Biological explanations and treatments for SZ

Question 1

What are the three studies that research schizophrenia and genetics?

Answer 1

Twin studies – where you investigate identical and non-identical twins one of whom has schizophrenia.

Family studies – family history is investigated where a relative has schizophrenia, the rate at which other relatives develop the same disorder is then calculated.

Adoption studies – adopted children of schizophrenic parents are investigated.

Question 2

What did Gottesman (1991) do and find?

Answer 2

Many years believed that SZ runs in families.

Gottesman (1991) has researched genetic similarity and the likelihood of both
developing SZ.

Strong relationship between degree of genetic similarity and shared risk of SZ. I.e. as genetic similarity increases, so does the probability of sharing SZ.

Question 3

What did Ketty et al (1988) do and find?

Answer 3

Adoption study - research on a schizophrenic patient (adopted)

14% of biological relatives were classified as schizophrenic

2.7% of their adopted relatives were classified as schizophrenic

Question 4

How do candidate genes link to schizophrenia?

Answer 4

Individual genes are believed to be associated with risk of inheritance.

It appears that SZ is polygenic because there are a number of genes which each
cause a small increased risk.

Polygenic- requires a number of factors to work in combination.

It is also aetiologically heterogeneous (different combination of factors can lead to the condition).

Question 5

What did Ripke et al (2014) do and find when researching candidate genes on schizophrenia?

Answer 5

Ripke et al, 2014 looked at previous data from studies that looked at whole human genome rather than particular genes of SZ.

Compared genetic makeup of 113,000 controls to 37,000 SZ patients.

108 separate genetic variations were associated with increased risk of SZ.

Question 6

What’s the dopamine hypothesis?

Answer 6

Dopamine (DA) widely thought to be involved.

DA is important in the functioning of several brain systems that may be implicated in the symptoms of SZ.

Hyperdopaminergic
Hypodopaminergia

Question 7

What’s hyperdopaminergic?

Answer 7

Too much dopamine

Links to hallucinations and speech poverty

Possible role of high levels / activity of dopamine in the sub -cortex (central areas
of the brain)

E.g. excessive dopamine in Broca’s area (responsible for speech production) may be associated with speech poverty and / or auditory hallucinations.

Question 8

What’s hypodopaminergia?

Answer 8

Not enough dopamine

Linked to delusions – links to decision making

Question 9

What did Goldman-Rakic et al (2014) do?

Answer 9

identified a role for low levels of DA in the prefrontal cortex (responsible for thinking and decision making) in the negative symps of SZ.

Question 10

What was the conclusion made over hyperdopaminergic and hypodopaminergia?

Answer 10

Both hyper and hypo are correct explanations – both high and low levels of DA are involved in SZ.

Question 11

What are neural correlates?

Answer 11

Measurements of the structure/function of the brain that correlate with an experience (ie SZ).

Both positive and negative symps of SZ have neural correlates.

Question 12

What are negative symptoms?

Answer 12

Motivation involves anticipation of a reward which is related to certain regions of the brain e.g. ventral striatum.

Question 13

What did Juckel et al (2006) find?

Answer 13

lower levels of activity in the ventral striatum of SZ sufferers than controls.

Negative correlation between ventral striatum activity levels and the overall severity of negative symptoms.

Question 14

What did Allen et al (2007) do, find and conclude?

Answer 14

Scanned patients experiencing auditory hallucinations and compared them to controls whilst they had to identify pre-recorded speech as theirs or others.

Found lower activation levels in the superior temporal gyrus and anterior cingulate gyrus of SZ patients than controls. They also made more errors.

Reduced activity in these two areas are a neural correlate of auditory hallucinations.

Question 15

What are the strengths of the biological explanations to SZ?

Answer 15

There are multiple sources of evidence for the genetic susceptibility of SZ:
Gottesman (2001) shows how genetic similarity and shared risk of SZ are closely
related.
Tienari et al, (2004), an adoption study showed that children of SZ sufferers are still at a heightened risk of SZ if adopted into a family with no history of SZ. Ketty concluded similar.

Biological explanation of schizophrenia is scientific.

Useful - treatments of SZ

L-Dopa – a drug for Parkinson’s disease actually increases dopamine – this in turn can produce symptoms of SZ.

Question 16

What are the limitations of the biological explanations to SZ?

Answer 16

Biologically reductionist. However this doesn’t consider how SZ can be explained in terms of the environment; such as stressful life events and parenting and family functioning in childhood. All of which are attributed as psychological / social causes. The probability of developing SZ even if your identical twin has it is less than 50%, suggesting there are other causes/ contributing factors. Can arise in the absence of a family history of the disorder.
We not get a clear picture of the cause and can therefore lead to ineffective treatments.

Causation problems - Anti Psychotic medication works as a treatment for schizophrenia this would suggest that there is a biological cause. However whether they treat the cause of schizophrenia or the symptoms of schizophrenia is a debatable concept.

Determinist.

There is no conclusive explanation that accounts for all experience of SZ. Therefore psychology explanations of SZ must be considered. This lends weight to the diathesis-stress model.

Question 17

What are the biological treatments of SZ?

Answer 17

Drug therapy: typical and atypical antipsychotics.

Question 18

What’s drug therapy?

Answer 18

Drugs are used to reduce the intensity of SZ symptoms particularly the positive symptoms.

Typical Antipsychotics: first generation of antipsychotic drugs, have been used since the 1950s.
They work as dopamine antagonists.
Main example: chlorpromazine

Atypical antipsychotics: developed after typical.
Typically target a range of neurotransmitters such as dopamine and serotonin.
Clozapine and Risperidone

Question 19

How do typical antipsychotics work?

Answer 19

Act as antagonists (chemicals that reduce the
effects of a neurotransmitter), blocks dopamine receptors in the synapse of the brain. When first taking, dopamine levels go up but then production is reduced. The dopamine antagonist effect normalises
neurotransmission in key areas of the brain which helps reduce symptoms like hallucinations.

Question 20

What was found about typical antipsychotics?

Answer 20

Strong association between the use of typical antipsychotics and the dopamine hypothesis.

Question 21

What’s clozapine?

Answer 21

Don’t all work in the same way.

Clozapine has smaller doses than typical antipsychotics. 350-400mg per day.

Regular blood tests are required as Clozapine is linked to a fatal blood condition (severely low white blood cells)

Binds to dopamine receptors like chlorpromazine but also acts on serotonin and glutamate receptors. – believed to help improve mood and reduce anxiety and may also improve cognitive functioning.

Often given to people who have SZ and are at a high risk of suicide because of its mood enhancing effects. (30-50% of people with SZ attempt suicide).

Question 22

What’s risperidone?

Answer 22

Developed later (1990s) with the hope of having less severe side effects than Clozapine.

Maximum dosage 12mg.

Question 23

How do risperidone tablets work?

Answer 23

Binds to dopamine and serotonin receptors, binds more strongly that other antipsychotics so a smaller dosage is required than other antipsychotics.

Evidence suggests that this leads to less side effects.

Question 24

What are the strengths of the biological treatments to SZ?

Answer 24

EffectiveintacklingsymptomsofSZ.Chlorpromazinewasassociatedwithbetteroverall functioning and reduced symptom severity. Relapse rate was also lower (Thornley et al, 2003).

Meltzer2012,Clozapineismoreeffectivethantypicalantipsychoticsandotheratypical.Was effective for 30-50% of treatment resistant cases where other medication has previously failed. … Link to individual and the economy.

Answer 25

Drugcompaniesfundtheresearchintotheeffectivenessofdrugs,alsotendtolookatshortterm effects without long term – why is this an issue? What is questioned? More independent research needed?
• Thereareserioussideeffectsoftakingtypicalandatypicalantipsychotics.Whatexampleshavewe looked at? Why is this a weakness? Link to treatment effectiveness, economy etc.
• OnlytreatsthesymptomsnotthecauseofSZ…whyisthisaproblem?
• Reductionist…whatisn’tconsidered,whyisthisaproblem?Wouldcombined/individually tailored treatment be more effective?