Topic 10: Schizophrenia Flashcards

(44 cards)

1
Q

Define schizophrenia

A

Schizophrenia is a type of psychosis characterised by a profound disruption of cognition and emotion.

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2
Q

Types of schizophrenia

A
  1. Paranoid Sz - feels extremely suspicious or grandiose.
  2. Catatonic Sz - person is withdrawn, mute, negative and often assumes very unusual body positions.
  3. Hebephrenic/disorganised Sz - primarily negative symptoms.
  4. Undifferentiated Sz - exhibits the characteristics of Sz but the overall picture is not one of catatonic type, paranoid type, or disorganised type Sz.
  5. Residual Sz - A subtype of schizophrenia in which the individual has suffered an episode of Sz but there are no longer any delusions, hallucinations, disorganized speech or behaviour.
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3
Q

Negative symptoms of schizophrenia

A

Negative symptoms appear to reflect a diminution or loss of normal functioning.

Examples:
- Speech poverty/alogia - The lessening of speech fluency & productivity, which reflects slowing or blocked thoughts.
- Avolition - The reuction, difficulty, or inability to initiate and persist in goal-directedbehaviour (lack of drive & motivation).
- Affected flattening - A reduction in the range & intensity of emotional expression, including facial expression, voice tone, eye contact & body language.
- Anhedonia - Loss of enjoymnet of activities that were previously pleasurable.
- Asociality - social withdrawal

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4
Q

Positive symptoms of schizophrenia

A

Positive symptoms appear to reflect an excess or distortion of normal function.

Examples:
- Hallucinations - Disotortions or exaggerations in any of the senses, most notably auditory hallucinations (A pereception of things that are not present).
- Delusions - fasle, sustained beliefs, which match reality. Delusions of grandeur = False, sustained beleif of importance or superiority. Delusions of persecution = False, sustained belief that others are trying to inflict suffering.
- Echolalia - Pathological repetition of the words of others.
- Disorganised thinking - can be speech, thinking or behaviour. Difficulties concentrating on things.

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5
Q

Diagnosing schizophrenia

A

Clinicians can use two diagnostic manuals: DSM and ICD
2 symptoms need to be present for 6 months or more & active for at least one month before a person can be diagnosed with scizophreniaa.

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6
Q

Measuring reliability of diagnosis

A

Reliability is measured by:
- Intra-rater reliability = How consistent one clinician is in diagnosing symptoms (test-retest).
- Inter-rater reliability = How similar diagnosis is between clinicians (measured by a statistic called a kappa score - 0.7 or above is considered good reliability.

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7
Q

Evaluation/discussion into reliability of diagnosis

A
  • In 1962, Beck found that diagnosis between different doctors were 52% similar, however measures of inter-rater reliability made in 2005 found that the diagnosis of Sz were 81% similar, so reliability has increased over time.
  • Whaley (2001) found inter-rater reliability correlations in the diagnostic of schizophrenia as low as 0.11.
  • Cultural differences in diagnosis: Copeland gave 134 US & 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed Sz but only 2% of the British ones gave the same diagnosis. This suggests a lack of consistency between American and British clinicians in diagnosing SZ. It also shows low concurrent validity between the DSM-V (primarily used in thd US) and the ICD (primarily used in the UK), suggesting that either one, or both, of the manuals are incorrectly measuring schizophrenia.
  • Gender bias: Loring and Powell: Gave male and female doctors identical descriptions of a patient but varied whether the pateint was described as male of female. When the patient was described as male 56% of doctors diagnosed the pateint with SZ, compared to only 20% when the patient was described as female. This indicates that there may be an alpha bias in diagnosing sz.
  • Cochrane (1977) conducted a review comparing the number of people diagnosed with schizophrenia in Britian and the Caribbean. The overall rate of schizophrenia was similar in the Caribbean and Birtian (around 1%). However, afro-caribean people were 7x more likely to be diagnosed with schizophrenia when living in Britian than when living in the Caribbean. Cochrane concluded that this was because of culutral bias by British doctors.
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8
Q

Problems with the validity of diagnosis

A
  • Symptom overlap refers to the fact that symptoms of a disorder may not be unique to that disorder but may also be found in other disorders (many symptoms of schizophrenia are also found in other disorders, such as depression or bipolar disorder), making accurate diagnosis difficult.
  • co-morbidity refers to the extent that two (or more) conditions ot diseases occur simultaneously in a patient. Substance abuse, anxiety and depression are common psychiatric co-morbitities among patients with Sz. Comorbidity can make it difficult to tell the difference between schizophrenia and other conditions, such as depression.
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9
Q

Evaluation/discussion of validity in diagnosis

A
    • Rosenhan: Got 8 healthy volunteers to pretend to have schizophrenia, by claiming they heard an unfamiliar voice in their head saying ‘empty’, ‘hollow’, and ‘thud’, in order to be admitted into a US psychiatric hospital. It took the doctors between 7 and 52 days to realise the diagnosis were wrong and that the volunteers were healthy. This indicates that the diagnosis of schizophrenia can lack validity.
  • Gender bias: Loring and Powell randomly selected 290 M & F psyhciatrists to offer their judgements on an account of patients’ behaviour. When patients were described as ‘male’ or their gender wasn’t shared, 56% gave a diagnosis of Sz. When patients were described as ‘female’, only 20% were given a diagnosis - alpha bias.
  • Symptom Overlap: Ellason and Ross compared the symptoms of patients with dissociative identitiy disorders and schizophrenia, and found that pateints with dissociative identity disorder displayed more schizophrenic symptons than people who had been diagnosed with schizophrenia. So the DSM’s diagnositic criterea might not be clear enough to provide a reliable or valid diagnosis.
  • Co-morbidity: Buckley et al estimate that co-morbid depression occurs in 50% of Sz patients, and 47% of patients have a lifetime diagnosis of co-morbid substance abuse and 23% had OCD. Therefore the criteria used to diagnose schizophrenia may lack valaidity as sz may not be a distinct mental disorder at all. Weber looked at nearly 6 million hospital discharge records and found evidence of many co-morbid non-psychiatric diagnoses including asthma, hypertension & type 2 diabetes.
  • Lacks predicitve validity - Variation in prognosis: Harrison (2001) found that 30% of patients showed improvement in some cases, but only 10% in others.
  • Cultural Bias: Cochrane conducted a review comparing the number of people diagnosed with Sz in Britian and the Caribbean. The overall rate of Sz was similar in the Caribbean and in Britian. Afro-Caribbean people were 7x more likely to be diagnosed with Sz when living in Britian than when living in the Caribbean. Cochrane concluded that this was because of culture bias by British doctors.
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10
Q

Measuring validity of diagnosis

A
  • The extent that a diagnosis actually reflects the actual disorder (how accurate the DSM/ICD is).
  • The extent which different assessement systems arrive at the same diagnosis for the same patient.
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11
Q

Cheniaux (2006)

A
  • 2 idependent psychiatrists diagnosede 100 patients using both DSM & ICD.
    Number of diagnosed schizophrenia cases:
  • 26 & 13 DSM = Lack of consistency between psychiatrists & therefore inter-rater reliability
  • 44 & 24 ICD
    There’s a discrepency between the number of diagnosis by DSM compared to ICD challenging the validity of the manuels.
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12
Q

Biological Explanation for schizophrenia: Genetics outline and evaluate

A

AO1: The genetic explanation of schizophrenia suggests that schizophrenia is a result of genetic fault and thus if more genes are shared there should be a greater concordance rate for schizophrenia. Thus it is often described as a heritable disorder.

Twin Studies:
For severe schizophrenia (involving 2+ years in hospital),Gottesman and shields found:
- CR for Mz twins = 75%
- CR for Dz twins = 24%
- General population = 1% risk
Eval:
If your romantic partner has Sz, your risk is twice that of the general population (2%). This suggest environment plays a role as they’re not genetically related.
Assumes that Mz twins and Dz twins have a similar amount of shared environment, however Mz twins are often treated more similarly, encounter similar environments & experience more identity confusion that Dz twins. Differences in CR’s may reflect environmental differences between the two types of twins

Family Studies:
Gottesman
- Children with 2 parents with Sz = 46% CR
- Children with 1 parent with Sz = 13% CR
- Siblings (where one has Sz) = 9% CR

Adoption Study:
Tienari et al
Of the 164 adoptees whose biological mothers had Sz, 11 (6.7%) also received a Sz diagnosis, compared to just 4 (2%) of the 197 control adoptees. Shows genetic liability to Sz.
Eval:
-Since these children were adopted at birth, any similarities between the child and their biological mother must be due to genetics rather than the environment. However adopted children are often matched with parents who are similar to their adoptive parents, and so any simmilarty between the child and their biological parents, might be caused by shared enviornmental factors as well as genetics.
- Adoptees may be selectively placed. A large adoption study into Sz took place in Oregon (1966), where it was assumed that procreation by any person admitted to a mental hospital would produce offspring with an inherited tendency to ‘insanity’. Therefore it is unlikely that the children born to women with Sz would have been placed in the same type of adoptive families as children without such a background.

Polygenetic (Ripke 2014):
Evidence that Sz is polygenic (a characteristic that is influenced by two or more genes).
P: He found the genetic makeup (genomes) of 37,000 patients and 113,000 controls.
F: 108 separate genetic variations were associated with increased risk of Sz. Link with genes which associated with number of neurotransmitters including dopamine.

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13
Q

Dopamine hypotheisis

A

Claims that an excess of the nuerotransmitter dopamine in certain areas of the brain is associated with the positive symptoms of scizophrenia.
Individuals with positive symptoms of Sz are likely to have high levels of dopamine and more dopamine receptors on the post-synaptic cell, increasing dopaminergic activity.

Th Revised dopamine hypothesis - Davis et al (1991):
Excess of dopamine (Hyperdopaminergia) in the mesolimbic pathway = positive symptoms
Deficit of dopamine (Hypodopaminergia) in areas of prefrontal cortex (area responsible for thinking, decision making etc) = Negative symptoms

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14
Q

Neural correlates hypothesis

A

Genes can cause abnormalities in the brain and according to the neural correlates explanantion of schizophrenia, schizophrenia is caused by abnormal brain structure (e.g. larger ventricles and smaller frontal cortex than normal)
Patterns of strucutre or function in the brain that correlate with a Sz experience. As they occur simultaneously this could lead us to believe that the patients observed are implicated in causing Sz.

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15
Q

neural correlates explanation of schizophrenia: evaluation and discussion

A
  • Torrey et al: results from an MRI scan found that on average the ventricles patients with schitzophrenia were 15% larger than the control group.
    This correlation doesn’t necessarily mean causation. The enlarges ventricles might be a side effect of taking medication to treat SZ.
  • There are individual differences in the brain abnormalities that patients with schizophrenia display and so studies suporting the role of large ventricles, haven’t always replicated.
  • Reduced myelation of white matter pathways in Sz patients, compared to controls (Due et al). Particularly in the neural pathways between the hippocampus & PFC.
  • Negative symptoms:Theventral striatumis involved with reward anticipation. Schizophrenia patients have been found to have less activity in this region- the lower the activity, the more severe the negative symptoms. This could explain avolition (loss of motivation).
  • Positive symptoms:Allenet al(2007) scanned the brains of patients experiencing hallucinations whilst they completed an auditory processing task. Lower activation levels were found in thesuperior temporal gyrusandanterior cingulate gyrus, and they made more errors, compared to a control group. Auditory hallucinations are therefore correlated with reduced activity in these areas.
  • Neural explanations have been criticised as reductionist, explaining schizophrenia at quite a simplistic level of explanation. The role of upbringing, learning and emotions is not considered, weakening this as a full explanation.
  • A neural correlates explanation of schizophrenia isan example of biological determinism as it assumes that specific brain structures and/or dopaminergic activity in the brain play a key role in the onset of schizophrenia
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16
Q

Evaluation of dopamine hypothesis

A

Strengths:
- Support from drug studies: Drugs that increase dopamine, like amphetamines cause hallucinations and delusions in healthy people. and drugs that decrease dopamine reduce the likelihood that pateints with schizophrenia will experience hallucinations and delusions.
- Practical Applications: Antipsychotic drugs, such as chlorpromazine, which reduce the symptoms of Sz work by inhibiting dopamine transmission. CP: Antipsychotic drugs only reduce all of the symptoms in around 20% of patients.
- Post-mortem (after death) examinations show schizophrenia patients have more dopamine receptors in the left amygdala (Falkai et al., 1988) and the caudate nucleus (Owen et al., 1978).

Weaknesses:
- Noll found that for 1/3 of pateints with schizophrenia, drugs that decrease the level of dopamine didn’t prevent hallucinations and dellusions. This suggests that high levels of dopamine in the mesolimbic system can cause positive symptoms but they aren’t the only cause of positive symptoms.
- Moncrieff conducted a review and claimed that the evidence supporting the dopamine hypothesis is inconclusive for two reasons: first, drugs like amphetamines, which cause positive symptoms, effect other neurotransmitters as well as dopamine - so we cannot be sure that it is the increased dopamine that is causing these symptoms. Second, not all post mortem studies support significant differences in levels of dopamine in schizophrenic patients mesolimbic systems.
- There is some evidence to suggest that dopamine is not the only neurotransmitter involved. Moghaddam & Javitt found evidence for the role of an NT called glutamate in which it appeared that Sz patients have a deficiency in glutamate function. Supports biological/neural explanation but challenges the simplicity of dopamine hypothesis on its own.
- Antipsychotics gradually reduce positive symptoms over several weeks, despite immediately blocking dopamine receptors. Suggests it’s not a direct cause and effect and challenges the simplicity of the theory.

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17
Q

Anti-psychotics

A
  • Drugs used for hyperdopaminergia to reduce positve Sz symptoms. Antipsychotic drugs bind to post synaptic dopamine receptors. This prevents dopamine from binding to receptors, reducing the overactivity of neurones in the mesolimbic system.
  • Typical (traditional) antipsychotics bind to dopamine receptors for long periods of time and thus have more side effects.
  • Atypical (newer) antipsychoticcs bind to dopamine receptors for shorter periods of time and sso have less side effects.
  • Examples: Chlorpromazinwe, clozapine, risperidone
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18
Q

Chlorpromazine

A
  • Typical antipsychotic (1950s)
  • Can be taken as tablets, syrups (absorbed faster than tablets), or injection.
  • Blocks dopamine receptors, reducing dopaminergic activity.
  • Reduced positive symptoms
  • Also an effective sedative, often used to calm patients with Sz and other mental disorders.
  • Side effects: dizziness, agitation, sleepiness, stiff jaw, weight gain, tardive dyskinesia, neruoleptic maligant syndrome (which can be fatal).
19
Q

Clozapine

A
  • Atypical antipsychotic (1970s)
  • Binds to dopamine receptors & acts on serotonine & glutamine receptors, providing mood-enhancing effects & improving cognition. Important as 30-50% of Sz patients attempt suicide.
  • Requires regular blood tests due to risk of fatal condition - agranulocytosis
  • Not available as an injection
20
Q

Risperidone

A
  • Atypical antipsychotic (1990s)
  • Binds to dopamine and serotonine receptors. More effective and requires smaller dosage due to stronger binding.
  • Tablets, syrup or injection
21
Q

Evaluate/discuss drug therapy as a treatment for schizophrenia

A
  • Typical antispychotics can have extra-pyramidal side effects (involuntary and uncontrollable movements), which can be distressing for patients and may cause them to stop taken the medication. They can also lead to an increased risk of heart problems, obesity and diabetes. However atypical antipsychotics are less likely to produce these extra-pyramidal effects and as a result patients are more likely to continue taking their medication & see a reduction in their symptoms.
  • Typical antispsychotics don’t treat negative symptoms of Sz
  • Leucht (2001) conducted a meta-analysis of 65 studies into the effectiveness of antipsychotic drugs. He found that antispsychotic drugs were more effective at treating Sz than placebo pills, and that patients taking the drugs were less likely to relapse and experience severe postitive symptoms.
  • Crossley (2010): meta-analysis of 15 studies comparing the effectiveness of typical and atypical antipsychotics. He found no difference in their overall effectiveness at preventing symptoms, but atypical antipsychotics had significantly fewer side effects than typical antipsychotics.
  • Patients are likely to relapse if they stop taking the drugs. - Schooler et al (2005) randomly allocated 555 patients in first episode of Sz, to either treatment with haloperidol or risperidone. In both groups 75% showed a reduction in symptoms. However he found a 55% relapse rate. Drug therapy is a short-term fix only because it only manages symptoms and doesn’t deal with the cause (Schooler’s relapse %). However it is possible to be used in combination with another treatment that may be longer term.
  • Drop out rates are high likely due to side effects like tardive dyskinesia and neuroleptic malignant syndrome, which can be fatal.
  • Antipsychotics are expensive: Globally, around $14.5bn is estimated to be spent on antipsychotics each year. This can lead to an problem of inequality. While wealthy individuals can afford acces to treatment, less fortunate individuals may be forced to suffer.
  • They help carers to look after patients with Sz. Mental Health nurses may rely on anti-psychotics to sedate & calm patients so that they are easier to work with. This can raise ethical issues of consent but also who the drugs are for. Are they being used to benefit the patients or the staff? While they can protect and help patients and nurses, it could also be unethical if misused. If given too high dosages too often patients may become zombie-like and withdrawn from reality, which doesn’t improve their lives and counteracts the purpose of treatment.
  • Barlow & Durand (1955) chlorpromazine is effective in reducing Sz symptoms in about 60% of cases. Most impact on positive symptoms; treated patients may still suffer from severe negative symptoms.
  • Emsley (2008) found that patients who were injected with risperidone early in the course of disorder has low relapse rates and high remission rates; 84% of patients showed at least a 50% reduction in both +ve and -ve symptoms and 64% went into remission.
22
Q

Double bind theory

A
  • Bateson (1956) suggests that children who frequently receive contradictory messages from their parents are more likely to develop Sz.
  • e.g. a mother saying ‘I love you’ but turning away in disgust.
  • These mixed & ambiguous messages cause confusion & mistrust - the child begins to question their own feelings and emotions as they cannot trust what their parent is telling them. These interactions prevent the development of an internally coherent construction of reality.
  • As a result the child grows up mistrusting all communication (paranoia) & withdrawing from society (asociality) which explains many of the symptoms of Sz.
23
Q

What are the psychological explanations for schizophrenia?

A
  • Family dysfunction: The presence of problems within a family that contribute to relapse rates in recovering schizophrenics, including lack of warmth between parents and child, dysfunctional communication patterns and parental overprotection.
  • Cognitive Explanations of mental disorders propose that abnormalities in cognitive function are a key component of Sz.
24
Q

The schizophrenic mother

A

Fomm-Reichmann (1948) suggested that a cold, rejecting, controlling mother causes tension and secrecy within the family and that this behaviour could lead to distrust and & later develops into paranoid delusions and ultimately schizophrenia.

Later revised into theories like double-blind and expressed emotion because of it’s social sensitivity & simplicity.

25
Expressed emotion & schizophrenia
Expressed emotion = A family communication style in which members of the family of a psychiatric patient talk about that patient in a critical or hostile manner or in a way that indicates emotional over-involvement or over-concern with the patient or their behaviour. **Brown** et al (1958) proposed that family interactions that involved high levels of expressed emotion (EE) & emotional over-involvement, including hostility & criticism could play a key role in **maintaining** the schizophrenic behaviours. EE includes: hostility towards the patient, verbal criticism and emotional over-involvement. High levels if EE can be a serious source of sress for patients triggering relapse or could trigger the onset of Sz in someone who is already vulnerbale (e.g. geneticallt)
26
Dysfunctional thought processing
Dysfunctional thought processing involves cognitive habits or beliefs that cause the individual to evaluate information innapropriately. A breakdown in the person's self-monitoring process makes it difficult for them to interpret their own thoughts & perceptions accurately, resulting in symptoms such as hallucinations and delusions. **Frith** identified two kinds of dysfunctional thought processings that could unerlie some symptoms: - **Meta representation** - The reflection of thoughts & behaviours as being our own. Individuals with schizophrenia may struggle to recognize their own actions and intentions, leading to feelings of being controlled by external forces. I.e. a pateint with Sz may close a door but then believe the door has been closed by someone else. - **Central control** - The ability to supress automatic responses & perform deliberate actions. I.e. Disorganized speech: Individuals with schizophrenia may struggle to control the flow of thoughts and speech, leading to jumbled sentences and frequent topic change **Stroop Effect**: The Stroop effect is a cognitive test that measures how well someone can inhibit irrelevant information. People with schizophrenia tend to show more interference on the Stroop task than people without schizophrenia. This is consistent with their tendency to be easily distracted. **Dysfunctional reasoning** can cause delusions: - **Jumping to conclusion bias**: tendency to jump to conclusions based on very little reasoning - **persecution bias**: the tendency to believe they are being single out or unfairly treated **Dysfuntional attention** can cause delusions and hallucinations: - Patients tend to overfocus on small irrelevant details and coincidences. But because of their dysfunction reasoning their explanation is irrational leading to a delusional belief. - A tendecny to overfocus on things they imagine can make them feel real leading to hallucinations Patients can become overwhelmed by hallucinationks and delusions causing them to want to avoid these abnormal experiences and as a result they may isolate themselves resulting in **negative symptoms of SZ**: avolition and speech poverty
27
CBT as a treatment for schizophrenia
-its aim is to help patients identify irrational thoughts and try to change them. -helps find coping mechanisms ,doesn’t get rid of the symptoms. -may involve argument /discussion of how likely the patient’s belief are to be true. - takes 5-20 sessions How CBT helps-it helps patients make sense of their delusions and hallucinations and how they impact their feelings and behaviour.Offers psychological explanations for the existence of hallucinations and delusions to help reduce this anxiety.Delusions can be challenged so the patient can learn that their beliefs are not based on reality. Step 1: Explanation - the patient explains their symptoms Step 2: Normalisation - the doctor normalises the pateints experiences Step 3: Challenging - the doctor challenges beliefs and expereinces Step 4: Alternative explanations - the patient is asked to develop alternative explanations for beliefs and expereinces. Ellis's model: A: Activating event or situation (the source of irrational belief) B: Beliefs (usually irrational) C: Consequences (The way a person feels in response to A+B) D: Disputation of the beliefs (Logical, empirical or pragmatic disupting) E: Effective new approach to dealing with the problem (Creating rational beliefs to replace irrational beliefs & using cognitive & behavioural modification techniques to reinforce the rational beliefs, improving mood over time.
28
Evaluate psychological explanations for SZ
Strengths: - Strong evidence for dysfunctional information processing - **Stirling** et al (2006) compared 30 patients with a diagnosis of schizophrenia with 18 no-patient controls on a range of cognitive tasks such as the stroop test, in which participants have to name the ink colours of colour words, suppressing the impulse to read the words in order to do this task. Patients took over twice as long to name the ink colours as the control group. - Family relationships: IN **Tienari's** adoption study, he found that children who has SZ biological parents were more likely to become ill themselves than were children with non-Sz biological parents. However, this difference only emerged in situations where the adopted family itself was rated as disturbed. - **Practical applications**: CBT & Family therapy. - **Berger** found that Sz's reported a higher recall of double-bind statements by their mothers than non Sz's. - **Linzen et all** found that a patient, who returns to a family high in hostility, criticism and emotional over-involvement in **4X** more likely to relapse than one who returns to a family that has a low amount of these characteristics. Limitations: - Weak evidence for family-based explanations-there is almost no evidence to support the importance of the schizophrenogenic mother or double blind. Both these theories are based on the clinical observation of patients. These explanations have led historically to parent-blaming (**social sensitivity**). Parents undergo further trauma for being blames. The shift in the 1980s from hospital to community care, often involving parent care, may be one of the factors leading to the decline of the schizophrenogenic mother and double bind theories. - Individual difference in vulnerability to expressed emotion: **Altorfer** et al found that 1/4 of patients they studied showed no physiological responses to stressful comments from their relatives. - **Alternative explanations**: Biological & drug therapies.
29
Family therapy
- Interventions aimed at the family of someone with Sz to reduce family conflict. - Aims to reduce rates of EE within families as EE increases likelihood of relapse. Steps: 1. **Educating** families about the illness, to help them better understand schizophrenia 2. **Teaching coping stratergies** - finding ways to support and resolve practical problems. 3. **Changing communication styles** to reduce the degree of expressed emotion in families.
30
Pharoah et al (2010)
- Meta-analysis: Reviewed 53 studies to investigate the effectiveness of family intervention. The studies compared outcomes from family therapy to 'standard care' (i.e. medication). Findings: - Mental state - Mixed findings - Compliance with medication - Increased with family intervention. - Social Functioning - Family intervention had some improvement on general functioning but not more concrete outcomes such as living independently or employment. - Reduction in relapse and readmission - Family intervention reduced the risk of relapse. There was a reduction in hospital admission during treatment and in the 24 months after. Methodological limitation: Not all studies in the meta-analysis had used randomisation or blinding. over 20% failed to use observers 'blind' to what treatments patients were receiving.
31
Evaluate Family Therapy as treatment for schizophrenia
Limitations: - Problems of practicability: Time-bound, difficulties getting the whole family together, family members may not be willing to take part or may have a negative response to therapy. Patient may not be honest & open up Infront of hostile family members and strategies may not work for everyone. - May be effective only because it improves compliance with antipsychotic medication. - Family therapy relies heavily on informed consent, and ethical boundaries may be crossed, patients may be uncomfortable sharing such details, and confidentiality issues may arise. - Due to the lengthy process, as family therapy can last up to a year, symptoms or incidents (such as disputes or conflicts in the family) may cause patients and family members to drop out of therapy. - Family therapy focuses on treating symptoms and improving the patient’s home life. It supports family relationships and helps family members cope with symptoms, but it is not a cure. Strengths: - Economic benefits: Extra cost of family intervention is offset by reduction of costs of hospitalisation associated with relapse. NCCMH found that there were significant cost savings when family therapy was combined with antipsychotic medication. However private treatment may result in class inequality as only those wealthy enough can afford the treatment. - Impact on family members: **Lobban** et al meta analysis of 50 studies into the results of family therapy on Sz. **60%** reported a positive impact on relatives.
32
Token Economy
- Form of behavioural therapy used in the management of Sz. - Uses tokens and exchange for rewards to increase target behaviours. - Uses operant conditioning principles and classical conditioning: Positive reinforcement - Tokens are secondary reinforcers exchanged for primary reinforcers (rewards). At first the token is neutral stimulus but after repeated pairings with the reward it becomes a conditioned stimulus and the pateint develops a conditioned response to the token. - Generalised secondary reinforcers more powerful (their reinforcing values are learned because they are associated with some primary reinforcer). - Patient trades token - timing of reinforcement is important (reinforcer needs to be delivered immediately after ther performance of the target behaviour).
33
Allyon & Azrin (1968)
Used a token economy on a ward with female Sz patients, whom had been hospitalised for many years. Findings: Increased the number of desirable behaviours they performed from 5 to 40 when rewarded with tokens.
34
Evaluate Token economy as a treatment for schizophrenia
- Ethical issues
35
Evaluate CBT as a treatment for schizophrenia
Strengths: - Review by **NICE** found that a combination of CBT and drugs was more effective than drugs alone at reducing symptoms and relapse. - Empirical evidence: **Tarrier et al.** (2005) investigated the effectiveness of CBT as a treatment for schizophrenia via a meta-analysis of 14 studies of CBT published between 1990 and 2004 involving 1,484 patients. Found that CBT significantly reduced positive symptoms and was especially beneficial to those suffering a short-term acute schizophrenic episode. Thus CBT is beneficial in the short-term. But is usually paired with drug treatment for maximum benefits. The empirical success of CBT has allowed it to become a viable alternative for patients who may not want to take antipsychotics (e.g. due to fear of addiction), thus widening the access for treatment. Limitations: - Many studies into the effectiveness of CBT are poorly designed, failing to use random allocation and blinding, potentially leading to confounding variables, and a lack of objectivity from the researchers. So the effectiveness of CBT might be over-exaggerated. In many studies, CBT is compared against a control treatment - TAU or 'treatment as usual' - and found to be superior. This difference may not be due to the effectiveness of CBT; it may be because TAU is positively harmful. - had contradictory evidence - **Jauhar** Jauhar et al. (2014) reviewed the results of 34 studies of CBT for schizophrenia. They concluded that CBT has a significant but fairly small effect on both positive and negative symptoms. **Morrison** found significant reduced symptoms in schizophrenics. Individual differences? Not a realiable treatment. - **Short term effectiveness** - when comparing CBT to standard care after 18 months the individuals all had the same relapse rates - effects are short lived - **Limited access** to CBT - psychiatrists may not offer CBT to those who do not believe them that their diagnosis is accurate. May not offer it to those that won't react well to the treatment. In many cases schizophrenics are unaware of their illness and refuse to believe or work with their therapists because of paranoia. Many patients with schizophrenia drop out of CBT. Patients need to be highly motivated because the treatment requires effort and commitment (unlike taking antipsychotic pills). - Time-consuming and expensive because it requires lots of one-to-one sessions with a therapist, which limits the availability of the treatment. However, **Kuipers** argues that while it may cost more initially, it will be beneficial in the long run as schizophrenics with CBT are less likely to need emergency help in the future.
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Problems with schizophrenia diagnosis and classification
- Due to the stigma surrounding schizophrenia, labelling make have a negative impact. **Roland Imhoff** found that calling an identical symptomatology 'schizophrenia' vs not labelling it led to greater perceptions of aggressiveness, less trust worthiness, more anxiety towards this person and stronger assumtions this person feels aggressive-related emotions. CP: A diagnosis can sometimes help an individual to understand their symptoms and provide access to treatments/support groups. - Culture and gender bias: more men are diagnosed than women - Longenecker et al. Aro-Caribbean Britons & African Americans are several times more likely to be diagnosed with Sz, despite rates of diagnosis not being high in Africa & the West Indies. In a lot of cultures it is considered normal to see or hear God or to talk with the dead.
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Diathesis-stress model
Explains mental disorders as the result of an interaction between biological (the diathesis) and environmental (stress) influences. This model proposes that individuals will develop schizophrenia if they have a biological predisposition and if they are exposed to stressful situation.
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How's has the diathesis-stress model changed over-time?
**Meehl's** (1962) original diathesis-stress model states: - Diathesis is entirely genetic - the result of a single schizogene, which led to a biological based schizotypic personality - one characteristic extremely sensitive to stress. No amount of stress will lead to Sz if the gene is not present. - Environmental stress linked to mother - It is now understood that multiple genes increase vulnerability to Sz. - Stress is no longer believed to be limited to dysfunctional parenting. - It is now acceptedthat vulnerability can be the result of early trauma as well as genetic-makeup and that stress can come in many forms including biological.
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Key study: Tienari et al (2004)
P: 145 adopted children of mothers with Sz compared with adopted children without this vulnerability. Assessed over a 21-year period; adoptive family also assessed using OPAS. F: 14 adoptees developed schizophrenia,11 from the schizophrenic group. Healthy family had protective effect, disturbed family likely to trigger Sz. C: In adoptees at high genetic risk of SZ, but not in those with low genetic risk, adoptive-family stress was a significant predictor of the development of SZ.
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Evaluate the interactionist approach as an explanation for schizophrenia
- Not reductionist because it looks at a range of influences of schizophrenia (holistic approach). This means that it doesn't ignore the complexity of human behaviour. However, it can be criticised for being less scientific. It's more hypothetical than lower level explanations and harder to measure individual elements. Difficulty isolating causal factors. - The original diathesis-stress model is over-simplistic: Ripke suggests that Sz is polygenic and in **Houston's** study childhood sexual trauma emerged as a vulnerability factor, while cannabis use was a trigger. This suggests that vulnerbilities can be psychological and triggers can be biological. - Practical Applications: Treatments accroding to interactionism, believe that a combination of therapy should be employed between antipsychotic drugs and psychological therapies like CBT (this is the standard practice in the UK, but medication alone is more common in the US). **Tarrier et al**. randomly allocated patients to either a medication plus CBT group, a medication plus supportive counselling group and a control group who just took medication. They found that patients in the two combination groups showed lower levels of symptoms than those in the control group, although there was no difference in hospital readmissions. This could be due to patients stopping their medication because of the side effects. This evidence suggests that taking an interactionist approach to treatment is beneficial and reduces suffering. However, the fact that combining treatment works does not necessarily mean that the interactionist approach is correct - it could be an error known as the treatment causation fallacy. - Studies like the Finnish Adoption Study by Tienari et al. provide evidence for the interactionist approach, showing that individuals with a genetic predisposition to schizophrenia are more likely to develop the disorder when exposed to high levels of family stress. 
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Neural Correlates in Schizophrenia: Ventricles
**Torrey** et al: results from an MRI scan found that on average the ventricles patients with schitzophrenia were **15%** larger than the control group. This correlation doesn't necessarily mean causation. The enlarges ventricles might be a side effect of taking medication to treat SZ.
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Outline and discuss/evaluate the cognitive explanantion for schizophrenia
AO1: According to the cogntive explanation, symptoms of Sz are caused by dysfunctional thought processes, including: dysfunctional attentions and dysfunctional reasoning. People with SZ display two types of dysfunctional reasoning: - The Jumping to conclusions bias - The tendency to believe that they are being singled out and unfairly treated - **the persecution bias** Due to dysfunctional attention, patients tend to overfocus on small irrelevant details and coincidences. The patient then tries to explain why all of these coincidences are happening, but because of their dysfunctional reasoning, their explanation is irrational, leading to a delusional belief. Patients may also overfocus on things that they imagine, making them feel real. As a result patients with Sz may struggled to tell the difference between things that they imagine and reality, leading to hallucinations Negative Symptoms: - when pateints become overwhelmed by hallucinations or delusions, they may want to avoid these abnormal experiences, and as a result may isolate themselves from people and the outside worrld, causing them to experience the negative symptoms of Sz - avolition and speech poverty AO3: - evidence for dysfunctional information processing - **Stirling** et al (2006) compared 30 patients with a diagnosis of schizophrenia with 18 no-patient controls on a range of cognitive tasks such as the stroop test, in which participants have to name the ink colours of colour words, suppressing the impulse to read the words in order to do this task. Patients took over twice as long to name the ink colours as the control group. - **O'Caroll reviewed studies that investigated mental dysfunction in Sz, and found that **75%** of patients displayed dysfunctional mental processes. O'Caroll then reviewed studies investigating people at risk of developing Sz. He found that people who went on to develop Sz, already had dysfunctional mental processes before they showed any symptoms. This suggests that the dysfunctional mental processes may have caused the symptoms. - However one limitation is that it doesn't account for biological factors (genetics, dopamine hypothesis, neural correlates) that may lead to sz. AO1: CBT as a treatment: - Aims to help patients identify irrational thoughts and try to change them. Takes 5-20 sessions. Step 1: Explanation - the patient explains their symptoms Step 2: Normalisation - the doctor normalises the pateints experiences Step 3: Challenging - the doctor challenges beliefs and expereinces Step 4: Alternative explanations - the patient is asked to develop alternative explanations for beliefs and expereinces. Ellis's model: A: Activating event or situation (the source of irrational belief) B: Beliefs (usually irrational) C: Consequences (The way a person feels in response to A+B) D: Disputation of the beliefs (Logical, empirical or pragmatic disupting) E: Effective new approach to dealing with the problem (Creating rational beliefs to replace irrational beliefs & using cognitive & behavioural modification techniques to reinforce the rational beliefs, improving mood over time. AO3: - Practical Applications: Review by **NICE** found that a combination of CBT and drugs was more effective than drugs alone at reducing symptoms and relapse. - Empirical evidence: **Tarrier et al.** (2005) investigated the effectiveness of CBT as a treatment for schizophrenia via a meta-analysis of 14 studies of CBT published between 1990 and 2004 involving 1,484 patients. Found that CBT significantly reduced positive symptoms and was especially beneficial to those suffering a short-term acute schizophrenic episode. Thus CBT is beneficial in the short-term. But is usually paired with drug treatment for maximum benefits. The empirical success of CBT has allowed it to become a viable alternative for patients who may not want to take antipsychotics (e.g. due to fear of addiction), thus widening the access for treatment. - - Many studies into the effectiveness of CBT are poorly designed, failing to use random allocation and blinding, potentially leading to confounding variables, and a lack of objectivity from the researchers. So the effectiveness of CBT might be over-exaggerated. In many studies, CBT is compared against a control treatment - TAU or 'treatment as usual' - and found to be superior. This difference may not be due to the effectiveness of CBT; it may be because TAU is positively harmful. - had contradictory evidence - **Jauhar** Jauhar et al. (2014) reviewed the results of 34 studies of CBT for schizophrenia. They concluded that CBT has a significant but fairly small effect on both positive and negative symptoms. **Morrison** found significant reduced symptoms in schizophrenics. Individual differences? Not a realiable treatment. - **Short term effectiveness** - when comparing CBT to standard care after 18 months the individuals all had the same relapse rates - effects are short lived - **Limited access** to CBT - psychiatrists may not offer CBT to those who do not believe them that their diagnosis is accurate. May not offer it to those that won't react well to the treatment. In many cases schizophrenics are unaware of their illness and refuse to believe or work with their therapists because of paranoia. Many patients with schizophrenia drop out of CBT. Patients need to be highly motivated because the treatment requires effort and commitment (unlike taking antipsychotic pills). - Time-consuming and expensive because it requires lots of one-to-one sessions with a therapist, which limits the availability of the treatment. However, **Kuipers** argues that while it may cost more initially, it will be beneficial in the long run as schizophrenics with CBT are less likely to need emergency help in the future.
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Outline and discuss/evaluate the family disfunction explanation for schizophrenia
AO1: Family conflict causes stress and confusion, which may cause schizophrenia. **Double bind**: When someone experiences two contradictory messages, meaning that they get confused about the correct way to behave. As a result the child grows up mistrusting all communication (paranoia) & withdrawing from society (asociality) which explains many of the symptoms of Sz. **High degree of expressed emotion**: When family's speak to each other in a negative way and express alot of criticism, complaints and over-involvement in each others lives AO3: - **Burger** (1965) conducted interviews and found that people with schizophrenia could recall more experiences of double binds during their childhood that people who didn't have schizophrenia. - **Vaughn and Leff** in an observational study found that when families display high levels of expressed emotion, peopl with schizophrenia were more likely to relapse after leaving the hospital. - The evidence about double binds might be unreliable: it's possible that patients may lack objectivity when reporting double binds as it relies of retrospective experiences and memory may be inaccurate, and may be impaired by the disorder. - There are individual difference is patients responses to expressed emotion: **Altorfer et al** (1988) observed schizoophrenic patients interacting with their families, and found that not all families displayed a high degree of expressed emotion, and even amongst the patients whose families displayed a high degree of expressed emotion, **1/4** of these patients didn't show a stress response when they were criticised. So a high degree of EE may just increase the risk of a person developing the disorder, rather than causing it. - Family relationships: In **Tienari's** adoption study, he found that children who has SZ biological parents were more likely to become ill themselves than were children with non-Sz biological parents. However, this difference only emerged in situations where the adopted family itself was rated as disturbed. - **Linzen et all** found that a patient, who returns to a family high in hostility, criticism and emotional over-involvement in **4X** more likely to relapse than one who returns to a family that has a low amount of these characteristics. - - Weak evidence for family-based explanations-there is almost no evidence to support the importance of the schizophrenogenic mother or double blind. Both these theories are based on the clinical observation of patients. These explanations have led historically to parent-blaming (**social sensitivity**). Parents undergo further trauma for being blames. The shift in the 1980s from hospital to community care, often involving parent care, may be one of the factors leading to the decline of the schizophrenogenic mother and double bind theories. AO1: Treatment: Family Therapy aims to reduce conflict: 1. **educating** families about the illness. 2. **Teaching coping stratergies** 3. **changing communication styles** to reduce the degree of expressed emotion in the family. AO3: - **Pharoah et al** reviewed studies that ivestigated the effectiveness of combining family therapy with medication, compared to just pescribing medication. They found that patients given family therapy were more likely to take their medication consistently and were less likely to relapse severe symptoms and return to hospital. However many studies in his review didn't use random allocation so participant variale weren't controlled, and in many studies the researchers weren't blind to the group and may have lacked objectivity. - Cost-effective as it reduces the likelihood of relapse. - Economic benefits: Extra cost of family intervention is offset by reduction of costs of hospitalisation associated with relapse. NCCMH found that there were significant cost savings when family therapy was combined with antipsychotic medication. However private treatment may result in class inequality as only those wealthy enough can afford the treatment. - Impact on family members: **Lobban** et al meta analysis of 50 studies into the results of family therapy on Sz. **60%** reported a positive impact on relatives. - Problems of practicability: Time-bound, difficulties getting the whole family together, family members may not be willing to take part or may have a negative response to therapy. Patient may not be honest & open up Infront of hostile family members and strategies may not work for everyone. Due to the lengthy process, symptoms or incidents (i.e family disuputes or conflicts) may cause patients or family members to drop out.
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Outline and discuss/evaluate the biological explanation for schizophrenia
GENETICS AO1: The genetic explanation of schizophrenia suggests that schizophrenia is a result of genetic fault and thus if more genes are shared there should be a greater concordance rate for schizophrenia. Thus it is often described as a heritable disorder. AO3: Twin Studies: For severe schizophrenia (involving 2+ years in hospital),**Gottesman and shields** found: - CR for Mz twins = **75%** - CR for Dz twins = **24%** - General population = **1%** risk Eval: If your romantic partner has Sz, your risk is twice that of the general population (**2%**). This suggest environment plays a role as they're not genetically related. Assumes that Mz twins and Dz twins have a similar amount of shared environment, however Mz twins are often treated more similarly, encounter similar environments & experience more identity confusion that Dz twins. Differences in CR's may reflect environmental differences between the two types of twins Family Studies: **Gottesman** - Children with 2 parents with Sz = **46%** CR - Children with 1 parent with Sz = **13%** CR - Siblings (where one has Sz) = **9%** CR Adoption Study: **Tienari et al** Of the **164** adoptees whose biological mothers had Sz, **11 (6.7%)** also received a Sz diagnosis, compared to just **4 (2%)** of the **197** control adoptees. Shows genetic liability to Sz. Eval: -Since these children were adopted at birth, any similarities between the child and their biological mother must be due to genetics rather than the environment. However adopted children are often matched with parents who are similar to their adoptive parents, and so any simmilarty between the child and their biological parents, might be caused by shared enviornmental factors as well as genetics. - Adoptees may be selectively placed. A large adoption study into Sz took place in Oregon (1966), where it was assumed that procreation by any person admitted to a mental hospital would produce offspring with an inherited tendency to 'insanity'. Therefore it is unlikely that the children born to women with Sz would have been placed in the same type of adoptive families as children without such a background. Polygenetic (Ripke 2014): Evidence that Sz is polygenic (a characteristic that is influenced by two or more genes). P: He found the genetic makeup (genomes) of 37,000 patients and 113,000 controls. F: **108** separate genetic variations were associated with increased risk of Sz. Link with genes which associated with number of neurotransmitters including dopamine. THE DOPAMINE HYPOTHESIS: AO1: Claims that an excess of the nuerotransmitter dopamine in certain areas of the brain is associated with the positive symptoms of scizophrenia. Individuals with positive symptoms of Sz are likely to have high levels of dopamine and more dopamine receptors on the post-synaptic cell, increasing dopaminergic activity. The Revised dopamine hypothesis - Davis et al (1991): Excess of dopamine (Hyperdopaminergia) in the mesolimbic pathway = positive symptoms Deficit of dopamine (Hypodopaminergia) in areas of prefrontal cortex (area responsible for thinking, decision making etc) = Negative symptoms AO3: Strengths: - Support from drug studies: Drugs that increase dopamine, like amphetamines cause hallucinations and delusions in healthy people. and drugs that decrease dopamine reduce the likelihood that pateints with schizophrenia will experience hallucinations and delusions. - Practical Applications: Antipsychotic drugs, such as chlorpromazine, which reduce the symptoms of Sz work by inhibiting dopamine transmission. CP: Antipsychotic drugs only reduce all of the symptoms in around **20%** of patients. - Post-mortem (after death) examinations show schizophrenia patients have more dopamine receptors in the left amygdala (**Falkai et al**., 1988) and the caudate nucleus (**Owen** et al., 1978). Weaknesses: - **Noll** found that for **1/3** of pateints with schizophrenia, drugs that decrease the level of dopamine didn't prevent hallucinations and dellusions. This suggests that high levels of dopamine in the mesolimbic system can cause positive symptoms but they aren't the only cause of positive symptoms. - **Moncrieff** conducted a review and claimed that the evidence supporting the dopamine hypothesis is inconclusive for two reasons: first, drugs like amphetamines, which cause positive symptoms, effect other neurotransmitters as well as dopamine - so we cannot be sure that it is the increased dopamine that is causing these symptoms. Second, not all post mortem studies support significant differences in levels of dopamine in schizophrenic patients mesolimbic systems. - There is some evidence to suggest that dopamine is not the only neurotransmitter involved. **Moghaddam & Javitt** found evidence for the role of an NT called glutamate in which it appeared that Sz patients have a deficiency in glutamate function. Supports biological/neural explanation but challenges the simplicity of dopamine hypothesis on its own. - Antipsychotics gradually reduce positive symptoms over several weeks, despite immediately blocking dopamine receptors. Suggests it's not a direct cause and effect and challenges the simplicity of the theory. NEURAL CORRELATES EXPLANATION: AO1: Genes can cause abnormalities in the brain and according to the neural correlates explanantion of schizophrenia, schizophrenia is caused by abnormal brain structure (e.g. larger ventricles and smaller frontal cortex than normal) AO3: - **Torrey** et al: results from an MRI scan found that on average the ventricles patients with schitzophrenia were **15%** larger than the control group. This correlation doesn't necessarily mean causation. The enlarges ventricles might be a side effect of taking medication to treat SZ. - There are individual differences in the brain abnormalities that patients with schizophrenia display and so studies suporting the role of large ventricles, haven't always replicated. - Reduced myelation of white matter pathways in Sz patients, compared to controls (Due et al). Particularly in the neural pathways between the hippocampus & PFC. - Negative symptoms: The **ventral striatum** is involved with reward anticipation. Schizophrenia patients have been found to have less activity in this region- the lower the activity, the more severe the negative symptoms. This could explain avolition (loss of motivation). - Positive symptoms: Allen et al (2007) scanned the brains of patients experiencing hallucinations whilst they completed an auditory processing task. Lower activation levels were found in the **superior temporal gyrus** and **anterior cingulate gyrus**, and they made more errors, compared to a control group. Auditory hallucinations are therefore correlated with reduced activity in these areas. - Neural explanations have been criticised as **reductionist**, explaining schizophrenia at quite a simplistic level of explanation. The role of upbringing, learning and emotions is not considered, weakening this as a full explanation. - A neural correlates explanation of schizophrenia is an example of **biological determinism** as it assumes that specific brain structures and/or dopaminergic activity in the brain play a key role in the onset of schizophrenia DRUG THERAPY AO1: - Drugs used for hyperdopaminergia to reduce positve Sz symptoms. Antipsychotic drugs bind to post synaptic dopamine receptors. This prevents dopamine from binding to receptors, reducing the overactivity of neurones in the mesolimbic system. - Typical (traditional) antipsychotics bind to dopamine receptors for long periods of time and thus have more side effects. - Atypical (newer) antipsychoticcs bind to dopamine receptors for shorter periods of time and sso have less side effects. - Examples: Chlorpromazinwe, clozapine, risperidone AO3: - Typical antispychotics can have extra-pyramidal side effects (involuntary and uncontrollable movements), which can be distressing for patients and may cause them to stop taken the medication. They can also lead to an increased risk of heart problems, obesity and diabetes. However atypical antipsychotics are less likely to produce these extra-pyramidal effects and as a result patients are more likely to continue taking their medication & see a reduction in their symptoms. - Typical antispsychotics don't treat negative symptoms of Sz - **Leucht** (2001) conducted a meta-analysis of 65 studies into the effectiveness of antipsychotic drugs. He found that antispsychotic drugs were more effective at treating Sz than placebo pills, and that patients taking the drugs were less likely to relapse and experience severe postitive symptoms. - **Crossley** (2010): meta-analysis of 15 studies comparing the effectiveness of typical and atypical antipsychotics. He found no difference in their overall effectiveness at preventing symptoms, but atypical antipsychotics had significantly fewer side effects than typical antipsychotics. - Patients are likely to relapse if they stop taking the drugs. - **Schooler et al** (2005) randomly allocated 555 patients in first episode of Sz, to either treatment with haloperidol or risperidone. In both groups **75%** showed a reduction in symptoms. However he found a **55%** relapse rate. Drug therapy is a short-term fix only because it only manages symptoms and doesn't deal with the cause (Schooler's relapse %). However it is possible to be used in combination with another treatment that may be longer term. - Drop out rates are high likely due to side effects like tardive dyskinesia and neuroleptic malignant syndrome, which can be fatal. - Antipsychotics are expensive: Globally, around $14.5bn is estimated to be spent on antipsychotics each year. This can lead to an problem of inequality. While wealthy individuals can afford acces to treatment, less fortunate individuals may be forced to suffer. - They help carers to look after patients with Sz. Mental Health nurses may rely on anti-psychotics to sedate & calm patients so that they are easier to work with. This can raise ethical issues of consent but also who the drugs are for. Are they being used to benefit the patients or the staff? While they can protect and help patients and nurses, it could also be unethical if misused. If given too high dosages too often patients may become zombie-like and withdrawn from reality, which doesn't improve their lives and counteracts the purpose of treatment.