EXPLANATIONS OF ANXIETY DISORDERS

1
EXPLANATIONS OF ANXIETY DISORDERS

• GAD PD
• a) Biological explanations
• Genetics-
• Balon et al (1989) 40 first degree relatives of
  a person with PD have the disorder themselves.
• Slater Shields (1969) twin study, 49 MZ
  concordance rate, 4 DZ concordance rate.
• BUT-
• Cant be sure that disorder is inherited -
  could be due to result of social (observational)
  learning from within the family environment.
• May not be the actual disorder that is being
  inherited may inherit a predisposition towards
  anxiety (a highly reactive autonomic nervous
  system). Supported by Eysenck (1967) - people
  with GAD demonstrate autonomic lability,
  i.e.more easily aroused by environmental stimuli.

2

• Direct biological causes-
• Papp et al (1993) PD triggered by a dysfunction
  in the receptors that monitor oxygen levels in
  the blood. Incorrectly inform brain that oxygen
  levels are low fear of suffocation
  hyperventilation.
• George Ballenger (1992) - locus coeruleus , in
  brain, is over sensitive to anything that is
  anxiogenic (anxiety inducing). This explains why,
  when people with PD are given sodium lactate
  during a biological challenge test, they often
  have a panic attack.
• (Lactic acid is a by product of muscle activity
  where oxygen is used up by the muscles and blood
  CO2 levels are increased. Lactic acid may also
  decrease the levels of serotonin and hence its
  calming effects).
• An oversensitive locus coeruleus would respond to
  these changes. Further evidence comes from the
  fact that anti-anxiety drugs block lactate
  effects.

3

• BUT-
• Sue et al (1994) said that the results of
  biological challenge tests may be affected by
  expectations.
• E.g. - people are told they will experience
  pleasant sensations report less anxiety than
  those told they will experience unpleasant
  sensations.
• This suggests that even if biological factors do
  play a part in anxiety disorders it is likely
  that they can be modified by cognitive factors.

4

• b) Cognitive explanations
• Internal triggers
• Belfer Glass (1992) certain
  thoughts/cognitions can act as triggers for PD.
  
• Clark (1993) main trigger is an abnormality in
  thinking
• (see next slide for diagram)
• As with PD , GAD is thought to be an over
  vigilance to physiological changes i.e. faulty
  interpretations of these changes.
• Pauli et al (1991) 28 Ps and 20 controls
  monitored heart rate fro 24 hours. Both noticed
  changes in HR.
• BUT Ps with PD showed increased HR following
  changes and feelings of anxiety not so for
  controls.
• However - some people do not report being aware
  of particular thoughts during a panic attack.

5

• e.g. Internal or external stressor
• Increased physiological activity
• Noticed and interpreted in catastrophic way
• (I am having a heart attack) abnormal
  thinking
• Causes increase in physiological activity
• Feedback loop
• Confirms catastrophic thoughts

6

• c) Psychodynamic explanations
• Unacceptable unconscious conflicts blocked by the
  ego. Powerful enough to produce constant tension
  and apprehension but unconscious, therefore
  person is not aware of the source of the anxiety.
  
• Defences used to block the conflicts include
  repression. Occasionally the defences are
  weakened and this can result in Panic disorder
  (panic attacks).
• Klein Rabkin (1981) result of unresolved
  separation anxiety. When a threat of separation
  is perceived or actually occurs in later life,
  this may result in PD.
• BUT-
• problems related to psychodynamic theory and the
  work of Freud also relate to this explanation.

7

• d) Behavioural explanations.
• Learning theory can explain the development of
  anticipatory anxiety. According to
  Clark(1993), external (environmental) cues can be
  associated with anxiety arousing situations.
• When these situations are avoided there is a
  reduction in the fear component of the disorder,
  thus the association between the cues and anxiety
  is reinforced giving rise to anticipatory
  anxiety.
• BUT-
• Sue et al (1994) point out that learning theory
  is not sufficient to explain all cases of GAD
  PD. In fact, it is thought that classical
  conditioning increases the severity of PD rather
  than causes it.

8

• Draw up a spider diagram summarising the four
  different explanations for GAD and PD.
• Biological
• Genetics Direct causes
• Cognitive Psychodynamic
• Behavioural

GAD PD
9

• Class exercise identify a phobia!
• Do the exercise on the handout in pairs. Prize
  for the pair with the most correct!!

10

• Alliumphobia- Fear of garlic.
• Arachibutyrophobia- Fear of peanut butter
  sticking to the roof of the mouth.
• Chronophobia- Fear of time.
• Consecotaleophobia- Fear of chopsticks.
• Euphobia- Fear of hearing good news.
• Geniophobia- Fear of chins.
• Genuphobia- Fear of knees.
• Ithyphallophobia- Fear of seeing, thinking about
  or having an erect penis.

11

• Hippopotomonstrosesquippedaliophobia- Fear of
  long words.
• Myxophobia- Fear of slime. (Blennophobia)
• Nostophobia- Fear of returning home.
• Optophobia- Fear of opening one's eyes.
• Phobophobia- Fear of phobias.
• Phronemophobia- Fear of thinking.
• Pteronophobia- Fear of being tickled by feathers.
• Stasibasiphobia or Stasiphobia- Fear of standing
  or walking. (Ambulophobia)
• Zemmiphobia- Fear of the great mole rat.

12
PHOBIAS

• a) Biological Explanations
• Genetics- Can phobias be inherited?
• Harris et al (1983) if a first degree relative
  has agoraphobia, the chance of developing
  agoraphobia is twice that of a person with no
  agoraphobia in a first degree relative.
• Solyam et al (1974) 45 of agoraphobia sufferers
  had another family member with agoraphobia, (19
  for non-agoraphobic controls).
• Even if agoraphobia was not in the family, 31
  of agoraphobics had a mother with another kind of
  phobia, 55 had a mother and 24 had fathers with
  other anxiety disorders (e.g. PD).
• Slater Shields(1969), 41 concordance rates
  among MZ twins, 4 among DZ twins

13
Explaining phobias.Supplementary notes taken
from Cardwell, M. Psychology for A level.

• Two basic explanations
• genetic /neurobiological
• social /psychological.
• For genetic /neurobiological explanations
  research focuses on two areas of study-
• Family studies and twin studies.
• Family studies
• look at recurrence of disorder between /within
  generations.
• Major problem rely on interviews with family of
  sufferer so accounts are retrospective and
  subjective.
• Also, dont actually prove a genetic link being
  brought up by someone with a phobia may teach a
  child to be phobic.

14

• Twin studies if rates of concordance (both
  twins affected) are higher with MZ rather than DZ
  twins then this is strong evidence for the
  predominant role of genetic rather than
  environmental factors.
• Consider - anxiety has an evolutionary basis
  fear is actually quite useful keeps us out of
  trouble! It is only fear out of all proportion to
  the actual situation that is classified as an
  anxiety disorder. Likely then that there will be
  a genetic component to phobias.

15
(No Transcript)
16

• What have the studies found?
• Family studies agoraphobia.
• Noyes et al (1986) - rates of agoraphobia and
  PD in first degree relatives.
• Fyer et al (1990) - of 49 Ps with specific
  phobias, 31 of first degree relatives also had
  phobias but only two had same type.
• Twin studies.
• Torgerson (1983) 31 concordance of PD and
  agoraphobia in 13 MZ pairs.
• 0 concordance in 16 DZ pairs.
• Overall difficult to interpret results one way
  or the other. Twin studies indicate genetic
  predisposition but very few studies done.
  Overall, little support for genetic transmission
  of anxiety disorders.

17
Neurological theories.

• Look at functioning of the ANS.
• Phobics tend to maintain high levels of arousal
• increased sensitivity to environment.
• Clearly there is an interaction between arousal
  level and environment but which came first?
• Are high arousal levels a result of, or the cause
  of phobias?
• Asso Beech (1975) - arousal makes it easier to
  acquire a conditioned response ? high arousal
  causes phobias.
• Lader Matthews (1968) high arousal more
  significant in agoraphobia and social phobia
  conditioning more significant in specific phobias.

18
Behavioural explanations.

• See handout for conditioning theories.
• Some phobias are more common than others are we
  biologically prepared to be frightened of
  certain things? (Seligmans preparedness theory)
• see handout for supporting research
• Also, Garcia Koelling rats easily conditioned
  to avoid shocks and toxic liquids, not so easily
  conditioned to avoid flashing lights.

You dont scare me with no flashing lights
dude!
19

• Common phobias e.g. heights, blood, dark, snakes
  etc do make a certain amount of sense all
  reasonable things to be wary of in survival
  terms!
• But these could still be learnt rather than
  biologically programmed in. see handout

20
Cognitive explanations.

• Extends the behavioural view into thinking.
• Ellis (1962) and Beck (1963)
• Irrational beliefs catastrophic thinking
  phobias
• E.g. Feel hemmed in in a lift
• I might suffocate
• Fear of lifts
• Fear of similar confined situations
• Claustrophobia.

21

• it is not only initial exposure to a fear
  producing situation but persons irrational
  thoughts about future situations which phobia.
• Major life events long regarded as a major
  factor in anxiety disorders.
• Holmes Rahe (1967) demonstrated cumulative
  effects of major life events.
• Kobasa (1979) pointed out the effects on minor
  everyday hassles.
• Kleiner Marshall (1987) 84 of agoraphobics
  had family problems prior to first panic attack.
• But, some people go through the most disastrous
  life situations and dont develop anxiety
  disorders why not?

22

• Diathesis stress model.
• Diatheses vulnerability factor an
  individuals stress tolerance level.
• How is this set?
• May be genetic (lability of the ANS) or may be
  due to early experiences?
• The model proposes an interaction between
  individual tolerance levels and degree of
  environmental stress.
• This interaction produces a negative correlation.

23

• Degree high
• of ill
• environmental
• stress medium
• well
• low
• low(a) medium(b) high(c)
• vulnerability

24

• Person (a) low vulnerability can cope with
  lots of
• stress without developing anxiety disorder. At
  high levels of environmental stress they are
  still OK but (b) and (c) have gone over the
  edge into illness.
• Person (b) medium vulnerability can cope with
  
• moderate stress but will become ill in situations
  where (a) is
• coping but stay well in situations where (c)
  becomes ill.
• Person (c) high vulnerability can only cope
  with low
• degree of environmental stress quickly pushed
  over the edge into illness and develops an
  anxiety disorder in situations where (a) and (b)
  are coping.

25

• Points to bear in mind stress is cumulative
  may be one small stressor which breaks the
  camels back!
• May cope with one serious life event better than
  lots of more minor hassles.
• Many other factors (e.g. support from family and
  friends) will influence coping. At very difficult
  times people rally round to help this may well
  not happen when there are lots of small problems
  even though the cumulative effect may be worse!
• (See notes on stress for more info)

26

• Class exercise
• Fill out the sheet given to you as honestly as
  possible do NOT discuss this with your
  neighbour it important we get your results
  only!
• We will then look at the results for the class as
  a whole after the following 3 slides.

27
(Continuation of notes from previous handout)

• Evolutionary explanation
• Basic fears have an evolutionary benefit -
  phobias are an excessive expression of this
  normal response.
• The evolutionary explanation a combination of
  the biological and the behaviourists
  (conditioning theory) approach.
• Seligman (1971) suggests a preparedness we
  are genetically prepared to fear things that were
  a source of danger in our evolutionary past.
• Based on three principles
• 1. Certain stimuli (that is, related to survival)
  condition more easily than others
• 2. The onset of the phobia is sudden
• 3. The phobia is resistant to extinction..

28

• Research evidence-
• Nesse Williams (1996) monkeys, shown video of
  another monkey making an alarm call in response
  to a snake the monkeys subsequently showed fear
  of snakes. The same fear could not be produced in
  response to flowers although the same procedure
  was followed.
• Hugdahl Ohman (1977) and Menzies(1995) have
  also shown that in laboratory conditions, people
  are more prepared to acquire fear reactions to
  some stimuli (such as snakes) than others.

29

• BUT -
• Studies do not show biological preparedness -
  many people react negatively towards certain
  animals so learning experiences rather than
  genetic factors may prepare us to fear these
  stimuli.
• Cannot account for all phobias e.g. social
  phobias no evolutionary benefit to not eating
  in public or meeting new people.
• Why do only some people develop phobias if
  there was an evolutionary basis then most people
  would have similar responses.
• Can not explain gender differences in phobias
• Often the phobia of spiders or snakes is not the
  fear of harm but of having a panic attack this
  doesnt fit in with this theory.

30

• Draw up a scattergram of the results we collected
  from the class exercise.
• What do they show?
• Do they support or refute the preparedness
  hypothesis?

31

• b) Cognitive explanations
• There is no specific cognitive explanation of
  phobias. However the general cognitive approach
  to all abnormal behaviour can be applied to
  phobias. A person with a phobia is seen to have
  unrealistic/irrational thoughts about the object
  /their response to the feared object.
• BUT -
• Most phobics are aware that their fear is
  irrational, therefore this is not a good
  explanation.

32
c) Psychodynamic explanations

• Phobias surface expression of a much deeper
  conflict between the id, ego and super ego - has
  origins in childhood.
• expressions of unacceptable wishes, fears and
  fantasies, displaced from their original,
  internal source onto some external object or
  situation that can be easily avoided.
• The famous case study - Little Hans phobia of
  horses kept him from going out of the house.
  Look back at AS notes textbook for details.

33

• BUT -
• Behaviourists challenged Freuds interpretation
  of the case of little Hans, - phobia may have
  been classically conditioned after Hans witnessed
  a terrible accident involving a horse pulling a
  cart at speed.
• There are many other criticisms relating to the
  work of Freud that throw doubts onto this
  explanation of phobias

34
d) Behaviourist explanations(Look back at your
AS notes on this approach)

• According to Wolpe (1969) Classical conditioning
  can be used to explain the development of all
  phobias.
• Support for this theory
• 1. Case of little Albert (Watson Raynor, 1920)
• 2. Some phobics can identify the pairing of a
  frightening experience with a neutral stimulus
  (which has now become the feared object) as the
  onset of their phobia.
• 3. The resilient nature of some phobias (their
  resistance to extinction) can also be explained
  in conditioning terms.
• 4. The success of behaviourist therapies in
  treating phobias.

35

• Mowrers (1947) two-process (or two-factor)
  theory - phobias acquired through classical
  conditioning (factor 1)

UCS
UCR
Neutral stimulus
UCS
UCR

CR
36

• maintained through operant conditioning (factor
  2).

R1
Not reinforced
S
R2
Reinforced
R3
Not reinforced
So Response 2 is the one that will be repeated
when the Stimulus occurs again
If Response 2 is run away and the Stimulus is
the feared object then the avoidance of the
stimulus will be reinforced
37

• The avoidance of the feared object/situation
  reduces the anxiety associated with the
  object/situation, this is negatively reinforcing.
  
• Rachman (1984) agrees with Mowrer a bit, but
  suggests that the avoidance of the
  object/situation bring feelings of safety, which
  is positively reinforcing.

38

• BUT-
• Some phobics can not recall any traumatic event
  which is linked to the onset of their phobia.
• Not all traumatic experiences lead to the
  development of a phobia.
• Can not explain why some stimuli are more easily
  made a conditioned stimulus than others this is
  explained by the preparedness theory.
• Draw up a summary diagram like the one for GAD
  and PD

39
OBSESSIVE-COMPULSIVE DISORDER

• Biological explanations
• Genetic
• Is there a genetic basis to OCD?
• Support
• Commings Commings (1987) people with OCD
  often have a first degree relative with an
  anxiety disorder.
• BUT-
• Shafran (1994) found that in over half the
  families of an OCD sufferer, members become
  actively involved in the rituals indicates the
  potential influence of learning - child with an
  OCD parent might see such rituals as the norm.

40

• Direct Biological causes
• There is a suggestion that OCD sufferers may have
  different patterns of brain activity to people
  who do not have OCD, specifically, increased
  metabolic activity in the frontal lobe of the
  left hemisphere.
• Support
• McGuire et al (1994) when drugs which reduce
  the activity of the frontal lobe are given to OCD
  sufferers, the symptoms of OCD decline.
• BUT -
• it is not clear whether this activity is the
  cause of OCD, the result of OCD or just a
  correlate with OCD.
• Fluoxetine (SSRI Specific serotonin re-uptake
  inhibitor which increases serotonin level in
  brain) can treat OCD. So is OCD due to serotonin
  deficiency? Studies are small but some sound
  evidence supports this idea.

41
See supplementary handout
Cingulate Cortex
C
A
B
Caudate Nucleus
Orbital Frontal Cortex
42

• b) Psychodynamic explanations
• According to psychodynamic theory, obsessions are
  defence mechanisms - occupy mind and displace
  more threatening thoughts.
• Laughlin (1967) - intrusion of obsessive thoughts
  prevent arousal of anxiety - act as a more
  tolerable substitute for a subjectively less
  acceptable thought or impulse.
• BUT-
• It is difficult to see what a thought of killing
  someone could be a more tolerable substitute for.
• Usual problems associated with psychodynamic
  approach apply to this explanation.

43

• Behaviourist explanations
• Anxiety reduction hypothesis explains how OCD
• is maintained - OCD is seen as a way of
• reducing anxiety.
• Rachmnan Hodgson (1980) compulsion
• provides a relief from the anxiety ( a type of
• negative reinforcement therefore more
• likely to be repeated).
• Relief is only temporary, when the anxiety
• builds up again the compulsion is repeated.
• The compulsions (as well avoidance and trying to
• suppress the obsession) increase the obsession.
  
• Sufferer is locked into a vicious obsession-
• compulsion cycle (Shafran, 1999).

44

• The superstition hypothesis
• Explains the development of OCD.
• Skinner(1948) - superstition develops as a
  result of chance associations between a behaviour
  and a reinforcer.
• He gave pigeons food at regular intervals
  irrespective of their behaviour. After a while
  the pigeons displayed individual peculiar
  movements, most likely because these were the
  movements they happened to be making at the time
  when the food was given.
• The superstition hypothesis can account for many
  compulsive rituals (OLeary Wilson, 1975). E.g.
  superstitious rituals performed by sports people
  before their event may occur because in the
  past they have been associated with success.

45

• BUT-
• This hypothesis may account for the development
  of some compulsive behaviours, it can not account
  for the development of intrusive thoughts.
• Cognitive-behavioural explanation
• Cognitive-behaviourists e.g.Beck(1976) take a
  combined approach to explaining OCD. Every one
  has obsessive thoughts from time to time.
  Sometimes these thoughts develop into
  obsessions when a persons thinking regarding
  those thoughts becomes faulty in some way.

46

• Perceived responsibility for harm- normal
  obsessions become abnormal when people
  interpret the occurrence and content of unwanted
  intrusive thoughts as indicating that they may be
  (have been or come to be) responsible for harm
  (i.e. a thought about harming something/someone)
  or for its prevention (i.e. preventing the harm
  being done).
• Support for this theory comes from Lopatka
  Rachman (1995).

47

• Thought-Action fusion (TAF) Rachman proposed
  the TAF theory of OCD.
• TAF involves two components-
• Likelihood TAF belief that thinking about an
  unacceptable or disturbing event makes it more
  likely to actually happen
• Moral TAF interpreting the obsessive thoughts
  and forbidden actions as morally equivalent. i.e.
  the thought is seen as bad as bad as the event
  (Only a wicked mother would have thoughts about
  harming her child).
• In both of these theories the compulsive
  behaviour becomes an attempt to deal with the
  interpretation of these thoughts. When the event
  is prevented from happening by the compulsion
  this provides a kind of negative reinforcement of
  the obsession.
• (Hence Cognitive-behavioural approach).

48

• Read through the other explanations for OCD on
  the supplementary handout.
• Do a summary diagram, as before of the
  biological, psychodynamic, behaviourist, and
  cognitive explanations of obsessive compulsive
  disorder.

49
Post Traumatic Stress Disorder

• All sufferers have experienced a profoundly
  traumatising event or events events may well be
  very different.
• But what makes one person develop PTSD while
  another who witnessed the same event does not
  develop it?
• a) Biological explanations
• Genetics-
• Genetic element in vulnerability to developing
  PTSD? Possibly.
• True et al (1993) USA Vietnam veterans- MZ
  twins had higher concordance rates for PTSD than
  DZ twins.
• But genetic component had a higher influence on
  higher levels of arousal anxiety ,but not
  re-experiencing the event among those with
  PTSD.
• i.e. the genetic link seems to be related to
  certain aspects of PTSD.

50

• Direct Biological Causes-
• Possible that sometimes the traumatic event
  causes a physical change in the individuals
  brain/brain chemistry.
• Evidence to suggest that this may be true-
• Noradrenergic burnout (van der Kolk et
  al,1984) the trauma leads to damage in the
  brain linked to the neurotransmitter
  noradrenaline.
• Result individual is more prone after the event
  to be startled and is thus less resilient to
  minor stress PTSD is an over reaction to every
  day events.
• Traumatic event large amount of adrenaline
  released.
• Adrenaline part of the fight or flight response
  involved in laying down emotional memories.
• The large amount of adrenaline released strong
  memories being laid down, thus making them easier
  to retrieve at any trigger.

51

• Support for this theory-
• Participants given beta-blockers suppresses the
  release of adrenaline, have a poorer recall of
  an emotional film than a control group who were
  not given beta-blockers.
• Overproduction of the bodys endorphins,
  released in response to pain, could produce
  feelings of numbness associated with PTSD.
• Trauma, the amygdala, part of the limbic system
  in the brain involved in emotion and arousal may
  be permanently in the on position.
• E.g. Startled by something amygdala switched
  on we become aroused.
• Recognise that what startled us is not dangerous
• amygdala turns off arousal levels decrease.
• For PTSD sufferer, may be that amygdala can not
  switch itself off.

52

• However, Molloy et al (1983) - USA Vietnam war
  veterans only showed excessive arousal in
  response to war related stimuli. Suggests that
  amygdala is probably not permanently in the on
  position.
• Alpha-2-receptors brain cell structures that
  slow down the release of adrenaline into the
  brain may be damaged as a result of the trauma.
• Evidence - PTSD sufferers have 40 fewer
  alpha-2-receptors than non-sufferers. (cited in
  Brewer, 2000).

53

• Hippocampus (a structure in the brain which is
  linked to memory) may be damaged during moments
  of overwhelming terror.
• Butler (1996) - three studies using MRI scans
• show significant reductions in the size of the
• hippocampus of traumatised people.
• Those with the smallest hippocampus displayed the
  most intense PTSD symptoms.
• Hippocampal damage may be caused by over
  production of cortisol due to prolonged stress.
• The locus coeruleus in the brain may be
  involved in PTSD Krystal et al (1989).

54

• BUT -
• Problems- some studies are correlational, thus
  interpretation of the findings must be done with
  care.
• How can we be sure that the changes in the brain
  are the result of the trauma ?
• Could they have been there before the trauma?
• Even if these changes are a result of the trauma,
  we still do not know why some individuals develop
  PTSD and some dont.
• (The Diathesis-stress model may give some insight
  into this).

55

• Diathesis-stress model - PTSD breakdown of the
  normal stress response (Butler, 1966) -repeated
  adrenalin rushes seems to progressively sensitise
  the brain chemistry, provoking even greater
  floods of adrenalin at lower thresholds.
• USA Vietnam war veterans who had been abused
  physically or sexually as children more likely to
  develop PTSD, than those without such a history.
• (BUT correlation evidence need to take care).
• USA Vietnam war veterans and a control group
  given identical injection of a drug that
  stimulates the secretion of noradrenalin. Control
  group reported a little heart pounding, whereas 9
  out of the 15 war veterans had panic attacks and
  6 had full blown flash-backs.

56

• Bremner et al (1993) - PTSD was more common in
  individuals with childhood experiences of
  poverty, parental separation, abuse or
  catastrophes.
• Psychodynamic explanations
• PTSD explained in terms of the trauma
  reactivating previously unresolved conflicts
  hidden in the unconscious mind.
• Symptoms of PTSD e.g. memories of the trauma etc.
  serve as defence mechanisms against the emergence
  of the unresolved childhood conflict into the
  conscious.
• BUT-
• Usual problems linked to Freudian theory. Also
  cant explain biological findings, behaviourist
  objections.

57

• Behaviourist explanations
• All PTSD sufferers have experienced a traumatic
  event. Classical conditioning can account for the
  learning of the responses to stimuli associated
  with the event.
• Hunt (1995) - some WWII veterans claimed that
  the 1994 anniversary ceremonies of the Normandy
  landings revived specific memories that were
  particularly distressing.
• BUT- not everyone who experiences the trauma
  develops PTSD, also, different traumatic events
  are more or less likely to lead to PTSD, so
  classical conditioning can not be the only
  explanation.
• Cognitive factors may be involved as well as the
  recovery environment (such as family support
  groups).

58

• Cognitive explanations
• Cognitive appraisal of the event is an important
  factor in whether or not PTSD will develop as a
  result of the trauma.
• Paton (1992) working with relief workers in
  Lockerbie Dixon et al (1993) Herald of Free
  Enterprise peripheral victims, suggested that
  the difference between what they expected to
  find at the scene of the event, and what they
  actually found was the source of stress
• BUT - what about biological findings
  behaviourists explanations?