Schizophrenia

Question 1

what is Schizophrenia?

Answer 1

chronic, severe, debilitating mental illness characterized by disordered
thoughts, abnormal behaviours, and anti-social behaviours.

Question 2

what type of disorder ?

Answer 2

is a psychotic disorder, where a person with schizophrenia does not identify with reality at times (APA).

Question 3

Features of Schz

Answer 3

• McGrath et al. (2008) - Schizophrenia affects about 1.1% of the world’s population.
• Women tend to be diagnosed later in life than men. Modal age of onset is between 18 - 25 for men and between 25 - 35 for women, with a second peak occurring around menopause.
• It affects men 1.5 times more than women.
• Tandon et al (2009) - Schizophrenia is broadly characterized by three core symptoms: positive symptoms, negative symptoms, and cognitive dysfunction.

Question 4

Phases of Schz

Answer 4

PAR

• Prodromal. This early stage is often not recognized until after the illness has progressed.
• Active. Also known as acute schizophrenia, this phase is the most visible. People will show the tell-tale symptoms of psychosis, including hallucinations, suspiciousness, and delusions.
• Residual. Though not a recognized diagnosis in the DSM-5, this term may still be used to describe a time when individuals with schizophrenia have fewer obvious symptoms (the psychos is is muted). However some symptoms are still present.

Question 5

Biological exp of schz

What is Dopamine?

Answer 5

a neurotransmitter that regulates mood and attention.

• High dopamine activity leads to acute episodes of sch and positive symptoms (delusions, hallucinations, confused thinking).
• Low dopamine activity leads to negative symptoms (avolition, speech poverty).

Question 6

What does the Dopamine Hypothesis (Van Rossum, 1967; Carlsson, 1970s) state?

Answer 6

• schizophrenia is caused by too much dopamine transmission, or increased dopamine (D2) receptors, in key areas of the brain.
• This causes the neurons that use dopamine to fire too often and transmit too many messages.

Question 7

Evidence/strengths of The Dopamine Hypothesis (Van Rossum,
1967; Carlsson, 1970s)

Answer 7

Owen et al (1987)- autopsies have found a large number of dopamine receptors and an increase in the amount of dopamine in the left amygdala (Falkai et al., 1988).

Antipsychotic drugs, dopamine antagonists, block the activity of dopamine in the brain and eliminate symptoms such as hallucinations and delusions.

Question 8

Evidence/limitations of The Dopamine Hypothesis (Van Rossum,
1967; Carlsson, 1970s)

Answer 8

+ This description is too simplistic - it failed to identify any specific brain areas where this would occur. Different dopamine receptors have different brain distributions, so more regional specificity is required.

+Davis et al. (1991)- Dopamine elevation is not universally higher in the brain. There are low levels of dopamine in pre-frontal area (negative symptoms) and higher levels of dopamine in subcortical areas (positive symptoms). This explains how dopamine causes both positive and negative symptoms.

Question 9

Davis’ Dopamine Hypothesis (version two) 1991

Answer 9

• schizophrenia presents itself after an increase in sub-cortical dopamine, especially in the striatum with the D2 receptor.
• It suggests that abnormalities in the prefrontal cortex, such as an abnormal volume of grey matter, may have caused the abnormalities in the limbic system.

Question 10

HYPOdopaminergia

Answer 10

Dopamine function in the mesocortical pathway may be responsible for the negative symptoms.

Question 11

HYPOdopaminergia - Aim of treatment

Answer 11

increase neurotransmission

Question 12

HYPERdopaminergia

Answer 12

Dopamine systems in the mesolimbic pathway contribute to the positive symptoms.

Question 13

HYPERdopaminergia- Aim of treatment

Answer 13

slow down neurotransmission

Question 14

Davis’ Dopamine Hypothesis (version two) 1991Evidence

Answer 14

• Davis et al. (1991) - Postmortem studies have shown high dopamine concentrations in various subcortical brain regions and greater than normal DA receptor densities in the brains of schizophrenic patients.
• Millan et al. (2014) - a decrease in grey matter volume of the temporal lobe has been associated with negative symptoms.

Question 15

Davis’ Dopamine Hypothesis (version two) 1991 - Evaluation

Answer 15

• This version was still deemed to be over simplified and biologically reductionist.
• Much of the evidence for version two has come from animal lesion or post-mortem studies which means that it has been indirectly collated.
• Findings cannot be generalised to humans as we cannot assume that the dead or animal brains will react to damage in the same way as living human brains.

Question 16

Further advancements led to a third version of the dopamine hypothesis (Howes and Kapur, 2009).

What had been identified?

Answer 16

identified that most schizophrenics have abnormally high presynaptic dopamine
production in their striatum due to also tending to have 10-20% higher levels, than usual, of D2 receptors there.

Question 17

third version of the dopamine hypothesis (Howes and Kapur, 2009) - Evidence

Answer 17

Brunello (1995) - D2 receptor occupancy linked to the development of psychosis was confirmed with the evidence from living schizophrenic human brains not just from the deceased or animals.

-Howes and Kapur (2009)-PETstudies show reduced cerebral blood flow in
frontal cortex that provides evidence of regional brain dysfunction in
schizophrenia.

Question 18

Evaluation of the Dopamine Hypothesis

Answer 18

• Haracz (1982) — postmortem of sch and found elevated dopamine levels in those who had received antipsychotic drugs before death. Those who had not received medication showed normal levels. (However, only correlational).
• Farde et al. (1990) found no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals.
• biologically deterministic. If the individual does have excessive amounts of dopamine then does it really mean that they will develop schizophrenia?
• Biologically reductionist as it oversimplifies the biology involved in the transmission of dopamine and does not take individual differences such as patients’ genetics and hormones into consideration.

Question 19

Conclusion of dopamine hypothesis

Answer 19

To understand schizophrenia and its causes more thoroughly we must consider the extensive role that our environment plays.

It must be acknowledged that our behaviour and experiences may lead to
abnormalities, as identified in the Diathesis Stress Model. In addition, aetiological validity should be considered, i.e., for a diagnosis to be valid, all patients diagnosed as schizophrenic should have the same cause for their disorder. This is not the case with schizophrenia: The causes may be one of biological or psychological or both.

Question 20

treatment

What is Drug therapy?

Answer 20

biological treatment for schizophrenia.

Question 21

Why are Antipsychotic drugs used?

Answer 21

to reduce the intensity of symptoms (particularly positive symptoms).

Question 22

How do Antiphsychotic drugs work ?

Answer 22

• work by binding to the dopamine receptor sites better than dopamine.
• When dopamine tries to bind with the receptor site, it finds that the site has already been filled by the drugs.
  -The reduces the number of receptors that are activated and reduces the effect of dopamine.

Question 23

What are the First-generation Antipsychotics called?

Answer 23

Typical antipsychotics, e.g., chlorpromazine.

Question 24

When are Typical antipsychotic drugs used?

Answer 24

to reduce the intensity of positive symptoms, blocking dopamine receptors in the synapses of the brain and thus reducing the action of dopamine.
- They arrest dopamine production by blocking the D2 receptors in synapses that
absorb dopamine, in the mesolimbic pathway thus reducing positive symptoms,
such as auditory hallucinations.

Question 25

What are the newer drugs called?

Answer 25

atypical antipsychotics, e.g., Risperidone and Clozapine,

Question 26

What do the atypical antipsychotics target?

Answer 26

D2 dopamine activity in the limbic system. They bind to dopamine,
serotonin, and glutamate receptors. They generally have fewer side effects, e.g.,
less effect on motor movement.

Question 27

Lobos (2010)
Wang (2013)

Answer 27

• Lobos (2010) - Clozapine is the only atypical antipsychotic that is effective for the management of positive and negative symptoms — it is used after other medication does not work due to serious risk - life-threatening hepatoxicity (liver damage).
• Wang (2013) - Atypical antipsychotic drugs work on negative symptoms,
  improving mood, cognitive functions and reducing depression and anxiety. This
  involves regulating monoamine, glutamate, gamma-aminobutyric acid (GABA),
  cortisol, and neurotrophic factors.

Question 28

Drug Therapy Evaluation
Benefits

Answer 28

• Antipsychotic medications have greatly improved treatment. Medications reduce positive symptoms particularly hallucinations and delusions; and usually allow the patient to function more effectively and appropriately.
• Thornley et al. carried out a meta-analysis comparing the effects of Chlorpromazine to placebo conditions and found chlorpromazine to be associated with better overall functioning — Drug therapy is an effective treatment for Sch.
• Offering drugs can lead to an enhanced quality of life as patients are given independence ~> Positive impact on the economy as patients can return to work and no longer need to be provided with institutional care.

Question 29

Drug Therapy Evaluation- Limitations

Answer 29

• Ethical issues — antipsychotics have been used in hospitals to calm patients and make them easier for staff to work with rather than for the patients’ benefit > Can lead to the abuse of the Human Rights Act (no one should be subject to degrading treatment).
  - Severe side effects — medication does not cure schizophrenia, rather they dampen symptoms down so that patients can live fairly normal lives in the community.
• Rege (2018) - research shows that one-third of individuals with sch do not respond to antipsychotics despite high levels of D2-receptor occupancy.
• Pills are not helpful with other symptoms, especially emotional problems.

Question 30

Biological Explanation of Schizophrenia

**Hypoglutamatergia (Glutamate) Hypothesis of Schizophrenia
**
what does glutamate control ?

Answer 30

As a neurotransmitter, glutamate controls memory and learning by binding to glutamate receptors (e.g., NMDA). These receptors are found everywhere in the brain. In very high quantities glutamate is toxic.

Question 31

Hypoglutamatergia (Glutamate) Hypothesis of Schizophrenia

What does glutamate seems to regulate?

Answer 31

• the behaviour of dopamine
• can act as an “accelerator” (increasing dopamine activity) or a “brake” (decreasing it).

Question 32

Hypoglutamatergia (Glutamate) Hypothesis of Schizophrenia

What may a lack of glutamate cause?

Answer 32

patients to have an exaggerated response to dopamine post-synapse.

Question 33

glutamate hypothesis

Carlsson

Answer 33

Low levels of glutamate (hypoglutamatergia) seem to link with both positive and
negative schizophrenic symptoms. This activity is in the striatum and in the cerebral cortex

Question 34

glutamate hypothesis

Coyle (1996)

Answer 34

hypofunction of NMDA receptors, located on GABAergic interneurons, lead to diminished inhibitory influence on neuronal function and contribute to schizophrenia.

Question 35

Evidence - glutamate hypothesis

Answer 35

• Miller & Abercrombie (1996) show that the release of dopamine is increased if glutamate activity is reduced
• Post-mortem studies have identified reduced density of NMDA in the pre-frontal cortex (Sokolov, 1998)
• **(Poels et al., 2014). **There is evidence of a deficit in NMDA receptor activity in the left hippocampus in unmedicated patients with sch

Question 36

Strengths of Glutamate hypthesis

Answer 36

• Not as reductionist as the Dopamine Hypothesis. As identified by Carlsson, the glutamate theory provides a more extensive explanation for sch. It considers other factors as an explanation for sch, not just dopamine.
• Stone (2011)- findings from small clinical trials support the NMDA receptor hypofunction hypothesis of sch.

Question 37

Limitations of glutamate hypothesis

Answer 37

Marsman et al., (2013) - Glutamate abnormalities may only be present in a subset of patients with sch, and possibly at a particular phase of illness in these individuals. Therefore, we can’t generalize to all who suffer from schizophrenia.

• There are no glutamatergic drugs currently on the market for sch, and trialsof glutamatergic treatments have not shown a conclusive or strong effects in most cases. Therefore,treatment programmes can’t be applied to patients.

Question 38

Biological exp of schz

what does the human genome comprimise ?

Answer 38

around 23000 genes.

Question 39

What may genetic variation may be responsible for?

Answer 39

some neurochemical irregularities.

Question 40

bio exp of schz

Schizophrenia as a heritable condition.
what does the explanation suggest?

Answer 40

schizophrenia is a heritable condition that passes from one generation to the next.

Question 41

biologiclal exp of scz - genetic - role of genes

Although specific genes have not been shown
to directly cause schizophrenia, numerous
chromosomes appear to be implicated,
including?

Answer 41

22.

Question 42

biologiclal exp of scz - genetic - role of genes

Some of the strongest
evidence suggests the importance of chromosomes..?

Answer 42

13 and 6

Question 43

biologiclal exp of scz - genetic - role of genes

Variations in numerous individual genes are thought to increase the risk of ?

Answer 43

an individual developing schizophrenia, including genes that regulate neurochemicals such as dopamine and serotonin.

Question 44

biologiclal exp of scz - genetic - role of genes

Gene mutations can be passed down from parents to their offspring or they happen spontaneously. In the latter
case, these changes may result from?

Answer 44

an environmental factor or an error during cell division,
such as a deletion or duplication of a strand of DNA.

Question 45

biologiclal exp of scz - genetic - role of genes

The link between schizophrenia and Di George may be due to the deletion of a specific gene called?

Answer 45

COMT

Question 46

biologiclal exp of scz - genetic - role of genes

what does the COMT gene provide?

Answer 46

instructions for the creation of an enzyme which breaks
down neurotransmitters, such as dopamine, in brain regions such as the prefrontal cortex, resulting in hallucinations and loss of reality.

Question 47

biologiclal exp of scz - genetic - role of genes

what does the COMT gene provide?

Answer 47

instructions for the creation of an enzyme which breaks
down neurotransmitters, such as dopamine, in brain regions such as the prefrontal cortex, resulting in hallucinations and loss of reality.

Question 48

biologiclal exp of scz - genetic - role of genes

What would the deletion of the COMT gene mean?

Answer 48

would mean that dopamine levels are poorly regulated resulting in positive schizophrenic symptoms.

Question 49

biologiclal exp of scz - genetic - role of genes

Evidence for Biological ex - genetic

Answer 49

Gottesman (1991) has found that schizophrenia is more common in the biological relatives of a schizophrenic, and that the closer the degree of genetic relatedness, the greater the risk (NATURE).

Gottesman (1991) found that MZ twins have a 48% risk of getting schizophrenia whereas DZ twins have a 17% risk rate. This is evidence that the higher the degree of genetic relativeness, the higher the risk of getting schizophrenia.

Tienari et al (2004) found that adopted children of biological mothers with sch were more likely to develop the disorder themselves than adopted children of mothers without schizophrenia, supporting the genetic link.

Question 50

Strengths of Biological genetic exp of schz

Answer 50

• Gottesman (1991) - When other psychiatric diagnoses were considered for the co-twin, the rate went up to 79% for MZ and 45% for DZs. The chance of being ‘psychologically normal’ was just 21% for the co-twins of MZs and 55% for the DZs. This shows that while schizophrenia is not entirely a genetic disorder, the fact that the concordance rate is greater for MZs than DZs, shows that biology certainly plays a significant part.

A strength of the suggestion that schizophrenia
may be linked to DISC1 and COMT is that:
- In a review of 14 studies, Tarik Dahoun et al. (2017) concluded that DISC1 is associated with presynaptic dopamine dysregulation.

• This shows how genetic variations underpin neurochemical differences which can predispose a person towards schizophrenia.

Question 51

Limitations of Biological genetic exp of schz

Answer 51

Nature-vs-Nurture. The fact that the concordance rates are not 100% means that schizophrenia cannot wholly be explained by genes, and it could be that the individual has a pre-disposition to schizophrenia and simply makes the ndividual more at risk of developing the disorder. This suggests that the biological account cannot give a full explanation of the disorder…

• Or it may be that the increased concordance rates in the Gottesman study were due to the increased chance of sharing the same environment as the person with schizophrenia. For example, identical twins share the same environment (and may be treated similarly), whereas first cousins would not. This means that it can’t be concluded that genetics has caused schizophrenia.
• there are methodological problems. Family, twin, and adoption studies must be considered cautiously because they are retrospective, and diagnosis may be biased by knowledge of the other family members who may have been diagnosed. This suggests that there may be problems of demand characteristics.

Question 52

Psychological Explanation of Schizophrenia

Freud’s Psychodynamic Explanation (1924).
psychodynamic approach. How is abnormality caused?

Answer 52

when trauma from unresolved conflict between the id, ego, and superego is repressed into the unconscious. This could be due to harsh or cold parenting.

Question 53

Psychological Explanation of Schizophrenia

According to Fromm-Reichman (1948), the schizophrenogenic mother is?

Answer 53

• a contributory factor in the development of schizophrenia — this is someone who is cold, dominant and creates conflict.
• These mothers are rejecting, overprotective, self-sacrificing, moralistic about sex and fearful of intimacy.
• This causes fixation or regression to an earlier stage of psychosexual development.

Question 54

Psychological Explanation of Schizophrenia

Schizophrenia was seen by Freud as?

Answer 54

an infantile state, linked to the oral stage; in particular,
a stage called primary narcissism during which the ego has not separated from the Id.

Question 55

Psychological Explanation of Schizophrenia

Because the ego is the rational part of the mind, if one regresses to a stage before it forms they will?

Answer 55

• stop operating on the reality principle and lose touch with reality.
• Fantasies become confused with reality, as the ego tries to gain control.
• This explains some of the symptoms of schizophrenia, especially hallucinations, delusions and disorganized thought and speech (very like the demanding and unsocialised behaviour of a baby/toddler).

Question 56

Psychological Explanation of Schizophrenia Evidence

Answer 56

There is no evidence to support a psychodynamic explanation of schizophrenia as the approach is based on supposition which has no scientific basis. It is empirically impossible,
i.e., unfalsifiable, to test concepts such as the Id, Ego, and Superego.

Question 57

Psychological Explanation of Schizophrenia - Freud’s Psychodynamic Explanation- treatment

What Treatment is used?

Answer 57

Psychoanalysis - Psychodynamic therapy

Question 58

Psychological Explanation of Schizophrenia - Freud’s Psychodynamic Explanation- Treatment

How does Psychoanalysis - Psychodynamic therapy help ?

Answer 58

helps the patient to gain self-awareness and understanding of the influence of the past on present behaviour, and it fosters new positive relationship experiences.

Question 59

Psychological Explanation of Schizophrenia - Freud’s Psychodynamic Explanation - Treatment

What techniques are involved in Psychoanalysis - Psychodynamic therapy?

Answer 59

free association or
the Rorschach inkblot test.

Question 60

Psychological Explanation of Schizophrenia - Freud’s Psychodynamic Explanation - Treatment

When is Art therapy often used?

Answer 60

often used with people who have schizophrenia.
If the client paints, they may be able to express what is wrong with them much better than they can in words. This helps with psychoanalysis, because the paintings may contain clues to the unconscious mind, but it also helps the client get rid of stress and anxiety, which tends to reduce the severity of symptoms too.

Question 61

Clinical Implications of The Psychoanalytic Theory of Schizophrenia

Answer 61

1. The classical psychoanalysis, which was and still is to some extent, a widely practiced form of treatment of schizophrenia is based on the psychoanalytic theory of schizophrenia.
2. This theory also explains some of the symptomatic manifestations of schizophrenia and provides an insight into understanding the phenomenology in individual patients, thereby facilitating treatment.

Question 62

Goals of Psychodynamic Psychotherapy in Schizophrenia

- want more detail look in book pg 18

Answer 62

• Psychodynamic psychotherapy focuses on affect and expression of emotion.
• Exploration of attempts to avoid distressing thoughts and feelings.
• Identification of recurring themes and patterns.
• Discussion of past experience
• Focus on interpersonal relations.
• Focus on the therapy relationship.

Question 63

Strengths of Psychodynamic explanation

Answer 63

• has face validity; the symptoms of schizophrenia do seem similar to some childlike behaviour, e.g., delusions where children believe in an imaginary friend.
• Rosenbaum (2012) psychodynamic therapy is still one of the most effective forms of treatment.
  Rosenbaum compared treatment as usual to treatment with supportive psychodynamic psychotherapy (SPP) in a sample of 269 adults admitted for psychosis. Rosenbaum found that the SPP group improved far more over the course of two years of treatment with respect to symptoms of psychosis.
  These findings demonstrate that psychodynamic therapy can still adequately serve the needs of many individuals with schizophrenia and other psychotic issues.

Question 64

Limitations of Psychodynamic explanation

Answer 64

Stirling and Hellewell (1999) suggest that the schizophrenic behaviour isn’t similar to an infants, which contradicts Freud’s theory. Stirling et al. (2006) believe the origins of thought disorder seem more closely linked to deficits in executive functioning and semantic processing.

• There is very little research to support Freud’s work in terms of schizophrenia. This is partly because the theory is based upon abstract ideas such as the subconscious.
• is unscientific in its analysis of human behaviour. Many of the concepts central to Freud’s theories are SUBJECTIVE, and as such, difficult to test scientifically.

Question 65

Family Therapy for Schizophrenia

What is Family therapy based on?

Answer 65

the theory that schizophrenia is associated with
a) schizophrenogenic mothers,
b) double bind communication
c) expressed emotion
or other dysfunction in the family.

Question 66

What is The aim in modern forms of family therapy ?

Answer 66

is to reduce the stress in the family environment so preventing relapse.

Question 67

Aims of Family Therapy

Answer 67

• To educate relatives about schizophrenia.
• To improve how the family communicates and handles the situation.

Question 68

Methods used in Family Therapy

Pharoah et al (2010) suggest that the following techniques, in which all of the family are involved, are used:

Answer 68

• A co-operative, trusting relationship with the family is established
• Therapist provides information about schizophrenia
• Family members contribute, all contributions valued
• Reducing anger and guilt
• Family is provided with practical coping skills to help deal with the disorder (to
  anticipate and solve problems)
• More constructive ways of interaction and communication encouraged (to avoid
  expressed emotion)
• Training to detect any signs of relapse in the patient

Question 69

Family Therapy for Schizophrenia
Evidence

Answer 69

Anderson etal. (1991) found a relapse rate of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy was used. The relapse rate was less than 5% when both were used together.

Pharaoh et al. (2003) meta - analysis found family interventions help the patient to understand their illness and to live with it, developing emotional strength and coping skills, thus reducing rates of relapse. (Yet, Pharoah et al. (2010) later found only moderate evidence to show that family therapy reduces relapse rates and hospital readmissions in schizophrenia patients).

Question 70

Strengths of Family therapy

Answer 70

Economic Benefits: Family therapy is highly cost effective because it reduces relapse rates, so the patients are less likely to take up hospital beds and resources. The NICE review of family therapy studies demonstrated that it was associated with significant cost savings when offered to patients alongside the standard care — Relapse rates are also lower which suggests the savings could be even higher.

Lobban (2013) reports that other family members felt they were able to cope better thanks to family therapy. In more extreme cases the patient might be unable to cope with the pressures of having to discuss their ideas and feelings and could become stressed by the therapy, or over-fixated with the details of their illness.

Question 71

Limitations of Family therapy

Answer 71

Simplistic - Family therapies may improve the quality of life for schizophrenia patients and their families, but do not provide a cure for schizophrenia, rather a management of the effects. This means it cannot be used to treat schizophrenia by itself.

Family therapy is based on the premise that nurture (upbringing) is a significant factor in schizophrenia. The biological basis for schizophrenia is therefore not addressed at all in the therapy, limiting its use (NATURE VS NURTURE).

The therapy works as long as the family is committed— they may choose not to follow the therapy

Family members may be resistant to confronting past actions and revisiting unpleasant times.

Question 72

The Interactionist Approach to Schizophrenia.
What does the interactionist approach attemp to explain schz as?

DO I HAVE TO KNOW THIS???????????????