The document discusses several biological explanations for schizophrenia, including genetics, biochemistry, and neuroanatomy. It summarizes evidence from twin and adoption studies that support a genetic influence but also the role of environmental factors. The document then focuses on the dopamine hypothesis, explaining that schizophrenia may involve excessive dopamine activity in the brain. Evidence from drugs, post-mortem studies, and PET scans is presented to support this hypothesis, though it is noted that other neurotransmitters may also be involved. Alternative biological explanations discussed include brain structure abnormalities, brain damage, viral infections, and birth complications.

1. Biological explanations
of Schizophrenia

2. Assumptions of biological
explanations
 All mental disorders have a physical
cause. (micro-organisms, genetics,
biochemistry or neuroanatomy)
 Mental illnesses can be described in
terms of clusters of symptoms.
 Symptoms can be identified, leading to
the diagnosis of an illness.
 Diagnosis leads to appropriate physical
treatments.

3. Schizophrenia: genetics
factors
Prevalence of schizophrenia is the same all over
the world (about 1%)
Supports a biological view as prevalence
does not vary with environment
However, there are variations within broad
geographical areas (e.g. Torrey 2002 –
found high rates of Sz in Ireland, 4% of the
population, the incidence is also high in
Croatia and Scandinavian countries but low
in Spain and Italy and very low in some
parts of Africa)

4. How do we study the influence
Concordance rate:
of genetic factors? the proportion of
pairs where both
If the concordance rate is individuals share a
100% in MZ twins it means certain characteristic.
that the characteristic is
genetically determined.
If it less than the 100% but
higher that DZ twins What
does it mean? Twin However they
However one studies might be
is usually treated
born bigger Dizygotic differently
Monozygotic
than the other twins
twins
Share as
Share the same many genes
genes and the as siblings
same but share
environment the same
environment

5. Family Adoption
studies studies
Children share 50% If the adopted children
of their genes with have a higher
each of their concordance rate for
parents. If one of Sz with their biological
their parent is parents than with their
schizophrenic has adoptive parents, does
the child more it support the
chance to be influence of genetic
schizophrenic? If factors?
he/she is Sz, are
only genetic factors
responsible?

6. Twin studies
 Gottesman and Shields ( reviewed the
results of 5 twin studies looking for
concordance rates for schizophrenia.
These studies looked at 210 MZ twins and
319 DZ twins
 It was found that in MZ twins there was a
concordance rate of 35-58% compared
with dizygotic (DZ) twin rates that ranged
from 9-26%. They also found a
concordance rate in MZ twins of 75-91%
when the sample was restricted to the
most severe form of schizophrenia.

7.  The milder forms of schizophrenia had
concordance rates of 17-33% suggesting
that there may be greater genetic loading
with severe forms of schizophrenia. The
twin studies have all assumed that the
shared environmental effects for MZ and
DZ twins are equal which may be incorrect
Twins are not representative of the wider
population. (gestational environment)
It is a very small sample. There are very few MZ
twins in the population and only 1% are Sz.
Are these diagnosis made using the same
criteria?

8. Adoption studies
Prevalence Prevalence
amongst among
biological adoptive
relatives relatives
Kety et al 13% 2%
(1968)
schizophrenia
only
Tienari et al 30% 15%
(1994) all
‘severe’ psych.
diagnoses
Could the psychiatrist making the diagnosis in the
WereHowtheyweretheir biological theythatregularly?
child Did influenced children when parents one offamily?
Weretheyolddiagnosishe/she using the same adopted?
be adopted by members of the were criteria?
these see if made is aware extended both
of the parents are Sz??

9. The overall picture
This seems to indicate an
influence of genetic factors
but also the importance of
environmental/ social
factors

10. So have we found a gene
responsible for Sz?
In 2006, an Edinburgh University team
found people carrying a variant of a gene
called neuregulin had a higher chance of
developing psychotic symptoms. However
since then research has shown that Sz
involves a huge number of genes with
each of them making only a small
contribution to the development of the
disorder according to Robin Murray a
leading schizophrenia researcher.

11. Risk rises with degree of genetic
relatedness
Spouse – 1% (same as general
population)
Child – 13%
DZ twin – 17%
MZ twin – 48%
Effect of shared environment?

12.  Substantial evidence for a genetic contribution
 Some evidence disputed:
Shared environment issues
Diagnostic criteria in adoption studies
All the evidence also suggests
environmental triggers: Epigenetics could
explain that the concordance rate is less
than 100% in MZ twinsHeritability is
similar with other major disorders
such as breast cancer, hypertension,
etc
 How is schizophrenia inherited and what
exactly is inherited?

13. DOPAMINE
HYPOTHESIS

14. Schizophrenia: Biochemical
 The dysfunction of several
neurotransmitter systems
 Dopamine,
 5-hydroxytryptamine (5-HT; Serotonin)
 Glutamate
 are thought to play a part in
schizophrenia.
 We will concentrate on the Dopamine
Hypothesis

15. Schizophrenia & dopamine
 The dopamine hypothesis:
Schizophrenia is caused by
excessive DA activity.
This causes abnormal functioning
of DA-dependent brain systems,
resulting in schizophrenic
symptoms
DA can increase or decrease brain
activity depending on the system
you’re looking at

16. Lets remind ourselves how
neurotransmitters work

17. DOPAMINE
HYPOTHESIS
The Dopamine hypothesis states that the
brain of schizophrenic patients produces
more dopamine than normal brains.
–Evidence comes from
–studies with drugs
–post mortems
–pet scans

18. Elevated Level of
Normal Level of
Dopamine In The Brain of a
Dopamine In The
Schizophrenic Patient
Human Brain
(specifically the D2 receptor)
 Neurons that use the transmitter ‘dopamine’ fire too often and
transmit too many messages or too often.
 Certain D2 receptors are known to play a key role in guiding
attention.
 Lowering DA activity helps remove the symptoms of
schizophrenia

19. 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

20. ROLE OF DRUGS
–Amphetamines (agonists) lead to increase
in DA levels
–Large quantities lead to delusions and
hallucinations
–If drugs are given to schizophrenic patients
their symptoms get worse

21. POST MORTEM
Falkai et al 1988
 Autopsies 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

22. 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

23. 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 cant be 100% sure about their
effects

24. EVALUATION
 There is a lack of correspondence between taking the drugs 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 the development in another.
 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 effective for 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.

25. Other possible causes
Brain structure
Brain damage
Viral infection
Birth complications

27. Brain structure
Swayze (1990) reviewed 50
studies of schizophrenics and
found that many had abnormally
large amounts of liquid in the
cavities of the brain. Suddath,
who supports this found the same
enlarged cavities when using MRI
scans on schizophrenic twins.

28. Structural abnormalities
 Unusually large corpus callosum
 High density of white matter in the right
frontal and parietal lobe
 Small amount of grey matter in the temporal
lobes
 A change in blood flow in the cerebral
hemisphere
 MRI scan show unusually large ventricular
enlargement but this is also seen in non-
schizophrenics
 Hippocampus and the thalamus are all
affected in the brains of schizophrenics

29. Brain Structure Evidence
Andreasen et 1990 –
conducted a very well
controlled CAT scan
study and found
significant enlargement
of the ventricles in
schizophrenics
compared to controls.
However this was only
the case for men and
not for women.
Therefore can’t
generalise the findings
to women.

30. Brain Structure
People with
schizophrenia have
abnormally large
ventricles in the
brain. Ventricles are
fluid filled cavities.
This means that the
brains of
schizophrenics are
lighter than normal.

32. Enlarged ventricles due to
medications?
Beng-Choon Ho (2010) However this was a
in a longitudinal correlational study so it
correlational study of does not show cause and
211 schizophrenics found effect. Lewis’s study was
that antipsychotic drugs carried out on animals so
have measurable we cannot extrapolate to
influence on brain tissue humans without caution.
loss over time. This was
supported by Lewis
(2009) who
administered
antipsychotic drugs to
primates and found a
brain volume loss of
10% .

33. Furthermore
If the reduction in
brain volume is the
cause of the
schizophrenic
symptoms then it
cannot explain why
after 30 years of the
initial onset, 35% of
the schizophrenics are
classified as "much
improved“ because
the cortex does not
grow back, if the
structural differences
were the cause then
no improvement
would be possible.

34. Brain plasticity
The brain is a
plastic organ
which changes
with the way we
use it so are the
differences in
structure the
cause or the result
of schizophrenia?

35. Brain Damage
Decreased rate of blinking
Staring
Lack of the blink reflex in
response to a tap on the
forehead
Poor visual pursuit movements
Poor pupil reactions to light

36. Viral Infection
In recent years, there has
been a build up of evidence
supporting the role of viral
infections in the development
of schizophrenia, including the
poliovirus, the flu virus and a
virus called encephalitis
lethargica ('inflammation of
the brain that makes you
tired‘).

37. Birth Complications
Complications during pregnancy,
abnormal foetal growth and
complications during delivery are
significant risk factors in the
development of schizophrenia.
Those that play a significant role in the
development of schizophrenia include:
bleeding, diabetes and pre-eclampsia
pregnancy complications

38. Birth Complications
abnormal foetal growth and
development problems including
conditions such as low birth weight
and reduced head circumference
complications of delivery including
asphyxia (lack of oxygen) and
emergency Caesarean section
However, the effect of such
complications is small in
comparison with factors such as
genetic pre-disposition to
schizophrenia.