PY4 - Psychology: Controversies, Topics and Applications
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Summary Schizophrenia Method of Modifying: Anti-Psychotics
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PY4 - Psychology: Controversies, Topics and Applications
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WJEC
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The Complete Companions for WJEC and Eduqas Year 2 A Level Psychology Student Book
A detailed description of anti-psychotics as a method of modifying schizophrenia. Includes evaluation points, as well as a straightforward explanation.
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PY4 - Psychology: Controversies, Topics and Applications
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Methods of Modifying Behaviour
Drug Therapy
Conventional Anti-Psychotics
- Anti-psychotics were first developed in the 1950s by Henri Laborit.
- Conventional anti-psychotics, such as chlorpromazine, work by blocking the neurotransmission of
dopamine.
- Chlorpromazine works as an antagonist for dopamine receptors, primarily D2.
- It is thought that schizophrenics produce too much dopamine or have more dopamine receptors
than non-schizophrenics. We cannot decrease the amount of dopamine, so blocking is the next
best thing.
- Conventional anti-psychotics work by blocking receptor sites on the postsynaptic neuron, thus
reducing activity in the post-synaptic neuron.
- Initially, this causes the pre-synaptic neuron increases the amount of dopamine it releases,
however in due course the production of dopamine drops because it is depleted and the amount
of dopamine in the synapse decreases.
- Lower levels of dopamine in the synapse, as well as the blockade provided by the anti-psychotic
leads to a substantial decrease in neural activity.
- Reduction of dopamine activity in the mesolimbic pathway is thought to be responsible for the
decline in positive symptoms.
- Chlorpromazine also affects serotonin receptors 5-HT1 and 5-HT2, but it is mainly a dopamine
antagonist.
Atypical Anti-Psychotics
- Atypical anti-psychotics, such as clozapine were first developed in the 1990’s.
- The mechanism of action of atypical antipsychotics is not yet fully known.
- Some report that atypical antipsychotics because they are received at less D2 receptors and more
D1 and D4 receptor sites.
- Kapur and Remington (2001): Atypical anti-psychotics do not involve serotonin or other
neurotransmitters, but only the dopamine system and the D2 receptors in particular. They
temporarily occupy D2 sites and dissociate quickly.
- Most atypical anti-psychotics also antagonise the serotonin receptor 5-HT2A to the same degree
that they block D2 sites.
- Phillip Seeman (2002): fast-off theory proposes that atypical anti-psychotics bind more loosely to
D2 receptor sites than conventional anti-psychotics.
- This means that the blockade has a therapeutic effect but it does not last for long enough to
produce some of the side effects produced by conventional anti-psychotics.
- The half-life of atypical antipsychotics is thought to be less than that of conventional psychotics.
Dosage
- Chlorpromazine can be prescribed as a tablet, oral solution, intramuscular injection or
suppository.
- The British National Formulary notes 1000mg as being the highest daily dose, but for children the
maximum dose ranges from 40-75mg.
- Clozapine is usually prescribed in tablet form, with a maximum daily dosage of 900mg.
- Patients taking clozapine, as well as the prescribing physicians and dispensing pharmacist must all
be registered with a specialised monitoring service because the drug carries a 3% risk of
agranulocytosis- a life threatening drop in white blood cells.
Evaluation
Effectiveness
Conventional Antipsychotics
- Jonathon Cole et al (1964): findings suggested that psychiatry could treat mental disorder in the
same way that physical disorders are treated.
They found that 75% of those given a conventional antipsychotic were considered ‘much
improved’ compared with only 25% of those given a placebo.
They also noted that none of the patients on antipsychotics got worse, while 48% of those
on the placebo did.
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