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Behavioral Sleep Medicine, 6:158–177, 2008
Copyright © Taylor & Francis Group, LLC
ISSN: 1540-2002 print/1540-2010 online
DOI: 10.1080/15402000802162539
Physiological–Emotional Reactivity to
Nightmare-Related Imagery in
Trauma-Exposed Persons With
Chronic Nightmares
Jamie L. Rhudy, Joanne L. Davis, Amy E. Williams,
Klanci M. McCabe, and Patricia M. Byrd
Department of Psychology
The University of Tulsa
Script-driven imagery was used to assess nightmare imagery-evoked physiological–
emotional reactivity (heart rate, skin conductance, facial electromyogram, subjective ratings) in trauma-exposed persons suffering from chronic nightmares. Goals
were to determine the efficacy of nightmare imagery to evoke physiological–
emotional reactivity, correlates (mental health, nightmare characteristics) of reactivity, and consequences (sleep and health problems) of reactivity. Nightmare
imagery resulted in significant reactivity relative to control imagery. No mental
health variable (posttraumatic stress disorder status, depressive symptoms, dissociation) or nightmare characteristic (months experienced, frequency, similarity to
trauma) was associated with reactivity level. However, nightmare imagery-evoked
autonomic responses were associated with greater sleep disturbance and reported
health symptoms, even when nightmare frequency was controlled. These results
suggest nightmare-related autonomic reactions may contribute to sleep and health
disturbance.
Chronic nightmares threaten psychological well-being, a fact that may be especially true for trauma-exposed persons. Presence of nightmares following trauma
exposure is associated with greater sleep disturbance (Resnick & Newton, 1992),
Correspondence should be addressed to Jamie L. Rhudy, Department of Psychology, The
University of Tulsa, 800 South Tucker Drive, Tulsa, OK 74104. E-mail: [email protected]
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NIGHTMARE-RELATED IMAGERY
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posttraumatic stress disorder (PTSD) symptom severity (Erman, 1987; Esposito,
Benitez, Barza, & Mellman, 1999), and functional impairment (Davis, Rhudy,
Byrd, & Wright, 2007; Schreuder, Kleijn, & Rooijmans, 2000). Nightmares
appear to be particularly problematic for trauma-exposed persons who go on
to develop PTSD. The presence of nightmares and sleep disturbances in the
immediate aftermath of a traumatic event are associated with current and consequent symptom severity (Koren, Arnon, Lavie, & Klein, 2002; Mellman, David,
Bustamante, Torres, & Fins, 2001). Specifically, studies find that the presence
and severity of nightmares after a trauma are associated with overall levels
of reported distress and overall severity of re-experiencing symptoms (Erman,
1987; Esposito et al., 1999; Schreuder et al., 2000). Research indicates that 50%
to 88% of individuals with PTSD report chronic nightmares (Forbes, Creamer, &
Biddle, 2001; Kilpatrick et al., 1998; Neylan et al., 1998), a prevalence rate that
is higher than the prevalence for trauma-exposed persons without PTSD (Neylan
et al., 1998). There is also evidence that among persons reporting chronic
nightmares, those with PTSD experience greater nightmare-related distress (van
der Kolk, Blitz, Burr, Sherry, & Hartmann, 1984). Although chronic nightmares
are particularly problematic for those with PTSD, PTSD-negative individuals still
experience significant nightmare-related psychological problems and difficulties
(Davis et al., 2007; Schreuder et al., 2000). Moreover, successful cognitivebehavioral treatments (CBTs) that specifically target chronic nightmares reduce
symptoms of PTSD, depression, and panic; therefore, chronic nightmares could
be a significant maintaining factor of psychological distress (Davis & Wright,
2007; Forbes et al., 2003; Germain & Nielsen, 2003; Krakow et al., 2001;
Krakow et al., 2000).
Although the negative effects of chronic nightmares likely stem from many
factors, physiological–emotional arousal subsequent to nightmare-related thoughts
and cues may contribute. For example, thoughts related to nightmares could elicit
significant physiological arousal that increases the latency to sleep, thus promoting nightmare-related distress, decreased sleep quality and quantity, and perhaps
nightmare maintenance. Moreover, chronic physiological arousal is known to
have a detrimental impact on physical and mental health (McEwen, 1998).
Thus, repeated exposure to nightmares and nightmare-related stimuli could place
patients at increased risk for developing chronic physical problems, such as
cardiovascular disease (Blanchard, 1990; Boscarino & Chang, 1999). Although
research finds heightened arousal in terms of panic symptoms upon waking from
a nightmare (Davis et al., 2007; Davis & Wright, 2007), it is unclear whether
heightened arousal may also be experienced with waking exposure to nightmare
cues. To date, no research has examined this issue.
By contrast, numerous studies have examined reactivity to trauma cues in
persons exposed to trauma. These studies consistently find that PTSD-positive
individuals have a heightened physiological response to trauma cues compared
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RHUDY ET AL.
with PTSD-negative individuals (Carson et al., 2000; Lindauer et al., 2006; Orr
et al., 1998; Pitman et al., 2001; Pole, 2007; Schmahl et al., 2004; Shin et al.,
2004). Research also finds that heightened reactivity is specific to trauma cues
and is not evidenced in response to other fear or stress–related stimuli (Orr
et al., 1998; Orr, Pitman, Lasko, & Herz, 1993; Pitman et al., 1990; Pitman,
Orr, Forgue, de Jong, & Claiborn, 1987; Shalev, Orr, & Pitman, 1993). Greater
physiological–emotional reactivity has further been shown to have relevance
in predicting chronic PTSD and treatment response, with heightened reactivity
generally being associated with better treatment outcome (Orr & Roth, 2000).
Although nightmare content is not always associated with traumatic events in
persons exposed to trauma (Halliday, 1987; Hartmann, 1998), nightmare content
is likely to evoke fear-like subjective and physiological reactivity. Thus, procedures used to study physiological–emotional reactivity to trauma cues in persons
with PTSD (e.g., script-driven imagery) can be adapted to study reactivity to
nightmare cues. If nightmare cues are found to elicit significant physiological–
emotional arousal, it would be possible to examine whether participant characteristics influence the degree of reactivity (e.g., PTSD status), whether individual
differences in the degree of physiological–emotional reactivity correlate with
health and sleep problems, or both.
The present study was designed to examine physiological–emotional reactivity to nightmare-related imagery relative to standard emotional imagery in
trauma-exposed persons (with and without PTSD) who experience chronic nightmares. Physiological reactivity was assessed via four measures. Activity in the
corrugator (frowning) and frontalis (outer eyebrow raise) muscles was assessed
by electromyogram (EMG) because activity in these muscles has been shown
to positively correlate with the subjective experience of negative affect (e.g.,
Lang, Greenwald, Bradley, & Hamm, 1993; Orr, McNally, Rosen, & Shalev,
2004). Heart rate (HR) and skin conductance (SC) were measured to assess
autonomic reactivity, with SC being specifically tied to sympathetic activation
(Dawson, Schell, & Filion, 2000). In addition, subjective emotional reactivity
was assessed from ratings of emotional valence (unpleasantness–pleasantness)
and arousal (calm–excited; Bradley & Lang, 1994).
We predicted that nightmare-related imagery would lead to significantly
greater physiological–emotional reactivity than other emotionally evocative
imagery. We also expected that poorer mental health (due to reduced coping
resources) and more severe nightmares would correlate with greater reactivity
to nightmare imagery. Because evidence suggests dissociation is associated with
reduced physiological reactivity to fear cues (Griffin, Resick, & Mechanic,
1997; Lanius et al., 2002; Pole et al., 2005), we predicted that dissociation
would be negatively associated with reactivity to nightmare imagery. Finally,
it was expected that greater physiological reactivity to nightmare imagery
would correlate with greater sleep disturbance and more self-reported health
NIGHTMARE-RELATED IMAGERY
161
problems. If these research hypotheses are supported, this study would represent
the first step toward developing methods to more comprehensively assess
psychophysiological variables that contribute to chronic nightmares and their
maintenance (Lang, 1988; Orr & Roth, 2000).
METHOD
Participants
Men .n D 10/ and women .n D 25/ from the community were recruited to
participate in an ongoing study evaluating the efficacy of a CBT for chronic
nightmares in trauma-exposed persons. Ages ranged from 22 to 63 years .M D
39; SD D 12:02/: Most were married (38%) or divorced (21%), and 82%
had at least some college education. The most frequent types of trauma reported were car accident (60%), unwanted sexual contact (57%), physical assault
with a weapon (51%), and physical assault without a weapon (49%). Thirtyeight percent met criteria for current PTSD, and 53% met criteria for lifetime
PTSD. Six participants dropped out before physiological assessments could be
conducted, and 1 participant was not exposed to their nightmare script due
to equipment problems; therefore, the final sample included 28 participants.
Participants were recruited by fliers, e-mail, and radio ads and were eligible to
participate if they were 18 years old, had previous exposure to a traumatic
event, and had nightmares 1 times per week for the previous 3 months.
Exclusion criteria were psychosis or mental retardation, active suicidality or
parasuicidal behaviors, and current drug or alcohol dependence. Participants
were asked to refrain from consuming alcohol, nicotine, or caffeine 24 hr prior
to the physiological assessments. Participants were not excluded for medication
use, but preliminary analyses suggested that neither psychotropic medications
nor other medications (e.g., beta blockers, analgesics) altered physiological–
emotional reactivity in the present study (all ps > .05). A $20 gift certificate
was provided for participation.
Procedure
All procedures were approved by the University of Tulsa instutional review
board. After an initial phone screening, eligible participants underwent a diagnostic evaluation (baseline psychological assessment) by a trained upper level
graduate student after informed consent was obtained. During this evaluation,
questionnaires and structured interviews (see later discussion) were administered
to assess inclusion or exclusion criteria as well as demographics, PTSD status,
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PTSD symptom severity and frequency, depressive symptoms, dissociative experiences, nightmare characteristics, sleep problems, and health problems. Furthermore, the Nightmare Content Interview (NCI) was used to obtain nightmare
content that was used later by different experimenters to generate a personalized
nightmare script for physiological assessment of script-driven imagery. (The
participant was not involved in the script generation.) Following this psychological evaluation, participants were randomly assigned to CBT for nightmares
or a waitlist control group and then scheduled for the baseline physiological
assessment conducted on a later day. For this study, only data collected during
psychological and physiological baseline assessments were used. Between the
psychological and physiological assessment, experimenters generated a 30-sec
script (approximately 100 words) from the nightmare content. This script and
the standard emotional scripts (see later discussion) were recorded onto the
computer in the voice of the third author (Amy E. Williams).
During the physiological assessment, participants were seated comfortably in
a recliner and instrumented for facial EMG, SC, and electrocardiogram (ECG)
following a thorough explanation of the procedures. Once the experimenter left
the room, the session started with a 5-min habituation period followed by a 3min relaxation training period (diaphragmatic breathing) that was presented by
computer. During script-driven imagery, five scripts (see later discussion) were
presented in random order during which physiological responses were recorded.
Physiological reactivity to each script was derived from a 2-min recording epoch
(30-sec baseline period, a 30-sec period during which the script was presented
over headphones by computer, a 30-sec imagery period in which the participant
was asked to engage in the script imagery “as if it were happening to them,”
and a 30-sec recovery period in which the participant was asked to clear their
mind and relax). After each recovery period, the participant rated their emotional
reaction to the script-driven imagery using the Self-Assessment Manikin (SAM;
Bradley & Lang, 1994), and then HR was monitored to ensure that it returned to
pre-script baseline before the next recording epoch began (generally 1–2 min).
Once all scripts were presented, participants were thanked for their time.
Emotional Scripts
Every script used to generate imagery was approximately 100 words long. The
script was recorded digitally in a slow-paced, monotone voice such that the
length was approximately 30 sec. Each participant’s personal nightmare script
was constructed from subjective and sensory content assessed by the NCI (see
later discussion) and written in second person. Non-personal, standard scripts obtained from other researchers using script-driven imagery (Peter Lang, personal
communication, April 16, 2004; Scott Orr, personal communication, January 27,
2004) were used as control stimuli and included the following content: pleasant
NIGHTMARE-RELATED IMAGERY
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(“You are lying on a sandy beach on a warm summer day: : : : You feel relaxed
and content, enjoying the warmth of the sun: : : : ”), neutral (“You are sitting in
a lawn chair on your porch on a summer afternoon: : : : ”), action (“: : : You are
riding your bicycle on a quiet country road. You breathe heavily and sweat runs
down your face: : : : ”), and fear (“: : : You have never addressed such a large
group before. Your palms have become sweaty, and you tense up: : : : ”).
Measures
Demographic questionnaire. The demographic questionnaire is a selfreport measure designed to obtain standard information about the participants
including age, marital status, educational achievement, ethnicity, vocational status, and household income.
Clinician-Administered PTSD Scale (CAPS; Blake et al., 1990). The
CAPS is a structured interview that assesses lifetime and current PTSD from
17 questions. The symptom endorsement method was used to determine current and lifetime PTSD diagnoses. This method has adequate sensitivity and
specificity rates (Weathers, Ruscio, & Keane, 1999) and good reliability (Blake
et al., 1990; Weathers et al., 1999). A CAPS total score was created by summing
frequency and intensity scores for all items.
Beck Depression Inventory–Second Edition (BDI–II; Beck, Steer, &
Brown, 1996). The BDI–II is a reliable, 21-item self-report inventory used
to assess depression symptoms. Responses are made on a 4-point scale, yielding
total scores ranging from 0 to 63.
Pittsburgh Sleep Quality Index (PSQI; Buysse, Reynolds, Monk,
Berman, & Kupfer, 1989). The PSQI is a reliable and valid self-report
instrument that assesses sleep problems and quality for the 1 month prior to
the assessment (Buysse et al., 1989). A global sleep problem score ranges from
0 to 21 (higher scores D poorer quality), and is obtained by summing seven
component scores for the following: subjective sleep quality, sleep latency, sleep
duration, habitual sleep efficiency, sleep disturbances, use of sleep medication,
and daytime dysfunction. Single items were used to assess minutes taken to fall
asleep and hours slept per night.
PSQI Addendum (PSQI-A) for PTSD (Germain, Hall, Krakow, Shear,
& Buysse, 2005). The PSQI–PTSD Addendum (PSQI-A) is a seven-item
scale that assesses PTSD-related sleep and nighttime behaviors. The items assess
frequency of sleep problems in the past month ranging from 0 (not during the
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past month) to 3 (three or more times per week). Scores range from 0 to 21.
The PSQI-A has an internal consistency of .85 and good convergent validity.
Modified PTSD Symptom Scale–Self-Report (MPSS–SR; Resnick,
Best, Kilpatrick, Freedy, & Falsetti, 1993). This reliable and valid instrument assesses the frequency (0 D not at all, 3 D five or more times per week/very
much/almost always) and severity (0 D not at all distressing, 4 D extremely
distressing) of 17 PTSD symptoms (Falsetti, Resick, Resnick, & Kilpatrick,
1992, as cited in Falsetti, Resnick, Resick, & Kilpatrick, 1993; Wright, Davis,
Inness, & Stem, 2003).
Trauma-Related Nightmare Survey (Davis, Wright, & Borntrager, 2001).
This scale assesses nightmare symptoms as well as nightmare-related cognitions, emotions, and behaviors. The panic upon waking subscale is a sum of
14 endorsed symptoms (e.g., chest pain or discomfort, numbness or tingling
sensations, derealization) assessed from the following prompt: “After waking
from the nightmare, do you experience any of the following symptoms?” Internal
consistency was ˛ D .83. A single item assessed whether nightmares were
“exactly or almost exactly like the trauma,” “similar to the trauma,” or “unrelated
to the trauma” (nightmares similar/replicates trauma).
Dissociative Experiences Scale (DES; Bernstein & Putnam, 1986).
The DES is a reliable, self-report questionnaire that assesses frequency of 28
dissociative experiences on a 0% to 100% scale with 10-point intervals (Carlson
& Putnam, 1993; Dubester & Braun, 1995).
Pennebaker Inventory of Limbic Languidness (PILL; Pennebaker,
1982). This reliable, 54-item, self-report questionnaire assesses the frequency
of common physical symptoms. It is scored using a 5-point Likert scale that
ranges from 0 (have never or almost never experienced the symptom) to 4
(experiencing the symptom more than once a week).
Nightmare Content Interview (NCI). This structured interview was used
to gather content from the participant’s most recurrent nightmare, or most recent
nightmare if a single recurring nightmare was not available, and create personal
nightmare scripts. Participants were asked, “First, I would like you to briefly
describe your recurrent nightmare,” and then follow-up questions probed for
additional cognitive (“Tell me what was going through your head: : : : ”), somatic
(“What is your heart doing, are you sweating‹ : : : ”), and sensory information
(“What did you hear, see, smell, taste?”).
NIGHTMARE-RELATED IMAGERY
165
Self-Assessment Mankin (SAM) (Bradley & Lang, 1994). A computerized version of the SAM (Rhudy, Williams, McCabe, Nguyen, & Rambo, 2005)
assessed affective valence (unpleasant–pleasant) and arousal (calm–excited)
reactions to script-driven imagery. The SAM is a two-item questionnaire that
consists of two sets of five pictographs depicting affective valence/pleasure and
arousal. To respond, an indicator was placed on or between any of the five
pictographs, and ratings ranged between 1 and 9 for each dimension (higher
scores D greater pleasure–valence or arousal).
Apparatus and Physiological Outcomes
Sound-attenuating headphones and a video camera allowed the experimenter
to communicate with and monitor the participant from an adjacent room. A
computer with dual 17-in. flat-panel monitors and A/D board (National Instruments, PCI–6036E) presented all script stimuli and SAM questionnaires, as
well as acquired and stored physiological data. One monitor was used by the
experimenter to assess physiological signals and experimental timing, whereas
the other monitor was used by the participant to complete the SAM questionnaire. All physiological signals were sampled at 250 Hz and collected
and filtered using a Grass Instruments Model 15LT Bipolar Amplifier with
Quad AC (15A54) and Dual DC (15A12) modules. SC was measured using
an adaptor (Grass, Model SCA1) for the 15A12 amplifier, and electrodes filled
with isotonic paste (EC33, Grass Instruments) were placed on the distal volar
surface of the nondominant index and middle fingers. Miniature electrodes to
measure corrugator EMG and lateralis frontalis EMG were placed, according
to the recommendations of Fridlund and Cacioppo (1986), on the left side of
the face. Electrodes for ECG were placed on the forearms. Facial EMG and
ECG electrodes were applied by degreasing the skin, followed by slight skin
abrasion using NuPrep gel to reduce impedances below 10 K, and then EC60
gel (Grass Instruments) was placed in the electrodes before application. Facial
EMG activity was used as a physiologic measure of negative affect (Orr et al.,
1998), whereas ECG and SC were used to assess autonomic reactivity (Dawson
et al., 2000).
Physiological Data Reduction and Analyses
ECG was converted offline to HR in beats per minute. The raw signals for
HR, SC, and facial EMG signals were visually inspected for artifacts in 5-sec
bins. Bins that did not contain artifacts were then averaged into 30-sec phases
(baseline, script, imagery, recovery). Physiological reactivity was defined as the
change in the raw physiological signals during imagery relative to baseline;
therefore, the averaged raw signal (for HR, SC, and facial EMG) during the
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baseline phase was subtracted from the averaged signal during the imagery
phase. These change scores were then subjected to statistical analysis.
Chi-square analyses (for nominal variables) and independent samples t tests
(for interval or ratio scale variables) were used to compare participants included
in the analysis to those not included on study variables, and to compare participants with and without a current diagnosis of PTSD. To assess whether
physiological–emotional reactivity was greater during personal nightmare imagery in persons with and without current PTSD, a 5 (Imagery Type: pleasant, neutral, action, fear, nightmare) 2 (PTSD Status) doubly multivariate
repeated measures analysis of variance was used to analyze all physiological
and subjective reactions simultaneously (to control Type-I error rate). (It is
noteworthy that results from this analysis were the same when lifetime PTSD
was used instead of current PTSD.) However, to interpret significant effects,
this analysis was followed up with individual analyses of variance (ANOVAs)
on each reaction. When necessary, Greenhouse–Geisser adjustments were used
to correct for violations of sphericity in ANOVA models. To control for Type-I
error rate, significant main effects of imagery type were followed up by a priori
contrasts that only compared nightmare imagery to standard imagery (i.e., comparisons among standard imagery were not conducted). All other significant
effects were followed up with Bonferroni adjusted comparisons. Partial eta
squared (2 ) is reported for the effect size of F tests. To provide a measure
of effect size for the degree of reactivity, Cohen’s d is reported for the comparison between reactions to nightmare imagery relative to standard fear script
imagery.
To determine whether poorer mental health, less dissociative tendencies, and
more severe nightmare characteristics correlated with greater physiological–
emotional reactivity to nightmare imagery, zero-order correlations were calculated between physiological–emotional reactivity outcomes and current or
lifetime PTSD status, PTSD severity, PTSD frequency, depressive symptoms, dissociative experiences, months since nightmares started, nightmare
frequency, and similarity of nightmare to trauma. To determine whether
physiological reactivity to nightmare imagery correlated with greater sleep
disturbance and more reported health problems, zero-order correlations were
also calculated between physiological and subjective reactions to nightmare
imagery and the global sleep quality index, PTSD-related sleep behaviors,
minutes taken to fall asleep, hours slept per night, panic upon awakening,
and health symptoms. For comparison, correlations between physiological–
emotional reactivity to fear imagery and consequences of nightmares were
also conducted. To interpret correlation analyses, a more stringent alpha
level .p :01/ was chosen that reduced family-wise Type-I error, but
also took into consideration the problem of augmenting a Type-II error
rate.
NIGHTMARE-RELATED IMAGERY
167
RESULTS
Characteristics of Participants Included in the Study
(Table 1)
The only significant difference found between persons included versus excluded
was that those included in the study reported sleeping longer (more hours) per
night .M D 4:57 vs. 5.96; t D 1:99; p D :05/: Participants without and with
current PTSD were similar on most variables (ps > .05) except global sleep
problems .M D 11:00 vs. 16.00; t D 3:27; p D :003/; CAPS total score .M D
44:05 vs. 82.14; t D 7:13; p < :001/; PTSD severity .M D 19:33 vs. 42.50;
t D 4:07; p < :001/; PTSD frequency .M D 17:47 vs. 34.50; t D 3:86; p D
:001/; depressive symptoms .M D 18:21 vs. 28.56; t D 2:12; p D :04/; and
TABLE 1
Sample Characteristics for Participants Included in the Study
Variable
Age, mean
Sex (female)
Race (White)
Relationship status (living with other or married)
Months since nightmare started (TRNS), mean
Nightmares per week (TRNS), mean
Nightmare similar to or replicates trauma (TRNS)
Panic upon waking (TRNS), mean
Global sleep problems (PSQI), mean
PTSD-related sleep behaviors (PSQI-A), mean
Minutes taken to fall asleep (PSQI), mean
Hours slept per night (PSQI), mean
CAPS total score, sum
PTSD current (CAPS)
PTSD lifetime (CAPS)
PTSD severity (MPSS–SR), mean
PTSD frequency (MPSS–SR), mean
Depressive symptoms (BDI–II), mean
Dissociative experiences (DES), mean
Health symptoms (PILL), mean
mean or %
39.64 (12.06)
68%
75%
46%
206.81 (140.87)
3.46 (1.82)
56%
5.44 (3.72)
12.80 (4.35)
9.70 (.90)
39.64 (28.67)
5.96 (1.54)
59.29 (24.32)
32%
46%
26.22 (17.04)
22.52 (12.96)
21.54 (12.80)
17.00 (15.60)
78.64 (31.61)
Note. N D 28: Standard deviations are shown in parentheses. TRNS D
Trauma-Related Nightmare Survey; PSQI D Pittsburgh Sleep Quality Index; PSQIA D PSQI-Addendum; CAPS D Clinician-Administered PTSD Scale; PTSD D
posttraumatic stress disorder; MPSS–SR D Modified PTSD Symptom Scale–SelfReport; BDI–II D Beck Depression Inventory–Second Edition; DES D Dissociative
Experiences Scale; PILL D Pennebaker Inventory of Limbic Languidness.
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RHUDY ET AL.
dissociative symptoms .M D 12:31 vs. 26.90; t D 2:53; p D :02/: Participants
with current PTSD had worse symptomatology.
Physiological–Emotional Reactivity to Nightmare Imagery
(Table 2)
The doubly multivariate analysis found a significant main effect of imagery
type, F .24; 305/ D 9:38; p < :001; 2 D :38: No other effects were significant
(ps > .17). To interpret this main effect, ANOVAs were conducted on each
physiological–emotional measure. A significant main effect of imagery type was
found for valence (pleasure) ratings, arousal ratings, HR, SC, and corrugator
EMG. Lateralis frontalis EMG was not significantly affected by imagery. Compared to all other standard imagery types, nightmare imagery resulted in lower
valence (greater displeasure) ratings (ps < .001), higher arousal ratings (ps .01), larger HR responses (ps < .01), and larger SC (ps < .004). Corrugator
reactivity was greater during nightmare imagery than pleasant and neutral (ps <
.005), but the comparisons of nightmare imagery to action .p D :07/ and fear
.p D :08/ imagery did not reach significance. Cohen’s d for the nightmare
versus fear imagery comparisons were as follows: valence D 1.37, arousal D
0.79, HR D 0.66, SC D 0.79, corrugator EMG D 0.62, and lateralis frontalis
EMG D 0.21. The PTSD status main effect was nonsignificant for all analyses
(F s < 1.78, ps > .18). The Imagery Type PTSD Status interaction was only
significant for HR, and suggested HR responses were lower for persons with
PTSD during pleasant and neutral imagery (ps < .03); but PTSD versus nonPTSD comparisons for action .p D :07/; fear .p D :59/; and nightmare imagery
.p D :15/ were nonsignificant. Together, these data suggest that nightmare
imagery resulted in significant physiological–emotional reactivity relative to
standard imagery, with medium to large effect sizes for most comparisons
between nightmare and fear imagery. It is interesting to note that PTSD status
did not have a significant effect on reactivity to nightmare imagery.
Correlates of Physiological–Emotional Reactivity to
Nightmare Imagery
No mental health or nightmare variable (PTSD status or symptoms, depressive
symptoms, dissociative experiences, or nightmare characteristics) was significantly related to physiological or subjective reactivity to nightmare imagery
at the p :01 level. The average correlations with outcome variables were
generally small (average r s: valence D .12, arousal D .16, HR D .27, SC D .18,
corrugator EMG D .09, lateralis frontalis EMG D .13). The only correlation that
approached significance was the relation between MPSS–SR PTSD symptom
frequency and HR .r D :42; p < :05/:
TABLE 2
Descriptive and Inferential Statistics (From Univariate ANOVAs) for Physiological and
Subjective Reactivity to Imagery Grouped by Imagery Type and PTSD Status
Physiological–Emotional Reactions
No Current PTSD
Variable
Subjective reactions
Valence ratings
Arousal ratings
Autonomic reactions
HR (bpm)
SC (S)
Facial EMG reactions
Corr. EMG (V)
Lat. Fr. EMG (V)
Pleas.
Neu.
ANOVA Results
Current PTSD
Act.
Fear
NM
Pleas.
Neu.
Act.
Imagery Type
Imagery PTSD
Fear
NM
F
2
F
2
77.53***
.76
0.79
.03
42.02***
.63
1.37
.05
13.02***
.35
3.91*
.14
15.84***
.39
0.85
.03
8.64**
.27
0.95
.04
1.02
.04
0.32
.01
M
SEM
M
SEM
7.83
0.34
1.89
0.44
7.94
0.37
1.67
0.44
5.61
0.45
5.06
0.47
3.61
0.46
6.00
0.51
1.72
0.25
7.61
0.38
8.00
0.48
2.56
0.62
7.78
0.53
3.33
0.62
6.78
0.63
5.22
0.67
4.00
0.65
6.11
0.72
1.56
0.35
7.11
0.54
M
SEM
M
SEM
0.70
0.71
0.17
0.06
0.86
0.45
0.14
0.05
2.56
0.85
0.02
0.09
2.20
0.72
0.28
0.20
4.09
1.52
0.96
0.28
2.34
1.07
0.24
0.09
2.43
0.68
0.21
0.07
0.35
1.27
0.22
0.13
1.48
1.08
0.23
0.30
8.19
2.28
1.44
0.42
M
SEM
M
SEM
0.43
0.44
0.15
0.13
0.63
0.31
0.04
0.08
1.19
0.98
0.14
0.09
1.22
0.61
0.25
0.14
5.71
1.85
0.99
0.81
2.03
0.65
0.36
0.20
0.74
0.45
0.00
0.12
2.64
1.43
0.16
0.13
3.04
0.88
0.53
0.20
4.07
2.70
0.27
1.21
Note. ANOVA D analysis of variance; PTSD D posttraumatic stress disorder; Pleas. D pleasant imagery; Neu. D neutral imagery; Act. D action
imagery; NM D personal nightmare imagery; HR D heart rate; bpm D change in beats per minute; SC D skin conductance; S D change in
microSiemens; EMG D electromyogram; Corr. D corrugator muscle; V D change in microvolts; Lat. Fr. D lateralis frontalis muscle.
*p < :05: **p < :01: ***p < :001:
169
170
RHUDY ET AL.
TABLE 3
Zero-Order Correlations Between Physiological–Emotional Reactions to
Nightmare Imagery and Problems With Sleep and Health
Reactions to Nightmare
Imagery
Valence rating
Arousal rating
HR (bpm)
SC (S)
Corr. EMG (V)
Lat. Fr. EMG (V)
Global
Sleep
Problems
(PSQI)
0.09
0.01
0.55*
0.33
0.18
0.01
PTSD
Sleep
Behaviors
(PSQI-A)
0.46***
0.17
0.20
0.19
0.05
0.18
Minutes
Taken
to Fall
Asleep
(PSQI)
0.25
0.31
0.41***
0.50*
0.41***
0.24
Hours Slept
Per Night
(PSQI)
0.02
0.04
0.59*
0.40***
0.13
0.26
Panic
Upon
Waking
(TRNS)
0.04
0.04
0.58*
0.63**
0.01
0.22
Health
Symptoms
(PILL)
0.09
0.06
0.54*
0.16
0.11
0.03
Note. Significant correlations are in bold type. PSQI D Pittsburgh Sleep Quality Index; PSQI-A D PSQIAddendum; TRNS D Trauma-Related Nightmare Survey; PILL D Pennebaker Inventory of Limbic Languidness;
HR D heart rate; bpm D change in beats per minute; SC D skin conductance; S D change in microSiemens;
Corr. D corrugator muscle; EMG D electromyogram; Lat. Fr. D lateralis frontalis; V D change in microvolts.
*p :01: **p :001: ***p :05:
Correlates of Negative Consequences of Chronic
Nightmares From Physiological and Subjective Reactivity
to Nightmare Imagery (Table 3)
Autonomic reactions were the most reliable correlates of poor sleep and health,
demonstrating large effect sizes. HR was associated with increased global sleep
problems, fewer hours slept per night, panic upon waking, and health symptoms.
SC was associated with time to fall asleep and panic upon awakening. It is
interesting to note that subjective reactions were unrelated to these variables.
For exploratory purposes, partial correlations were conducted that controlled
for number of nightmares per week (nightmare chronicity). All relationships
remained significant. More important, physiological–emotional reactions to fear
imagery were unrelated to any of these outcomes, with the strongest correlation
being between valence ratings and PTSD-related sleep behaviors .r D :28; p >
:05/: Moreover, Fisher’s r -to-z tests for non-independent correlations indicated
nightmare and fear imagery correlations were different at p :01; except
between SC and minutes taken to fall asleep .p D :13/: Therefore, autonomic
reactions to nightmare imagery appear related to sleep disturbance and health
symptomatology.
DISCUSSION
The present study examined physiological–emotional reactions to nightmare
imagery in trauma-exposed persons suffering from chronic nightmares. Results
NIGHTMARE-RELATED IMAGERY
171
suggested nightmare imagery increased reports of displeasure (lower valence)
and arousal, as well as increased HR, SC, and corrugator (frowning) muscle
activity. Lateralis frontalis muscle activity was not affected. Of particular interest
is the fact that PTSD status did not moderate reactivity to nightmare imagery.
This suggests nightmares may have a significant physiological–emotional impact
on all sufferers, regardless of comorbid psychopathology. Although PTSD status
did interact with imagery type for HR, this stemmed from the fact that HR
decelerated in persons with PTSD during pleasant and neutral imagery compared
to persons without PTSD. Results from the ANOVA suggested HR reactivity to
nightmare imagery did not differ by PTSD status. This analysis was supported
by correlational analyses showing that PTSD symptomatology (current–lifetime
PTSD diagnosis, symptom severity, symptom frequency) was not associated
with nightmare imagery-evoked HR. One possible explanation for this lack of
moderation by PTSD could have been that participants with PTSD had greater
anxious apprehension about being exposed to their nightmare. This apprehension
could have elevated resting HR, making it difficult to evoke greater reactivity
above baseline (i.e., a ceiling effect). This could also explain why HR decelerated
during relaxing and pleasing imagery (neutral, pleasant). To minimize anticipation and emotional carry-over effects associated with our within-subjects design,
script order was randomized between individuals. However, this tactic may not
have eliminated all anticipatory and carry-over effects in the PTSD-positive
individuals.
Our prediction that mental health would influence the level of nightmare
imagery-evoked physiological–emotional reactivity was not supported. Neither
PTSD nor depressive symptoms were significant correlates. This is surprising
given that mental health problems in trauma-exposed persons are typically associated with impaired coping (e.g., Stallard & Smith, 2007) and heightened
physiological–emotional reactivity to stressful events (Keane et al., 1998; Orr
et al., 2004; Shalev, Orr, & Pitman, 1992). Analyses also suggested that dissociative tendencies were not associated with blunted physiological–emotional
responses (Griffin et al., 1997). However, this may have resulted from the explicit
instructions to engage in imagery rather than avoid it. Future research could
address this issue by varying the instruction set.
Results also did not support our prediction that greater nightmare chronicity
(months since nightmares started, number of nightmares per week) and similarity of the nightmare to a previously experienced trauma would be associated
with greater reactivity. However, these null results need to be interpreted with
caution because our small sample size may have reduced our power to detect
significant relations (e.g., some correlations between HR reactivity and mental
health had medium effect sizes). Power analyses, however, suggested that a large
sample size (between 250 and 2,800) would have been needed to detect most
of the correlational effects determined to be nonsignificant in the current study.
172
RHUDY ET AL.
Even the correlations with HR would have required over 100 participants. In
addition, our one-time assessment of physiological reactivity to scripts during
this baseline assessment may have led to low reliability and stability of our
dependent variables. Inconsistent with this interpretation however, we did find
that individual differences in physiological reactivity to nightmare imagery was
associated with sleep and self-reported health problems. Consistently, greater
HR reactivity was associated with poor sleep and health outcomes. Also, greater
SC was associated with longer time taken to fall asleep and greater panic upon
waking. It is interesting to note that participants’ subjective or facial emotional
reactions were unrelated to sleep and health problems. Therefore, autonomic
arousal resulting from nightmare-related thoughts and imagery may play an
important role in sleep disturbance. For example, increased autonomic arousal
could interfere with getting to sleep, returning to sleep upon awakening from
a nightmare, and amount of restful sleep (sleep quality). Indeed, sleep latency
has been found to positively correlate with contemporaneous HR (Bonnet &
Arand, 2005). In addition, frequent and exaggerated autonomic arousal may
increase allostatic load, thus resulting in poorer health (McEwen, 1998). In
particular, the finding of increased HR reactivity may place persons suffering
from chronic nightmares at increased risk of developing cardiovascular disease
(Blanchard, 1990; Boscarino & Chang, 1999). Given the potential importance of
autonomic reactivity in nightmare-related problems, this suggests future studies
should consider other, more dynamic, measures of autonomic reactivity, such as
HR variability.
Together, these results suggest that reducing nightmare-related autonomic
arousal could improve sleep and health. However, longitudinal studies are needed
to determine the direction of the relations noted in these cross-sectional analyses (perhaps greater sleep disturbance and health problems result in greater
nightmare-related autonomic reactivity). Our laboratory is currently following
these participants after they undergo CBT for nightmares to determine whether
physiological–emotional arousal is impacted by psychological treatment. If so,
this would add to the extant literature suggesting psychological (e.g., Davis &
Wright, 2007; Forbes, Phelps, & McHugh, 2001; Germain & Nielsen, 2003)
and pharmacological (e.g., Raskind et al., 2003) interventions are efficacious for
reducing nightmare-related problems.
Study Limitations
In addition to the limitations noted earlier, there are a few other issues worthy of
mention. The present study used personal nightmare content to evoke nightmare
imagery. In future studies, another personally relevant script unrelated to the
nightmare should be used to control for physiological–emotional reactivity due
to personal relevance. Although the present design did not allow us to con-
NIGHTMARE-RELATED IMAGERY
173
trol for personal relevance, reactivity to the nightmare imagery was large and
significantly different from all other imagery types.
In the majority of studies, script-driven imagery is used to examine
physiological–emotional reactivity to fear cues, including trauma-reminders. For
the present study, we assume that nightmare content, regardless of its relation
to an experienced trauma, would serve as a fear cue to elicit physiological–
emotional reactivity. Our results are consistent with this hypothesis and suggest
that nightmare-related thoughts could promote avoidance of sleep (during which
exposure to nightmare content is imminent). Nonetheless, it is important to note
that nightmare imagery is different from most other fear cues in that it does not
represent a specific environmental or sensory event.
For 56% of participants, the nightmare imagery was trauma related (the
nightmare was similar to, or replicated, the participant’s trauma experience).
Although analyses suggested the trauma similarity of the nightmare was not
associated with the degree of physiological–emotional reactivity to nightmare
imagery, our sample size was not large enough to determine whether PTSD
status interacted with trauma similarity of the nightmare. For example, it is
possible that persons who are PTSD-positive and whose nightmares are related
to their trauma have greater physiological–emotional reactivity to nightmare
imagery than persons who are PTSD-negative.
Finally, to assess subjective reactions to imagery, the SAM was used. Although the SAM is well-validated and commonly used in studies of subjective reactivity (e.g., Bradley, Codispoti, Cuthbert, & Lang, 2001; Bradley &
Lang, 1994), single items are used to measure valence and arousal. Moreover,
participants generally rated their nightmare imagery as highly unpleasant (low
valence) and arousing, thus limiting response variability. These issues could have
impacted our ability to detect significant relations between subjective emotional
reactivity and other study variables.
Despite these limitations, this study contributes to our understanding of chronic
nightmares and their impact in trauma-exposed persons. It is the first study, to
our knowledge, to use script-driven imagery to examine physiological–emotional
reactivity to nightmare imagery in persons suffering from chronic nightmares.
Although preliminary, these data suggest physiological reactivity may be an
important variable to consider when assessing and treating chronic nightmares.
In particular, nightmare cue-evoked autonomic reactivity may be an important
therapeutic target.
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