The Psychophysiology of Posttraumatic Stress Disorder: A Meta-Analysis
University of Michigan
This meta-analysis of 58 resting baseline studies, 25 startle studies, 17 standardized trauma cue studies,
and 22 idiographic trauma cue studies compared adults with and without posttraumatic stress disorder
(PTSD) on psychophysiological variables: facial electromyography (EMG), heart rate (HR), skin con-
ductance (SC), and blood pressure. Significant weighted mean effects of PTSD were observed for HR
(r ? .18) and SC (r ? .08) in resting baseline studies; eyeblink EMG (r ? .13), HR (r ? .23), and SC
habituation slope (r ? .21) in startle studies; HR (r ? .27) in standardized trauma cue studies; and
frontalis EMG (r ? .21), corrugator EMG (r ? .34), HR (r ? .22), and SC (r ? .19) in idiographic
trauma cue studies. The most robust correlates of PTSD were SC habituation slope, facial EMG during
idiographic trauma cues, and HR during all study types. Overall, the results support the view that PTSD
is associated with elevated psychophysiology. However, the generalizability of these findings is limited
by characteristics of the published literature, including its disproportionate focus on male veterans and
neglect of potential PTSD subtypes.
Keywords: posttraumatic stress disorder (PTSD), psychophysiology, hyperarousal, startle, trauma cues
Posttraumatic stress disorder (PTSD) is a common psychiatric
condition (Kessler et al., 2005) triggered by exposure to an in-
tensely distressing traumatic event and characterized by more than
1 month of re-experiencing, avoidance, and hyperarousal symp-
toms (Diagnostic and Statistical Manual of Mental Disorders, 4th
ed., text revision; DSM–IV–TR; American Psychiatric Association
[APA], 2000). Psychophysiological symptoms have always been a
prominent feature of this disorder (Kardiner, 1941; Mott, 1919)
even before it was officially codified into the American psychiatric
nomenclature (3rd ed.; DSM–III; APA, 1980). Unlike most psy-
chiatric symptoms, which can be assessed only by patient self-
report or clinical observation, psychophysiological symptoms can
be independently corroborated by using laboratory methods. Re-
searchers have taken advantage of this opportunity and have gen-
erated a substantial literature on objective psychophysiological
correlates of PTSD. This literature has received several qualitative
reviews (e.g., Orr, Metzger, Miller, & Kaloupek, 2004; Prins,
Kaloupek, & Keane, 1995; Shalev & Rogel-Fuchs, 1993), but it
has not yet received a quantitative meta-analytic review. The
absence of a meta-analysis of the psychophysiology of PTSD is
notable given the presence of several meta-analyses of other cor-
relates of PTSD (Brewin, Andrews, & Valentine, 2000; Karl,
Malta, & Maercker, 2006; Ozer, Best, Lipsey, & Weiss, 2003).
Such meta-analyses have proven useful to the increasing number
of social scientists interested in understanding PTSD. Moreover,
because of advances in computer technology over the past decade,
psychophysiological measurement is now more accessible to a
broader range of social scientists than ever before (Orr et al.,
2004). Thus, the time may now be ripe for a meta-analytic review
of the psychophysiology of PTSD in Psychological Bulletin.
The diagnostic criteria for PTSD treat psychophysiology as a
unitary construct, but laboratory assessments of psychophysiology
typically involve the noninvasive, simultaneous recording of sep-
arate biological processes. In the PTSD literature, these processes
commonly include facial electromyography (EMG; muscle con-
tractions), heart rate (HR; cardiac activity), skin conductance (SC;
sweat gland activity), systolic blood pressure (SBP; the force of
blood in the circulatory system when the heart contracts), and
diastolic blood pressure (DBP; the force of blood in the circulatory
system when the heart is at rest). Under conditions of intense
distress, all of these measures would be expected to show in-
creases. Yet, each measure has its own biological underpinning
and somewhat unique interpretation that may be informative about
the pathophysiology of PTSD. For example, a dominant relation-
ship between PTSD and EMG may point to specific abnormalities
in the expression of negative emotions (frontalis or corrugator
EMG), positive emotions (zygomaticus EMG), or the startle reflex
(orbicularis oculi EMG; Blumenthal et al., 2005; Lang, Bradley, &
Cuthbert, 1998). Dominant relationships in either SC or HR may
imply a special role of the sympathetic (SNS) or parasympathetic
(PNS) nervous systems. SC is primarily governed by the SNS. HR
is regulated by both the SNS and the PNS such that increases in
HR could be due to sympathetic activation, parasympathetic with-
drawal, or both (Bernston, Cacioppo, & Quigley, 1993). Thus, a
I wish to thank Scott P. Orr and William Lamb for their consultation on
this meta-analysis; Adam Bernstein for his helpful meta-analysis program
that calculated many of the results presented in this article; Daniel Weiss,
Suzanne Best, Mindy Miller, Madhur Kulkarni, and Wendy D’Andrea-
Merrins for their helpful critiques on a draft of this article; and Jeb
Northern, Lauren Wecshler, Olga Slavin, Adam Bramoweth, Baxter Allen,
Ted Miin, Marina Abayev, and Lindsay Duggan for their assistance with
gathering, hand searching, coding, and managing the data involved in this
project. Thanks also to Danny G. Kaloupek, Richard McNally, Roger K.
Pitman, and Terry M. Keane for their help in interpreting some of the
findings of this meta-analysis. Finally, thanks to Delores Carter Pole for
her special contributions.
Correspondence concerning this article should be addressed to Nnamdi
Pole, Department of Psychology, University of Michigan, 530 Church
Street, 2260 East Hall, Ann Arbor, MI 48109-1109. E-mail:
2007, Vol. 133, No. 5, 725–746
Copyright 2007 by the American Psychological Association
stronger association between PTSD and HR than between PTSD
and SC could imply an important parasympathetic contribution.
Finally, a dominant finding in SBP relative to DBP blood pressure
could indicate a key physiological disturbance during heart con-
traction relative to heart relaxation. A finding of the reverse could
imply the opposite. The pathophysiological implications of psy-
chophysiological findings have been relatively neglected in the
PTSD literature. However, a meta-analytic review may clarify this
pathophysiology by identifying the dominant relationships.
Psychophysiological measures have been assessed in a variety
of laboratory studies designed to evoke specific PTSD symptoms.
Many of these studies have involved one or more of the following
four procedures: resting baseline, exposure to startling sounds,
exposure to standardized trauma cues, and/or exposure to idio-
graphic trauma cues. It is common to find that groups with and
without PTSD may differ in a particular psychophysiological
measure in one procedure but not another (e.g., Keane et al., 1998).
These differences may reflect the different theoretical and clinical
significance ascribed to each procedure (as described in detail
Types of Studies Included in the Meta-Analysis
Resting Baseline Studies
Because the diagnostic criteria for PTSD include a variety of
hyperarousal symptoms, investigators have wondered whether
PTSD patients show persistently elevated psychophysiological
levels in the absence of obvious stressful stimuli. In resting base-
line studies, psychophysiology is assessed while participants with
and without PTSD rest quietly. Notably, such data are sometimes
obtained shortly before the participants face a stressful challenge.
Though resting baseline studies have yielded inconsistent results,
a meta-analysis of this literature concluded that groups of patients
with PTSD show higher resting HR and higher resting DBP than
do their counterparts without PTSD, even though their resting
SBPs are similar (Buckley & Kaloupek, 2001). The finding of
group differences in DBP without corresponding differences in
SBP implies that PTSD exerts stronger effects on the resting phase
of the cardiac cycle than the activation phase of this cycle. This
finding echoes recent evidence showing that the relationship be-
tween PTSD and elevated resting HR may be primarily mediated
by reduced parasympathetic activity rather than increased sympa-
thetic activity (Hopper, Spinazzola, Simpson, & van der Kolk,
2006; Sack, Hopper, & Lamprecht, 2004). Unfortunately, Buckley
and Kaloupek’s study did not examine resting SC or EMG, which
may have further clarified the pathophysiology of resting arousal.
Three potential explanations were proposed by Buckley and
Kaloupek (2001) for their findings: (a) long-term alteration in the
structure or function of physiological systems in PTSD patients
because of frequent physiological hyperreactivity (e.g., Lovallo &
Gerin, 2003); (b) anticipatory anxiety about stressful challenges
that the PTSD patients would face after the resting period (e.g.,
Prins et al., 1995); and/or (c) physiological effects of comorbid
substance dependence (Keane & Wolfe, 1990). The long-term
alteration theory was supported by evidence of larger effect sizes
in studies involving patients who had been suffering from PTSD
for over a decade. Neither the anticipatory anxiety theory nor the
comorbid substance dependence theory was supported by their
data. The former theory was refuted by findings of a relationship
between PTSD and elevated psychophysiological levels in the
absence of a stressful postbaseline challenge. The latter theory
went untested because there were too few studies involving
substance-dependent PTSD participants.
Psychophysiological Responses to Startling Sounds
Of the 17 symptoms that may contribute to a PTSD diagnosis,
exaggerated startle (Criterion D5; APA, 2000) is one of the most
commonly reported by PTSD patients (Davidson, Hughes, Blazer,
& George, 1991). The etiology of exaggerated startle in PTSD is
uncertain. Some prospective evidence suggests that exaggerated
startle may reflect a pretrauma propensity for excessive uncondi-
tioned responding (Guthrie & Bryant, 2005), whereas other evi-
dence suggests that exaggerated startle emerges as a result of
posttraumatic neuronal sensitization (Shalev et al., 2000). Still
other evidence has indicated that some components of exaggerated
startle in PTSD may result from excessive negative emotions
(Lang et al., 1998) triggered by hypersensitivity to contextual
threat cues (Grillon, Morgan, Davis, & Southwick, 1998a, 1998b;
Pole et al., in press; Pole, Neylan, Best, Orr, & Marmar, 2003).
The startle reflex is measured in the psychophysiology labora-
tory by presenting sudden, loud sounds through headphones at
random intervals and recording short latency electromyogram re-
sponses at the orbicularis oculi (a muscle group involved in eye-
blinks; e.g., Morgan, Grillon, Southwick, Davis, & Charney,
1996). Secondary, longer latency, defensive responses in SC and
HR are also commonly measured (e.g., Orr, Solomon, Peri, Pit-
man, & Shalev, 1997). In addition, some investigators have as-
sessed tertiary startle parameters such as habituation and prepulse
inhibition. Habituation reflects the rate at which individuals show
diminished psychophysiological responses to repeated presenta-
tions of the same startling sound. It is usually expressed as either
the slope of the line representing the diminution of responses over
time or the number of trials (i.e., sound exposures) required before
achieving a predefined nonresponse criterion (e.g., Shalev, Orr,
Peri, Schreiber, & Pitman, 1992). Because habituation, in part,
indicates how quickly an organism can regulate its response to
repeated aversive stimuli, PTSD patients are expected to show
slower habituation rates than do their counterparts without PTSD.
Prepulse inhibition refers to the amount of eyeblink response
reduction caused by the introduction of a less intense, nonstartling
stimulus just prior to the startling stimulus (e.g., Grillon, Morgan,
Southwick, Davis, & Charney, 1996). Because prepulse inhibition
is reduced in some individuals who have difficulty blocking un-
wanted thoughts (e.g., schizophrenic patients), theorists have spec-
ulated that it might be reduced in PTSD.
Laboratory studies have yielded mixed evidence of relationships
between PTSD and these startle measures. Some inconsistencies
have been attributed to unmeasured variability in contextual threat
(Grillon et al., 1998a). A meta-analysis of 11 startle studies con-
cluded that PTSD is associated with larger eyeblink, HR, and SC
responses and slower SC habituation (Metzger et al., 1999). There
are no published meta-analytic estimates of the relationships be-
tween PTSD and either prepulse inhibition or habituation of other
psychophysiological measures. Moreover, no meta-analyses have
examined whether contextual threat moderates startle effect sizes.
Psychophysiological Responses to Standardized Trauma
Elevated psychophysiological reactivity to reminders of trauma
(Criterion B5) has been cited as the most common symptom
reported by PTSD patients (Davidson et al., 1991). A two-factor
learning theory (Keane, Zimering, & Caddell, 1985) has been
proposed to explain why this symptom occurs in response to
external trauma cues. This theory holds that (a) trauma reminders
are classically conditioned to evoke the intense psychophysiolog-
ical reactions that occurred at the time of the trauma and (b) these
responses fail to become extinguished because of operantly con-
ditioned avoidance behaviors. This symptom has been corrobo-
rated by several laboratory studies examining differences between
groups with and without PTSD in their psychophysiological re-
sponses to standardized audiovisual representations of their trau-
matic event. For example, combat veterans have been exposed to
combat sounds (e.g., Liberzon, Abelson, Flagel, Raz, & Young,
1999), and motor vehicle accident survivors have been exposed to
videotapes of car crashes (e.g., Blanchard, Hickling, Taylor, Loos,
& Gerardi, 1994). Though these studies have never been subjected
to a meta-analysis, qualitative reviews suggest they have generally
found elevated psychophysiological reactivity in groups with
PTSD as compared with those without PTSD (for reviews, see
Blanchard, 1990; Shalev & Rogel-Fuchs, 1993).
The differences between psychophysiological responses of
PTSD and non-PTSD participants to trauma cues have been sub-
stantial enough that investigators have wondered whether these
responses could be used as diagnostic markers of PTSD. An
important consideration in this regard is to first determine whether
psychophysiological responses consistent with PTSD can be faked.
Researchers have found that individuals without PTSD can vol-
untarily mimic some psychophysiological features of PTSD (Ger-
ardi, Blanchard, & Kolb, 1989; Orr & Pitman, 1993) and that
PTSD patients can decrease some of their psychophysiological
responses to simulate the responses of nonpatients (Laor et al.,
1998). However, it appears that even with these efforts of simu-
lation in place, PTSD patients can still be distinguished from
nonpatients by using discriminant function analyses with between
75% and 89% overall accuracy (Gerardi et al., 1989; Orr &
In the absence of deliberate simulation, some studies have
reported that psychophysiological measures can accurately classify
between 80% and 100% of participants into either PTSD or non-
PTSD groups (Keane, Wolfe, & Taylor, 1987). However, gener-
ally speaking, specificity outstrips sensitivity. For example,
whereas it has not been unusual for investigators to accurately
classify between 80% and 100% of participants in the non-PTSD
group, up to 40% of participants diagnosed with PTSD via struc-
tured interviews have been misclassified on the basis of their
psychophysiological responses (Keane et al., 1998; Laor et al.,
1998). Explanations for these so-called “nonresponders” range
from speculations about errors in the diagnostic or psychophysio-
logical measurement process (Laor et al., 1998) to empirical evi-
dence showing that such nonresponders either deny having exag-
gerated physiological reactivity to trauma cues (Pitman et al.,
1990) or report having less severe PTSD symptoms than do their
counterparts who are correctly classified (e.g., Blanchard, Kolb,
Taylor, & Wittrock, 1989; Keane et al., 1998). An important
alternative explanation that is also consistent with the two-factor
learning theory is that some kinds of traumatic experiences (e.g.,
repeated and inescapable childhood trauma) may trigger different
but functionally appropriate (Lang, Davis, & Ohman, 2000) re-
sponses such as psychophysiological hypoarousal and/or dissoci-
ation. These responses are viewed as being consistent with “help-
lessness or freezing” rather than “fight or flight” (Nijenhuis,
Vanderlinden, & Spinhoven, 1998). Because of classical condi-
tioning, these kinds of trauma responses would be expected to
re-emerge in the laboratory as hypoarousal responses to trauma
reminders (e.g., Griffin, Resick, & Mechanic, 1997; Lanius et al.,
2002; Pole et al., 2006). Thus, a different physiological response
profile would be required for accurate classification of these
Psychophysiological Responses to Idiographic Trauma
A limitation of the standardized trauma cue studies is that they
can be used only to elicit reminders of trauma that can be depicted
by standard stimuli. Idiosyncratic aspects of trauma experiences
may be more difficult to capture. To address this issue, investiga-
tors have measured psychophysiological reactivity in participants
with and without PTSD as they recall the details of their personal
traumatic event. The most common paradigm uses a highly struc-
tured, individually tailored, script-driven imagery procedure (e.g.,
Pitman, Orr, Forgue, de Jong, & Claiborn, 1987). The investigator
and participant create a brief narrative account of the participant’s
traumatic event following a standardized format. The participant
listens to his or her script as it is read in the present tense and is
instructed to mentally relive the event while psychophysiological
responses are recorded.
Because internal representations of the trauma are the eliciting
cue in this paradigm, Lang’s (1985) bioinformational theory of
emotion is commonly used to explain it. In this theory, exagger-
ated psychophysiological responses in PTSD are viewed as part of
an associated network of responses that are activated by internal or
external trauma reminders. Consistent with the two-factor theory,
the network recapitulates the responses that occurred during the
trauma. Idiographic trauma cue studies have never been subjected
to a meta-analysis, but qualitative reviews indicated they have
consistently found groups with PTSD to show larger psychophys-
iological responses than do their non-PTSD counterparts (e.g., Orr,
Pitman, Lasko, & Herz, 1993; Orr, Lasko, et al., 1998; Pitman et
al., 1987, 1990; Shalev, Orr, & Pitman, 1993). Psychophysiolog-
ical data from idiographic trauma cue studies have also been
examined for their potential as biological markers of PTSD. The
results have been similar to those achieved with standardized
trauma cue studies, that is, the measures show very good speci-
ficity, but up to 40% of PTSD patients are incorrectly classified on
the basis of their psychophysiological responses (Orr & Roth,
The Present Meta-Analysis
The goals of the present meta-analysis were to determine (a)
whether PTSD is reliably related to aggregate laboratory measures
of persistent hyperarousal, abnormal startle responding, and ele-
vated reactivity to standardized and idiographic trauma cues; (b)
PSYCHOPHYSIOLOGY OF PTSD META-ANALYSIS
which specific psychophysiological measures are reliably and
most robustly related to PTSD; (c) which psychophysiological
measures show a dominant relationship with PTSD and with each
other under specific laboratory conditions; and (d) what variables
moderate the relationships between PTSD and psychophysiologi-
cal arousal and reactivity.
Selection of Studies Included in the Meta-Analysis
I selected studies in English, published between 1980 (the year
that PTSD formally entered the psychiatric nosology) and 2004,
comparing adults with and without PTSD on at least one of the
following psychophysiological dependent measures: HR, SC,
SBP, DBP, orbicularis oculi EMG (O-EMG), frontalis EMG
(F-EMG), corrugator EMG (C-EMG), or zygomaticus EMG
(Z-EMG). Studies were identified with computer databases (i.e.,
PsycArticles, PsycINFO, PILOTS, MEDLINE, and PubMed), re-
view articles, and book chapters (e.g., Orr et al., 2004; Prins et al.,
1995). Each issue of all journals that had previously published
pertinent articles was hand searched, beginning with the 1980
issue.1The Introduction and Discussion sections of all included
studies were also examined for additional relevant studies.
Studies Excluded From the Meta-Analysis
Unpublished dissertations, masters theses, and conference pre-
sentations were excluded from this meta-analysis, which is con-
sistent with other meta-analyses of the PTSD literature (e.g.,
Brewin et al., 2000; Ozer et al., 2003). Duplicate publications (e.g.,
Morgan, Grillon, Lubin, & Southwick, 1997a, 1997b) or studies
reporting on the same sample (e.g., Beckham et al., 2000; Beck-
ham et al., 2002) were counted only once. Studies that did not
report results in terms of a PTSD group (e.g., Medina, Mejia,
Schell, Dawson, & Margolin, 2001) or a non-PTSD group (e.g.,
Blanchard, Hickling, & Taylor, 1991; Hyer, Albrecht, Boudewyns,
Woods, & Brandsma, 1993; Shalev & Rogel-Fuchs, 1992) were
also excluded unless the authors were able to reanalyze their data
in terms of a comparison between groups with and without PTSD
(e.g., Pole et al., 2003). Studies were excluded if they reported
psychophysiology data that were exclusively ambulatory (i.e.,
obtained while the participant engaged in normal daily activities;
e.g., Beckham et al., 2003) or prospective (i.e., obtained before the
participants met diagnostic criteria for PTSD; e.g., Bryant, Harvey,
Guthrie, & Moulds, 2000). Excluded studies were checked by an
independent research assistant to ensure adherence to the exclusion
Calculation of Effect Sizes
Studies were included in the meta-analysis only if enough
information could be gleaned to calculate at least one effect size
representing the difference between groups with and without
PTSD on one of the designated psychophysiological variables.
Some studies compared PTSD groups with more than one type of
control group. These studies typically included both a control
group that was exposed to the same index trauma as the PTSD
group and a control group that was not exposed to such trauma.
Whenever possible, effect sizes were calculated with respect to a
trauma-exposed control group. This was done with the expectation
that such effect sizes would provide the most conservative estimate
of the effects of PTSD status over and above the effects of mere
trauma exposure. When insufficient information was presented in
the published report, some authors supplied the data required to
compute the target effect sizes (e.g., Orr, Lasko, et al., 1998; Orr,
Meyerhoff, Edwards, & Pitman, 1998; Orr & Pitman, 1993; Tara-
brina et al., 2001). In other cases, the appropriate effect sizes were
gleaned from secondary sources, that is, books (e.g., Blanchard &
Hickling, 2004), review articles (e.g., Prins et al., 1995), or other
meta-analyses (e.g., Buckley & Kaloupek, 2001). When such
information could not be gleaned for any relevant psychophysio-
logical measure, the study was excluded (e.g., Grillon & Morgan,
1999; Laor et al., 1998; Malloy, Fairbank, & Keane, 1983; Mc-
Durmut, Haaga, & Kirk, 2000; McNally et al., 1987).
Meta-analyses normally include only one effect size per con-
struct per study. In the present meta-analysis, the concept of
construct was defined so that each psychophysiological response
measure was viewed as a separate construct. Thus, several effect
sizes were often derived from a given study, each representing a
different construct. For example, the HR response to an idio-
graphic trauma cue was defined as a separate construct from the
SC response to the same trauma cue. Similarly, the HR response to
an idiographic trauma cue was defined as a separate construct from
the HR response to a standardized trauma cue even when these
measures were assessed in the same study. When more than one
measure was reported for a particular construct (e.g., several
measures of startle eyeblink), the mean response (e.g., mean
O-EMGR to all startling sounds) was used to calculate the effect
size. In addition to the separate effect sizes for each psychophys-
iological measure, an aggregate psychophysiological effect size
was obtained for each task by calculating the mean of all psycho-
physiological effect sizes assessing responses to the same task
(e.g., all physiological measures of responses to standard trauma
All study effect sizes were calculated following standard meta-
analytic procedures and expressed in terms of r (Rosenthal, 1994).
1The hand-searched journals included American Journal of Psychiatry,
Annals of Behavioral Medicine, Annals of the New York Academy of
Sciences, Applied Psychophysiology and Biofeedback, Archives of General
Psychiatry, Australian and New Zealand Journal of Psychiatry, Behavior
Research and Therapy, Behavior Therapy, Behavioural and Cognitive
Psychotherapy, Biofeedback and Self Regulation, Biological Psychiatry,
British Journal of Psychiatry, Clinical Psychology and Psychotherapy,
Comprehensive Psychiatry, Depression and Anxiety, European Archives of
Psychiatry and Clinical Neuroscience, Integrative Physiological and Be-
havioral Science, International Journal of Psychophysiology, Israel Jour-
nal of Psychiatry and Related Sciences, Journal of Abnormal Psychology,
Journal of Anxiety Disorders, Journal of Behavior Therapy and Experi-
mental Psychiatry, Journal of Clinical and Experimental Neuropsychol-
ogy, Journal of Clinical Psychiatry, Journal of Clinical Psychology, Jour-
nal of Clinical Psychopharmacology, Journal of Consulting and Clinical
Psychology, Journal of Nervous and Mental Disease, Journal of Neuro-
psychiatry, Journal of Russian and East European Psychology, Journal of
Traumatic Stress, Life Sciences, Neuropsychobiology, Neuropsychophar-
macology, NeuroReport, Psychiatric Annals, Psychiatric Quarterly, Psy-
chiatry, Psychiatry Research, Psychological Reports, Psychopathology,
Psychopharmacologia, Psychophysiology, Psychosomatic Medicine, and
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Received March 6, 2006
Revision received March 20, 2007
Accepted March 26, 2007 ?