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European Journal of Psychotraumatology
ISSN: (Print) (Online) Journal homepage: https://www.tandfonline.com/loi/zept20
Trauma-related dissociation and the autonomic
nervous system: a systematic literature review
of psychophysiological correlates of dissociative
experiencing in PTSD patients
Sarah Beutler, Yoki L. Mertens, Liliana Ladner, Julia Schellong, Ilona Croy &
Judith K. Daniels
To cite this article: Sarah Beutler, Yoki L. Mertens, Liliana Ladner, Julia Schellong, Ilona
Croy & Judith K. Daniels (2022) Trauma-related dissociation and the autonomic nervous
system: a systematic literature review of psychophysiological correlates of dissociative
experiencing in PTSD patients, European Journal of Psychotraumatology, 13:2, 2132599, DOI:
10.1080/20008066.2022.2132599
To link to this article: https://doi.org/10.1080/20008066.2022.2132599
© 2022 The Author(s). Published by Informa
UK Limited, trading as Taylor & Francis
Group
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Published online: 02 Nov 2022. Submit your article to this journal
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REVIEW ARTICLE
Trauma-related dissociation and the autonomic nervous system: a systematic
literature review of psychophysiological correlates of dissociative
experiencing in PTSD patients
Sarah Beutler
a
*, Yoki L. Mertens
b
*, Liliana Ladner
a,c
, Julia Schellong
a
, Ilona Croy
a,d
and Judith K. Daniels
b
a
Department of Psychotherapy and Psychosomatic Medicine, Medical Faculty, Technical University of Dresden, Dresden, Germany;
b
Department of Clinical Psychology and Experimental Psychopathology, University of Groningen, Groningen, Netherlands;
c
Virginia Tech
Carilion School of Medicine, Roanoke, VA, USA;
d
Department of Clinical Psychology, Friedrich-Schiller University Jena, Jena, Germany
ABSTRACT
Background: Neurophysiological models link dissociation (e.g. feeling detached during or
after a traumatic event) to hypoarousal. It is currently assumed that the initial passive
reaction to a threat may coincide with a blunted autonomic response, which constitutes the
dissociative subtype of post-traumatic stress disorder (PTSD).
Objective: Within this systematic review we summarize research which evaluates autonomic
nervous system activation (e.g. heart rate, blood pressure) and dissociation in PTSD patients
to discern the validity of current neurophysiological models of trauma-related hypoarousal.
Method: Of 553 screened articles, 28 studies (N= 1300 subjects) investigating the physiological
response to stress provocation or trauma-related interventions were included in the final
analysis.
Results: No clear trend exists across all measured physiological markers in trauma-related
dissociation. Extracted results are inconsistent, in part due to high heterogeneity in
experimental methodology.
Conclusion: The current review is unable to provide robust evidence that peri- and post-
traumatic dissociation are associated with hypoarousal, questioning the validity of distinct
psychophysiological profiles in PTSD.
La disociación relacionada con el trauma y el sistema nervioso
autónomo: Una revisión bibliográfica sistemática de los correlatos
psicofisiológicos de la experiencia disociativa en pacientes con TEPT
Antecedentes: Los modelos neurofisiológicos vinculan la disociación (por ejemplo, la
sensación de desapego durante o después de un evento traumático) con la hipoactivación.
Actualmente se asume que la reacción pasiva inicial ante una amenaza puede coincidir con
una respuesta autonómica embotada, lo que constituye el subtipo disociativo del trastorno
de estrés postraumático (TEPT).
Objetivo: En esta revisión sistemática resumimos las investigaciones que evalúan la activación
del sistema nervioso autónomo (por ejemplo, la frecuencia cardíaca, la presión arterial) y la
disociación en pacientes con TEPT para discernir la validez de los modelos neurofisiológicos
actuales de la hipoactivación relacionada con el trauma.
Método: De 553 artículos seleccionados, se incluyeron en el análisis final 28 estudios (N=1300
sujetos) que investigaban la respuesta fisiológica a la provocación del estrés o a las
intervenciones relacionadas con el trauma.
Resultados: No existe una tendencia clara en todos los marcadores fisiológicos medidos en la
disociación relacionada con el trauma. Los resultados extraídos son inconsistentes, en parte
debido a la alta heterogeneidad en la metodología experimental.
Conclusión: La presente revisión no puede aportar pruebas sólidas de que la disociación peri y
postraumática esté asociada a la hipoactivación, lo que cuestiona la validez de los distintos
perfiles psicofisiológicos en el TEPT
创伤相关解离和自主神经系统：一项对PTSD 患者解离体验的心理生理相
关因素的系统文献综述
背景：神经生理学模型将解离（例如，在创伤事件期间或之后感到超然）与低唤起联系起
来。目前假设对威胁的初始被动反应可能与迟钝的自主反应同时发生，这构成了创伤后应
激障碍(PTSD) 的解离亚型。
ARTICLE HISTORY
Received 3 June 2022
Revised 29 August 2022
Accepted 13 September
2022
KEYWORDS
Biomarkers; autonomic
nervous system; dissociative
experiencing; threat
responding; defense
cascade; freeze; immobility;
heart rate; blood pressure;
skin conductance response
PALABRAS CLAVE
Biomarcadores; Sistema
Nervioso Autónomo;
Experiencia disociativa;
Respuesta a la amenaza;
Cascada de defensa;
Congelación; Inmovilidad;
Frecuencia cardíaca; Presión
arterial; Respuesta de
conductancia de la piel
关键词
生物标志物;自主神经系
统;解离体验;人格解体;现
实解体;威胁反应;防御级
联;冻结;不动;心率;心率
变异性;血压;皮肤电导反
应
HIGHLIGHTS
•There is no consensus on
physiological biomarkers
of trauma-related
dissociation.
•Peri- and post-traumatic
dissociation are
physiologically distinct
from stress reactions in
chronic states.
•Standardized
methodologies may
increase the
reproducibility and
specificity of
psychophysiological
biomarkers of dissociation.
© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which
permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
CONTACT Judith K. Daniels j.k.daniels@rug.nl Department of Clinical Psychology and Experimental Psychopathology; University of Groningen,
Grote Kruisstraat 2, 9712 TS Groningen, Netherlands
*These authors contributed equally to this work.
Supplemental data for this article can be accessed online at https://doi.org/10.1080/20008066.2022.2132599.
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
2022, VOL. 13, 2132599
https://doi.org/10.1080/20008066.2022.2132599
目的：在本系统综述中，我们总结了评估PTSD 患者自主神经系统激活（例如心率、血
压）和解离的研究，以认清当前创伤相关低唤起神经生理模型的有效性。
方法：在553 篇筛选出的文章中，28 项研究（N= 1300 名受试者）考查了对应激刺激或创
伤相关干预的生理反应，并被纳入最终分析。
结果：在创伤相关解离中，所有测量的生理标志物都没有明显的趋势。提取的结果不一
致，部分原因是实验方法的高度异质性。
结论：本综述无法提供稳健的证据表明创伤前后解离与低唤起有关，质疑了不同心理生理
特征在PTSD 中的有效性。
1. Introduction
‘Does anyone know of research documenting large
heart-rate decrease during episodes of psychological
dissociation?’. This question, posted in ResearchGate
(2016), incited an ongoing debate in the psychotrau-
matology community by calling into question the
accepted notion that dissociation is related to psycho-
physiological hypoarousal (Iffland et al., 2020; Pole,
2007). This article thus seeks to provide a systematic
and comprehensive overview on autonomic markers
of trauma-related dissociation. In the following, we
will (1) briefly summarize key theoretical models
related to the psychophysiology of peri- and post-trau-
matic dissociation, and (2) systematically review exist-
ing findings on the relationship between dissociation
and the autonomic nervous system (ANS) in PTSD.
1.1. Psychophysiology of post-traumatic stress
disorder and dissociation
PTSD is diagnosed when a person experiences auto-
nomic hyperarousal and symptoms of vivid re-experi-
encing, avoidance, and negative changes in mood and
thought within one month of the traumatic incident.
Hyperarousal refers to an active stress response to a per-
ceived threat characterized by hypervigilance, exagger-
ated startle response, irritability, disturbed sleeping
patterns, and the inability to concentrate (American
Psychiatric Association, 2013). Early studies (Orr,
1997;Orretal.,2002; Orr & Roth, 2000) demonstrated
that most PTSD patients experience increased heart rate
under stressful conditions. Yet, a subset of traumatized
individuals (approximately one third) do not show such
hyperreactivity to threat cues. Other studies found auto-
nomic responses in PTSD patients to be either physio-
logically similar to controls or reduced from baseline
(Cuthbert et al., 2003;D’Andrea et al., 2013;Limberg
et al., 2011; McTeague & Lang, 2012). This divergence
from the standard hyperarousal phenotype of PTSD
towards a more blunted psychophysiological response
was later termed hyporeactivity or hypoarousal (D’An-
drea et al., 2013; Frewen & Lanius, 2006b; Terpou et al.,
2019). Further research by Lanius and colleagues
(Lanius et al., 2002; Lanius et al., 2005; Lanius et al.,
2006) employing trauma memory recall supports the
idea of two different PTSD profiles and paved the way
for the inclusion of a new diagnosis by the American
Psychiatric Association (2013) (might need to update
citation here). PTSD patients with decreased affective
and physiological responses, concomitant with altered
brain activity in fronto-limbic circuits were labeled
‘physiological non-responders’and would later fall
into the dissociative subtype of PTSD (American Psy-
chiatric Association, 2013; Lanius et al., 2010; Lanius
et al., 2012; Spiegel et al., 2011; Terpou et al., 2019).
1.2. Peri- and post-traumatic dissociation
Previous metanalyses demonstrate a robust link
between dissociative experiencing and exposure to
trauma (Rafiq et al., 2018; Vonderlin et al., 2018).
Trauma-related dissociation may be an innate defense
mechanism to cope with and detach from trauma or
trauma-related cues (Dalenberg & Carlson, 2012;
Lanius et al., 2012). Dissociation is characterized by a
sense of psychological detachment (Holmes et al.,
2005) which can manifest as depersonalization (i.e. feel-
ing disconnected from the surroundings), derealization
(i.e. feeling disconnected from the surroundings),
emotional numbing (Frewen & Lanius, 2006a), analge-
sia (Ludascher et al., 2010; Mickleborough et al., 2011;
Strigo et al., 2010), and immobility (Volchan et al.,
2011; Volchan et al., 2017). One can distinguish
between peritraumatic dissociation and post-traumatic
dissociation by the timing of dissociation relative to
the traumatic event (e.g. during or after). Post-trau-
matic dissociation includes dissociative reactions
towards a real or experimental threat within a short
time scale (e.g. within the hour) (Carlson et al., 2018).
If these acute reactions occur repeatedly over time,
they may blend into a chronic state where dissociation
is experienced daily (i.e. trait dissociation). Between 6
and 45% of dissociative PTSD patients (Hansen et al.,
2017) exhibit more severe psychological symptoms
(more re-experiencing, higher suicidality, and impaired
role functioning) than non-dissociative PTSD patients
(e.g. Stein et al., 2013). It remains unclear which psy-
chobiological mechanisms underlie or illicit peri- and
post-traumatic dissociation. We will subsequently high-
light several theories which implicate acute defensive
reactions and altered ANS activity as the drivers of dis-
sociation in PTSD.
2S. BEUTLER ET AL.
1.3. The autonomic nervous system
The ANS, consisting of the sympathetic nervous sys-
tem (SNS) and parasympathetic nervous system
(PNS), regulates heart rate, respiratory rate, blood
pressure, and galvanic skin response. Broadly speak-
ing, an increase in SNS activity corresponds with phys-
iological arousal, as measured by elevated heart rate,
respiratory rate, blood pressure and skin conductance
(Bandler et al., 2000). Meanwhile, a decrease in SNS
activity and/or an increase in PNS activity corre-
sponds with the relative slowing of heart rate and low-
ering of blood pressure and skin conductance. In
addition, reduced SNS activity is associated with
increased heart rate variability parameters like the
high-frequency band or the root mean square succes-
sive, which can represent autonomic hypoarousal (see
Table 1). It should be noted, though, that sympathetic
and parasympathetic activity are not reciprocal, but
interact in a loosely coupled fashion (e.g. Billman,
2013; de Geus et al., 2019). Thus, blunted physiological
responses may reflect parasympathetic hyperactivity,
sympathetic hypoactivity or both (Bandler et al.,
2000), warranting a detailed assessment of quantifiable
biomarkers which underlie altered autonomic
responses in dissociation (see Table 1). In the follow-
ing, we will summarize key theoretical models that
have shaped the current scientific and clinical dialogue
on the psychophysiology of threat processing and
trauma-related dissociation.
1.4. Psychophysiological models
1.4.1. Defense cascade model
Incorporating animal research (for an overview see
https://fanselowlab.psych.ucla.edu/predatory-immine
nce-continuum/) and Mobbs’threat processing model
(Mobbs et al., 2009), the defense cascade model by
Lanius and colleagues (2018) posits that humans
under severe threat initially respond with an active
defense response (‘fight-and-flight’, characterized by
sympathetic dominance and endocannabinoid release)
and then exhibit SNS/PNS co-activation (‘tonic immo-
bility’). With a limited chance of escape, humans exhi-
bit a passive defensive response, characterized by
depersonalization/derealization symptoms (‘unre-
sponsive immobility’) and opioid release. Simul-
taneously the heart rate, blood pressure and skeletal
muscle tone go down (tonic immobility) (McKinnon
et al., 2016), which may be mediated by increased
top-down modulation of limbic brain regions includ-
ing the amygdala and periaqueductal gray (Lanius
et al., 2018; Nicholson et al., 2017).
Table 1. Abbreviations, full names, and short definitions of included physiological parameters.
Abbreviation Full name Definition
Cardiovascular parameters
BP Blood pressure Force of circulating blood on the walls of the arteries reported as a ratio: systolic/diastolic;
hypertension is related to increased sympathetic and decreased parasympathetic tone
SBP Systolic blood pressure Pressure when heart beats (BP is at its highest)
DBP Diastolic blood pressure Pressure when heart is at rest (BP at its lowest)
CRD Cardiovascular response discordance Measure for discrepancy; Low BP while HR is high, calculation = subtracting each
standardized BP score from the corresponding standardized HR score
FPV Finger pulse volume Via infrared plethysmography measured pulse wave obtaining information about HR and
peripheral volume blood flow; changes in FPV serve as indicator of sympathetic arousal
HR Heart rate How many times the heart beats in a given time period (typically one minute); sympathetic
and parasympathetic innervation
HRV Heart rate variability Variation in the time interval between consecutive heartbeats; reflects the regulation of
autonomic balance, blood pressure, gut, heart, vascular tone
HF-HRV High frequency heart rate variability Power of the high-frequency band (0.15–0.4 Hz); frequency domain; higher units are
associated with parasympathetic drive; magnitude of RSA
LF-HRV Low frequency heart rate variability Power of the low-frequency band (0.04–0.15 Hz); frequency domain; sympathetic and
parasympathetic involvement; but increased when dominant sympathetic drive
LF/HF-ratio Ratio of low frequency to high frequency
heart rate variability
Ratio of LF-to-HF power; frequency domain; value of interaction of parasympathetic (HF) and
sympathetic (LF) drive; increased ratio = increased sympathetic activity; decreased ratio =
increased parasympathetic and decreased sympathetic activity
RMSSD Root mean square successive difference Root mean square of successive interbeat intervals; time domain; is associated with the
parasympathetic drive
RSA Respiratory sinus arrhythmia Heat rate variability synchronized with breathing, increases with inhalation, and decreases
with exhalation; proposed indirect measure of vagal tone
IBI Interbeat interval Time between two heart beats; Conversion between HR and IBI: 60,000 / beats per minute =
one beat in milliseconds; same drive as HR
PEP Pre-ejection period Length of time between the contraction of the heart (onset of systole) and the ejection of
blood out of the heart and into the aorta (onset of left ventricular ejection); shorter PEP is
associated with an increase in sympathetic drive
Electrodermal parameters
SC Skin conductance Measurement of the skin’s ability to conduct electricity; based on activity of eccrine sweat
glands controlled by the sudomotor nerves; Synonym = electrodermal activity; sympathetic
drive
NSCF Number of skin conductance fluctuations Number of spontaneous fluctuations in skin conductance
SCL Skin conductance level Measure of the basal level of sweat gland activity; tonic, continuous, and slowly changing
SCR Skin conductance response Measure of changes in sweat gland activity as discrete responses to stimuli; highly correlated
with sympathetic activity; indicator of emotional arousal/distress
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 3
The proposed psychophysiological defense stages
correspond to the severity of dissociation. Following
a threat, the type of defensive response in PTSD
(hyper- vs. hypoarousal) depends on the severity of
dissociative symptomatology (Terpou et al., 2019). In
sum, this model conceptualizes dissociation in terms
of depersonalization, derealization and emotional/
physical numbing and suggests that the initial peri-
traumatic reaction (i.e. shock) can become a con-
ditioned response, triggered by trauma cues or
stressors (Lanius et al., 2018) in accordance with the
inescapable shock model (van der Kolk, 1988). Follow-
ing this rationale, the initial psychophysiological
response to a trauma (peritraumatic) and to a trauma
cue/stressor (acute post-traumatic dissociation) may
over time result in a chronic dissociative state. To
date, few neurophysiological studies have assessed
peritraumatic, acute, and trait dissociation within
one cohort (e.g. Bichescu-Burian et al., 2017;
Hauschildt et al., 2011), and longitudinal research is
warranted to better understand the hypothesized etio-
logical continuity of passive defensive responding in
humans.
1.4.2. Shutdown model
The shutdown model by Schauer and Elbert (2010) clo-
sely resembles the defense cascade model, but classifies
six distinct stages of threat response. After an initial
orienting response (1. ‘freeze’), the body under threat
prepares to escape (2. ‘flight’), then attack (3. ‘fight’). If
both options fail to eliminate the threat, the body sub-
verts to a state of unresponsive immobility (4. ‘tonic
immobility’), and shut-down (5. ‘flag’) which may pro-
gress to fainting mediated by disgust (6. ‘faint’) as the
body surrenders to the threat (i.e. the attacker). Simi-
lar to the defense cascade model (Lanius et al., 2010;
Lanius et al., 2012), the shutdown model describes
two distinct response profiles: the Type 1 ‘uproar-
PTSD’, characterized by dominant sympathetic acti-
vation, and Type 2 ‘shutdown-PTSD’, characterized
by dominant parasympathetic activation and includ-
ing patients who follow the cascade at least until
stage 4. The authors propose that the initial threat
response informs subsequent physiological reactivity,
where the hypersensitized trauma-related fear net-
work is easily reactivated, eliciting the initial psycho-
physiological defense response. Thus, an individual
who exhibits a parasympathetic-dominant reaction
(e.g. flag or faint) to the trauma is more likely to
experience an acute post-traumatic dissociative
response, accompanied by inhibition of the SNS, acti-
vation of the PNS, and reduction in heart rate and
blood pressure. For instance, a study of PTSD patients
demonstrated that experiencing acute dissociation
during trauma recall (via personalized trauma audio-
scripts) is associated with reduced heart rate (Sack
et al., 2012). It is unknown whether these individuals
experienced a similar initial peritraumatic response.
The model does not explicitly state that the (repeated)
PNS-dominant physiological reactions to trauma cues
share similar features to chronic post-traumatic dis-
sociation. However, the characterization of the shut-
down model of PTSD suggests that the stable
dissociative response pattern may be a conditioned
automatic response to stressors and perceived threat
(Schauer & Elbert, 2010).
1.4.3. Freeze and tonic immobility
Another model of threat-responding is one in which
two alternative pathways lead to tonic immobility
(Hagenaars et al., 2014; Roelofs, 2017). In this mode,
the initial orienting response to a threat is followed
by either the fight/flight response or the freeze
response. The latter is characterized by immobility,
bradycardia and increased muscle tonus accompanied
by concomitant SNS-PNS activation. The authors
describe that rapid shifting between the two defensive
behaviors of fight/flight and freeze is possible. If both
options fail, the body enters a state of tonic immobility
(‘death feigning’or ‘playing dead’), characterized by
motor inhibition, muscle rigidity and the inability to
express oneself vocally (Kuiling et al., 2019). Tonic
immobility (i.e. hypotension or unresponsiveness) is
conceptualized as a more passive defensive response
as opposed to freezing. In this model freezing is associ-
ated with, and is thus measurable via, reduced body
sway (see also Volchan et al., 2017;2011). Roelofs
(2017) emphasizes the lack of evidence on the physi-
ology of tonic immobility in humans but suggests
that freezing may be linked to a maladaptive
emotional response which precedes the development
of PTSD, necessitating further longitudinal research
in this field. Importantly, this model does not associate
defensive behavior with dissociation, but portrays dis-
sociation and tonic immobility as related but different
constructs (Abrams et al., 2009; Hagenaars, 2016;
Lima et al., 2010).
1.4.4. Polyvagal theory
The polyvagal theory, developed by Stephen Porges
(2003,2007,2011), has received substantial attention
in the psychotraumatology field. Porges emphasizes
the evolutionary relevance of the vagal nerve in facil-
itating arousal states, mobilization and immobiliz-
ation, and social engagement. According to Porges,
the vagus nerve can be differentiated into three differ-
ent branches with evolutionarily selective advantages
in regulating autonomic functioning (2003). First,
the unmyelinated vagus branch (e.g. the dorsal vagal
complex) is associated with immobilization (e.g.
fainting, shutdown, dissociation), bradycardia and
decreased muscle tone. The second branch, the sym-
pathetic-adrenal branch, is active during mobiliz-
ation behaviors (e.g. fight/flight) when under attack.
4S. BEUTLER ET AL.
The final branch, themyelinatedbranch(e.g.theven-
tral vagal complex), regulates cardiac vagal activity
and withdrawal via inhibition of the sympathetic
branch, which corresponds with decreased arousal,
social engagement and (self-)soothing behaviors
(Porges, 2007). Through this framework, dissociative
responding in humans is purely a defensive immobil-
ization response modulated by the dorsal vagal com-
plex and associated with large heart rate decreases.
This immobilization response occurs when behaviors
initiated by the ventral vagal complex (e.g. social
engagement) or the sympathetic-adrenal pathway
(e.g. active defensive behavior) are not possible.
Indirect support for this model is seen in studies
which have proven that trait dissociation is nega-
tively correlated with heart rate during experimen-
tally-induced social stress (Powers et al., 2021;
Simeon et al., 2008).
1.4.5. Window of tolerance
The window of tolerance model (Corrigan et al.,
2011; Ogden et al., 2006;Siegel,1999) states that
trauma, particularly prolonged childhood trauma,
can result in high autonomic sensitivity towards
stressors and an imbalance in the dopaminergic sys-
tem associated with rapid, uncontrolled shifting
between two distress dipoles (also termed ‘biphasic
rollercoaster’, Corrigan et al., 2011, p. 20). When
exposed to trauma cues, patients switch between
an SNS-dominated high-arousal state of active
defensive responding (e.g. fear, anger, impulsivity,
vigilance) and a PNS-dominated low-arousal ‘pas-
sive defensive’state of emotional coping (e.g. sub-
mission, depression, and numbing). To manage
these extremes, the window of tolerance represents
a zone of psychological and autonomic flexibility: a
balanced psychophysiological state allowing for
flexible shifting, regulation, and integration of
emotions, so they become tolerable.
In regards to dissociation, this model hypothesizes
a noradrenergic lateral tegmental limbic forebrain –
midbrain circuit (Bergmann, 2008), which activates
the PNS and downregulates affect (both positive and
negative), leading to emotional numbing and cogni-
tive dissociation. Indirect support for this hypothesis
was found in a study by Krause-Utz and colleagues
(2018). This study found a strong positive association
between acute dissociation and PNS-mediated heart
rate variability when patients (with comorbid PTSD
and borderline personality disorder) were instructed
to downregulate emotion, but passively viewing affec-
tive pictures. Although not explicitly stated, the
authors draw a clear link between the initial physio-
logical effects of trauma and subsequent SNS and
PNS-mediated responses, with the latter including
numbing, collapse, and dissociation.
1.5. Summary and study aim
Taken together, current theories of ANS-mediated
defensive behaviors share a common framework,
mainly in that dissociation is (a) a defensive reaction
to traumatic stressors or reminders, (b) related to
parasympathetic dominance, and (c) associated with
a muted psychophysiological response (i.e. hypoarou-
sal; Pole, 2007). However, these theories differ in their
use of terminology, such as the meaning of freezing
and its corresponding physiological correlates. In the
shutdown model, freezing is part of the orienting
response, but Hagenaars and colleagues (2014) dis-
tinguish these two physiological states as unique
experiences. Additionally, this model does not men-
tion other defensive stages following tonic immobility,
as suggested by the shutdown model (e.g. flag) and
defense cascade model (e.g. collapsed freeze). On the
other hand, congruity across models can be found in
their neurophysiological correlates of threat response.
Importantly, some of these theories either do not
address dissociation at all or fail to specify how they
conceptualize dissociation. It remains unclear whether
acute dissociation as a defensive response shares simi-
lar psychophysiological characteristics with peritrau-
matic (i.e. during a trauma) or post-traumatic
dissociation (e.g. a stable behavioral pattern following
the trauma). Another general criticism of the afore-
mentioned models, particularly the polyvagal theory
(see Grossman & Taylor, 2007), concerns the oversim-
plification of biological processes and the assumption
of similarity between human and animal psychophy-
siology, due to its basis on partially outdated theoreti-
cal conceptualizations of human evolutionary biology
(see Barrett, 2020, for critical reflection; for instance,
the triune brain theory by MacLean, 1990)
The current study aims to provide more clarity on
the question of whether dissociation in PTSD patients
is related to autonomic hypoarousal. To this end, a
systematic literature search was conducted on research
in human subjects evaluating both psychophysiologi-
cal markers, (e.g. heart rate, blood pressure, and skin
conductance) and dissociative experiences in PTSD
patients.
2. Methods
2.1. Search strategy
This systematic review was conducted with studies pub-
lished until 21 March 2022, following the Preferred
Reporting Items for Systematic Review and Meta
Analysis for Individual Patient Data (PRISMA-IPD;
Stewartetal.,2015) procedures. 801 articles were
identified through searches in Web of Science,
PubMed, PsycArticles, and PTSDpubs, using keywords
which combined dissociative symptoms according to
the dissociative subtype (dissociat*, dissociative,
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 5
depersonali#ation, dereali#ation, DP/DR), PTSD (PTSD,
post-traumatic stress disorder, posttraumatic stress dis-
order, post-traumatic stress disorder) and ANS-related
physiological markers (heart rate, HR, HRV, ECG, elec-
trocardiogram, cardiac, cardiovascular, skin conduc-
tance, SC, SCR, electrodermal blood pressure, BP,
systolic,diastolic,temperature,eye,pupilsize,pupillary
dilatation, pupil* diameter, startle response, respiratory
sinus arrhythmia, respira*, breath*, ANS, autonomic
nervous system, parasympath*, sympath*, PNS, SNS,
visceral nervous system). Keywords within one concept
were combined with the ‘OR’command, while the con-
cepts (dissociation, PTSD, and physiological markers)
were combined with the ‘AND’command. Search
terms on muscle tension (muscle tone, muscle tension,
body sway, electromyography, EMG) were also included.
Although skeletal muscles are not part of the ANS, they
are of interest as part of the physiologic stress response.
However, this search term revealed no studies worthy of
inclusion.
Of all 801 articles, 204 were duplicates and 44 were
not peer reviewed articles. Once removed, this left 553
relevant peer reviewed articles for further evaluation.
All 553 articles were screened by two independent
reviewers using the title, abstract, and methods (inter-
rater reliability: 0.83). Inclusion criteria were: (a)
study participant age equal to or greater than 18, (b)
at least 5 patients with a PTSD diagnosis or meeting cri-
teria for PTSD diagnosis included, (c) experimental
studies with trauma-related interventions (e.g. recall,
script, film) or stress provocation (e.g. Trier Social
Stress Test, acoustic startle), (d) with measurable and
specific autonomic outcomes, and (e) designed in either
a correlative (e.g. dissociation and physiological mar-
ker) or comparative (e.g. physiological marker across
low dissociation vs. high dissociation subgroups) man-
ner. Exclusion criteria were (a) animal studies, (b) dis-
sociation not assessed, (c) assessment of treatment
outcome or baseline/resting state only, and (d) PTSD
assessment after experimental intervention (prospective
design). In the case of diverging ratings, which did
occur for 21 articles, they were assigned by mutual con-
sensus. After the initial screening process, 65 relevant
studies remained to be analyzed further. Four studies
were excluded in this step for other reasons (see
Figure 1). For 49 of the remaining 61 studies, authors
were contacted to acquire missing patient data or ana-
lyses which could support the current review. We con-
tacted authors at least twice and 65% replied. A total of
28 studies were included in the final analysis (Table 2 &
Figure 1; for a list of non-included studies see Sup-
plemental Table S1).
2.2. Data extraction
A study coding spreadsheet was utilized to collect data
from each included study. Within the coding
spreadsheet was data on basic study information
(e.g. authors, year, title), sample characteristics (e.g.
sample size, mean age, gender, trauma history, PTSD
diagnosis or meeting criteria), experimental condition
(e.g. traumatic content, stress evoking, acoustic star-
tle), on which value scores were based (e.g. change
score –trauma condition minus neutral condition,
change score –trauma condition minus baseline,
specific trials), as well as indices (e.g. kind and score
of effect sizes, significances) of the physiological par-
ameters (see Table 1 for an overview of all parameters
included). It should be noted that, although we
focused on physiological activity during an interven-
tion, we also reviewed baseline scores (see Table S2
in the supplement). The spreadsheet also included
comments to further define specific trials, as well as
notes on our statistical procedures if effect sizes were
not directly taken from the original publication.
2.3. Publication bias
Publication bias remains an important issue in
psychological and medical research (Head et al.,
2015; Thornton & Lee, 2000). However, Pole (2007),
who conducted the most comprehensive meta-analy-
sis on psychophysiological markers and PTSD, argued
that studies measuring psychophysiological activity
may be less affected by publication bias because they
often report multiple physiological measures, increas-
ing the likelihood of non-significant results or results
contrary to the hypothesis. Although an earlier
meta-analysis on heart rate variability and anxiety dis-
orders in general (Chalmers et al., 2014) and PTSD
(Nagpal et al., 2013) supported this assumption,
newer publications reveal publication bias in studies
on heart rate variability and PTSD (Ge et al., 2020;
Schneider & Schwerdtfeger, 2020). The influence of
publication bias still needs to be carefully considered.
Therefore, we did not only screen titles and abstracts
for physiological and dissociative measurements, but
also the methods section of each of the 553 peer
reviewed articles to overcome possible biases in data
collection and interpretation. Frequently, dissociation
was reported as a descriptive sample characteristic, but
not further included into a study’s analysis. If a disso-
ciative physiological measurement was reported in the
methods but not results of a study, we asked the
authors for additional data or calculations on this
parameter.
2.4. Data structuring and presentation
Our examination revealed great heterogeneity
between included studies on several characteristics,
including experimental condition, physiological par-
ameters, score calculation of physiological parameters,
and sample characteristics. Therefore, we have
6S. BEUTLER ET AL.
structured this systematic review as follows: articles
included are grouped according to the temporal
classification of dissociation as trait, peritraumatic,
or acute dissociation. Studies that report multiple tem-
poral classifications are included in more than one cat-
egory (see Table 2). Subsections for each dissociative
classification are clustered along with physiological
parameters. Within these subsections we also differen-
tiate between stimuli in experimental trauma stimuli
and more general stress (See Supplemental materials
4a–e for an additional graphical overview).
We aim to be as precise and accurate as possible in
the presentation of its results. Therefore, we have
obtained all available effect sizes (ror Cohens d)to
elucidate the magnitude of reported differences in dis-
sociation and physiological reactivity. If effect sizes
were not available, they were calculated by means
and standard deviation via the Psychometrica website
Figure 1. PRISMA Flowchart of literature search and study identification.
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 7
(Lenhard & Lenhard, 2016). In a few cases, the calcu-
lation approach differed from this procedure. This is
indicated in Supplemental Table S3. For the study of
Kaufman et al. (2002), we were not able to match an
appropriate sample size with each physiologic variable
and have therefore conservatively based our calcu-
lation on the smallest reported sample sizes. Signifi-
cance levels were taken from the original studies and
may therefore differ in their accuracy.
3. Results
3.1. Trait dissociation
3.1.1. General study characteristics
In total, 13 articles were identified that examined car-
diovascular or electrodermal reactions to trauma- or
stress-related interventions in the context of trait dis-
sociation. Sample sizes varied (n=14ton= 134) and a
combined 508 participants were studied. Mean age
varied from 23.86 years to 46.95 years. Five studies
examined female participants only, one study males
only, and the percentage of female participants in
other studies varied (8% to 95%). In eight studies, all
participants had been diagnosed with PTSD (for
detailed information see Supplemental Table S3).
The remaining articles included some patients with
PTSD, non-PTSD trauma-exposed participants and
non-exposed controls (one study) (compare Table 3
for more detailed information).
To assess trait dissociation, the majority of the
studies used the Dissociative Experiences Scale (DES;
Bernstein & Putnam, 1986), the most commonly
used dissociation self-report questionnaire (Lyssenko
et al., 2018). Other questionnaires included the Trait
Dissociation Questionnaire (TDQ; Murray et al.,
2002), the Shutdown Dissociation Scale (Shut-D;
Schalinski et al., 2015), the Multidimensional Inven-
tory of Dissociation (MID; Dell, 2006), and the Multi-
scale Dissociation Inventory (MDI; Briere et al., 2005).
To provoke physiologic reactions, seven studies
used personalized trauma-related content and one
study used videos with trauma-associated content of
varying emotional valence. General stress stimuli
were used in five studies, including mirror confronta-
tion, the Trier Social Stress Test (TSST), white noise,
and acoustic startle probes.
All but two studies examined heart rate (HR). Par-
ameters of heart rate variability (HRV) were assessed
in four studies, including root mean square successive
difference (RMSSD), high frequency HRV (HF-HRV),
low frequency HRV (LF-HRV), the ratio of low fre-
quency to high frequency (LF/HF-ratio) and respirat-
ory sinus arrhythmia (RSA), which can be interpreted
as an HRV marker (Berntson et al., 1997). Two studies
measured systolic (SBP) and diastolic blood pressure
(DBP), and one the pre-ejection period (PEP). Five
studies measured skin conductance (SC) parameters,
which include skin conductance level (SCL), skin con-
ductance response (SCR), and numbers of skin con-
ductance fluctuations (NSCF).
Six studies examined physiological reactions during
the experimental condition only. Seven studies either
additionally or solely reported a change score, which
Table 2. Included studies.
Study specification Trait Dissociation Peritraumatic Dissociation Acute Dissociation
Barnow et al. (2012) X
Bichescu-Burian, Steyer, Steinert, Grieb, & Tschoke (2017)X X X
Castro-Chapman et al. (2018)X
Chou, La Marca, Steptoe, & Brewin (2018) X
D’Andrea, Pole, DePierro, Freed, & Wallace (2013) X
Duesenberg et al. (2019) X
Ebner-Priemer et al. (2009) X
Halligan, Michael, Wilhelm, Clark, & Ehlers (2006)X X
Hauschildt, Peters, Moritz, & Jelinek (2011)XXX
Hetzel-Riggin & Wilber (2010)X
Hyer, Albrecht, Boudewyns, Woods, & Brandsma (1993)X
Kaufman et al. (2002) X
Krause-Utz, Walther, Lis, Schmahl, & Bohus (2018) X
Ladwig et al. (2002) X
Lanius et al. (2002) X
Malta et al. (2021) X
Metz et al. (2020) X
Pole et al. (2006) X
Powers et al. (2021)X
Rhudy, Davis, Williams, McCabe, & Byrd (2008 X
Sack, Cillien, & Hopper (2012) X
Schäflein, Sattel, Schmidt, & Sack (2018)X X
Schalinski, Elbert, & Schauer (2013)X
Schmahl et al. (2004)X X
Seligowski et al. (2019)X
Simeon, Yehuda, Knutelska, & Schmeidler (2008)X
Sledjeski & Delahanty (2012)X
Vermes et al. (2020)X X
Note: X = Study assessed this dissociation measure.
8S. BEUTLER ET AL.
Table 3. Trait dissociation –Study characteristics and results.
HR HRV BP SC
Study NPatients
Mean
age
Sex
distribution
(% women)
Dissociation
measurement
Physiological
parameter Symptom provocation
Comparison
Specification HR PEP RMSSD HF LF
LF/
HF-
ratio RSA
BP
(s/d) SCL SCR NSCF
Personalized trauma stimuli
Bichescu-
Burian
et al. (2017)
21 BPD patients with
comorbid PTSD
23.86 100 DES HR, SCRa, SCRf Personalized trauma-
content
Correlation •*•
Castro-
Chapman
et al. (2018)
134 Veterans with combat
exposure (on
average moderate
PTSD symptom
severity)
37.64 8 DES HR Personalized trauma-
content
Correlation •*
Halligan et al.
(2006)
61
a
Assault survivors (41%
met criteria for PTSD)
39.0 46 TDQ HR Personalized trauma-
content
Correlation –
full sample
(n= 54)
•*
Correlation –
females
(n= 25)
•*
Correlation –
males
(n= 29)
•*
Hauschildt
et al. (2011)
70 n= 26 trauma-exposed
with PTSD,
n= 26 trauma-
exposed without
PTSD,
n= 18 non-exposed
controls
32.7
b
71 DES RMSSD, HF-
HRV, LF-HRV
Video with emotional
valence (neutral,
negative, positive,
trauma-related)
Correlation •••
Hyer et al.
(1993)
57
(n=19
low diss.,
n=17
medium
diss.,
n=21
high diss.)
Veterans with chronic
PTSD
40.2 0 DES HR Personalized trauma-
content
High vs.
medium
dissociation
↑
•*
High vs. low
dissociation
•
•*
Rhudy et al.
(2008)
28 Trauma-exposed with
chronic nightmares
(32% current PTSD,
46% lifetime PTSD)
39.0 68 DES HR, SCL Personal nightmare
scripts
Correlation •*•*
Schmahl
et al. (2004)
14 PTSD patients with
history of sexual &
/or physical abuse
36.2 100 DES HR, BP, NSCF Personalized trauma-
content
Correlation •*↑*/•*•*
Vermes et al.
(2020)
21 PTSD patients 34.7 95 DES SCR Personalized trauma-
content
Correlation •
(Continued)
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 9
Table 3. Continued.
HR HRV BP SC
Study NPatients
Mean
age
Sex
distribution
(% women)
Dissociation
measurement
Physiological
parameter Symptom provocation
Comparison
Specification HR PEP RMSSD HF LF
LF/
HF-
ratio RSA
BP
(s/d) SCL SCR NSCF
General stress stimuli
Powers et al.
(2021)
19 Trauma-exposed with
diabetes
46.95 100 MDI HR, LF/HF-
ratio, RSA
Trier Social Stress Test Correlation ↓••
Schäflein
et al. (2018)
18 DDNOS patients with
comorbid PTSD
41.7 94 DES HR, lnRMSSD,
PEP
mirror confrontation
(only, or combined
with positive or
negative cognitions)
Correlation •••
Schalinski
et al. (2013)
31 Refugees with multiple
traumatic
experiences & PTSD
(6% did not meet the
avoidance criterion)
36.45 100 Shut-D HR White noise Correlation •
Seligowski
et al. (2019)
19 General medical
hospital in-patients
with PTSD
37.68 100 MDI HR, RSA, SCR Fear-potentiated
startle paradigm
Correlation •*•
c
*↓
d
20 Psychiatric hospital in-
patients with PTSD
39.75 100 MID Correlation •*•
c
*↑
e
Simeon et al.
(2008)
21 New York City
residents highly
exposed to 9/11
(33% met criteria for
PTSD)
40.4 38 DES HR, BP Trier Social Stress Test Correlation ↓•/•
Note: Arrow directions indicate increase ↑or decrease ↓during provocation condition, parentheses indicate non-significant results, * = results indicated by change score, •=noeffect. If studies reported results during condition and change
scores, both are presented in the table; BP (s/d): (systolic or diastolic) blood pressure, BPD: Borderline Personality Disorder, DDNOS: Dissociative Disorder Not Otherwise Specified, DES: Dissociative Experience Scale, HF-HRV: high frequency
heart rate variability, HR: heart rate, HRV: heart rate variability, LF-HRV: low frequency heart rate variability, LF/HF-ratio: ratio of low frequency to high frequency heart rate variability, lnRMSSD: natural logarithm of root mean square
successive difference; MDI: Multiscale Dissociation Inventory, MID: Multidimensional Inventory of Dissociation, NSCF: number of skin conductance fluctuations, PEP: pre-ejection period, PTSD: Posttraumatic-Stress Disorder, RMSSD: root
mean square successive difference, RSA: respiratory sinus arrhythmia, SC: skin conductance, SCL: skin conductance level, SCR: skin conductance response, SCRa: amplitude of skin conductance response, SCRf: frequency of skin conductance
response, Shut-D: Shutdown Dissociation Scale, TDQ: Trait Dissociation Questionnaire.
a
Correlation with trait dissociation is available for 54 participants.
b
N-adjusted mean value weighted by size of subgroups.
c
Significant positive correlations were only found in trait dissociation subscales of depersonalization in the general hospital sample and derealization in the psychiatric sample.
d
For danger signal.
e
For safety signal.
10 S. BEUTLER ET AL.
was corrected by physiological activity during a base-
line or neutral condition. In these studies, the baseline
or neutral physiological response was subtracted from
the experiment response, reducing the amount of
interference from the baseline or default activity.
3.1.2. Effects on heart rate
With respect to heart rate, no trend across studies was
observed. Of the 11 studies investigating the relation-
ship between trait dissociation severity and HR, only
three reported significant results. Using personalized
trauma stimuli, only Hyer et al. (1993) found a higher
HR in a high dissociative group than in a medium dis-
sociative group under a trauma condition (p< .050, d
= 0.34), which was no longer present when the calcu-
lation was based on the change score (p> .050, d=
0.10). Neither under the trauma condition (p> .050,
d= 0.27) nor based on the change score (p> .050, d
= 0.37) were there any differences between the high
vs. low dissociation group. Under baseline conditions,
HR in the high dissociation group was increased as
compared to the medium (p< .010, d= 0.44) and
low dissociation groups (p< .050, d= 0.26; see Sup-
plemental Table S2). None of the other studies using
personalized trauma reminders (Bichescu-Burian
et al., 2017; Castro-Chapman et al., 2018; Halligan
et al., 2006; Schmahl et al., 2004) or nightmare scripts
(Rhudy et al., 2008) found a relationship between HR
and trait dissociation.
Using general stress stimuli, Simeon et al. (2008)
found that trait dissociation correlated negatively
and with moderate effect to HR (r=−.48, p< .050)
measured during the TSST but not at baseline (r=
−.08, p> .050; for baseline see Supplemental Table
S2). This negative correlation (r=−.65, p= .009)
between trait dissociation and HR during the TSST
was confirmed by Powers et al. (2021), who observed
this relationship even at baseline (r=−.52, p= .047).
The remaining studies reported no significant change
in HR to mirror confrontation (Schäflein et al., 2018),
white noise (Schalinski et al., 2013), or fear-poten-
tiated startle (Seligowski et al., 2019).
3.1.3. Effects on heart rate variability
Seligowski et al. (2019) demonstrated a positive corre-
lation between RSA and depersonalization/derealiza-
tion subscales (with MDI depersonalization subscale
in the general hospital sample: r= .35, p< .010; with
MID depersonalization/derealization mean in the psy-
chiatric sample: r= .33, p< .010) during fear-poten-
tiated startle, but not with overall trait dissociation
(in the general hospital sample: r= .16, p> .050; in
the psychiatric sample: r= .10, p> .050).
None of the other studies found correlations
between HRV and trait dissociation after exposure
to trauma related material (Hauschildt et al., 2011)
or general stress stimuli (Powers et al., 2021; Schäflein
et al., 2018).
3.1.4. Effects on blood pressure
Only one study examined blood pressure during
trauma exposure (Schmahl et al., 2004), demonstrat-
ing a positive correlation between trait dissociation
and SBP (change score: r= .65, p= .032), but not
DBP (r= .48, p= .137).
One study examining blood pressure under a more
general stress stimulus (Simeon et al., 2008) showed
neither a correlation for SBP (r=−.24, p> .050) nor
for DBP (r=−.37, p> .050) during TSST. However,
this study demonstrated a correlation between trait
dissociation and SBP at baseline (r=−.54, p< .010),
but not with DBP (r=−.24, p> .050; for baseline see
Supplemental Table S2).
3.1.5. Effects on skin conductance
No study utilizing personalized trauma stimuli found
a relationship between SC and trait dissociation
(Bichescu-Burian et al., 2017; Rhudy et al., 2008;
Schmahl et al., 2004; Vermes et al., 2020).
Under non-personalized stress stimuli, Seligowski
et al. (2019) showed a moderate correlation between
SCR and trait dissociation during a fear-potentiated
startle paradigm. These results varied according to
the sample population and presented stimuli. In the
general hospital sample, trait dissociation correlated
negatively with the SCR response to the danger signal
(r=−.39, p< .010), but not the SCR response to the
safety signal (r=−.28, p> .050). On the contrary, in
the psychiatric hospital sample, trait dissociation cor-
related positively with the SCR to the safety signal (r
= .38, p< .010), but not the SCR to the danger signal
(r= .20, p> .050).
3.2. Peritraumatic dissociation
3.2.1. General study characteristics
In total, 8 articles were identified that examined cardi-
ovascular or electrodermal reactions to trauma- or
stress-related interventions in the context of peritrau-
matic dissociation. Sample sizes varied (n=19 to n=
200) and 581 participants were studied. Mean age var-
ied from 18.74 years to 61.0 years. Three studies exam-
ined female participants only, one study males only,
and the percentage of female participants in the
other studies varied (12% to 69%). In two studies, all
participants had been diagnosed with PTSD (for
detailed information see Supplemental Table S3).
The remaining articles included some patients with
PTSD and non-PTSD trauma-exposed participants
(compare Table 4 for more detailed information).
To assess peritraumatic dissociation, almost all
included studies used the Peritraumatic Dissociative
Experience Questionnaire (PDEQ; Marmar et al.,
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 11
Table 4. Peritraumatic dissociation –Study characteristics and results.
HR HRV BP SC
Study NPatients
Mean
age
Sex distribution
(% women)
Dissociation
measurement
Physiological
parameter Symptom provocation
Comparison
Specification HR PEP RMSSD HF LF RSA
BP
(s/d) CRD SCL SCR
Personalized trauma stimuli
Bichescu-Burian
et al. (2017)
21 BPD patients with comorbid
PTSD
23.86 100 PDEQ-SRV HR, SCRa, SCRf Personalized trauma-content Correlation ↓*•
Halligan et al.,
(2006)
61
a
Assault survivors (41% met
criteria for PTSD)
39.0 46 SDQ HR Personalized trauma-content Correlation –full
sample (n= 60)
•*
Correlation –females
(n= 33)
•*
Correlation –males
(n= 27)
•*
Hauschildt et al.
(2011)
52 n= 26 trauma-exposed with
PTSD,
n= 26 trauma-exposed
without PTSD
33.1
b
69 PDEQ-SRV RMSSD, HF-HRV,
LF-HRV
Video with emotional valence
(neutral, negative, positive,
trauma-related)
Correlation •••
Hetzel-Riggin &
Wilber (2010)
86 Sexual assault victims (22%
met criteria for PTSD)
18.8 100 PDEQ-SRV HR, SCR, SCL Personalized trauma-content Correlation (full
sample)
•*•*↑*
Correlation (n=19
PTSD subsample)
↑
•*
•
•*
Kaufman et al.
(2002)
187–200
(n=51–56
low diss.,
n= 136–
144 high
diss.)
Vietnam veterans with PTSD 42.8
b
0 PDEQ-RA
4
HR, SCL, BP Standardized combat scenes &
personally relevant combat
situations
High vs. low
dissociation
•••
Pole et al. (2006)19
(n= 10 with
low diss.,
n= 9 with
high diss.)
Trauma-exposed (53% met
criteria for PTSD)
44.3
b
47 PDEQ-RA
10
HR, BP, CRD Personalized trauma-content High vs. low
dissociation
•↓
c
/•↑
Sledjeski &
Delahanty
(2012)
39 Trauma-exposed
undergraduates (51% met
criteria for PTSD)
18.74
b
100 PDEQ-SRV HR, RSA, PEP Personalized trauma-content Correlation ↑*↓*•*
General stimuli
Ladwig et al.
(2002)
103
(n= 71 no/
low diss.,
n= 32 high
diss.,
n= 19 high
diss. - PTSD,
n= 11 high
diss. + PTSD)
Survivors of life-threatening
cardiac event
61.0 12 PDEQ-RA
8
SCR Acoustic startle High vs. no/low
dissociation
↑
High dissociation
without vs. with
PTSD
•
Note: Arrow directions indicate increase ↑or decrease ↓during provocation condition, * = results indicated by change score, •=noeffect. If studies reported results during condition and change scores, both are presented in the table; BP (s/d): (systolic or
diastolic) blood pressure, BPD: Borderline Personality Disorder, CRD: cardiovascular response discordance, HF-HRV: high frequency heart rate variability, HR: heart rate, HRV: heart rate variability, LF-HRV: low frequency heart rate variability, PDEQ-SRV:
Peritraumatic Dissociative Experience Questionnaire as self-report version, PDEQ-RA
4, 8, 10
: Peritraumatic Dissociative Experience Questionnaire as rater-administered version with 4, 8, or 10 items length, PEP: pre-ejection period, PTSD: Posttraumatic-
Stress Disorder, RMSSD: root mean square successive difference, RSA: respiratory sinus arrhythmia, SC: skin conductance, SCL: skin conductance level, SCR: skin conductance response, SCRa: amplitude of skin conductance response, SCRf: frequency of skin
conductance response, SDQ: Sate Dissociation Questionnaire
a
Correlation with state dissociation during the traumatic event available for 60 participants.
b
N-adjusted mean value weighted by size of subgroups.
c
Only in thinking about trauma condition.
12 S. BEUTLER ET AL.
1994; Marmar et al., 1997). Several modifications to
this instrument were made: four studies used the 10-
item self-report version, and three studies used a
rater-administrated version with varied item length.
One study used the State Dissociation Questionnaire
(SDQ; Murray et al., 2002) to assess peritraumatic
experiences like derealization, depersonalization,
detachment, altered time sense, and emotional numb-
ing during the traumatic experience (Halligan et al.,
2003).
To provoke physiological reactions, five studies
used personalized intrusive content. One study of
combat veterans used standardized audiovisual com-
bat scenes as well as scripts describing combat situ-
ations. One study used videos with trauma-
associated content of varying emotional valence.
Only one study used more general stressors in the
form of acoustic startle probes.
Six articles examined HR. HRV was assessed in two
studies as RMSSD, HF-HRV, LF-HRV and RSA. Two
studies measured SBP and DBP, of which one also
introduced the cardiovascular response discordance
(CRD), a subtraction of standardized BP scores from
standardized HR scores. One study measured PEP
and four examined SC via SCL and SCR.
Four studies examined physiological reaction
during experimental conditions, while four reported
baseline or neutral condition-corrected change scores
(either alone or in combination).
3.2.2. Effects on heart rate
The relationships between peritraumatic dissociation
and HR during trauma exposure were mixed, although
there was a tendency towards a positive correlation.
Sledjeski and Delahanty (2012) report a positive corre-
lation between peritraumatic dissociation and HR (r
= .34, p= .034), and a negative correlation between
peritraumatic dissociation and the PEP score (r=
−.42, p= .008), which corresponds to a faster HR.
Additionally, Hetzel-Riggin and Wilber (2010)
demonstrate a large positive correlation between peri-
traumatic dissociation and HR in a PTSD subsample
during the trauma condition (r= .52, p= .023). How-
ever, with a change score this correlation is non-sig-
nificant (r= .11, p= .661). On the other hand,
Bichescu-Burian et al. (2017) used a change score to
demonstrate a large negative correlation between peri-
traumatic dissociation and HR during an intervention
(r=−.54, p= .010). No effects of experimentally-
induced peritraumatic dissociation on HR were
observed by Halligan et al. (2006), Pole et al. (2006),
and Kaufman et al. (2002).
3.2.3. Effects on heart rate variability
There was no correlation with peritraumatic dis-
sociation and the assessed HRV parameters in the
study by Hauschildt et al. (2011) or with RSA in the
study by Sledjeski and Delahanty (2012).
3.2.4. Effects on blood pressure
At baseline, Pole et al. (2006) found lower SBP (p
< .050, d=−1.09), and DBP (p< .050, d=−1.15) for
the high dissociation group compared to the low dis-
sociation group (for baseline see Supplemental Table
S2). This effect persisted while participants thought
about their trauma for SBP (p< .050, d=−1.19), but
not for DBP in the same condition (p> .050, d=
−0.68). Neither SBP (p> .050, d=−0.75) nor DBP
(p> .050, d=−0.39) differed while talking about the
trauma condition. The authors of this study addition-
ally calculated the CRD. In this regard, they found that
in the high dissociation group HR was elevated rela-
tive to their associated trauma SBP, which was not
observed in the low dissociation group during both
the trauma and baseline conditions (for baseline see
Supplemental Table S2). Kaufman et al. (2002)
found no effects of peritraumatic dissociation on BP.
3.2.5. Effects on skin conductance
No study found associations between SCL and peri-
traumatic dissociation when participants were
exposed to personalized trauma stimuli (Hetzel-Rig-
gin & Wilber, 2010; Kaufman et al., 2002). However,
there is some evidence of elevated SCR in relation to
peritraumatic dissociation. Hetzel-Riggin and Wilber
(2010) found a positive correlation between SCR and
peritraumatic dissociation in a sample of female
assault victims (r= .24, p< .050) but not in the subset
who had a diagnosis of PTSD (r= .19, p= .434). Con-
trarily, during an intervention Bichescu-Burian et al.
(2017) found no effects of peritraumatic dissociation
on SCR amplitude or frequency.
Using general stress stimuli, Ladwig et al. (2002)
found increased SCR in participants with high levels
of dissociation as compared to participants with no/
low dissociation during an acoustic startle probe (p
= .017, d= 0.42). Furthermore, when dissociation
was high, the presence or absence of PTSD did not
affect SCR (p= .878, d= 0.17).
3.3. Acute dissociation
3.3.1. General study characteristics
In total, 15 articles examined cardiovascular or elec-
trodermal reactions to trauma- or stress-related inter-
ventions in the context of acute state dissociation.
Sample sizes varied (n=14 to n= 61). A combined
482 participants were studied. Mean age varied from
18.8 years to 42.4 years. One study examined predomi-
nantly male participants, seven studies examined
female participants only, and the percentage of female
participants in the other studies was high (65% to
95%).
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 13
In five studies all participants were diagnosed with
PTSD. Another five studies included trauma-exposed
participants of which some met criteria for PTSD
(for detailed information see Supplemental Table
S3). In contrast to trait and peritraumatic dissociation,
there are more studies on acute dissociative reactions
during symptom provocation in BPD patients. This is
expected, as dissociation is classified as a pathological
reaction in BPD (American Psychiatric Association,
2013). However, most of the BPD patients in the
included studies report a history of trauma and/or
PTSD symptoms. This is to be expected due to the
high comorbidity of the two disorders (Jowett et al.,
2020). Accordingly, four studies assessed acute dis-
sociation in patients with BPD, where all or a relevant
proportion of the participants reported comorbid
PTSD. However, one study reported correlations in
an overall sample of BPD-patients with and without
comorbid PTSD, as well as healthy controls (compare
Table 5 for more detailed information).
To evaluate acute dissociation, four studies used the
Dissociation-Tension Scale-acute (DSS-acute; Stigl-
mayr et al., 2003; Stiglmayr et al., 2010), consisting
of dissociation-related items from the DES (Bernstein
& Putnam, 1986), somatoform dissociation from the
Somatoform Dissociation Questionnaire (SDQ-20;
Nijenhuis et al., 1996), and 1–3 items of inner tension.
Two studies used the related short version, the DSS-4
(Stiglmayr et al., 2009). Two studies used the dis-
sociation subscale of the Responses to Script-Driven
Imagery Scale (RSDI-SSD; Hopper, Frewen, Sack
et al., 2007). This self-report rating was developed to
assess post-traumatic reactions during experimental
trauma confrontation on the subscales of re-experien-
cing, avoidance, and dissociation. Three studies used
the Clinician-Administered Dissociative States Scale
(CADSS; Bremner et al., 1998), which is rated by the
subject and by an observer, either on a 4-point scale
or as a dichotomy (present vs. absent). One study
used the Dissociation State Scale (DSS), a self-rating
adaptation of the CADSS (Bremner et al., 1998), and
one study modified the PDEQ (Marmar et al., 1997)
into an 8-item version they termed the State Dis-
sociation Scale (SDS). Malta et al. (2021) designed a
study-specific Dissociation Scale, including 3 items
assessing dissociation related experiences (e.g. losing
sense of time, losing track of events, and feeling
emotionally numb) on a 7-point scale.
To provoke physiological reactions to trauma
stimuli, six studies used personalized intrusive content
and one study used videos with trauma-associated
content of varying emotional valence. Malta et al.
(2021) used a novel approach, incorporating virtual
reality simulations of combat stressors. Seven studies
used more general stress stimuli, including the TSST,
white noise, acoustic startle probes, mirror confronta-
tion, idiographic aversive scripts with startle probes,
emotion regulation (with pictures of varying
emotional valence) and aversive differential delay con-
ditioning. Regarding the results of the latter, we
focused on stress-eliciting interventions and therefore
only report the psychophysiology for the initial reac-
tivity within this conditioning paradigm.
Eight studies examined HR, one of which focused
on HR acceleration and HR deceleration (defined as
peak and lowest HR) following the experimental
stimulus. Five studies assessed HRV parameters,
including RMSSD, HF-HRV, LF-HRV and LF/HF-
ratio. Three studies examined BP, one PEP and one
finger pulse volume (FPV). Six studies examined SC
parameters, including SCL, SCR and NSCF.
3.3.2. Effects on heart rate
Regarding personalized trauma stimuli, only one
study (Sack et al., 2012) showed a moderate negative
correlation between maximum HR in the trauma con-
dition and acute dissociation (r=−.30, p< .050), also
reflected by the baseline corrected change scores (r=
−.23, p< .050). Additionally, they used median split-
ting of the RSDI-SSD to divide the full sample into
high and low acute dissociation groups and, sub-
sequently, into high re-experiencing and low re-
experiencing groups. Focusing here on the high re-
experiencing group, those with high dissociation
exhibited significantly lower maximum HR than
those with low dissociation (p= .002, d=−1.11) a
finding confirmed by significantly different HR change
scores across groups (p= .002, d=−1.11). Other
studies (Bichescu-Burian et al., 2017; Chou et al.,
2018; Lanius et al., 2002; Malta et al., 2021; Schmahl
et al., 2004) found no correlation between HR and
alterations in acute dissociative states. Lanius et al.
(2002) found no differences in HR between trauma-
exposed patients without PTSD and PTSD patients
with comorbid Dissociative Disorder Not Otherwise
Specified (DDNOS), but the authors interpreted this
as the absence of an increase in HR that would be
expected in PTSD patients.
For general stress stimuli, no correlation was found
between HR and acute dissociation (D’Andrea et al.,
2013; Schäflein et al., 2018).
3.3.3. Effects on heart rate variability
Studies using personalized trauma stimuli demon-
strate inconsistent and contradictory findings on
HRV changes in acute dissociation. Sack et al. (2012)
found no correlation between the RMSSD acute dis-
sociation in the overall sample (r=−.21, p< .050),
but did find differences in RMSSD across participants
with high vs low dissociation (p= .029, d=−0.80).
More specifically, the high dissociation group exhib-
ited a smaller decrease in RMSSD from the neutral
to the trauma condition, reflecting less PNS adapta-
bility. Chou et al. (2018) found a negative correlation
14 S. BEUTLER ET AL.
Table 5. Acute dissociation –Study characteristics and results.
Study NPatients
Mean
age
Sex
distribution
(% women) Dissociation
Physiological
parameter
Symptom
provocation
Comparison
Specification HR PEP RMSSD HF LF
LF/
HF-
ratio
BP
(s/
d) FPV SCL SCR NSCF
Personalized trauma stimuli
Bichescu-
Burian et al.
(2017)
21 BPD patients with
comorbid PTSD
23.86 100 DSS-4 HR, SCRa, SCRf Personalized
trauma-content
Correlation •*•
Chou et al.
(2018)
22 Volunteers with
current PTSD
42.36 68.2% DSS HR, HF-HRV,
LF-HRV, LF/
HF-ratio
Personalized
trauma-content
Correlation •*•*•*↓*
Hauschildt
et al. (2011)
52 n= 26 trauma-
exposed with
PTSD,
n= 26 trauma-
exposed
without PTSD
33.1
c
69 DSS-acute RMSSD, HF-
HRV, LF-HRV
Video with
emotional
valence (neutral,
negative, positive,
trauma-related)
Correlation •••
Lanius et al.
(2002)
17
(n= 7 with
PTSD &
comorbid
DDNOS,
n=10
without
PTSD)
Trauma-exposed 35.4
a
94 CADSS
dich
HR Personalized
trauma-content
Patients vs.
controls
•*
Malta et al.
(2021)
32 Combat trauma-
exposed
veterans, 34%
with PTSD
30.28 16 Dissociation
Scale
HR VR simulation
including
standardized
combat segments
Correlation •
Sack et al.
(2012)
61
(n= 16 high
re-exp. with
high.;
n= 15 high
re-exp. with
low diss.)
Trauma-exposed,
69% met criteria
for current PTSD
34.5 77 RSDI-SSD HR, lnRMSSD,
FPV
Personalized
trauma-content
Correlation (full
sample)
↓
↓*•*↑*
High re-exp.
with high vs.
with low
dissociation
↓
↓*
↓*
•*
Schmahl et al.
(2004)
14 PTSD patients
with history of
sexual & /or
physical abuse
36.2 100 CADSS HR, BP, NSCF Personalized
trauma-content
Correlation •*•*/
•*
•*
Vermes et al.
(2020)
21 PTSD patients 34.7 95 CADSS SCR Personalized
trauma-content
Correlation •
General stress stimuli
Barnow et al.
(2012)
59 n= 21 BPD
patients with
comorbid PTSD
n= 12 BPD
patients without
comorbid PTSD
23.66
a
100 DSS-acute SCL Idiographic aversive
scripts including
startle probe
Correlation ↑*
(Continued)
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 15
Table 5. Continued.
Study NPatients
Mean
age
Sex
distribution
(% women) Dissociation
Physiological
parameter
Symptom
provocation
Comparison
Specification HR PEP RMSSD HF LF
LF/
HF-
ratio
BP
(s/
d) FPV SCL SCR NSCF
n= 26 healthy
controls
D’Andrea
et al. (2013)
54
(n= 27 high
diss.,
n= 27 low
diss.)
Trauma-exposed
African
American
college
students, 37%
with lifetime
PTSD
18.8 65 SDS HRaccel,
HRdecel, SCR
Acoustic startle High vs. low
dissociation •
d
•
e
•*
d
•*
e
•
↓*
Duesenberg
et al. (2019)
49 BPD patients, 45%
with comorbid
PTSD
28.7 100 DSS-4 BP Trier Social Stress
Test
Correlation •*/
•*
Ebner-
Priemer
et al. (2009)
21
(n= 10 diss.,
n= 11 non-
diss.)
BPD patients, 27%
of the diss., 50%
of the non-diss.
subgroup with
current PTSD
27.8
b
100 DSS-acute SCR Aversive differential
delay
conditioning
Dissociatives vs.
non-
dissociatives
•
Krause-Utz
et al. (2019)
20 BPD patients with
comorbid PTSD
34.16 100 DSS-4 HF-HRV Emotional
regulation task
with neutral,
positive, &
negative pictures
Correlation •
f
↑
g
•
h
Metz et al.
(2020)
21 PTSD patients 39.7 100 DSS-acute BP Trier Social Stress
Test
Correlation •/•
Schäflein et al.
(2018)
18 DDNOS patients
with comorbid
PTSD
41.7 94 RSDI-SSD HR, lnRMSSD,
PEP
mirror
confrontation
(only, or
combined with
positive or
negative
cognitions)
Correlation •••
Note: Arrow directions indicate increase ↑or decrease ↓during provocation condition, * = results indicated by change score, •=noeffect. If studies reported results during condition and change scores, both are presented in the table; BP (s/
d): (systolic or diastolic) blood pressure, BPD: Borderline Personality Disorder, CADSS: Clinician-Administered Dissociative States Scale, CADSS
dich
: dichotomous version of Clinician-Administered Dissociative States Scale, DDNOS: Disso-
ciative Disorder Not Otherwise Specified, DSS: Dissociation State Scale, DSS-acute: Dissociation Tension scale acute, DSS-4: Dissociation Tension Scale acute as short version, FPV: finger pulse volume, HF-HRV: high frequency heart rate
variability, HR: heart rate, HRaccel: heart rate acceleration, HRdecel: heart rate deceleration, HRV: heart rate variability, LF-HRV: low frequency heart rate variability, LF/HF-ratio: ratio of low frequency to high frequency heart rate variability,
lnRMSSD: natural logarithm of root mean square successive difference, NSCF: number of skin conductance fluctuations, PEP: pre-ejection period, PTSD: Posttraumatic-Stress Disorder, RMSSD: root mean square successive difference, RSDI-
SSD: subscale dissociation of the Responses to Script-Driven Imagery Scale, SC: skin conductance, SCL: skin conductance level, SCR: skin conductance response, SCRa: amplitude of skin conductance response, SCRf: frequency of skin
conductance response, SDS: State Dissociation Scale, VR: virtual reality.
a
N-adjusted mean value weighted by size of subgroups.
bMean age of all 33 BPD patients, while medium dissociative subgroup (n= 12) was not further reported.
cN-adjusted mean value weighted by size of subgroups.
d
HR acceleration.
e
HR deceleration.
f
Non-regulation condition.
g
Regulation of negative pictures.
h
Regulation of positive pictures.
16 S. BEUTLER ET AL.
between dissociation and LF/HF-ratio (r=−.53, p
< .050), reflecting increased parasympathetic activity,
but no correlation with HF-HRV (r= .16, p> .050)
or LF-HRV (r=−.28, p> .050). Hauschildt et al.
(2011) found no correlation between HRV and acute
dissociation.
Regarding general stress stimuli, Schäflein et al.
(2018) found no correlation between acute dis-
sociation and RMSSD in the mirror confrontation
task. Krause-Utz et al. (2018) also demonstrated no
effects of acute dissociation on HF-HRV while partici-
pants watched pictures with varying emotional
valence. However, when participants were asked to
downregulate their emotions while viewing, there
was a robust correlation between acute dissociation
and HF-HRV for negative pictures (r= .66, p= .025)
but not for positive pictures (r= .32, p= .614).
3.3.4. Effects on blood pressure and finger pulse
volume
There was no correlation between acute dissociation
and BP during trauma confrontation (Schmahl et al.,
2004) or stress provocation (Duesenberg et al., 2019;
Metz et al., 2020).
However, Sack et al. (2012) found a positive corre-
lation between acute dissociation and FPV (r= .33, p
< .010). This effect was not observed in participants
with high re-experiencing when comparing high vs.
low dissociation (p> .050, d=−0.79).
3.3.5. Effects on skin conductance
With respect to studies using personalized trauma
stimuli, no effects of acute dissociation on SC were
observed (Bichescu-Burian et al., 2017; Schmahl
et al., 2004; Vermes et al., 2020).
When general stress stimuli were utilized, findings
were inconclusive. In a mixed sample including BPD
patients with and without comorbid PTSD as well as
healthy controls, Barnow et al. (2012) demonstrated
a positive correlation between acute dissociation and
SCL change score (r= .14, p= .001). Neither D’Andrea
et al. (2013) nor Ebner-Priemer et al. (2009) found
group differences in SCL at baseline (for baseline see
Supplemental Table S2). Regarding SCR, D’Andrea
et al. (2013) demonstrated that SCR was moderately
decreased in the high dissociation group (p= .040, d
=−0.57).
4. Discussion
We systematically reviewed 28 articles (n= 1300 sub-
jects) with the hope of identifying the psychophysiolo-
gical correlates of trait, peritraumatic, and acute
dissociation. Due to conflicting results within and
between studies, we found no clear pattern or trend
for physiological markers of trauma-related dis-
sociation. Studies on trait dissociation demonstrated
contradicting physiological reactions. Two studies
using TSST (Powers et al., 2021; Simeon et al., 2008)
found a decrease in heart rate during stress induction
which was associated with trait dissociation, whereas
two other studies (Hyer et al., 1993; Schmahl et al.,
2004) demonstrated hyperactive autonomic responses
to traumatic content. These inconsistencies allude that
the type of intervention and stress arousal (social
stress vs. traumatic stress) may drive specific physio-
logical responses. However, this divergence was only
observed in relation to chronic trait dissociation. For
peritraumatic dissociation, one study depicted a sig-
nificantly decreased heart rate in comorbid PTSD-
BPD patients (Bichescu-Burian et al., 2017). Other
studies showed a slight trend towards hyperarousal
associated with the retrospectively assessed dissocia-
tive reactions experienced during the initial traumatic
event (Hetzel-Riggin & Wilber, 2010; Ladwig et al.,
2002; Sledjeski & Delahanty, 2012). Contrary to this,
several studies investigating acute post-traumatic dis-
sociation depicted a tendency towards a hypoaroused
autonomic reactivity (Chou et al., 2018;D’Andrea
et al., 2013; Krause-Utz et al., 2018; Sack et al.,
2012), suggesting that peri- and post-traumatic dis-
sociation may be physiologically distinct from each
other.
According to the defense cascade (Lanius et al.,
2018)andshutdown models (Schauer & Elbert,
2010), individuals who experience dissociation
during the initial traumatic event should bypass the
tonic immobility state and enter a hypoaroused
state. Additionally, an individual’s initial physiologic
response to a traumatic event will determine their
subsequent responses to trauma cues and stressors
(see Introduction). Current research assessing peri-
traumatic and/or acute dissociation has not yet pro-
vided sufficient support for this idea. As previously
stated, only a single study on peritraumatic dis-
sociation demonstrated a significantly decreased
heart rate, reflecting a hypoaroused autonomic state
(Bichescu-Burian et al., 2017). Contrarily, several
other studies on peritraumatic dissociation found a
tendency towards increased arousal. With regards
to acute post-traumatic dissociation, findings were
similarly inconsistent, although there was some evi-
dence of an attenuated response (based on heart
rate, heart rate variability and skin conductance)
(Chou et al., 2018;D’Andrea et al., 2013;Krause-
Utz et al., 2018;Sacketal.,2012). Based on our
assessment of the reviewed studies, we conclude
that peritraumatic dissociation and acute posttrau-
matic dissociation are neither associated with PNS-
mediated hypoarousal, nor follow the proposed
physiologic trajectory in which the initial passive
response to a trauma predicts one’sresponsestosub-
sequent stressors or trauma reminders. At this point,
there is insufficient evidence to prove a consistent
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 17
association beyond spurious findings, raising the
question: why do well-prepared experimental studies
fail to extract psychophysiological markers of
dissociation?
One possible answer might lie in the inconsistent
assessment of psychophysiological parameters across
studies. Outcomes may be influenced by varying adap-
tation times, measurement durations, baseline con-
ditions, artifact editing, and post-experiment
processing. For instance, a review (Beauchaine et al.,
2019) reported high inconsistencies across studies
which used the RSA as a measure of transpathological
dimensions, which they attribute to a lack of methodo-
logical standardization. Contrarily, psychophysiologi-
cal markers of PTSD have been extensively
investigated and respected for their easy and afford-
able implementation into clinical, ambulatory, and
laboratory research (see Pineles & Orr, 2018).
Additionally, if PTSD is examined without consider-
ation of dissociative symptoms, there is consistent
support for increased autonomic activity while resting
and across experimental paradigms, as measured by
HR, HRV parameters, and SC (Ge et al., 2020; Nagpal
et al., 2013; Schneider & Schwerdtfeger, 2020). How-
ever, when the dissociative subtype of PTSD is
extracted, the psychophysiological fingerprint remains
elusive.
A recent extensive systematic review focused on the
psychophysiological markers (among others) of
pathological dissociation in a broader, transdiagnostic
view (Roydeva & Reinders, 2021). This review
confirmed our findings, citing inconclusive results
due to most studies reporting no effects. The authors
further concluded that none of the reviewed physio-
logical measures could be recommended as a bio-
marker of pathological dissociation (Roydeva &
Reinders, 2021). The same is true for markers of
post-traumatic dissociation at the level of brain acti-
vation or anatomy. A review on this topic failed to
establish a clear trend across studies (Lotfinia et al.,
2020). Although analyses on resting-state brain acti-
vation tentatively support the idea of an overmodu-
lated fear network (see defense cascade and shutdown
models) through reports of altered functional connec-
tivity between prefrontal and subcortical areas in dis-
sociative PTSD patients (Nicholson et al., 2017;
Nicholson et al., 2019; Rabellino et al., 2018), exper-
imental studies are lacking. The few experimental neu-
roimaging studies to date (Daniels et al., 2012;
Felmingham et al., 2008; Hopper, Frewen, van der
Kolk et al., 2007; Mertens et al., 2022) either report
inconsistent brain regions associated with trauma-
related dissociation or fail to present any associated
neural regions at all. Ultimately, this undermines the
proposed neurobiological basis (e.g. Lanius et al.,
2010; Terpou et al., 2019) of the defense cascade
model and the dissociative subtype as a whole.
Other factors which may influence the assessment
of valid objective markers of dissociation are the
inconsistent conceptualization and measurement of
dissociation. Within this review alone, we include
studies with 14 unique measures of dissociation,
which each emphasize different aspects of dis-
sociation. The resulting sum scores are therefore dri-
ven by a spectrum of symptoms, from those
considered less pathological (e.g. absorption) to
those considered more pathological (e.g. identity frag-
mentation). When correlating such a sum score with
psychophysiological measures, any true effect of
depersonalization and derealization could be masked
by the influence of these other symptoms. Hence, het-
erogeneity in our results may be driven by the diver-
sity of dissociation assessment techniques.
Additionally, the meaning of hypoarousal is not
consistent in the dissociation literature. Most of the
aforementioned models defined hypoarousal as equiv-
alent to parasympathetic dominance; however physio-
logical research shows that alterations in heart rate or
heart rate variability may be steered by both SNS and
PNS activity (de Geus et al., 2019). Multimodal assess-
ments incorporating psychophysiological measures
reflective of both SNS and PNS activation are thus
highly recommended to disentangle these complex
interactions (e.g. as in Schmahl et al., 2004; Seligowski
et al., 2019).
The initial pilot studies describing alternating phys-
iological reactions to individualized trauma scripts in
chronic PTSD patients (Lanius et al., 2001; Lanius
et al., 2002) interpreted the data as supportive for
two distinct subtypes ‘each representing unique path-
ways to chronic stress- related psychopathology’
(Lanius et al., 2006, p. 710). In these studies, patients
with elevated heart rates (70%) were characterized as
intrusive subtypes whereas the 30% without elevated
heart rates were characterized as dissociative subtypes,
reflective of derealization or depersonalization. Here,
dissociative hypoarousal was characterized as the
absence of the PTSD-pathognomonic hyperarousal
state. It should be noted that these findings were
based on small samples (N≤10). Another study
from the same research group found that although
some dissociative PTSD patients had unchanged (or
not increased) HR during trauma exposure, there
was no clinical difference between these patients and
those who exhibited decreased or increased HR
(Lanius et al., 2005). Meanwhile, other studies
employed the term ‘active suppression’to reflect sig-
nificant heart rate deceleration (D’Andrea et al.,
2013) or reduced heart rate reactivity (Sack et al.,
2012) concurrent with parasympathetic dominance
(Lanius et al., 2018; Schauer & Elbert, 2010). Due to
these inconsistencies in language, we implore future
researchers in this field to clearly state whether they
define hypoarousal as the absence of an increase in
18 S. BEUTLER ET AL.
HR, a relative decrease in HR within-subjects (e.g.
from baseline or within tasks), or a decrease in HR
between-groups (e.g. compared to trauma-exposed
controls).
4.1. Limitations and strengths
Several limitations are present in the current review.
First, this qualitative review did not include a quanti-
tative meta-analysis of the reviewed studies’findings.
Although the search resulted in sufficient data to be
quantitatively reviewed, it was not deemed sensible
due to the high heterogeneity in sample characteristics
(e.g. PTSD severity, gender, comorbidity), experimen-
tal interventions, dissociation assessment tools, and
physiological measures. With this variation, a meta-
analysis would run the risk of hastily simplifying a
complex phenomenon. Thus, a systematic overview
of these heterogenetic studies seemed to be more
appropriate.
This review specifically focused on post-traumatic
dissociation and therefore concentrated on search
terms according to derealization/depersonalization.
However, except for the RSDI-SSD, none of the
reported instruments solely measured derealization/
depersonalization. Therefore, no clear distinction
could be made between physiological reactions
specific to derealization/depersonalization vs. those
associated with ‘compartmentalization’(Holmes
et al., 2005). Hence, these results can only be inter-
preted to a limited extent. Additionally, we have lim-
ited information on the differences between
dissociators vs non-dissociators with PTSD to verify
the postulated opposing subtypes. Only one study on
these opposing groups was identified within in each
included dissociative modality (e.g. acute, trait, and
peritraumatic dissociation). We observed lower auto-
nomic activity in people with high acute dissociation
(Sack et al., 2012), higher HR in those with high
trait dissociation (Hyer et al., 1993), and no physio-
logic effect in those with high peritraumatic dis-
sociation (Kaufman et al., 2002).
One of the main limitations to the reviewed studies
is the low sample sizes and thus limited statistical
power to detect subtle changes in sensitive measures
of psychophysiological activity. Additionally, the het-
erogeneity of physiological indices and dissociation
measures employed across studies impedes our ability
to make any direct comparisons or generalizations.
Specifically, only five studies included at least two
types of dissociation modalities (e.g. assessed both
peritraumatic and acute dissociation). Most studies
related dissociation to mean scores of psychophysiolo-
gical measurements. In future studies, temporal
changes in physiology should be included to highlight
any fluctuations or trends that may support current
models of defense response (e.g. progression of an
initial increased HR followed by reduced HR/hypoten-
sion as suggested by the defense cascade model).
This review has several strengths and provides novel
insight into the psychophysiology of dissociation in
PTSD. One strength is that we included only exper-
imental studies that employed symptom provocation
or stress-induction paradigms. This is of significance
as all defense response models underscore the impor-
tance of dissociation as a defensive reaction to a clear
stressor or trauma reminder. To our knowledge, this
is the first review to summarize the relationship
between dissociation and experimentally induced
acute physiological responses. Furthermore, we cat-
egorize findings according to distinct dissociation mod-
alities, thus permitting a clear comparison of
physiological responses across peri-, acute, and chronic
post-traumatic dissociation. In doing so, we begin to
disentangle dissociation-related psychophysiological
reactions from the moment the trauma occurs, gets
reactivated, and develops into a chronic pattern.
4.2. Conclusion and future outlook
In sum, the current review investigates psychophysio-
logical correlates of dissociation in PTSD through a
well-defined and narrow scope. From the extracted lit-
erature, we find (a) an association between a hyperac-
tive defensive response and peritraumatic dissociation,
(b) an association between a hypoactive defensive
response and acute post-traumatic dissociation, and
(c) a possible impact of the type of stressor on physio-
logic responses in chronic trait dissociation. However,
there is no evidence for a clear link between a hypoar-
oused ANS and peri- and post-traumatic dissociation
across studies. Furthermore, it should be noted that
none of the studied physiological parameters are
pathognomonic predictors of trauma-related dis-
sociation as similar reactive patterns have been
observed across various psychiatric disorders (see
Chalmers et al., 2014 for anxiety; see Koenig et al.,
2016 for BPD). As recommended by Roydeva and
Reinders (2021), future research should aim to
increase the specificity of biomarkers to PTSD-related
dissociation, for instance by testing the robustness of
these psychophysiological correlates across other psy-
chopathologies (e.g. depression or anxiety).
To overcome the gap between theoretical models
and empirical evidence, studies are needed which
have clear inclusion criteria (e.g. PTSD or post-trau-
matic stress symptoms), control for PTSD severity,
and use longitudinal designs to assess symptom vari-
ation. Particularly, studies which assess peritraumatic
dissociation as early as possible after a trauma will
reduce the risk of retrospective bias. Ambulatory
assessment strategies like ecological sampling (e.g.
wireless HR monitoring) may overcome the necessity
of provoking PTSD and dissociation symptoms. These
EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY 19
findings would be far more applicable to the PTSD
patient population.
Acknowledgments
The authors would like to thank Christina Schulte for taking
part in the rating process as independent rater and Margaret
Engstrom for language proofreading. The authors express
our gratitude to all authors of the original publications for
supporting this work by providing additional information,
calculations, and their interest in this research topic.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Funding
This research was funded by the German Research Foun-
dation (Deutsche Forschungsgemeinschaft, DFG), Grant
number: CR 479/9–1 (http://www.dfg.de/). This work was
supported by the EU Rosalind-Franklin Fellowship granted
to J. K. Daniels. The work by Sarah Beutler was supported by
Fellowship of the Heinrich Böll Foundation. Liliana
R. Ladner was supported by the Deutscher Akademischer
Austauschdienst (DAAD) Research Internships in Science
and Engineering Program.
Data availability
Supplementary material, including a data file with the
effect sizes and detailed descriptions of the studies
reported (see Supplementary Table 3), can be found in
the online version, at https://doi.org/10.1080/20008066.
2022.2132599.
ORCID
Judith K. Daniels http://orcid.org/0000-0001-6304-2310
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