SCHIZOPHRENIA ESSAYS
Outline and evaluate biological therapies for schizophrenia
Antipsychotics are a biological way of treating schizophrenia. There are
two types – typical antipsychotics and atypical antipsychotics. Typical
antipsychotics have been around since the 1950s. The most common
typical antipsychotic is chlorpromazine. This works by reducing the action
of dopamine – it blocks the dopamine receptors in the synapses of the
brain, which reduces the action of dopamine. When a patient starts taking
chlorpromazine, the levels of dopamine build up, but after time the
production is reduced. As a result, the neurotransmission in key areas of
the brain is normalised, leading to the reduction of symptoms such as
hallucinations. Chlorpromazine also has a sedation effect as it affects
histamine receptors. Therefore it is also used to calm anxious patients
when they are admitted to hospital. Atypical antipsychotics are newer
drugs which were developed to improve the effectiveness of drugs in
suppressing psychotic symptoms, and to minimise side effects. One
example in clozapine. This binds to dopamine receptors, in the same way
as chlorpromazine, but also acts on serotonin and glutamate receptors.
This drug was more effective than typical antipsychotics by reducing
depression and anxiety, as well as improving cognitive functioning. It also
improves mood which is important as many as 50% of schizophrenics can
attempt suicide. Another drug, risperidone, was developed because
clozapine was involved in the deaths of some people with a blood
condition. Risperidone binds more strongly to dopamine receptors, so is
more effective in smaller doses and has fewer side effects.
One strength of antipsychotics is that there is evidence for their
effectiveness. Thornley et al. reviewed data from 13 trials (1121
participants) and found that chlorpromazine was associated with better
functioning and less severe symptoms than a placebo. There is also
support for the benefits of atypical antipsychotics. Meltzer concluded that
clozapine is more effective than typical antipsychotics and is effective in
30-50% of cases that had resisted treatment. This demonstrates that
antipsychotics work, and adds validity to treating schizophrenia
biologically. However, most of these studies only look at short-term
effects and some of the data has been published many times, which
exaggerates the amount of evidence that exists. Also, some of the
benefits could be due to the calming effects of the drugs rather than
actual; effects on symptoms. This means that evidence for antipsychotic’s
effectiveness may not be as impressive as it looks.
A limitation of antipsychotic drugs is the likelihood of side effects. Typical
antipsychotics are associated with side effects such as weight gain,
dizziness or sleepiness. Long-term use can lead to lip smacking and
grimacing due to dopamine sensitivity, known as tardive dyskinesia. The
most serious side effect is NMS, caused by blocking dopamine in the
hypothalamus, which can be fatal consequently, antipsychotics can do
, harm as well as good, which can lead to sufferers avoiding them which
reduces their effectiveness, as they are not being taken.
Another limitation of antipsychotics is that we don’t know why they work.
The drugs have been developed and used based on the dopamine
hypothesis and the belief that levels of dopamine in the subcortex are too
high. However, there is evidence to suggest that this may be incorrect
and dopamine levels in other prats of the brain are too low, which could
mean that antipsychotics shouldn’t work. Consequently, antipsychotics
may not be the best treatment to use for all patients suffering from
schizophrenia. Also, when they do work, there might be another factor
involved in why they are successful.
It is possible that antipsychotics are used in hospitals to calm
schizophrenic patients down, in order to make it easier for the staff to deal
with them. This questions who really benefits from the treatment.
Nevertheless, calming people down who are experiencing hallucinations
and delusions probably does make them feel better and allows them to
engage with other treatments such as CBT.
Outline and evaluate psychological explanations for schizophrenia
One psychological explanation for schizophrenia is the family dysfunction
explanation. This is divided into three more explanations: The
schizophrenogenic mother suggests that mothers who are cold, rejecting
and controlling create an atmosphere of tension and secrecy in the family.
This leads to feelings of distrust and paranoid delusions, ultimately
leading to schizophrenia. The double-bind theory is based on problems of
communication within the family. Bateson suggested that a child could be
in a situation where they are scared to do the wrong thing but receive
mixed signals about what is right or wrong. When they do get it wrong this
leads to a withdrawal of love and the child learns that the world is
confusing, leading to disorganised thinking and delusions. Expressed
emotion is when family members act negatively – usually verbal criticism,
acting hostile or being overly emotionally involved in the person’s life.
High levels of expressed emotion causes stress, which can trigger the
onset of schizophrenia or a relapse.
Cognitive explanations for schizophrenia involve dysfunctional thought
processing, metarepresentation and central control. Dysfunctional thought
processing is when lower levels of information processing in the brain
suggest that there is a problem with cognition. Metarepresentation is the
cognitive ability to think about your thoughts and behaviour. It is
suggested that having problems with being able to do this explains why
schizophrenics experience hallucinations and delusions. Central control is
the cognitive ability to suppress automatic responses when you are
performing deliberate actions. Frith et al. suggested that schizophrenics
have a problem being able to do this, which explains speech poverty.
Outline and evaluate biological therapies for schizophrenia
Antipsychotics are a biological way of treating schizophrenia. There are
two types – typical antipsychotics and atypical antipsychotics. Typical
antipsychotics have been around since the 1950s. The most common
typical antipsychotic is chlorpromazine. This works by reducing the action
of dopamine – it blocks the dopamine receptors in the synapses of the
brain, which reduces the action of dopamine. When a patient starts taking
chlorpromazine, the levels of dopamine build up, but after time the
production is reduced. As a result, the neurotransmission in key areas of
the brain is normalised, leading to the reduction of symptoms such as
hallucinations. Chlorpromazine also has a sedation effect as it affects
histamine receptors. Therefore it is also used to calm anxious patients
when they are admitted to hospital. Atypical antipsychotics are newer
drugs which were developed to improve the effectiveness of drugs in
suppressing psychotic symptoms, and to minimise side effects. One
example in clozapine. This binds to dopamine receptors, in the same way
as chlorpromazine, but also acts on serotonin and glutamate receptors.
This drug was more effective than typical antipsychotics by reducing
depression and anxiety, as well as improving cognitive functioning. It also
improves mood which is important as many as 50% of schizophrenics can
attempt suicide. Another drug, risperidone, was developed because
clozapine was involved in the deaths of some people with a blood
condition. Risperidone binds more strongly to dopamine receptors, so is
more effective in smaller doses and has fewer side effects.
One strength of antipsychotics is that there is evidence for their
effectiveness. Thornley et al. reviewed data from 13 trials (1121
participants) and found that chlorpromazine was associated with better
functioning and less severe symptoms than a placebo. There is also
support for the benefits of atypical antipsychotics. Meltzer concluded that
clozapine is more effective than typical antipsychotics and is effective in
30-50% of cases that had resisted treatment. This demonstrates that
antipsychotics work, and adds validity to treating schizophrenia
biologically. However, most of these studies only look at short-term
effects and some of the data has been published many times, which
exaggerates the amount of evidence that exists. Also, some of the
benefits could be due to the calming effects of the drugs rather than
actual; effects on symptoms. This means that evidence for antipsychotic’s
effectiveness may not be as impressive as it looks.
A limitation of antipsychotic drugs is the likelihood of side effects. Typical
antipsychotics are associated with side effects such as weight gain,
dizziness or sleepiness. Long-term use can lead to lip smacking and
grimacing due to dopamine sensitivity, known as tardive dyskinesia. The
most serious side effect is NMS, caused by blocking dopamine in the
hypothalamus, which can be fatal consequently, antipsychotics can do
, harm as well as good, which can lead to sufferers avoiding them which
reduces their effectiveness, as they are not being taken.
Another limitation of antipsychotics is that we don’t know why they work.
The drugs have been developed and used based on the dopamine
hypothesis and the belief that levels of dopamine in the subcortex are too
high. However, there is evidence to suggest that this may be incorrect
and dopamine levels in other prats of the brain are too low, which could
mean that antipsychotics shouldn’t work. Consequently, antipsychotics
may not be the best treatment to use for all patients suffering from
schizophrenia. Also, when they do work, there might be another factor
involved in why they are successful.
It is possible that antipsychotics are used in hospitals to calm
schizophrenic patients down, in order to make it easier for the staff to deal
with them. This questions who really benefits from the treatment.
Nevertheless, calming people down who are experiencing hallucinations
and delusions probably does make them feel better and allows them to
engage with other treatments such as CBT.
Outline and evaluate psychological explanations for schizophrenia
One psychological explanation for schizophrenia is the family dysfunction
explanation. This is divided into three more explanations: The
schizophrenogenic mother suggests that mothers who are cold, rejecting
and controlling create an atmosphere of tension and secrecy in the family.
This leads to feelings of distrust and paranoid delusions, ultimately
leading to schizophrenia. The double-bind theory is based on problems of
communication within the family. Bateson suggested that a child could be
in a situation where they are scared to do the wrong thing but receive
mixed signals about what is right or wrong. When they do get it wrong this
leads to a withdrawal of love and the child learns that the world is
confusing, leading to disorganised thinking and delusions. Expressed
emotion is when family members act negatively – usually verbal criticism,
acting hostile or being overly emotionally involved in the person’s life.
High levels of expressed emotion causes stress, which can trigger the
onset of schizophrenia or a relapse.
Cognitive explanations for schizophrenia involve dysfunctional thought
processing, metarepresentation and central control. Dysfunctional thought
processing is when lower levels of information processing in the brain
suggest that there is a problem with cognition. Metarepresentation is the
cognitive ability to think about your thoughts and behaviour. It is
suggested that having problems with being able to do this explains why
schizophrenics experience hallucinations and delusions. Central control is
the cognitive ability to suppress automatic responses when you are
performing deliberate actions. Frith et al. suggested that schizophrenics
have a problem being able to do this, which explains speech poverty.
