Psychopathology: Evaluation Flashcards
Statistical Infrequency AO3
+ appropriate: used in clinical practice, part of formal diagnosis, way to assess severity of symptoms, diagnosis of intellectual disability disorder requires IQ of below 70 (bottom 2%)
- can be positive: individuals with IQ above 130 statistically infrequent, not considered abnormal to have high IQ, wouldn’t think of someone with very low depression score on BDI as abnormal, being at one end of psychological spectrum doesn’t necessarily make someone abnormal
Deviation From Social Norms AO3
+ distinguishes between desirable and undesirable behaviours: social deviance model considers effect behaviour has on others, defined in terms of transgression of social rules established to help people live together, abnormal behaviour damages others
- relates to context: being nude on a nudist beach is normal but being nude in public may be abnormal and indication of mental disorder, degree important, shouting loudly and persistently deviant behaviour but only indication of mental disorder if excessive
Failure to Function Adequately AO3
+ includes subjective experience: allows us to view mental disorders from pov of person experiencing it, recognises importance of experience of patient, difficult to assess distress, WHODAS’ objective criteria makes relatively easy to judge objectively because can list behaviours (can dress self, can prepare meals)
- easy to label non-standard lifestyle as abnormal: can be hard to say someone really failing to function and simply chosen to deviate from social norms, not having job or permanent address might seem like failing to function, people with alternative lifestyles choose to live ‘off-grid’, favour high-risk leisure activities or unusual spiritual practices classed as irrational and perhaps danger to self
Deviation From Ideal Mental Health AO3
+ focuses on positives: offers alternative perspective on mental disorder that focuses on ‘ideal’, what’s desirable rather than what’s undesirable, Jahoda’s ideas never really taken up by mental health professionals, ideas have had some influence and are in accord with ‘positive psychology’ movement
- applies principles of physical health to mental health: physical illnesses have physical causes, virus or bacterial infection, makes relatively easy to detect and diagnose, some mental disorders also have physical causes (e.g., brain injury or drug abuse), many don’t, consequence of life experiences.
Two Process Model for Phobias AO3
+ successful treatments: systematic desensitisation behavioural treatment for phobias, gradually introduces patient to phobic stimulus, counter-conditioning occurs and fear replaced with relaxation due to use of relaxation techniques, flooding successful exposure therapy, immediately exposed to phobic stimulus, avoidance prevented, adrenaline levels eventually subside after enough time
+ research support for link between bad experiences and phobias: Ad De Jongh et al (2006) found 73% of people with fear of dental treatment experienced traumatic experience, mostly involving dentistry (others experienced being victim of crime), control group of people with low dental anxiety only 21% had experienced traumatic event
- doesn’t explain all phobias or not developing phobia after trauma: Seligman (1970) suggested humans more likely to develop phobias to things that would have been dangerous in evolutionary past, fire, predators, heights, Bregman (1934) tried to condition ‘fear response’ in infants to block of wood, paired block with loud bell to try and condition wood to produce response loud bell produces, failed
- not complete explanation: need cognitive factors to explain why some people don’t develop phobias after exposure to frightening stimuli, DiNardo (1988) found some who had traumatic experience developed phobia of dogs others didn’t, with phobia more likely to believe would have similar negative experience in future, high level of anxiety lead to catastrophising, found only half of people who had traumatic experiences develop phobia
Systematic Desensitisation for Phobias AO3
+ research successful and effective: McGrath et al. (1990) reported 75% of patients with phobias respond to this treatment, success lie with actual contact with feared stimulus, in vivo techniques more successful than using pictures or imagining feared stimulus (Choy et al 2007), number of exposure techniques involved- in vivo, in vitro and modelling, patient watches someone else coping well with feared stimulus (Corner 2002)
+ faster, cheaper, less effort: CBT requires willingness for people to think deeply about mental problems, not true for behavioural therapies, lack of ‘thinking’ means that technique useful for people who lack insight into motivations or emotions, patients with learning difficulties, can be self administered, successful with social phobia (Humphrey 1973)
- not effective for all phobias: Ohman et al (1975) suggest sd not as effective in treating phobias that have underlying evolutionary survival component (e.g. dark, heights or dangerous animals), than in treating phobias acquired as result of personal experience
Flooding for Phobias AO3
+ effective: Choy et al reported both SD and flooding effective but flooding more effective of two at treating phobias, Craske et al 2008 concluded SD and flooding equally effective in treatment of phobias
+ faster, cheaper, less effort: CBT requires willingness for people to think deeply about mental problems, not true for behavioural therapies, lack of ‘thinking’ means that technique useful for people who lack insight into motivations or emotions, patients with learning difficulties, can be self administered, successful with social phobia (Humphrey 1973)
- isn’t for every patient: highly traumatic procedure, made aware of beforehand, may quit during treatment which reduces ultimate effectiveness of therapy for some
ABC Model and Negative Triad for Depression AO3
+ successful therapies: Beck and Ellis’ explanations led to different types of CBT, Beck’s patients identify automatic thoughts about world, self, and future, then challenged directly with therapist, for homework reality testing done to allow them to question negative beliefs, Ellis’s ABC model has led to REBT, therapist working with client to dispute and challenge irrational beliefs
+ research support: view depression is linked to irrational thinking, Hammen and Krantz (1976) found depressed ps made more errors in logic when asked to interpret written material than non-depressed ps, Bates et al (1999) found depressed ps who given negative automatic-thought statements became more and more depressed, supporting view negative thinking leads to depression, issue of bidirectional ambiguity as is correlation, can’t be sure if negative thoughts caused depression or depression caused negative thoughts
- machine reductionist: uses theoretical models, fails to take other approaches into account, biological approach to understanding mental disorder suggests genes and neurotransmitters cause depression, research supports role of low levels of neurotransmitter serotonin in depressed people, also found gene related to this 10x more common in people with depression (Zhang et al, 2005), success of drug therapies for treating depression suggests neurotransmitters play important role
- blames individual: suggests client responsible for disorder, good thing because gives client power to change way things are, lead client or therapist to overlook situational factors, not considering how life events or family problems may have contributed to mental disorder, simply in client’s mind, recovery lies in changing that, rather than considering how client/therapist might change other aspects of client’s environment and life
CBT for Depression AO3
+ research support: Ellis (1957) claimed 90% success rate for REBT, average of 27 sessions to complete, REBT and CBT in general done well in outcome studies of depression, review by Cuijpers et al (2013) of 75 studies found CBT superior to no treatment, Ellis recognised therapy wasn’t always effective, suggested could be because some didn’t put revised beliefs into action (Ellis 2001), therapist competence appears to explain significant amount of variation in CBT outcomes (Kuyken and Tsivrikos 2009)
+ supoprt for behavioural action: belief that changing behaviour can go some way to alleviating depression supported by study on beneficial effects of exercise, Babyak et al (2000) studied 156 adult volunteers diagnosed with major depressive disorder, randomly assigned to 4 month course of aerobic exercise, drug treatment or combination of the two, clients in all 3 groups exhibited significant improvement at end of 4 months, 6 months after end of study those in exercise group significantly lower relapse rates in medication group
- individual differences: less suitable for people who have high levels of irrational beliefs both rigid and resistant to change (Elkin et al 1985), less suitable in situations where high levels of stress in individual reflect realistic stressors in person’s life that therapy can’t resolve (Simons et al 1995), Ellis explained possible lack of success in terms of suitability, some don’t want direct sort of advice CBT practitioners dispense, prefer to share worries with therapist without getting involved in cognitive effort associated with recovery (Ellis 2001)
Genetic Explanations for OCD AO3
+ research support: Pauls and Leckman (1986) studied genes of patients with Tourette’s and families, concluded OCD is form of expression of same gene that determines Tourette’s, obsessional behaviour of OCD and Tourette’s also found in children with autism, who display stereotyped behaviours and rituals as well as compulsions, diagnosing harder when only looking at genes as could be something else
+ twin studies support: Nestadt et al (2000) reviewed twin studies of OCD, found concordance rate for MZs 68%, 31% for DZs, if fully genetic concordance rate would be 100% and 50%
- alternative explanations: Cromer et al (2007) conducted structured clinical interviews of 265 people with OCD, 54% reported experiencing least one traumatic life event in lifetime, those who reported traumatic life events tended to have more severe symptoms of OCD
- polygenic: COMT and SERT not only genes which contribute to OCD, understanding of human genome advancing all the time, more genes being discovered which contribute to OCD, many of these genes contribute very small risk of OCD, many of have many other functions
Neural Explanations for OCD AO3
+ successful treatments: Pigott et al (1990) found serotonin agonists (which stimulate production) and several SSRIs effective at reducing symptoms of OCD, anxiety reducing drugs that don’t affect serotonin not effective, Szechtman et al (1999) gave rats dopamine agonist, started to exhibit compulsive “repetitive behaviour”, resembles ritualistic OCD behaviour in humans, gave dopamine antagonist (to decrease production), “repetitive behaviour” reduced
+ use of brain scans: Saxena and Rauch (2000) reviewed studies of OCD that used PET, fMRI, and MRI neuro-imaging techniques, found consistent evidence of association between the OFC and OCD symptoms
- comorbidity: depression thought to involve disruption to serotonin system, leaves us with logical problem when comes to serotonin system as possible basis for OCD, serotonin system disrupted in many patients with OCD because depressed as well, issue of bidirectional ambiguity in these correlations as biological abnormalities could be result of OCD, not cause
- unclear evidence: not clear exactly what neural mechanisms involved in OCD, studies shown neural systems involved in decision making are same systems that function abnormally in OCD (Cavedini et al, 2002), some research also identified other brain systems that may sometimes be involved in OCD, no system found that always plays role in OCD
Drug Therapy for OCD AO3
+ research support for effectiveness: researchers use randomised, double-blind control trial, using both real drug and the placebo, Somoro (2008) reviewed 17 studies of SSRIs finding them more effective than placebos up to 3 months after, most studies on drug effectiveness are short-term, little long-term data exists
+ little effort and less time: CBT patient must attend regular meetings and think about how to tackle problem, drugs also cheaper than CBT, require little monitoring from pov of NHS, patients may still benefit from fact that talking to doctor in consultations may help
- side effects: nausea, headaches, insomnia common in SSRIs, may choose not to take drug, hallucinations and irregular heartbeats common in tricyclics, only used when SSRIs fail, issues of addiction, particularly with BZs, only prescribed for approx 4 weeks
- CBT should be tried first: Koran (2007) suggested this after comprehensive review of OCD treatments sponsored by APA, drugs may be effective in short-term but don’t provide lasting cure for OCD, Maina (2001) suggested people relapse when drug is stopped
