Schizophrenia

What is schizophrenia?

Schizophrenia is a thought process disorder. It is characterised by a disruption to a person's perceptions, emotions and beliefs.

Type 1 - more acute, has more of the positive symptoms, but repsonds better to treatment.

Type 2 - chronic, has more of the negative symptoms and is less responsive to treatment. It affects mood, though processes and the ability to determine what is reality.

A psychosis is a severe mental disorder in which thoughts and emotions are so impaired that contact is lost with external reality.

A neurosis means to have excessive and irrational anxiety or obsession.

Will sufferers recover? 25% will get better after one episode of the illness, 50-65% will improve, but continue to have bouts of the illness, the remainder will have persistent difficulties (Stirling & Hellewell, 1999).

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How do we classify schizophrenia?

We classify schizophrenia with manuals.

The ICD (International Classification of Diseases) recognises a range of subtypes.

The DSM (Diagnostic and Statistical Manual of Psychiatric Disorder) recognises subtypes.

 

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The 5 subtypes

Disorganised schizophrenia: disorganised speech, behaviour and flattened effect; inappropriate/unexpected behaviour; strange mannerisms & gestures; causes signfiicant dysfunction in daily life, self-care, and interaction with others.

Catatonic schizophrenia: assume peculiar postures and are usually speechless; rigidness and motionless or agitated and moving constantly; strange facial expressions and mimic the behaviour of others.

Paranoid schizophrenia: delusions that have a theme; auditory hallucinations may accompany them; anger, irritable, anxiety are prominent symtpoms; violent; able to live, work and care for themselves; the onset is often later in life.

Undifferentiated schizophrenia: given to a lack of catatonic, paranoia or disorgansied speech; may resemble other illnesses; tend to have an insight.

Residual schizophrenia: positive symptoms have disappeared; negative symptoms remain and may be interrupted only briefly by mildly disorganised speech or strange behaviour; symptoms can last indefinitely, or they can lead to complete recovery, though this is rare.

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Symptoms of schizophrenia

Positive symptoms are behaviours that are additional to normal life experiences and concern losing touch with reality.

Examples of positive symptoms: hallucinations, delusions, delusions of grandeur, paranoia, disorganised speech, delusions of control, catatonic behaviour.

Negative symptoms are behaviours that detract from normal life experiences; a lack of something.

Examples of negative symptoms: withdrawal, language impairments, avolition, lack of emotion, stereotyped behaviours, psychomotor disturbance, affective flattening, anhedonia.

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What are the diagnostic books?

ICD & DSM.

Criteria A symptoms for the DSM: delusions, hallucinations, disorganised speech, catatonic behaviour, negative symptoms.

Criteria B symptoms for the DSM: social/occupational dysfunction; significant portion of time since onset, one or more major areas of functioning are below expected.

Criteria C symptoms for the DSM: duration; continuous sign of disturbance for at least 6 months.

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Symptom overlap & co-morbidity

Symptom overlap - when the symptoms of two mental illnesses are very similar. It's problematic between schizophrenia and bipolar disorder. Also with depression, intoxication through drugs and autism.

Co-morbidity - the co-existence of two separate conditions/illnesses at the same time. It complicates the diagnosis and may mean that different treatment programmes are needed side by side.

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Definitions of abnormality

Deviation from social norms - social norms are implicit rules about how we ought to behave in society. Anything that violates these are abnormal.

Statistical deviation - if behaviour is statistically unusual, it is classed as abnormal.

Deviation from ideal mental health - a list of criteria that we would consider normal, and therefore an absence of any of these would help us define abnormality.

Failure to function adequately - inability to carry out everyday tasks and lead what would be considered a 'normal' life.

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Symptoms of phobias

Emotional

Marked & persistent fear, excessive & unreasonable, anxiety & panic, triggered by the thought of it.

Behavioural:

Avoidance, freeze, faint, fight-or-flight response.

Cognitive:

Irrational thoughts and an insight.

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Symptoms of depression

Emotional:

Empty, sadness, worthless, low self-esteem, loss of interest, anger, hopeless.

Behavioural:

Reduced/increased level of activity, reduced energy, tiredness, insomnia, agitated & restless, loss of appetite/too much.

Cognitive:

Irrational thoughts, guilt, worthlessness, suicidal thoughts, an insight.

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Symptoms of OCD

Emotional:

Anxiety, distressed, aware they're excessive, embarrassment, shame.

Behavioural:

Compulsive behaviours, repetitive & unconcealed, they have to do it, not in a realistic way, avoidance.

Cognitive:

Recurrent & intrusive thoughts, uncontrollable ideas, doubts, impulses or images, an insight.

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Difficulties of diagnosing schizophrenia

Schizophrenia patients don't have an insight; they believe it's the same for everyone. This makes it difficult to diagnose schizophrenia as they believe that what they are seeing/hearing is real.

If diagnosis is reliable, we should be able to get the same diagnosis from different professionals.

If diagnosis is valid, there should be a genuine measurement of schizophrenic symptoms.

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The biological approach: assumptions

The role of genetics and neurochemicals.

It gathers scientific evidence.

It states that the chances of developing schizophrenia is less than 1% for an individual, but if you have a close relative with schizophrenia, the risk increases to between 6 and 17%.

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Gottesman, Joseph & Tiernari

Gottesman's family study found that children with 2 schizophrenic parents had a concordance rate of 46%, children with 1 schizophrenic parent had a rate of 13%, and siblings a concordance rate of 9%.

Gottesman's research shows that schizophrenia is more common among biological relatives of a person with schizophrenia and that the closer the degree of genetic relatedness, the greater the risk. 

Joseph's twin study found that the pooled data for all schizophrenic twin studies carried out prior to 2001, showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins.

Joseph's research shows that a concordance rate for MZ twins that is many times higher than that for DZ twins,

Tiernari's adoption study found that of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 6.7% also received a diagnosis of schizophrenia, compared to just 2% of the 197 control adoptees.

Tienari's research shows that the genetic liability to schizophrenia had been 'decisively confirmed'.

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Evaluation of genetic explanations

- Concordance rates: do show a genetic link, however, they clearly show genetics is not the only explanation. Adoption studies (1% chance to 6%).

- Variables: can't establish cause & effect; not all are controlled (environment?); age adopted at; can't account for all factors; type?

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The dopamine hypothesis

The dopamine hypothesis suggests that an excess of dopamine in the brain is associated with the positive symptoms. If you have too much dopamine, it leads to the positive symptoms of schizophrenia.

Drugs that increase dopaminergic activity: amphetamine. 'Normal' people that are exposed, develop the positive symptoms.

Parkinson's disease: some people with Parkinson's disease, characterised by low dopamine levels, who take the drug L-dopa to raise their levels, have been found to develop positive schizophrenic symptoms.

Drugs that decrease dopaminergic activity: if reduced too much, can develop Parkinson's disease. However, antipsychotic drugs can take away the positive symptoms.

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The revised dopamine hypothesis

The revised dopamine hypothesis (Davis & Kahn, 1991) suggests that positive symptoms are caused by an excess of dopamine. The negative symptoms are thought to arise from a deficit of dopamine in areas of the prefrontal cortex.

Supporting evidence comes from neural imaging (Patel, 2010): PET scans to assess dopamine levels in schizophrenic patients and 'normal' individuals found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls.

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Evaluation of the dopamine hypothesis

+ Scientific evidence: brain scans to show increased levels of dopamine. The genetic explanation does not have scientific evidence to support it. It has led to treatment; drugs used to reduce the levels of dopamine and it has been successful.

- No account for negative symptoms: which came first? Did schizophrenia cause high dopamine levels or were some people born before noticing high levels of dopamine. Can's establish cause & effect.

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The cognitive approach: assumptions

Behaviour comes from our mental processes; which causes schizophrenia. 

Input - Processing - Output.

How could our family be a possible cause for schizophrenia? Stress can trigger an episode.

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Cognitive explanations of schizophrenia

1. Propose that abnormalities in cognitive function are a key component of schizophrenia. Not enough information received = faulty processing. Delusions - interpretations of their experiences are controlled by inadequate information processing.

2. Hallucinations - excessive attention on auditory stimuli and so have a higher expectancy for the occurrence of a voice. Assume that every sound they hear is real.

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Evaluation of cognitive explanations

+ Supportive evidence for the cognitive model of schizophrenia: Sarin & Walin - review of research; positive symptoms - origins in faulty cognition. E.g. schizophrenics with hallucinations had impaired self-monitoring. Negative symptoms also displayed dysfunctional thought processes.

- An integrated model of schizophrenia: model deals with one aspect, but ignores other aspects (Haves & Murray). Early vulnerability factors and exposure to social stressors, sensitises the dopamine system, causing it to release dopamine. Results: paranoia & hallucinations.

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Family dysfunction: double bind theory

Family dysfunction - the presence of problems within a family that contribute to relapse rates in recovering schizophrenics, including lack of warmth between parents & children, dysfunctional communication patterns and parental over protection.

Double bind theory: contradictory messages from parents & children (Bateson, 1956). Prevent the development of an internally coherent construction of reality, and in the long run, this manifests itself as schizophrenic symptoms (negative).

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Family dysfunction: expressed emotion

Expressed emotion: family of a psychiatric patient talk about them in a critical or hostile manner or in a way that indicates emotional over-involvement. Patients have a lower tolerance for intense environmental stimuli, particularly intense emotional comments and interactions with family members. Negative emotional climate in these families arouses the patient and leads to stress.

Kuipers (1983): EE relatives talk more and listen less. High levels are most likely to influence relapse rates. A patient returning to a family with high EE is above four times more likely to relapse than a patient whose family is in EE.

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Evaluation of family dysfunction

- Family relationships: Tiernari - adopted children with schizophrenic biological parents are more likely to develop it. However, only emerged in situations where the adopted family was rated as disturbed. It suggests that appropriate environmental conditions are needed. Genetics aren't the only cause.

+ Double bind theory: Berger - schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics. May be affected by their schizophrenia.

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Drug therapy

What is the basic principle of drug therapy? Drugs to reduce levels of dopamine in the brain.

When was drug therapy for schizophrenia introduced? In the 1950s. Before this, patients would be imprisoned.

When/why is drug therapy recommended? Medical condition - medication so it legitimises it. Patients feel better as it takes the blame away. Good as it is a short-term solution to calm the symptoms down in order to start talking.

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Types of antipsychotics

Typical antipsychotics were introduced in the 1950s. They reduce the effects of dopamine; reduce symptoms; dopamine antagonists; block action; 60-75% of dopamine receptors must be blocked for effectiveness.

Side effects of typical antipsychotics: cause movement problems; Parkinson's disease symptoms; Tardive dyskinesia; urinary problems.

Examples of typical antipsychotics: chlorpromazine, fluphenazine, haloperidol.

Atypical antipsychotics are newer drugs. They carry a lower risk of side effects; beneficial effect on negative symptoms and cognitive impairment; suitable for treatment-resistant patients; block action; reduce levels of dopamine temporarily.

Side effects of atypical antipsychotics: weight gain; diabetes; cardiovascular conditions; reduced white blood cell count (using clozapine).

Examples of atypical antipsychotics: clozapine, quetiapine, olanzapine.

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Evaluation of drug therapy

- Can't treat all cases: typical antipsychotics reduce dopamine levels by 75% so symptoms of schizophrenia are reduced, but they develop Parkinson's disease symptoms as a side effect.

+ Effective: drugs work quickly. A review of 6,000 cases. Swapped their medication for a placebo. 64% relapsed within a few months. Unethical study. Effective - has to keep taking drugs.

- Side effects: vary with typical & atypical drugs. Typical drugs reduce dopamine levels, but are reduced by 75% which leads to Parkinson's disease; lose emotion; don't feel 'normal'. Increases dropout rates = less successful.

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What is cognitive behavioural therapy?

CBT - a combination of cognitive therapy and behavioural therapy.

What are the basic principles of CBT? Depression is caused by irrational/faulty thinking. 

Aims: correct irrational thoughts.

Ellis' ABC model.

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What is CBT for psychosis?

The basic assumption is that people have distorted beliefs, which influence their feelings and behaviours in maladaptive ways.

The nature of CBTp: therapist lets the patient develop their own alternatives to the previous maladaptive beliefs. Alternative explanations & coping strategies. Patients trace back the origins of their symptoms to see how they might have developed.

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Steps for CBTp

1. Assessment: patient expresses their own thoughts about their experiences.

2. Engagement: the use of Socratic questioning and empathy creates a therapeutic relationship. A good relationship is needed; unconditional positive regard.

3. ABC model: patient can organise their thoughts and feelings. (A) activating event - identify stressors; (B) belief - irrational thoughts; (C) consequence - behaviour.

4. Normalisation: de-catastrophising psychotic experiences which are placed on a continuum with normal experiences, making the possibility of recovery seem less distant. Make them aware of other sufferers.

5. Critical collaborative analysis: once trust is formed, gentle questioning is used to help the patient appreciate maladaptive beliefs. Challenge irrational thoughts. Unconditional positive regard.

6. Developing alternative explanations: the patient should develop their own alternatives to previous maladaptive assumptions. Look at coping strategies. Unconditional positive regard; work together.

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Evaluation of CBTp

- Drugs vs CBTp: (D) calms symptoms; anyone with a doctor can get access to antipsychotics. (CBTp) cost per session; wait to be referred; have to build rapport or patient won't talk; not easily accessible.

+ Advantages: unconditional positive regard - rapport built between therapist & patient; trust = communicate more; someone to talk to; self-awareness; long-term.

- Preference for drug therapy: calms symptoms down before talking; takes blame away; suggests there is a cause.

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Family therapy

What are the main aims of family therapy for schizophrenia? It's a long-term strategy. It helps every member of the family to have a greater understanding of schizophrenia, supports them and the patient is left feeling not as isolated.

NICE: "All individuals diagnosed with schizophrenia who are in contact with or live with family members." 

The nature family therapy: 3-12 months; 10+ sessions; reduce the level of expressed emotion (relapse); provides families with information; supports them; resolves practical problems; involves the patient; benefits everyone; not just the patient.

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Strategies used for family therapy

1. Psychoeducation - greater understanding of schizophrenia. Dealing with it in a better way.

2. Alliances - with those who care for the patient.

3. Emotional climate - reduce the burden of care for the family members.

4. Solving problems - anticipate ways to solve problems.

5. Anger/guilt - reduce the feelings of anger and guilt.

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Supporting evidence for family therapy: Pharoah (2

Procedure: 53 studies to investigate the effectiveness of family intervention. In Europe, Asia & North America. Compared them to 'standard care'.

Findings

  • Compliance with medication - more likely to continue their drug therapy when receiving family therapy. 
  • Reduction in relapse & readmission - during treatment and in the 24 months after.
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Family therapy vs drug therapy

Family therapy is an extra therapy; drugs first to get the patient thinking more rationally.

Drug therapy is just for the patient, whereas family therapy supports everyone as it changes the environment.

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Family therapy vs CBTp

Both cost a lot of money and take a lot of time.

For family therapy, it may be difficult to get all the family together (e.g. jobs), whereas CBTp is just for the patient.

Family therapy gives the patient a voice; it's directed by them, not the therapist.They talk about what is beneficial to them; how they want their family to help them.

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Evaluation of family therapy

+ Economic benefits: less chance of a relapse because there is no hospitalisation, so they save money. The patient can go back to work and start earning money again. Therapy is expensive, but the savings outweigh it for not being hospitalised. The patient and family can save a lot of money.

+ Positive impact on family members: provides support and removes the burden of care that family members may feel. It educates the family members and allows them to develop coping strategies and it improves the family situation. It is less reductionist as everyone is involved. It is beneficial as stress is removed, which can prevent a schizophrenic episode.

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What are token economies?

Token economies - a form of therapy where desirable behaviours are encouraged by the use of selective reinforcements. Rewards are given as secondary reinforcers when individuals engage in socially desirable behaviours; can be exchanged for primary reinforcers.

Where are they used? In hospitals to help institutionalised people with schizophrenia to gain more control over their daily lives and increase positive behaviours.

What are they based on? The operant conditioning theory.

Primary reinforcers - anything that give pleasure (e.g. food) or remove unpleasant states. Do not depend on learning in order to acquire their value.

Secondary reinforcers - initially have no value to the individual, but aqcuire their reinforcing properties as a result of being paired with primary reinforcers.

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The token economy cycle

1. Tokens are paired with rewarding stimuli and so become secondary reinforcers.

2. Patient engages in 'target' behaviours or reduces inappropriate ones.

3. Patient is given tokens for engaging in these target behaviours.

4. Patient trades these tokens for access to desirable items or other privileges.

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Supporting evidence for token economies: Ayllon

Procedure: ward of female schizophrenics; hospitalised for years. Given plastic tokens with 'one gift' on, which could be exchanged for privileges.

Findings: the use of token economies with these patients increased dramatically the number of desirable behaviours that the patients performed each day.

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The token

Assigning value: to give the neutral token some 'value', it needs to first be repeatedly presented alongside or immediately before the reinforcing stimulus.

Result of assigning value: the neutral tokens become secondary reinforcers, and so can be used to modify behaviour.

Reinforcing target behaviours: when patients perform the desirable target behaviours, the clinician awards them tokens. When a token can be exchanged for a variety of different privileges and rewards, it is referred to as a generalised reinforcer.

Supporting evidence for reinforcing target behaviours: Sran and Borrero (2010) found that all participants had higher rates of responding in the sessions where tokens could be exchanged for a variety of items.

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Trading the tokens

The rewards include food, sweets or privileges, such as watching a movie. During the early stages, frequent exchange periods meant that patients can be quickly reinforced and target behaviours can then increase in frequency.

Supporting evidence for trading token economies: Kazdin (1977) found that the effectiveness of the token economy may decrease if more time passes between presentation of the token and exchange for the backup reinforcers.

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Evaluation of token economies

- Ethics: do patients have the same list of 'target' behaviours? Some patients may already wash themselves, for example, and some may not and if they get rewarded, then they will too. If they already did that; won't learn it's a desirable behaviour. It's not fair.

- Less useful for patients living in the community: it has only been shown to work in a hospital setting. It is difficult to administer care and support to outpatients compared to hospitalised patients who receive 24 hour care.

- Ethical concerns: clinicians may exercise control over important primary reinforcers, such as food, privacy or access to activities that alleviate boredom. It is generally accepted that all human beings have certain basic rights to food and privacy.

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The diathesis-stress model

Diathesis-stress model - explains mental disorders as the result of an interaction between biological (diathesis) and environmental (stress) influences.

Diathesis: genetic component for vulnerability. Identical twins: 50% chance; environment plays a role too in whether the twin develops schizophrenia.

Stress: stressful life events can trigger schizophrenia. Can be childhood trauma or living in a highly urbanised environment.

Diathesis + stress: genetic blueprint + live in an overcrowded environment = stress = schizophrenia.

The additive nature of DSM: vulnerable person - lots of minor stressful events + highly vulnerable individual = schizophrenia.

The additive nature of DSM: not so vulnerable - one major stressful event + individual who has a low vulnerability = schizophrenia.

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Evaluation of the diathesis-stress model

- Diatheses may not be exclusively genetic: it emphasises vulnerability in genetic influence. It causes neurochemical abnormalities that result in an increase risk. It can also be a result from brain damage from environmental factors.

+ Urban environments are not necessarily more stressful: living in densely populated urban areas is a stress factor, however, a study found that there weren't differences in rural-urban areas in mental health among women in New Zealand. This study, however, is not generalisable to men.

- Limitations of Tiernari: assessing family functioning at one given time only. Doesn't reflect developmental changes. It is impossible to determine how much stress observed is assigned to the family.

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