Schizophrenia Flashcards

1
Q

Diagnosis and Classification: DSM-5

A

One positive symptom must be present (delusions, hallucinations or speech disorganisation).

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2
Q

Diagnosis and Classification: ICD-10

A

Two or more negative symptoms are sufficient for diagnosis (e.g. avolition or speech poverty).

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3
Q

Positive symptoms

A

Additional experiences beyond those of ordinary existence.

  • Hallucinations: sensory experiences. No real basis in reality or distorted perceptions of real things. E.G. hearing voices/ seeing people who aren’t there.
  • Delusions: beliefs. No real basis in reality. Behaving in ways that makes sense to sufferers only. E.G. beliefs about being a very important person.
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4
Q

Negative symptoms

A

Loss of usual abilities and experiences.

  • Avolition: severe loss of motivation to carry out everyday tasks. Lowered activity levels, unwillingness to carry out goal-directed behaviours.
  • Speech poverty: reduction in the amount and quality of speech. (Delay inverbal responses). DSM emphasises speech disorganisation and incoherence.
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5
Q

Issues in Diagnosis

A

Reliability: extent to which diagnosis is consistent.
Validity: extent to which diagnosis and classification techniques measure what they are designed to measure.
Co-morbidity: occurrence of two illnesses together confuses diagnosis and treatment.
Symptom overlap: e.g. depression and schizophrenia.

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6
Q

Evaluation of diagnosis and classification

A

✗ Diagnosis has low reliability - Cheniaux et al. had 2 psychiatrists independently diagnose 100 patients using both DSM and ICD criteria. Inter-rater reliability was poor. One diagnosed 26 using DSM and 44 using ICD. Another diagnosed 13 with DSM and 24 using ICD.
✗ Validity - this study shows that schizophrenia is more likely diagnosed with ICD. People are either over-diagnosed or under-diagnosed.
✗ Co-morbidity - Buckley et al. found half of patients with diagnosis of schizophrenia also have a diagnosis of depression.
✗ Gender bias - Cotton et al. found female patients typically function better. Some women escape diagnosis - interpersonal functioning may bias practitioners to under-diagnose.

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7
Q

Biological Explanations: Genetic Basis

A

Schizophrenia runs in families.
Gottesman’s family study found MZ twins have a 48% shared risk of schizophrenia. DZ twins have a 17% shared risk and siblings have a 9% shared risk.
- Schizophrenia is polygenetic and aetiologically heterogenous.
- Ripke et al. studied 37,000 patients and found 108 separate genetic variations associated with increased risk; many coded for the dopamine neurotransmitter.

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8
Q

Biological Explanations: Dopamine Hypothesis

A

Dopamine is featured in the functioning of brain systems related to the symptoms of schizophrenia.

  • Hyperdopaminerga linked to subcortex associated with hallucinations and poverty of speech (excess of dopamine receptors in Broca’s area).
  • Hypodopaminergia linked to prefrontal cortex responsible for thinking and decision making.
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9
Q

Biological Explanations: Neural Correlates

A

Measurements of the structure of function of the brain that correlate with the positive or negative symptoms of schizophrenia.

  • Ventral Striatum: anticipation of reward (motivation). Loss of motivation may be explained by low levels of activity here. Juckel et al. found a negative correlation between ventral striatum activity and overall negative symptoms.
  • Superior Temporal Gyrus: Allen et al. found patients experienced auditory hallucinations recorded lower activation levels in STG and anterior cingulate gyrus.
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10
Q

Evaluation of Biological Explanations

A

✓ Strong evidence for genetic vulnerability - Gottesman family study shows how genetic similarity and shared risk are closely related. Adoption studies (Tienari) show children of people with schizophrenia are still at a heightened risk if adopted into family histories without schizophrenia.

✗ Mixed support for dopamine hypothesis - dopamine agonists (amphetamines) that increase dopamine can induce schizophrenic-like symptoms in people without schizophrenia. However, some of the candidate genes identified code for the production of other neurotransmitters - glutamate.

✗ The environment is also involved - family functioning during childhood and other factors can also play a role in the development of schizophrenia. Combination of biological and psychological approaches.

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11
Q

Psychological Explanations: Family Dysfunction (Schizophrenogenic Mothers)

A

Fromm-Reichmann’s psychodynamic explanation based on patients’ early experiences of SM - these mothers are cold, rejecting and controlling and create family tension and secrecy.

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12
Q

Psychological Explanations: Family Dysfunction (Double-bind Theory)

A

Bateson et al. found a child may be trapped in situations where they fear doing the wrong thing, but they receive conflicting messages about what counts as wrong.

When they ‘get it wrong’ they are often punished by withdrawal of love - they learn the world is confusing, leading to disorganised thinking and delusions.

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13
Q

Psychological Explanations: Family Dysfunction (Expressed Emotion)

A

The level of emotion expressed towards the schizophrenic patient and includes:

  • Verbal criticism of patient
  • Hostility towards them
  • Emotional over-involvement in their life

High levels = stress, a primary explanation for relapse.

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14
Q

Psychological Explanations: Cognitive Explanations (Dysfunctional thought processing)

A

Cognition is impaired e.g. reduced processing in ventral striatum associated with negative symptoms.

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15
Q

Psychological Explanations: Cognitive Explanations (Metarepresentation)

A

Ability to reflect on thoughts and behaviour. Dysfunction leads to hallucinations and delusions as it disrupts our ability to recognise our own.

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16
Q

Psychological Explanations: Cognitive Explanations (Dysfunction of central control)

A

Frith et al. suggests this leads to speech poverty.

Central control = the cognitive ability to suppress automatic responses while performing deliberate actions.

17
Q

Evaluation of Psychological Explanations

A

✗ Evidence for family relationships is often retrospective: Read et al. reviewed 42 studies and concluded that 69% of all adult female inpatients with schizophrenia had a history of physical and/or sexual abuse in childhood.

But most of this evidence is based on information about childhood experiences gathered after diagnosis. May question validity - distorted recall.

✗ Biological factors are sometimes overlooked: both factors can produce schizophrenia.

✗ Evidence for family-based explanations is weak: poor childhood experiences may be associated with schizophrenia, but there is little evidence to support the importance of schizophrenogenic mothers, expressed emotion or double-bind.
- Theories are mainly based on clinical observation of patients - undermines the credibility of this explanation.

18
Q

Biological Therapies: Drug Therapy - Typical antipsychotics

A

(e. g. chlorpromazine).
- Work by acting as antagonists in the dopamine system and aim to reduce the action of dopamine are strongly associated with dopamine hypothesis.
- Block dopamine receptors in the synapses in the brain, reducing the action of dopamine.
- They normalise neurotransmission in key areas of the brain, which in turn reduces symptoms like hallucinations.
- Chlorpromazine has an effect on histamine receptors, which appears to lead to a sedation effect

19
Q

Biological Therapies: Drug Therapy - Atypical antipsychotics

A

(e. g. clozapine).
- Aim was to improve effectiveness of drugs suppressing psychoses and also minimise side effects.
- Typically target a range of neurotransmitters - dopamine and serotonin.
- Clozapine binds to dopamine receptors as chlorpromazine does, but also acts on serotonin and glutamate receptors.
- Reduces depression and anxiety as well as improving cognitive functioning.
- Improves mood.

20
Q

Biological Therapies: Drug Therapy - Risperidone

A

Developed because of the deaths caused by clozapine.

  • Binds to dopamine and serotonin receptors more strongly and effectively in smaller doses than most antipsychotics.
  • Fewer side effects.
21
Q

Evaluation of Drug Therapy

A

✓ Evidence shows antipsychotics are effective - Thornley et al. reviewed data from 13 trials and found chlorpromazine was associated with better functioning and reduce symptom severity compared with placebo.
✓ Meltzer et al. concluded that clozapine is more effective than typical antipsychotics. 30-50% more effective in treatment-resistant cases. Therefore it is reasonably effective.

✗ Side effects - typical antipsychotics: associated with dizziness, agitation, sleepiness, weight gain, etc. Long term use can lead to lip smacking and grimacing due to dopamine super-sensitivity. Can also lead to neuroleptic malignant syndrome.
✗ Antipsychotic drugs may be a ‘chemical cosh’ - may have been used in hospitals to calm patients down and make them easier for staff to work with rather than to benefit the patients. Raises ethical issues in use of these drugs in schizophrenia patients.

22
Q

Psychological Therapies: CBT

A
  • Aims to identify and change irrational beliefs.
  • CBT helps patients to understand their symptoms: making sense of delusions and hallucinations.
  • Offering explanations for these symptoms reduces anxiety and helps the patients realise their beliefs aren’t based on reality.
23
Q

Psychological Therapies: Family Therapy

A
  • Reduce expressed emotion in the family.
  • Aims to improve communication and interaction and reduce stress within the family that may contribute to relapse risk.
  • Improve family functioning: Pharaoh et al. identified a range of strategies family therapists use to reduce likelihood of relapse:
    1) Reduce stress of caring for relative
    2) Improve ability of family to anticipate and solve problems
    3) Reduce guilt and anger in family members
    4) Improve beliefs about behaviour towards schizophrenia
24
Q

Psychological Therapies: Token Economies

A

Reward systems (operant conditioning) used to manage the behaviour of patients who spend long periods in psychiatric hospitals.

  • Tokens are given to patients who carry out desirable behaviours (e.g. getting dressed).
  • This reinforces the behaviour and prevents ‘delay discounting.’
  • Tokens are secondary reinforcers - swapped for rewards (e.g. a walk outside). Only have value due to learned association (classical conditioning) with innate primary reinforcers.
25
Q

Evaluation of Psychological Therapies

A

✗ Limited benefits: Jauhar et al. found CBT had a significant but small effect on positive and negative symptoms. McMonagle and Sultana found only one of three studies of token economies that used random allocation showed improvement.

✗ May help but not cure: Reduces stress of living with it, biological therapies may be more desirable for coping.

✗ Ethical issues: Token economy systems are controversial - severely ill patients can’t get privileges as they are less able to comply with desirable behaviours. CBT may challenge a person’s paranoia but might interfere with their freedom of thought.

✗ Under-researched: unclear on effectiveness.

✗ Limited quality of some evidence: small-scale studies have found positive results. But these often lack a control group or random allocation to conditions.

26
Q

Interactionist Approach: Diathesis-Stress Model

A

Vulnerability + stress trigger = schizophrenia.
• Meehl original model: someone without the ‘schizogene’ should never develop it, no matter how much stress they are exposed to. But a person with the gene is vulnerable to the effects of chronic stress.

27
Q

Interactionist Approach: Modern Diathesis-Stress Model

A
  • Modern understanding of diathesis: many genes increase vulnerability. Diathesis doesn’t have to be genetic, could be early psychological trauma affecting brain development. E.G. child abuse affects the hypothalamic-pituitary-adrenal system, making a child vulnerable to stress.
  • Modern understanding of stress: includes anything that risks triggering schizophrenia. E.G. cannabis use can increase risk up to 7 times as it interferes with dopamine system.
28
Q

Treatment according to interactionist approach

A

Turkington et al. found antipsychotic medication and CBT is effective.
In Britain it is increasingly standard procedure to treat patients with a combination of drugs and CBT. In the US there is more of a conflict between psychological and biological methods - slower adoption of interactionist approach.

29
Q

Strengths of the interactionist approach

A

✓ Support for the dual role of vulnerability and stress: Tienari et al. studied children adopted away from schizophrenic mothers. Adoptive parents’ parenting styles were assessed and compared with a control group of adoptees with no genetic risk. Child-rearing style with high levels of conflict and low levels of empathy implicated in the development of schizophrenia for children with high genetic risk.

✓ Usefulness in treatment: Tarrier et al. randomly allocated 315 patients. Patients in combination groups of medication + CBT/ medication + counselling showed lower symptom levels than those in control group.

30
Q

Limitations of the interactionist approach

A

✗ Treatment-causation fallacy: Turkington et al. argued the fact that combined therapies are more effective than on their own. This error of logic is treatment-causation fallacy.
- The superior outcomes of combined therapies shouldn’t be over-interpreted in terms of evidence in support of the approach.

✗ Diathesis-stress model is too simplistic: Housten et al. found childhood sexual trauma was a diathesis and cannabis use a trigger. The original idea of diathesis as biological and stress as psychological is too simplistic.