Biological Therapies for Schizophrenia Flashcards
(18 cards)
AO3 (1) biological therapies for schizophrenia
— The development of antipsychotics was mainly based upon the dopamine hypothesis, and so their
use depends on this theory too. For example, if antipsychotics appear to alleviate symptoms by
reducing the action of dopamine, this makes sense considering the original dopamine hypothesis i.e.
hyperdopaminergia in the subcortex. However, this action is not in line with the revised version of the
dopamine hypothesis, which suggests that abnormally low levels of dopamine in the cortex are
responsible for symptoms. Therefore, a further reduction in dopamine levels should make symptoms
worse, and not better. This paradox has caused some to question the validity of the use of
antipsychotics, as well as the accuracy of the dopamine hypothesis as an explanation for
schizophrenia.
AO3 (2) biological therapies for schizophrenia
— A serious consideration which must be made when using antipsychotics is thinking about the side
effects. The short-term side effects of typical antipsychotics are relatively mild (e.g. agitation and
weight gain), whilst the long-term risk include tardive dyskinesia (characterised by involuntary
contraction and relaxation of the facial muscles) and neuroleptic malignant syndrome (NMS). NMS is
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characterised by fever, altered mental states, muscle rigidity and autonomic dysfunction and is
thought to be caused by dopamine receptor blockage or central nervous system infections. These
side effects are not offset by atypical antipsychotics, where agranulocyotis remains a serious concern
for those taking Clozapine, whose state must be continually monitored using blood tests. Therefore, a
cost-benefit analysis should be carried out to consider whether the benefit of symptom reduction
outweighs the cost of side effects for each specific patient.
AO3 (3) biological therapies for schizophrenia
Despite there being a range of evidence supporting the use of typical (Thornley et al, 2003) and
atypical antipsychotics (Meltzer, 2012), these studies still suffer from problems of validity, as suggested
by Healy (2012). For example, since Chlorpromazine has particularly powerful sedative effects, then
this suggests that studies reviewing the effectiveness of antipsychotics in terms of symptom reduction
may actually be measuring how calm and functional the patient appears to be - simply suppressing
the symptoms is not a way of controlling them, and so such studies may lack validity due to not
accurately assessing the actual effectiveness of antipsychotics in treating the proximal cause of SZ.
Secondly, drug companies are selective about what type of information they publish: many focus on
the short-term benefits as opposed to the long-term risks, and use inappropriate control groups, such
as patients suffering from withdrawal symptoms as they have stopped taking their medication. This
distorted focus brings into question, yet again, the validity of research into the effectiveness of
antipsychotics.
Q: What are the two types of antipsychotic drugs used to treat schizophrenia?
A: Typical (first generation) and Atypical (second generation) antipsychotics.
How do antipsychotics work?
They are dopamine antagonists that bind to dopamine receptors on postsynaptic membranes, preventing dopamine from binding and reducing action potential
What is the result of antipsychotic drugs blocking dopamine receptors?
Neurotransmission returns to normal levels, especially in the prefrontal cortex and subcortices.
What are typical antipsychotics also known as?
First generation antipsychotics.
What is the main example of a typical antipsychotic?
Chlorpromazine
What are the effects of Chlorpromazine?
It has calming and sedative effects by acting on dopamine and histamine receptors.
Why is Chlorpromazine commonly used in institutions?
Because of its tranquilising effect, which helps manage agitation and aggression.
What are atypical antipsychotics also known as?
Second generation antipsychotics.
How do atypical antipsychotics differ from typical ones?
They also act on other neurotransmitter receptors such as serotonin and glutamate, not just dopamine.
What receptors does Clozapine act on?
Dopamine, serotonin, and glutamate receptors.
What are the key benefits of Clozapine?
Improves cognitive functioning and mood, useful for patients with schizophrenia and depression.
What is a serious risk of taking Clozapine?
Agranulocytosis – a life-threatening drop in white blood cells (leukopenia).
What receptors does Risperidone act on?
Dopamine and serotonin receptors.
What is the advantage of Risperidone over Clozapine?
Requires smaller doses because it acts more strongly on dopamine receptors.
Who is Risperidone best suited for?
Patients without depression but with a history of blood-related illnesses.
