Learning Objectives Week 1: Nothing so Practical as a good Theory
1. Explain the critical features of “good” theories and why theories can be best seen
as disposables (are not forever)
Making sense of loose facts and observations: Understanding the origin of
psychopathology (predict who and under what type of conditions -prevention);
Understanding factors involved in the persistence of psychopathology (predict
for whom and under what conditions symptoms will or will not persist -
interventions)
Guides further inquiries
Criteria / characteristics of a “good” theory? NECESSARY FEATURES:
External criteria:
Is consistent with known facts
Testable / falsifiable
Internal criteria:
Internally consistent (no conflicting predictions)
As simple as possible (parsimony)
The fewer the number of assumptions the better (“Occam’s razor”)
Many different theories in psychopathology:
Complementary (additional): social anxiety disorder - Genetic theory
(Behavioral Inhibition); Developmental psychological theory; Associative
learning theory
“Convertible”: gen x development x learning experiences
Incompatible: only one can be the best!
The case of Panic Disorder: explained ahead-→ two theories:
1. Psychiatric ‘theory’: they increase CO2 in a rat brain → hyperarousal Locus
Coeruleus (LC) → panic symptoms? – Panic Disorder is caused by a
neurophysiological defect that renders people hypersensitive for increase in
CO2 – levels. How can this theory be tested? – If A leads to B –
Induce/heighten A and examine if B occurs/increases. **Experimental lactate
studio: results suggest that panic disorder is a biological disease. (lactate goes
up, CO2 levels go up). effective intervention via clonidine (LC inhibition)
2. Hyperventilation theory of PD: hyperventilation symptoms are kinda the
same. Lowering CO2 --> Panic Attack, Thus PA elicited by hyperventilation?
(A leads to B, therefore A?). Therefore PA due to hyperventilation? Next step:
Is indeed in naturalistic contexts PA accompanied by reduction in CO2 level?
effective “bag” intervention.
Both predictive value, but: 1. Incompatible 2. No optimal summary of available data.
,Theories are disposables – no theory has eternal value. Basically because they
can be incompatible – as this PD example – and change over time all the time
because both kinda make sense – As soon there is a better theory available ->
exchange ->Theory that can cope with the findings that … →panic disorder →Both
increase and reduction of CO2 -> PA + Selectivity (why PA in PD’s but not in
controls) Both “bag” and clonidine work…
2. Explain why it is critical/important for therapists to know how and why their
interventions work
No theory? Rash empiricism! – (eg., Electro convulsion therapy
(ECT)/“Antidepressive” medication).
Theory yes, but defective. – ted talk Jim van Os – explains that madness has
been misrepresented as a 'devastating genetic brain disease', referred to as
'schizophrenia', that is said to leave the person 'completely disabled'. In fact,
modern science has discovered that subtle states of madness - psychosis -
are quite common in the general population, and linked to social and
emotional factors. Madness, therefore, is about human variation. We can all
connect to it, using novel mobile apps that track thoughts and experience in
daily life.
Optimal interventions are techniques derived from optimal theories. Without (optimal)
theories, therapy is Hocus Pokus. Therefore…. Beware of pragmatists who don’t
want to know why their interventions work, Beware of people who hold on to theories
that cannot stand the test of empirical scrutiny.
3. Describe and explain the arguments that have been raised against EMDR.
EMDR (eye movement desensitization and reprocessing). EMDR seems to
therapeutically exploit the fact that memories become labile during recall and that
reconsolidation is affected by the nature of the recall. Recalling an episode depends
on working memory (WM) resources that are limited. If a secondary task 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. Eye movements are held to serve as such a ‘secondary’ task that
taxes WM. WM rightly predicts that individuals who are bad at multitasking derive
more benefit from eye movements. Whereas EMDR has been advocated as
treatment for past trauma, the WM theory implies that negative images about future
events (‘flashforwards’) can be treated as well.
The WM/CE (central executive –part of the WM) account of the eye movements
component of EMDR implies that therapeutic changes in memories are due to the
degree of CE taxation during recall – so can it be auditive or tactil as well? Other
secondary tasks and how they affect – Whats best – experiments.
,4. Explain the contribution of Marcel van den Hout’s experiments for our
understanding of how EMDR might work.
Eye movements and beeps (auditory stimuli) were directly compared on the
degree to which they taxed the CE.
1 st experiment: The aim of the first experiment was to test whether eye
movements tax the CE, measured by the slowing down of RTs to auditory
cues. this is the first experiment that directly shows that the CE is taxed during
eye movements.
2 nd experiment: The question whether, and to what degree, binaural
stimulation taxes the CE. To allow for conclusions about CE taxing vs.
loading the phonological loop, the auditive stimulation in the RT task could not
be used here. It was replaced by a visual RT discrimination task.
3 rd experiment: experiment III, an RIR (a Random Interval Repetition) task
instead of a stimulus discrimination RT task was used. We wanted to directly
compare the taxing effects of beeps and eye movements. RTs were
recorded under three conditions: no dual-task, binaural stimulation, and eye
movements. 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.
4 th experiment: WM theory suggests that the RT tasks used in experiments I-
III tap the same process that is responsible for the beneficial effects of EMDR
and related interventions. It follows from WM theory that the effects of eye
movements on memory are larger than those of binaural stimulation, while the
binaural stimulation should have no or little effect. Testing these predictions
was the aim of experiment IV. III, and had relatively small effects on vividness
in experiment IV. Eye movements taxed the CE considerably more than
binaural stimulation, and had substantially larger effects on vividness
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 auditive 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. Hence, we predicted that, in terms of reduced
vividness and emotionality of negative memories, eye movements would outperform
binaural stimulation, while the latter would have no or small effects. Eye movements
had no stronger effects than the other conditions on emotionality. Findings support
, a working memory account of EMDR and suggest that effects of beeps on
negative memories are inferior to those of eye movements.
5. Describe Clark’s cognitive model of panic disorder and explain how the various
components of the model have been tested.
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). 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 (anxiety
disorders which are characterized by panic attacks respond to imipramine while
anxiety disorders which are not characterized by panic attacks fail to respond to
imipramine. This ‘pharmacological dissociation’ led Klein (1981) to propose that panic
anxiety is qualitatively different from non-panic anxiety).
They made a study investigating 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. This suggests that
the various pharmacological and physiological agents which have been shown to
promote panic in patients may not have direct panic-inducing effects but instead
may provoke panic only if the bodily sensations which they induce are interpreted in
a particular fashion.
how the components of the model have been tested:
Ideational components of panic anxiety) – the subjects that had panic attacks
thought about the possibilities of being dead and the ones that didn’t just
thought about that fear. the ideational content of those experiencing panic
attacks can be understood as a reaction to the somatic symptoms.
Perceived sequence of events in a panic attack : patients frequently report
that the first thing they notice during an episode of anxiety is a physical
feeling. In addition, Hibbert found that this sequence of events was reported
significantly more often by patients with panic attacks than by patients without
panic attacks (53 and O%, respectively)
The role of hyperventilation in panic attacks: hyperventilation only induces
panic if the bodily sensations which it induces are perceived as unpleasant
and interpreted in a catastrophic fashion.
