Wednesday, September 13, 2006

Got An Anxiety Problem? Need Help?

A general anxiety disorder can be defined as a “state of uneasiness and apprehension, as about future uncertainties”. It can be extremely debilitating, and dealing with general anxiety disorders can vary enormously from person to person.

Heres a few suggestions of some things that many people find useful in dealing with general anxiety disorders.

1. Meditation. This is a form of relaxation for most people. One of the most effective methods of dealing with anxiety and depression can be relaxation. By focusing on ones inner self you can let go of the problems and the fears that seem to plague our lives and forget for a while, and this can foster a deeper form of relaxation. This can allow for a clearer view of a problem, and often after some time practicing meditation people can come up with their own solutions to their own problems. But it can certainly be relaxing and calming, both of which are useful for anyone suffering from general anxiety disorders.

2. Exercise can also be extremely useful. Vigorous exercise can pick you up and leave you feeling great. This is the opposite of how a debilitating anxiety attack can leave you. Often after anxiety attacks you are left feeling depressed and run down, and exercise can pick you up out of this rut and reinvigorate you. It makes those endorphins zing around you body leaving you feeling happier, more relaxed and less anxious.

3. Yoga is a form of exercise, but low impact exercise. It is a slower form of more fluid movements which tend to be more stretching than vigorous exercise. It is a discipline of fluidity and is extremely relaxing and calming, but still produces some of the benefits of the endorphins that more vigorous exercise produces.

4. Talking it out. Sometimes when afflicted by some form of general anxiety disorder it is useful to talk about the things that are making you feel anxious. By letting the feelings out it can help to lighten them. Find someone you really trust to let it all hang out to and unburden yourself. By vocalizing your feelings of anxiety you can help reduce them, with the right person.

5. Any other form of relaxation that works for you. Everyone has their own relaxation. Find out what yours is. Take a bath, or a long walk. Watch a movie or just read a book. General forms of anxiety disorders can leave us feeling on edge and strung out, and sometimes some good relaxation can help.

Many of these suggestions will help, and if you combine 2 or 3 you may be surprised. They may not be a complete answer but they will certainly give your life a boost that it may need.
To find out more about Anxiety visit Peter's Website Anxiety Attack Relief at http://www.anxietyattackrelief.com/ and find out about recognising anxiety signs and more about anxiety relief
Article Source: http://EzineArticles.com/?expert=Peter_Crump

Sunday, September 03, 2006

Please Add Your Panic Attack Or Anxiety Attack Tips For My Local Readers

I am looking for support from the internet community to add there tip or coping skill for panic and anxiety attacks for my local readers. Any suggestion you could give would be greatly appreciated, just leave it in the comment section.

Thank You

Saturday, September 02, 2006

Interesting Panic Attack Study

Behavioural and Cognitive Psychotherapy, 1999, 27, 353–367
Cambridge University Press. Printed in the United Kingdom

THE PSYCHOBIOLOGICAL CORRELATES OF
PANIC ATTACKS DURING IN VIVO EXPOSURE

Nigar G. Khawaja


Queensland University of Technology, Brisbane, Australia
Tian P. S. Oei

University of Queensland, Brisbane, Australia

Abstract. This study examined in detail the psychobiological correlates of panic attacks
experienced in panic disorder with agoraphobia. The cognitions, affect, and physiology
of the six patients were monitored during in vivo exposure to their phobic situations.
The results from these case studies showed that catastrophic cognitions are the key
component of panic attacks. However, there was no clear-cut evidence to support an
interaction among cognitions, affect, and physiology, which has been postulated by
cognitive theories to be the central component of panic attacks and panic disorder with
agoraphobia.

Keywords: Panic attacks, psychobiological, in vivo, exposure, panic disorder,
agoraphobia.
Introduction

In the latest version of the Diagnostic and statistical manual of mental disorders IV
(DSM-IV; American Psychiatric Association, 1994) panic attacks are defined as a discrete
period of intense fear or discomfort accompanied by at least 4 symptoms out of
a list of 13. The list includes symptoms such as palpitations, sweating, and fear of losing
control. The panic attack has a sudden onset and usually peaks within 10 minutes or
less. Thus, as defined, panic is a rather ubiquitous phenomenon found in most of the
anxiety disorders. However, it is a key feature of panic disorder without agoraphobia
(PD) and panic disorder with agoraphobia (PDA).

In recent years, panic attacks have been a focus of behavioural research (Barlow,
1988). One purpose of investigating panic attacks was to increase the understanding of
PD and PDA. Initially influenced by the biological models (Klein, 1981; Sheehan &
Sheehan, 1983), researchers studied panic attacks to examine and quantify their physiological
correlates (Freedman, Ianni, Ettedgui, & Puthezhath, 1985; Margraf, Taylor,
Ehlers, Roth, & Agras, 1987; Shear et al., 1992). These investigations were unable to
Reprint requests to Professor Tian P. S. Oei, School of Psychology, University of Queensland, Brisbane,

Queensland 4072, Australia. E-mail: oei@psy.uq.edu.au
Ó 1999 British Association for Behavioural and Cognitive Psychotherapies
354 N. G. Khawaja and T. P. S. Oei
provide empirical evidence of the biological markers of PD or PDA. Other possible
explanations of this phenomenon were therefore explored, leading to the emergence of
cognitive models (Beck, Emery, & Greenberg, 1985; Clark, 1988; Rapee, 1993; Salkovskis,
1988).

Cognitive models highlight the importance of cognitions in the occurrence of panic
attacks (Khawaja & Oei, 1998a). According to cognitive theories (Beck et al., 1985;
Clark, 1988; Rapee, 1993; Salkovskis, 1988), the physiological changes that initiate
panic may occur as a result of an internal (e.g., physical effort, emotional responses,
drug intake) or external (e.g., environmental stresses) trigger. These sensations, when
interpreted as an indication of imminent danger, create anxiety (Khawaja & Oei,
1998a). This in turn exacerbates the somatic sensations and heightens the anticipation
of threat, with the result that the spiralling anxiety develops into a panic attack. The
cognitive process of attributing a threatening meaning to autonomic arousal and
experiencing the resultant catastrophic cognitions is considered a vital characteristic of
panic attacks (Zoellner, Craske, & Rapee, 1996). Catastrophic cognitions are defined
as thoughts with the theme of danger or threat (Beck et al., 1985). Empirical evidence
has demonstrated that these catastrophic cognitions are involved in panic attacks and
PD (Khawaja & Oei, 1998a, b).

Although cognitive explanations emphasize the vital role of cognitive elements in the
occurrence of panic attacks, it is important to note that other dimensions are also
thought to be involved (for a review see Whittal, Goetsch, & Eifert, 1996). For example,
physiological factors are also taken into account when evaluating a panic experience.
Somatic sensations are regarded as a primary trigger of panic attacks and evidence of
a link between autonomic arousal and panic attacks has been demonstrated by several
researchers (e.g., Clark et al., 1988; Ehlers, Margraf, Roth, Taylor, & Birbaumer, 1988;
Margraf, Barlow, Clark, & Telch, 1993; Margraf & Ehlers, 1989; Rachmann, Lopatka,
& Levitt, 1988). Moreover, panic attacks are manifested by severe physical symptoms
(Krystal, Woods, Hill, & Charney, 1991; Sanderson, Rapee, & Barlow, 1988). There is
consensus among cognitive theories that PD and PDA patients experience panic by
misperceiving a benign autonomic reaction as catastrophic (Beck et al., 1985; Clark,
1988). The affect experienced by the individual during a panic attack is also thought
to be linked with the physiology and cognitions. Affect is reflected by the subjective
distress felt by the person (Whittal et al., 1996). The hypothesized involvement of cognitions,
physiology, and affect indicate the importance of investigating the relationship
of PDA patients’ cognitions with respect to their autonomic arousal and affect.
The relationship among the components of panic attacks (i.e., cognitions, affect, and
physiology) has recently been examined using several procedures (Khawaja & Oei,
1998a). The majority of researchers have relied on retrospective methods. Unfortunately,
retrospective reports can be biased (Beurs, Lange, & Dyck, 1992; Rapee, Craske,
& Barlow, 1990). A more sophisticated method of assessing the various dimensions of
panic was introduced by a group of researchers (Kenardy, Evans, & Oei, 1988; 1989;
Kenardy, Oei, Weir, & Evans, 1993). These researchers investigated the relationship
among PDA patients’ cognitions, affect, and physiology by monitoring these responses
as they occurred in the natural environment or in phobic situations. Physiology, in the
form of heart rates, was monitored by microprocessor in epochs as brief as 5 seconds.
Participants were asked to verbalize their thoughts and distress levels (affect) and these

Panic attacks 355were recorded by a microcassette recorder. In order to interpret the cognitions and tomake them more meaningful, they were classified on a number of dimensions by anindependent coder using the classification system developed by Last, Barlow and
O’Brien (1985). In the case of PDyPDA these classifications are often made in terms
of the presence or frequency of negative andyor catastrophic cognitions. The in vivo
assessment of the ongoing responses increased the reality of the situation.
The initial studies shed light on the relationship among the different variables (i.e.,
cognitions, affect, and physiology) at the time of the panic attack and elevated anxiety.

However, further investigation of this relationship phenomenon by Khawaja, Oei and
Evans (1993) failed to show a significant relationship among these variables. It is
important to note that the preliminary studies were not free from limitations. The
findings were either based on limited data (Kenardy et al., 1988) or on data that was
not collected continuously (Kenardy et al., 1989). Two of these studies (Kenardy et al.,
1993; Khawaja et al., 1993) conducted statistical analyses on responses recorded during
elevated anxiety. These analyses presented an overall global picture with reference to
the high anxiety of the patients. However, elevated anxiety, compared to panic attacks,
may not be an accurate reflection of PD or PDA. Furthermore, the absence of any
significant relationship in the study by Khawaja et al. (1993) may have been due to
methodological problems, because the cognitions reported by the patients were classified
by an independent normal coder. Further examination of this methodology indicated
that the normal coder may not be accurate in reflecting the perspective of the
patients who reported the cognitions (Oei & Khawaja, 1999). In view of this finding, it
was suggested that the patients who report the cognitions should be involved in the
process of coding.

The present research was designed to investigate the components of PD or PDA by
addressing the shortcomings of the previous studies. First, the relationship among the
variables postulated to be important by the cognitive models of PD or PDA has not
been studied extensively by the monitoring of ongoing panic responses recorded during
the time the panicker is exposed to the phobic situation. Second, it is important to
investigate the interaction among the components of PD or PDA by focusing on panic
attacks. The aim of the present study was therefore to examine the relationship among
the cognitions, physiology, and affect of the PDA patients by concentrating on their
detailed responses during panic attacks. Detailed observations of panic are considered
a useful method of collecting meaningful data about the characteristics of panic attack
(Whittal et al., 1996). Patients’ responses were monitored using cognitive sampling and
ambulatory monitoring during in vivo exposure to the phobic settings. These procedures
have been shown to be useful in collecting the spontaneous data (Margraf, 1990; Kenardy
et al., 1989; Turnip, 1990). To increase the interpretability of the information
about the inter-relationship of the components of panic attacks, the data for each
patient were plotted graphically and examined visually. Finally, because patients who
reported the cognitions have been shown to be better at coding their own data (Oei &
Khawaja, 1999), the psychobiological correlates of panic attacks were investigated by
incorporating these recent developments into the coding system. Based on previous
research, it was expected that panic attacks would be characterized by catastrophic
cognitions, elevated affect, and physiology. Thus, cognitions, physiology and affect
were expected to be interrelated during panic attacks.
356 N. G. Khawaja and T. P. S. Oei

Method

Participants

Six patients meeting the DSM-III-R (American Psychiatric Association, 1987) diagnostic
criteria for panic disorder with agoraphobia (300.21) participated in the study. The
patients reported experiencing between 1 and 3 panic attacks per week. All participants
were housewives with secondary education. Their mean age was 43.33 years (SDG
11.63 years; rangeG29 to 57 years). The mean duration of their illness was 16.5 years
(SDG11.55 years; rangeG1 to 32 years). The participants were not receiving any treatment
at the time of the study.
Measures
Ambulatory monitoring. Ambulatory monitoring was recorded using the Vitalog
PMS-8 (Vitalog Corp., 1982). The Vitalog is an ambulatory microprocessor that
records heart rate and activity level when worn by the participant (in epochs as brief
as 5 seconds). Physical activity ranges from 0 (no movement) to 6 (walking at a fast
pace). The event marker of this device is a button, which can be pressed to record any
panic attack onset. The Vitalog is a small and portable device that is carried in a pouch
on the waist. These procedures were similar to those reported in the earlier studies (e.g.,
Khawaja et al., 1993).

Cognitive sampling. The spontaneous cognitions of particpants were sampled every
minute, cued by a two second repeated tone generated by a timing watch. Cognitions
occurring immediately prior to the tone cue were to be reported by the participant.
After the first cue, following a 10 second interval, there was a second cue on which
participants were to report their subjective distress level (SUD) on a scale from 0–10.
A microrecorder recorded participants’ cognitions and subjective distress level throughout
the exposure. These procedures were similar to those used in the earlier studies
(Kenardy et al., 1989; Khawaja et al., 1993).

Procedure

Patients reporting panic attacks were selected for the present study. The selection and
experimental procedures are described in detail in Khawaja et al., 1993. Briefly, participants
were selected from the two clinics associated with the University of Queensland:
the Anxiety Disorder Clinic and the Psychology Clinic. The patients from the Anxiety
Disorder Clinic were referred by health practitioners. These patients went through routine
pre-assessment in the clinic. A psychologist or a psychiatrist interviewed the
patients using a semi-structured interview according to the DSM-III-R. The duration
of the interview was approximately one hour. These procedures are similar to those
outlined in previous studies (Kenardy et al., 1989; Oei, Moylan, & Evans, 1991). Participants
recruited from the Psychology Clinic responded to advertisements appearing
in the local newspapers of the Brisbane metropolitan area. Those who appeared to be
suitable, on the basis of a screening interview conducted by telephone, were mailed a
package containing brief information about the study, a consent form, and a set of

Panic attacks 357
questionnaires. They were asked to bring the completed questionnaires to the Psychology
Clinic, University of Queensland. On their visit to the clinic, the first author
on the basis of SCID-NP interviewed them. Participants were informed about the
nature of the study and it was emphasized that they were free to discontinue at any
time, without prejudice.
The selected participants reported to the Clinic on the day of the experiment. The
procedure was explained in detail and all queries were answered (see Khawaja et al.,
1993, for a full description of the procedure). Prior to the exposure, they were provided
with training in reporting cognitions and subjective distress levels. They were further
instructed to record any panic attack onset by pressing the event marker, or reporting
aloud. Panic attacks were explained to the subjects according to the DSM-III-R
criteria. After satisfactory training, a baseline recording was done for a period of 10
minutes. During this phase, each participant was asked to report her cognitions and
subjective distress levels, first while sitting alone in a clinic room for 5 minutes, and
then walking around the clinic at a normal pace with the experimenter for another 5
minutes. Heart rates and activity were automatically being recorded. Subsequently,
assessment was conducted during a period of exposure to situations of self-reported
high anxiety and avoidance. The first author accompanied participants to their feared
situations. They were then asked to remain on their own in the in vivo situation for
approximately 15 to 20 minutes. Participants were then debriefed at the end of the
exposure. The total duration of the experiment was approximately 70 minutes. A
second appointment, within the next 3–5 days, was arranged with the participant. During
this interval the tapes with the participants’ recorded cognitions were transcribed.
On the second visit, participants were asked to classify the cognitions they had reported
during the exposure, using the simplified version of the Last and colleagues’ classification
system (Last et al., 1985). This simplified form is fully described elsewhere (Oei
& Khawaja, 1999). Participants were instructed to categorize their own thoughts, which
they had reported when taken out to a situation that was anxiety provoking for them.
It was further stated in the instructions that their thoughts could be classified into
different types on the basis of the categories listed (i.e., catastrophic, negative affect,
escape, approach, coping, positive affect, descriptive, and irrelevant). Finally, subjects
were offered group cognitive behaviour therapy at the end of the study.

Results

Seven panic attacks were reported by the six participants. One participant (Subject 1)
experienced a panic attack twice during the exposure phase. In order to study the
cognitive, affective, and physiological correlates of panic attacks in detail, the data
were examined visually. Responses 10 minutes prior to, until 10 minutes after, the
reported onset of the panic attacks were selected. As panic attacks have a sudden onset
and generally last for a few minutes, this duration was considered a reasonable time to
investigate the attacks. Figures 1 to 6 present responses of the six subjects as they
occurred during the selected time period. These responses consist of cognitions, heart
rate, SUDS, and physical activity. Heart rate and SUDS, which were recorded every 5
seconds, were averaged across each minute. Physical activity, which originally ranged
from 0–6, was multiplied by 10 in order to prepare the graphs. The averaged heart
358 N. G. Khawaja and T. P. S. Oei

Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 1. Panic attacks of Subject 1
rates and physical activity per minute were plotted in the graph along with the coinciding
cognition and SUD. The graphs also show the situations in which the patients
experienced the panic attacks. These situations were extremely fearful for the participants
as compared with the other phases of the exposure.
As can be seen from the Figures, six out of the seven panic attacks were experienced
when the patients were alone. The first panic attack of Subject 1 occurred whilst
accompanied by the experimenter. Cognitions coinciding with the onset of panic
attacks had a catastrophic content (see Figures 1 to 6). As shown by the graphs, the
thoughts reported before and after the panic attacks were generally of a negative type
(e.g., catastrophic, negative affect, and escape). Inspection of the data in Figures 1 to
6 indicates that positive (coping and approach) and neutral (description and irrelevant)
cognitions were also occasionally reported.
The data reveal that the distress levels were not reported consistently by the participants.
SUDS were moderate at the time of four of the panic attakcs (Figures 1, 2, 3,
and 5). High SUDS (7 or above on the scale of 1 to 10) were reported by two participants
(Figures 1 and 6). One participant did not report her subjective anxiety levels
(see Figure 4). There was no fluctuation in the heart rate at the time of five panic
attacks (Figures 1, 2, 3, 5, and 6). In the case of Subject 4, there was a sudden increase
in the heart rate one minute before the onset of the panic attack (see Figure 4). A sharp
acceleration in the heart rate occurred only in the first panic attack of Subject 1 (see
Figure 1). Physical activity was either absent (Figures 1, 3, and 5) or minimal (Figures

Panic attacks 359
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 2. Panic attacks of Subject 2

1, 2, and 6) at the time of six of the panic attacks. The first participant (see Figure 1)
was walking slowly in the shopping centre before reporting a panic attack. The fourth
participant (see Figure 4) walked for a few minutes towards the bus stop before
reporting the panic attack.

Concurrent relationships

Overall, the data show that only one panic attack, the first panic attack of Subject 1
(see Figure 1), was marked by a catastrophic cognition, high subjective distress, and
an elevated heart rate without an impact of physical activity. The panic attack experienced
by Subject 4 was marked by a catastrophic cognition along with an increased
heart rate one minute before the onset of the attack (see Figure 4). However, the heart
rate of this participant may have been confounded by physical activity. Catastrophic
cognitions and moderate SUDS were the main features of the remaining panic attacks
(Figures 1, 2, 3, 5, and 6).

Discussion

The present study presents an in-depth analysis of panic attacks as they occurred during
in vivo exposure using ambulatory monitoring and cognitive sampling. Graphic presentation
of the data highlights the vital features of the panic attacks. The majority (85%)
360 N. G. Khawaja and T. P. S. Oei
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 3. Panic attacks of Subject 3
of the attacks occurred after the researcher had left the patients alone in the phobic
situations. Apparently, the aversiveness of the environment increased when patients
were on their own and without a safety figure (Rachmann, 1984). This may have
increased their attention to the potential dangers of the situations andyor to their fearful
bodily sensations (Borden, Lowenbruan, Wolff, & Jones, 1993). A lack of perceived
control over these internal andyor external-threatening events may have aggravated
their autonomic arousal (Rapee, Craske, Brown, & Barlow, 1996). Anticipation of the
panic and an exaggerated appraisal of the negative consequences of anxiety may thus
have escalated into a panic attack (Telch, Brouillard, Telch, Agras, & Taylor, 1989).
This is consistent with the outcome of recent studies that have indicated that absence
of the safe person led to a marked increase in anxiety, fear, heart rate, panic, and
catastrophic cognitions in PDA patients (Carter, Hollon, Carson, & Shelton, 1995;
Rapee, Telfer, & Barlow, 1991).

Cognitions were revealed as the prominent feature of panic attacks. Ideation reported
at the time of the panic attack had a catastrophic content, reflecting the patients’ tendency
to misinterpret internal and external cues as dangerous and likely to lead to a
disaster (Beck, 1988; Clark, 1988; Westling & Ost, 1993). This finding is consistent with
the cognitive theories of PDyPDA (for reviews see McNally, 1994; Taylor, 1995;
Khawaja & Oei, 1998). Furthermore, the attack onsets were generally preceded, and
followed by, negative cognitions with a theme of danger, unpleasant mood, or escape
from the in vivo situation. This indicates that anxiety was marked immediately before
Panic attacks 361

Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 4. Panic attacks of Subject 4
and after the panic attacks. The content of the negative cognitions shed light on the
physical symptoms and the unpleasant emotions experienced by patients (Marks, Basoglu,
Alkubaisy, Sengun, & Marks, 1991). For example, cognitions with a content of
escape were suggestive of participants’ compulsion to leave the in vivo situation. This
finding is consistent with a previous study by Genest, Bowen and Dudley (1990), who
hypothesized that escape or avoidance may be linked to high levels of anxiety. Barlow
and colleagues (Barlow, Brown, & Craske, 1994) have described the ‘‘urge to escape’’
as an important feature of panic, which prepares the organism for action. However,
because it is a subjective experience, it is expressed through self-report (see Whittal et
al., 1996, for a discussion of the limitations of this method). Participants in the present
study also reported neutral or positive cognitions, which acted as coping mechanisms,
either by reassuring or distracting the person. Coping mechanisms have been shown to
be associated with negative ideation and elevated anxiety (Stoler & McNally, 1991).
The subjective distress of the patients was generally moderate at the time of most
(85%) of the panic attacks. This finding indicates that the patients experienced anxiety
and emotional responses at the time of these attacks (cf. Barlow, 1988; Ley, 1992).
However, it appears that like the other self-report procedures, SUDS were reported in
an inconsistent manner. This was one of the measures, where there was a substantial
amount of data missing. It seems that the subjects’ major emphasis was on reporting
the cognitions and they probably forgot to report the SUDS. Distress levels reported
within the moderate range could be due to the fact that the subjects were engrossed
362 N. G. Khawaja and T. P. S. Oei
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 5. Panic attacks of Subject 5
with the task of reporting cognitions and reported the SUDS inattentively. It is also
important to note that the ambulatory monitoring procedures do not point out the
exact time at which the SUDS were reported. There is no certainty that they reported
immediately after the cue. It is possible that they reported them after a delay when
they experienced a decrease in their subjective distress.
Limited information about autonomic arousal (in the form of fluctuating heart rate)
was provided by the present study. There was little evidence of an elevated heart rate
at the time of the panic attacks. Most of the panic attacks (71%) were not characterized
by fluctuations in heart rates. The absence of variability in the heart rate could be due
to one of several factors. First, it is important to note that not all panic attacks are
marked by sudden changes in heart rate. Previous findings have shown that increases
in heart rate occurred only in a subgroup (50%) of all panic attacks (Margraf et al.,
1987; Taylor et al., 1986). In those studies, not all monitored panic attacks were associated
with heart rate changes. Therefore, absence of increased cardio-vascular activity
at the time of a panic attack is consistent with previous findings based on panic induction
(Ehlers, Margraf, & Roth, 1988; Ehlers, Margraf, Taylor, & Roth, 1988) and
physiological ambulatory monitoring procedures (Shear et al., 1992).
Second, fluctuation in heart rate is only one of the physical symptoms of panic
attacks. Patients who reported panic attacks may have responded with symptoms other
than those of a cardio-vascular nature and these symptoms were not monitored (Light,
1990). A variety of physiological responses could not be measured due to equipment

Panic attacks 363
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 6. Panic attacks of Subject 6
limitations. Vitalog stores data regarding heart rate, physical activity, and event markers.
However, it does not have the capacity to store more than three modalities. Therefore,
information about other physiological correlates could not be obtained using the
Vitalog equipment.

Third, it is possible that the crucial feature of panic attacks is the perception of
sensations, which need not be highly correlated with actual physiological changes (Margraf
& Ehlers, 1989). Patients might have experienced subtle physical changes that were
not detected by the cardiovascular measure. Furthermore, there is substantial empirical
evidence that patients allocate attentional resources to their internal milieu (Cloitre,
Heimberg, Holt, & Liebowitz, 1992; McNally, Riemann, Louro, Lukach, & Kim,
1992), suggesting they might have noticed the bodily changes even when these were
subtle (Ehlers, 1993; Rapee, 1994). Thus, perception and catastrophic misinterpretation
of subtle bodily changes (i.e., not detected by the cardiovascular measure) may be a
significant feature of panic attacks.

Fourth, it is important to note that heart rates were recorded after 5 seconds. In
order to manage the data the heart rates recorded during one minute were averaged to
obtain one value for each minute. This value was then compared with the other
responses occurring during that minute. It is possible that within each minute there
were minor fluctuations in the heart rate, which were lost as a result of converting a
number of recordings into one average value.
364 N. G. Khawaja and T. P. S. Oei

Concurrent relationships among cognitions, affect, and physiology were not often
observed in the present data. A moderate association between cognitions and SUDS
was found. This is in line with previous findings (Michelson, 1988). However, only
marginal links of heart rates with SUDS and cognitions were apparent. It is important
to note that the monitoring procedures may not be sensitive enough to evaluate the
relationships among the different variables because the timing intervals used may be
too coarse to reveal such associations. For example, it is difficult to know if the cognitions
were reported at the time indicated or if they were concurrent with the subjective
or physiological responses recorded at that time. The exact time at which a cognition
of SUD is reported is not evident, making it difficult to link them to their concurrent
heart rate. It is also difficult to determine which cognition or SUD is affecting which
heart rate and vice versa. Furthermore, it is difficult to determine the extent to which
heart rates are confounded by other factors such as physical activity or metabolism. In
view of these issues, it appears that the relationships among cognitions, affect, and
physiology cannot be effectively investigated by employing ambulatory monitoring and
cognitive sampling in their current forms. However, the present research has demonstrated
the utility of these methods in the assessment of ongoing cognitions, subjective
distress, and heart rate responses in anxiety or panic as they occur during in vivo
exposure.

In summary, the present study demonstrates that catastrophic cognitions are the
most important attribute of panic attacks. This finding indicates the importance of
catastrophic cognitions in PD and PDA. The present results also suggest that SUDS
may play a secondary role in panic attacks and that there is some overlap of SUDS
with cognitions. The influence of physiology, in the form of heart rate fluctuations, in
the panic attacks was minor. However, this may have been due to the limitations of
the monitoring equipment. The Vitalog is confined to data that can be evaluated separately
and it fails to provide information about the synchronization among different
types of responses. In conclusion, catastrophic cognitions appear to be the primary
feature of a panic attack. The use of in vivo cognitive assessment in the present research
showed it is a valuable procedure for investigating these ongoing cognitions. Furthermore,
involving the patient reporting the cognitions in the process of classifying the
cognitions enhanced the methodology accuracy. Nevertheless, the results of the present
study should be considered with some caution as they are based on a relatively small
sample of panic attacks.

Acknowledgements

We would like to thank the patients for their participation in the study. Our thanks
also to the staff of the Anxiety Disorder Clinic, in particular Dr L. Evans, for their
assistance in data collection. This research was supported by a grant from the British
Red Cross Society. Dr Khawaja, who was on leave from the University of Punjab, was
supported by a grant from the Pakistan Government. She is now at Queensland University
of Technology.
References
AMERICAN PSYCHIATRIC ASSOCIATION (1987). DSM-III-R: Diagnostic and statistical manual of
mental disorders ± revised (3rd R). Washington, DC: Author.
Panic attacks 365
AMERICAN PSYCHIATRIC ASSOCIATION (1994). DSM-IV: Diagnostic and statistical manual of
mental disorders ± revised (4th Edn). Washington, DC: Author.
BARLOW, D. H. (1988). Anxiety and its disorders: The nature and treatment of anxiety and panic.
New York: Guilford Press.
BARLOW, D. H., BROWN, T. A., & CRASKE, M. G. (1994). Definitions of panic attacks and
panic disorder in the DSM-IV: Implications for research. Journal of Abnormal Psychology,
103, 553–564.
BECK, A. T. (1988). Cognitive approaches to panic disorder: Theory and therapy. In S. Rachmann
& J. Maser (Eds.), Panic: Psychological perspectives (pp. 91–109). Hillsdale, New Jersey:
Erlbaum Associates.
BECK, A. T., EMERY, G., & GREENBERG, R. L. (1985). Anxiety disorders and phobias: A cognitive
perspective. New York: Basic Books.
BEURS, E. D., LANGE, A., & DYCK, R. V. (1992). Self-monitoring of panic attacks and retrospective
estimates of panic: Discordant findings. Behaviour Research and Therapy, 30, 411–
413.
BORDEN, J. W., LOWENBRAUN, P. B., WOLFF, P. L., & JONES, A. (1993). Self-focused attention
in panic disorder. Cognitive Therapy and Research, 17, 413–425.
CARTER, M. M., HOLLON, S. D., CARSON, R., & SHELTON, R. C. (1995). Effects of a safe
person on induced distress following a biological challenge in panic disorder with agoraphobia.
Journal of Abnormal Psychology, 104, 156–163.
CLARK, D. M. (1988). A cognitive approach to panic. In S. Rachmann & J. Maser (Eds.), Panic:
Psychological perspectives (pp. 71–89). Hillsdale, New Jersey: Erlbaum Associates.
CLARK, D. M., SALKOVSKIS, P. M., GELDER, M. G., KOEHLER, C., MARTIN, M., ANASTASIADES,
P., HACKMANN, A., MIDDLETON, H., & JEAVONS, A. (1988). Tests of a cognitive
theory of panic. In I. Hand & H. U. Wittchen (Eds.), Panic and phobias (pp. 149–158). New
York: Springer-Verlag.
CLOITRE, M., HEIMBERG, R. G., HOLT, C. S., & LIEBOWITZ, M. R. (1992). Reaction time to
threat stimuli in pain disorder and social phobia. Behaviour Research and Therapy, 30, 609–
617.
EHLERS, A. (1993). Introception and panic disorder. Advances in Behaviour Research and Therapy,
15, 3–21.
EHLERS, A., MARGRAF, J., & ROTH, W. T. (1988). Interaction of expectancy and physiological
stressors in a laboratory model of panic. In D. Hellhammer, I. Florin & H. Weiner (Eds.),
Neurobiological approaches to human disease (pp. 379–384). Toronto: Huber.
EHLERS, A., MARGRAF, J., ROTH, W. T., TAYLOR, C. B., & BIRBAUMER, N. (1988). Anxiety
produced by false heart rate feedback in patients with panic disorder. Behaviour Research and
Therapy, 26, 1–11.
EHLERS, A., MARGRAF, J., TAYLOR, C. B., & ROTH, W. T. (1988). Cardiovascular aspects of
panic disorder. In T. Elbert, W. Langosch, A. Steptoe & D. Vaiti (Eds.), Behavioral medicine
in cardiovascular disorders. New York: Wiley and Sons.
FREEDMAN, R. R., IANNI, P., ETTEDGUI, E., & PATHEZHATH, N. (1985). Ambulatory monitoring
of panic disorder. Archives of General Psychiatry, 42, 244–248.
GENEST, M., BOWEN, R. C., & DUDLEY, J. (1990). Assessment of strategies for coping with
anxiety: Investigations. Journal of Anxiety Disorders, 4, 1–14.
KENARDY, J., EVANS, L., & OEI, T. P. S. (1988). The importance of cognitions in panic attacks.
Behavior Therapy, 19, 471–483.
KENARDY, J., EVANS, L., & OEI, T. P. S. (1989). Cognition and heart rate in panic disorders
during everyday activity. Journal of Anxiety Disorders, 3, 33–43.
KENARDY, J., OEI, T. P. S., WEIR, D., & EVANS, L. (1993). Cognitions in panic disorder with
agoraphobia: Temporal changes and relationships with heart rate and subjective distress.
Journal of Anxiety Disorders, 7, 359–371.
366 N. G. Khawaja and T. P. S. Oei
KHAWAJA, N. G., & OEI, T. P. S. (1998a). Catastrophic cognitions in panic disorder with and
without agoraphobia: A review. Clinical Psychology Review, 18, 341–365.
KHAWAJA, N. G., & OEI, T. P. S. (1998b). Catastrophic cognitions and clinical outcome: Two
case studies. Behavioral and Cognitive Psychotherapy, 26, 271–282.
KHAWAJA, N. G., OEI, T. P. S., & EVANS, L. (1993). Comparison between the panic disorder
with agoraphobia patients and normal controls on the basis of cognitions, affect and physiology.
Cognitive and Behavioral Psychotherapy, 21, 199–217.
KLEIN, D. (1981). Anxiety reconceptualized. In D. F. Klein & J. RABKIN (Eds.), Anxiety: New
research and changing concepts. New York: Raven Press.
KRYSTAL, J. H., WOODS, S. W., HILL, C. L., & CHARNEY, D. S. (1991). Characteristics of panic
attack subtypes: Assessment of spontaneous panic, situational panic, sleep panic, and limited
symptom attacks. Comprehensive Psychiatry, 32, 474–480.
LAST, C. G., BARLOW, D. H., & O’BRIEN, G. T. (1985). Assessing cognitive aspects of anxiety:
Stability and agreement between several methods. Behavior Modi®cation, 9, 72–93.
LEY, R. (1992). The many faces of pan: Psychological and physiological differences among three
types of panic attacks. Behaviour Research and Therapy, 30, 347–357.
LIGHT, K. C. (1990). Ambulatory clinical psychophysiological monitoring: A brief summary and
commentary. Journal of Psychophysiology, 4, 339–341.
MARGRAF, J. (1990). Ambulatory psychophysiological monitoring of panic attacks. Journal of
Psychophysiology, 4, 321–330.
MARGRAF, J., BARLOW, D. H., CLARK, D.M., & TELCH, M. J. (1993). Psychological treatment
of panic: Work in progress and outcome, active ingredients, and follow-up. Behaviour
Research and Therapy, 31, 1–8.
MARGRAF, J., & EHLERS, A. (1989). Etiological models of panic: Psychological and cognitive
aspects. In R. Baker (Ed.), Panic disorder: Theory, research and therapy (pp. 205–225).
London: Wiley & Sons.
MARGRAF, J., TAYLOR, C. B., EHLERS, A., ROTH, W. T., & AGRAS, W. S. (1987). Panic attacks
in a natural environment. Journal of Mental and Nervous Disease, 175, 558–565.
MARKS,M. P., BASOGLU, M., ALKUBAISY, T., SENGUN, S., &MARKS, I. M. (1991). Are anxiety
symptoms and catastrophic cognitions directly related? Journal of Anxiety Disorders, 5, 247–
254.
MCNALLY, R. J. (1994). Panic disorder: A critical analysis. New York: Guilford Press.
MCNALLY, R. J., RIEMANN, B. C., LOURO, C. E., LUKACH, B. M., & KIM, E. (1992). Cognitive
processing of emotional information in panic disorder. Behaviour Research and Therapy, 30,
143–149.
MICHELSON, L. (1988). Cognitive, behavioral, and psychophysiological treatments and correlates
of panic. In S. Rachmann & J. D. Maser (Eds.), Panic: Psychological perspectives (pp. 138–
162). Hillsdale, New Jersey: Erlbaum Associates.
OEI, T. P. S., & KHAWAJA, N. G. (1999). Cognitive assessment by the independent normal coders:
Accuracy and usefulness. Manuscript submitted for publication.
OEI, T. P. S., MOYLAN, A., & EVANS, L. (1991). Validity and clinical utility of Fear Questionnaire
for anxiety disorder patients. Psychological Assessment: A Journal of Consulting and
Clinical Psychology, 3, 391–397.
RACHMANN, S. (1984). Agoraphobia: A safety-signal perspective. Behaviour Research and Therapy,
1, 59–70.
RACHMANN, S., LOPATKA, C., & LEVITT, K. (1988). Experimental analyses of panic-II: Panic
patients. Behaviour Research and Therapy, 26, 33–40.
RAPEE, R. M. (1993). Psychological factors in panic disorder. Advances in Behaviour Research
and Therapy, 15, 85–102.
Panic attacks 367
RAPEE, R. M. (1994). Detection of somatic sensations in panic disorder. Behaviour Research and
Therapy, 32, 825–831.
RAPEE, R. M., CRASKE, M. G., & BARLOW, D. H. (1990). Subject-described features of panic
attacks using self-monitoring. Journal of Anxiety Disorders, 4, 171–181.
RAPEE, R. M., CRASKE, M. G., BROWN, T. A., & BARLOW, D. H. (1996). Measurement of
perceived control over anxiety-related events. Behaviour Therapy, 27, 279–293.
RAPEE, R. M., TELFER, L. A., & BARLOW, D. H. (1991). The role of safety cues in mediating
the response to inhalations of CO2 in agoraphobic. Behaviour Research and Therapy, 29, 353–
355.
SALKOVSKIS, P. M. (1988). Phenomenology, assessment, and the cognitive model of panic. In S.
Rachmann & J. D. Maser (Eds.), Panic: Psychological perspectives (pp. 111–136). New York:
Erlbaum Associates.
SANDERSON, W. C., RAPEE, R.M., & BARLOW, D. H. (1988). Panic induction via inhalation of
5.5% of CO2 enriched air: A single subject analysis of psychological and physiological effects.
Behaviour Research and Therapy, 26, 333–335.
SHEAR, M. K., POLAN, J. J., HARSHFIELD, G., PICKERING, T., MANN, J. J., FRANCES, A., &
JAMES, G. (1992). Ambulatory monitoring of blood pressure in heart rate and panic patients.
Journal of Anxiety Disorders, 6, 213–221.
SHEEHAN, D. V., & SHEEHAN, H. M. (1983). The classification of phobic disorders. International
Journal of Psychiatric Medicine, 12, 243–266.
STOLER, L. S., & MCNALLY, R. J. (1991). Cognitive bias in symptomatic and recovered agoraphobics.
Behaviour Research and Therapy, 29, 539–545.
TAYLOR, S. (1985). Anxiety sensitivity: Theoretical perspectives and recent findings. Behaviour
Research and Therapy, 33, 243–258.
TAYLOR, C. B., SHEIKH, J., AGRAS, W. S., ROTH, W. T., MARGRAF, J., EHLERS, A., MADDOCK,
R. J., & GOSSARD, D. (1986). Ambulatory heart rate changes in patients with panic
attacks. American Journal of Psychiatry, 143, 478–482.
TELCH, M. J., BROUILLARD, M., TELCH, C. F., AGRAS, W. S., & TAYLOR, C. B. (1989). Role
of cognitive appraisal in panic-related avoidance. Behaviour Research and Therapy, 27, 373–
383.
TURNIP, G. (1990). Ambulatory clinical psychophysiology: An introduction to techniques and
methodological issues. Journal of Psychopathology, 4, 299–304.
VITALOG CORPORATION (1982). PMS-8 Owners manual. Mountain View, CA: Author.
WESTLING, B. E., & OST, L. B. (1993). Relationship between panic attack symptoms and cognition
in panic disorder patients. Journal of Anxiety Disorders, 7, 181–194.
WHITTAL, M. L., GOETSCH, V. L., & EIFERT, G. H. (1996). Introduction of a dynamic, idiographic
model for identifying panic. Journal of Anxiety Disorders, 10, 129–144.
ZOELLNER, L. A., CRASKE, M. G., & RAPEE, R. M. (1996). Stability of catastrophic cognitions
in panic disorder. Behaviour Research and Therapy, 34, 399–402.
Behavioural and Cognitive Psychotherapy, 1999, 27, 353–367
Cambridge University Press. Printed in the United Kingdom
THE PSYCHOBIOLOGICAL CORRELATES OF
PANIC ATTACKS DURING IN VIVO EXPOSURE

Nigar G. Khawaja


Queensland University of Technology, Brisbane, Australia
Tian P. S. Oei

University of Queensland, Brisbane, Australia

Abstract. This study examined in detail the psychobiological correlates of panic attacks
experienced in panic disorder with agoraphobia. The cognitions, affect, and physiology
of the six patients were monitored during in vivo exposure to their phobic situations.
The results from these case studies showed that catastrophic cognitions are the key
component of panic attacks. However, there was no clear-cut evidence to support an
interaction among cognitions, affect, and physiology, which has been postulated by
cognitive theories to be the central component of panic attacks and panic disorder with
agoraphobia.

Keywords: Panic attacks, psychobiological, in vivo, exposure, panic disorder,
agoraphobia.
Introduction

In the latest version of the Diagnostic and statistical manual of mental disorders IV
(DSM-IV; American Psychiatric Association, 1994) panic attacks are defined as a discrete
period of intense fear or discomfort accompanied by at least 4 symptoms out of
a list of 13. The list includes symptoms such as palpitations, sweating, and fear of losing
control. The panic attack has a sudden onset and usually peaks within 10 minutes or
less. Thus, as defined, panic is a rather ubiquitous phenomenon found in most of the
anxiety disorders. However, it is a key feature of panic disorder without agoraphobia
(PD) and panic disorder with agoraphobia (PDA).

In recent years, panic attacks have been a focus of behavioural research (Barlow,
1988). One purpose of investigating panic attacks was to increase the understanding of
PD and PDA. Initially influenced by the biological models (Klein, 1981; Sheehan &
Sheehan, 1983), researchers studied panic attacks to examine and quantify their physiological
correlates (Freedman, Ianni, Ettedgui, & Puthezhath, 1985; Margraf, Taylor,
Ehlers, Roth, & Agras, 1987; Shear et al., 1992). These investigations were unable to
Reprint requests to Professor Tian P. S. Oei, School of Psychology, University of Queensland, Brisbane,

Queensland 4072, Australia. E-mail: oei@psy.uq.edu.au
Ó 1999 British Association for Behavioural and Cognitive Psychotherapies
354 N. G. Khawaja and T. P. S. Oei
provide empirical evidence of the biological markers of PD or PDA. Other possible
explanations of this phenomenon were therefore explored, leading to the emergence of
cognitive models (Beck, Emery, & Greenberg, 1985; Clark, 1988; Rapee, 1993; Salkovskis,
1988).

Cognitive models highlight the importance of cognitions in the occurrence of panic
attacks (Khawaja & Oei, 1998a). According to cognitive theories (Beck et al., 1985;
Clark, 1988; Rapee, 1993; Salkovskis, 1988), the physiological changes that initiate
panic may occur as a result of an internal (e.g., physical effort, emotional responses,
drug intake) or external (e.g., environmental stresses) trigger. These sensations, when
interpreted as an indication of imminent danger, create anxiety (Khawaja & Oei,
1998a). This in turn exacerbates the somatic sensations and heightens the anticipation
of threat, with the result that the spiralling anxiety develops into a panic attack. The
cognitive process of attributing a threatening meaning to autonomic arousal and
experiencing the resultant catastrophic cognitions is considered a vital characteristic of
panic attacks (Zoellner, Craske, & Rapee, 1996). Catastrophic cognitions are defined
as thoughts with the theme of danger or threat (Beck et al., 1985). Empirical evidence
has demonstrated that these catastrophic cognitions are involved in panic attacks and
PD (Khawaja & Oei, 1998a, b).

Although cognitive explanations emphasize the vital role of cognitive elements in the
occurrence of panic attacks, it is important to note that other dimensions are also
thought to be involved (for a review see Whittal, Goetsch, & Eifert, 1996). For example,
physiological factors are also taken into account when evaluating a panic experience.
Somatic sensations are regarded as a primary trigger of panic attacks and evidence of
a link between autonomic arousal and panic attacks has been demonstrated by several
researchers (e.g., Clark et al., 1988; Ehlers, Margraf, Roth, Taylor, & Birbaumer, 1988;
Margraf, Barlow, Clark, & Telch, 1993; Margraf & Ehlers, 1989; Rachmann, Lopatka,
& Levitt, 1988). Moreover, panic attacks are manifested by severe physical symptoms
(Krystal, Woods, Hill, & Charney, 1991; Sanderson, Rapee, & Barlow, 1988). There is
consensus among cognitive theories that PD and PDA patients experience panic by
misperceiving a benign autonomic reaction as catastrophic (Beck et al., 1985; Clark,
1988). The affect experienced by the individual during a panic attack is also thought
to be linked with the physiology and cognitions. Affect is reflected by the subjective
distress felt by the person (Whittal et al., 1996). The hypothesized involvement of cognitions,
physiology, and affect indicate the importance of investigating the relationship
of PDA patients’ cognitions with respect to their autonomic arousal and affect.
The relationship among the components of panic attacks (i.e., cognitions, affect, and
physiology) has recently been examined using several procedures (Khawaja & Oei,
1998a). The majority of researchers have relied on retrospective methods. Unfortunately,
retrospective reports can be biased (Beurs, Lange, & Dyck, 1992; Rapee, Craske,
& Barlow, 1990). A more sophisticated method of assessing the various dimensions of
panic was introduced by a group of researchers (Kenardy, Evans, & Oei, 1988; 1989;
Kenardy, Oei, Weir, & Evans, 1993). These researchers investigated the relationship
among PDA patients’ cognitions, affect, and physiology by monitoring these responses
as they occurred in the natural environment or in phobic situations. Physiology, in the
form of heart rates, was monitored by microprocessor in epochs as brief as 5 seconds.
Participants were asked to verbalize their thoughts and distress levels (affect) and these

Panic attacks 355were recorded by a microcassette recorder. In order to interpret the cognitions and tomake them more meaningful, they were classified on a number of dimensions by anindependent coder using the classification system developed by Last, Barlow and
O’Brien (1985). In the case of PDyPDA these classifications are often made in terms
of the presence or frequency of negative andyor catastrophic cognitions. The in vivo
assessment of the ongoing responses increased the reality of the situation.
The initial studies shed light on the relationship among the different variables (i.e.,
cognitions, affect, and physiology) at the time of the panic attack and elevated anxiety.

However, further investigation of this relationship phenomenon by Khawaja, Oei and
Evans (1993) failed to show a significant relationship among these variables. It is
important to note that the preliminary studies were not free from limitations. The
findings were either based on limited data (Kenardy et al., 1988) or on data that was
not collected continuously (Kenardy et al., 1989). Two of these studies (Kenardy et al.,
1993; Khawaja et al., 1993) conducted statistical analyses on responses recorded during
elevated anxiety. These analyses presented an overall global picture with reference to
the high anxiety of the patients. However, elevated anxiety, compared to panic attacks,
may not be an accurate reflection of PD or PDA. Furthermore, the absence of any
significant relationship in the study by Khawaja et al. (1993) may have been due to
methodological problems, because the cognitions reported by the patients were classified
by an independent normal coder. Further examination of this methodology indicated
that the normal coder may not be accurate in reflecting the perspective of the
patients who reported the cognitions (Oei & Khawaja, 1999). In view of this finding, it
was suggested that the patients who report the cognitions should be involved in the
process of coding.

The present research was designed to investigate the components of PD or PDA by
addressing the shortcomings of the previous studies. First, the relationship among the
variables postulated to be important by the cognitive models of PD or PDA has not
been studied extensively by the monitoring of ongoing panic responses recorded during
the time the panicker is exposed to the phobic situation. Second, it is important to
investigate the interaction among the components of PD or PDA by focusing on panic
attacks. The aim of the present study was therefore to examine the relationship among
the cognitions, physiology, and affect of the PDA patients by concentrating on their
detailed responses during panic attacks. Detailed observations of panic are considered
a useful method of collecting meaningful data about the characteristics of panic attack
(Whittal et al., 1996). Patients’ responses were monitored using cognitive sampling and
ambulatory monitoring during in vivo exposure to the phobic settings. These procedures
have been shown to be useful in collecting the spontaneous data (Margraf, 1990; Kenardy
et al., 1989; Turnip, 1990). To increase the interpretability of the information
about the inter-relationship of the components of panic attacks, the data for each
patient were plotted graphically and examined visually. Finally, because patients who
reported the cognitions have been shown to be better at coding their own data (Oei &
Khawaja, 1999), the psychobiological correlates of panic attacks were investigated by
incorporating these recent developments into the coding system. Based on previous
research, it was expected that panic attacks would be characterized by catastrophic
cognitions, elevated affect, and physiology. Thus, cognitions, physiology and affect
were expected to be interrelated during panic attacks.
356 N. G. Khawaja and T. P. S. Oei

Method

Participants

Six patients meeting the DSM-III-R (American Psychiatric Association, 1987) diagnostic
criteria for panic disorder with agoraphobia (300.21) participated in the study. The
patients reported experiencing between 1 and 3 panic attacks per week. All participants
were housewives with secondary education. Their mean age was 43.33 years (SDG
11.63 years; rangeG29 to 57 years). The mean duration of their illness was 16.5 years
(SDG11.55 years; rangeG1 to 32 years). The participants were not receiving any treatment
at the time of the study.
Measures
Ambulatory monitoring. Ambulatory monitoring was recorded using the Vitalog
PMS-8 (Vitalog Corp., 1982). The Vitalog is an ambulatory microprocessor that
records heart rate and activity level when worn by the participant (in epochs as brief
as 5 seconds). Physical activity ranges from 0 (no movement) to 6 (walking at a fast
pace). The event marker of this device is a button, which can be pressed to record any
panic attack onset. The Vitalog is a small and portable device that is carried in a pouch
on the waist. These procedures were similar to those reported in the earlier studies (e.g.,
Khawaja et al., 1993).

Cognitive sampling. The spontaneous cognitions of particpants were sampled every
minute, cued by a two second repeated tone generated by a timing watch. Cognitions
occurring immediately prior to the tone cue were to be reported by the participant.
After the first cue, following a 10 second interval, there was a second cue on which
participants were to report their subjective distress level (SUD) on a scale from 0–10.
A microrecorder recorded participants’ cognitions and subjective distress level throughout
the exposure. These procedures were similar to those used in the earlier studies
(Kenardy et al., 1989; Khawaja et al., 1993).

Procedure

Patients reporting panic attacks were selected for the present study. The selection and
experimental procedures are described in detail in Khawaja et al., 1993. Briefly, participants
were selected from the two clinics associated with the University of Queensland:
the Anxiety Disorder Clinic and the Psychology Clinic. The patients from the Anxiety
Disorder Clinic were referred by health practitioners. These patients went through routine
pre-assessment in the clinic. A psychologist or a psychiatrist interviewed the
patients using a semi-structured interview according to the DSM-III-R. The duration
of the interview was approximately one hour. These procedures are similar to those
outlined in previous studies (Kenardy et al., 1989; Oei, Moylan, & Evans, 1991). Participants
recruited from the Psychology Clinic responded to advertisements appearing
in the local newspapers of the Brisbane metropolitan area. Those who appeared to be
suitable, on the basis of a screening interview conducted by telephone, were mailed a
package containing brief information about the study, a consent form, and a set of

Panic attacks 357
questionnaires. They were asked to bring the completed questionnaires to the Psychology
Clinic, University of Queensland. On their visit to the clinic, the first author
on the basis of SCID-NP interviewed them. Participants were informed about the
nature of the study and it was emphasized that they were free to discontinue at any
time, without prejudice.
The selected participants reported to the Clinic on the day of the experiment. The
procedure was explained in detail and all queries were answered (see Khawaja et al.,
1993, for a full description of the procedure). Prior to the exposure, they were provided
with training in reporting cognitions and subjective distress levels. They were further
instructed to record any panic attack onset by pressing the event marker, or reporting
aloud. Panic attacks were explained to the subjects according to the DSM-III-R
criteria. After satisfactory training, a baseline recording was done for a period of 10
minutes. During this phase, each participant was asked to report her cognitions and
subjective distress levels, first while sitting alone in a clinic room for 5 minutes, and
then walking around the clinic at a normal pace with the experimenter for another 5
minutes. Heart rates and activity were automatically being recorded. Subsequently,
assessment was conducted during a period of exposure to situations of self-reported
high anxiety and avoidance. The first author accompanied participants to their feared
situations. They were then asked to remain on their own in the in vivo situation for
approximately 15 to 20 minutes. Participants were then debriefed at the end of the
exposure. The total duration of the experiment was approximately 70 minutes. A
second appointment, within the next 3–5 days, was arranged with the participant. During
this interval the tapes with the participants’ recorded cognitions were transcribed.
On the second visit, participants were asked to classify the cognitions they had reported
during the exposure, using the simplified version of the Last and colleagues’ classification
system (Last et al., 1985). This simplified form is fully described elsewhere (Oei
& Khawaja, 1999). Participants were instructed to categorize their own thoughts, which
they had reported when taken out to a situation that was anxiety provoking for them.
It was further stated in the instructions that their thoughts could be classified into
different types on the basis of the categories listed (i.e., catastrophic, negative affect,
escape, approach, coping, positive affect, descriptive, and irrelevant). Finally, subjects
were offered group cognitive behaviour therapy at the end of the study.

Results

Seven panic attacks were reported by the six participants. One participant (Subject 1)
experienced a panic attack twice during the exposure phase. In order to study the
cognitive, affective, and physiological correlates of panic attacks in detail, the data
were examined visually. Responses 10 minutes prior to, until 10 minutes after, the
reported onset of the panic attacks were selected. As panic attacks have a sudden onset
and generally last for a few minutes, this duration was considered a reasonable time to
investigate the attacks. Figures 1 to 6 present responses of the six subjects as they
occurred during the selected time period. These responses consist of cognitions, heart
rate, SUDS, and physical activity. Heart rate and SUDS, which were recorded every 5
seconds, were averaged across each minute. Physical activity, which originally ranged
from 0–6, was multiplied by 10 in order to prepare the graphs. The averaged heart
358 N. G. Khawaja and T. P. S. Oei

Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 1. Panic attacks of Subject 1
rates and physical activity per minute were plotted in the graph along with the coinciding
cognition and SUD. The graphs also show the situations in which the patients
experienced the panic attacks. These situations were extremely fearful for the participants
as compared with the other phases of the exposure.
As can be seen from the Figures, six out of the seven panic attacks were experienced
when the patients were alone. The first panic attack of Subject 1 occurred whilst
accompanied by the experimenter. Cognitions coinciding with the onset of panic
attacks had a catastrophic content (see Figures 1 to 6). As shown by the graphs, the
thoughts reported before and after the panic attacks were generally of a negative type
(e.g., catastrophic, negative affect, and escape). Inspection of the data in Figures 1 to
6 indicates that positive (coping and approach) and neutral (description and irrelevant)
cognitions were also occasionally reported.
The data reveal that the distress levels were not reported consistently by the participants.
SUDS were moderate at the time of four of the panic attakcs (Figures 1, 2, 3,
and 5). High SUDS (7 or above on the scale of 1 to 10) were reported by two participants
(Figures 1 and 6). One participant did not report her subjective anxiety levels
(see Figure 4). There was no fluctuation in the heart rate at the time of five panic
attacks (Figures 1, 2, 3, 5, and 6). In the case of Subject 4, there was a sudden increase
in the heart rate one minute before the onset of the panic attack (see Figure 4). A sharp
acceleration in the heart rate occurred only in the first panic attack of Subject 1 (see
Figure 1). Physical activity was either absent (Figures 1, 3, and 5) or minimal (Figures

Panic attacks 359
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 2. Panic attacks of Subject 2

1, 2, and 6) at the time of six of the panic attacks. The first participant (see Figure 1)
was walking slowly in the shopping centre before reporting a panic attack. The fourth
participant (see Figure 4) walked for a few minutes towards the bus stop before
reporting the panic attack.

Concurrent relationships

Overall, the data show that only one panic attack, the first panic attack of Subject 1
(see Figure 1), was marked by a catastrophic cognition, high subjective distress, and
an elevated heart rate without an impact of physical activity. The panic attack experienced
by Subject 4 was marked by a catastrophic cognition along with an increased
heart rate one minute before the onset of the attack (see Figure 4). However, the heart
rate of this participant may have been confounded by physical activity. Catastrophic
cognitions and moderate SUDS were the main features of the remaining panic attacks
(Figures 1, 2, 3, 5, and 6).

Discussion

The present study presents an in-depth analysis of panic attacks as they occurred during
in vivo exposure using ambulatory monitoring and cognitive sampling. Graphic presentation
of the data highlights the vital features of the panic attacks. The majority (85%)
360 N. G. Khawaja and T. P. S. Oei
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 3. Panic attacks of Subject 3
of the attacks occurred after the researcher had left the patients alone in the phobic
situations. Apparently, the aversiveness of the environment increased when patients
were on their own and without a safety figure (Rachmann, 1984). This may have
increased their attention to the potential dangers of the situations andyor to their fearful
bodily sensations (Borden, Lowenbruan, Wolff, & Jones, 1993). A lack of perceived
control over these internal andyor external-threatening events may have aggravated
their autonomic arousal (Rapee, Craske, Brown, & Barlow, 1996). Anticipation of the
panic and an exaggerated appraisal of the negative consequences of anxiety may thus
have escalated into a panic attack (Telch, Brouillard, Telch, Agras, & Taylor, 1989).
This is consistent with the outcome of recent studies that have indicated that absence
of the safe person led to a marked increase in anxiety, fear, heart rate, panic, and
catastrophic cognitions in PDA patients (Carter, Hollon, Carson, & Shelton, 1995;
Rapee, Telfer, & Barlow, 1991).

Cognitions were revealed as the prominent feature of panic attacks. Ideation reported
at the time of the panic attack had a catastrophic content, reflecting the patients’ tendency
to misinterpret internal and external cues as dangerous and likely to lead to a
disaster (Beck, 1988; Clark, 1988; Westling & Ost, 1993). This finding is consistent with
the cognitive theories of PDyPDA (for reviews see McNally, 1994; Taylor, 1995;
Khawaja & Oei, 1998). Furthermore, the attack onsets were generally preceded, and
followed by, negative cognitions with a theme of danger, unpleasant mood, or escape
from the in vivo situation. This indicates that anxiety was marked immediately before
Panic attacks 361

Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 4. Panic attacks of Subject 4
and after the panic attacks. The content of the negative cognitions shed light on the
physical symptoms and the unpleasant emotions experienced by patients (Marks, Basoglu,
Alkubaisy, Sengun, & Marks, 1991). For example, cognitions with a content of
escape were suggestive of participants’ compulsion to leave the in vivo situation. This
finding is consistent with a previous study by Genest, Bowen and Dudley (1990), who
hypothesized that escape or avoidance may be linked to high levels of anxiety. Barlow
and colleagues (Barlow, Brown, & Craske, 1994) have described the ‘‘urge to escape’’
as an important feature of panic, which prepares the organism for action. However,
because it is a subjective experience, it is expressed through self-report (see Whittal et
al., 1996, for a discussion of the limitations of this method). Participants in the present
study also reported neutral or positive cognitions, which acted as coping mechanisms,
either by reassuring or distracting the person. Coping mechanisms have been shown to
be associated with negative ideation and elevated anxiety (Stoler & McNally, 1991).
The subjective distress of the patients was generally moderate at the time of most
(85%) of the panic attacks. This finding indicates that the patients experienced anxiety
and emotional responses at the time of these attacks (cf. Barlow, 1988; Ley, 1992).
However, it appears that like the other self-report procedures, SUDS were reported in
an inconsistent manner. This was one of the measures, where there was a substantial
amount of data missing. It seems that the subjects’ major emphasis was on reporting
the cognitions and they probably forgot to report the SUDS. Distress levels reported
within the moderate range could be due to the fact that the subjects were engrossed
362 N. G. Khawaja and T. P. S. Oei
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 5. Panic attacks of Subject 5
with the task of reporting cognitions and reported the SUDS inattentively. It is also
important to note that the ambulatory monitoring procedures do not point out the
exact time at which the SUDS were reported. There is no certainty that they reported
immediately after the cue. It is possible that they reported them after a delay when
they experienced a decrease in their subjective distress.
Limited information about autonomic arousal (in the form of fluctuating heart rate)
was provided by the present study. There was little evidence of an elevated heart rate
at the time of the panic attacks. Most of the panic attacks (71%) were not characterized
by fluctuations in heart rates. The absence of variability in the heart rate could be due
to one of several factors. First, it is important to note that not all panic attacks are
marked by sudden changes in heart rate. Previous findings have shown that increases
in heart rate occurred only in a subgroup (50%) of all panic attacks (Margraf et al.,
1987; Taylor et al., 1986). In those studies, not all monitored panic attacks were associated
with heart rate changes. Therefore, absence of increased cardio-vascular activity
at the time of a panic attack is consistent with previous findings based on panic induction
(Ehlers, Margraf, & Roth, 1988; Ehlers, Margraf, Taylor, & Roth, 1988) and
physiological ambulatory monitoring procedures (Shear et al., 1992).
Second, fluctuation in heart rate is only one of the physical symptoms of panic
attacks. Patients who reported panic attacks may have responded with symptoms other
than those of a cardio-vascular nature and these symptoms were not monitored (Light,
1990). A variety of physiological responses could not be measured due to equipment

Panic attacks 363
Note: AV HRGaverage bpm; AV ACGaverage activity level per minute; SUDSGsubjective
distress level per minute; activity and SUDS are multiplied by 10; cognitions: 1Gcatastrophic,
2Gescape, 3Gnegative affect, 4Gcoping, 5Gapproach, 6Gpositive affect, 7Gdescription, 8G
irrelevant; Gaps in cognitions and curves showing AV HR, AV AC and SUDSGmissing datay
no response

Figure 6. Panic attacks of Subject 6
limitations. Vitalog stores data regarding heart rate, physical activity, and event markers.
However, it does not have the capacity to store more than three modalities. Therefore,
information about other physiological correlates could not be obtained using the
Vitalog equipment.

Third, it is possible that the crucial feature of panic attacks is the perception of
sensations, which need not be highly correlated with actual physiological changes (Margraf
& Ehlers, 1989). Patients might have experienced subtle physical changes that were
not detected by the cardiovascular measure. Furthermore, there is substantial empirical
evidence that patients allocate attentional resources to their internal milieu (Cloitre,
Heimberg, Holt, & Liebowitz, 1992; McNally, Riemann, Louro, Lukach, & Kim,
1992), suggesting they might have noticed the bodily changes even when these were
subtle (Ehlers, 1993; Rapee, 1994). Thus, perception and catastrophic misinterpretation
of subtle bodily changes (i.e., not detected by the cardiovascular measure) may be a
significant feature of panic attacks.

Fourth, it is important to note that heart rates were recorded after 5 seconds. In
order to manage the data the heart rates recorded during one minute were averaged to
obtain one value for each minute. This value was then compared with the other
responses occurring during that minute. It is possible that within each minute there
were minor fluctuations in the heart rate, which were lost as a result of converting a
number of recordings into one average value.
364 N. G. Khawaja and T. P. S. Oei

Concurrent relationships among cognitions, affect, and physiology were not often
observed in the present data. A moderate association between cognitions and SUDS
was found. This is in line with previous findings (Michelson, 1988). However, only
marginal links of heart rates with SUDS and cognitions were apparent. It is important
to note that the monitoring procedures may not be sensitive enough to evaluate the
relationships among the different variables because the timing intervals used may be
too coarse to reveal such associations. For example, it is difficult to know if the cognitions
were reported at the time indicated or if they were concurrent with the subjective
or physiological responses recorded at that time. The exact time at which a cognition
of SUD is reported is not evident, making it difficult to link them to their concurrent
heart rate. It is also difficult to determine which cognition or SUD is affecting which
heart rate and vice versa. Furthermore, it is difficult to determine the extent to which
heart rates are confounded by other factors such as physical activity or metabolism. In
view of these issues, it appears that the relationships among cognitions, affect, and
physiology cannot be effectively investigated by employing ambulatory monitoring and
cognitive sampling in their current forms. However, the present research has demonstrated
the utility of these methods in the assessment of ongoing cognitions, subjective
distress, and heart rate responses in anxiety or panic as they occur during in vivo
exposure.

In summary, the present study demonstrates that catastrophic cognitions are the
most important attribute of panic attacks. This finding indicates the importance of
catastrophic cognitions in PD and PDA. The present results also suggest that SUDS
may play a secondary role in panic attacks and that there is some overlap of SUDS
with cognitions. The influence of physiology, in the form of heart rate fluctuations, in
the panic attacks was minor. However, this may have been due to the limitations of
the monitoring equipment. The Vitalog is confined to data that can be evaluated separately
and it fails to provide information about the synchronization among different
types of responses. In conclusion, catastrophic cognitions appear to be the primary
feature of a panic attack. The use of in vivo cognitive assessment in the present research
showed it is a valuable procedure for investigating these ongoing cognitions. Furthermore,
involving the patient reporting the cognitions in the process of classifying the
cognitions enhanced the methodology accuracy. Nevertheless, the results of the present
study should be considered with some caution as they are based on a relatively small
sample of panic attacks.

Acknowledgements

We would like to thank the patients for their participation in the study. Our thanks
also to the staff of the Anxiety Disorder Clinic, in particular Dr L. Evans, for their
assistance in data collection. This research was supported by a grant from the British
Red Cross Society. Dr Khawaja, who was on leave from the University of Punjab, was
supported by a grant from the Pakistan Government. She is now at Queensland University
of Technology.
References
AMERICAN PSYCHIATRIC ASSOCIATION (1987). DSM-III-R: Diagnostic and statistical manual of
mental disorders ± revised (3rd R). Washington, DC: Author.
Panic attacks 365
AMERICAN PSYCHIATRIC ASSOCIATION (1994). DSM-IV: Diagnostic and statistical manual of
mental disorders ± revised (4th Edn). Washington, DC: Author.
BARLOW, D. H. (1988). Anxiety and its disorders: The nature and treatment of anxiety and panic.
New York: Guilford Press.
BARLOW, D. H., BROWN, T. A., & CRASKE, M. G. (1994). Definitions of panic attacks and
panic disorder in the DSM-IV: Implications for research. Journal of Abnormal Psychology,
103, 553–564.
BECK, A. T. (1988). Cognitive approaches to panic disorder: Theory and therapy. In S. Rachmann
& J. Maser (Eds.), Panic: Psychological perspectives (pp. 91–109). Hillsdale, New Jersey:
Erlbaum Associates.
BECK, A. T., EMERY, G., & GREENBERG, R. L. (1985). Anxiety disorders and phobias: A cognitive
perspective. New York: Basic Books.
BEURS, E. D., LANGE, A., & DYCK, R. V. (1992). Self-monitoring of panic attacks and retrospective
estimates of panic: Discordant findings. Behaviour Research and Therapy, 30, 411–
413.
BORDEN, J. W., LOWENBRAUN, P. B., WOLFF, P. L., & JONES, A. (1993). Self-focused attention
in panic disorder. Cognitive Therapy and Research, 17, 413–425.
CARTER, M. M., HOLLON, S. D., CARSON, R., & SHELTON, R. C. (1995). Effects of a safe
person on induced distress following a biological challenge in panic disorder with agoraphobia.
Journal of Abnormal Psychology, 104, 156–163.
CLARK, D. M. (1988). A cognitive approach to panic. In S. Rachmann & J. Maser (Eds.), Panic:
Psychological perspectives (pp. 71–89). Hillsdale, New Jersey: Erlbaum Associates.
CLARK, D. M., SALKOVSKIS, P. M., GELDER, M. G., KOEHLER, C., MARTIN, M., ANASTASIADES,
P., HACKMANN, A., MIDDLETON, H., & JEAVONS, A. (1988). Tests of a cognitive
theory of panic. In I. Hand & H. U. Wittchen (Eds.), Panic and phobias (pp. 149–158). New
York: Springer-Verlag.
CLOITRE, M., HEIMBERG, R. G., HOLT, C. S., & LIEBOWITZ, M. R. (1992). Reaction time to
threat stimuli in pain disorder and social phobia. Behaviour Research and Therapy, 30, 609–
617.
EHLERS, A. (1993). Introception and panic disorder. Advances in Behaviour Research and Therapy,
15, 3–21.
EHLERS, A., MARGRAF, J., & ROTH, W. T. (1988). Interaction of expectancy and physiological
stressors in a laboratory model of panic. In D. Hellhammer, I. Florin & H. Weiner (Eds.),
Neurobiological approaches to human disease (pp. 379–384). Toronto: Huber.
EHLERS, A., MARGRAF, J., ROTH, W. T., TAYLOR, C. B., & BIRBAUMER, N. (1988). Anxiety
produced by false heart rate feedback in patients with panic disorder. Behaviour Research and
Therapy, 26, 1–11.
EHLERS, A., MARGRAF, J., TAYLOR, C. B., & ROTH, W. T. (1988). Cardiovascular aspects of
panic disorder. In T. Elbert, W. Langosch, A. Steptoe & D. Vaiti (Eds.), Behavioral medicine
in cardiovascular disorders. New York: Wiley and Sons.
FREEDMAN, R. R., IANNI, P., ETTEDGUI, E., & PATHEZHATH, N. (1985). Ambulatory monitoring
of panic disorder. Archives of General Psychiatry, 42, 244–248.
GENEST, M., BOWEN, R. C., & DUDLEY, J. (1990). Assessment of strategies for coping with
anxiety: Investigations. Journal of Anxiety Disorders, 4, 1–14.
KENARDY, J., EVANS, L., & OEI, T. P. S. (1988). The importance of cognitions in panic attacks.
Behavior Therapy, 19, 471–483.
KENARDY, J., EVANS, L., & OEI, T. P. S. (1989). Cognition and heart rate in panic disorders
during everyday activity. Journal of Anxiety Disorders, 3, 33–43.
KENARDY, J., OEI, T. P. S., WEIR, D., & EVANS, L. (1993). Cognitions in panic disorder with
agoraphobia: Temporal changes and relationships with heart rate and subjective distress.
Journal of Anxiety Disorders, 7, 359–371.
366 N. G. Khawaja and T. P. S. Oei
KHAWAJA, N. G., & OEI, T. P. S. (1998a). Catastrophic cognitions in panic disorder with and
without agoraphobia: A review. Clinical Psychology Review, 18, 341–365.
KHAWAJA, N. G., & OEI, T. P. S. (1998b). Catastrophic cognitions and clinical outcome: Two
case studies. Behavioral and Cognitive Psychotherapy, 26, 271–282.
KHAWAJA, N. G., OEI, T. P. S., & EVANS, L. (1993). Comparison between the panic disorder
with agoraphobia patients and normal controls on the basis of cognitions, affect and physiology.
Cognitive and Behavioral Psychotherapy, 21, 199–217.
KLEIN, D. (1981). Anxiety reconceptualized. In D. F. Klein & J. RABKIN (Eds.), Anxiety: New
research and changing concepts. New York: Raven Press.
KRYSTAL, J. H., WOODS, S. W., HILL, C. L., & CHARNEY, D. S. (1991). Characteristics of panic
attack subtypes: Assessment of spontaneous panic, situational panic, sleep panic, and limited
symptom attacks. Comprehensive Psychiatry, 32, 474–480.
LAST, C. G., BARLOW, D. H., & O’BRIEN, G. T. (1985). Assessing cognitive aspects of anxiety:
Stability and agreement between several methods. Behavior Modi®cation, 9, 72–93.
LEY, R. (1992). The many faces of pan: Psychological and physiological differences among three
types of panic attacks. Behaviour Research and Therapy, 30, 347–357.
LIGHT, K. C. (1990). Ambulatory clinical psychophysiological monitoring: A brief summary and
commentary. Journal of Psychophysiology, 4, 339–341.
MARGRAF, J. (1990). Ambulatory psychophysiological monitoring of panic attacks. Journal of
Psychophysiology, 4, 321–330.
MARGRAF, J., BARLOW, D. H., CLARK, D.M., & TELCH, M. J. (1993). Psychological treatment
of panic: Work in progress and outcome, active ingredients, and follow-up. Behaviour
Research and Therapy, 31, 1–8.
MARGRAF, J., & EHLERS, A. (1989). Etiological models of panic: Psychological and cognitive
aspects. In R. Baker (Ed.), Panic disorder: Theory, research and therapy (pp. 205–225).
London: Wiley & Sons.
MARGRAF, J., TAYLOR, C. B., EHLERS, A., ROTH, W. T., & AGRAS, W. S. (1987). Panic attacks
in a natural environment. Journal of Mental and Nervous Disease, 175, 558–565.
MARKS,M. P., BASOGLU, M., ALKUBAISY, T., SENGUN, S., &MARKS, I. M. (1991). Are anxiety
symptoms and catastrophic cognitions directly related? Journal of Anxiety Disorders, 5, 247–
254.
MCNALLY, R. J. (1994). Panic disorder: A critical analysis. New York: Guilford Press.
MCNALLY, R. J., RIEMANN, B. C., LOURO, C. E., LUKACH, B. M., & KIM, E. (1992). Cognitive
processing of emotional information in panic disorder. Behaviour Research and Therapy, 30,
143–149.
MICHELSON, L. (1988). Cognitive, behavioral, and psychophysiological treatments and correlates
of panic. In S. Rachmann & J. D. Maser (Eds.), Panic: Psychological perspectives (pp. 138–
162). Hillsdale, New Jersey: Erlbaum Associates.
OEI, T. P. S., & KHAWAJA, N. G. (1999). Cognitive assessment by the independent normal coders:
Accuracy and usefulness. Manuscript submitted for publication.
OEI, T. P. S., MOYLAN, A., & EVANS, L. (1991). Validity and clinical utility of Fear Questionnaire
for anxiety disorder patients. Psychological Assessment: A Journal of Consulting and
Clinical Psychology, 3, 391–397.
RACHMANN, S. (1984). Agoraphobia: A safety-signal perspective. Behaviour Research and Therapy,
1, 59–70.
RACHMANN, S., LOPATKA, C., & LEVITT, K. (1988). Experimental analyses of panic-II: Panic
patients. Behaviour Research and Therapy, 26, 33–40.
RAPEE, R. M. (1993). Psychological factors in panic disorder. Advances in Behaviour Research
and Therapy, 15, 85–102.
Panic attacks 367
RAPEE, R. M. (1994). Detection of somatic sensations in panic disorder. Behaviour Research and
Therapy, 32, 825–831.
RAPEE, R. M., CRASKE, M. G., & BARLOW, D. H. (1990). Subject-described features of panic
attacks using self-monitoring. Journal of Anxiety Disorders, 4, 171–181.
RAPEE, R. M., CRASKE, M. G., BROWN, T. A., & BARLOW, D. H. (1996). Measurement of
perceived control over anxiety-related events. Behaviour Therapy, 27, 279–293.
RAPEE, R. M., TELFER, L. A., & BARLOW, D. H. (1991). The role of safety cues in mediating
the response to inhalations of CO2 in agoraphobic. Behaviour Research and Therapy, 29, 353–
355.
SALKOVSKIS, P. M. (1988). Phenomenology, assessment, and the cognitive model of panic. In S.
Rachmann & J. D. Maser (Eds.), Panic: Psychological perspectives (pp. 111–136). New York:
Erlbaum Associates.
SANDERSON, W. C., RAPEE, R.M., & BARLOW, D. H. (1988). Panic induction via inhalation of
5.5% of CO2 enriched air: A single subject analysis of psychological and physiological effects.
Behaviour Research and Therapy, 26, 333–335.
SHEAR, M. K., POLAN, J. J., HARSHFIELD, G., PICKERING, T., MANN, J. J., FRANCES, A., &
JAMES, G. (1992). Ambulatory monitoring of blood pressure in heart rate and panic patients.
Journal of Anxiety Disorders, 6, 213–221.
SHEEHAN, D. V., & SHEEHAN, H. M. (1983). The classification of phobic disorders. International
Journal of Psychiatric Medicine, 12, 243–266.
STOLER, L. S., & MCNALLY, R. J. (1991). Cognitive bias in symptomatic and recovered agoraphobics.
Behaviour Research and Therapy, 29, 539–545.
TAYLOR, S. (1985). Anxiety sensitivity: Theoretical perspectives and recent findings. Behaviour
Research and Therapy, 33, 243–258.
TAYLOR, C. B., SHEIKH, J., AGRAS, W. S., ROTH, W. T., MARGRAF, J., EHLERS, A., MADDOCK,
R. J., & GOSSARD, D. (1986). Ambulatory heart rate changes in patients with panic
attacks. American Journal of Psychiatry, 143, 478–482.
TELCH, M. J., BROUILLARD, M., TELCH, C. F., AGRAS, W. S., & TAYLOR, C. B. (1989). Role
of cognitive appraisal in panic-related avoidance. Behaviour Research and Therapy, 27, 373–
383.
TURNIP, G. (1990). Ambulatory clinical psychophysiology: An introduction to techniques and
methodological issues. Journal of Psychopathology, 4, 299–304.
VITALOG CORPORATION (1982). PMS-8 Owners manual. Mountain View, CA: Author.
WESTLING, B. E., & OST, L. B. (1993). Relationship between panic attack symptoms and cognition
in panic disorder patients. Journal of Anxiety Disorders, 7, 181–194.
WHITTAL, M. L., GOETSCH, V. L., & EIFERT, G. H. (1996). Introduction of a dynamic, idiographic
model for identifying panic. Journal of Anxiety Disorders, 10, 129–144.
ZOELLNER, L. A., CRASKE, M. G., & RAPEE, R. M. (1996). Stability of catastrophic cognitions
in panic disorder. Behaviour Research and Therapy, 34, 399–402.

Thursday, August 31, 2006

Anxiety And How To Overcome It By Jason Rickard

Feeling anxious every now and then is normal for everyone. What is not normal, is if it controls your whole life and it affects your choices in a negative way. If this happens, then you should seek professional advice as Anxiety is a condition that needs medical attention.

Anxiety can be healed non-medically but for some advanced cases, either a physician or a psychiatrist may need to be summoned. To free yourself from anxiety, you can try the good old method of easy and correct breathing. If you feel that you are close to succumbing to anxiety, breath as calmly as you possibly can. Do it until you can sense that your breathing and heartbeat becomes normal again.

Making decisions during the early phases of your anxiety can be dangerous. Your decision at that point may not be correct and certainly may not be the wisest. Try clearing your mind. If you are gripped with anxiety, you may act overly impulsive. Try to calm down and free your mind. Whisk away all your worries and try to focus more on the problem at hand.
You have to slow things down as an anxious person will have a tendency is to hurry things up.

Anxiety triggers adrenaline that can make a person have the necessary power to think and work in a single snap. This may affect a person in a positive or negative way but it its best to think before you act.

Do not heed the anxious voice you hear at the back of your head. Most of the time, anxiety arises in the way you perceive things. Anxiety is both felt and thought. Try not to think of things that will make matters worst and exaggerate things all the more.
Solicit the help of your family and friends. When anxiety strikes, that’s the time you needed somebody the most. They should be able to lead you towards the right path. During this time, your own judgment is not that accurate, so you cannot really trust it. Shift your trust to somebody you deeply know.

Anxiety has to be taken out of your senses because it could just lead you to a situation far more dangerous situation than you could have ever imagined. Be mentally sound at all times and there is never a need to be anxious.

Jason Rickard is the owner of Your Favourite Shop - Offering White Noise and Relaxation CDs -

Visit Hapa Health for more articles

Article Source: http://EzineArticles.com/?expert=Jason_Rickard

Tuesday, August 29, 2006

Reduce Your Anxiety By Carolyn Chambers Clark

Anxiety is the number one mental health problem for women (and second only to alcohol and drug abuse for men).

What is anxiety and what causes it?

Anxiety is a technical term for worry, that butterflies in the stomach feeling that can easily escalate. Anxiety comes in many forms---from feeling fearful something terrible is going to happen, to stammering and getting tongue-tied, to stress incontinence, to not wanting to leave the house, to test anxiety, panic attacks, and post traumatic stress reactions.
Anxiety’s a big problem today because the world is so much more stressful than it used to be.

The increased pace of society, increased rate of technological change, absence of traditional value, barrages of inconsistent world views, terrorism threats and more make for a lack of consistency. The result is increased stress and anxiety or worry. There are other factors that can cause anxiety from being born an excitable reactive type of person, to a childhood of being around overly cautious or overly critical people, and to a stressful lifestyle.

How to reduce anxiety

There are anti-anxiety drugs to take, but unfortunately, many of them have negative side effects and they can be addictive. Fortunately, anxiety is a learned behavior, and can be unlearned. Safe and effective self-care measures abound. One of the best ways to begin to reduce your anxiety is to see how you might be perpetuating anxiety.
Major ways you might be adding to your anxiety include: avoiding situations that cause anxiety, talking to yourself in a negative way (“I’ll never be able to deal with this!”), negative beliefs (I can’t trust anyone), denial of your feelings, lack of assertiveness, muscle tension (if you relax your body, your mind will follow), lack of self-nurturing, poor nutrition, stressful lifestyle, and not having a purpose for your life.

Dr. Clark teaches in the Health Services doctoral program at Walden University. Her web site at http://www.carolynchambersclark.com offers free articles and newsletters. This article is extracted with permission from her book, Living Well with Anxiety, What Your Doctor Doesn't Tell You...That You Need To Know (HarperCollins, 2006).
Article Source: http://EzineArticles.com/?expert=Carolyn_Chambers_Clark

Monday, August 28, 2006

Please Leave Your Comment

I am looking for any of you that have tips on dealing with panic attacks or anxiety attacks to leave a comment or two to help myself and the rest of the readers. Please feel free to do so. Thanks
BlogRankings.com