Psychophysiology, 40 (2003), 407–422. Blackwell Publishing Inc. Printed in the USA.
Copyright r 2003 Society for Psychophysiological Research
The psychophysiology of anxiety disorder:
Fear memory imagery
BRUCE N. CUTHBERT, PETER J. LANG, CYD STRAUSS, DAVID DROBES,
CHRISTOPHER J. PATRICK, and MARGARET M. BRADLEY
Center for the Study of Emotion and Attention, University of Florida, Gainesville, Florida, USA
Abstract
Psychophysiological response to fear memory imagery was assessed in specific phobia, social anxiety disorder, panic
disorder with agoraphobia, post-traumatic stress disorder (PTSD), and healthy controls. Heart rate, skin conductance,
and corrugator muscle were recorded as participants responded to tone cues signaling previously memorized descriptor
sentences. Image contents included personal fears, social fears, fears of physical danger, and neutral (low arousal)
scenes. Reactions to acoustic startle probes (eyeblink) were assessed during recall imagery and nonsignal periods.
Participants were significantly more reactive (in physiology and report of affect) to fear than neutral cues. Panic and
PTSD patients were, however, less physiologically responsive than specific phobics and the socially anxious. Panic and
PTSD patients also reported the most anxiety and mood symptoms, and were most frequently comorbidly depressed.
Overall, physiological reactivity to sentence memory cues was greatest in patients with focal fear of specific objects or
events, and reduced in patients characterized by generalized, high negative affect.
Descriptors: Anxiety, Imagery, Startle, Depression, Panic, PTSD
Furthermore, because network representations are associatively
connected, only a few matches may be needed to activate an
entire memory structure. In this way, pictures, movies, poetry,
and narrative text cue emotional memories, and the reflex
physiology of emotion can be primed by no more than words on
a page or the flickering light of film and television screens.
This memory model has been extensively studied in normal
participants instructed to process verbal descriptions of a fear
context (e.g., Lang, Levin, Miller, & Kozak, 1983; Miller et al.,
1987). In this research, perceptual-motor memories were consistently activated by text cues, with an accompanying efferent
reaction that varied in strength with reports of emotional
arousal. The process was modulated by imagery instructions,
training, and variations in text content. Optimal physiological
responses resembled preparation to avoid/escape, as it occurs in
an actual fearful encounter. Curiously, however, in pilot studies
with anxiety patients, the efferent effects were greatly diminished
in some disordersFeven with recall of patients’ primary clinical
fears. These seemingly counterintuitive data prompted Lang
(1985) to speculate that anxiety disorders might differ in memory
organization, according to principal diagnosis. He proposed a
continuum in the coherence of fear memory networks, varying
over anxiety diagnoses from high to low associative network
strength. In this view, phobia is characterized by fear networks of
high associative strength, with specific, reliable cues to active
avoidance, assuring strong physiological activation at memory
recall; the fear networks of socially anxious patients are somewhat less coherent, with many more stimulus and meaning
representations, but with a lower overall associative strength;
coherence is further reduced in panic, and lowest in generalized
It has been suggested (Lang, 1979, 1985, 1994) that vivid recollection of an emotional event depends on central processing of an
associative information network. Emotional networks include
three classes of information (or types of representations):
information about the physical stimulus context in which the
event occurred, interpretive associations that elaborate the
event’s meaning, and most importantly for the current investigation, procedural representations of the efferent reflexesFvisceral
and somaticFthat define expressed emotion. Given the presence
of procedural representations (and assuming high strength of
association among network elements), retrieval of an emotional
memory is expected to prompt actual activation of the
represented muscles and glands, albeit generally below the
threshold of overt action.
Network processing (memory retrieval) is instigated by
external stimuli that match some network representations.
Bruce Cuthbert is currently at the National Institute of Mental Health
in Bethesda, MD. Peter Lang, Cyd Strauss, and Margaret Bradley are at
the University of Florida, Center for the Study of Emotion and Attention
in Gainesville, FL. David Drobes is at the University of South Florida,
Department of Interdisciplinary Oncology in Tampa, FL, and Christopher Patrick is at the University of Minnesota, Department of
Psychology in Minneapolis, MN. This work was supported by National
Institute of Mental Health (NIMH) Grants MH 37757, MH 43975, and
P50 MH 52384.
Address reprint requests to: Peter Lang, Center for the Study of
Emotion and Attention, Box 100165, Health Sciences Center, University
of Florida, Gainesville, FL 32610, USA. E-mail: [email protected].
ufl.edu.
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anxiety disorder. These variations in network coherence determine a parallel variation in strength of physiological reaction
at memory recall.
A hypothesized practical consequence of low network
coherence is that emotional language is less likely to activate
emotional expression in the context of psychological treatments.
For example, imagery methods would be less effective in cognitive and exposure therapy. Findings consistent with this view
have been reported, showing that participants who respond
physiologically in emotional imagery have a better therapeutic
outcome (Bryant, Sullivan, Strauss, Cuthbert, & Lang, 1997;
Lang, 1970).
Studying Emotional Memory in Anxious Patients
The present research is a broader reconsideration of an experimental problem first addressed by Cook, Melamed, Cuthbert,
McNeil, and Lang (1988). Consistent with the network
hypothesis, they found that panic disorder patients with agoraphobia did not show robust autonomic response to emotional
imagery of their fears, as was consistently found for specific phobics and, to a lesser extent, for social phobics. This difference was
not apparent in verbal report of emotional arousal during
imagery.
In research with normal participants, language descriptive of
a fear context (with imagery instructions) has been shown to
activate perceptual-motor memories that include metabolic
mobilization, presumably preparatory to active avoidance as it
would occur in an actual fearful encounter (e.g., Lang, 1979,
1994; Lang et al., 1983; Miller et al., 1987). The observed absence
of cardiovascular arousal and skin conductance activation in
panic patientFwho, nevertheless, report intense fearFsuggests
that for this diagnosis, language cues are not strongly associated
with a procedural physiology. This appears to involve both a
reduced effectiveness of instructional and descriptive verbal input
and an output discordance between the reactive physiology and
evaluative language.
In examining their data, Cook et al. (1988) noted other differences between phobia and panic. On questionnaire measures
of anxiety and depression, panic patients consistently had significantly higher scores than phobics. That is, diagnoses characterized by high ‘‘negative affect’’ (as defined by Tellegen, 1985; see
also Clark, Watson, & Mineka, 1994), nevertheless showed
the smallest physiological response. Curiously, this apparent
association between high negative affect and low autonomic
reactivity was not seen if diagnosis was ignored. That is, when the
entire sample of anxiety patients was considered as a single
group, correlations between physiological reactivity and questionnaire scores were low and nonsignificant. Furthermore, there
was no significant covariation of these variables within the panic
sample.
McNeil, Vrana, Melamed, Cuthbert, and Lang (1993) followed up this experiment using a similar methodology, studying
fearful normal and anxious participants. The research results suggested that this population could be divided into two different groups
with characteristics similar to those distinguishing specific phobics from panic patients. One group was characterized predominantly by fear, that is, an active avoidance of a specific
fear object or group of objects. These subjects showed clear
physiological arousal, concordant with verbal report of affective
intensity, during fear image processing. The second group, like
the panic patients, reported strong fear but also had higher scores
on scales evaluating more generalized symptoms of anxiety and
B.N. Cuthbert et al.
social distress (e.g., passive avoidance, restlessness, negative selftalk). The physiological response to imagery text of this
‘‘anxious’’ group was small, discordant with verbal report, and
significantly less than that of the ‘‘fear’’ group.
The Experimental Protocol
The present psychophysiological protocol was originally developed in studies of normal participants (e.g., Vrana, Cuthbert, &
Lang, 1986; Vrana & Lang, 1990), and differs in important ways
from the one employed in previous studies of anxiety patients.
Instead of using a paragraph of text to prompt fear imagery (e.g.,
Cook et al., 1988; McNeil et al., 1993; see also Orr et al., 1998),
the image cues were simplified by reducing them to single,
descriptive sentences. To further assure that the textual cues were
understood, and to eliminate the possibility that the physical
properties of auditory presentation (which can vary with speaker
and sentence content) might compromise imagery measurement,
participants memorized the sentence material in advance.
Subsequently, during psychophysiological assessment, imagery
was cued by brief auditory tones high or low in frequency,
distinguishing two previously learned sentences of either fearful
or neutral content.
The array of physiological measures studied here was
expanded to include somatic as well as the autonomic responses
(heart rate and skin conductance) previously reported. Thus,
potentials from the corrugator (‘‘frown’’) muscle were measured
as a covert index of facial expression. Furthermore, the eyeblink
component of the startle reflex was recorded, as evoked by brief
acoustic stimuli presented both during imagery processing and in
the intertrial intervals (ITI). The potentiation of the startle reflex
during fearful states, based upon extensive animal models
documenting the involvement of the amygdala and other limbic
structures (e.g., Davis, 1992), has been extensively documented
in recent years both for perceptually presented stimuli (Lang,
Bradley, & Cuthbert, 1997; Vrana, Spence, & Lang, 1988) and in
imagery (Bradley, Lang, & Cuthbert, 1991; Cook, Hawk, Davis,
& Stevenson, 1991; Vrana & Lang, 1990).
Research Aims and Hypotheses
The primary aim of the present experiment is to further explore
emotional memory differences among anxiety disorders, first
determining if the previously observed phenomena are reliable.
That is, do phobic disorders differ from other anxiety diagnoses
(e.g., panic disorder) in psychophysiological response to fear
memory imagery? Are higher questionnaire scores in anxiety and
depression found for diagnoses that also show reduced physiological reactivity? A further aim was to better understand the
determinants of, and the relationship between, these phenomena.
In advancing this aim, another anxiety disorder, post-traumatic
stress disorder (PTSD), was included in the study sample and the
several diagnostic groups were compared with a normal control
group. Finally, the relationship between depression comorbidity
and physiology was assessed for both base level activity and
imagery response.
It was anticipated that autonomic reactivity to personal fear
imagery would again be diminished in panic patients relative to
specific phobics and socially anxious patients. This analysis was
performed for all physiological measures of image processing. To
evaluate the generality of effect, participants also imagined two
standard fear contents, involving situations that are dangerous
(an automobile accident, threat of physical violence) and
situations that are socially difficult and distressing (giving a
Fear imagery and anxiety
speech, suffering verbal abuse). It was anticipated that socially
anxious patients would show greater reactivity to the standard
social scripts than the other diagnoses. All diagnoses and
controls may be expected to react strongly to the danger
sentences.
The reactions of PTSD patients in the present context were
not easily predicted. Researchers have observed significant
autonomic reactivity to fear imagery in these patients, relative
to controls (e.g., Pitman, Orr, Gorgue, de Jong, & Claiborn,
1987) and more marked startle probe potentiation in the context
of a shock threat (e.g., Morgan & Grillon, 1998). However, there
are few data comparing the fear reactions of PTSD patients with
other anxiety diagnoses. Thus, for example, previous data
indicate that PTSD patients show greater heart rate increases
when imaging combat scenes than veteran controls without
PTSD (Pitman et al., 1987). However, it is not clear that the
responses of PTSD patients are greater than, for example,
specific phobics responding to their own fear content. Similarly,
it has not been shown that PTSD patients are more reactive than
normal controls when both groups respond to image cues of their
own worst fears.
Considering the hypothesis that high cue specificity is the key
feature determining a strong psychophysiological response,
PTSD patients might be expected to show a marked reaction
similar to that of specific phobics. On the other hand, PTSD is
characterized by high comorbidity with other anxiety disorders
and depression. From this perspective, previous results suggest
that they would show a diminished reaction similar to panic
disorder.
Method
Participants
Participants were seen at the University of Florida Fear and
Anxiety Disorders Clinic (N 5 130). The sample included 106
patients, grouped by principal diagnoses: 28 specific phobia (5
men), 30 social anxiety disorder (17 men), 26 panic disorder with
agoraphobia (10 men), and 22 PTSD (8 men). These patients
were predominantly Caucasian, and between 30 and 40 years of
age. They presented for treatment following referral by a
physician or other health care worker or in response to clinic
advertisements. In addition to the patients, 24 controls (9 men)
without behavior disorders were recruited through a newspaper
advertisement and paid for their participation. Potential
participants who showed active psychotic symptoms or had
health problems that would compromise the physiological
recording were excluded. However, 3 patients were included in
the sample that had a past history of bipolar disorder (1 in the
social and 2 in the panic groups).
Interviews were conducted using the Anxiety Disorders
Interview Schedule–Revised (ADIS-R; DiNardo & Barlow,
1988) in order to assign diagnoses according to the Diagnostic
and Statistical Manual of Mental Disorders (DSM-III-R;
American Psychiatric Association, 1987).1 The ADIS has been
used extensively by senior members of the research team (see
Cook et al., 1988; Lang et al., 2001; McNeil et al., 1993). They
monitored uniformity in its use and interpretation, and trained
and supervised new assessors. Diagnostic categories for all
1
At the inception of this research, DSM-IV was not yet in general use.
After the revision’s publication, considering that the changes would not
significantly affect patient groupings, it was elected not to alter criteria in
midstream.
409
participants were independently rated by two of three clinical
psychologists on the evaluation team, who either conducted the
evaluation interview or observed it (live or on videotape). Using
the ADIS-R data, each anxiety and mood disorder was assigned
a severity score ranging from 0 to 5; the numbers 1 or 2
represented levels of subsyndromal features, and codes of 3 to 5
denoted presence of a diagnosable disorder with one of three
increasing levels of severity. Axis II disorders were assigned
according to presenting symptomatology, although time constraints precluded structured Axis II interview measures. A
‘‘principal diagnosis’’ was assigned according to the patient’s
chief presenting complaintF‘‘the condition established after
study to be chiefly responsible for occasioning the admission
of the individual.’’ (American Psychiatric Association, 2000,
p. 3). Additional diagnoses were assigned as appropriate in
decreasing order of severity or impairment. Any assessment
differences were resolved at a meeting of the full evaluation
team; the interrater agreement on principal diagnoses was high
(Kappa 5 .86). Control participants were free of any Axis I or II
disorders.
Anxiety disorder comorbidity was similar in pattern to that
reported by Brown, Campbell, Lehman, Grisham, and Mancill
(2001), that is, over half of all patients had another anxiety
diagnosis in addition to their principal diagnosis. Patients in the
panic group had the highest anxiety comorbidity (76%); specific
phobics were the least likely to have an additional anxiety
diagnosis (32%). Social anxiety disorder and specific phobia
were the additional anxiety diagnoses showing the greatest
overlap among experimental groups: 26% of the patients had an
additional diagnosis of social anxiety disorder (highest incidence
for the panic group, n 5 10); 17% had specific phobia as an
additional diagnosis (highest incidence in the social phobic
group, n 5 6). Additional diagnoses of panic with agoraphobia
or PTSD were rareF5% and 4%, respectively. Other than the
four diagnoses that defined the patient groups, generalized
anxiety disorder was the additional diagnosis most frequently
assigned (27% of the patient sample, highest incidence in the
panic group, n 5 11). The incidence of comorbid mood disorder
(major depressive episode or dysthymia) was lowest for specific
phobia (11%) and highest for panic disorder (42%) and PTSD
(55%). Axis II additional diagnoses were not significant in
number.
Procedure
Upon arrival at the Fear and Anxiety Disorders Clinic and after
providing informed consent, participants were interviewed
(ADIS-R) and administered a questionnaire battery. The questionnaires included the Beck Depression Inventory (BDI; Beck,
Ward, Mendelsohn, Mock, & Erbaugh, 1961); the Fenz–Epstein
manifest anxiety questionnaire, assessing autonomic, somatic,
and psychosocial symptom reports (FEQ; Fenz & Epstein,
1965); the Marks–Mathews self-rating scale of phobic symptoms
(Marks & Mathews, 1979); and the Fear Survey Schedule of
reactions to a catalogue of phobic objects (FSS; Wolpe & Lang,
1964). A temperament questionnaire assessing negative emotionality (EASI; Buss & Plomin, 1975) was added to the battery
after data collection had begun, and was administered to the last
97 participants.2
2
The EASI was introduced after the research was already underway.
Therefore there are only data for 74 patient participants who were
administered the measure, at least half of each diagnostic group.
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Stimulus materials consisted of 12 one- or two-sentence
imagery scripts, 6 each describing fearful and neutral scenes. Two
of the fear scripts were personalized for each participant, based
on interview and on Scene Construction forms filled out during
the initial session just after the ADIS-R interview. For the latter,
both patients and controls were first asked to describe their
‘‘worst fear experience.’’ For patients, the content of the fear
scripts was their central, clinical fear (e.g., having a panic attack
or confronting the phobic object); for control participants, these
sentences described what they reported to be their ‘‘worst fear
experience.’’ For all participants, guided by the bio-informational view of affective imagery (Foa & Kozak, 1986; Lang,
1979, 1994), the fear report was used to construct sentences that
specifically included stimulus events (who, what, where), meaning (reported feelings and interpretations), and response
information (expressive physiology and actions) coded in fear
B.N. Cuthbert et al.
memory. The second personalized script comprised another
scene related to the central clinical fear for patients, and another
severe fear experience for controls. Examples are provided in
Table 1.
In addition to these personal fear sentences, four standard fear
imagery sentences and six standard neutral sentences were identical
for all participants (Table 1). Standard fear scenes included two
common social fear situations, that is, giving a speech and being
humiliated in front of others, and two danger-oriented situations,
that is, hearing an intruder while home alone and seeing a friend
struck by a moving car. As for personal fear scripts, standard
scenes included details of stimulus events, meaning, and response
information. The six low-arousal neutral sentences described
clearly nonfearful, normal, mildly pleasant situations, for example,
relaxing in a chair at home or waking up on a weekend morning.
Each of the 12 sentences was typed on an index card.
Table 1. Standard Fear and Neutral Scenes and Sample Personal Fear Scenes
Standard fear scenes
1. My heart pounds in the suddenly silent room; everyone is watching me, waiting impatiently to hear what I will say. (social)
2. I’m wrong. They say, ‘‘Stupid! You never get anything right!’’; my face is hot, and I have to stand there and take it. (social)
3. I flinch at the screech of brakes; my companion is struck by a speeding car: Her leg is crushed, bone protruding, and blood pumps onto the road.
(danger)
4. Taking a shower, alone in the house, I hear the sound of someone forcing the door, and I panic. (danger)
Standard neutral/low arousal pleasant scenes
1. I am relaxing on my living room couch looking out the window on a sunny autumn day.
2. I am sitting in a lawn chair on the front porch watching the soft summer breeze sway the leaves on the trees.
3. Soft music is playing on the stereo as I snooze lazily on my favorite chair.
4. I am lying on the sand on a warm day, listening to children playing down the beach, their soft voices mingling with the sound of the waves.
5. I am lying in bed on a Sunday morning, half asleep and listening to the distant sound of bells, relaxing on my day off.
6. A wood fire dances in the hearth, I feel snug and warm in the cabin, reading the book on my lap, enjoying a well-deserved rest.
Examples of personal fear scenes (clinically relevant for patients)
Specific phobia
1. I feel tense all over and I fight back the tears as I walk past all the birds in the park; my eyes are closed and I feel so frightened I want to scream.
2. I tense my arms when I wait to receive the shot from the nurse to treat the spider bite; my heart races and my palms become sweaty.
3. I feel closed in and like I am losing control as I sit in my car at the traffic light with cars all around me.
4. My heart quickens and my veins constrict as the lab tech wraps the rubber band around my arm; my face is flushed and when I see the needle I begin
to feel sick.
Social anxiety
1. I’m jittery, with heart pounding and stomach knotted, as I scan the room full of people for the disapproving looks that I know will come when I do
something wrong.
2. As I wait to give my report on the conference call, I progressively feel nervous and unable to breathe; I put them on hold twice but still am unable to
catch my breath.
3. My voice quivers and I begin to hyperventilate as I give a speech in front of a large group of people who are watching me uneasily.
4. After rehearsal, I gather together with the other members of our church choir to talk; my face feels as if it is swelling, my heart races and I am unable to
articulate ideas properly.
Post-traumatic stress disorder
1. My heart beats faster as I hear the robbers in the front room; one of them shoots me and I want to scream.
2. I panic, as the man starts toward me; my hands tremble and I feel dizzy; I want to get away.
3. My eyes water and my stomach is in a knot as I share a last cigarette with my best friend; I know he won’t survive his stomach wound, but I can’t leave
him. My heart pounds as I lift the gun to shoot him in the head.
4. While reading a book, I freeze as I hear someone forcing the door, my heart pounds, my body shakes and I feel nauseous.
Panic disorder with agoraphobia
1. After jumping out of the car, I start to have a severe panic attack, I become clammy, I am in a knot, and I feel tense all over.
2. My heart races and blood rushes to my head as I pull into the parking space; I approach the store with cautious steps, legs trembling, and I feel I must
escape.
3. My heart pounds, I feel nauseous, and I am shaking as I drive myself to the doctor; I am worried that I am going to die as I am unsure if I am sick or
experiencing a panic attack.
4. At the baseball park, I am walking and suddenly I feel an intense rush of fear; my heart is pounding, my breath is labored, and my stomach is in a
knot.
Control participants
1. I feel jittery when my brother tells me a tornado is coming. My heart races as the tornado passes over my house.
2. My heart races as my boyfriend punches my best friend in the nose. He hits him again and again. I want to scream.
3. My stomach is in a knot as my new car begins to hydroplane. My palms are clammy and my jaw is clenched as I lose control of the car.
4. My heart races as I awake. A man is standing over my bed. I am screaming; I am afraid of dying.
Fear imagery and anxiety
Imagery assessment began 1–2 hr after the diagnostic session
and lasted approximately 2 hr (several patients, due to scheduling
conflicts, were seen at a later time). Participants were seated in a
reclining chair in a dimly lit room and given a brief introduction
to the procedure, followed by placement of the recording
electrodes. Overall, the session consisted of six trial blocks. For
each trial block, the participant’s task was to memorize two
sentences (one fearful and one neutral in content), and when
subsequently cued, separately recall each of the sentences and
imagine its content ‘‘vividly, as a personal experience.’’ The
selection of fear and neutral sentences for the six trial blocks was
determined randomly for each subject, as was the order of trials
within a block.
The tone-cued recall task. Before each trial block, two
sentences were memorized to a criterion of one perfect repetition.
Participants were then instructed to close their eyes and listen to a
series of brief, soft nonsignal tones presented at regular intervals,
one every 6 s (0.5 s at 1000 Hz, 70 dB, 50 ms rise time, using
Coulbourn Instruments S24-05 Tone Generator, S84-04 Rise
Time Gate, and S82-24 Gated Amplifier). Participants were told
to relax during these tones, breathe out slowly, and say the word
‘‘one’’ to themselves as in a secular meditation exercise (Benson,
1975). This had the general effect of reducing and stabilizing
background physiological activity.
From time to time in the series of nonsignal stimuli, tones
occurred that were discriminably higher or lower in pitch (700 or
1500 Hz, respectively). Participants were instructed that these
special cue tones signaled that they were to recall and image the
event described by one of the memorized sentences. Assignment of
high or low tones to fear or neutral sentences was balanced across
participants. Signal tones were always presented in a sequence of
two 6-s intervals: Participants were instructed to silently articulate
the sentence in the 6-s processing period following the first cue tone
and to actively imagine the scene described at the second tone. A
series of nonsignal tones then ensued.
Recall of each sentence was cued four times across a trial
block, with a perceptually random fear–neutral order of presentation. A rapid double-tone signaled the end of a trial block.
Participants were instructed to then open their eyes and to
provide self-assessments of their emotional experience during
imagery. Participants judged their feelings of pleasure and
arousal, separately for fear and neutral sentences. They also
rated imagery vividness, ‘‘interest’’ in the sentence, and chose one
of seven specific emotions best representing their affective state.
All six fear–neutral sentence pairs were presented in this manner,
each with its own trial block. After the final block of trials,
electrodes were removed and participants were debriefed.
The startle probe. Acoustic startle probes were 50-ms, 95-dB
white noise bursts with instantaneous rise time, presented over
Telephonics TDH-49 earphones using a Coulbourn Instruments
S81-02 White Noise Generator and S82-24 Gated Amplifier.
Over the course of the imagery assessment session, 48 probes
were presented: Across the four trials for each sentence, probes
were presented once during the silent articulation period, once
during the imagery period, once during both periods, and once
for neither period. Twelve probes were presented during the
intertrial interval between sentence processing periods, two in
each block of trials. Participants were told that the extra noises
would sometimes occur, but that they were irrelevant to their
experimental tasks.
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Experimental Control and Data Collection
A PC-compatible computer and VPM software (Cook, Atkinson, & Lang, 1987) were used for timing, stimulus presentation,
and physiological and rating data acquisition. Analog physiological measures were digitized at 20 Hz throughout each trial.
Coulbourn Instruments S75-01 bioamplifiers and S76-01 contour-following integrators were used to record electromyographic (EMG) potentials from over the left orbicularis oculi
and the left corrugator regions (bandpass of 90–1000 Hz, time
constants of 125 and 500 ms, respectively). For more accurate
recording of the blink response, the orbicularis channel was
digitized at 1000 Hz from 50 ms before until 250-ms after-startle
probe; eyeblinks were scored with an interactive computer
program that scored each blink for latency and peak. Skin
conductance was recorded from electrodes placed adjacently on
the hypothenar eminence of the nondominant hand, using
Sensormedics standard electrodes filled with K-Y Jelly; the signal
was transduced by a Coulbourn S71-22 skin conductance
amplifier calibrated for a range of 0–40 mS. The ECG was
recorded using electrodes placed on each forearm, amplified
through a Coulbourn S75-01 bioamplifier; heart rate was
recorded with a Schmitt trigger that interrupted the computer
to record R-R intervals to the nearest 1 ms. The data were edited
with an off-line program, and then transformed to beats/minute
averages for each half-second. Ratings were acquired using the
Self-Assessment Manikin (Bradley & Lang, 1994; Hodes, Cook,
& Lang, 1985; Lang, 1980), an interactive computer graphics
display that records judgments along the affective dimensions of
valence and arousal on 21-point scales. In addition, participants
used a computerized line rating display to report their judgments
of ‘‘imagery vividness.’’
Data Reduction and Analysis
Statistical analyses for all measures were accomplished with the
SYSTAT package; all repeated measures with more than two
levels employed the Wilks’ Lambda multivariate calculation. For
demographic data and questionnaires, diagnostic group differences (specific, social, PTSD, panic, and control) were assessed
with univariate analyses of variance (ANOVA) and follow-up
Tukey Honestly Significant Difference (HSD) tests. The VPM
software was used for reduction and initial processing of all
physiological data.
Direct measures: Physiology and ratings. Physiological responses evoked directly by sentence imageryFi.e., heart rate,
skin conductance, and corrugator EMGFwere scored for each
trial as the average activity during the combined silent
articulation and imagery periods, deviated from the 6-s period
immediately preceding silent articulation. For all three measures,
a single value was derived for each category (personal, danger,
social, and neutral) by averaging scores for the two sentences
within each fear category, and for all six neutral trials. Skin
conductance and corrugator data were lost for 3 and 4
participants, respectively, due to equipment failures.
Given the specific hypotheses, separate analyses of the three
fear categories comprised the primary analytic focus. However,
initial omnibus tests were conducted to verify the expectation
that across all contents, fear categories would prompt palpably
larger physiological effects, as well as higher arousal and lower
pleasantness/dominance ratings. Accordingly, physiological responses directly evoked by sentence imagery were all analyzed
initially with mixed-model ANOVA, followed by planned com-
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B.N. Cuthbert et al.
parisons and Tukey HSD tests where appropriate; diagnostic
group was the between-subjects factor and sentence content
(personal, social, danger, neutral) the within-subjects factor.
These were followed by the separate tests of diagnostic
differences for the specific fear contents (danger, social, and
personal), assessing prior hypotheses.
Similarly, participants’ imagery ratings were analyzed in overall Diagnosis Image Type ANOVAs (separately for valence,
arousal, and vividness). These were followed by individual
ANOVAs of each fear image category, again followed up by
Tukey tests.
sentence from the same trial. As for the other measures, analyses
began with omnibus ANOVAs including diagnosis and content.
Then, based on the a priori hypotheses, fear/neutral differences
were separately tested for social, danger, and personal fear
contents. Initial analyses were conducted to examine differences
in response between the silent articulation and imagery periods.
No systematic pattern of effects could be found (perhaps due to a
relatively limited number of startle probes in each period), and so
these two periods were combined in estimating participants’
reactions to the different contents.
The startle probe. Eyeblink magnitude was measured as the
maximum excursion in microvolts of the orbicularis oculi signal
from the level immediately prior to the response. Trials with clear
artifacts were rejected, and trials with no response were scored as
zero-magnitude blinks; 14 subjects were excluded from startle
analyses for failing to meet the criterion of measurable blinks on
at least 40% of all trials. Differences in base reflex reactivity
between groups were examined using the absolute startle
response magnitudes obtained during the intertrial intervals.
For the analyses of startle potentiation during imagery trials,
standardized scores were computed (i.e., T scores with a mean of
50 and standard deviation of 10) using the mean and standard
deviation of each subject’s ITI startle responses as the reference
distribution. This normalization procedure (Bonnet, Bradley,
Lang, & Requin, 1995; Requin & Bonnet, 1993) is designed to
reduce the influence of arbitrary, between-subjects variance in
reflex size while preserving probe response differences that
occurred in the context of sentence imagery.
As was found here, the basic startle circuit is characterized by
marked habituation (Davis & File, 1984); however, despite the
overall reduction in reflex amplitude, emotional startle modulation (presumably due to amygdala projections) appears to be
preserved over trials (see Bradley, Lang, & Cuthbert, 1993).
These findings were considered in analyzing imagery content
effects, so fear sentences were always compared with the neutral
Questionnaire Measures
As expected, the intercorrelations among questionnaires used to
measure various aspects of anxiety and depressive pathologies
were all positive and uniformly high (ranging from .79 to .46).
Mean questionnaire scores for each scale, by diagnosis, are
presented in Table 2. The overall difference among groups was
significant, F(4,124) 5 18.0, po.0001, based on analysis of Z
scores for the four measures for which there are complete data
(FSS, BDI, FEQ, Marks–Mathews scale). Overall, specific
phobics were not different from controls and both these groups
were significantly lower in Tukey pairwise comparisons than the
social anxiety, PTSD, and panic groups; panic patients had the
most elevated scores, differing from all other groups except PTSD.
This pattern was remarkably consistent when questionnaires
were considered individually. Control and specific phobics had
the lowest scores on each measure and were not themselves
significantly different. In contrast, the PTSD and panic patient
groups had the highest mean scores on all questionnaires, and
also did not differ from each other. Furthermore, both these high
scoring diagnoses differed significantly from both specific
phobics and controls on manifest anxiety and the Beck
Depression Inventory. In addition, the panic group differed
from the low scorers on both phobia measures, whereas the
PTSD group differed significantly in negative emotionality.
Social phobics were intermediate, and not discriminable from
Results
Table 2. Means and Standard Deviations of Questionnaire Measures, by Diagnostic Group
Diagnosis
Age
F-E Manifest
Anxiety Scale
Marks–Mathews
Phobia Quest.
Fear Survey
Schedule
Negative Emotionality
(Scale from the EASI)
Beck Depression
Inventory
% comorbidity
(additional anxiety
and/or mood disorder)
% comorbidity (additional
mood disorder)
Control (n 5 24)
Specific (n 5 28)
Social (n 5 30)
PTSD (n 5 22)
Panic-A (n 5 26)
Overall F, p
34.2 (9.7)
94.7 a (21.9)
33.2 (13.2)
109.4 a (22.3)
32.0 (11.1)
131.5 b (32.4)
36.5 (15.2)
135.0 b (27.9)
34.2 (11.2)
142.0 b (38.7)
n.s.
11.0,o.0001
15.5 a (12.3)
23.9 ab (13.3)
35.4 bc (14.7)
38.4 cd (23.0)
40.2 d (26.5)
12.9,o.0001
167.7 a (39.3)
202.8 ab (44.1)
225.8 bc (57.7)
229.9 bc (57.7)
262.9 c (75.5)
9.6,o.0001
22.2 a (5.5)
26.6 ab (7.2)
28.6 bc (5.7)
33.8 c (7.0)
30.9 bc (6.3)
9.3,o.0001
3.9 a (3.5)
9.2 ab (7.7)
15.2 bc (9.7)
19.5 c (7.5)
21.0 c (12.0)
16.5,o.0001
39.3
60.0
81.8
84.6
15.62,o.002
10.7
26.7
54.5
42.3
12.61,o.006
Notes. Values sharing a common letter do not differ at po.05, Tukey HSD post hoc test. SD in parentheses. A Chi-square tests were used to assess
differences in the percent of patients with an additional anxiety disorder or comorbid mood disorder (either current major depressive episode or
dysthymia, including patients with partial remission). The EASI (Buss & Plomin, 1975) consists of four Scales, Emotionality, Activity, Sociability, and
Impulsivity. The Emotionality Scale is an estimate of negative affect, and includes both fear and anger related items.
413
Fear imagery and anxiety
either the high or low groups on almost all the assessment
instruments. Only on the Manifest Anxiety Scale was the social
phobic group’s mean score significantly higher than the mean of
the specific phobics.
The co-occurrence of additional diagnoses of anxiety or
depression was similar to what has been observed in other clinical
samples of the anxiety disorders. That is, the specific phobia and
social anxiety groups showed a comorbidity incidence (at least
one additional diagnosis) of approximately 40 and 60%,
respectively, whereas the incidences for PTSD and panic were
82 and 85%. Similarly, the specific incidence of current major
depression was only 11% for specific phobics. In contrast, panic
and PTSD patients both showed an incidence of major
depression that was over 40%. Social phobics were again
intermediate, at 27%.
Physiological Activity Levels
Base startle magnitude. ITI responses provided an estimate of
participants’ base reflex reactivity (Table 3, ITI probes). The F
test of differences between diagnoses was not quite statistically
reliable, F(4,116) 5 2.31, po.07. Interestingly, however, the
pattern of mean values was similar to that seen for the anxiety
and depression questionnaires: Control subjects and simple
phobic patients had the smallest probe responses, panic and
PTSD patients the largest, and social phobics were intermediate.
Prestimulus activity in autonomic and facial EMG measures.
Heart rate base levels were recorded during the interval that
immediately preceded the tones that cued sentence recall. As
shown in Table 3, these initial levels differed significantly over the
experimental groups, F(4,125) 5 7.7, po.0001. Panic patients had
the highest base values, significantly higher than both social
phobics and controls; control subjects showed the slowest heart
rates, significantly slower than both specific phobics and panic
patients. The PTSD patients were not statistically different from
the other groups. Base skin conductance levels were also
statistically significant across groups, F(4,122) 5 2.75, po.04
(see Table 3). However, only the extreme groups, controls and
panic patients, differed significantly in the Tukey pairwise analyses.
Pre-onset levels of corrugator activity did not vary greatly
across groups, and no test of diagnostic group difference approached significance.
Sentence Imagery: Evaluative Judgments
Affective reports. Sentence image ratings are presented in
Table 4. For most patient groups, the personally relevant fear
images were rated maximally unpleasant, with danger images
next in aversiveness, followed by social fear imagery, fear
sentence type F(2,124) 5 38.97, po.0001. Social phobics were an
exception, Fear Sentence Type Diagnosis F(8,248) 5 5.58,
po.0001: Not unexpectedly, they rated social fear images more
unpleasant than did the other groups, F(4,125) 5 5.98, po.0005,
and equivalent in aversiveness to the other fear images. Groups
did not differ significantly in valence ratings of clinical or danger
imagery.
Arousal ratings were distributed in a similar pattern by
diagnosis and fear imagery content, fear sentence type
F(2,124) 5 24.68, po.0001; Fear Sentence Type Diagnosis
F(8,248) 5 3.96, po.0005. All patients rated the personal fear
images most arousing, and there was no significant difference
among groups. Danger images generally received high ratings,
though less for panic disorders, diagnosis, F(4,125) 5 3.29,
po.02. Paralleling their strong judgments of unpleasantness,
social phobics rated social fear images more arousing than did
the other groups, F(4,125) 5 4.52, po.002.
Vividness reports. Groups did not show a significant overall
difference in reports of imagery vividness, whereas clinical fear
imagery was rated as more vivid than the other two fear contents,
F(1,124) 5 16.93, po.0001. As can be seen in Table 3, all groups
gave nearly equivalent ratings to social and danger images. For
clinical fear imagery, however, social phobics failed to show the
greater image vividness reported by the other diagnostic groups,
DiagnosisFear Sentence Type F(8,248)52.31, po.03. Uniquely
for this groupFperhaps because of redundancy with the
standard social fear cuesFthere was no significant difference
among their ratings of the three fear contents. Overall, fear
images were rated as less vivid than neutral images, F(1,125) 5
7.02, po.01.
Sentence Imagery: Potentiation of the Startle Reflex
As anticipated, the omnibus analysis of the startle probe reflex
indicated larger blinks overall for fear sentences than for neutral
sentences, F(1,112) 5 42.30, po.0001 (see Table 5). Furthermore, reflex potentiation during fear imagery (all contents
together) varied with diagnosis, Fear versus Neutral Diagnosis
F(4,112) 5 3.44, po.02: The finding of greater startle magnitude
during fear contents (relative to neutral) was highly reliable for
control subjects and for specific and social phobics, all pso.002.
The same test for PTSD patients also indicated reliable fear
potentiation, po.03; however, the overall difference in probe
response between fear and neutral sentence contents was
borderline for panic patients, po.06.
Table 3. Startle Magnitude during Intertrial Intervals and Preimagery Base Values for Physiological Measures by
Diagnostic Group
Diagnosis
Control
ITI startle
magnitude (mV)
Heart rate (B/M)
Skin conductance
(micromhos)
Corrugator
muscle (mV)
2.9 (4.1)
63.8 a (8.9)
2.4 a (2.1)
6.2 (1.0)
Specific
2.6 (2.8)
76.4 bc (11.8)
2.9 ab (2.6)
7.0 (4.1)
Social
3.1 (3.1)
69.7 ab (11.4)
4.0 ab (3.9)
7.1 (3.7)
PTSD
4.1 (3.8)
71.4 abc (10.6)
2.9 ab (2.6)
7.3 (3.3)
Panic-A
5.9 (6.6)
79.5 c (12.2)
4.9 b (3.5)
7.2 (3.3)
Notes. Values sharing a common letter do not differ at po.05, Tukey HSD post hoc test. SD in parentheses.
F, p
2.3, n.s.
7.7,o.0001
2.8,o.04
o1, n.s.
414
B.N. Cuthbert et al.
Table 4. Evaluative Judgments of Memory Imagery by Content and Diagnosis: Mean and Standard Deviations
Diagnosis
Control (n 5 24) Specific (n 5 28)
Social (n 5 30)
PTSD (n 5 22)
Panic-A (n 5 26)
F, p
5.13 (2.51)
3.43 ab (3.08)
3.98 (3.57)
7.96 a (3.08)
16.93 ab (2.16)
4.38 (2.09)
5.12 a (3.33)
3.95 (3.03)
4.15 b (2.95)
15.26 b (2.18)
5.26 (2.95)
3.59 ab (3.83)
4.68 (3.18)
7.50 a (3.93)
16.05 ab (2.56)
4.34 (2.82)
2.60 b (2.99)
4.42 (3.78)
5.87 ab (3.34)
15.28 b (4.12)
n.s.
2.19o.08
n.s.
5.98o.0002
3.94o.005
15.92 ab (2.98)
15.96 (4.56)
16.75 b (4.03)
14.94 ab (3.65)
2.56 (2.11)
15.59 ab (3.76)
17.95 (3.66)
16.04 ab (4.20)
12.80 a (5.40)
2.88 (2.66)
16.57 a (3.03)
17.45 (3.20)
15.75 ab (4.27)
16.67 b (3.89)
4.01 (2.76)
14.02 ab (3.99)
16.18 (4.77)
13.77 ab (4.99)
12.11 a (4.59)
4.09 (3.19)
13.99 b (3.80)
17.00 (2.81)
12.62 a (5.93)
12.62 a (5.67)
3.34 (3.28)
2.84o.03
n.s.
3.39o.02
4.52o.002
n.s.
14.27 (2.66)
15.98 b (3.29)
13.73 (3.46)
13.06 (3.08)
15.22 b (2.78)
13.32 (2.59)
14.64 ab (3.74)
13.70 (3.22)
11.63 (3.65)
14.37 ab (2.56)
12.28 (3.64)
12.18 a (4.31)
12.02 (3.97)
12.47 (4.82)
12.62 a (3.32)
12.48 (3.63)
13.98 ab (5.39)
12.25 (3.09)
11.20 (3.96)
12.75 ab (3.95)
12.86 (3.56)
14.23 ab (4.12)
11.92 (4.12)
12.54 (4.11)
13.41 ab (3.44)
n.s.
2.90o.03
n.s.
n.s.
2.99o.03
Affective valence ratings
All fear
4.46 (2.29)
Personal
3.90 ab (3.24)
Danger
3.44 (2.61)
Social
5.98 ab (3.08)
Neutral
17.72 a (2.30)
Arousal ratings
All fear
Personal
Danger
Social
Neutral
Vividness ratings
All fear
Personal
Danger
Social
Neutral
Notes. All ratings were administered by computer and are based on a 21-point scale. Valence and arousal ratings are from the SelfAssessment Manikin (SAM; Lang, 1980). Values sharing a common letter do not differ at po.05, Tukey HSD post hoc test. SD in
parentheses. Lower scores on valence ratings indicate greater unpleasantness.
among fear scenes was found for the danger content: Reliable
potentiation was seen for control participants, specific phobics,
social anxiety disorder, and panic patients, although it was less
strong for PTSD, po.09.
As previously noted, the groups did not differ significantly in
baseline reflex magnitude. However, the pattern of means
(largest for PTSD and panic patients) suggested that baseline
magnitude might contribute to the overall pattern (base/change
score r 5 .19). However, this hypothesis was not supported
by a subsequent covariance analysis of these same data,
which produced the same results reported above. We also
speculated that finding no potentiation during personal fear
imagery for some of the patients might be attributed to the
averaging of probe responses to the two personal scenes (on the
assumption that one of the scenes was, by chance, less pertinent
or less engaging). Thus, a post hoc analysis was conducted
using only each participant’s largest personal fear startle
reflex (which could have occurred during either of the two
personal fear sentences). Startle potentiation was again not
significant for panic patients, Fo1, and borderline for PTSD
patients, po.09.
Fear imagery potentiation varied significantly with the
specific fear content [Fear vs. Neutral Fear Sentence Type
F(2,111) 5 3.75, po.03], and was largest overall for danger
scenes and smallest for social fear scenes. The three-way
interaction was not significant. Based on a priori hypotheses,
however, separate analyses of diagnostic differences were
conducted for each fear content. To illustrate these effects, fear/
neutral difference scores are presented in Table 5 along with
statistical results.
For personal fear imagery, a significant difference in
potentiation was confirmed among diagnostic groups [Fear vs.
Neutral Diagnosis F(4,112) 5 2.28, po.006; see Figure 1].
When tested separately, control and specific and social phobics
all showed significant fear potentiation, but this was not observed
for panic or for PTSD patients. For social fear scenes, the
interaction with group did not reach significance, po.13.
Nevertheless, the potentiation differences across diagnoses were
similar to the findings for personal scene content, that is, social
fear scene potentiation was significant for control participants
and specific and social phobics, but did not approach significance
for panic and PTSD patients. The most consistent potentiation
Table 5. Startle Reflex Potentiation during Fear Memory Imagery: Means, Standard Deviations, and Significance Tests
Diagnosis
Control (n 5 22)
Specific (n 5 27)
Social (n 5 28)
PTSD (n 5 19)
Panic-A (n 5 21)
Personal
5.82 (7.68)
11.72 (17.00)
3.57 (8.07)
2.03 (9.27)
0.81 (8.57)
5.13 ab (11.51)
po.002
po.002
po.03
n.s.
n.s.
Danger
6.10 (9.15)
9.78 (15.72)
7.88 (10.67)
3.26 (7.68)
4.94 (7.44)
6.71 b (11.0)
Social
po.01
po.005
po.001
n.s.
po.01
5.22 (6.31)
7.33 (18.37)
3.83 (5.12)
0.63 (5.93)
1.12 (3.99)
3.89 a (10.17)
po.001
po.05
po.001
n.s.
n.s.
5.71 ab (5.86)
9.61 a (13.95)
5.09 ab (5.65)
1.97 b (3.58)
2.29 b (5.05)
Notes. Reflex potentiation is defined as the T value difference (fear minus neutral imagery). The significance of these differences is
given for each diagnostic group for each image content. Tukey tests of the pairwise differences between groups in potentiation
magnitude over all contents are given with the marginal values in the right column. Potentiation differences between contents over all
participants are based on pairwise within-subjects tests (bottom row). For all these marginal values, a common lowercase letter
indicates the absence of a significant difference.
415
Fear imagery and anxiety
Fear minus Neutral (T-Score difference)
Startle Potentiation during Fear Memory Imagery
12
Personal Fear
All Fear
8
4
0
Control
Specific
Social
PTSD
Diagnostic Group
Panic-A
Figure 1. Startle potentiation during fear imagery by diagnostic group.
The data presented include the magnitude of startle during personal
imagery, and the average magnitude of all fear imagery contents (T score
differences from neutral imagery). The between-group ANOVA for
personal fear was F(4,112) 5 3.44, po.007; and for all fear contents,
F(4,112) 5 3.44, po.02.
An analysis was conducted for the Social Anxiety Disorder
group to determine if there might be subtype differences within
this diagnosis (N 5 30). Unfortunately, only 4 members of the
group could be classified as of the Specific Social Phobic type,
precluding a meaningful statistical analysis of potentiation; the
remainder were Generalized. Nonetheless, reflex potentiation
during imagery of personal scenes for these 4 patients was indeed
high, T score 5 12.61, and similar to the Specific Phobia group
(see Table 5). Furthermore, when these 4 subjects were removed
from the sample and the Social Anxiety Disorder group was
reanalyzed (N 5 26), personal scene potentiation was no longer
significant, po.16. Finally, startle potentiation to personal fear
scenes was significant for the Social Anxiety group participants
with only a single Social Anxiety Disorder diagnosis (N 5 12;
po.01), but not significant for patients with additional diagnoses
(N 5 18; Fo1).
Sentence Imagery: Physiological Responses to Image Processing
Heart rate. The amount of heart rate change prompted by
the sentence imagery task differed significantly over diagnoses,
F(4,125) 5 3.43, po.02, and the four different image contents,
F(3,123) 5 33.43, po.0001 (see Table 6). As expected, there was
a general increase in heart rate during fear imagery, contrasted,
for most participants, with a slight heart rate decrease for neutral
imagery, which was confirmed by the planned contrast, fear
versus neutral, F(1,125) 5 92.62, po.0001. When neutral image
processing was analyzed alone, heart rate change did not vary
significantly over diagnostic groups. However, heart rate
increase during fear imagery differed significantly over diagnoses, F(4,125) 5 3.25, po.02, and also differed among the three
fear categories, fear sentence type F(2,124) 5 14.18, po.0001.
Specific and social phobics responded consistently with the
greatest increases to all fear images, controls were intermediate,
and PTSD and panic patients were the least responsive during
fear imagery (see Figure 2). A retest of this analysis, covarying
for base heart rate, produced the same result.3
The planned contrasts of panic versus specific and social
phobic patients were significant for both personal fear and
danger imagery. Consistent with the startle data, the heart rate
imagery response of panic patients to both these contents was
markedly less acceleratory than for the two phobic groups,
pso.02. The social fear content test (social anxiety disorder vs.
all groups) only approached significance, F(1,125) 5 3.89,
po.06.
Corrugator. The initial overall analysis again showed a
strong difference among imagery contents, F(3,119) 5 10.5,
po.0001, with corrugator muscle activity significantly greater
for fear than neutral content, F(1,121) 5 31.14, po.0001.
Furthermore, this effect interacted with diagnosis,
F(4,121) 5 3.14, po.02. In follow-up tests, the effects of
diagnosis were only marginal for neutral and for fear contents,
both pso.11. Following this effect further with separate analyses
of each fear type, only the diagnostic group test for personal fear
scenes approached significance, F(4,121) 5 2.25, po.07. Specific
phobia and PTSD patients showed a markedly greater mean
corrugator response when processing clinically relevant fear
imagery than did the other groups, contrast F(1,121) 5 8.46,
po.005.
Skin conductance. This measure was consistent with heart
rate and corrugator EMG activity in revealing palpable
differences among contents, F(3,120) 5 8.49, po.0001, with fear
imagery prompting significantly larger responses than neutral
imagery, F(1,122) 5 23.32, po.0001. However, the overall
analysis and the separate analyses for fear and neutral content
were not significant for diagnosis, nor were the analyses of
individual fear contents. The only significant planned contrast
was for social content: Social phobics responded with greater
skin conductance increase to social fear imagery than did the
other groups, F(1,122) 5 4.7, po.04.
Depression Comorbidity and Physiological Response
Participants were divided into two groups, those having a current
mood disorder diagnosis and those without (see Table 2 for
percentage by diagnosis). For heart rate change during imagery,
depressed and noncomorbid participants did not differ significantly for heart rate, skin conductance, or corrugator muscle.
Similarly, these groups did not differ in startle potentiation
during fear imagery, relative to neutral imagery. However, the
magnitude of base startle reflexes (ITI) was significantly larger
for anxiety patients with mood disorder (5.3 mV) than for
patients without depression (3.1 mV), F (1, 93) 5 5.11, po.03.
Furthermore, prestimulus corrugator muscle activity was greater
3
The overall correlation between base heart rate and imagery response
was .13. A covariance analysis (using base heart rate as the covariate)
did not change the significance of the results reported here for ANOVA.
This is consistent with an inspection of the means, in that higher base level
differences among groups did not prompt reduced reactivity: Specific
phobics recorded the second-highest base levels and the largest fearrelated increases, whereas panic patients were average among the groups
in baseline and the lowest reactivity. For skin conductance also, baseline
levels failed to show a significant relationship to reactivity for any of the
fear contents, and again covariance did not change the results of any
analyses.
416
B.N. Cuthbert et al.
Table 6. Means and Standard Deviations of Autonomic and Somatic Reactions in Imagery, by Diagnosis
Diagnosis
Personal
Danger
1.10 (1.74)
1.79 (2.20)
2.18 (1.82)
0.66 (1.80)
0.90 (1.44)
0.88 (1.60)
1.31 (1.85)
1.58 (1.78)
0.10 (1.74)
0.36 (1.68)
0.67 (1.51)
0.80 (1.68)
1.17 (1.82)
0.42 (1.70)
0.25 (1.15)
0.17 (1.02)
0.40 (0.61)
0.09 (1.27)
0.47 (0.95)
0.53 (1.05)
Corrugator muscle (microvolts change)
Control (n 5 24)
0.09 (0.24)
Specific (n 5 27)
0.38 (0.84)
Social (n 5 29)
0.17 (0.43)
PTSD (n 5 22)
0.50 (1.05)
Panic-A (n 5 24)
0.04 (0.23)
0.13 (0.28)
0.25 (0.46)
0.21 (0.42)
0.36 (0.66)
0.13 (0.52)
0.16 (0.29)
0.21 (0.34)
0.09 (0.27)
0.22 (0.38)
0.07 (0.30)
0.01 (0.18)
0.11 (0.24)
0.04 (0.21)
0.07 (0.17)
0.01 (0.21)
Skin conductance (micromhos)
Control (n 5 24)
Specific (n 5 28)
Social (n 5 28)
PTSD (n 5 22)
Panic-A (n 5 25)
0.05 (0.17)
0.01 (0.08)
0.06 (0.14)
0.01 (0.06)
0.05 (0.16)
0.05 (0.17)
0.00 (0.07)
0.07 (0.16)
0.002 (0.06)
0.01 (0.09)
0.01 (0.06)
0.02 (0.05)
0.01 (0.09)
0.01 (0.04)
0.04 (0.08)
Heart rate (bpm change)
Control (n 5 24)
Specific (n 5 28)
Social (n 5 30)
PTSD (n 5 22)
Panic-A (n 5 26)
0.01 (0.09)
0.04 (0.11)
0.11 (0.27)
0.03 (0.09)
0.10 (0.33)
in amplitude for patients with comorbid depression than for
nondepressed participants, F(1,100) 5 4.5, po.04.
Moderator Variables
There were no interactions between diagnostic differences and sex
of the participant in analyses of either physiological change or base
scores. The only significant gender effect found was that men had
higher base skin conductance levels than women, po.03.
All subjects were instructed to avoid prescription medications
taken on an as-needed basis and recreational drug use 24 hr prior
to psychophysiological evaluation. (Patients were not instructed
to discontinue antidepressant medications.) Current use of
medication was recorded at interview. Fifteen patients reported
use of antidepressant medications (tricyclics or SSRIs; 3 each in
Heart Rate Increase during Fear Memory Imagery
Personal Fear
All Fear
∆ Heart Rate (bpm)
2.0
Social
Neutral
the specific phobia and social anxiety groups, 8 panic patients,
and 1 PTSD). Although these numbers were too small to permit
reliable comparisons between subgroups (drug/no-drug), reanalyses of startle potentiation by diagnostic groupFincluding only
patients not on medicationsFshowed no change in the results.
Specific phobic, social phobic, and PTSD patients showed
significant potentiation for all fear versus neutral content,
pso.03, whereas the result for panic patients no longer
even approached significance, po.19. For personal fear scenes,
startle was again strongly potentiated for the two phobic
groups, but not at all for PTSD and panic patients, Fso1.
Similarly, the pattern of results for heart rate was unchanged in
the reanalysis of diagnostic groups, with patients on antidepressants excluded.
Eleven patients reported use of antianxiety medications
(primarily benzodiazepines) in the 24 hr preceding the session
(2, 1, 7, and 1 for specific phobia, social anxiety, panic, and
PTSD, respectively). With these patients excluded, the overall
pattern of results was again highly similar to the results obtained
with the full sample. The same general startle potentiation effects
were apparent, although the response of social phobics to
personal fear scenes was now just below the significance level,
po.07. Heart rate outcomes were unchanged. In summary, the
psychophysiological results of the study were not affected to any
appreciable extent by medication use.
Discussion
1.0
0.0
Control
Specific
Social
PTSD
Panic-A
Diagnostic Group
Figure 2. Heart rate change during fear imagery by diagnostic group.
Change scores from base are shown for personal imagery and for the
average of all fear contents. The between-group ANOVA for personal
fear was F(4,125) 5 3.23, po.02; and for all fear contents,
F(4,125) 5 3.25, po.02.
The overall results are consistent with the view that reactions to
fear memory cues differ significantly among the anxiety
disorders. As hypothesized by the network coherence model,
phobic participants were overall the most physiologically
responsive at memory retrieval and panic patients tended to be
the least reactive across all measures. However, the data are open
to a variety of interpretations, as to the specific factors that may
determine diagnostic differences in emotional expression.
The present findings replicate and extend the Cook et al.
(1988) results: Panic patients consistently scored higher than
phobics or the socially anxious on depression and anxiety
questionnaires (see also Turner, McCann, Beidel, & Mezzich,
Fear imagery and anxiety
1986), consistent with high trait negative affect (Zinbarg &
Barlow, 1996). In the present research, furthermore, patients
diagnosed with panic had a higher incidence of comorbid
depression (42%) and additional anxiety disorder (77%). PTSD
patients also differed from phobia and socially anxious patients,
reporting more anxiety symptoms on questionnaires and at
interview, and they also showed a high incidence of mood
disorder (55%). Finally, these groups with higher questionnaire
scores and greater comorbidity, panic and PTSD patients, also
differed from the other groups in showing smaller heart rate
changes and no startle potentiation to personal fear memories.
Base Levels
Panic patients tended to have somewhat higher base physiological levels than the other diagnoses. Their mean values were the
highest of all groups for heart rate and skin conductance (only
base heart rate differed significantly over diagnosis, with values
for panic patients significantly greater than normal controls and
the social anxiety group). Panic patients were also highest in base
startle response (with PTSD second), although again the overall
analysis of the group means fell short of significance.
Startle Potentiation
In numerous studies with animals and humans (Davis, 1992;
Davis & Lang, 2003), probes presented during exposure to fearconditioned stimuli potentiate the startle reflex. In the present
clinical experiment, the normal control, specific phobic, and
social anxiety disorder groups showed a similar, significant probe
startle potentiation during personal fear imagery. Potentiation
was not generally found for panic or PTSD patients. Furthermore, additional analyses of the social anxiety patients showed
patients diagnosed specific/social phobic subtype were critical to
the positive findings for social anxiety group. That is, when the
few specifics were dropped from the analysis, potentiation during
personal fear scenes could not be confirmed for the social anxiety
group. Thus, it is increasingly clear that fear text imagery
instigates a stronger, more reliable fear physiology in focal
phobics, relative to other anxiety diagnosesFconsistent with
Cook et al. (1988) and McNeil et al. (1993).
Negative Affect
Overall, the data suggest that the high negative affect seen in
panic and PTSD patients, defined here by a higher incidence of
comorbidity and higher scores on the questionnaires (see Watson
& Clark, 1984), might directly determine their reduced reaction
to fear cues. Furthermore, the internal analysis of the social
anxiety groups lends support to this hypothesis. Patients from
this group with additional anxiety diagnoses (greater anxiety
comorbidity) were similar to panic patientsFi.e., they did not
show the significant startle potentiation during fear scenes that
was found in patients with the single, primary diagnosis of social
anxiety.
Despite the above, several factors suggest that the relationship
between negative affect and a reduced fear imagery response, if
truly causal, is complex and indirect. First, when the correlations
between questionnaires and physiology were computed, independent of diagnosis, the resulting values were low and
nonsignificant. Second, although comorbid mood disorder was
significantly associated with base corrugator activity and
noncued (ITI) startle magnitude, it was not independently
related to any measure of reactivity. Furthermore, although the
PTSD and panic groups had similar questionnaire scores and
417
incidence of comorbidity, patterns of physiological response over
fear imagery contents were different for the two diagnoses. For
example, PTSD patients showed the highest corrugator
(‘‘frown’’) muscle reactivity to personal fear memories (along
with specific phobics, significantly greater than all other groups).
On the other hand, significant startle potentiation to danger
scenes was found for panic, but not for PTSD. These findings
suggest that different factors orchestrate physiological responding in the two diagnoses.
PTSD, Panic, and Nonanxious Controls
The mean baseline activation of the normal control participants
was the lowest of all experimental groups, and for heart rate and
skin conductance, significantly less than panic patients. The
other anxiety diagnoses did not differ consistently from controls
in base values. Furthermore, controls, social anxiety patients,
and specific phobics showed similar reactivity to fear memories.
For these three groups, the defense motive system was generally
functioning normally: They responded with appropriate arousal
to fear cuesFhowever inconvenient or inappropriate the fears
might be. Interestingly, these groups had the lowest scores on all
questionnaire measures of psychopathology and the lowest
incidence of comorbid depression. In contrast, panic and PTSD
patients showed a broader, more severe affective pathology, but
a hyporeactive physiology in fear imagery. The findings suggest
that defense responding in these disordersFcharacterized by a
more general pathologyFis somehow compromised.
Considering the fact that an exaggerated sensitivity to startle
cues is a pathognomic sign of PTSD in DSM-IV, the startle
results appear to merit particular comment. In fact, laboratory
studies of traumatized patients have not produced results wholly
consistent with the broad DSM view. For example, Grillon,
Morgan, Davis, and Southwick (1998) reported that base blink
reflex magnitude did not differ between Vietnam combat
veterans with PTSD and either veteran or civilian non-PTSD
controls. Furthermore, although the veterans showed a relatively
greater increase in startle when under ‘‘threat of shock,’’ the
actual increase, compared to a safe condition, did not differ
among the three groups. Using a different measure, parallel
response inconsistencies in conditioning were noted by Machulda
(1999). In brief, the role of startle in PTSD continues to be a work
in progress, particularly in terms of comparative startle
sensitivity among anxiety disorders.
Physiological Hyporeactivity in Anxiety
The finding of a reduced physiological fear reaction in the most
distressed patients seems at first counterintuitive, and one
naturally first looks for explanation in possible differences
among the personal texts. These texts were developed in
collaboration with each participant. It was emphasized that the
fear text should describe their ‘‘worst fear’’ experience. The
consistency in participant’s emotional ratings across groups
suggests that they generally followed this instruction (panic
patients actually had the most extreme negative valence ratings,
and their arousal ratings were within the same high range as the
social anxiety and phobic groups). As can be seen from the
examples in Table 1, although scenes varied in specific content,
the texts for all participants contain cues to physiological
reactions, as well as to the sensory context and cognitive
elaborations reported to be part of the fear experience. In all
cases, the patient is confronting the feared event or it is imminent
and physiological and behavioral distress is ongoing. Never-
418
theless, despite imaging evocative texts that were similar in rated
affect to those of the other groups, panic and PTSD showed
reduced startle and heart rate responses. Moreover, it appears to
be a characteristic image/text processing reaction for these
patients, as their mean physiological response to standard fear
scenes was also generally lower than the other experimental
groups.4
Autonomic flexibility. Discordance between affective or
physiological symptom reports in anxious patients, and measured behavioral or physiological reactivity, has frequently been
observed (e.g., Lang, 1968, 1978; Mandler, Mandler, Kremen,
& Sholiton, 1961; Pennebaker, 1982). Furthermore, there are
data suggesting that it is associated with a more generalized
pathology. Relative to normal controls, patients with Generalized Anxiety Disorder (GAD) or panic have shown reduced
reactivity on a variety of tasks in Hoehn-Saric, McLeod, and
Zimmerli (1989, 1991). Roemer and Borkovec (1993) also
reported reduced autonomic reactivity in GAD. Kirsch and Geer
(1988) found a similar reduced response in women with PostMenstrual Syndrome.
Hoehn-Saric and McLeod (2000) have suggested that anxiety
patients have a chronically less flexible autonomic nervous
system (ANS). A related view is held by Thayer and colleagues
(e.g., Friedman & Thayer, 1998), who found that patients with
Generalized Anxiety Disorder show less heart rate variability at
rest than normals. They suggest that this reflects a deficit in the
parasympathetic branch of the ANS: Autonomic balance is
chronically weighted in a sympathetic direction, associated with a
sustained arousal but impaired reactance. This physiological
pattern is seen to be a consequence of the patient’s cognitive style
(e.g., Borkovec & Inz, 1990). That is, GAD patients are
characterized by persistent worryFlanguage processing that
has the effect of elevating and flattening the heart rate sinus
arrhythmia. Friedman, Thayer, Borkovec, and Tyrell (1993)
have reported a resting cardiac pattern in panic patients that is
similar to that found for GAD, whereas this reduced heart rate
variability was not found in specific (blood) phobics. An affinity
between panic (with agoraphobia) and generalized anxiety
disorder, compared to more focused phobic states, is suggested
4
There is now considerable psychophysiological evidence that
patterns of response vary with the imminence of threat (temporal, spatial
distance from danger or pain) in animals (Blanchard & Blanchard, 1989;
Campbell, Wood, & McBride, 1997), and to some extent in humans
(Lang et al., 1997). In the context of patient’s fears, however, the time/
distance parameter is often reduced to a symbolic analogue that is
difficult to quantify. What seems clear, nevertheless, is that for all
participants, their ‘‘worst fear’’ involved a reported active visceral and
somatic physiology, which may be the best index of symbolic, close
‘‘imminence.’’ None of the scenes included what might be considered
blunting, cognitive symptoms of anxiety. Scenes for all groups were
similar. They were immediately anticipatory or at full engagement with
the fear event, that is, in the Fanselow (1994) circa-strike zone (see Table
1). An important related feature is the degree of event predictability/
controllability possessed by the victim. In the real world, things are
generally less predictable for the panic patient. In this laboratory context,
however, all the panic texts involved an already developed fear
physiology. Phasic unpredictability can heighten activationFat least at
first. However, persistent, chronic uncontrollability of aversive events
will, over time, produce a state of ‘‘learned helplessness’’ (Seligman,
1975), characterized by a general blunted sympathetic reaction to
uncertain fear cues. The view would not be inconsistent with the finding
that panic and PTSD patients are less physiologically reactive to their fear
memories.
B.N. Cuthbert et al.
by studies of personality questionnaire patterns (e.g., Turner et al.,
1986). Thus, different habitual patterns of worry and an
associated reduced cardiac variability, along with high negative
affect, could be a determinant of the response reactivity
differences seen here between panic and phobia.
Brain function and the anxiety response. Gray (1987) has
proposed an elaborate theory of brain function in anxiety that
might also accommodate the hyporesponding observed in the
present experiment. In Gray’s conceptual brain, a ‘‘behavioral
activation system’’ (BAS) mediates reactivity to motivationally
relevant stimuli, presumably including the abrupt metabolic
mobilization that precedes and accompanies ‘‘fight or flight.’’
This is contrasted with the ‘‘behavioral inhibition system’’ (BIS),
mediating passive avoidance, and approach–avoidance conflict.5
In a recent revision of the theory (McNaughton & Gray,
2000), the amygdala circuit described by Davis (1992; see also
LeDoux, 1992; Fanselow, 1994)Fwhich also determines
potentiated startleFis seen as the activation system mediating
the ‘‘fear’’ response. In contrast, the BIS is a septal-hippocampal
circuit mediating suppression of approach and an excessive
avoidance of threat. Davis (1992; see also, Lang, Davis, &
Öhman, 2000; Davis & Lang, 2003) has also proposed an
‘‘anxiety’’ path that is separate from ‘‘fear,’’ but one different
from the BIS, and involving the bed nucleus of the stria
terminalis.
As Fowles (2000) points out, the BAS/BIS systems seem to
map on to Barlow’s (1988) distinction between fear and anxiety.
From this perspective, phobia might be determined by the
amygdala fear circuit, whereas GAD is the prototypic ‘‘anxiety’’
disorder. However, more than phobia, Barlow views panic as
specifically driven by the fear system. The panic attack is defined
by ‘‘a subjective sense of extreme fear or impending doom
accompanied by a massive autonomic surge and strong flight-orfight behavioral action tendencies’’ (Bouton, Mineka, & Barlow,
2001, p. 7). Furthermore, as Craske (1999, p. 26) states, ‘‘In
contrast to worry, ...anticipatory anxiety, elicited by an
approaching feared stimulus, is associated with definite autonomic arousal relative to baseline conditions.’’ Thus, the
memory of an imminent or ongoing panic attack should prompt
an associated somato-visceral response. The present data set
suggests that, on the contrary, the reactivity of panic patients is
more like GADFa blunted autonomic and somatic response. It
5
Based on research using the electroencephalogram to analyze brain
asymmetry, Heller, Nitschke, and colleagues have defined two anxiety
trait characteristics in the normal population that appears to parallel
Gray’s two systems (e.g., Nitschke, Heller, Palmieri, & Miller, 1999; see
also Bruder, Fong, Tenke, & Leite, 1997). They propose that a
fundamental distinction can be made between a trait pattern of ‘‘anxious
arousal (somatic anxiety)’’ and ‘‘anxious apprehension (worry).’’
Participants with apprehension anxiety (defined by the Penn State Worry
Questionnaire: Meyer, Miller, Metzger, & Borkovec, 1990) are held to
show greater posterior hemisphere brain activity than right, whereas it is
predicted that participants characterized by anxious arousal will show
greater right posterior activity. The supporting data are suggestive, but
mixed (e.g., Nitschke et al., 1999). A possible mechanism for the brain
effects hypothesized for anxious apprehension might be: Worry involves
persistent language processing. Language processing centers are generally
left lateralized. Thus, greater activity would be seen in the left hemisphere.
Furthermore, if this cognitive pattern characterizes panic and GAD, and
not phobics, these diagnoses might show differences in brain asymmetry
that parallel those expected for anxious apprehension and anxious
arousal.
Fear imagery and anxiety
is not obvious, however, that there is a common mechanism.
Panic patients may either fail to accurately encode panic attacks
(e.g., input to the distance receptors that cues a phobic could be
more readily encoded verbally than the physiological response
information that may cue panic) or succumb to some inhibitory
interference or disattention at the retrieval stage that compromises the verbally mediated, reevocation of a fear experience.
Attention, cognition, and language processing. Distraction is a
possible fear–cue countermechanism.6 If the brain is continuously occupied processing worries, cognitive resources are not
available to attend to external cues or to retrieve the relevant fear
memories. It is also known that the ‘‘spotlight of attention’’ can
be directed to one part of the perceptual field, to the neglect of
other features that might otherwise be salient (Posner & Petersen,
1990). For PTSD patients, particularly, such an altered
attentional state is described as dissociationFrelated to a dulling
of responsivity, emotional ‘‘numbing.’’ Feeny, Zoellner, Fitzgibbons, and Foa (2000) reported that severity of initial and
chronic PTSD-assaulted women was related to patterns of
depression, numbing, and dissociation (Dissociative Experiences
Scale: Bernstein & Putnam, 1986). The dissociative mechanism is
sometimes considered to be an effortful suppression of fear cue
information, or alternatively, an automatic process by which fear
information is rendered unavailable (see Wenzlaff & Wegner,
2000).
Differences in the prevalence of suppression/dissociation might
explain the apparently greater heart rate responsivity seen in
PTSD veterans (e.g., Pitman et al., 1987), than was observed here
in predominantly female, nonveteran patients. These variables
clearly need further study. Ehlers, Mayou, and Bryant (1998), for
example, found evidence that patients injured in auto accidents
who tried to suppress thoughts about the trauma were more likely
to show PTSD symptoms 1 year later. Unfortunately, the present
sample of PTSD subjects (N 5 22) lacks the power for an analysis
of subtypes (dissociative vs. nondissociative; suppressors vs.
nonsuppressors) that might help to clarify these issues.
At present, it is not known how an inhibitory reaction to
emotional cues can be generally achieved. Autonomic arousal is a
frequently observed response in thought suppression experiments
(e.g., Gross & Levenson, 1993). It is not clear, however, if the
observed arousal is an emotional reaction, expressed despite
suppression, or alternatively, an arousal physiology that is the
product of the effort of suppression. Vrana, Cuthbert, and Lang
(1989) studied college student subjects, using a paradigm similar to
the one employed here, in which participants were asked to delay
their imagery response (not respond immediately to the tone cue).
These healthy subjects were indeed able to considerably reduce
6
Disattention to fear cues is a process that has long been enshrined in
clinical lore. It is, however, unclear exactly how disattention might
function, given that a stimulus activates the sensory system of a sentient
organism. For normal control participants, if a topic is cued, it is very
difficult to prevent it becoming the focus of cognitive processing (e.g.,
‘‘Don’t think about white bears’’: Wegner, 1989). Furthermore, it has
been repeatedly shown that affectively arousing stimuli (associated with
sympathetic activation) are better recalled than less emotional events
(e.g., eye-witness testimony: Deffenbacher, 1983; verbal materials: Bock
& Klinger, 1986; pictures: Bradley, Greenwald, Petry, & Lang, 1992). In
addition, there are many studies suggesting that threat cues (even single
words) are actually more intrusive for anxious individuals, capturing
their attention much more readily than that of nonanxious subjects (e.g.,
Mathews & McLeod, 1985).
419
their heart rate response during this delay period, but not so much
that the fear–neutral difference was completely eliminated.
Encoding fear memories. It has been suggested (Lang, 1979,
1985, 1994; see also Foa & Kozak, 1986) that fear-event
memories have an associative structure that includes three broad
categories of information: These are information about the
evoking stimulus, as a sensory event; information about the
reacting individual’s responsesFbehavioral acts and somatic
and autonomic patterns of affective arousal; and associated
semantic elaboration (about where, when, what, how) that
broaden the context and define its meaning as a fearful event. It is
clear that many of these data are not encoded linguisticallyFparticularly stimulus and response information. Human
beings can report, for example, only a fraction of the enormous
data set that is transmitted from retina to occipital cortex, when a
visual stimulus impinges on the eye. The computation that occurs
during perceptual processing, resolving image into object, is also
unavailable for comment. Similarly, the complex changes in the
cardiovascular system and the assembly of muscle actions
involved in an escape response are, in the main, completely
unknown to the actor. Furthermore, it is probable that most
associative connections that link the units of a fear representation
are formed independently of language mediation. That is, the
learning of patterns of autonomic and somatic arousal, escape
and avoidance, the creation of event memories that determine
future behavior, appear to follow conditioning processes that are
essentially the same in humans and in organisms that wholly lack
any capacity for language.
The semantic elaborations (‘‘All snakes are dangerous’’; I’m
having a heart attack’’; ‘‘The audience probably thinks I’m
ridiculous’’), that is, meaning information, are mainly coded
linguistically. We often view such language as a kind of carryall
that can transfer an affective reaction (behavioral and physiological) to contexts that are remote from the stimulus environment in which the primary association was formed (e.g., the
cognitive theories of Beck, Emery, & Greenberg, 1985; Clark,
1996). On the other hand, the relationship of verbal responses to
the other information (behavioral and physiological) can be
tenuous, absent, or unidirectional in associative strength (e.g.,
physiological activation might prompt descriptive language, but
language might not evoke the physiology). In the present
experiment an effort was made to assure that the patient
had, at least, coded the verbal description of the fear event in
memory. That is, patients memorized their personal fear
sentences beforehand to a common criterion. Furthermore,
the sentences were based on information from a structured
interview and contained descriptive language for all three
elements in the fear structureFstimulus, response, and meaning
information. Finally, all patients, regardless of diagnoses,
reported their fear imagery experiences to be affectively negative
and highly arousing. Nevertheless, as noted, diagnoses characterized by a broad range of neurotic complaints (panic and
PTSD) failed to respond to these prompts with a robust
physiology of fear.
To summarize, assuming that the patient’s conditioning
history is a major determinant of anxiety disorder (e.g., Bouton
et al., 2001), we may conjecture that some patients have not
acquired language representations that are strongly associated
with the efferent and sensory (perhaps, interoceptive) memories
of fear. Thus, fear language input (‘‘Tell me about your fear.’’)
gets fear language output (a report of a fear experience)
420
B.N. Cuthbert et al.
according to a propositional grammar, but the visceral and
somatic foundations of fear remain untouched. A related view is
that the physiological responses seen in panic patients during
imagery of panic scenes are not in fact part of a retrieved, primary
fear network (i.e., they are not fear memories of a panic
response). Instead, they reflect an associated state of worry and
vague apprehension that is characterized by response inhibition.
That is, if the event is truly unpredictable and uncontrollable,
reviewing a verbal description of the panic experience may only
be a reminder that panic can occurFprompting reflection and
vigilance in a helpless patient. It would then not result in the
directed, mobilization of the body that is the defense response to
imminent danger or pain.
It is important to note in conclusion that, although there has
been much speculation concerning physiology’s role in determining the different anxiety pathologies, there are as yet very few
data comparing physiological reactivity across the spectrum of
anxiety disorders, considering the wide range of relevant tasks
and challenges. To decide among the various explanatory
models, we will need to repair this deficit. It is only with a view
from a larger data platform that we will be able to determine if
diagnostic differences like those observed here reflect variations
in attentional patterns, language processing, associative learning,
efferent inhibition, or some interaction of all these factors with
the dynamics of memory retrieval.
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(Received August 6, 2002; Accepted November 2, 2002)