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OCD:Psychopathology - Coggle Diagram
OCD:Psychopathology
Diathesis stress model:
Individuals may have a genetic vulnerability to a disorder but it is not set in stone
Individual may only develop the disorder if there is some environmental trigger
Diathesis = genes (how close they are to the edge)
Stress = life event (how hard you are pushed)
Explaining OCD:
Behavioural characteristics:
Behavioural component = compulsive behaviour
Compulsions are repetitive and reduce anxiety
Avoidance (can interfere with everyday life)
Emotional characteristics:
Anxiety
Guilt/disgust
Accompanying depression
Cognitive characteristics:
Approach concerned with the two ways in which people process information
Obsessional and catastrophic thoughts
Cognitive coping strategies
Hypervigilance
The Biological Approach to explaining OCD:
Neutral Explanations:
The serotonin hypothesis:
Serotonin is a transmitter
Serotonin is known to regulate mood
Low levels of brain serotonin have been proposed as the cause of OCD = the serotonin hypothesis
How do we know this?
SSRI increase serotonin levels
SSRI drugs reduce OCD
SSRI = selective serotonin reuptake inhibitors
Evaluation of the serotonin hypothesis:
Could just be co-morbidity with depression
Too simplistic - drugs that block dopamine help SSRIs work better
1/3 of patients don't respond to SSRIs
Cause/ effect is hard to establish (treatment aetiology fallacy)
Psychological therapies can be effective
Brain neuropathology:
Frontal lobe
Part of the brain responsible for decision making and logical reasoning - overactive functioning linked to OCD
Parahippocampal gyrus
Left part (associated with processing unpleasant emotions) is overactive in OCD - account for emotional characteristics
Evaluation of brain neuropathology:
S - Overactive areas tend to become normal when patients receive effective treatment
W - Is brain activity a cause or effect of OCD
W - No overactive brain area plays a role in all patients
Genetic Explanations:
Studies that support a genetic link to OCD:
Lewis (1939) - observed from his patients that 37% had parents with OCD + 21% had siblings with OCD
Nestadt et al (2010) - found a 68% concordance rate for MZ twins and 31% for DZ twins
Candidate gene - SERT gene is mutated in OCD (gene that creates vulnerability)
Study that supports the role of environmental factors in OCD:
Cromner et al (2007) -found that OCD pts in their sample had a traumatic event in their past (OCD was more severe in those with more than one trauma)
Evaluation of genetic explanations:
The Biological Approach to treating OCD:
Assumptions:
Drugs to treat OCD increase serotonin
Biological treatments include drug treatments
If a disorder is thought to have a biological cause, a biological treatment would be offered
Selective Serotonin Reuptake Inhibitors:
SSRI side effects:
B - body weight increase
A - anxiety and aggression
D - dizziness
S - sedation
S - stimulated CNS
R - reproductive/sexual dysfunction
I - insomnia
Effectiveness (efficacy):
Somro et al 2009:
17 studies showed significantly better results for SSRI's than placebo
Most effective when combined with CBT
Around 70% respond
S - Cost effective, non disruptive
W - Treatment aetiology fallacy (lack of drugs does not equal cause of the problem)
At the synapse these block the reuptake molecules - this has a overall effect on increase serotonin levels
Less serotonin =sufferer
SSRI added = more serotonin = treatment (blocks reuptake of molecules)
3-4 months before symptoms reduce, often used alongside CBT
The cycle of OCD:
Obsessive thought >> Anxiety >> Compulsive behaviour >> Temporary relief