Schizophrenia

Positive symptoms - Symptoms they only experiences after becoming ill.

Hallucinations - Perceptual, sensory experiences that do not exist in reality. E.g hearing voices(often critical, instructive).

Delusions - Disturbances in the content of thought, irrational beliefs commonly linked to paranoia. E.g persecution - people re out to get you.

Disorganised speech - Derailent: Shift themes constantly. Word salad: invent words/phrases. Incoherence: illogical speech.

Disorganised/catatonic behav - Disorganised: Move quickly, pace or engage in repetitive movements.

Catatonic:Adopt strange postures, immobile for periods like a statue.

Negative symptoms - Things someone can no longer experience

Affective flattening - Poor range of emotional expression, lack sensitivity.

Speech poverty - Reduction in quantity and quality of speech, impaired linguistic ability.

Avolition - Loss of drive and motivation to carry out activities.

Diagnostic reliability

The consistency of a measuring instrument, such as a questionnaire to assess something such as the severity of sz symptoms.

Inter-rater reliability evidence

Whether 2 independent assessors give similar diagnosis of the same person independently. Classification systems have become reliable over time such as DSM-III due to multi axial system, as more psychologists can agree when someone has it. Sooderberg et al - 81 perc agreement using DSM. Osario - inter-rater reliability of +0.97 in 180 indiv using DSM5.

Test-retest reliability evidence

Whether tests used to deliver these diagnoses are consistent over time allowing a clinician to make the same diagnosis on separate occasions. Osario - +0.92 in 180 indiv using DSM5.

Rosenhan - ‘On Being sane in insane places’

Wanted to find whether medical staff could judge between mental normality/abnormality. First study - 8 ppl to hospital, claimed hear voices saying empty hollow and thud, seven admitted with diagnosis of sz, then when asked for help, ignored, everything interpreted as symptoms.

second study - hospital warned pseudopatiends would come in, none were caught but 10 perc of real patients susespected.

Reliability factors/evaluation

-Cultural diff’s cause variations with diagnosis.Coupeland - gave 134 US and 194 british psychiatrists desc of patient, 69 perc of US diagnosed sz, 2 perc of british did. So, could be due to the difference in healthcare systems, in the NHS, less time and resources, so they are ‘rushed’ and may only admit the most serious cases. So, reliability is low due to the lack of inter rater reliability across countries.

-Subjectivity is an issue. Mojtabi + Nicholson asked 50 US psychiatrists to distinguish bizarre and non-bizzarre delusions, correlation was low at 0.4. So central diagnostic requirement lacks sufficient reliability to distinguish sz and non-sz patients. So psychiatrists may require a more objective classification or more training.

-Sz too broad a category.

Diagnostic validity

The extent that sz represents something that is real and distinct from other disorders and the extent that a classification such as the ICD measures what it claims to meausre.

Criterion validity

The extent to which using different classification systems produces the same diagnosis in the same patient. Chenieuz et al - 2 psychiatrists independently rate 100 clients using DSM4 and ICD10, 68 diagnosed using ICD and 39 with DSM, so criterion validity is low.

Factors that affect validity - Comorbidity

The extent that 2(or more) conditions co-occur in the same indi.Makes diagnostic validity difficult to achieve as suggests sz may not be separate, as if conditions occur together, may be a single condition. Buckley et al - found comorbid depression occurs in 50 perc of sz patients, 23 perc OCD, 29 perc PTSD.

Factors that affect validity - Symptom overlap

Symptoms in sz are also found inother conditions. Bi-polar also involves delusions and avolition. Leads to innacurate diagnoses. Not pathogomonic - Doesnt have unique symptoms making it hard to differentiate from other disorders.

Validity evaluation

-Culture bias. High bias to people from African-Caribbean descent in the uk, Pinto and Jones estimate its 9 times higher in british people of this descent over white british groups. So, could be due to the psychosocial factors and stressors - poor housing, unemployment and social isolation, but likely that british psychiatrists are white and biased. So, validity low as its over diagnosed cross culturally.

-Gender bias. Men more commonly diagnosed with sz than women. Loring + Powell - randomly selected 290 male + female psychiatrists to read two case articles of patient behav and asked to diagnose, when patient was ‘male’ or no info on gender, 56 perc given diagnosis of sz, but when ‘female’ only 20 perc were given diagnosis of sz, this was not evident amongst the females asked. So, diagnosis influenced by gender of patient aswell as gender of clinician(men hold bias). So validity is low as men may withhold diagnosing women, and men over represented.

Biological explanations of sz:Genetics(Family studies)

Gottesman children with 2 szparents have concor rate of 46 perc, one parent13 perc,siblings 9 perc. Suggests sz runs in families, but could be env factors.

Biological explanations of sz:Genetics(Twin studies)

Joseph - Calculated that all pooled data for all sz twin studies prior to 2001 showed a concordance rate of MZ twins of 40 perc and 7 perc for DZ.

+All twin studies point out higher conc in MZ twins.

-Mz experience more equal env due to them being identical.

Bio exp of sz:Neural correlates

Early research attention has focused on ppl with sz having abnormally large ventricles in the brain. Ventricles are fluid filled cavities between brain areas that keep everything in place through internal pressure. If dmg to parts of brain, parts of it die and ventricles enlarge to fill the space. Enlarged ventricles associated with dmg to central brain and PFX, associated with neg symptoms such as avolition and the organisation of thoughts.

Bio exp of sz:Neural correlates evaluation

-Extent of brain abnormalities is unclear. The relationship is not as simple as it seems,some non sz have enlarged ventricles, while not all sz do. So, challenges the idea of sz being caused by a loss of brain tissue. So, exp lacks population valid as could have diff causes. H:Torrey found ventricles are 15 perc bigger in sz than normal.

-Existence of neural correlates tells us little about the cause. Weinberger - evidence still inconclusive as to whether brain structure is diff before they have symptoms or as a result of it. Bc sz who do not respond to medication mainly exhibit enlarged ventricles. So, efect of suffering from sz over long period of time could lead to physical brain dmg rather than brain dmg leading to sz.

-Enlarged ventricles could be due to medication which may dmg brain tissue. Ho - longitudinal, correlational study of 211 first-time sz, scanned their brains every 3 years over 14 year period, concluding antipsychotic drugs have measureable influence on brain tissue loss over time. So medication could be the damaging cause, not the illness. So, more research needs to be done.

Bio exp of sz: The original dopamine hypothesis

Stated sz’s release more dopamine into synapse than ppl without sz, causing neurons that use the transmitter to fire too often and transmit too many messages as more dopamine binded to post-synamptic neuron. Initially thought to have abnormally high D2 recepters in subcortex(explaining speech poverty - brocas area).

Bio exp of sz: The updated dopamine hypothesis (Davis et al)

High levels of dopamine are not found in all sz’s because of modern drug clozapine only blocks dopamine a little but works effectively against the disorder. Low levels of dopamine now found in prefrontal cortex(responsible for thinking and decision making) which only contains D1 receptors.Reduced dopamine in frontal areas causes neg symptoms of sz.

The dopamine hypothesis - Evidence

Anti-psychotics - Block dopamine activity and have high success rates in treating pos symptoms.

Amphetamines - Such as speed, cocaine, are dopamine antagonists causing synapse to be flooded with dopamine. Large doses lead to delusions and hallucinations in non-schizophrenia.

The dopamine hypothesis:evaluation

-Studies indicate that there may be other neurotransmitters involved. Barlow + Durand - both dopamine + serotonin involved, and recent attention given to glutamate, which sends signals to other cells, and it is important in interacting with dopamine, with severalk candidate genes for sz involved in glutamate production(Javitt). So, explains that the theory may not actually explain the root neurological cause. So theory lacks validity + credibility.

-Reductionist. Reduces it to simple neurotransmitters could be so much more such as env factors.

-Dopamine theory is correlational. Only emerged after discovered that anti-psychotics lessen the symptoms. So must be cautious in presuming the cause and effect relationsh. So theory lacks plausability

-Takes a nature side of the debate.