Understanding Psychopathology
Week 1: Nothing as practical as a good theory (3 art.)
A cognitive approach to panic
Summary
A cognitive model of panic is described. Within this model panic attacks are said to
result from the catastrophic misinterpretation of certain bodily sensations. The sensations
which are misinterpreted are mainly those involved in normal anxiety responses (e.g.
palpitations, breathlessness. dizziness etc.) but also include some other sensations. The
catastrophic misinterpretation involves perceiving these sensations as much more
dangerous than they really are (e.g. perceiving palpitations as evidence of an impending
heart attack). A review of the literature indicates that the proposed model is consistent with
the major features of panic. In particular, it is consistent with the nature of the cognitive
disturbance in panic patients, the perceived sequence of events in an attack, the occurrence
of ‘spontaneous’ attacks, the role of hyperventilation in attacks, the effects of sodium lactate
and the literature on psychological and pharmacological treatments. Finally, a series of direct
tests of the model are proposed.
The phenomenology of panic attacks
A panic attack consists of an intense feeling of apprehension or impending doom
which is of sudden onset and which is associated with a wide range of distressing physical
sensations. These sensations include breathlessness, palpitations, chest pain, choking,
dizziness, tingling in the hands and feet, hot and cold flushes, sweating, faintness, trembling
and feelings of unreality. Panic attacks occur in both phobic and non-phobic anxiety
disorders; can follow a clearly identifiably precipitating event or short period of anxious
rumination, or come ‘out of the blue’. The majority of people who suffer frequent panic
attacks fall into the DSM-III categories of panic disorder or agoraphobia with panic. In
order to be diagnosed as suffering from panic disorder an individual must have had at least
three panic attacks in the last 3 weeks and these attacks must not be restricted to
circumscribed phobic situations. In order to be diagnosed as suffering from agoraphobia with
panic, an individual must show marked fear and avoidance of the agoraphobic cluster of
situations and also have a history of panic attacks.
A cognitive model of panic attacks
The success of pharmacological and physiological agents (e.g. lactate, yohimbine,
isoproterenol) at producing panic attacks in panic patients and their less marked effects on
normals have been taken to indicate that certain biochemical changes have a direct panic
inducing effect, and that individuals who are vulnerable to the agents have a biochemical
disorder.
Other recent studies suggest an alternative, psychological, explanation for the panic-
inducing effects of these diverse agents. These studies investigated the effects of two panic-
inducing agents: hyperventilation and CO2 inhalation. It was found that individuals varied
considerably in their affective response to the procedures and there was tentative evidence
that the extent to which individuals experienced the procedures as pleasurable or aversive
was determined by cognitive factors such as expectation and the recall of previous
experiences with the induced sensations.
, Cognitive theory of panic: proposes that panic attacks result from the catastrophic
misinterpretation of certain bodily sensations. The sensations which are misinterpreted are
mainly those which are involved in normal anxiety responses (e.g. palpitations,
breathlessness, dizziness etc.) but also include some other bodily sensations. The
catastrophic misinterpretation involves perceiving these sensations as much more
dangerous than they really are.
Cognitive model of panic attacks:
Trigger stimulus (internal or external) -> perceived threat -> apprehension -> body
sensations -> interpretation of sensations as catastrophic -> perceived threat …(vicious
circle of misinterpretation).
A brief review of research on panic attacks
Having presented a cognitive model of panic, I will now briefly review the literature on
panic to determine the extent to which it is consistent with the proposed model.
1) Ideational components of panic anxiety:
Panic patients were significantly more likely than non-panic patients to have thoughts
concerned with the anticipation of illness, death or loss of control (includes ‘going mad’), but
did not differ from non-panic patients in the frequency of thoughts concerned with general
feelings of being unable to cope or with the anticipation of social embarrassment.
2) Perceived sequence of events in a panic attack:
As the cognitive model specifies that panic attacks result from the catastrophic interpretation
of bodily sensations, one would expect that a bodily sensation would be one of the first
things which individuals notice during an attack (=confirmed by research).
3) The role of hyperventilation in panic attacks:
Hyperventilation plays an important role in the production of panic attacks, but doesn’t per se
produce panic. Hyperventilation only induces panic if the bodily sensations which it induces
are (a) perceived as unpleasant and (b) interpreted in a catastrophic fashion.
4) Lactate-induced panic:
Infusions of sodium lactate are the most frequently used technique for inducing panic attacks
in the laboratory. Between 60-90% of panic patients and 0-20% of normals and non-panic
anxious patients experience an attack when given an i.v. infusion of OS-l.0 M racemic
sodium lactate; lactate infusions are accompanied by a wide range of physiological and
biochemical changes. As some of these changes in bodily function are likely to be perceived,
the cognitive model could account for the panic-inducing effects of lactate by proposing that
individuals who panic do so because they catastrophically interpret the induced sensations.
5) Effects of psychological treatment:
The cognitive-behavioral approach would involve identifying patients’ negative
interpretations of the bodily sensations which they experience in panic attacks, suggesting
alternative non-catastrophic interpretations of the sensations and then helping the patient to
test the validity of these alternative interpretations through discussion and behavioral
experiments. The behavioral approach would capitalize on the observation that fear of
specific stimuli can often be treated by repeated, controlled exposure to those stimuli and
would consist of graded exposure to the body sensations which accompany panic.
6) The role of biological factors in panic:
By specifying that the catastrophic interpretation of certain bodily sensations is a necessary
condition for the production of a panic attack, the cognitive model provides a different
perspective to that offered by biological models of panic and also provides a rationale for
psychological approaches to treatment. However, it would be wrong to assume that
,biological factors have no role to play in panic attacks. In principle, there are at least three
ways in which biological factors might increase an individuals’ vulnerability to the vicious
circle: 1) biological factors may contribute to the triggering of an attack (often triggered by
bodily sensations); 2) biological factors are likely to influence the extent to which a perceived
threat produces an increase in bodily sensations (e.g. reduced efficiency of central
adrenergic α2-autoreceptors); 3) the extent to which bodily sensations which accompany
anxiety are interpreted in a catastrophic fashion will largely be determined by psychological
factors. However, biological factors may also have a role to play in this aspect of the vicious
circle. For example, the hypothesized deficiency in central α2-adrenergic autoreceptors
would mean that individuals would be more likely to experience sudden surges in
sympathetic activity and surges in activity may be more likely to be interpreted in a
catastrophic fashion than gradual build-ups.
7) Effects of pharmacological treatment:
So far, three drugs (propranolol, diazepam and imipramine) have been investigated in
controlled trials which include measures of panic. Propranolol appears to be ineffective,
even when given in doses which are sufficient to effect β-blockade. High doses of diazepam
(up to 30 mg) were effective in reducing panic frequency over a period of 2 weeks but they
failed to provide data on the long-term effectiveness (still doubts). More positive results have
been obtained with imipramine. It is found that imipramine is more effective than an
inert placebo in reducing the frequency of panic attacks in agoraphobics with panic. It can be
that imipramine may not have direct anti-panic effects, but instead simply potentiates the
effects of self-initiated and/or therapist-initiated graded exposure.
EMDR: Eye movements superior to beeps in taxing working memory and
reducing vividness of recollections
Abstract
Posttraumatic stress disorder (PTSD) is effectively treated with eye movement
desensitization and reprocessing (EMDR) with patients making eye movements during
recall of traumatic memories. Many therapists have replaced eye movements with bilateral
beeps, but there are no data on the effects of beeps. Experimental studies suggest that eye
movements may be beneficial because they tax working memory, especially the central
executive component, but the presence/degree of taxation has not been assessed directly.
Using discrimination Reaction Time (RT) tasks, we found that eye movements slow down
RTs to auditory cues (experiment I), but binaural beeps do not slow down RTs to visual cues
(experiment II). In an arguably more sensitive “Random Interval Repetition” task using tactile
stimulation, working memory taxation of beeps and eye movements were directly compared.
RTs slowed down during beeps, but the effects were much stronger for eye movements
(experiment III). The same pattern was observed in a memory experiment with healthy
volunteers (experiment IV): vividness of negative memories was reduced after both beeps
and eye movements, but effects were larger for eye movements. Findings support a working
memory account of EMDR and suggest that effects of beeps on negative memories are
inferior to those of eye movements.
Introduction
, About 20 years ago, eye movement desensitization and reprocessing (EMDR)
was introduced as a treatment for posttraumatic stress disorder (PTSD), and it has met with
considerable skepticism. However, methodologically strict and rigorous meta-analyses of
clinical trials have indicated that EMDR is an effective treatment for PTSD, and is equally
effective as cognitive behavior therapy.
Studies suggest how EMDR affects emotional memories: During recall, emotional
memories become ‘labile’, and their reconsolidation is affected by experiences during recall.
Recalling an episode depends on working memory (WM) resources that are limited. If a
secondary task (e.g. eye movements) is executed during recall that shares this dependence,
fewer resources will be available for recalling an episode and the memory will be
experienced as less vivid and emotional. Interestingly, memories are not only blurred during
the eye movements, but also during recollections immediately after the eye movements
session.
Crucially, the same effects occur if WM is taxed during recall with non-eye-movement
secondary tasks, like listening to a series of non-words (auditory shadowing), drawing a
complex figure, or counting. Tasks that are presumably hardly taxing, like simple finger
tapping, do not have beneficial effects.
WM is typically held to consist of 3 subsystems: 1) The “central executive” (CE)
allocates and divides attention between tasks, selects retrieval strategies, activates
memories, and inhibits distractors. Furthermore, two “slave systems” are postulated: 2) the
visuospatial sketchpad (VSSP), involved in the processing of visuospatial information, and
3) the phonological loop (PL) that processes verbal information.
EMDR therapists have started to use ‘binaural stimulation’ as an alternative to eye
movements. During ‘binaural stimulation’, the patient wears a headphone and hears beeps
alternating Left-Right beeps, typically one per s (the no engagement in active cognitive or
motor operations raises the question whether this stimulation taxes WM, and how this
compares to the effect of for example eye movements).
Experiment I, II, III, IV (results)
I) Eye movements induced a substantial slowing down of RTs to auditory cues, which
implies that eye movements tax the CE.
II) The slowing of RTs to visual cues during arithmetic shows that it taxed the CE.
During binaural stimulation, however, there was no trace of increased RTs compared to no
dual-task. The findings contrast with the data displayed in Fig. 1 (experiment 1). This
suggests that, compared to eye movements, unattended binaural stimulation does not
require CE capacity. If binaural stimulation would have beneficial clinical effects, this would
not be readily explicable in terms of WM theory.
III) The data show that, relative to the no dual-task condition, eye movements
produced a substantial interference with the RIR task, which replicates the effect found in
experiment I. Making eye movements is an active task that requires concentration and motor
operations. Although this does not hold for binaural stimulation, the latter also interfered with
the RIR performance. This contrasts with the absence of an effect of binaural stimulation on
the discrimination task of experiment II. It seems plausible that the task difference (RIR task
vs. discrimination RT task) was responsible for these difference effects. Taken together, the
data from experiment II and III suggest that binaural stimulation requires CE resources, but
the effect is subtle and small compared to eye movements.
IV) With regard to vividness of the memories, the data reflect the pattern found in
experiment III: binaural stimulation taxed the CE a little in experiment III, and had relatively
