Download y-dopamine-hypothesis

Starter:
Rosenhan questions
1. Who were Rosenhan’s participants for his
study?
2. How many hospitals did they visit?
3. What did these pseudopatients have to do?
4. What did they do once they gained admission?
5. What were the two aims of the study?
6. What were the main findings?
Follow-up questions
(a) In his original study, all but one of the patients were given
the label of paranoid schizophrenia with the other patient
being labelled as bipolar. How does this show that there are
issues with the reliability of diagnosis?
(b) Rosenhan did a follow-up study where he told the psychiatric
institutions that he would send them more pseudopatients
(fake patients) over the next three months and they had to
detect them. After three months they were confident that
approximately a third of the new patients they were sent
were pseudopatients and were shocked when they found
out that Rosenhan had not actually sent any! Explain how
this further highlights the poor validity
(c) What were the implications of this study for the psychiatric
profession?
1.
2.
3.
4.
5.
7 students – 4 male, 3 female
12 in 5 different states
State hearing same sex “empty hollow thud” voice
Acted normal and said symptoms have gone
Aim 1: investigate whether psychiatric labels would
be used in situations where they weren’t
appropriate
Aim 2: investigate whether the experience of
being hospitalised in a psychiatric ward
6. None were ever detected as being pseudo- patients
and the longest stay was 2 months
Additional questions
• The diagnosis of the different psychiatrists were
inconsistent when they were presented with the
same symptoms of Sz
• Shows psychiatrists were unsure what Sz actually
was as they were labelling someone with the
disorder (insane) when they were actually sane
• It brought widespread distrust in the ability of
psychiatrists to accurately diagnoses mental
illnesses
– it also brought about a revision of the classification
systems to incorporate a more in depth overview of
mental illness
1. Negative symptoms of
schizophrenia represent the
loss of a usual experience
T/F
2. Match the term to the definition
A: A loss of motivation and
lowered activity levels
1. Hallucinations
2. Delusions
3. Avolition
4. Poverty of speech
B: Reduced frequency and quality
of speech
C: Sensory experiences that have
no basis in reality, e.g. hearing
voices
D: Beliefs that have no basis in
reality, for example thinking they
are someone else or that they are
the victim of a conspiracy
3. Co-morbidity is how
commonly two or more
conditions occur on their own
T/F
4. Which of the following is an example of
delusions?
1. Hearing voices.
2. Thinking that the neighbours are
plotting to kill you
3. Lacking a desire to wash and go to work
4. Reduced frequency of speech.
5. White psychiatrists may tend
to over-interpret symptoms of
schizophrenia in black patients
T/F
Answers
1. True
2. 1 C
2D
3A
4B
3. False
4. 2
5. True
Explanations of
Schizophrenia
Specification details:
Biological explanations for
schizophrenia:
1. the dopamine hypothesis
2. genetics,
3. neural correlates.
Biological approach offers useful
suggestions as to how it is caused.
LEARNING OBJECTIVES
• Describe / Draw the role of Dopamine (DA)
in Sz
• Outline / articulate evidence to support this
hypothesis
• Evaluate, using CASTLES the Dopamine
Hypothesis
• Outline the role of genes in Sz
• Evaluate the role of genes using research
evidence
DOPAMINE
HYPOTHESIS
Draw the following:
- Endocrine system
- Nervous system
- Neuron
Human nervous
system
Peripheral
nervous system
(PNS)
Autonomic nervous
system
Somatic nervous
system
Sympathetic
nervous system
Parasympathetic
nervous system
Central nervous
system (CNS)
Brain
Spinal cord
Lets remind ourselves how
neurotransmitters work
1
5
2
4
3
Lets remind ourselves how
neurotransmitters work
What is dopamine?
• known to be active in
the limbic system - an
area of the brain
governing emotion
• Regulates attention if this process is
disturbed may lead to
problems with
attention, perception
and thought
DOPAMINE HYPOTHESIS
The Dopamine hypothesis states that the
brain of schizophrenic patients produces
more dopamine than normal brains.
Evidence for this comes from
studies with drugs
post mortems
pet scans
Dopamine Hypothesis
Although the original
Dopamine Hypothesis
states that the brain of
schizophrenic patients
produces more dopamine
than the brain of a
“normal” person.
It is now thought that
schizophrenics have an
abnormally high number of
D2 receptors.
Normal Level of
Dopamine In The
Human Brain
Elevated Level of Dopamine
In The Brain of a
Schizophrenic Patient
(specifically the D2 receptor)
 Neurons that use the transmitter ‘dopamine’ fire too often and
transmit too many messages.
 There may be an excess of DA receptors at the synapse in
schizophrenics
 Lowering DA activity helps remove the symptoms of schizophrenia
ROLE OF DRUGS
Amphetamines (agonists – prevent the
breakdown of dopamine) lead to increase in DA levels
Large quantities lead to delusions and hallucinations
If these drugs are given to schizophrenic patients
their symptoms get worse
Randrup et al
Rats given
amphetamines
developed
schizophrenia
type symptoms
Parkinson’s disease
• Parkinson’s sufferers have
low levels of dopamine
• L-dopa raises DA activity
• People with Parkinson's
develop schizophrenic
symptoms if they take too
much L-dopa
Chlorphromazine (given to schizophrenics) reduces the
symptoms by blocking D2 receptors
Post-mortems
Iversen (1979) and Seidman (1990)
Post-mortem (after death) examinations have found
that people with schizophrenia have a larger than
usual number of dopamine receptors.
Increase of DA in brain structures and receptor
density (left amygdala and caudate nucleus
putamen)
Concluded that DA production is abnormal for
schizophrenia
What is a strength and weakness of a postmortem study?
PET SCANS
Lindstroem et al (1999)
• Radioactively labelled a chemical L-Dopa
• administered to 10 patients with
schizophrenia and 10 with no diagnosis
• L-Dopa taken up quicker with
schizophrenic patients
• Suggests they were producing more DA
than the control group
PET Scans
Gjedde and Wong (1987)
There are more than twice as many dopamine
receptors in schizophrenics compared to controls.
Farde et al. (1990)
There is no difference in the number of dopamine
receptors between schizophrenics and controls.
What is the main strength of a PET scan?
What conclusions can be drawn from the research
findings?
Chickens
hatch from
eggs, but a
mother
chicken must
keep an egg
warm in order
for it to hatch
Which Came First?
The Chicken or the Egg?
Schizophrenia or Faulty
Chemicals?
Faulty chemicals cause
schizophrenia but schizophrenia
may cause faulty chemicals
Drugs may influence other systems that impact on
schizophrenia so we cannot be 100% sure about their
effects
There are lots of problems with
the dopamine hypothesis!
• The research is inconclusive… ensure you have
both sides in your notes
• There is a lack of correspondence between taking
phenothiazines and signs of clinical effectiveness. It
takes 4 weeks to see any sign that the drugs are
working when they begin to block dopamine
immediately. We cannot seem to explain this time
difference.
• It could be that the development of receptors in
one part of the brain may inhibit their development
in another
Other EVALUATION POINTS
• Type 1 cases respond well to conventional anti-psychotic drugs.
Drugs such as CHLOPROMAZINE: Only effective at relieving the
Positive Symptoms of the Illness.
• Not good at explaining negative symptoms. Therefore suggested that
Type 2 is related to a different kind of abnormality such as brain
structure.
• PET scans have suggested that drugs did not reduce symptoms of
patients diagnosed with disorder for 10 yrs or more
• There may be other neurotransmitters involved.
• Possible that social and environmental factors trigger the condition.
TASK: read, absorb and understand some of the evaluation points using your text books.
Make notes and ensure you can describe and evaluate the explanation: complete pgs in
your packs
GENETIC EXPLANTION
• What is the logic behind conducting twin
studies when investigating schizophrenia?
• What is the logic behind conducting
adoption studies when investigating
schizophrenia?
• What do we mean by concordance rate?
Do you remember what
concordance rate means?
The probability of one twin having the disorder
if the other already has it - expressed as a
percentage
MZ and DZ twins
MZ = Monozygotic
• Come from one egg
• Identical twins – share 100% of their
genes
DZ = Dizygotic
• Come from two eggs
• Non-identical twins – share 50% of their
genes
Genetic vulnerability
• Genetic explanation suggest that component to
schizophrenia which predisposes some individuals to
the illness
• whether a person develops schizophrenia is at least
partly due to their genes
– may explain why patients often have other family members
with schizophrenia
• Look at:
– Family studies
– Twin studies
– Adoption studies
1. Family Studies
A01
• find individuals who have schizophrenia and
determine whether their biological relatives are
similarly affected more often than non-biological
relatives
Large-scale family study - Gottesman (1991) –
additional material on the Blog
• concluded if both parents suffer from schizophrenia, 46%
chance of also developing the disorder (compared to a
1% chance for the general population)
• Findings have shown greater degree of genetic
relatedness, greater risk of developing schizophrenia
1. Family studies
A03
• genes do play an important factor - however if
genes were the only cause of schizophrenia then
the percentages should be 100%
Deterministic; just because we are ‘predisposed’
by our genes cannot mean we necessarily get the
disorder schizophrenia
• researchers accept that schizophrenia concordance
rates in families to do with common rearing patterns or
other environmental factors that have nothing to do
with heredity
2. Twin Studies
A01
• Twin studies help researchers work out whether
nature or nurture has the greatest influence
• Gottesman and Shields (1972) found that the
concordance rate for schizophrenia in MZ twins
was 48% compared to 17% for DZ twins.
• He therefore suggests that schizophrenia is
inherited through genes.
• Also Joseph (2004) – showed concordance rate
of 40.4% MZ and 7.4% for DZ.
2. Twin Studies
A03
• Twin studies seem to indicate that there is a strong
genetic component to the disorder
• Twin studies demonstrate may be a predisposition to
develop schizophrenia, however, both twins do not
always develop schizophrenia suggesting
environmental factors
• Concordance rate for twins are not 100% therefore
schizophrenia cannot be accounted for by genetics
alone
• Sample sizes of such twin studies always going to be very
small…. difficult to generalise to the general population
2. Twin studies
A03
L - higher concordance between MZ twins could be explained by
greater environmental similarity rather than genetic similarity – MZ
twins elicit more similar treatment than DZ twins (so can be
explained by other theories)
E - No single gene has been identified for schizophrenia,
questioning genetics as a valid explanation for schizophrenia.
S - Evidence for concordance rates for schizophrenia are based on
older twin studies which are less reliable due to changes in the
diagnostic criteria
diagnosis is much rigorous than it was 40 years ago so some of those
diagnosed as schizophrenic 40 years ago might not meet the criteria now
3. Adoption Studies
A01
• genetically related individuals who have been reared
apart due to being adopted
• allow researchers to overcome the problem of
disentangling genetic and environmental influences
– Heston (1966) compared 47 adopted children whose
biological mother had schizophrenia with a control group of
adopted children with no history of schizophrenia in their
biological family.
– None of the control group was diagnosed with the illness;
16% of the offspring of schizophrenic mothers were
diagnosed
3. Adoption studies
A03
• results of adoption studies only reveal small
percentages
– still support the idea that genes must play a role within
schizophrenia.
• Tienara (1991)
– 155 adoptees whose biological mothers had been
diagnosed with schizophrenia , 10% also received a
diagnosis of schizophrenia,
– compared to just 1% of the 185 control adoptees (page
213) – this provides supporting evidence also
• However, Tienara conducted his study within
Finland, therefore we are not able to generalise this
study to the rest of the world
Genetic explanation
overview
Through research, Candidate genes have been implicated in the
development of schizophrenia.
Schizophrenia is thought to be polygenic – this means that its
development is not determined by a single gene but a few (maybe as
many as 108 genes) – this means that there is little predictive power
from this explanation.
Genes associated with the increased risk included those coding for
the functioning of a number of neurotransmitters including dopamine
Link to previous theory …
Additional material to help you form
an argument for or against the
biological explanation of Sz
Schizophrenia: stolen minds stolen lives:
https://www.youtube.com/watch?v=Rv0b1unxUp
M
A specific gene that increases the risk of Sz >>>
https://www.youtube.com/watch?v=fME16W4kc_
Q
Neural Correlates: Brain dysfunction
• Brain scanning techniques have made it possible to investigate
living Sz brains
• Both positive and negative symptoms have correlates
Neural correlates of negative
Neural correlates of positive
•Activity in the ventral striatum •Reduced activity in the superior
linked to the development of
temporal gyrus and anterior
avolition (loss of motivation)
cingulate gyrus linked to the
•ventral striatum believed to be development of auditory
hallucinations
involved in anticipation of a
•Patients with auditory hallucinations
reward
– if there is abnormality in areas
such as the ventral striatum,
then this would result in a lack
of motivation (avolition)
showed lower activation levels in these
areas than controls
– reduced activity in these areas of
the brain is a neural correlate of
auditory hallucinations
Suggested that the ventricles
are 15% larger in Sz
Ventricles:
cavities that
supply
nutrients and
remove waste
Enlarged ventricles
associated with
negative rather than
positive symptoms:
Activity - Put the key phrases below
in the appropriate part of the table:
• Located deep inside the brain and affects movement and thinking skills.
• Process information received from the eyes and the ears.
• Schizophrenics have the same activity in these areas when they hallucinate
as sane people do when they have genuine visual and auditory experiences.
• Many schizophrenics have lower activity in this area, which could be linked to
delusions and disorganised thoughts.
• High levels in brain areas are linked to positive symptoms.
• Smaller in schizophrenics so can link to loss of emotion (affective flattening).
• Research has shown that this structure is larger in schizophrenics, which
could cause motor dysfunction.
• Responsible for basic feelings such as fear, lust and hunger.
• Helps people think logically and organise their thoughts.
• Low levels in certain brain areas are linked to negative symptoms as these
are linked to a loss of pleasure.
• Responsible for feelings of pleasure and also affects thinking and
movement.
Using your picture in the pack
Match the text in the table to the areas of the brain.
A
Low levels of dopamine (hypodopaminergia) in the prefrontal
cortex (responsible for thinking and decision making) in the
negative symptoms of schizophrenia.
B
An excess of dopamine receptors in Broca’s area (which is
responsible for speech production) may be associated with
poverty of speech and/or the experience of auditory
hallucinations.
C
Lower activation levels in the superior temporal gyrus and
anterior cingulate gyrus are correlated with hallucinations.
D
Abnormality of areas like the ventral striatum may be involved
in the development of avolition.
Neural correlates of
schizophrenia - evaluation
A03
• Findings are inconsistent and therefore inconclusive
• MRIs have made it possible to investigate living brain
images which is an advance on merely having to rely
on post mortems
• However issues of causality.
– Cause and effect can not be established with brain
abnormalities - it is still uncertain whether structural
abnormalities/reduced functioning predispose to
schizophrenia, or whether the onset of the clinical
symptoms causes these changes.
Evaluation Summary
• Biological explanations do account for schizophrenia,
however the fact that there is no conclusive explanation
that accounts for all schizophrenics - research is difficult
to interpret and there have been contradictory findings.
• It is difficult to establish cause and effect – as many
participants have suffered from schizophrenia for a
while and have been undergoing treatment.
• Enlarged ventricles may be the result of taking antipsychotic medication for example
• Biological explanations are reductionist in attempting to
explain a complex multi- faceted disorder at the level of
cells, genes and chemicals
Evaluation Summary
• Biological explanations are deterministic in the
assumption that the disorder can be inherited and
unavoidable
• Biological explanations do account for schizophrenia,
however the fact that there is no conclusive explanation
that accounts for all schizophrenics means that
psychological explanations need to be considered.
• A ‘diathesis-stress’ relationship may be at work – an
individual may have a genetic predisposition for
schizophrenia but it may be due to environmental factors
that lead to the onset of the condition
What have I learnt?
On a post it note:
5 key words each
• What is the genetic explanation?
• What is the dopamine H1 explanation?
• What is the neural correlates explanation?
to leave
ACTIVITY
• Describe and evaluate the biological
explanation of schizophrenia
• You must comment on how the evidence you use supports or
challenges the explanation
• You should comment on evidence both for and against the
explanation
• You could use your own skills and knowledge to make
additional critical and evaluative points.