OCD (PSYCHOPATHOLOGY 4/4) Flashcards
OCD definition
obsessive compulsive disorder is an anxiety disorder where suffers experience persistent and intrusive thoughts (obsessions), compulsions or a combination of both
most realise obsessive ideas and compulsions are excessive and inappropriate but cannot consciously control them, resulting in high levels of anxiety
symptoms can overlap with other conditions (autism, Tourettes), question whether it exists as a separate disorder
can become very time consuming, interfering with ability to conduct everyday activities
obsessions
things people think about
recurrent and persistent thoughts, urges or images that are inappropriate and aren’t based in reality
lead to extreme anxiety
compulsions
results of obsessions
repetitive behaviours or mental acts which are intense and uncontrollable
attempt to reduce distress or prevent feared events, even though there is little chance of them happening or being reduced by compulsions
can reduce compulsions but are only temporary solutions, but rely on them as a short-term solution as there is no other way of coping
e.g. avoiding situations that trigger obsessive ideas or images
prevalence
2% of UK population
no real gender difference
preoccupations with contaminations and cleaning are more common in females
males focus more on religious and sexual obsessions
more common among male children - earlier, gradual onset
females generally have later, sudden onset with fewer severe symptoms
behavioural characteristics
REPETITIVE COMPULSIONS - compulsions to repeat a behaviour, commonly hand washing, praying, tidying or ordering objects
ANXIETY-REDUCING COMPULSIONS - 10% of sufferers have compulsive behaviours alone, no obsessions, just a general sense of irrational anxiety, performed to manage anxiety e.g. hand-washing in response to fear of germs
AVOIDANCE - attempt to reduce anxiety by avoiding situations that trigger it, can interfere with leading an ordinary life
emotional characteristics
EXTREME ANXIETY AND DISTRESS - anxiety accompanies both obsessions and compulsions, obsessive thoughts are unpleasant and frightening, anxiety overwhelming, urge to repeat a behaviour creates anxiety
ACCOMPANYING DEPRESSION - low mood and lack of enjoyment, compulsive behaviours bring some relief from anxiety but is only temporary
GUILT AND DISGUST - involves other negative emotions such as irrational guilt (e.g. over moral issues) or disgust directed at something external or at self
cognitive characteristics
OBSESSIVE/RECURRENT THOUGHTS - 90% of sufferers experience obsessive thoughts as major cognitive feature, vary but always unpleasant e.g. contaminated by dirt, certainty a door in unlocked, impulses to hurt someone
COGNITIVE COPING STRATEGIES - respond to obsessions by adopting coping strategies, religious person tormented by excessive guilt may respond by praying or meditating, may help manage anxiety but can make them appear abnormal and distract from everyday tasks
INSIGHT/AWARENESS OF IRRATIONAL BEHAVIOURS AND ANXIETY - aware of irrationality of obsessions and compulsions, necessary for diagnosis, experience catastrophic thoughts about worst-case scenarios, tend to be hypervigilant (maintain constant alertness and keep attention focused on potential hazards)
explaining OCD - genetics
evidence that OCD is inherited
those with disorder inherited specific genes related to onset
concordance rates
COMT gene
SERT gene
diathesis-stress model
OCD is polygenic
concordance rates
2% of UK population at risk
Lewis observed 37% of OCD patients had parents with OCD, 21% with siblings with OCD, suggesting that it runs in families
may be a vulnerability passed on, not absolutely certainty
Pauls found that risk was greater in first-degree relatives of OCD patients compared to relatives of controls without OCD (10% vs 1.9%)
COMT gene
catechol-o-methyltransferase
candidate gene that can be inherited and increase vulnerability to OCD
involved in production of an enzyme regulating production of neurotransmitter dopamine
one form is more common in OCD patients - lower activity and higher dopamine (rewards - positive reinforcement)
SERT gene
candidate gene
affects transport and take-up of serotonin (causes anxiety, resulting in compulsions performed to reduce anxiety)
lower levels and activity of serotonin implicated in OCD
diathesis-stress model
genes interact with environment to bring about development of OCD
suggests that individual genes cause vulnerability for OCD (diathesis)
other factors affect development (stressors)
some possess genes but never suffer
genetics play part in development, but interaction with environment is key
OCD is polygenic
caused by combination of genetic variations that increase vulnerability
Taylor analysed findings and found that up to 230 genes may be involved
genetic explanation of OCD strengths (supporting evidence)
supporting evidence
Ozaki found mutation of SERT gene in two unrelated families, where 6/7 family members had OCD
supports idea that SERT gene increases risk of developing OCD, caused by genetics
supporting evidence
Nestadt reviewed twin studies and reported that 68% of identical twins shared OCD as opposed to 31% of non-identical twins
supports idea of inheritance - share 100% of DNA so if one has OCD, the other’s risk of developing OCD is higher
proves inheritance and affected by genetics
genetic explanation of OCD weaknesses
cannot rule out environmental influence
living in similar environments may affect OCD development
social learning theory - if one family member has OCD, others may view behaviour as normal and learn from each other, increasing likelihood of development
concordance rates
not purely genetic - in twins the risk should be 100% as they share same DNA
genetic explanation of OCD weaknesses
few details about genetic mechanisms well understood, although heritable (Pato)
one group of genes may cause OCD in one person, but another group in someone else
lacks validity and applicability - hard to find consistent treatment
OCD is more genetic in nature when originating in childhood than adulthood
genetic element for both
may be different types of OCD and different causes
neural explanation of OCD
abnormal levels of neurotransmitters
- dopamine
- serotonin
abnormal brain circuits / functioning
- worry circuit
- links to neurotransmission
-parahippocampal gyrus
dopamine
pleasure hormone
abnormally high
Szetchman found that enhanced levels of dopamine induced repetitive checking in rats, resembling compulsive behaviours
serotonin
satisfaction, optimism, happiness
low levels
antidepressants that increase activity reduce symptoms
the worry circuit
orbitofrontal cortex (OFC) sends worry signals to the thalamus via caudate nucleus (in basal ganglia)
minor worry signals normally suppressed by caudate nucleus, but if damaged, thalamus is alerted and confirms worry, bringing about repetitive and compulsive behaviours
OCD patients show heightened activity in OFC
links to neurotransmission
serotonin and dopamine linked to regions of frontal lobe
serotonin plays role in operation of OFC and caudate nucleus –> abnormal levels may cause malfunction
dopamine main neurotransmitter of basal ganglia –> high levels lead to overactivity
parahippocampal gyrus
associated with abnormal functioning in left parahippocampal gyrus, normally process unpleasant emotions
neural explanations strengths
research evidence to support role of abnormal serotonin functioning
Zohar gave mCPP, a drug that reduces serotonin functioning to 12 patients and 20 non-OCD patients and found that symptoms were significantly enhanced
suggests that low levels of serotonin implicated as symptoms worsened
suggests neural explanations are valid
evidence to support role of abnormal brain structures
Saxena and Pauch reviewed studies that used neuroimaging techniques and found an association between OFC and OCD symptoms
supports idea that when OFC relays messages to thalamus, the caudate nucleus is not able to suppress the worry - supporting validity
but weak evidence because no cause and effect established - cannot say for certain that issues with worry circuit cause OCD while other factors may have an effect
drug treatments increasing levels of serotonin effective in treatment - supporting role of serotonin
antidepressants (SSRIs) which inhibit serotonin reuptake reduce OCD symptoms
strengthens neural explanation as effects of drug suggest low levels of serotonin linked to OCD, increasing validity
but SSRIs ineffective in reducing symptoms in everyone - not all linked to or caused by serotonin, must be other factors
neural explanations weaknesses
OCD can be explained by psychological explanations
two-process model of phobias also applied
neutral stimulus repeatedly associated with a UCS, producing anxiety, creating a CS and CR of anxiety, maintained by avoiding anxiety-inducing stimulus, or negatively reinforced through compulsive behaviours to reduce anxiety
weakness as neural explanation doesn’t account for environmental occurrences affecting development
reductionist - only take biological factors into account
issues with cause and effect
findings e.g. serotonin, worry circuit only show correlation and do not indicate causing OCD
cannot be entirely sure of true causes, or whether the OCD causes these abnormal functions - can’t develop most effective treatments, reducing applicability
drug therapy
increase or decrease levels of neurotransmitters in the brain
aim to decrease anxiety and arousal levels - lowering blood pressure, heart rate, cause OFC to function normally
- antidepressants (SSRIs)
- SNRIs
- antidepressants (tricyclics)
- anti-anxiety drugs (BZs)
usually lasts 12-16 weeks, but most need treatment for at least a year
antidepressants (SSRIs)
selective serotonin reuptake inhibitors
elevate levels of neurotransmitters, by preventing reuptake of serotonin into presynaptic neurone
increase serotonin activity in synapse and serotonin will continue to stimulate receptors on post-synaptic neurone
reduces anxiety by normalising the worry circuit
most commonly fluoxetine (Prozac)
SNRIs
serotonin-noradrenaline reuptake inhibitors prescribed when SSRIs are ineffective
work on both serotonin and noradrenaline
antidepressants (tricyclics)
tricyclic clomipramine
block transporter mechanism in reuptake of serotonin and noradrenaline in presynaptic neurone
more NTs in synapse, prolonging activity
target more than one NT
greater negative side effects - only used as second treatment if SSRIs are ineffective
anti-anxiety drugs (BZs)
benzodiazepines used to lower anxiety levels
enhance activity of GABA, which has inhibitory effect on brain
stops and slows down neurones
general quietening influence on the brain
consequently reduce anxiety
drug therapy strengths
research support
SSRIs more effective than placebos in 17 trials
clearly effective and useful
cost effective
drugs easy and cheap to administer / mass produce
limited time with professional
CBT needs 1 hour sessions - many sessions, very expensive
CBT requires motivation, drugs are non-disruptive and can be taken until symptoms subside
less motivation needed
easy and time-efficient
no commitment to attend sessions
more likely to complete treatment, more success
drug therapy weaknesses
negative side effects
BZs highly addictive, increased aggression and long-term memory impairments
only prescribed for short term treatment
decreases likeliness of finishing course, decreasing effectiveness
root of problem and relapse rates
Simpson 45% treated with relapsed wighin 12 weeks of completion
treat symptoms, not the cause
SSRIs increase levels of serotonin, reduce anxiety, alleviate symptoms, fail to address and treat cause of lack of serotonin, leading to relapse
controversial treatment
SSRIs are effective, side effects short term
research may be biased due to sponsors
companies may selectively publish positive outcomes of drug sponsors
reductionism
biological treatments work on assumption that OCD is biological in origin, range of other causes
drug therapy not always appropriate (trauma)
drug therapy weaknesses
negative side effects
BZs highly addictive, increased aggression and long-term memory impairments
only prescribed for short term treatment
decreases likeliness of finishing course, decreasing effectiveness
root of problem and relapse rates
Simpson 45% treated with relapsed wighin 12 weeks of completion
treat symptoms, not the cause
SSRIs increase levels of serotonin, reduce anxiety, alleviate symptoms, fail to address and treat cause of lack of serotonin, leading to relapse
controversial treatment
SSRIs are effective, side effects short term
research may be biased due to sponsors
companies may selectively publish positive outcomes of drug sponsors
reductionism
biological treatments work on assumption that OCD is biological in origin, range of other causes
drug therapy not always appropriate (trauma)
