SZ

Question 1

Classification

Answer 1

organising symptoms into categories based on which symptoms cluster together in sufferers i.e. categorising the symptoms of schizophrenia.

Question 2

Diagnosis

Answer 2

deciding whether someone has a particular mental illness using the classifications.

Question 3

Positive symptoms

Answer 3

These aren’t “positive” because they’re good - they’re things that are ADDED and which “normal” people don’t have…

Hallucinations - seeing/hearing
Delusions/Paranoia/Grandeur - false cognitions
Disorganized speech - “word salad”
Disorganized/catatonic behaviour - completion/motivation issues

Question 4

negative symptoms

Answer 4

Sometimes known as “deficits” if they’re present for at least a year; these are things people have LOST …

Avolition - reduced motivation/goal-directed behaviour where options are present
Speech Poverty (Alogia) - loss of fluency/productivity. They don’t know less, they just produce less in a given time
Affective Flattening - Reduced range/intensity of emotions, even body language
Anhedonia - Loss of interest/pleasure, or reduced reaction to things that are pleasurable. Social aspect confused with depression - only physical anhedonia is reliable for schizophrenia (Sarkar et al., 2010)

Question 5

Delusions

Answer 5

Delusions of persecution – the belief that others want to harm, threaten or manipulate you e.g. the government, aliens.

Delusions of grandeur – the belief that they are an important individual, even god-like and have extraordinary powers e.g. the belief that they are Jesus Christ.

Delusions of control – the belief that their body is under external control e.g. being controlled by aliens or the government (e.g. have implanted radio transmitters).

Delusions of reference – the belief that events in the environment appear to be directly related to them e.g. special personal messages are being communicated through the TV.

Question 6

DSM-5 criteria

Answer 6

Two or more of the symptoms for at
least 1 month

Some signs of the disorder must last
for a continuous period of at least 6
months

Schizoaffective disorder and bipolar
or depressive disorder with
psychotic features have been ruled
out

The disturbance is not caused by
the effects of a substance or another
medical condition

Question 7

Peak on set period and % of population

Answer 7

25-30 years (younger in males, older in females)

1%

Question 8

What do we need to rule out before making a SZ diagnosis?

Answer 8

Autism Spectrum Disorder & communication deficits

Substance (drug) effects & other medical issues

Schizoaffective disorder, bipolar disorder and depression

Question 9

Being sane in insane places

Answer 9

Covert participant observation (1973) 5 states

Students (N=7) reported only “dull thud” - not an actual symptom (DSM-II)
All were diagnosed with SZ and hospitalised

They were given meds/treatment and not allowed to leave until the university intervened - in some cases after 2 months

Inter-rater reliability was good but internal validity was very poor.

Rosenhan later phoned hospitals and said he was sending more fake patients over soon. Over the next 2 weeks, 21% of patients were labelled “pseudopatients” and released.

Rosenhan actually never sent any more people to the hospital.

Question 10

evaluation of diagnostic systems

Answer 10

Inter-rater reliability r = 0.11 (Whaley, 2001)
Rosenhan “Being Sane in Insane Places” study shows…
Subjective criteria not cross-culturally reliable (r = 0.4 for judgement of “bizarre” in experienced clinicians)
Internal validity, Nomothetic/idiographic, beta bias…

Gender Bias (beta bias)
Significant difference in diagnosis for M (56%) and F (20%) examples (Loring et al., 1988)
Culture bias too - spiritualist cultures…
Determinism and reductionism related to male bias in research. Economic costs…

Comorbidity issues
Depression, anxiety disorders, personality disorders, PTSD…
Symptom overlap also an issue (dissociative personality disorder - DID especially)
Application issues - treat with wrong drugs; make condition worse

Question 11

Dopamine receptor genes (D2, DRD2)

Answer 11

Affects number of dopamine receptor sites and transport proteins for dopamine. Associated with both positive and negative symptoms (Davis & Khan, 1991)

Question 12

Glutamate receptor genes (NMDA/AMPA)

Answer 12

Affects number of glutamate receptor sites. Especially important in the ventral striatum (part of basal ganglia). Associated with negative symptoms (Sorg et al., 2013)

Question 13

G-protein coupled receptor kinase (GRK)

Answer 13

Makes epigenetic and sensitivity changes to receptors for a number of excitatory neurotransmitters. Higher levels increase effects. (Funk et al., 2014)

Question 14

Family genetic factors

Answer 14

Gottesman (1991)

Studied concordance rates in children with SZ parent(s) or siblings

2x SZ parents - 46% concordance

1x SZ parent - 13% concordance

1x SZ sibling - 9% concordance

Question 15

Twin genetic factors

Answer 15

Joseph (2004)

Meta-analysis of data on MZ vs DZ twin concordance for SZ (studies before 2001)

MZ concordance - 40.4%

DZ concordance - 7.4%

Modern studies use “blind” researchers (why?)
They show a lower, but still big, difference

Question 16

Adoption genetic factors

Answer 16

Tienari et al. (2000)

Compared siblings raised together vs apart. (Why?)

164 adoptees had SZ mothers. Of these, 6.7% also developed SZ.

197 adoptees were in control group. 2% of them developed SZ.

Conclusion - genetic liability for SZ is “decisively confirmed”

Question 17

The Dopamine Hypothesis

Answer 17

This hypothesis states that SZ is caused by imbalances of dopamine. Either:
They have too many D2 receptors
Their D2 receptors are too sensitive/fire too often
They produce too much dopamine
This explains positive symptoms only

Question 18

HYPER dopaminergia

Answer 18

too much

Hyperdopaminergia in subcortex is associated with positive symptoms

Broca’s area produces speech. Too much dopamine here leads to the speech and hearing-related symptoms

Question 19

HYPO dopaminergia

Answer 19

too little

Hypodopaminergia in cortex is associated with negative symptoms

Prefrontal cortex (PFC) is the central executive (cognitive processes/decisions). Too little here leads to avolition/catatonia.

Question 20

Typical antipsychotics

Answer 20

Developed in 1950s
Stop hallucinations/delusions

e.g. chlorpromazine are dopamine antagonists – they bind to (and so block) dopamine receptors but don’t stimulate them, reducing the action of dopamine. Initially dopamine levels build up but then production is reduced. This normalises neurotransmission in key areas of the brain, by reducing stimulation of the dopamine system reducing positive symptoms such as hallucinations.

Question 21

Atypical antipsychotics

Answer 21

More modern (popular since 1980s)
Treat positive AND negative symptoms
Work on “hard-to-treat” patients

e.g. clozapine and risperidone also block dopamine receptors like typical antipsychotics. However, they only temporarily occupy the receptors and then rapidly dissociate to allow normal dopamine transmission. This is thought to be responsible for fewer side effects. They also act on other neurotransmitters, particularly serotonin and they address negative symptoms e.g. avolition as well as positive symptoms.

Question 22

The double bind

Answer 22

“schizophrenogenic mother”

Bateson et al. (1956) says contradictory messages are responsible for children becoming schizophrenic.

Eg. If your mother says she loves you while she physically punishes you then you can get confused about what the reality is.

Question 23

Dysfunctional families

Answer 23

Families with high “emotional expression” can trigger psychotic episodes
These families describe SZ relatives in hostile, critical terms
EE level in family/friends is strongly correlated with relapse rates

Negative emotions can trigger SZ episodes in vulnerable people. Supportive environments may be protective. This is a diathesis-stress model.

Question 24

Dysfunctional thought processing

Answer 24

stage 1:
Cognitive processing biases
(Hyperdopaminergia in/around MLP)

stage 2:
Misattribution of consequences to causes
(Hypodopaminergia in ACG and PFC)

stage 3:
Failure to test reality with memory or logic
(DLPFC - Hippocampus link atrophy or dysfunction (glutamate))

Question 25

cognitive explanations

Answer 25

Delusions:
Inadequate information processing
Egocentric bias
Failure to contextualise events
Patients unable to perform “reality testing” (Beck & Rector, 2005)

Hallucinations:
Hypervigilance
Higher expectancy of voices
Patients can’t distinguish between sensory info and internal images (Aleman, 2001)
They misattribute the source of internal images to external sources (Baker & Morrison, 1998)
They don’t see disconfirming evidence as they don’t reality check.

Question 26

CBTp

Answer 26

-aims to help patients to identify irrational thoughts and challenge them (including the origin of ‘voices’) and reality testing them to reduce distress.

-uses the ABCDE model

-Critical collaborative analysis – the therapist uses gentle questioning to help the patient to understand and challenge illogical deductions and conclusions e.g. ‘if your voices are real, why can no one else hear them?’
Rather than ‘getting rid’ of schizophrenia, CBTp helps patients to cope better with their symptoms because it reduces distress.

Question 27

ABCDE model

Answer 27

identifying activating events (A) and the resulting beliefs (B)
from these events that appear to cause their emotional and behavioural consequences (C). These beliefs can then be rationalised, disputed (D)
and changed through critical collaborative analysis, leading to the effect (E) of restructured beliefs.

Question 28

ACT therapy

Answer 28

Rather than using behavioural techniques to correct irrational thoughts, patients are encouraged to embrace and embody their thoughts and feelings

The goal is building resilience and confidence - patients must live with their condition and if they cannot face their difficulties they’re more likely to need drug treatments

Question 29

family therapy

Answer 29

It’s so successful at reducing relapse that NICE recommends it for all SZ families
It’s based on the finding that hostile/overly expressive families –> more relapses
Family therapy reduces chance of relapse by up to 50% (Garety et al., 2008)

Lasts from 3-12 months (at least 10 sessions)

Question 30

token economy

Answer 30

Token economy is a form of behavioural therapy used in the management of schizophrenia. It is used to shape and manage behaviour so that patients in long stay hospitals are easier to manage

It involves desirable behaviours being encouraged through selective reinforcement.
Rewards (tokens) are given immediately as secondary reinforcers when patients engage in desirable behaviours e.g. getting dressed in the morning, making a bed, taking medication etc.

Although these tokens have no value in themselves, they can be swapped later for more tangible rewards (primary reinforcers). For example, sweets, magazines, privileges such as a walk outside the hospital. Therefore, this encourages the desirable behaviour to be repeated because they have become associated with rewards and privileges.

Whilst modifying these behaviours doesn’t cure schizophrenia, it improves the patients’ quality of life and makes it more likely that they can live outside a hospital setting.

Question 31

Diathesis-Stress

Answer 31

The diathesis (vulnerability) for schizophrenia is entirely genetic. Genes are assumed to cause neurochemical abnormalities that in turn, result in an increased risk for schizophrenia.
If a person does not have the genetic vulnerability, no amount of stress would lead to schizophrenia.
The stress (trigger) for schizophrenia is negative psychological experience e.g. dysfunctional parents and stressful life events (e.g. going to university, moving house etc.).

Question 32

Key Study: Tienari et al. (2004)

Answer 32

To see whether genetic factors moderate susceptibility to environmental risks associated with adoptive family functioning. Two-tailed hypothesis - investigation.

Checked hospital records to identify women who’d had a psychotic episode. They noted who’d given kids for adoption.

145 high-risk adoptees compared with 158 “control” adoptees.

Both groups assessed after 12 years and followed up at 21 years. Family functioning was also assessed.

Interviewers were kept blind about status of the biological mother - to avoid investigator effects.