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Peritraumatic Heart Rate and Posttraumatic Stress Disorder in Patients With Severe Burns

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Previous studies have suggested a link between heart rate (HR) following trauma and the development of posttraumatic stress disorder (PTSD). This study expands on previous work by evaluating HR in burn patients followed longitudinally for symptoms of acute stress disorder (ASD) and PTSD. Data were collected from consecutive patients admitted to the Johns Hopkins Burn Center, Baltimore, Maryland, between 1997 and 2002. Patients completed the Stanford Acute Stress Reaction Questionnaire (n = 157) to assess symptoms of ASD. The Davidson Trauma Scale was completed at 1 (n = 145), 6 (n = 106), 12 (n = 94), and 24 (n = 66) months postdischarge to assess symptoms of PTSD. Heart rate in the ambulance, emergency room, and burn unit were obtained by retrospective medical chart review. Pearson correlations revealed a significant relationship between HR in the ambulance (r = 0.32, P = .016) and burn unit (r = 0.30, P = .001) and ASD scores at baseline. Heart rate in the ambulance was related to PTSD avoidance cluster scores at 1, 6, 12, and 24 months. In women, HR in the ambulance was correlated with PTSD scores at 6 (r = 0.65, P = .005) and 12 (r = 0.78, P = .005) months. When covariates (gender, β-blockers, Brief Symptom Inventory Global Severity Index score) were included in multivariate linear regression analyses, ambulance HR was associated with ASD and PTSD scores at baseline and 1 month, and the interaction of ambulance HR and gender was associated with PTSD scores at 6 and 12 months. Multivariate logistic regression results were similar at baseline and 12 months, which included an HR association yet no interaction at 6 months and a marginal interaction at 1 month. While peritraumatic HR is most robustly associated with PTSD symptom severity, HR on admission to burn unit also predicts the development of ASD. Gender and avoidance symptoms appear particularly salient in this relationship, and these factors may aid in the identification of subgroups for which HR serves as a biomarker for PTSD. Future work may identify endophenotypic measures of increased risk for PTSD, targeting subgroups for early intervention.
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Gould et al
539 J Clin Psychiatry 72:4, April 2011
Peritraumatic Heart Rate and Posttraumatic Stress Disorder
in Patients With Severe Burns
Neda F. Gould, PhD; Jodi B. McKibben, PhD; Ryan Hall, MD; Nida H. Corry, PhD;
Nicole A. Amoyal, BA; Shawn T. Mason, PhD; Una D. McCann, MD; and James A. Fauerbach, PhD
Objective: Previous studies have suggested a
link between heart rate (HR) following trauma and
the development of posttraumatic stress disorder
(PTSD). This study expands on previous work by
evaluating HR in burn patients followed longitudi-
nally for symptoms of acute stress disorder (ASD)
and PTSD.
Method: Data were collected from consecutive
patients admitted to the Johns Hopkins Burn
Center, Baltimore, Maryland, between 1997 and
2002. Patients completed the Stanford Acute Stress
Reaction Questionnaire (n = 157) to assess symp-
toms of ASD. The Davidson Trauma Scale was
completed at 1 (n = 145), 6 (n = 106), 12 (n = 94),
and 24 (n = 66) months postdischarge to assess
symptoms of PTSD. Heart rate in the ambulance,
emergency room, and burn unit were obtained by
retrospective medical chart review.
Results: Pearson correlations revealed a sig-
nificant relationship between HR in the ambulance
(r = 0.32, P = .016) and burn unit (r = 0.30, P = .001)
and ASD scores at baseline. Heart rate in the ambu-
lance was related to PTSD avoidance cluster scores
at 1, 6, 12, and 24 months. In women, HR in the
ambulance was correlated with PTSD scores at 6
(r = 0.65, P = .005) and 12 (r = 0.78, P = .005) months.
When covariates (gender, β-blockers, Brief Symp-
tom Inventory Global Severity Index score) were
included in multivariate linear regression analyses,
ambulance HR was associated with ASD and PTSD
scores at baseline and 1 month, and the interaction
of ambulance HR and gender was associated with
PTSD scores at 6 and 12 months. Multivariate logis-
tic regression results were similar at baseline and
12 months, which included an HR association yet
no interaction at 6 months and a marginal interac-
tion at 1 month.
Conclusions: While peritraumatic HR is most
robustly associated with PTSD symptom severity,
HR on admission to burn unit also predicts the
development of ASD. Gender and avoidance symp-
toms appear particularly salient in this relationship,
and these factors may aid in the identification of
subgroups for which HR serves as a biomarker for
PTSD. Future work may identify endophenotypic
measures of increased risk for PTSD, targeting sub-
groups for early intervention.
J Clin Psychiatry 2011;72(4):539–547
© Copyright 2010 Physicians Postgraduate Press, Inc.
Submitted: May 31, 2009; accepted September 28, 2009.
Online ahead of print: October 19, 2010 (doi:10.4088/JCP.09m05405blu).
Corresponding author: Neda F. Gould, PhD, Johns Hopkins University
School of Medicine, Department of Psychiatry and Behavioral Sciences,
4940 Eastern Ave, Asthma and Allergy Center, 5B.71B, Baltimore,
MD 21224 (ngould1@jhmi.edu).
Acute stress disorder (ASD) and posttraumatic stress
disorder (PTSD) are frequently observed after ex-
posure to traumatic events and they can be extremely
debilitating disorders. Posttraumatic stress disorder occurs
in approximately 20% of trauma victims, often resulting in
significant impairment in physical, occupational, and so-
cial functioning,1 and 80% of individuals with ASD may
go on to develop PTSD.2 Given the devastating impact of
PTSD, efforts to understand the psychological and physi-
ologic variables associated with fear conditioning provide
an opportunity for advances in treatment. Currently, at-
tempts to identify individuals at risk for the development
of ASD and PTSD after a trauma have produced inconsis-
tent findings. Although self-report and clinician-assessed
infor mation are useful, identification of biologic markers or
endophenotypes3 associated with these disorders may yield
more accurate diagnosis and highlight the dynamic interplay
between traumatic events, time parameters, psychological
interpretation, and physiologic reactivity.
Acute physiologic responses following trauma may
provide useful markers for predicting subsequent PTSD.
Increased arousal is a necessary criterion in the diagnosis
of PTSD, and physiologic reactivity is a common form of
re-experiencing associated with the disorder according to
the Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition, Text Revision (DSM-IV-TR).4 In fact, hyper-
arousal symptoms often remain even after the remission of
other symptoms.5 It has been postulated that sympathetic
arousal immediately after a traumatic event may lead to
overconsolidation of trauma memories6 and that hyperac-
tivity of the sympathetic nervous system may prevent normal
memory processing.7 Memory processing is believed to be
mediated by overstimulated endogenous stress hormones
and neuromodulators after the traumatic event.6 This series
of events may ultimately lead to the development of PTSD.7
Indeed, preclinical research has revealed that epinephrine
may enhance the consolidation of learning of a traumatic
memory and fear conditioning in both human6 and animal
models.8,9 As such, understanding the pathophysiology of
hyperarousal may lead to a clearer understanding of the
development of PTSD.
Elevated heart rate (HR) is among the most salient
by-products of increased sympathetic arousal. However, to
date, there has been some inconsistency in extant investiga-
tions of the relationship between HR and the development
of PTSD. In their initial study, Shalev et al10 reported that
elevated HR after trauma was predictive of the subsequent
development of PTSD. This finding was replicated in
adults11,12 and children,13 and, most recently, in an elegantly
Peritraumatic Heart Rate and PTSD in Severe Burns
J Clin Psychiatry 72:4, April 2011 540
designed, large, multisite study by Bryant and colleagues.14
In contrast, in a study by Blanchard et al,15 elevated HR was
not predictive of PTSD. In fact, in this latter study, patients
with elevated HR were less likely to develop PTSD.
Possible reasons for discrepancies across studies include
differences in methodology, such as symptom assessment (self
vs clinician report), composition of samples, and timing of
PTSD assessment,16 as well as the temporal assessment of HR,
injury severity, and PTSD symptom criteria.17 In this regard,
even minor differences in patient samples may result in dif-
ferences across studies.17 Nevertheless, recent meta- analytic
reviews have revealed a significant association between PTSD
and elevated HR18 and have identified HR as one of the most
reliable psychophysiological correlates of PTSD.19
Thus, the purpose of the present study was to more clearly
elucidate factors involved in the relationship between physio-
logic arousal and the development and maintenance of PTSD.
The present study expands on previous work in this realm by
examining the relationship between HR and blood pressure
(BP) and both in-hospital ASD and PTSD through 2-year
follow-up in a group of trauma survivors who underwent
a similar type of trauma, therefore minimizing the variabil-
ity within the study sample. To our knowledge, this study
is the first to examine this relationship that (1) examines a
sample of adult patients with severe burn injury, (2) assesses
the potential relationship between HR and BP and specific
symptom clusters of ASD and PTSD (a largely unexamined
topic), (3) accounts for the role of relevant demographic
(eg, gender) and clinical (eg, use of β-blockers) variables, and
(4) obtains HR and BP measurements at various time points
following the trauma (ie, in the ambulance, emergency room,
and burn unit).
METHOD
Sample
Data were collected from consecutive patients admitted
to the Johns Hopkins Burn Center, Baltimore, Maryland,
between 1997 and 2002. Eligible participants met at least
1 criterion for major burn injury as determined by the
American Burn Association, and they were at least 18 years of
age. The American Burn Association criteria for major burn
injury included deep second and third degree burns with the
following variations: greater than 10% total body surface area
(TBSA) in patients over 50 years old; greater than 20% TBSA
in other age groups; burns with serious threat of functional
or cosmetic threat that involve face, hands, feet, genitalia,
perineum, or major joints; third degree burns greater than
5% TBSA in any age group; deep electrical burns, in cluding
lightning injury; inhalation injury with burn injury; or cir-
cumferential burns of the extremity or chest. Participants
were excluded if they presented with cognitive limitations
precluding adequate consent, comprehension, or benefit, or
if their level of fluency in English would prevent them from
understanding the consent or protocol. Additionally, patients
were excluded from further participation if they were incar-
cerated after discharge.
Our sample included 167 adult burn patients (mean
age = 40.2 years, SD = 14.4) who were predominantly male
(71.9%), white (60.5%), had an average TBSA of 15.5%
(SD = 14.8), and the majority of whom worked at the time
of injury (74.3%). The primary etiology of burn injuries in
our sample was due to flame/fire (55.1%), followed by scald
(18.0%), grease (9.0%), and thermal contact (6.6%) burns
(sample demographic characteristics and descriptive statis-
tics for variables are presented in Table 1). Participation in
this study was voluntary, and the protocol was approved by
the Johns Hopkins University School of Medicine Institu-
tional Review Board.
Measures
Psychiatric measures. The Davidson Trauma Scale
(DTS)20 is a 17-item self-report measure based on the
Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition (DSM-IV).21 Frequency and severity items for symp-
toms are rated on a 0–4 scale, with higher scores indicative
of greater severity or frequency. Analyses of the DTS have
demonstrated test-retest reliability with a coefficient of 0.86
(P < .01) and high internal consistency (α = .99) for the fre-
quency and severity items.20 Furthermore, the DTS has been
shown to reliably predict PTSD diagnosis as measured by
the Structured Clinical Interview for the DSM-IV when a
diagnostic cutoff score of 40 is used.20
The Stanford Acute Stress Reaction Questionnaire
(SASRQ)22 is a 30-item self-report measure used for the
Table 1. Sample Demographics and Descriptive Statistics
(total N = 167)
Variable n (%)
Sex, male 120 (71.9)
Ethnicity
White 101 (60.5)
African American 56 (33.5)
Hispanic 4 (2.4)
Other 1 (0.6)
Participants employed 124 (74.3)
Etiology of burn
Flame 92 (55.1)
Scald 30 (18.0)
Grease 15 (9.0)
Hot object 11 (6.6)
Chemical 4 (2.4)
Electricity 5 (3.0)
Tar 4 (2.4)
Other 6 (3.6)
Mean (SD)
Age, y 40.2 (14.4)
Length of hospital stay, d 16.8 (14.1)
Heart rate measurement, locationa
Ambulance 105.0 (16.2)
Emergency room 94.7 (17.3)
Burn unit 87.3 (18.0)
SASRQ total score 39.5 (29.0)
DTS total score, time postdischarge
1 mo 33.2 (31.4)
6 mo 31.9 (31.6)
12 mo 28.3 (29.3)
24 mo 28.7 (30.2)
aHeart rate values reported in beats per minute.
Abbreviations: DTS = Davidson Trauma Scale, SASRQ = Stanford Acute
Stress Reaction Questionnaire.
Gould et al
541 J Clin Psychiatry 72:4, April 2011
assessment of ASD. Frequency of symptoms, including
re-experiencing, dissociation, avoidance, hyperarousal, and
impairment in functioning were rated on a Likert-type scale
ranging from 0 to 5. A previously published algorithm was
used on the basis of the DSM-IV criteria23 that indicate a
diagnostic cutoff score of 3 for each of the items and require
the endorsement of 3 of the 5 dissociative symptoms (that
correspond to the 5 DSM-IV dissociative symptoms), and 1
symptom each from the reexperiencing, avoidance, hyper-
arousal, and impairment domains. Table 2 shows clinical
characteristics of participants dichotomized by SASRQ and
DTS cutoff scores. α Coefficients for the SASRQ demonstrate
high internal consistency for anxiety and dissociative symp-
toms (α = .91 and α = .90, respectively22).
The Brief Symptom Inventory (BSI)24 is a 53-item version
of the Symptom Checklist 90-Revised25 that measures severity
of psychological distress over the previous 7 days. Respon-
dents rate how much they were distressed by each symptom
using a 5-point Likert scale (0 = not at all, 4 = always). The
BSI has good internal consistency and retest reliability.24
The Global Severity Index (GSI) is the BSI’s most sensitive
index of psychological distress,26 and it has been shown to
discern among clinical and normative populations.27 The
GSI was dichotomized at T-score ≥ 63 (high distress) versus
T-score < 63 (low distress). This GSI cutoff has been shown to
be a valid and reliable marker for the presence of a significant
psychiatric condition (ie, clinically significant psychological
distress) warranting evaluation and possible intervention24
and has been used in other large-scale, multisite studies in
injured populations.28 Rather than a gold-standard structured
clinical interview, a self-report psychological assessment tool
was used—primarily to minimize the burden on participants
given the long-term nature of the study.
Cardiovascular Measures
Heart rate and BP were measured manually by stethoscope
and sphygmomanometer administered by the emergency
medical technicians in the ambulance during transporta-
tion to the hospital. A Simmons monitor (Siemens, Danvers,
Massachusetts) was used to assess HR and BP in the emer-
gency room and inpatient intensive care unit (ICU). Both
Simmons and Spacelab monitoring equipment (Spacelab
Medical Inc, Issaquah, Washington) were used to measure
HR and BP during the patients’ stay in the surgical interme-
diate care center, a step-down inpatient unit from the ICU.
Procedures
This study was part of a national study targeting the
assessment and treatment of patients with major burn injuries.
As part of a larger, multisite study, participants’ demographic
and clinical variables including age, gender, TBSA, ethnicity,
etiology, location of burn, and employment were obtained
by chart review. Patients were approached for consent within
72 hours of accessibility during their stay in the inpatient
unit if they met eligibility criteria. All participants were
18 years or older and met American Burn Association cri-
teria for severe burns, as described above.
Participants completed the SASRQ and BSI at dis-
charge (n = 157), and the DTS, BSI, and other psychological
questionnaires at 1 month (n = 145), 6 months (n = 106),
12 months (n = 94), and 24 months (n = 66) after discharge
from the hospital. A retrospective medical chart review
was conducted to acquire participants’ HR, systolic BP, and
diastolic BP in the ambulance and on admission to the emer-
gency room and burn unit. Total body surface area burned
was also gathered from chart review.
Statistical Analyses
Normality of data distribution for all outcome measures
was established by evaluating skew and kurtosis, which
ranged from 0.60 to 1.1, well within the normal range.
Pearson correlations were calculated to assess the
relationship between HR and BP at each of the time points
(ie, ambulance, admittance to emergency room, transfer to
burn unit) with total SASRQ and DTS scores at 1, 6, 12,
and 24 months. In addition, SASRQ and DTS subscale
scores were analyzed. Subscales for the SASRQ included
reexperiencing, avoidance, arousal, and dissociative symptom
clusters; while the DTS included re-experiencing, avoid-
ance, and hyperarousal symptom cluster scores. Finally, post
hoc analyses assessed HR correlations for male and female
patients separately.
To test the hypothesis that HR is predictive of posttrau-
matic stress symptom severity, linear regression analyses
Table 2. Clinical Characteristics of Participants Dichotomized by SASRQ and DTS Cutoff Scoresa
Characteristic
SASRQ <
Diagnostic
Cutoff
(n = 119)
SASRQ
Diagnostic
Cutoff
(n = 38)
DTS < 40,
1 mo
(n = 91)
DTS 40,
1 mo
(n = 54)
DTS < 40,
6 mo
(n = 70)
DTS 40,
6 mo
(n = 36)
DTS < 40,
12 mo
(n = 65)
DTS 40,
12 mo
(n = 29)
DTS < 40,
24 mo
(n = 45)
DTS 40,
24 mo
(n = 21)
Age, y 38.0 (14.6) 38.1 (10.5) 37.6 (13.5) 39.3 (12.5) 40.4 (15.5) 36.5 (10.8) 39.5 (15.0) 36.1 (11.7) 38.7 (15.0) 36.2 (10.7)
Heart rateb
Ambulance
101.8 (14.8) 110.7 (17.1) 103.8 (13.8) 108.9 (17.1) 101.5 (14.8) 113.4 (16.3) 103.2 (16.8) 107.8 (16.5) 100.4 (18.1) 111.2 (11.9)
Emergency
room
93.2 (16.2) 98.6 (19.9) 95.3 (17.2) 96.8 (15.5) 94.6 (18.2) 96.0 (18.3) 92.7 (20.4) 93.5 (18.6) 93.2 (18.5) 92.6 (14.3)
Burn unit
85.0 (16.5) 93.3 (21.3) 86.5 (16.0) 90.0 (19.7) 86.1 (17.1) 90.3 (20.4) 84.2 (17.4) 87.8 (20.7) 86.1 (17.3) 88.8 (19.7)
SASRQ total
score
27.3 (19.3) 77.5 (19.9)
DTS total score 12.4 (11.2) 68.2 (21.6) 12.3 (11.8) 70.2 (20.9) 11.0 (10.7) 67.1 (18.4) 11.3 (12.2) 65.8 (22.6)
aAll values reported as means and standard deviations.
bHeart rate values reported in beats per minute, in locations where heart rate was measured.
Abbreviations: DTS = Davidson Trauma Scale, SASRQ = Stanford Acute Stress Reaction Questionnaire.
Peritraumatic Heart Rate and PTSD in Severe Burns
J Clin Psychiatry 72:4, April 2011 542
were used to evaluate the role of HR readings in the ambu-
lance in accounting for SASRQ and DTS continuous scores
at 1, 6, 12, and 24 months. Logistic regression analyses were
used to examine SASRQ and DTS dichotomous variables
(ie, diagnostic status) across assessment periods. Due to
attrition, a ubiquitous problem among longitudinal stud-
ies, only a limited subset of covariates were included in the
analyses, and they were selected on the basis of theoreti-
cal significance. Thus, the following variables were used as
predictors in the regression analyses: gender, β-blockers
(present or absent), BSI GSI score (high and low distress, as
defined above), and the HR × gender interaction. Goodness
of fit for each of the models was evaluated using the Hosmer-
Lemeshow statistic.
All tests were 2-tailed and considered significant at P < .05.
Analyses were conducted using SPSS version 16.0 (SPSS Inc,
Chicago, Illinois) and Stata Statistical Software, Release 9.2
(StataCorp LP, College Station, Texas).
RESULTS
Pearson correlations revealed a significant relationship
between HR in the ambulance and SASRQ (r = 0.32, P = .016,
n = 58) and total DTS scores at 6 months (r = 0.44, P = .003,
n = 44). In addition, burn unit HR was significantly corre lated
with total SASRQ score (r = 0.30, P = .001, n = 112) (Figure 1).
Importantly, when the aforementioned relationships were
assessed by gender, a significant HR × gender interaction
was revealed whereby HR in the ambulance corresponded
to higher total DTS scores at 6 (r = 0.65, P = .005, n = 17) and
12 (r = 0.78, P = .005, n = 11) months in women only. These
findings were not significant for male participants. Blood
pressure was not related to SASRQ or DTS scores.
When SASRQ and DTS overall scores were divided
into their respective subscales, HR in the ambulance was
significantly related to the following continuous subscale
scores: DTS avoidance at 1, 6, 12, and 24 months and DTS
reexperiencing and arousal at 6 months. Thus, initial HR
measurements in the ambulance appear to be most consis-
tently related to PTSD/DTS avoidance symptom clusters up
to 2 years postinjury (Table 3). When dichotomized into
those meeting and not meeting criteria for ASD, the SASRQ
reexperiencing cluster was significantly correlated with HR
in the ambulance, and the arousal cluster was correlated with
HR on the burn unit.
Linear Regression Analyses
An important objective of this study is to determine
whether HR (obtained in the ambulance) would predict
ASD scores at baseline (as assessed with the SASRQ) and
PTSD scores (as assessed with the DTS) at 1, 6, 12, and
24 months. First, simple/crude linear regression analyses
were completed, and the results indicated significant asso-
ciations between HR and ASD/PTSD scores at baseline and
6 months (Tables 4A and 4B). In the multiple linear regres-
sion analyses used to address the question above, HR and the
Table 3. Significant Correlations Between Ambulance
Heart Rate and DTS Subscale Scores at Various Time Pointsa
DTS Subscale Pearson R P Value n
Avoidance, at 1 mo 0.274 .039 57
Avoidance, at 6 mo 0.461 .001 45
Avoidance, at 12 mo 0.330 .033 42
Avoidance, at 24 mo 0.344 .021 45
Reexperiencing, at 6 mo 0.397 .037 28
Arousal, at 6 mo 0.414 .005 44
aAll variables are continuous.
Abbreviation: DTS = Davidson Trauma Scale.
Figure 1. Significant Correlations Between Heart Rate (HR)
and Continuous Outcome Variables
Abbreviations: bpm = beats per minute, DTS = Davidson Trauma Scale,
SASRQ = Stanford Acute Stress Reaction Questionnaire.
140.00
120.00
100.00
80.00
60.00
Ambulance HR, bpm
0.00 20.00 40.00 60.00 80.00 100.00 120.00
SASRQ Total Score
140.00
120.00
100.00
80.00
60.00
Ambulance HR, bpm
0.00 25.00 50.00 75.00 100.00 125.00
DTS Total Score at 6 mo
140.00
120.00
100.00
80.00
60.00
40.00
Burn Unit HR, bpm
0.00 20.00 40.00 60.00 80.00 100.00 120.00
SASRQ Total Score
Gould et al
543 J Clin Psychiatry 72:4, April 2011
Table 4B. Results of Linear Regression Analyses Relating Heart Rate to SASRQ (algorithm-based cutoff) and DTS (cutoff 40)a
12 Months Postdischarge (n = 41) 24 Months Postdischarge (n = 27)
Predictors at Baseline Crude Bb (95% CI) Adjusted Bc (95% CI) Crude B (95% CI) Adjusted B (95% CI)
Heart rate
1-unit increase 0.42 (–0.08 to 0.91) 0.13 (–0.40 to 0.66) 0.54 (–0.14 to 1.21)
1-SD increase 6.93 2.18 9.36
Gender, male vs female 9.75 (–9.03 to 28.52) –130.45* (–253.97 to –6.92) 20.83 (–3.41 to 45.07) 23.16* (2.14 to 44.17)
Heart rate × genderd
1-unit increase 1.45* (0.42–2.48) … …
1-SD increase 24.13
BSI score, ≥ 63 vs < 63 14.39 (–2.26 to 31.04) 24.33* (0.65 to 48.01)
β-blockers, yes vs no 16.73 (–5.02 to 38.48) 39.55* (9.58 to 69.53) 41.82** (13.93 to 69.71)
aSASRQ used at baseline; DTS used at 1, 6, 12, and 24 months postdischarge. bUnivariate association between predictors and SASRQ. cMultivariate association between predictors and SASRQ/DTS after adjusting
for all remaining predictors in the model. dValues displayed are for women.
*P < .05; **P < .01; ***P < .001.
Abbreviations: BSI = Brief Symptom Inventory, DTS = Davidson Trauma Scale, SASRQ = Stanford Acute Stress Reaction Questionnaire.
Symbol: … = not included in model.
Table 4A. Results of Linear Regression Analyses Relating Heart Rate to SASRQ (algorithm-based cutoff) and DTS (cutoff 40)a
Predictors at Baseline
Baseline (n = 56) 1 Month Postdischarge (n = 52) 6 Months Postdischarge (n = 44)
Crude Bb (95% CI) Adjusted Bc (95% CI) Crude B (95% CI) Adjusted B (95% CI) Crude B (95% CI) Adjusted B (95% CI)
Heart rate
1-unit increase 0.55* (0.06 to 1.05) 0.67*** (0.33 to 1.02) 0.43 (–0.13 to 1.00) 0.52* (0.004 to 1.04) 0.89** (0.33 to 1.45) 0.51 (–0.07 to 1.09)
1-SD increase 9.00 10.94 6.54 7.94 14.43 8.24
Gender, male vs female 14.90 (–1.85 to 31.66) 13.73 (–3.48 to 30.94) 20.28* (0.65 to 39.92) –130.95* (–250.41 to –11.49)
Heart rate × genderd
1-unit increase 1.93* (0.97 to 2.88)
1-SD increase 31.36
BSI score, ≥ 63 vs < 63 41.81*** (29.08 to 54.54) 43.80*** (32.43 to 55.17) 24.32** (7.71 to 40.92) 26.12** (9.90 to 42.34) 11.66 (–8.65 to 31.96) 17.60* (1.11 to 34.09)
β-blockers, yes vs no 29.85* (7.43 to 52.28) 21.22 (–2.02 to 44.45) 23.60 (–1.38 to 48.58)
aSASRQ used at baseline; DTS used at 1, 6, 12, and 24 months postdischarge. bUnivariate association between predictors and SASRQ. cMultivariate association between predictors and SASRQ/DTS after adjusting
for all remaining predictors in the model. dValues displayed are for women.
*P < .05; **P < .01; ***P < .001.
Abbreviations: BSI = Brief Symptom Inventory, DTS = Davidson Trauma Scale, SASRQ = Stanford Acute Stress Reaction Questionnaire.
Symbol: … = not included in model.
aforementioned covariates (ie,
gender, β-blockers, and BSI) were
used. Once missing data across
the predictor variables were ac-
counted for, 56 cases remained
for the analysis at baseline, 52 for
the 1-month follow-up period,
44 at 6 months, 41 at 12 months,
and 27 at 24 months. The initial
model contained all covariates.
Using a backward elimination
linear regression procedure, co-
variates were removed on the
basis of the Wald tests. In the
case of significant interactions,
all lower-order covariates in the
interaction were retained in the
model, regardless of significance.
When all eligible nonsignificant
covariates were removed, the fol-
lowing variables were retained in
models assessing the relationship
of ambulance HR with ASD and
PTSD: Heart rate and BSI score
at baseline (adjusted R2 = 0.55,
σ̂ = 20.63); HR and BSI score
at 1 month (adjusted R2 = 0.18,
σ̂ = 27.86); HR, gender, BSI score,
and HR × gender at 6 months
(adjusted R2 = 0.36, σ̂ = 26.00);
HR, gender, and HR × gender at
12 months (adjusted R2 = 0.14,
σ̂ = 24.40); and gender and
β-blockers at 24 months (adjusted
R2 = 0.31, σ̂ = 24.87).
At baseline and 1 month post-
discharge, a 1-unit increase in
HR was associated with a 0.67
increase in the total SASRQ score
and an increase of 0.52 in the
total DTS score (see Tables 4A
and 4B). In order to put this
finding into perspective, it may
be useful to consider an SD in-
crease in HR as well (SD = 16.22
at baseline and 15.15 at 1 month).
A 1-SD increase in HR was asso-
ciated at baseline and 1 month
with an increase of 10.94 in
the total SASRQ score and an
increase of 7.94 in the total DTS
score. At 6 and 12 months, there
were differential effects across
sex/gender. For men and women,
a unit increase in HR was associ-
ated at 6 months with a 0.51 and
a 1.93 increase in the total DTS
Peritraumatic Heart Rate and PTSD in Severe Burns
J Clin Psychiatry 72:4, April 2011 544
score, respectively. A 1-SD increase in HR was associated
at 6 months (SD = 16.26) with an increase of only 8.24 for
men but 31.36 for women in total DTS scores. Further, for
men and women, a unit increase in HR was associated at
12 months with a 0.13 and 1.45 increase in the total DTS
score, respectively. For a 1-SD increase in HR (SD = 16.63),
the increases in the total DTS scores at 12 months were 2.18
and 24.13, respectively.
Logistic Regression Analyses
The aforementioned analyses were replicated with the
dichotomous PTSD and ASD diagnostic status dependent
variables described above. Once again, simple/crude logistic
regression analyses were completed, and the results indi cated
significant associations between HR and the PTSD cutoff
score at 6 months (see Tables 5A and 5B). In the multiple
logistic regression analyses, HR and the aforementioned pre-
dictor variables (ie, gender, β-blockers, and BSI score) were
used once again and the number of cases available for each of
the time periods was the same as indicated above. The initial
model contained all covariates. Using a backward elimina-
tion procedure, covariates were removed on the basis of the
likelihood ratio tests. In the case of significant interactions,
all lower-order covariates in the interaction were retained in
the model, regardless of significance. When all eligible non-
significant covariates were removed, the following variables
were retained in models assessing the relationship of ambu-
lance HR with ASD and PTSD: HR and BSI score at baseline
(Nagelkerke R2 = 0.31); BSI score at 1 month (Nagelkerke
R2 = 0.19); HR at 6 months (Nagelkerke R2 = 0.19); and HR,
gender, BSI score, and HR × gender at 12 months (Nagelkerke
R2 = 0.36). No variables were retained at the 24-month time
period. The Hosmer-Lemeshow goodness of fit χ2 statistics
were shown to be nonsignificant for the aforementioned
logistic regression analyses with the exception of the 1-month
time period. However, if an alternative model that includes
BSI score and a trend for HR × gender (P = .07), along with
HR and gender, is considered, then the Hosmer-Lemeshow
is nonsignificant (Nagelkerke R2 = 0.30).
A 1-unit increase/1-SD increase in HR (SD = 16.23) was
associated with it being 1.05 times/2.18 times more likely
for participants to have an SASRQ score above the cutoff
for ASD at baseline (Tables 5A and 5B). Heart rate was not
correlated with PTSD at 1 month. However, in the previ ously
mentioned model that included a trend for HR × gender at
1 month, a 1-unit increase in HR was associated with it
being 1.00 times as likely for men and 1.08 times more likely
for women to have a DTS score above the cutoff for PTSD.
Table 5A. Results of Logistic Regression Analyses Relating Heart Rate to SASRQ (algorithm-based cutoff) and DTS (cutoff 40)a
Predictors at Baseline
Baseline (n = 56) 1 Month Postdischarge (n = 52) 6 Months Postdischarge (n = 44)
Crude ORb (95% CI)
Adjusted ORc
(95% CI) Crude OR (95% CI)
Adjusted OR
(95% CI) Crude OR (95% CI)
Adjusted OR
(95% CI)
Heart rate
1-unit increase 1.03 (1.00 to 1.07) 1.05* (1.01 to 1.10) 1.01 (0.98 to 1.05) 1.06* (1.01 to 1.12) 1.06* (1.01 to 1.12)
1-SD increase 1.72 2.18 1.22 2.51 2.51
Gender, male vs
female
1.64 (0.53 to 5.08) 1.91 (0.61 to 6.09) 2.45 (0.65 to 9.58)
Heart rate × genderd
1-unit increase
1-SD increase
BSI score, ≥ 63 vs < 63 5.57** (1.76 to 19.33) 8.01** (2.23 to 35.44) 5.36** (1.63 to 19.31) 5.36** (1.63 to 19.31) 1.56 (0.41 to 5.89)
β-blockers, yes vs no 3.67 (0.80 to 19.83) 3.22 (0.70 to 17.49) 5.83* (1.18 to 33.92)
aSASRQ used at baseline; DTS used at 1, 6, 12, and 24 months postdischarge. bUnivariate association between predictors and SASRQ/DTS.
cMultivariate association between predictors and SASRQ/DTS after adjusting for all remaining predictors in the model. dValues displayed are for
women.
*P < .05; **P < .01; ***P < .001.
Abbreviations: BSI = Brief Symptom Inventory, DTS = Davidson Trauma Scale, SASRQ = Stanford Acute Stress Reaction Questionnaire.
Symbol: … = not included in model.
Table 5B. Results of Logistic Regression Analyses Relating Heart Rate to SASRQ (algorithm-based cutoff) and DTS (cutoff 40)a
Predictors at Baseline
12 Months Postdischarge (n = 41) 24 Months Postdischarge (n = 27)
Crude ORb (95% CI) Adjusted ORc (95% CI) Crude OR (95% CI) Adjusted OR (95% CI)
Heart rate
1-u
nit increase 1.01 (0.97 to 1.06) 0.99 (0.94 to 1.04) 1.03 (0.98 to 1.10)
1-
SD increase 1.28 0.82 1.67
Gender, male vs female 1.33 (0.29 to 5.65) 6.94e-10** (9.53e-20 to 0.01) 2.50 (0.37 to 17.29)
Heart rate × genderd
1-
unit increase 1.20** (1.04 to 1.72) … …
1-
SD increase 21.40
BSI score, ≥ 63 vs < 63 4.00* (1.03 to 17.10) 5.18* (1.15 to 27.25) 6.40 (0.96 to 57.70)
β-blockers, yes vs no 1.80 (0.31 to 9.69) 4.75 (0.46 to 51.20)
aSASRQ used at baseline; DTS used at 1, 6, 12, and 24 months postdischarge. bUnivariate association between predictors and SASRQ/DTS.
cMultivariate association between predictors and SASRQ/DTS after adjusting for all remaining predictors in the model. dValues displayed are for
women.
*P < .05; **P < .01; ***P < .001.
Abbreviations: BSI = Brief Symptom Inventory, DTS = Davidson Trauma Scale, SASRQ = Stanford Acute Stress Reaction Questionnaire.
Symbol: … = not included in model.
Gould et al
545 J Clin Psychiatry 72:4, April 2011
A 1-SD increase in HR (SD = 15.15) resulted in it being
0.94 times less likely for men and 3.29 times more likely for
women to be above the DTS cutoff for PTSD at 1 month. A
1-unit increase/SD increase in HR (SD = 16.26) was associ-
ated at 6 months with it being 1.06 times/2.51 times more
likely for patients to be above the DTS cutoff for PTSD.
Finally, at 12 months, there were differential effects across
sex/gender. For men and women, a 1-unit increase in HR
was associated with it being 0.99 times less likely and 1.20
times more likely to be above the DTS cutoff for PTSD. A
1-SD increase (SD = 16.63) in HR resulted in it being 0.82
times less likely for men and 21.40 times more likely for
women to be above the DTS cutoff for PTSD.
DISCUSSION
The present study is the first to assess the predictive value
of HR and BP for the subsequent development of ASD and
PTSD in patients with severe burns. Our results revealed
that increased HR immediately following major burn injury
was associated with higher rates of ASD and PTSD 6 months
after hospital discharge. Further, elevated HR levels during
hospital admission were associated with the development of
ASD. An interactive effect for gender indicated that elevated
HR at the time of hospital admission was associated with
more PTSD symptoms at 6 and 12 months after discharge
for females only. This finding suggests that gender influences
the relationship between elevated HR following trauma and
subsequent PTSD severity. This gender finding is of particu-
lar importance given that the type of trauma was consistent
across sexes and less gender-specific than previously studied
traumas.
Gender differences in the association between peritrau-
matic physiologic markers and the later development of
PTSD may be better understood if placed in the context of
the complex relationship between gender and PTSD. Previous
research in the field of PTSD has not consistently reported
gender differences because they were not of central interest
in those studies29; however, several previous studies shed
light on the influence of gender on PTSD development. De-
spite the fact that men experience more trauma during their
lifetime, PTSD is more prevalent among women. Several
explanations have been posited to account for this discrep-
ancy, including women’s increased exposure to traumas that
often involve developmental disruptions (ie, sexual abuse and
violation of physical integrity) and may increase vulnerabil-
ity to develop PTSD and other psychopathology. Compared
to men, women tend to engage in more ruminative styles
of coping, which are associated with more prolonged or
severe depressive episodes30 and also predict PTSD.31 Bio-
logic explanations include endogenous opioid peptides,
which vary across the menstrual cycle for women and
coincide with observed changes in PTSD symptoms. Women
have been found to be more physiologically reactive than
men to trauma,32 and previous research has revealed that
specific symptom clusters, such as hyperarousal and numb-
ing, are particularly salient in women.33 It is well-established
that women have higher resting HR,34 longer corrected QT
intervals,35–37 and a shorter sinus node recovery time38
than men, possibly due to differences in exercise tolerance,
autonomic modulation, sinus node properties, and gender
hormones.39 Nevertheless, while women have been shown to
have higher HRs34 and a higher incidence of PTSD,40,41 our
findings revealed a significant relationship between ambu-
lance HR and PTSD scores at 6 and 12 months even while
controlling for gender. Although the clinical significance of
these gender differences in cardiac variables is unclear, we
can speculate that women may tend to have greater sym-
pathetic arousal and release of stress hormones during a
trauma, due to baseline physiologic differences.
Consistent with several previous studies,10,11,14 BP
immediately following trauma and during hospital stay was
not significantly related to total ASD or PTSD symptoms
at any subsequent assessments in the current study (ie, 1,
6, 12, or 24 months). The lack of predictive utility of BP in
light of significant HR findings suggests that PTSD may be
influenced by excessive adrenergic activation via enhanced
memory consolidation rather than noradrenergic activa-
tion.10 The lack of a relationship between BP and subsequent
ASD or PTSD in the current study could also be attributed
to a potentially larger representation of patients whose stress
response patterns involve more cardiac- than vascular-based
reactivity.42
A unique finding of the current study was that peritrau-
matic HR was most consistently related to PTSD avoidance
symptoms up to 2 years after hospital discharge. As noted in
a recent synthesizing review, avoidance cluster symptoms are
emerging as the strongest indicators for PTSD risk.43 Given
this finding, it is potentially of great importance that future
investigations examine the means by which early HR is
related to increased severity of future avoidance symptoms.
Fear-conditioning models suggest that, after a traumatic
event, cues reminiscent of the trauma result in the resur-
gence of anxiety symptoms,44 and that these symptoms are
maintained through negative reinforcement associated with
avoidance of these cues.45 Indeed, increased HR, along with
other psychophysiological responses, may reflect changes
in amygdala activation, and conditioned fear and contin-
ued avoidance may contribute to a failure to extinguish
emotional responses to trauma-related cues.46 Thus, our
findings may represent impaired extinction pathways and
processes. Of great interest is the identification of subgroups
of individuals with PTSD on the basis of varying physiologic
and psychological response patterns (eg, specific symptom
clusters), which may help elucidate the contributions of vari-
ous markers to the development of PTSD. In accordance
with our current findings, different biologic markers may
be related to different subgroups of patients (eg, those with
greater endorsement of avoidance symptoms). Thus, clinical
literature on human responses following traumatic injury
should continue to conduct mechanistic studies to identify
the basic processes and pathways to clarify how, when, and
for what clinical subphenotypes HR serves as a biomarker
for PTSD.
Peritraumatic Heart Rate and PTSD in Severe Burns
J Clin Psychiatry 72:4, April 2011 546
Limitations
It is important to note that these findings must be inter-
preted in light of several limitations of the present study.
Inherent to retrospective analyses, the number and type
of variables available for examination were limited. Most
notably, preinjury measures of psychological and physi-
ologic function or indications of pretrauma arousal (eg,
HR and BP) were not available. For example, data on
previous traumas or PTSD diagnosis in our sample are
unknown, a factor that could have impacted the current
findings. Also unavailable was medical information such
as premorbid aerobic health, respiratory disease, cardio-
vascular disease, and presence of stimulants such as illicit
drugs, as well as other medications that have been shown to
impact the development of PTSD (eg, morphine in trauma
patients).47,48 Variability in the measurement and collection
of physiologic data was also likely. For example, the time lag
from burn injury to emergency care and variation in the
measurement of HR and BP between emergency care per-
sonnel were not known. Although not possible for this study,
some authors have suggested obtaining multiple assessments
at each time point to account for the natural variability of
HR.49 Although the DTS has been well- examined in burn
samples and has an established cutoff score for clinically
significant distress,50 more exact diagnostic information
was not available (eg, structured clinical interviews). Sta-
tistical analyses were also limited by the sample size and
attrition, in that power was only suitable to examine
a small number of covariates or predictors. Finally, the
timing of symptom assessment is inherent to all trauma
studies and may account for mixed findings in the literature.
For example, initial nonpathological distress following an
injury may augment endorsement of symptoms if measured
immediately after the event.16 Clearly, empirical investiga-
tion of this topic is challenging due to the life-threatening
nature and emergency care needed for many traumatic
events. Despite confounds, our findings reveal a relation-
ship between immediate posttrauma physiologic markers
and the later development of traumatic stress symptoms.
It remains premature at this time to use HR as a mecha-
nism to identify at-risk individuals in a clinical setting.14
The accumulating evidence in this area encourages further
examination of the role of acute HR in the development of
PTSD. Utilizing multiple methods for assessing sympathetic
tone (eg, HR, HR responsivity, HR variability) would refine
the utility of a predictive algorithm.51 Understanding the
changes in HR pretrauma and posttrauma (ie, determining
if individuals with PTSD had higher HR levels long before
their trauma or simply higher HR around the time of the
trauma) will be critical to our understanding of the role of
HR as a reliable predictor of PTSD development. Substantial
work remains to be done elucidating the processes, pathways,
and modulators by which risk and resilience after traumatic
injuries are linked to cognitive and behavioral responses (eg,
catastrophizing, approach/avoidance,52 perceived controlla-
bility53,54 and environmental qualities (eg, support, safety).55
Future work that incorporates these considerations may
help to refine knowledge regarding endophenotypes iden-
tifying groups of trauma-exposed individuals at increased
risk of developing PTSD.3,56 This knowledge may, in turn,
provide additional targets for early psychological and phar-
macologic intervention. In this regard, while studies have
assessed the role of secondary preventive pharmacologic
agents for PTSD,47,48,57 this area of research remains in its
infancy. Promising avenues of future work will optimally
assess biologic, cognitive, and behavioral correlates and
predictors of PTSD symptoms in an effort to elucidate
mechanisms in the development of PTSD.46 The pathophysi-
ology of PTSD can only be understood in the context of such
related and co-occurring factors.17
Author affiliations: Department of Psychiatry and Behavioral Sciences,
Johns Hopkins University School of Medicine, Baltimore, Maryland (Drs
Gould, Hall, Corry, Mason, McCann and Fauerbach and Ms Amoyal);
and Department of Psychiatry, Uniformed Services University of the
Health Sciences, Bethesda, Maryland (Dr McKibben).
Potential conflicts of interest: Dr McCann has been a consultant to and
served on the speakers/advisory board for Jazz. Drs Gould, McKibben,
Hall, Corry, Mason, and Fauerbach and Ms Amoyal report no potential
conflicts of interest to disclose relative to the subject of this article.
Funding/support: This project was funded by Burn Model Systems Grant
(H133A070045) supported by the National Institute of Disability and
Rehabilitation Research, Office of Special Education and Rehabilitation
Services in the US Department of Education.
Disclaimer: The views expressed in this article are those of the
authors and do not reflect official policy or position of the Department
of Defense, the U.S. Government, or any of the institutional affiliations
listed.
Previous presentation: Previously presented at the 41st annual meeting of
the American Burn Association; March 24–27, 2009; San Antonio, Texas.
REFERENCES
1.
Olatunji BO, Cisler JM, Tolin DF. Quality of life in the anxiety disorders:
a meta-analytic review. Clin Psychol Rev. 2007;27(5):572–581.
doi:10.1016/j.cpr.2007.01.015 PubMed
2.
Harvey AG, Bryant RA. The relationship between acute stress disorder
and posttraumatic stress disorder: a prospective evaluation of motor
vehicle accident survivors. J Consult Clin Psychol. 1998;66(3):507–512.
doi:10.1037/0022-006X.66.3.507 PubMed
3.
Gottesman II, Gould TD. The endophenotype concept in psychiatry: ety-
mology and strategic intentions. Am J Psychiatry. 2003;160(4):636–645.
doi:10.1176/appi.ajp.160.4.636 PubMed
4.
American Psychiatric Association. Diagnostic and Statistical Manual
of Mental Disorders, Fourth Edition, Text Revision. Washington, DC;
American Psychiatric Association; 2000.
5.
Blanchard EB, Hickling EJ, Vollmer AJ, et al. Short-term follow-up
of post-traumatic stress symptoms in motor vehicle accident victims.
Behav Res Ther. 1995;33(4):369–377.
doi:10.1016/0005-7967(94)00067-T PubMed
6.
Pitman RK. Post-traumatic stress disorder, hormones, and memory.
Biol Psychiatry. 1989;26(3):221–223.
doi:10.1016/0006-3223(89)90033-4 PubMed
7.
Yehuda R, McFarlane AC, Shalev AY. Predicting the development of
posttraumatic stress disorder from the acute response to a traumatic
event. Biol Psychiatry. 1998;44(12):1305–1313.
doi:10.1016/S0006-3223(98)00276-5 PubMed
8.
Cahill L, Prins B, Weber M, et al. Beta-adrenergic activation and memory
for emotional events. Nature. 1994;371(6499):702–704.
doi:10.1038/371702a0 PubMed
9.
McGaugh JL. Peripheral and central adrenergic influences on brain
systems involved in the modulation of memory storage. Ann N Y
Acad Sci. 1985;444:150–161.
doi:10.1111/j.1749-6632.1985.tb37586.x PubMed
10. Shalev AY, Sahar T, Freedman S, et al. A prospective study of heart rate
response following trauma and the subsequent development of posttrau-
matic stress disorder. Arch Gen Psychiatry. 1998;55(6):553–559.
doi:10.1001/archpsyc.55.6.553 PubMed
11. Bryant RA, Harvey AG, Guthrie RM, et al. A prospective study of
psychophysiological arousal, acute stress disorder, and posttraumatic
stress disorder. J Abnorm Psychol. 2000;109(2):341–344.
doi:10.1037/0021-843X.109.2.341 PubMed
12. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective
evaluation. Am J Psychiatry. 2005;162(6):1188–1191.
doi:10.1176/appi.ajp.162.6.1188 PubMed
13. Kassam-Adams N, Garcia-España JF, Fein JA, et al. Heart rate and post-
traumatic stress in injured children. Arch Gen Psychiatry. 2005;62(3):
335–340.
doi:10.1001/archpsyc.62.3.335 PubMed
14. Bryant RA, Creamer M, O’Donnell M, et al. A multisite study of initial
Gould et al
547 J Clin Psychiatry 72:4, April 2011
respiration rate and heart rate as predictors of posttraumatic stress
disorder. J Clin Psychiatry. 2008;69(11):1694–1701.
doi:10.4088/JCP.v69n1104 PubMed
15. Blanchard EB, Hickling EJ, Galovski T, et al. Emergency room vital signs
and PTSD in a treatment seeking sample of motor vehicle accident survi-
vors. J Trauma Stress. 2002;15(3):199–204.
doi:10.1023/A:1015299126858 PubMed
16. Kuhn E, Blanchard EB, Fuse T, et al. Heart rate of motor vehicle accident
survivors in the emergency department, peritraumatic psychological reac-
tions, ASD, and PTSD severity: a 6-month prospective study. J Trauma
Stress. 2006;19(5):735–740.
doi:10.1002/jts.20150 PubMed
17. Shalev AY, Segman RH. Commentary: biological findings in PTSD—too
much or too little? Prog Brain Res. 2008;167:187–199.
doi:10.1016/S0079-6123(07)67013-7 PubMed
18. Buckley TC, Kaloupek DG. A meta-analytic examination of basal cardio-
vascular activity in posttraumatic stress disorder. Psychosom Med. 2001;
63(4):585–594.
PubMed
19. Pole N. The psychophysiology of posttraumatic stress disorder:
a meta-analysis. Psychol Bull. 2007;133(5):725–746.
doi:10.1037/0033-2909.133.5.725 PubMed
20. Davidson JR, Book SW, Colket JT, et al. Assessment of a new self-rating
scale for post-traumatic stress disorder. Psychol Med. 1997;27(1):153–160.
doi:10.1017/S0033291796004229 PubMed
21. American Psychiatric Association. Diagnostic and Statistical Manual of
Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric
Association; 1994.
22. Cardeña E, Koopman C, Classen C, et al. Psychometric properties of the
Stanford Acute Stress Reaction Questionnaire (SASRQ): a valid and reli-
able measure of acute stress. J Trauma Stress. 2000;13(4):719–734.
doi:10.1023/A:1007822603186 PubMed
23. Koopman C, Gore-Felton C, Classen C, et al. Acute stress reactions to
everyday stressful life events among sexual abuse survivors with PTSD.
J Child Sex Abuse. 2002;10(2):83–99.
doi:10.1300/J070v10n02_05
24. Derogatis LR. BSI: Brief Symptom Inventory. 3rd ed. Minneapolis, MN:
National Computer Systems; 1993.
25. Derogatis LR. SCL-90-R: Administration, Scoring, and Procedures Manual.
3rd ed. Minneapolis, MN: National Computer Systems, Inc; 1994.
26. Boulet J, Boss MW. Reliability and validity of the Brief Symptom
Inventory. Psychol Assess. 1991;3(3):433–437.
doi:10.1037/1040-3590.3.3.433
27. Piersma HL, Reaume WM, Boes JL. The Brief Symptom Inventory (BSI)
as an outcome measure for adult psychiatric inpatients. J Clin Psychol.
1994;50(4):555–563.
doi:10.1002/1097-4679(199407)50:4<555::AID-JCLP2270500410>3.0.CO;2-G PubMed
28. McCarthy ML, MacKenzie EJ, Edwin D, et al; LEAP study group.
Psychological distress associated with severe lower-limb injury.
J Bone Joint Surg Am. 2003;85-A(9):1689–1697.
PubMed
29. Gavranidou M, Rosner R. The weaker sex? gender and post-traumatic
stress disorder. Depress Anxiety. 2003;17(3):130–139.
doi:10.1002/da.10103 PubMed
30. Nolen-Hoeksema S. Epidemiology and theories of gender differences
in unipolar depression. In: Seeman MV, ed. Gender and Psychopathology.
Washington, DC: American Psychiatric Association; 1995: 63–87.
31. Ehlers A, Mayou RA, Bryant B. Psychological predictors of chronic post-
traumatic stress disorder after motor vehicle accidents. J Abnorm Psychol.
1998;107(3):508–519.
doi:10.1037/0021-843X.107.3.508 PubMed
32. Norris FH, Perilla JL, Ibanez GE, et al. Sex differences in symptoms of
posttraumatic stress: does culture play a role? J Trauma Stress. 2001;14(1):
7–28.
doi:10.1023/A:1007851413867
33. Fullerton CS, Ursano RJ, Epstein RS, et al. Gender differences in post-
traumatic stress disorder after motor vehicle accidents. Am J Psychiatry.
2001;158(9):1486–1491.
doi:10.1176/appi.ajp.158.9.1486 PubMed
34. Liu K, Ballew C, Jacobs DR Jr, et al. Ethnic differences in blood pressure,
pulse rate, and related characteristics in young adults: The CARDIA study.
Hypertension. 1989;14(2):218–226.
PubMed
35. Bazette H. An analysis of the time relations of electrocardiograms.
Heart. 1920;7:353–370.
36. Ashman R. The normal duration of the QT interval. Am Heart J. 1942;
23(4):522–534.
doi:10.1016/S0002-8703(42)90297-7
37. Molnar J, Zhang F, Weiss J, et al. Diurnal pattern of QTc interval: how
long is prolonged? possible relation to circadian triggers of cardiovascular
events. J Am Coll Cardiol. 1996;27(1):76–83.
doi:10.1016/0735-1097(95)00426-2 PubMed
38. Kadish AH. The effect of gender on cardiac electrophysiology and
arrhythmias. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From
Cell to Bedside. 2nd ed. Philadelphia, PA: WB Saunders; 1995: 1268–1275.
39. Yarnoz MJ, Curtis AB. More reasons why men and women are not the
same (gender differences in electrophysiology and arrhythmias).
Am J Cardiol. 2008;101(9):1291–1296.
doi:10.1016/j.amjcard.2007.12.027 PubMed
40. Breslau N. Epidemiologic studies of trauma, posttraumatic stress disorder,
and other psychiatric disorders. Can J Psychiatry. 2002;47(10):923–929.
PubMed
41. Breslau N. Gender differences in trauma and posttraumatic stress
disorder. J Gend Specif Med. 2002;5(1):34–40.
PubMed
42. Manuck SB, Kamarck TW, Kasprowicz AS, et al. Stability and patterning
of behaviorally evoked cardiovascular reactivity. In: Blascovic J, Katkin
ES, eds. Cardiovascular Reactivity to Psychological Stress and Disease.
Washington, DC: American Psychological Association; 1995:111–134.
43. North CS, Suris AM, Davis M, et al. Toward validation of the diagnosis
of posttraumatic stress disorder. Am J Psychiatry. 2009;166(1):34–41.
doi:10.1176/appi.ajp.2008.08050644 PubMed
44. Charney DS, Deutch AY, Krystal JH, et al. Psychobiologic mechanisms of
posttraumatic stress disorder. Arch Gen Psychiatry. 1993;50(4):295–305.
PubMed
45. Keane TM, Zimmering RT, Caddell JM. A behavioral formulation of post
traumatic stress disorder in Vietnam veterans. Behav Therapist. 1985;8:
9–12.
46. Bryant RA. Early predictors of posttraumatic stress disorder.
Biol Psychiatry. 2003;53(9):789–795.
doi:10.1016/S0006-3223(02)01895-4 PubMed
47. Bryant RA, Creamer M, O’Donnell M, et al. A study of the protective
function of acute morphine administration on subsequent posttraumatic
stress disorder. Biol Psychiatry. 2009;65(5):438–440.
doi:10.1016/j.biopsych.2008.10.032 PubMed
48. Saxe G, Stoddard F, Courtney D, et al. Relationship between acute
morphine and the course of PTSD in children with burns. J Am Acad
Child Adolesc Psychiatry. 2001;40(8):915–921.
doi:10.1097/00004583-200108000-00013 PubMed
49. Buckley TC, Holohan D, Greif JL, et al. Twenty-four-hour ambulatory
assessment of heart rate and blood pressure in chronic PTSD and
non-PTSD veterans. J Trauma Stress. 2004;17(2):163–171.
doi:10.1023/B:JOTS.0000022623.01190.f0 PubMed
50. Fauerbach JA, McKibben J, Bienvenu OJ, et al. Psychological distress
after major burn injury. Psychosom Med. 2007;69(5):473–482.
doi:10.1097/psy.0b013e31806bf393 PubMed
51. Cohen H, Benjamin J, Geva AB, et al. Autonomic dysregulation in
panic disorder and in post-traumatic stress disorder: application of
power spectrum analysis of heart rate variability at rest and in response to
recollection of trauma or panic attacks. Psychiatry Res. 2000;96(1):1–13.
doi:10.1016/S0165-1781(00)00195-5 PubMed
52. Ehlers A, Clark DM. A cognitive model of posttraumatic stress disorder.
Behav Res Ther. 2000;38(4):319–345.
doi:10.1016/S0005-7967(99)00123-0 PubMed
53. Ehlers A, Clark DM, Dunmore E, et al. Predicting response to exposure
treatment in PTSD: the role of mental defeat and alienation. J Trauma
Stress. 1998;11(3):457–471.
doi:10.1023/A:1024448511504 PubMed
54. Kushner MG, Riggs DS, Foa EB, et al. Perceived controllability and the
development of posttraumatic stress disorder (PTSD) in crime victims.
Behav Res Ther. 1993;31(1):105–110.
doi:10.1016/0005-7967(93)90048-Y PubMed
55. Charuvastra A, Cloitre M. Social bonds and posttraumatic stress disorder.
Annu Rev Psychol. 2008;59(1):301–328.
doi:10.1146/annurev.psych.58.110405.085650 PubMed
56. Broekman BF, Olff M, Boer F. The genetic background to PTSD. Neurosci
Biobehav Rev. 2007;31(3):348–362.
doi:10.1016/j.neubiorev.2006.10.001 PubMed
57. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary pre-
vention of posttraumatic stress disorder with propranolol. Biol Psychiatry.
2002;51(2):189–192.
doi:10.1016/S0006-3223(01)01279-3 PubMed
... Prior literature has identified many preexisting and post hoc risk factors for development of PTSD (Ozer et al. 2003;Marmar et al. 2006;Cukor et al. 2011;Clark et al. 2013;Glatt et al. 2013;Eraly et al. 2014;Yurgil et al. 2014). However, limitations in the individual-based predictive value of these factors have prompted particular interest in the immediate peritraumatic response after trauma exposure as an individual specific robust predictor of PTSD development (McNally 2003;Ozer et al. 2003;Briere et al. 2005;Marmar et al. 2006;Breh and Seidler 2007;Lensvelt-Mulders et al. 2008;Bovin and Marx 2011;Gould et al. 2011) (Fig. 1). In particular, the first hours following the trauma may be a critical window for interventions aimed at the prevention or reduction of posttraumatic anxiety (Bryant 2003;Ehring et al. 2008) and have been characterized as the "golden hour(s)" after trauma (Zohar et al. 2009). ...
... Peritraumatic stress reactions refer to the specific stress-associated behavioral, emotional, cognitive, and physiological symptoms during and immediately following a traumatic event and include fear of dying, fear of losing emotional control, tachycardia, sweating, shaking, dizziness and dissociation symptoms, reduction of awareness, etc. (Fig. 2). These reactions have repeatedly demonstrated a strong and consistent association with the subsequent development of posttraumatic stress symptoms in prior research (McNally 2003;Ozer et al. 2003;Briere et al. 2005;Marmar et al. 2006;Breh and Seidler 2007;Lensvelt-Mulders et al. 2008;Bovin and Marx 2011;Gould et al. 2011). Peritraumatic panic symptoms are associated with activation of the sympathetic nervous system, with several studies showing that elevated heart rate during or immediately after the trauma is prospectively associated with an increased risk of developing PTSD symptoms (Fig. 2) (Shalev et al. 1998;Bryant et al. 2000Bryant et al. , 2007Birmes et al. 2003;Bryant 2003;Kassam-Adams et al. 2005). ...
Chapter
The postwar fiscal burden for treatment of posttraumatic stress disorder (PTSD) and PTSD-related mental, physical, and social outcomes can be high, and the liability can persist for decades post-armistice. Thus, any advancement in early detection and prevention of PTSD promise substantial benefits. There is strong confirmation that peritraumatic stress reactions are robust posttrauma predictors of PTSD development. This fact provides evidence to warrant training for the recognition and evaluation of peritraumatic stress. However, although instruments for measuring peritraumatic symptoms exist, they were not specifically developed to assess combat-related peritraumatic reactions and may insufficiently capture the wide range of possible reactions in the immediate aftermath of a combat-related trauma. In addition, these measures also all rely on subjective, retrospective self-report. To redress this problem, we developed the Peritraumatic Behavior Questionnaire (PBQ). The ultimate goal was to generate a military-specific observer-rating scale for corpsman and medics in theater to facilitate the early detection of combat-related peritraumatic distress symptoms in actively deployed service members and to unify underlying peritraumatic symptom dimensions to reliably assess combat-related peritraumatic reactions as a general construct. Before assessing an observer-rated version of the PBQ (PBQ – Observer Rated, PBQ-OR), we initially investigated the psychometric and predictive properties of the self-rated PBQ version (PBQ – Self Report, PBQ-SR). We considered that the establishment of good psychometric properties for the SR version would be important before introducing the additional complexities of observer ratings. Here we report the development of the PBQ and summarize the recently reported psychometric properties of the PBQ-SR, as well as our findings and conclusions from the in-theater evaluation procedure of the PBQ-OR. Our data confirm the ability of the PBQ to unify the underlying peritraumatic symptom dimensions and reliably assess combat-related peritraumatic reactions as a general construct. Both PBQ-SR and PBQ-OR showed high correlation to various PTSD-specific as well as PTSD-related symptoms and demonstrated promise as a potential standard screening measure in military clinical practice.
... e., dissociation around the time of trauma; for a review see Cardeña & Classen, in press) predicted acute stress and higher scores on the SASRQ (Hunt et al., 2008). Furthermore, higher heart rate during a stressful event was associated with later acute stress and high scores on the SASRQ (Gould et al., 2011). One study indicated that participants who believed that a certain event would have a big impact on the future tended to score higher on the SASRQ (Maldonado et al., 2002) Gelkopf, Berger andRoe (2016). ...
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The fourth edition of the Diagnostic and Statistical Manual introduced the diagnosis of Acute Stress Disorder (ASD) for acute pathological reactions including dissociative ones, following a traumatic event. Various measures of ASD have been developed, with the Stanford Acute Stress Reaction Questionnaire (SASRQ) being one of the most commonly used across the world. This paper systematically covers more than 20 years of research with it and 90 papers in different languages. The main conclusion is that the SASRQ and its translations to other languages have consistently shown convergent, divergent, and predictive validity, besides exhibiting good reliability. We finish the paper by advancing suggestions for future development including the use a new SASRQ version that follows DSM-5 criteria, evaluating whether distinct items or subscales differentially predict different types of acute- and long-term posttraumatic symptomatology, and assessing its clinical usefulness.
... Previous work also suggests that cardiovascular arousal plays an important role in PTSD symptom development [27]. In particular, clinical studies revealed that PTSD was associated with increases in heart rate (HR), as an indicator of psychophysiological arousal, shortly after trauma (i.e. in ambulance/emergency room after major burn injuries) [28] and in response to trauma-related stimuli [29]. Similarly, decreases in heart rate variability (HRV), as an indicator of elevated sympathetic activity relative to parasympathetic activity, were associated with PTSD diagnosis in veterans [30]. ...
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The angiotensin-II antagonist losartan is a promising candidate that has enhanced extinction in a post-traumatic stress disorder (PTSD) animal model and was related to reducing PTSD symptom development in humans. Here, we investigate the neurocognitive mechanisms underlying these results, testing the effect of losartan on data-driven and contextual processing of traumatic material, mechanisms proposed to be relevant for PTSD development. In a double-blind between-subject design, 40 healthy participants were randomised to a single oral dose of losartan (50 mg) or placebo, 1 h before being exposed to distressing films as a trauma analogue while heart rate (HR) was measured. Peritraumatic processing was investigated using blurry picture stimuli from the films, which transformed into clear images. Data-driven processing was measured by the level of blurriness at which contents were recognised. Contextual processing was measured as the amount of context information retrieved when describing the pictures’ contents. Negative-matched control images were used to test perceptual processing of peripheral trauma-cues. Post-traumatic stress symptoms were assessed via self-report questionnaires after analogue trauma and an intrusion diary completed over 4 days following the experiment. Compared to placebo, losartan facilitated contextual processing and enhanced detail perception in the negative-match pictures. During the films, the losartan group recorded lower HR and higher HR variability, reflecting lower autonomic stress responses. We discuss potential mechanisms of losartan in preventing PTSD symptomatology, including the role of reduced arousal and increased contextual processing during trauma exposure, as well as increased threat-safety differentiation when encountering peripheral trauma-cues in the aftermaths of traumatic events.
... The Pearson product-moment correlation (r) was used to determine the strength and direction of the relation between acute posttraumatic risk markers and PTSD symptoms or disorder. For studies reporting data for pairings of continuous and dichotomous variables, including presence or absence of PTSD diagnosis at follow-up (Bryant et al., 2008;Coronas et al., 2011;De Young et al., 2007;Shalev & Freedman, 2005;Yehuda et al., 1998), PTSD symptom cutoff scores (Alarcon et al., 2011;Gould et al., 2011), or cut-off scores for risk markers (Bryant et al., 2008;Zatzick et al., 2005), formulas were used to impute point-biserial correlations (Lipsey & Wilson, 2001). All r values were transformed using the Fisher's Z r transform (Hedges & Olkin, 1985) and associated standard errors and inverse variance weights were computed for each effect size. ...
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Individuals with posttraumatic stress disorder (PTSD) typically exhibit altered hypothalamic–pituitary-adrenal (HPA) function and sympathetic nervous system (SNS) activity. The goals of this study were to determine whether HPA and SNS alterations in the immediate aftermath of trauma predict subsequent PTSD symptom development and whether inconsistencies observed between studies can be explained by key demographic and methodological factors. This work informs secondary prevention of PTSD by identifying subgroups of trauma survivors at risk for PTSD. This meta-analysis (26 studies, N = 5186 individuals) revealed that higher heart rate measured soon after trauma exposure was associated with higher PTSD symptoms subsequently (r = 0.13). Neither cortisol (r = − 0.07) nor blood pressure (diastolic: r = − 0.01; systolic: r = 0.02) were associated with PTSD symptoms which may be influenced by methodological limitations. Associations between risk markers (heart rate, cortisol, systolic blood pressure) and PTSD symptoms were in the positive direction for younger samples and negative direction for older samples. These findings extend developmental traumatology models of PTSD by revealing an age-related shift in the presentation of early risk markers. More work will be needed to identify risk markers and pathways to PTSD while addressing methodological limitations in order to shape and target preventive interventions.
... This analysis represents the largest review of satisfaction with life after burn to date, and includes follow-up for up to 2 years. The majority of psychosocial, burn-related research has focused on psychopathology associated with burn-injury, for example post-traumatic stress, depression, and anxiety [13][14][15][16][17][18][19]. More recently after burn quality of life has been investigated, although the data is not robust; and with respect to satisfaction with life after burn [20][21][22][23][24], only one study has previously examined this outcome [11]. ...
Article
Objectives: While mortality rates after burn are low, physical and psychosocial impairments are common. Clinical research is focusing on reducing morbidity and optimizing quality of life. This study examines self-reported Satisfaction With Life Scale scores in a longitudinal, multicenter cohort of survivors of major burns. Risk factors associated with Satisfaction With Life Scale scores are identified. Methods: Data from the National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR) Burn Model System (BMS) database for burn survivors greater than 9 years of age, from 1994 to 2014, were analyzed. Demographic and medical data were collected on each subject. The primary outcome measures were the individual items and total Satisfaction With Life Scale (SWLS) scores at time of hospital discharge (pre-burn recall period) and 6, 12, and 24 months after burn. The SWLS is a validated 5-item instrument with items rated on a 1-7 Likert scale. The differences in scores over time were determined and scores for burn survivors were also compared to a non-burn, healthy population. Step-wise regression analysis was performed to determine predictors of SWLS scores at different time intervals. Results: The SWLS was completed at time of discharge (1129 patients), 6 months after burn (1231 patients), 12 months after burn (1123 patients), and 24 months after burn (959 patients). There were no statistically significant differences between these groups in terms of medical or injury demographics. The majority of the population was Caucasian (62.9%) and male (72.6%), with a mean TBSA burned of 22.3%. Mean total SWLS scores for burn survivors were unchanged and significantly below that of a non-burn population at all examined time points after burn. Although the mean SWLS score was unchanged over time, a large number of subjects demonstrated improvement or decrement of at least one SWLS category. Gender, TBSA burned, LOS, and school status were associated with SWLS scores at 6 months; scores at 12 months were associated with LOS, school status, and amputation; scores at 24 months were associated with LOS, school status, and drug abuse. Conclusions: In this large, longitudinal, multicenter cohort of burn survivors, satisfaction with life after burn was consistently lower than that of non-burn norms. Furthermore mean SWLS scores did not improve over the two-year follow-up period. This study demonstrates the need for continued efforts to improve patient-centered long term satisfaction with life after burn.
Chapter
Psychiatric problems frequently occur during burn treatment and can complicate recovery. In addition, preexisting psychiatric disorders are often present and sometimes will have contributed to the burn injury. Pain, itching, and stress during burn recovery can complicate treatment and recovery. It is therefore essential that members of the burn treatment team recognize, assess, and treat psychiatric problems in patients with burn injury. More severe psychiatric disorders in patients may result from the injury and treatment, such as posttraumatic stress disorder and depression. It is useful to have mental health professionals as part of the treatment team. Quick detection and treatment of psychiatric problems contribute to overall recovery and reduce complications.
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Patient-reported outcome measures (PROMs) are vital for evaluating patient needs and therapeutic progress. This review aimed to identify the PROMs used in adult burn care and establish their quality. Computerized bibliographic searches of Psychinfo, Social Sciences Citation Index, Cinahl, Psycharticles, AMED, Medline, and HAPI were used to find English-language articles using English-language PROMs from January 2001 to September 2016. Psychometric quality assessment of the PROMs was conducted. A total of 117 studies achieved the entry criteria and reported using 77 different PROMs (71 generic and 6 burn-specific). Overall, the psychometric quality of the PROMs was low; only 17 (13 generic and 4 burn-specific) had psychometric evidence appropriate to adults with burn injuries completing an English language version of the PROM. Although this review identified a number of generic and burn-specific PROMs that have some psychometric evidence with adult burn patients, research is still needed to further examine these preexisting measures and validate them in different languages. This will enable researchers and clinicians to better understand the potential impact of a burn injury on adults, and evaluate the effectiveness of therapeutic interventions.
Article
Objectives: While mortality rates after burn are low, physical and psychosocial impairments are common. Clinical research is focusing on reducing morbidity and optimizing quality of life. This study examines self-reported Satisfaction With Life Scale scores in a longitudinal, multicenter cohort of survivors of major burns. Risk factors associated with Satisfaction With Life Scale scores are identified. Methods: Data from the National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR) Burn Model System (BMS) database for burn survivors greater than 9 years of age, from 1994 to 2014, were analyzed. Demographic and medical data were collected on each subject. The primary outcome measures were the individual items and total Satisfaction With Life Scale (SWLS) scores at time of hospital discharge (pre-burn recall period) and 6, 12, and 24 months after burn. The SWLS is a validated 5-item instrument with items rated on a 1-7 Likert scale. The differences in scores over time were determined and scores for burn survivors were also compared to a non-burn, healthy population. Step-wise regression analysis was performed to determine predictors of SWLS scores at different time intervals. Results: The SWLS was completed at time of discharge (1129 patients), 6 months after burn (1231 patients), 12 months after burn (1123 patients), and 24 months after burn (959 patients). There were no statistically significant differences between these groups in terms of medical or injury demographics. The majority of the population was Caucasian (62.9%) and male (72.6%), with a mean TBSA burned of 22.3%. Mean total SWLS scores for burn survivors were unchanged and significantly below that of a non-burn population at all examined time points after burn. Although the mean SWLS score was unchanged over time, a large number of subjects demonstrated improvement or decrement of at least one SWLS category. Gender, TBSA burned, LOS, and school status were associated with SWLS scores at 6 months; scores at 12 months were associated with LOS, school status, and amputation; scores at 24 months were associated with LOS, school status, and drug abuse. Conclusions: In this large, longitudinal, multicenter cohort of burn survivors, satisfaction with life after burn was consistently lower than that of non-burn norms. Furthermore mean SWLS scores did not improve over the two-year follow-up period. This study demonstrates the need for continued efforts to improve patient-centered long term satisfaction with life after burn.
Chapter
The elderly as a general population are frequently understudied for both diagnostic criteria and responses to therapeutic interventions. When it comes to medications, the pharmacokinetic (e.g., medication concentration) and pharmacodynamic (e.g., receptor affinity) properties are often different for the elderly which at times may limit how effective medications are as well as side effects experienced. In addition, geriatric patients’ brains are undergoing loss of neuronal reserve related to aging and increased prevalence of neurodegenerative diseases. In short, the elderly are a unique population when it comes to susceptibility of side effects from medications. This chapter reviews how these factors impact the prescribing of medications for PTSD in the elderly as well as potential complications which can occur.
Chapter
The elderly as a general population are frequently understudied for both diagnostic criteria and responses to therapeutic interventions. When it comes to medications, the pharmacokinetic (e.g., medication concentration) and pharmacodynamic (e.g., receptor affinity) properties are often different for the elderly which at times may limit how effective medications are as well as side effects experienced. In addition, geriatric patients’ brains are undergoing loss of neuronal reserve related to aging and increased prevalence of neurodegenerative diseases. In short, the elderly are a unique population when it comes to susceptibility of side effects from medications. This chapter reviews how these factors impact the prescribing of medications for PTSD in the elderly as well as potential complications which can occur.
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Posttraumatic stress disorder (PTSD) is a common reaction to traumatic events. Many people recover in the ensuing months, but in a significant subgroup the symptoms persist, often for years. A cognitive model of persistence of PTSD is proposed. It is suggested that PTSD becomes persistent when individuals process the trauma in a way that leads to a sense of serious, current threat. The sense of threat arises as a consequence of: (1) excessively negative appraisals of the trauma and/or ist sequelae and (2) a disturbance of autobiographical memory characterised by poor elaboration and contextualisation, strong associative memory and strong perceptual priming. Change in the negative appraisals and the trauma memory are prevented by a series of problematic behavioural and cognitive strategies. The model is consistent with the main clinical features of PTSD, helps explain several apparently puzzling phenomena and provides a framework for treatment by identifying three key targets for change. Recent studies provided preliminary support for several aspects of the model.
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Defines posttraumatic stress disorder (PSD), which has been used to circumscribe the varied symptoms reported by combatants, and briefly presents a conditioning model for the development of PSD. The model explains PSD as a combination of high-order conditioning and stimulus generalization. The benchmark symptoms for a diagnosis of PSD are (1) intrusive thoughts regarding the traumatic event, (2) vivid recollections of the traumatic event wherein the individual reports that he/she feels that the trauma is actually reoccurring, and (3) terrifying nightmares that contain specific details of the event. A previous study by the authors (unpublished) is reported in which several symptoms were assessed by evaluating Ss' performance on cognitive and behavioral tasks and by questionnaires selected for their relationship to specific symptoms to the disorder. Responses of PSD veterans on these tasks were compared to those of well-adjusted Vietnam combat veterans without PSD. Results show that performance on 5 of the 6 tasks was effective in distinguishing Vietnam veterans with PSD from those who were well adjusted: PSD Ss demonstrated increased physiological arousal; motoric agitation; intrusive, combat-related cognitions when exposed to cues resembling the original traumatic event; poor concentration; and poor performance on emotion identification. (26 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
Posttraumatic stress disorder (PTSD) is a psychiatric condition that is directly precipitated by an event that threatens a person's life or physical integrity and that invokes a response of fear, helplessness, or horror. In recent years it has become clear that only a proportion of those exposed to fear-producing events develop or sustain PTSD. Thus, it seems that an important challenge is to elucidate aberrations in the normal fear response that might precipitate trauma-related psychiatric disorder. This paper summarizes the findings from recent studies that examined the acute and longer term biological response to traumatic stress in people appearing to the emergency room immediately following trauma exposure. In the aggregate, these studies have demonstrated increased heart rate and lower cortisol levels at the time of the traumatic event in those who have PTSD at a follow-up time compared to those who do not. In contrast, certain features associated with PTSD, such as intrusive symptoms and exaggerated startle responses, are only manifest weeks after the trauma. The findings suggest that the development of PTSD may be facilitated by an atypical biological response in the immediate aftermath of a traumatic event, which in turn leads to a maladaptive psychological state.
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A reliable and valid measure is needed for assessing the psychological symptoms experienced in the aftermath of a traumatic event. Previous research suggests that trauma victims typically experience dissociative, anxiety and other symptoms, during or shortly after a traumatic event. Although some of these symptoms may protect the trauma victim from pain, they may also lead to acute stress, posttraumatic stress, or other disorders. The Stanford Acute Stress Reaction Questionnaire (SASRQ) was developed to evaluate anxiety and dissociation symptoms in the aftermath of traumatic events, following DSM-IV criteria for acute stress disorder. We present data from multiple datasets and analyses supporting the reliability and construct, convergent, discriminant, and predictive validity of the SASRQ.
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This study was presented in part at the 42nd Annual Scientific Session of the American College of Cardiology, Anaheim, California, March 1993. Dr. Molnar is a visiting research fellow from the State Hospital for Cardiology, Balatonfured, Hungary and was supported by a grant from Marquette Electronics, Inc., Milwaukee, Wisconsin. This study was supported in part by the Reingold Estate and the Cooley Charitable Trust, Chicago, Illinois. Dr. Rosenthal is a member of the Feinberg Cardiovascular Research Institute, Northwestern University Medical School, Chicago, Illinois.
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Substantial evidence from animal studies suggests that enhanced memory associated with emotional arousal results from an activation of beta-adrenergic stress hormone systems during and after an emotional experience. To examine this implication in human subjects, we investigated the effect of the beta-adrenergic receptor antagonist propranolol hydrochloride on long-term memory for an emotionally arousing short story, or a closely matched but more emotionally neutral story. We report here that propranolol significantly impaired memory of the emotionally arousing story but did not affect memory of the emotionally neutral story. The impairing effect of propranolol on memory of the emotional story was not due either to reduced emotional responsiveness or to nonspecific sedative or attentional effects. The results support the hypothesis that enhanced memory associated with emotional experiences involves activation of the beta-adrenergic system.
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The reliability and validity of the Brief Symptom Inventory (BSI) was examined for a group of 501 forensic psychiatric inpatients and outpatients. Alpha coefficients for the 9 primary symptom dimensions revealed a high degree of consistency among the items that compose each scale. Scores on the 9 BSI dimensions were found to correlate with both analogous and nonanalogous measures of the Minnesota Multiphasic Personality Inventory (MMPI), indicating a limited convergent validity and a poor discriminant validity for the instrument. Reactivity to response bias was demonstrated by prominent correlations between the BSI dimensions and the MMPI validity scales. The significant intercorrelations among the BSI symptom subscales indicated the inappropriateness of BSI profile analysis in this sample. The BSI may hold some promise as a general indicator of psychopathology but further research is needed to justify its use as a clinical psychiatric screening tool. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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We discuss the gender-specific differences for traumatic events and Post-Traumatic Stress Disorder (PTSD) as found in the epidemiological literature. Recent research literature consistently reports three interesting findings: 1) men experience traumatic events more often, 2) women and men differ in the type of traumatic experiences they experience, and 3) women more often develop PTSD after the experience of a traumatic event. In the second part of the present article we provide some explanations for these differences. The reported higher vulnerability of women for PTSD could be due to the methodology used, the higher prevalence of childhood sexual abuse and rape in women, the different coping styles of women and men, or the more limited socio-economic resources of women. Depression and Anxiety 17:130–139, 2003. © 2003 Wiley-Liss, Inc.