Schizophrenia

• what is schizophrenia?


  psychotic disorder where a person loses touch w/ reality (has a 'split mind' - meaning split from reality)

  - rare = only around 1% of people in world have it
• what does 'positive' symptoms mean ?

  additional experiences beyond those of 'ordinary existence
• what does 'negative' symptoms mean?

  involve the loss of usual abilities and experiences
• what are the positive symptoms of schizophrenia?

  HALLUCINATIONS = sensory experiences of stimuli that have either no basis in reality or are distorted perceptions of things that are there (eg. auditory hallucinations (hearing voices) - often critical (most common)/ distorted facial expressions/ seeing people who aren't there)

  DELUSIONS = irrational beliefs about world that aren't true

  eg. 'delusions of grandeur' - believing they are important political/religious figure (eg. Jesus)/ belief that they or part of them is under external control/ paranoid delusions (eg. belief doctor is trying to kill u)

  (DISORDERED THINKING - disjointed, not logical speech )

  (DISORGANISED/ ABNORMAL MOTOR BEHAVIOUR - agitation, lack of goals or responses, excessive movement)
• what are the negative symptoms of schizophrenia?

  AVOLITION = loss of motivation to carry out tasks/ lowered activity levels/ lethargic (eg. poor hygiene/ lack of persistence in work/ lack of energy)

  ANHEDONIA = loss of interest/ pleasure in everyday life/ activities

  SPEECH POVERTY (alogia) = reduced frequency + quality of speech
• what are the 2 classification manuals?

  - diagnostic statical manual (DSM-5)

  - international classification of diseases (ICD) 11
• What are the subtypes of schizophrenia? (extra info)

  - DISORGANISED SZ = delusions, hallucinations, disordered thinking (+ poor hygiene - avoliton)

  - PARANOID SZ = (paranoid) delusions, delusions of grandeur

  - CATATONIC SZ = motor control problems (posturing like a statue is common) (+ hallucinations)

  - SIMPLE SZ = all neg. symptoms (only recognised by ICD)

  - UNDIFFERENTIATED SZ = range of symptoms that don't fall into the other sub types

  (many other sub-types)
• how is speech poverty described differently in the 2 manuals?

  ICD = says it's a NEG. symptom (reduced amount/ quality)

  DSM = says it's a POS. symptom (speech disorganisation/ incoherent speech/ changing topic mid sentence)
• what is the DSM?

  DIAGNOSTIC STASTICAL MANUAL

  - American psychiatric association

  - 1 POSITIVE SYMPTOM must be present for diagnosis of SZ
• what is the ICD?

  INTERNATIONAL CLASSIFICATION OF DISEASES

  - world health organisation

  - 2 NEGATIVE SYMPTOMS must be present for diagnosis of SZ

  - recognises subtypes of SZ = hebephrenic/ paranoid/ catatonic
• what is validity?


  the extent to which we are measuring what we intend to measure (ie. is schizophrenia actually being diagnosed)
• what is symptom overlap? how does this affect validity of diagnosis of SZ?

  - when there are the same symptoms for multiple illnesses (eg. avolition/ loss of energy/ anhedonia/ low mood = symptoms of depression and SZ) (depression, bipolar, SZ most overlap)

  - MISDIAGNOSIS - could lead to WRONG TREATMENT - so patient DON'T GET BETTER (research = misdiagnosis - can lead to yrs delay in correct treatment)
• what is co-morbidity? how does this affect validity of diagnosis of SZ?


  - when ONE DISORDER EXISTS ALONGSIDE ANOTHER DISORDER (occurrence of 2 illnesses/ conditions together - eg. patient has depression and SZ)

  - SZ may not be a separate disorder (ie. depression + SZ is 1 illness)/ decreases validity (boundaries between disorders artificially drawn up)/ neg. implications for patients - range of 'labels' + prescribed range of medicine/ issues of construct validity
• what is the study of co-morbidity (+ symptom overlap/ validity)?

  BUCKLEY ET AL.

  - 50% of SZ patients also diagnosed w/ DEPRESSION

  (- 47% diagnosed w/ SUBSTANCE ABUSE)

  (- 29% diagnosed w/ PTSD)

  (- 23% diagnosed w/ OCD)
• what is reliability?


  the extent to which classification and diagnosis is consistent
• who did the study on reliability of SZ diagnosis and what was the procedure?

  - ROSENHAN

  - 8 HEALTHY ps (5M/3F) went to 12 psychiatric hospitals

  - complained of HEARING INDISTINCT VOICES saying 'empty'/ 'hollow'/ 'thud'

  - ONLY SYMPTOM reported + after reporting, acted completely normally
• what were the findings for Rosenhan's reliability study?

  - ALL were diagnosed + institutionalised w/ SZ (but 1 - bipolar)

  - NONE of Ps were identified as 'FAKE' PATIENT

  - held in hospital, for some cases 3 MONTHS + were classified as 'schizophrenia in remission' upon discharge

  (poor reliability - all same symptoms, not all diagnosed w/ SZ - 1 bipolar/ + no fake patients identified)
• what was Rosenhan's follow-up study?


  - told staff at hospital, MORE FAKE PS would TRY GAIN ADMITTANCE

  - hospital said they would identify them this time

  - after 1 MONTH, hospital claimed 41 PATIENTS WERE FAKE (of 193 admitted)

  - ALL PATIENTS WERE REAL (rosenhan sent 0 fake patients)

  (poor reliability - could not identify diff. between real and fake symptoms/ patients)
• how is SZ diagnosis inconsistent across cultures (reliability)?

  (Copeland et al) = cultural variations in diagnosis study

  - gave same patient description to 134 AMERICAN + 194 BRITSH PSYCHIATRISTS

  - 69% of AMERICAN psychiatrists diagnosed SZ

  - 2% of BRITISH psychiatrists diagnosed SZ

  = UNRELIABLE ACROSS CULTURES (large diff. 69-2%)

  = UNRELIABLE WITHIN CULTURES (only 69% identified SZ not 100% or near 100% so inconsistent)
• what is the inter-rater reliability for SZ diagnosis?

  - POOR INTER-RATER RELIABILITY

  - Whaley = found correlations as low as 0.11 (v bad)

  (0.8 = good inter-rater reliability)
• what are the contradictions between the DSM + ICD?

  CHENIUX ET AL

  - 2 psychiatrists independently diagnosed 100 patients using DSM + ICD criteria

  PSYCHIATRIST 1 = 26 w/ SZ (according to DSM)/ 44 w/ SZ (ICD)

  PSYCHIATRIST 2 = 14 w/ SZ (DSM)/ 24 w/ SZ (ICD)

  - POOR INTER-RATER RELIABILITY between manuals + psychiatrists
• what is predictive validity?

  the ability to test or other measurement to predict a future outcome (eg. behaviour, performance, recovery after treatment)

  - SZ = can be gauged by effectiveness of successful recovery

  - if its valid + identifiable disorder = those diagnosed + w/ treatment should recover

  - CARDWELL + FLANAGAN = suggest only 10% of diagnosed SZ patients fully recover (low predictive validity)

  (- some psychiatrists argue whatever treatment given, it won't be effective because SZ may be biological/ encoded in genes)
• gender bias questioning reliability of SZ diagnosis (evaluation)

  prevelance of SZ - found men more often diagnosed w/ SZ than women

  - possibly due to gender bias

  - female patients = typically HIGHER FUNCTIONING (more likely to work/ have good fam. relationships)

  - women may be more under diagnosed due to GOOD FUNCTIONING + MASKING OF SYMPTOMS

  (weakens validity of diagnosis - biased towards male presentation of SZ)
• cultural bias questioning reliability of SZ diagnosis (evaluation)

  - african Americans + ppl of afro-american origin = several times more likely to be diagnosed w/ SZ than white people - even though rates in africa/ West Indies isn't high

  - pos. symptoms (eg. hearing voices) more accepted in African cultures due to cultural beliefs (communication w/ ancestors) so ppl more accepting of these experiences (more normalised)

  - in western cultures = seen as bizarre + irrational so more likely to be diagnosed w/ SZ

  (- over-diagnosis of these cultures weakens validity, cultural backgrounds of patients not taken into account)
• why is validity + reliability important?

  - if not can lead to MISDIAGNOSIS w/ serious implications: - wrong treatment/ medicine w/ can have side effects

  - damaging 'labels' that r difficult to get rid of affecting how others view + treat them

  - economic implications w/ misdiagnosis - expensive to give treatments that might not be needed/ could stop people from working when they r health enough, impacting economy
• what are the biological explanations for SZ?

  - genetics (genetic explanation)

  - dopamine hypothesis

  - neural correlates
• what is the genetic explanation for SZ?

  - tends to RUN IN FAMILIES - ppl may be GENETICALLY PREDISPOSED to develop sz

  - GOTTESMAN = strong relationship between DEGREE OF GENETIC SIMILARITY + SHARED RISK OF SZ (highest likelihood w/ identical twins = 48%)

  - CANDIDATE GENES/ POLYGENIC/ AETIOLOGICALLY HETEROGENOUS
• what are candidate genes?

  individual genes believed to be associated w/ risk of inheritance (of SZ)
• what does polygenic mean?

  - multiple genes associated w/ SZ

  (multiple genes appear to carry small inc. risk of SZ)
• what dos aetiologically heterogenous mean?

  different combinations of genes can lead to sz (different studies identified different genes cause sz)

  (as well as other factors)
• what happens at the synapse (genetic explanation for SZ)?

  - electrical impulse arrives at end of neurone

  - neurotransmitter released into synaptic cleft/ synapse + sit in appropriately shaped receptor sites on post-synaptic neurone, stimulating it

  - chemical charge (threshold reached) triggering electrical impulse to fire along neurone + process continues across other neurones

  - when neurone fired, brief moment of rest where neurone can't fire = refectory period + excess neurotransmitter cleared from synapse

  - excess neurotransmitters reabsorbed by pre-synaptic neurone (reuptake) or broken down + recycled elsewhere

  
• what are the synapses called in reference to DOPAMINE?

  pre-synaptic cleft = D1 receptor (may cause over activation of DA due to releasing too much DA into synaptic cleft)

  post-synaptic cleft = D2 receptor (may cause over activation by being too sensitive +/or too numerous + so 'fire' too readily)
• what are the 2 explanations of the dopamine hypothesis?

  - HYPERdopaminergia in the SUBCORTEX

  - HYPOdopaminergia in the CORTEX

  (both hyper- + hypo- may be correct explanations for sz because it involves diff. brain regions)
• how does HYPERdopaminergia explain SZ? (dopamine hypothesis)

  (original version of DA hypothesis)

  - HIGH LEVELS OF DA in SUBCORTEX (central areas of brain)

  - eg. excess of DA receptors in Broca's area (responsible for speech production)

  - may be associated w/ SPEECH POVERTY +/or AUDITORY HALLUCINATIONS
• how does HYPOdopaminergia explain SZ? (dopamine hypothesis)

  (newer version of DA hypothesis)

  - LOW LEVELS OF DA in PREFRONTAL CORETX (responsible for thinking + decision making)

  - may be associated w/ NEGATIVE SYMPTOMS of SZ
• what are neural correlates?

  measurements of the STRUCTURE OR FUNCTION of the BRAIN that CORRELATE W/ AN EXPERIENCE

  (ie. structure of brain cause certain symptoms of sz)
• how are negative symptoms of sz connected to neural correlates?

  - AVOLITION (lack of motivation) = VENTRAL STRIATUM (part of brain)

  (motivation involves anticipation of rewards + VS involved in this)

  - LOWERED ACTIVITY LEVELS IN VS (cause the symptoms)
• how are positive symptoms of sz connected to neural correlates?

  - LOWER ACTIVATION LEVELS in ANTERIOR CINGULATE GYRUS + SUPERIOR TEMPORAL GYRUS in ppl w/ HALLUCINATIONS
• what is SUPPORTING research for the GENETIC EXPLATION of sz? (evaluation of bio. explanation)

  GOTTESMAN:

  - large scale fam. study looking at risk of developing sz + genetic relatedness

  - strong relationship between degree of genetic similarity + risk of sz

  - (MZ (identical) twins = 48% risk/ parent = 6% risk of developing sz)

  ADOPTION STUDIES (TIENARI ET AL):

  - investigated whether Finnish (Finland) kids adopted from SZ mothers developed SZ

  - adoptive parents assessed for childrearing style + rates of SZ + compared against control group (w/out genetic risk)

  - found kids more affected by childrearing style if they had a heightened genetic risk (already predisposed to SZ so childrearing style just inc. already present risk)

  RIPKE ET AL:

  - genome wide study - genetic makeup of 37,000 patients compared to 113,000 controls

  - 108 separate variations (of genes) associated w/ inc risk of sz (so its polygenic)
• what is the research AGAINST the GENETIC EXPLANATION for sz? (evaluation of bio. explanation)

  ENVIRONMENT: (counterpoint - gottesman)

  - families also share environment (as well as genes)

  - could be similar environment which causes sz rather than genetics

  ADOPTION: (counterpoint - tienari)

  - only certain types of ppl will be open to adopting children predisposed to sz

  - so childrearing practices will be similar between all/most adoptive parents (not completely random allocation