clinical

• DSM


  • current version- dsm-v
  • brought in in 2013
• DSM-V


  • removed confusing multiaxial system and focuses on 3 main sections: 1= instruction section, 2= main disorders, 3= “work in progress section” for disorders not currently recognised and cultural differences
• Reliability of diagnosis


  every clinician needs to diagnose the same disorder consistently
• reliability of diagnosis 


  -Beck et al (1961) found 54% of 153 patients were diagnosed consistently between 2 psychiatrists

  +Stinchfield (2003) questionnaire based on DSM for 803 people and 259 people on treatment programmes. results sorted gamblers from non

  -Lee (2006) ADHD in korean children, found accurate diagnosis from dsm. girls didn’t fit criteria. construct validity.

  -Hoffman (2002) looked at diagnosis of alcohol dependence. dsm interview was valid and interview data supported dependence was more severe than abuse
• patient factors in diagnosis

  info provided may be inaccurate due to memory problems, denial or shame

  psychological factors such as disordered thinking also impacts this
• clinician factors 


  some clinicians may unconsciously ask/focus on the wrong symptoms or ask questions which lead the patient the wrong way
• concurrent validity 


  if evidence from multiple studies are the same and in agreeance
• aerological validity 


  the extent to which a disorder has the same cause/causes eg if a known genetic cause, psychiatrist can look at family history
• predictive validity 


  the extent to which results from a test (dsm) or study can predict future behaviour, eg someone newly prescribed antipsychotics would be expected to improve in 3 weeks
• cultural differences


  • icd=european dsm=american
  • some guides developed to help generalise to other cultures
  • arguments that dsm-v has been influenced by pharmaceutical companies
• social control 


  changing someone’s mind using therapy or medication, mental health sectioning
• psychological understanding over time

  dsm and ice symptoms have been altered over time, some conditions eg homophobia have been removed, validity has increased over time
• 4 D’s

  • deviance
  • distress
  • dysfunction
  • danger
  • (5th duration)
• deviance


  wether someone is deviating from societal norms
• danger


  if someone is a danger to themselves or others
• distress


  wether their symptoms are causing distress
• dysfunction 


  if someone is struggling to function normally in society
• using the 4 D’s to diagnose

  • potential for subjectivity- how do we decide what is abnormal
  • not fully reliable- clinician interviews are not always reliable, this could be due to the clinician or patient
• cognitive explanation for schizophrenia

  we ignore many cognitive impulses that go on at a level beyond our conscious awareness- too exhausting to not (cognitive noise)

  sz patients are unable to ignore these so have an increased cognitive awareness that they can’t make sense of, leading to further delusions and worsening symptoms
• social drift theory


  evidence suggests sz is more prevalent in lower social classes due to the symptoms making it difficult to hold down jobs, achieve well in education and maintain relationships so they drop down classes

  there is more availability of cheap housing, food, help services in cities, adding to conc of sz in poorer areas
• cognitive psychology acknowledges: 


  biological bases of behaviour, especially positive symptoms of sz. when the patient tries to make sense of the experience they begin to experience other symptoms

  explains why patients with psychosis develop fears of radio waves, aliens, ect as they are trying to make sense of their condition
• evaluation of cognitive explanation

  + gold and harvey (1993) people with sz score lower on tests of attention, memory and problem solving

  + mcguigan (1996) identifies immediately before auditory hallucinations, some sz patients showed vocal centre activation. may suggest they misinterpreted their own “inner voice”

  + corcoran (1995) found patients with sz showed deficits requiring “theory of mind”- the cognitive skill associated with ability to read and interpret the intentions of other people’s behaviour
• evaluation of cognitive explanation

  -Beck et al (2009) dopamine reduction on “cognitive loading”- reduced levels of NT causes the brain to struggle more into processing info, leading to cognitive insufficiency, then development of psychosis. may be a pre-existing bio risk factor which a stressor is the final trigger for sz

  -sitskoom et al (2002) cognitive deficits found in patients with sz were also found in relatives of the patients without the disorder

  -doesn’t take into account negative symptoms
• dopamine hypothesis

  states the brain of sz patients produces too much dopamine compared to a normal brain, this causes positive symptoms
• mesolimbic pathway

  if overactive, produces positive symptoms

  associated with addictive behaviour
• mesocortical pathway

  negative symptoms when underactive

  associated with motivation and emotion
• support for dopamine hypothesis

  +sz often cooccurs with depression and substance misuse

  +parkinsons: dont have enough dopamine and display similar negative symptoms to sz

  +sz can develop genetically or by brain injury

  +randrup and munkvad 1966:

  animal study, injected rats with amphetamines (inc dopamine) and they showed behavioural indicators of sz. this was replicated with many other animals

  +pet scans- gjedde and wong 1987 more than twice as many dopamine receptors in sz compared to control
• evaluation of dopamine hypothesis

  -evidence only gathered after diagnosis

  -reductionist- brown and birley 1968 found 50% of szs had a major life event in 3 weeks prior to relapse

  -antipsychotic drugs cause upregulation in dopamine

  +hardcz 1982 in post mortem studies, sz who took antipsychotics brains had raised levels of dopamine

  -drugs dont work for 4 weeks even though they block dopamine immediately, why?

  +could be development of NTs in one area inhibiting the development of other NTs

  -pet scans suggest antipsychotics dont work for szs of 10 years or more

  -possible social and environmental features
• genetic explanation for sz

  identical twin risk of sz: 48%

  first degree relative: 6-17%

  greater risk of developing sz if you are more genetically related to a sufferer

  -joseph 2004 found higher risk of birth defects in twins. mz are raised more similarly than dz, maybe the environment is more of an influence

  -tamminga and schulz 1991 cant find a single gene causing sz

  +harrison and owen 2003 up to 6 genes involved in development of sz

  -harrison and weinberger 2004 result of genetic effect on synapses, which changed how brain works
• positive evaluation of genetic explanation for sz

  +gottesman 1991 fact that mz twins show such an increase in concordance suggests genes must play a role

  +tienari et al 2000 almost 7% of adoptees with sz had a bio mother with sz and 2% werent sz but mothers were, some genetics

  +kendler 1983 30.9% concordance rate for mz and 6.5% for dz

  +disorder could be the result of the expression of multiple genes

  +adoption studies remove the problem of influence of the environment
• negative evaluation for genetic explanation of sz

  -failure to isolate a single dominant or recessive gene

  -family studies criticised for failing to acknowledge sz in families may have environmental influence

  -adoptions arent randomly placed, often put with families of similar background

  -is sz a learned condition? evidence of dysfunctional families with patterns of sz caused by negative emotions

  -twin studies dont use same diagnostic criteria

  -genetically identical twins should have 100% concordance rate if genetic