Explaining Schizophrenia

Question 1

Genetic causes of schizophrenia

Answer 1

Inherited through generations/transmissions of genes and DNA, runs in families and likely polygenic
NRG1 contributes as glutamatergic signalling regulates NMDA receptor (excitatory neurotransmitter in brain), also NRG3 is a susceptibility gene
Ripke meta-analysed studies of candidate genes of sufferers, 37k sufferers vs 11k controls, finding 108 genetic variations associated with increased risk. High levels of dopamine can cause schizophrenia and these genes also seemed to code for dopamine functioning (including NRG1 and 3)

Question 2

Ripke/ genetics eval

Answer 2

• Need to be cautious when looking at genetics alone as a cause, other factors can exist e.g learning abnormal behaviours via environment (behavioural approach)
• Not a full explanation as to how schizophrenia is transmitted, if someone has the gene they do not automatically get illness (if the gene is recessive) so diathesis stress makes more sense i.e environmental trigger of illness
  + Lots of research support and robust studies e.g Gottesman and Kety so genetics cannot be ignored as a cause
• Schizophrenia can occur in the absence of genetic history e.g mutation in parental DNA causing schizophrenia in future offspring (e.g radiation, poison, viral cell damage), also age a risk factor, fathers under 25 have 0.7% chance of schizophrenia child compared to 2% over 50
  + Supported by dopamine hypothesis which states that high level of dopamine in D1 and D2 receptors cause schizophrenia- Ripke work can be praised by linking biological mechanism (genes/neurotransmitters) that cause schizophrenia

Question 3

Gottesman and Shields - twin study

Answer 3

106 MZ and 118 DZ twins investigated (129 male 104 female) with average age 46yrs and range of ethnic backgrounds, longitudinal study over 25yrs where diagnosis using in depth interviews, doctors case notes and the DSM. One twin already had schizophrenia and they tracked whether the other one did
48% of MZ both concordance by the end of the study vs 17% of DZ so clear genetic basis to some extent , even for DZ where risk factor much higher than general population (1%)

Question 4

Gottesman and Shields eval

Answer 4

+ population validity/representative sample
+ longitudinal so prospective study, looked at both before and after diagnoses so was holistic and didn’t rely on potentially flawed recall of e.g memories
- ignores behavioural approach i.e identical twins often copy/model behaviour (SLT) or learn the same behaviour through shared growing environments rather than genes
+ reliable and valid sources of data wi5 in depth interviews, notes, DSM also high inter-rater reliability/ validity
- Schizo patients often struggle with speech/communications so may have struggled to communicate symptoms effectively in interviews, so diagnosis/classification may be inaccurate

Question 5

Kety - adoption study

Answer 5

prospective longitudinal study from 1972 - 1989 in Denmark, 207 high risk adopted children studied whose bio mums had schizophrenia diagnosis, matched (age, gender, race, socioeconomic status) control group of 104 adoptives, low risk
16.2% of high risk schizo diagnosis and 18.8% for schizotypal personality disorder (35% total) compared to 1.9% schizophrenia and 5% schizotypal (6.9% total)

Question 6

Kety eval

Answer 6

+ Similar new york high risk project study conducted over 25 years and similar results to Kety
+ Longitudinal and prospective so holistic and accurate
+ Carefully matched pairs helps to reduce confounding variables that could affect the schizophrenia diagnosis
- Cannot fully separate genes from environment as the children would have shared the environment for a short time before adoption - this needs to be carefully considered when interpreting results
- Problematic reliability - mothers were diagnosed before systems like DSM, so some critics suggest that they would have had schizotypal personality disorder instead (as similar symptoms) so their kids would also not be as high risk

Question 7

Davis and Neale - Dopamine hypothesis

Answer 7

Excess levels of dopamine neurotransmitter in subcortical area - increases firing of neurons (hyperdopaminergia) - can give phenothiazines to block dopamine but then only positive symptoms reduce
L-dopamine increases dopamine and is seen to induce symptoms - also e.g LSD and amphetamines (dopamine antagonists) - post mortem studies found schizophrenia patients had increased amounts of dopamine in receptors and left amygdala
Glutamatergic another neurotransmitter in brain/CNS - excitatory and major role in learning/memory but schizophrenia patients have struggles with making and using it
Abnormal dopamine metabolisms - can be monitored using position emission tomography (PET) - brain activity/imaging

Question 8

Dopamine hypothesis eval

Answer 8

+ When schizo patients given L-dopa their symptoms got worse and intensifies (obvious ethical issues)
- Unclear cause and effect - perhaps investigate further with (longitudinal?) PET scanning
- Dopamine also associated with mania (bipolar depression) which can also be alleviated by phenothiazines - so dopamine has complex role - ideas of symptom overlap?
- Biologically reductionist as reduces complex phenomenon down to a singular neurotransmitter - other biological factors e.g neuroanatomy of brain or psychological factors e.g family dysfunction, behaviourist approach
+ Research into dopamine uses scientific methods e.g PET and fMRI which are highly valid and reliable

Question 9

Neural correlates

Answer 9

Correlation between brain structure and function and symptoms of schizophrenia
Schizophrenia patients given cognitive and memory tasks and compared to control patients during fMRI scan
Swayed reviewed 50 patient scans and examined brain images to find common structural abnormalities - decrease in brain weight, enlarged ventricles (filled with water), smaller hypothalamus, less grey matter (where intelligence is held) and structural abnormalities in prefrontal cortex (where personality is held)

Question 10

Neural correlates eval

Answer 10

• The extent to which ventricles are enlarged is not significant so little difference in that neural correlate
• Cause and effect unclear - schizophrenia may cause brain structure to alter
  +- lots of evidence to suggest schizophrenia caused by neural correlates changing during pre natal development (in womb) but fails to explain why schizophrenia occurs in early adulthood and not infancy - ideas include that pre frontal cortex develops during adolescence so damage to this part of the brain only noticeable at/after this time (when symptoms become apparent)
• sufferers of mania also have enlarged ventricles so those alone cannot cause schizophrenia but rather a risk factor - can link to diathesis stress model
  + Research involves scientific and objective techniques like fMRI - valid/reliable

Question 11

Bateson - double bind theory of communication

Answer 11

Disturbed patterns of communication and family dysfunction as a risk factor of schizophrenia- double bind hypothesis means children are given mixed messages from parents and feel they cannot do anything right. E.g be loving one time or critical another, give conditional love or say positive things in a cruel way - creates confusion, withdrawal, self doubt where children cannot construct an internally coherent sense of reality
May develop schizophrenic symptoms e.g withdrawal,disorganised thinking, paranoia, delusions (of persecution?)
Also can be caused by a marital schism where parents argue in front of children (and even involve them) which causes distress and confusion

Question 12

Double bind eval

Answer 12

• Criticism as theory used retrospective studies so relied on potentially faulty/inaccurate recollection of memories
• Unclear cause and effect - schizophrenia may cause friction and e.g double bind in families
  + Research found that schizophrenia patients reported a higher recall of double bind statements by mothers than non-schizophrenics
• Ethical issues when studying family dysfunction - can cause psych harm if a family told their behaviour helped cause schizophrenia - also need to be aware of invading privacy and keeping info confidential and anonymous
  + Research found people with difficult childhood families had increased schizophrenia risk in adulthood - studies found 69% of females and 59% of male adult schizo patient had history of physical or sexual abuse in childhood
  + Support from psychodynamic theories recognising a schizophrenogenic mother who is cold, controlling, rejecting leading to excessive stress - can be main factor that helps develop schizo. But this theory suggests passive involvement from father, alpha bias and temporally invalid

Question 13

Kavanagh - Expressed emotion

Answer 13

Negative emotional interactions/climates as a key role in causing and maintaining symptoms of schizophrenia- set of traits where family members talk to/about patient in a critical/hostile/emotionally over-involved manner - this can cause relapse in person recovering from schizophrenia esp if returning home after hospital stay (x4 chance vs low EE)
Families with high EE talk more than listen so patient has low tolerance for emotional stimuli e.g intense comments, causing stress
Can also cause relapse of other mental disorders e.g depression and eating disorders
More typical in developed countries rather than developing ones (despite more access to resources/treatments)

Question 14

Expressed emotion eval

Answer 14

+ Research by Brown supports that high EE households more likely to cause/aid relapse of schizophrenia
+ Support and well established maintenance model for schizophrenia since 1990s, and research agreed in many different cultures - idea is so strong that families with high EE encouraged to undergo education/training to reduce EE - temporal/cultural validity
+ Applications i.e family therapy to help alleviate symptoms and increase support/awareness
- Critics suggest that schizophrenia patient have minimal contact with families e.g if they are institutionalised and lack familial contact or due to family withdrawal, so low chance of EE being a causal factor of schizophrenia
- Cause and effect unclear - schizophrenia in one member may cause family members to have high EE
- Ignores biological factors causing schizophrenia - main causes tend to be biological and this is supported by the most research e,g Ripke, Gottesman, Kety
- Family dysfunction as a maintenance model rather than an onset explanation, where difficult dynamics prolong and perhaps worsen symptoms but do not cause them alone

Question 15

Cognitive view by Frith

Answer 15

i.e cognitive impairments and maladaptive thinking linked to developing positive symptoms - central control deficits (cognitive inability to filter, suppress, or override automatic thoughts, actions, and speech)
Delusions of control/auditory hallucinations due issues w self monitoring/info processing
Cannot distinguish between internal actions/thoughts from external - causes distress
Therefore dysfunctional thought processes - cannot recognise cognitive distortions (biases)
Poor at recognising own output e,g drawings and understanding their own thinking (metacognition) as distinct from environmental stimuli
Symptoms can be explained with 3 factors of metarepresentation (ability to reflect on thoughts and experiences) - inability to generate and monitory voluntary action, inability to monitor beliefs and intentions of others
Card prediction task (if red or black) given to schizophrenia vs control - schizophrenia patients produced more stereotypical choices e.g all red all black or alternating, while control had more random choices - suggests problems generating immediate action and supports lack of self control due to cognitive impairments

Question 16

Cognitive view eval

Answer 16

+ Explains why symptoms are developed (metarepresentation) not just how or what - seems a reasonable account face valid i.e if thoughts don’t come from us they may be hallucinations
- Reductionist ideas of metarepresentation by reducing schizo to 3 basic individual cognitive symptoms
- Ignores the underlying cause of schizophrenia which is mainly biological - only explains some aspects of schizophrenia thinking/suffering and ignores other approaches - diathesis stress
- Cause and effect unclear - schizophrenia sufferers may develop dysfunctional thought processes due to illness
- Can be seen as more of a list of symptoms that will be developed/ already have been, rather than explaining exactly what causes schizophrenia
+ Cognitive approach research usually lab experiment so results are scientific and objective and helps establish clear IV DV effects with one variable as schizo

Question 17

Hemsley - Schemas and dysfunctional thoughts

Answer 17

Healthy people have a good combo of perception and memory but schizophrenia patients have a poor combo (esp memory)
Breakdown between stored info in LTM (schemas) and new info, so schemas (which are used to interpret and deal with current situations based on experience/knowledge) cannot be accessed - breakdown in cognitive processing and possible sensory overload where they cannot decide what to focus on/ignore - leading to disorganised/delusional thinking/behaviour

Question 18

Schema theory eval

Answer 18

+- Consideration of nature-nurture debate - dysfunctional thoughts due to biology or environment/upbringing, maybe diathesis stress
- Ethical issues using schizophrenia patients in research - may be unable to give fully informed consent or communicate effectively when they wish to withdraw - or psych harm/discomfort of being tested for cognitive functioning
+ Schizophrenia vs control given stroop test (say the word not the colour) and schizophrenia patients had a central control dysfunction and took 2x the time to say the correct word
- While it makes sense how faulty schema/ central control dysfunction leads to schizophrenia, not all patients suffer from dysfunctional thoughts so it is not a complete explanation
- Beck and rector had a more unified/ interactionism approach - biological (brain) abnormality leads to schizo, thus leading to vulnerability to more stressful experiences which leads to the dysfunctional thoughts - cognitive causes alone do not cause schizophrenia