psychopathology

Question 1

define abnormality

Answer 1

term used to label + control ‘difficult’ people

Question 2

what are the 4 definitions of abnormality?

Answer 2

• deviation from ideal mental health
• failure to function adequately
• deviation from social norms
• statistical infrequency

Question 3

deviation from social norms?

Answer 3

• social norms [can be (un)/written rules in society] → they’re mostly accepted & can vary between cultures
• social norms = regulation of ‘normal’ social behaviour → they’re socially constructed
• [anyone who differs from the standards of acceptable social behaviour] = deemed ‘abnormal’
• eg -> overtime, homosexuality & between culturs - hearing voices {schiz example}

Example: antisocial personality or affectionless psychopathy (from disruptions in attachment) → lack emptying (failure to conform to culturally ethical behaviour)

Question 4

failure to function adequately?

Answer 4

• when one cannot go about their day-to-day life
• can’t function properly = causes distress + suffering to individual and sometimes, the surrounding ppl
  – the individual may not be aware that they’re distressed if they have a mental disorder
• their behaviour = unpredictable // irrational
• behaviour prvents them from attaining social // occupational goals
• Rosenhan + Seligman formed the criteria for ‘failure to function adequately’
  ↳ observer discomfort // irrational behaviour // vividness (others see behaviour as odd) // unpredictability // violation of moral codes // suffering // maladaptiveness (their behaviour prevents them from reaching their desires)

Example: schizophrenia

Question 5

deviation from ideal mental health?

Answer 5

• jahoda formed the 6 categories of good mental health:
  ↳ self-attitude // personal growth // integration // autonomy // having an accurate perception of reality // mastery of the environment
• according to her, if one doesn’t have these, they’re considered to be abnormal (and can potentially have a mental disorder)

Example: depression

Question 6

statistical infrequency?

Answer 6

• ‘normal’ = referring to the typical value
• descriptive stats (aka, mean / mode / median) = used to rep typical value
• helps to identify anomalies

Example: intellectual disability disorder [ppl w IQs below 70 have limited intellectual and social functioning]

Question 7

evaluate deviation from social norms

Answer 7

(D) the definition = era dependent
- social norms = constantly changing
– (e.g. - homosexuality was once considered a mental disorder, in current times ppl = more accepting so it’s now a social norm)
↳ due to the constant changes / updates, it may be difficult to judge certain things as there may be lots of conflicting opinions → suggesting that there’s a lack of consensus between generations

(D) behaviour = subjective + context specific
- what is considered norm in one sitch can be seen as abnorm by others & the behaviour in diff sitchs can be sen as normal in one or abnormal in the others#

Question 8

evaluate failure to function adequately

Answer 8

(D) focuses on how someone copes → some abnormal behaviour may be missed
- ppl may physically appear fine (as they fit social standards), but their thinking may distorted → causing them inner distress

(D) despite the use of a criteria, can there’s still subjectivity -> what other ppl view as norm may not be the same as others {individual diffrences}

(D) can be culturally bias -> not genrealisable to all cultures (individualisitic vs individualist)

Question 9

evaluate deviation from ideal mental health

Answer 9

(D) the criteria of autonomy make collectivist cultures seem abnormal
↳ collectivist cultures = where helping others & thinking as / for groups is ideal - rather than making yourself (the individual) the priority
- meaning, non-western cultures cannot relate to jahoda’s criteria (it’s not globally applicable)
- the criteria outlined by jahoda makes ideal mental health practically impossible to achieve (when it should be normal) → suggesting, (according to jahoda) the majority of the population would be abnormal

(A) focuses on what’s needed + desirable → provides goals people can meet → can better lives

(D) criteria can be subjective
- it’s vague + hard to asses → rely on subjective judgements

Question 10

evaluate statistical infrequency

Answer 10

(A) Provides an objective view → defining / seeking abonormalities can be done by using a cut-off point
- there’s no judgement → e.g. → looking @ data for homosexuality, it would be less frequent than hetrosexuality , but it would be seen as ‘wrong’

• the definition doesn’t distinguish what is desirable or undesirable behaviour (what is considered abnormal & what isn’t)
  ↳ some behaviours are seen as abnormal even though they’re frequent (like depression)

(D) can be culturally biased
- what is considered normal in one culture (like hearing voices in African cultures) is rare another culture

Question 11

list 3 types of mental disorders

Answer 11

phobias, OCD (obsessive compulsive disorder), depression

Question 12

define phobia

Answer 12

• a persistent anxiety disorder which interferes w daily life
• an instance of irrational fear that produces constant avoidance
• person will avoid it at all costs
• irrational & aware of it

Question 13

define OCD

Answer 13

• an anxiety diorder than is ade up of 3 componenets:
  -> obessions [recurring / persitant / disturbing thoghts abt certain topics] (internal components) -> cogntive symp
  -> guilt + anxiety -> for having intrusive / impulsive thoughts -> emotional symp
• feelings of embarrassed / shame / disgust {aware of irrational thoughts}
  -> compulsions -> [repetitive actions until urge = satisifed] (external components) -> behavioural symp
• help relieve guilt + anxiety of intrusive thoughts / obsession
• irrational thoughts & aware of it
• obsessional themes / thoughts –> germs

Question 14

explain + evaluate the neural explanation of OCD

biological explanations of OCD

Answer 14

neuroanatomy:
- orbitofrontal cortex = detects worrying stimuli
- basal ganglia = monitors the outcome of actions (after task has been done) => inhibits neural activity in orbitofrontal cortex {satisfied w taks + actions}
- ppl w OCD = impaired communication between basal ganglia + orbitofrontal conrtex
– when comm = impaired -> singal sent to OC = much weaker {nerual activity in OC = less inhibited} => urge to still act (discomfort) = still there / persistant {obssession => compulsions} due to hyperactive orbitofrontal cortex

(A) PET scans show pp w OCD = higher activity

(D) research = identified areas of the brain = consistently found to be related to OCD (correlation)
- there’s no cause and effect R between brain structure abnormalities + OCD (issues w causality)

(A) research support from case studies
- case studies [detailed investigatoins into 1 individual // small grp]
- Max et al (1995) conducted case study of 12yr patient w OCD symps after being hit by a car (brain damage)
- MRI scan [shows structure of brain] -> showed there was damage to the basal ganglia
-> hence showing support for neuroatonmy => OCD symps
(CP) case study => may not apply to everyone -> just a oneoff -> lmited relaibility

(D) inconsistent findings
- when studies = replicated => findings = diff
- Aylward et al (1996) conducted BI study using MRIs -> to investigate brains of those w OCD -> compared them to ppl’s w/out OCD
- found: no sig difference in basal ganglias in boht grp -> contradicting Max et al’s study
- suggesting that damage to basal ganglia = not only exp

(A) research supprt from brain imaging studies
- neuroimaging techniques [shows different activation patterns - when peforming diff tasks + behaviours - within the brain]
– used to view neural activity of pp w OCD -> then comparedto ppl w/out OCD
- Saxena + Rauch (2000) reviewed all BI studies of adults w OCD
- found: inc-ed activity in OC compared to control ptts

nerurotransmitters: [chemical messengers that transmit nerve impulses from cells to others, accross the synapse]
- ppl w OCD = low S levels + high D levels
– S = neurotransmitter, released from pre-synaptic terminal during synaptic transmissions
– S = main NT that’s released in OC (after BG sends signals to inhibit OC’s activity) => OC = hyperactive => signal in response to worrying stimuli = persistant {=> obsession + anxiety + compulsions}

(A) piggott et al (1990) found: SSRIs [incs S in synaptic gap] = effective when treating OCD
(A) Szchetman et al (1998) found: high doses of D icn-ing drugs induce movements that resemble compulsive behaviours
-> these both show how drugs = effectove when treating OCD -> bio solutions -> neurotransmitters play a role in causing OCD

S = inhibitory -> low S = overactive OC => OCD symps

Question 15

the genetic explanation + evaluation of OCD

biological explanations of OCD

Answer 15

• genetic predispositions han be genetically inherited
  – hence, there are many specific alleles associated w OCD
• behaviours = due to combo of diff genes
• genetic influence = complex, evniro factors play a role as well

SERT gene: [controls level of S available @ synapse]
- SERT produces a re-uptake protein [carries S back into pre-synaptic membrane after synaptic transmission]
– more SERT prodcution => less S in synapse
2 alleles of SERT gene:
- short allele = produces less {=> more S availbale in synapse => nerual activity = more inhibited}
- long allele = produces more {=> less S available => less inhibited => overactive OC} -> hence associted w OCD

COMT gene: [COMT regulates D}
- a variation of this gene => high D levels -> hence, more common in OCD patients

(A) research support from Ozaki et al (2003)
- mutation of SERT gene = found in 2 unrelated families where 6/7 = OCD

(A) research support from Hu et al (2006)
- conducted gene study: DNA analysis of OCDs -> compared w control grp
- found: OCDs = more likely to carry long variation of SERT gene

(A) supporting research from twin studies
- the bigger the diff in CC rates => the more influence genetic variation has {MZ >.DZ = genetic factors}
- Billet et al (1998) -> reviewed twin studies that compare CC rates of MZ + DZ w OCD
– MZ = 68% CC & DZ = 31% {MZ > DZ -> large diff in CC rates => OCD = partially due to genetic influence}
(CP) TS assumes MZ + DZ = similar amount of shared environment & impact of environment on phenotype = similar for MZ + DZ
- MZ = treated more simialrly {=> maybe more similar enviro} > DZ
– hence, diff CC rates may be due to diff enviro factors as well - not just bio

(A) supporting research from family studies
- Nesdtadt et al (2000) -> investigate if OCD = inherited
- recuited OCD patients & control grp -> then interviewed family of ptts to see how many of fam had OCD
- found: 12% of OCD patients = 1 relaitve w OCD
– 3% of control grp - relative w OCD

-> if 1 person in fam = OCD => other members = likely to have it
-> OCD = likely partially genetic

Question 16

define depression

+ symptoms

Answer 16

[mood disorder]

• loss of pleasure -> stop doing activites one used to enjoy // lack of interest
• person will feel sad {low moods}
• may have difficulty sleeping (chnage in sleep patterns), eating (chnage in appetite) and/or* concentrating*
• irrational negative beliefs (negative thoughts)
• social withdrawal

manic dep:
- depressive episode [period of low - for at least 1w]
- manic ep [period of high mood - for at least 1w]
- manic depression [cycles between deppressive + manic episodes] -> same as bipolar disorder

Question 17

what are the characteristics of depression?

when diagnosing

Answer 17

• emotional -> the emotional backlash(?) that’s felt a result of the disorder
  – like low mood // loss of pleasure
• behavioural -> how the disorder impacts the individual’s behaviour
  – social withdrawal, changes in sleeping + eating
• cognitive -> how the disorder impacts the way info is processed (the thought process // thinking pattern)
  – irrational (-) beliefs + difficulty concentrating
• to be diagnosed -> one must experience low mood or loss of pleasure

{refer to pic in notes for full detail + examples}

Question 18

models for depression?

A01 + A03

Answer 18

Ellis’ ABC model: [cognitive approach to exp depression]
- states: good mental health = result of rational thinking {dep = result of (-) irrational beliefs
process:
(A)ctivating event -> the event that has occured
(B)elief -> the interpretation of the event
- can be rational / irrational
(C)onsequnces -> the (emotional / behavioural / cognitive) result due to the belief

Beck’s negative traid:
- Beck’s cog exp has 3 components:
-> cognitive bias -> found that dep ppl = more likely to focus on (-) aspects-> prone to ditorting + misinteroreting info
-> (-) self-schemas -> ppl w this = likely to interpret info abt themselves in a (-) may {=> can lead to cogntive bias}
- schemas = norm develop in childhood -> neg schemas may come from (-) experiences (like critism)
-> negative triad -> CBs + S-Ss maintain the negative triad + irrational views of us + future + the world
- {negative view of ourselves} -> {negative view of future - “never be able to do this …”} -> {negative view world - “everything is like this - don’t try”}

eval:
(A) real life application
- cog exos = used to develop effective treatments (like CBT + REBT)
– developed from the ABC model
– attempts to identify + challenge (-) irrational thoughs / beliefs -> successfully treats cases w depression
(CP) ppl must have motivation to attend (due to avolition & others) - they may not show up => not beneficial

(A) supporting research
- Boury et al (2001) found: dep patients = more likely to misinterpret info negatively (CB) + feel hopeless abt their future (negative triad)
- Bates et al (1999) made dep patients read (-) automatic thought statements => worsens symps
- therefore -> showing (-) thinking = involved in dep

(D) alternative exps
- there are biological causes, like genes + neurotransmitters {low S + D}
- research shows low S = found in dep patients
- drug therapies show bio factors impact dep levels
– SSRIs (inc S) = effective in treating dep
- hence, cog = not sole exp

(D) doesn’t explain cause of irrational thoughts / beliefs
- most research = correlational {no causality}
– dk what causes what & if there’s other variables

Question 19

treating depression?

A01 + A03

Answer 19

CBT:
- based on how irrational thinking = makes one vulnerable to depression
- aim = identify + challenge + coorect neg thoughts

process:
intial assessment -> patient + therapist identify the patient’s irrational thoughts -> explain to them (rationalise / dispute)
goal setting -> they agrre of realistic goals + plan action to achieve {behavioural assignments outside of session}
identifying + challenging thoughts -> diff methods using diff cog exps if dep
-> Beck’s CBT:
- therapist help to identify (-) thoughts realted themselves + their future + world
- then try to challenge this -> discussing evidence + dispute
-> Ellis’ rational emotive behaviour therapy
- ABC + (D)ispute + (E)ffect (emotionall + cog + behaviourally)
– logical D -> questions patient’s logic (does it make sense?)
– emprical D -> questions their evidence of their belief
-> homework -> patient identifies their irrational beliefs + proves them wrong (they change to rational thinking)

• identify neg beliefs
• challenge
• test hypothesis (done thru HW + gathering evidence on their beliefs)
• evaluate evidence is next sessions

eval for CBT:
(A) study support from review - Cuijpers et al (2013)
- looked @ all US studies abt effectiveness of CBT as a treatment of depression
- in all studies: 2 grps of ptts
– 1 grp = depressed & given CBT (experimental)
– 2 grp = depressed & not given any treatment (control)
- ptts w CBT = sig imporovement w symps > control gro
- hence, CBT = more effective than no treatment
(CP) culture bias => less generalisable
(CP) same levels of severity? {standardised?}

(D) individual diffrences
- for those w social difficulties (social-anxiety // social-phobias) -> hard for them to open up + express themslves - esp to stranger -> CBT may not help
- ppl w diff concentrating (dysfunctional attention?) -> several steps involved w CBT may be overwhelming {not able to keep up => may induce more neg feelings abt ‘failing’ therapy => worsens symps}
- appts require energy + motivati9on + willingness to attend + imporove - >may be diff w low moods + other symps

(D) npt as effective as other treatments
- genetics ==> development of major dep -> hence, using cog-based treatments = not as much help
– treatments aimed @ bio causes = used instead
- depressed ppl = low S -> may used antidepressants - SSRIs (they higher S levels)

Question 20

behavioural approach to phobias

Answer 20

extinction -> after a number of presentations of the CS (conditioned stimulus) in the absence of the UCS (unconditioned stimulus), it loses it ability to produce the CR (conditioned response)

spontaneous recovery -> following extinction, if the CS + UCS are paired again, the connection = made quicker

stimulus generalisation = [after conditioning, animals respond to stimuli that are similar to the CS]

Question 21

how does classical conditioning explain phobias?

Answer 21

• the little albert experiment whatson + rayner: learning thru association
  stage one: loud noise (UCS) → fear response (UCR)
  stage two: loud noise + rat (UCS) + (NS) → fear response (UCR)
  stage three: rat (CS) → fear response (CR)
• albert (the participant) developed a phobia of objects that shared similar characteristics with the rat (e.g → fur coats // cotton wool)

Question 22

how does operant condition explain phobias?

Answer 22

• phobias = maintained thru reinforcement
  ↳ e.g - avoiding a feared stimulus means the individual is rewarded with their anxiety dissipating

Question 23

the two process model?

Answer 23

• fear = developed thru classical conditioning → maintained thru operant conditioning
• escape = lessens anxiety (negative reinforcement)
• attention = positive reinforcement

Question 24

evaluate the behaviourist approach

Answer 24

(A) has research support
- watson + rayner (1920) → conditioned Little Albert to have a phobia of a white rat (& anything that resembled it)
↳ this was done thru associating it with a pre-existing fear of Albert’s
- therefore supports the behavioural approach to phobias → it demonstrates how a phobia can be acquired thru association → demonstrating the 1st step of the two-process-model
- however - study was only done on Little Albert → no guarantee that the results would be the same for others → results drawn from this exp cannot be generalised → limits the behavioural approach as support

(A) application to therapy
- behaviourist ideas = used to develop effective treatments → eg, systematics desensitisation + flooding
↳ SD = helps to unlearn fears using classical conditioning
↳ flooding = prevents ppl from avoiding their phobias & stops negative reinforcement from happening
- these therapies = successful when used to treat phobias → has credibility due to how the treatments = made for behaviour, implying that it works

(D) considered to be too simplistic
- it ignores the role of cognition in the formation of a phobia → phobias can be developed due to irrational thoughts - not just learning
- eg → those who suffer from claustrophobia may think they will be trapped and suffocated in the lift, which is an irrational thought and is not taken into consideration in the behaviourist explanation
- the cognitive approach = led to the development of cognitive behavioural therapy (CBT) → which is considered to be more successful than behaviourist treatments
- therefore … ??????

(D) ignores evolutionary factors that contribute to the development of phobias
- Seligman = humans are biologically prepared & have an innate tendency to acquire certain fears which would’ve been a source of danger in our evolutionary past (like snakes // spiders // heights)
- the facts the approach overlooks these biological influences ..

Question 25

what is flooding?

Answer 25

[when a person = exposed to the most frightening situation immediately]
↳ e.g → a person w a phobia of dogs is placed in a room w a dog & is asked to stroke / pet it right away

2 types:
- in vivo → actual exposure
- in vitro → imaginary exposure
- a patient = taught relaxation techniques → these are then applied to the most feared situations through either vivo (direct) or vitro (imagined) exposure

process:
- at first → person = in state of extreme anxiety → then exhaustion sets in, meaning anxiety levels will decrease
- person = unable to avoid their phobia → thru continuous exposure, anxiety levels decrease (aka negative reinforcement) → limiting the amount of anxiety associated with their phobia
- one session = 2-3 hrs
↳ in some cases, only 1 long session = needed to cure a phobia

Question 26

evaluate flooding

Answer 26

(A) it’s cost effective
- therapy = found to be effective → sessions aren’t expensive - flooding can cure a phobia in just one session
- hence why flooding may be a better treatment for phobias compared to others → like cognitive behavioural therapy (CBT) due to the economic implications it has on health care services

(A) has research support
- Choy et al… investigated the effectiveness of both systematic desensitisation + flooding → found that flooding = most effective out of the two @ treating phobias
- suggests that flooding = a more effective method of treating phobias

(D) can be seen as unethical
- although patients provide informed consent, may don’t complete their treatment → experience = too stressful
↳ exposing patients directly to their phobias can sometimes cause more anxiety → doing more harm than good in the process of trying to help
- hence why, flooding = sometimes a waste of time + money if patients don’t finish their entire therapy process

(D) not all phobias are the same type → meaning the treatment may not work for all phobias
- eg → social phobias consists of mainly cognitive aspects
- more complex phobias cannot be treated by behaviourist treatments - instead, it would be affected by cognitive behavioural {treats irrational thinking}

Question 27

systematic desensitisation?

A01

Answer 27

a method that uses reverse counter-conditioning to unlearn the maladaptive response to a situation / object - by instead, eliciting another response

3 components:
- fear hierarchy [rank the phobic situations that involve them interacting with their fear, from least to most terrifying]
– the patient will gradually move up their FH until they’re completely relaxed in their most feared situations → SD would’ve been successful at this point

• relaxation training
  – after the fear hierarchy has been completed, the patient is taught relaxation techniques
  ↳ eg → breathing techniques // muscle relaxation strategies // mental imagery techniques
  – these are used when the patient is ‘facing’ / confronting their phobia(s)
• reciprocal inhibition
  – SD states = 2 emotional states cannot exist @ the same time (AKA reciprocal inhibition → suggesting an individual = unable to be relaxed and anxious at the same time → when the exhaustion sets in - the relaxation should overtake the fear

Question 28

(Q) fully explain the process of systematic desensitisation(4 marks)

Answer 28

• the process of SD consists of: FH, RT, RI
• FH → when the client ranks their phobic situation from least to most terrifying
• afterwards, the client is taught many RTs → used when they confront their phobia

Question 29

evaluate systematic desensitisation

Answer 29

(A) supporting research from Gilroy et al (2002):
↳ he examined 42 patients w arachnophobia
↳ each patient = treated using 3x 45min SD sessions
↳ they were examined again 3 & 33 months later → the SD group = less fearful than the control group (CG = only taught relaxation techniques)
- this provides support for the effectiveness of SD → there’s long time effects of the treatment
- however → the study only investigated arachnophobia → meaning there’s no guarantee that SD will work in the same way w other phobias → weakening Gilroy’s study as support for SD as a treatment

(A) it’s less time consuming & may require less effort compared to other treatments - (like CBT)
- Cognitive Behavioural Therapy requires a lot of will power from the patient
↳ aim = to deal w the cognitive elements of phobias → whereas, SD deals w exposure (rather than cognition & it’s a lot quicker)
- for a quicker treatment of phobias - SD = best choice
- however it could be argues that SD doesn’t deal w the root cause of the phobia → thus limiting the treatment

(D) pracitcal issues
- For sd to work it relies of the client’s ability to imagine their fearful situation → for those who can’t create a vivid & realistic image, sd won’t be effective

(D) theoretical issue
- Sd is only effective when the phobia is learned through anxiety
↳ when dealing with serious issues (like depression // schizophrenia) sd may not be effective

(D) ethical issues
- Sd causes very high levels of anxiety (when the client is initially exposed to their phobia)
↳ this questions ethics & appropriateness

Question 30

treatments of OCD

A01

Answer 30

drug therapy = main form of treatment [aims to restore chemical imablances in the brain - as its assumed to be the main cause]

SSRIs - antidepressants:
- bio exp: low S in the brain => OCD -> hence, - treatment aim = to inc S levels @ OC
- (Selective Serotonin Re-uptake Inhibitors) = preferred treatment
process:
- S that’s not absorbed in the post-synaptic neurone = reabsorbed (by SERT’s re-uptake protein) into sending cell
- blocks the re-uptake of S @ synapse => more S available @ synapse => more inhibition of neural activity : post-synaptic neuron => dec-ed hyperactivity of neurons in OC
- inc-ed S in synapse => improves concentration of brain;s chem receptor sites on post-synaptic neuron => intense stimulation on the recieving nerve

BZs - anti-anxiety drugs:
- Benzodiazepines (BZs) = enhance actions of the neurotransmitter GABA
– GABA [tell neurons in b rain to ‘slow down’ // ‘stop firing’ {inhibiting} -> appx 40% of neurons in brain respond to GABA -> meaning GABA = ‘quieting’ influence on brain => reduces anxiety => dec-ed obsessions
- some neurons = have GABA receptor sites @ synapses -> when GABA lock otno this -< flow of chloride ions = inc-ed
- chloride ion = make it diff for recieving neurons to be stimulated by other future NTs => nervous system = slowed => patients = relaxed

Question 31

evalute treatment of OCD

A03

Answer 31

(A) study support
- many studies that investigate the effectiveness of SSRIs
- procedure: ptts = OCD patients-> divide them into grps
– 1grp = SSRIs & 2 grp = placebo pills
- Soomro et al (2008) reviewed results of 17 studies
- found = SSRIs = more effective > placebp sugar pills
– 70% of SSRI grp = improvment in symps (less frequent obsessions + comulsions) . control grp
(CP) the studies = critisised for only investigating ST effectiveness of drug treatments

(A) cost effective (cheaper than therapy)
- drugs can be mass produced -> cheaper to produce + pruchase + easier accesss to patients => encourages use (unlike therapy, as it can be time + money consuming + mentally draining)

(D) side effects
- SSRIs block S re-uptake sccross whole body -> even where theyre aren’t abnormalities = >side effects
- in Soomro’s study ->SEs = headaches + nausea + sleeping difficulties => can discourage ppl from taking meds => relapse
- BZs = highy addictive & can cause inc-ed agg + LT memory impairments
– hence why BZs = reccommended for ST use (up to 4 weeks)

(D) patients take drus indefinitely to avoid relapse
- research sows when ppl stop taking meds, symps come back quick {relapse}
- meds have to be taken indefinitely - so they may have to always suffer from SEs

(D) not as effective as other treatments
- if ppl = bound to relapse after stopping meds -> drugs = not treating / solving prob
- O’Conner et al (1999) compared grp of OCD adults that wer given diff treatments
- grp 1 = CBT, grp 2 = SSRIs, grp 3 = both
- all grps = imroved symps
- grp 3 = biggest reduction in symps -> hence OCD = caused by combo of diff factors (bio + cog)