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Psychology 1
Psychopathology
OCD
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OCD
A range of
disorders
, characterised by either
obsessions
,
compultions
or both
OCD Examples
Trichotiyomania
: compulsive hair pulling
Hoarding
disorder
Exocoriation
disorder
OCD
REMEMBER!
A
compulsion
is a behaviour
An
obsession
is a compulsion
OCD: Behavioural characteristics
Compulsions
Repetition
They can reduce
anxiety
(short term)
Avoidance
: attempting to reduce
anxiety
by keeping
away
from situations that
trigger
it
OCD: Emotional characteristics
Anxiety
and
distress
,
unpleasant
and
overwhelming
Accompanying
depression
, low
mood
, lack of
enjoyment
Guilt
and
disgust
, at
oneself
or things around
you
OCD: Cognitive characteristics
Obsessive
thoughts, vary
Mediation or
praying
to deal with thoughts
Insight into excessive
anxiety
(aware that their
compulsions
and
obsessions
are
irrational
)
Hypervigilant
Biological approach to explaining
OCD
Caused by faulty biological processes
Two main explanations:
Genetic
and
Neural
Genetic explanations
OCD
is
inherited
from your parents
Heritable: There is a
genetic
component which
increase
an individual's genetic vulnerability to developing OCD
Candidate
genes: Genes which, through
research
, have been implicated in the development of OCD
Polygenic
OCD
is
polygenic
: more than 1 gene has been identified in the onset of OCD
The COMT gene
Regulates the function of dopamine, mutated in individuals with OCD (
Mutation
:
increased dopamine
)
The
SERT gene
Helps to transport
serotonin
, also mutated in individuals with OCD (mutation:
decreased
serotonin)
Aetiologically Heterogeneous
Different combinations of
genes
are implicated in the disorder
Investigation of OCD:
Twin studies
Concordance rate:
Monozygotic
twins share
100
% of DNA whereas dizygotic twins share 50% of DNA
Evaluation: Genetic explanation AO3
Supporting evidence:
Strength
Family/twin studies
Nestadt
et al.
2010
Reviewed previous twin studies
Monozygotic
OCD concordance:
68
%
Dizygotic
OCD concordance:
31
%
There is a
genetic
component to the disorder
Research
support
COUNTER:
Diathesis-stress
model, flaws of using
twin
studies
Diathesis-stress
model
Suggests that people gain a vulnerability towards
OCD
through
genes
but an environmental stressor is also required
Evaluation: Genetic Explanation AO3
Too many candidate genes:
Limitation
Too many genes involved
Psychologists have still not successfully pinned down every gene
Taylor (2013) -> Meta analysis (found around
230
genes implicated in developing
OCD
)
Each genetic variation only increases the risk of
OCD
by a fraction (little
predictive
power)
Neural explanations
Psychological characteristics are determined by behaviour of the nervous system, in particular the
brain
as well as
individual neurons
Neurotransmitters
These are chemical messangers that transmit nerve impluses from one cell across the
synapse
to another cell
Serotonin
Lower levels of serotonin found in
OCD
sufferers
Dopamine
Levels are high in people with
OCD
Serotonin is a mood regulators and dopamine triggers your mind to believe you are going to receive a
reward
->
Dependancy
The Worry circuit
The
orbitofrontal cortex
: tell your body there is a danger
thalamus
: What needs to occur to escape that danger
Caudate nucleus
: bodyguard for thalamus (filter that blocks worry signals)
people with
OCD
have an unfunctional
caudate nucleus
, not able to filter messages
Overactive
worry circuit
The Neural explanation: Evaluations
Research support:
Strength
Antidepressants
which contain serotonin reduce symptons of
OCD
Proves that
lower
levels serotonin triggers
OCD
The Neural explanation: Evaluations
Co-morbidity issues:
Limitation
Yap
et al (2012) -> depression is linked to a lack of
serotonin
Serotonin disrupted because they are
depressed
(not suffering from
OCD
)
The Neural explanation: Evaluations
Correlation vs Causality:
Limitation
Both OCD and neural abnormality may be influenced by a
third
factor
No established
cause
of explanation
Drug therapy
most common
biological therapy
this therapy assumes there is a
chemical
imbalance in the
brain
This can be corrected by
drugs
, which increase or decrease the levels of
neurotransmitters
in the brain
SSRIs
Selective Serotonin
reuptake inhibitors
venting the
reabsorption
of
serotonin
by preventing this
reabsorption
, SSRIs effectively increase its levels in the synapse and thus continue to stimulate the
post synaptic neuron
Examples include
Prozac
and
Paxil
Combining SSRIs with other treatment
Drugs
are often used alongside
CBT
The drugs reduce the sufferers
emotional
symptoms
Patient can engage better/more
effectively
with CBT
Alternative to
SSRIs
SSRI not effective,
dose
can be increased after
3
or 4 months or combined with other drugs
Tricyclics
-> same effect with more
side effects
SNRIs -> increase levels of
serotonin
and
noradrenaline
Evaluations of treating OCD
Effectiveness: Strength
Using
placebo
vs
drugs
, the drug is effective
Soomro
et al. (2009) reviewed
17
studies of the use of SSRIs with OCD patients across different measures
Typically, symptoms
decreased
by
70
%
More
effective
when paired with
CBT
COUNTER
Skapinakis
et al. (2016) did a review
Findings:
cognitive
and
behavioural
techniques were more effective than SSRIs at treating OCD
Reduces
validity
Evaluations of treating OCD
Side effects:
Weakness
Common side effects of
SSRIs
are headaches, nausea, insomnia and
reduced sex drive
Tricyclics: more serious,
hallucinations
,
irregular heartbeat
Such factors may reduce effectiveness and cause people to
stop
taking the
medication
Evaluations of treating OCD
Not a lasting cure:
Limitation
Marina
et al (2001) found that
relapse
is common
Turner
et al. (2008) -> publication is biased towards studies that show a
positive
outcome
More research is funded by
drug
companies
Selective
publication -> lead doctors to make
inappropriate
treatment decisions
Validity
issues