) specifically mentioned repressed memory in their study while others specifically stated dissociative amnesia; The instructions
category were only added for studies using functional imaging tools and refers to the instructions that the subjects received during imaging. Review papers are
added at the end of the Table. All studies including comparison groups used healthy control participants except for the paper by Harrison et al. (2017)
Running head: NEUROSCIENCE, DISSOCIATIVE AMNESIA, AND REPRESSSED
MEMORY 19
Alternative Explanations
We next consider the important issue to discuss of whether neuroscientific studies on
dissociative amnesia can be explained by alternative, more plausible explanations for patient
reports of memory loss. For example, Mangiulli and colleagues (2022) found that organic brain
damage, instead of psychological coping mechanisms for trauma, could explain many of the
cases of reported autobiographical memory loss. In the reviewed studies (Table 1), Harrison et
al. (2019) also shared this view. They reviewed 53 patients with purported dissociative amnesia
and the authors found that “a history of past head injury was actually more common” (p. 2498).
Thus, it might well be the case that their autobiographical memory loss did not have a
psychological origin but was caused by, for example, head injury.
Another alternative explanation for the neural correlates found in some dissociative
amnesia cases is that the detected regions are actually related to other cognitive mechanisms. We
already mentioned the possibility of metamemory beliefs explaining reports of dissociative
amnesia (Huntjens et al., 2022). As another example, functional MRI research on motivated
forgetting has shown that similar brain areas are recruited during such forgetting (i.e., prefrontal
cortex) as the areas observed in the reviewed papers (Anderson & Hanslmayr, 2014). Thus, 21
(64%) of the identified papers mentioned involvements of the prefrontal cortex and some (or all)
of them might have nothing to do with dissociative amnesia but instead be linked to motivated
forgetting. Put another way, these areas may involve the conscious suppression of events people
do not want to recall.
FMRI studies have shown that the prefrontal cortex is involved in memory suppression
(Anderson & Hanslmayr, 2014). Although there is debate on the robustness of the memory
suppression effect (e.g., Bulevich et al., 2006; Wessel et al., 2020) and the motivated forgetting
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
20
effect (Patihis & Place, 2018), there is a possibility that the observed brain areas in the reviewed
studies are not related to dissociative amnesia but instead to active memory suppression, or
cognitive control more generally. It is important to stress here that memory suppression is
different from dissociative amnesia as the latter purportedly involve unconscious forms of
memory loss whereas suppression is an intentional act to forget memories. Also, research shows
that people who have experienced trauma frequently try to forget the trauma (McNally, 2005)
and therefore, some neuroscientific studies on dissociative amnesia might actually involve cases
of memory suppression or cognitive control.
The claimed involvement of the prefrontal cortex in dissociative amnesia might also be
indicative of deception in some cases (e.g., malingering). Specifically, investigations into brain
areas involved in deception have revealed the prefrontal cortex to play a chief role (e.g., Abe,
2011). This perspective fits well with concerns that some cases of autobiographical memory loss
might be due to deceitful attempts to claim amnesia (Jelicic, 2018; Mangiulli et al, 2022). To
recap, although the reviewed papers sometimes reported that the prefrontal cortex might be
related to dissociative amnesia, we argue that memory suppression might equally apply as an
alternative explanation.
To examine whether the authors of the included studies considered alternative
explanations, we coded all case studies in terms of whether or not the authors ruled out the
possibility that the claimed memory loss was due to normal forgetting, encoding failure, or
malingering. Importantly, the alternative explanations of normal forgetting and encoding failure
can only be coded for case studies in which the amnesia was localized (memory loss for a
specific period) or selective (remembrance of some aspects of an event but not all; APA, 2013)
(see Mangiulli et al., 2022). For these case studies, none mentioned that the memory loss might
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
21
be attributable to normal forgetting or encoding failures. Regarding malingering, only 37% (n =
19) of the case studies mentioned this as a possible alternative explanation. However, of these 19
cases, most did not elaborate on potential malingering and, for example, did not refer to the
context in which malingering might be a plausible explanation (e.g., criminal context, n = 17;
90%) or did not state how malingering was tested (n = 13; 68%). In short, only limited
information was present in the case studies concerning alternative explanations of the claimed
memory loss.
Conceptual and Methodological Problems
In this final section, we concentrate on several conceptual and methodological problems
that underlie neuroscientific investigations concerning dissociative amnesia and repressed
memory. First, the aim to find a structural biomarker of dissociative amnesia is incompatible
with the nature of the phenomenon (e.g., Dimitrova et al., 2021; Li et al., 2021; see Huntjens et
al., 2022 for a critical commentary on this issue). The DSM-5 definition is that dissociative
amnesia is always potentially reversible due to successful storage of the memory. It is for this
reason that some neuroscientific investigations have attempted to exclude structural brain
damage when diagnosing dissociative amnesia (e.g., Brand et al., 2009).
Second, neuroscientific studies on dissociative amnesia and repressed memory suffer
from other methodological limitations such as small sample size and lack of comparison groups.
For example, a minority of studies included comparison groups (n = 11; 33%). Furthermore, as
can be seen in Table 1, it is not uncommon that only a few patients were tested and that
conclusions were based on small sample sizes. Nonetheless, the small samples are
understandable given the alleged low prevalence of the disorder and the difficulty in recruiting
these patients who suffer great impairment in daily functioning. However, recent work has
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
22
suggested that published studies on biomarkers for psychological phenomena might yield
erroneous conclusions as many more participants are needed in such studies to obtain reliable
results (Marek et al., 2022). This possibility is echoed by recent work conducted by Mertens et
al. (2022) on the neural correlates of posttraumatic dissociation. The authors stressed that small
sample sizes in this area limited the interpretation of neuroscientific research into dissociation.
Their research contained the largest sample size using fMRI to identify neural regions of
dissociation and they did not observe any reliable neural marker of dissociation. Moreover, most
studies did not include corrections for multiple testing or make use of alternatives like robust
testing, further compounding these problems (Huntjens et al., 2022).
Additionally, the extant research (a) usually did not entail structural clinical interviews in
the diagnostic procedure, (b) did not consistently examine the role of comorbid psychopathology
as a determinant of outcomes secured or as a source of variability across studies; (c) did not
consistently include control groups of individuals matched for general psychopathology, distress,
arousal, and/or negative affect who do not report dissociative amnesia (Lynn et al., 2019; 2022);
and (d) was not based on longitudinal studies that ascertain whether patterns of brain structure,
activation, or anomalies implicated in dissociative amnesia are present prior to the onset of
amnesia or traumatic events. Moreover, what a biomarker is versus a correlate of dissociative
amnesia is rarely defined and specified, and as stated, the study designs sometimes lacked
(clinical) comparison groups (e.g., PTSD present/dissociative amnesia absent group) necessary
to rule out confounds that may have accounted for the detected neurobiological patterns.
Finally, even if these conceptual and methodological limitations were remedied, the
aforementioned investigations speak to relative differences in the magnitude of brain structures
or activity in people with and without dissociative amnesia, but they do not suggest empirically
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
23
based cut-off specifications needed to verify of dissociative amnesia, thereby showing limited
utility in legal and clinical arenas. The correlations researchers report are generally so weak that
they cannot be used for diagnostic purposes (see Huntjens et al., 2022)—in essence they are not
biomarkers to the same extent that medicine has reliable biomarkers for diseases (e.g., blood
tests for diabetes). To summarize, conceptual and methodological issues strongly limit the
interpretation of neuroscientific investigations of dissociative amnesia and repressed memory.
Conclusions and Recommendations
Debate continues regarding whether traumatic memories can be unconsciously repressed
(Brewin et al., 2019; Otgaar et al., 2019). To investigate the potential mechanisms underpinning
dissociative amnesia and repressed memory, researchers have examined the neural correlates of
dissociative amnesia and repressed memory. We provided a critical discussion of these
neurobiological studies on dissociative amnesia and repressed memory. Our main conclusion is
that these studies fall short on many different levels (e.g., conceptual and methodological).
Therefore, we argue that at present, these neuroscientific studies tell us little about whether
traumatic memories can be unconsciously blocked. Importantly, none of these proposed
biomarkers are sufficiently reliable for diagnosis in clinics or legal arenas. We will briefly
summarize the main problems and we will then end with several recommendations for future
research.
First, we have shown that neuroscientific studies have revealed a large number of brain
regions potentially involved in dissociative amnesia and repressed memory. This heterogeneity
makes it difficult to pinpoint whether any specific regions are involved in the purported
traumatic memory loss. Second, it is questionable whether the reviewed case studies really are
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
24
genuine dissociative amnesia cases—frequently they did not match the DSM–5 criteria. Third,
alternative explanations involving ordinary mechanisms can oftentimes better explain traumatic
memory loss, compared to the extraordinary mechanisms proposed by the dissociative amnesia
concept. This criticism is crucial because explanations such as malingering, metamemory beliefs,
and/or cognitive control might be candidates for the observed brains regions claimed to be
involved in dissociative amnesia. Finally, it can be said that many of the neurobiological studies
are plagued by methodological flaws such as small sample sizes. All in all, the research on the
purported neurological markers that underpin dissociative amnesia and repressed memory is
poorly developed.
To improve the status of neuroscientific research in this area, we offer several
recommendations. To begin with, considering the uncertain cause of the alleged memory loss,
one might wonder why the term “dissociative” is needed to describe this form of amnesia.
Mangiulli and colleagues (2022) proposed to use the term “amnesia of uncertain etiology” to
describe extreme forgetting with no organic cause. We concur with this suggestion, and we have
seen that researchers are already slowly using this terminology when describing unique case
studies concerning unclear autobiographical memory loss (Basagni et al., 2022). Furthermore,
using such a more neutral term would also benefit interpretating the possible causes of the
traumatic loss. That is, at present, discussions of dissociative amnesia often gravitate to whether
it has an organic, feigned, or dissociative etiology. According to Kopelman (2000), such
dichotomies might be too simplistic as case studies on extreme forgetting might be due to an
amalgam of organic, faked, and other reasons (see also Mangiulli et al., 2022). Second, because
we have noticed that neuroscientific studies on dissociative amnesia and repressed memory are
plagued by small sample sizes, we believe it is imperative that investment be made in team
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
25
science in this area (Forscher et al., in press). That is, since cases of alleged traumatic memory
loss are exceptional, working together with other teams worldwide would increase the amount of
cases in one particular study thereby increasing statistical power and obtaining more reliable
results.
Finally and relatedly, the field of dissociative amnesia (and repressed memory) would
benefit from more transparency and adherence to open science practices. Future neuroscientific
research on dissociative amnesia should include preregistration of research protocols that
stipulate in advance (a-priori) hypotheses, sample size, details of the methodology, planned
analyses, and cut-offs for ascertaining a biological marker. Additionally, post-research
implementation should make data available for other interested researchers to inspect, re-
analyze, and verify. Doing so is important because, as we have seen, in research in this area
many of these essential steps are not taken, and multiple analyses are often conducted on the
same data set, which might inflate false positive results (see Huntjens et al, 2022 for a detailed
discussion). Preregistration might increase research transparency regarding which analyses were
planned and which were done post-hoc in an exploratory fashion.
To conclude, we critically discussed neuroscientific research on dissociative amnesia and
repressed memory and argued that this research must be interpreted with great caution and
numerous caveats. Considering the fact that this area has been the subject of a controversial
debate regarding whether traumatic memories can be blocked and accurately surface after many
years, it is vital that neuroscientific research in this field is sound. At this time, there are no
consistent or reliable biomarkers of dissociative amnesia. Accordingly, biomarkers cannot be
used in diagnosis, and even the existence of the concept as a disease category still remains in
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
26
doubt. Therefore, we encourage researchers to collaborate in order to critically examine the
factors that underlie claims of extreme forgetting.
NEUROSCIENCE BEHIND DISSOCIATIVE AMNESIA AND REPRESSED MEMORY
27
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