Psychopathology- OCD Flashcards
What is the genetic similarity with MZ twins? and how many eggs are there?
share 100% of their genes and are identical twins, one egg that is split into two
what is the gentic similarity for DZ twins? how many eggs are there?
share 50% of their genes and are fraternal (non-identical) twins. 2 eggs
what are concordance rates?
indicates the percentage of twins pairs or other pairs of relatives who exhibit the same disorder
Migel et al (2005)- what were the concordance rates for MZ and DZ twins in terms of OCD? and what does this suggest?
MZ- if one identical twin has OCD there is a 53-87% chance that the other twin will also develop it
DZ- if one non-identical twin has OCD there is a 22-47% the other twin will also develop it
It suggests that OCD is more of a genetics factor rather than an environmental factor
Lewis 1936- what were his findings and conclusions about OCD?
genes are involved in vulnerability for OCD
of his OCD patients, 37% had parents with OCD and 21% had siblings with OCD. suggests it runs in families
Pauls et al (1995)- findings and conclusions?
the risk of OCD was significantly greater in first-degree relatives of OCD subjects as compared to relatives of psychiatrically normal controls
Diathesis stress model- what does this suggest causes OCD?
certain genes leave people more likely to suffer from a mental health disorder but not certain- some environmental stress is necessary to trigger the condition
candidate genes- what do these genes create? what system fo some of them regulate/control?
genes create vulnerability for OCD, some are involved in regulating the serotonin sytem
SERT gene- what is this responsible for?
the transport of serotonin across synapses, causing lower levels of serotonin which is also associated with OCD
COMT gene- what is this responsible for? what is one variation of this gene associated with?
regulating the neurotransmitter dopamine. one variation of the COMT gene results in higher levels of dompamine and this variation is more common in patients with OCD
GE- Nestadt et al (2010) found what?
review of twin studies examining OCD found 68% concordance rates for OCD in MZ twins and 31% concordance rate for DZ twins experience OCD
GE- Counter argue Nestadt et al by saying concordance rates are not 100%
environment in which people are bought up in play an important role in the development of OCD
GE- genes are implicated in OCD- using evidence support this statement
samuels et al (2007) used gene mapping and found OCD sufferers who exhibited compulsive hoarding behaviour linked to chromosome 14 behaviour- shows OCD sufferers have a genetic component to their OCD
GE- what does aetiologically heterogenous mean?
different combinations of genes are implicated in the disorder- what causes it in person A may not cause it in person B
GE- a genetic explanation is unlikely to provide predictive value- what does this mean?
cannot identify a definitive causing factor of the disorder- cant change peoples genetic makeup
GE- limitations of twin studies as a research method?
may overemphasise the role of genes when comparing concordance rates of MZ and Da twins, assume higher concordance rates in mz twins indicates a genetic component for a disorder but mz are more likely to be treated similarly than dz twins- bc identical and share same gender
GE- reductionism -environment risk factors
OCD is associated with trauma, so it is clearly not entirely genetic in origin. Cromer (2007)- over half ocd patient had experienced a traumatic event in their past, was most severe in those who had suffered more than one trauma
GE- what is the diathesis stress model?
the theory that mental and physical disorders develop from a genetic or biological predisposition for that illness (diathesis) combined with stressful conditions that play a precipitating or facilitating
GE- determinism- it is biologically deterministic: predetermined what genes you inherit, therefore may inherit genes for OCD, what does this remove?
removes accountability- ignores environmental factors and free-will
NE- what is serotonin?
a neurotransmitter- a chemical messenger in the brain
NE- what are the 6 AO1 points for neural explanations?
- low levels of serotonin link to OCD
- SERT gene is responsible for transport of serotonin across synapse
- high levels of activity in orbital frontal cortex (“worry circuit”), cannot switch off areas
- ignorning impulses in turn end up as obsessions
- COMT gene, high levels of dopamine which is also linked to OCD
- candidate genes make people more vulnerable
NE- research evidence for the neural explanation of OCD
Zohar et al (1987)- a drug reduces serotonin was given to OCD patients which enhanced their symptoms- suggests low levels of serotonin directly impacts ocd, perhaps disorder does have a biological cause
NE-but not all sufferers respond positively to serotonin enhancing drugs, relapse is high- explain Simpson et al (2004)
up to 45% of patients treated with Clomipramine relapsed within 12 weeks of completing medication, which lessens the support for this neurotransmitter being the sole cause of the disorder- maybe masking symptoms rather than the cause, must be other causes
NE- causation? relate to serotonin levels
unable to establish if OCD is caused by low serotonin, or if having OCD influences your serotonin levels
NE- determinism?
same as genetic explanation- removes accountability, ignores environmental factors and free-will
what are SSRI’s?
selective serotonin reuptake inhibitor- antidepressants that increase levels of serotonin at the synapse
what can you to to SSRI’s to achieve optimum results
combine SSRI’s with CBT or other drugs
what does tricyclic mean?
any class of antidepressant drugs having molecules with three fused rings
what is GABA and what does it do?
GABA is a neurotransmitter that tells neurons in the brain to ‘slow down’ and ‘stop firing’ around 40% of the neurons in the brain respond to GABA
what does SNRI stand for?
serotonin-norepinephrine reuptake inhibitor
how long does drug treatments usually last?
12-15 weeks- dosage can be changed depending on person if not working
The use of drug treatments for OCD in 6 AO1 points:
-general aim to increase or decrease level of neurotransmitter activity at synapse to reduce arousal/anxiety
- SSRIs prevent the reuptake of serotonin In pre-synaptic neuron so activity in synapse is increased
– increased stimulation of the post-synaptic neuron so normalises the worry circuit in the brain
- BZs enhance activity of GABA- quietening influence on brain
– SNRIs work on serotonin and norepinephrine given if SSRIs don’t work
– 12-15 weeks, return to doctor, may increase dosage etc
What is a placebo drug?
a placebo is made to look exactly like a real drug but is made of an inactive substance
DT- describe Soomro et al (2008) experiment
conducted a review of the research examining effectiveness of SSRI’s and found SSRI’s were more effective than placebos in the treatment of ocd, in 17 different trails suggesting that they are a successful treatment for OCD
DT- cost effective?
compared to psychological treatments drugs are cheap and non-disruptive
DT- side effects?
can have side effects; indigestion, blurred vision and loss of sex drive- worse for clomipramine
DT- motivation?
Less motivation than psychological therapies- easy to administer. No commitment to attending sessions. More likely to complete the course!
DT- root of the problem and relapse rates?
drugs fail to address the root cause of the OCD especially if it was a traumatic life experience - a relapse may occur when drugs are not taken as the drugs are not masking the symptoms any more
