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Psych (1.5) Psychopathology > OCD - Explanation > Flashcards

OCD - Explanation Flashcards

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1
Q

From which key approach is the explanation to psychology drawn?

A

The biological approach.

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2
Q

What are the two forms of Biological explanations that can be used to explain the OCD behaviours?

A
  • Genetic explanations,

- Neural explanations.

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3
Q

What are neural explanations?

A

The genes associated with OCD are likely to affect the levels of key neurotransmitters as well as structures of the brain, these are neural explanations.

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4
Q

Lewis (1936) observed that of his OCD patients, ____% had parents with OCD and ____% had siblings with OCD.

A

37% and 21%:

Lewis (1936) observed that of his OCD patients, 37% had parents with OCD and 21% had siblings with OCD.

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5
Q

Which model can explain how certain genes leave some people more likely to suffer a mental disorder?

A

The diathesis-stress model.

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6
Q

What are candidate genes?

A

Researchers have identified genes, which create a genetic vulnerability for OCD, these are called candidate genes.

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7
Q

What are the three parts of the genetic approach?

A
  • Candidate genes,
  • OCD is polygenic,
  • Different types of OCD.
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8
Q

T / F:
Lewis (1936) found that of his OCD patients, 37% had parents with OCD, this means that there is a gene which makes you have OCD.

A

False - What is probably being passed down through generations is a genetic vulnerability as the number is not 100%.

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9
Q

Candidate genes that have been identified by researchers usually have what type of function in the body?

A

They are mostly involved in regulating the development of the dopamine or seratonin system. (e.g. the gene 5HT1-D beta which is implicates in the efficiency of transport of seratonin across synapses.)

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10
Q

What did Lewis’ findings (1936) suggest about the nature of OCD?

A

His findings suggested OCD runs in families, although what is probably passed down is a genetic vulnerability and OCD is not definite.

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11
Q

Researchers have identified candidate genes such as ‘5HT1-D beta’, what is the role of this gene and why may damage to it suggest OCD could develop?

A

It is implicated in the efficiency of seratonin transport across synapses, seratonin regulates anxiety, mood etc and therefore less efficient transport means more unstable moods and anxiety levels.

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12
Q

OCD, like many conditions is polygenic, what does this mean?

A

This means OCD is caused not by one single gene but several genes are involved.

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13
Q

Who found evidence on the polygenic nature of OCD?

A

Taylor (2013) analysed findings of previous studies and found evidence that up to 230 different genes may be involved in OCD.

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14
Q

Dopamine and Serotonin have both been studied in relation to OCD, what do they have in common?

A

They are both neurotransmitters believed to have a role in regulating mood.

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15
Q

What does it mean that OCD is aetiologically heterogeneous?

A

This means one group of genes may cause OCD in one person but a different group of genes may cause the disorder in someone else.

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16
Q

Breakdown the word:

‘aetiologically heterogeneous’.

A

aetiologically = origin (of OCD gene),
heterogeneous = different causes,
Therefore, all together means genes have different causes in each person in relation to OCD.

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17
Q

Due to the polygenic nature of OCD, one group of genes can cause OCD is one person but a different group of genes may cause the disorder in someone else. What is the name for this?

A

‘aetiologically heterogeneous’.

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18
Q

Describe the findings of Taylor (2013):

A

Taylor analysed findings of previous studies and found evidence that up to 230 different genes may be involved in OCD.

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19
Q

What are the two main neural explanations?

A

The role of seratonin,

Decision-making systems.

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20
Q

What evidence is there for the genetic basis of OCD?

A

OCD tends to run in families, suggesting there is a genetic influence. Research support for this has come from twin studies and family studies.

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21
Q

T / F:

OCD has a 100% concordance rate in MZ twins.

A

False - we NEVER find a 100% concordance rate.

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22
Q

What do biopsychologists say about the relationship between concordance rates and inheritance of a trait?

A

They say that the higher the concordance rates between two people, the more likely it is the trait was inherited.

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23
Q

In twin and family studies we never see 100% concordance, what is meant by concordance?

A

The “similarity” between data sets, expressed as a percentage.

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24
Q

If a trait has a biological (genetic) basis, then would we expect MZ twins or DZ twins to have higher concordance rates and why?

A

we would expect MZ twins to have higher concordance rats than DZ twins as MZ are genetically identical.

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25
Q

Research has found that OCD tends to run in families, what type of studies would support this finding?

A

Twin and family concordance studies.

26
Q

Explain gene-mapping studies (in relation to OCD sufferers):

A

They compare the genetic material from OCD sufferers with non-sufferers.

27
Q

Research has shown what about the heritability of different types of OCD?

A

Different types of OCD have different heritability co-efficients.

28
Q

The neural explanation is based around neurotransmitters, what are they?

A

They are chemical messengers.

29
Q

Serotonin is a neurotransmitter linked to OCD, what is its simple function?

A

It sends mood relevant information.

30
Q

What can be said about the levels of seratonin in those with OCD (and depression)?

A

They are extremely low.

31
Q

What are SSRI’s?

A

Selective Serotonin Re-uptake Inhibitors.

32
Q

What three brain structures have been linked to OCD?

A
  • Orbito-frontal cortex,
  • Thalamus,
  • Caudate nucleus.
33
Q

What is the implication of damage to the caudate nucleus?

A

The damaged nucleus fails to suppress ‘minor’ signals and this leads to obsessive thoughts and anxiety.

34
Q

What is the role of the Orbito-frontal cortex?

A

Decision-making and noticing something abnormal.

35
Q

What is the role of the Thalamus?

A

Directs signals in the brain to where they can be interpreted.

36
Q

What is the role of the Caudate nucleus?

A

Regulates signals between the O-FC and the thalamus.

37
Q

T / F:

Environmental factors can also have an increase on the risk of developing OCD.

A

True.

38
Q

Researchers have found candidate genes that may have an impact in the genetics behind OCD, name one of these candidate genes:

A

5HT1-D beta.

39
Q

In terms of the nature / nurture debate, what are the issues with using family studies and twin studies to support biological explanations of OCD?

A

Discounts the nurture argument because twins from the same family are likely to have the same environment growing up.

40
Q

What did Gomer (2007) find about hte effect of environmental factors in OCD?

A

Gomer (2007) found that over 50% of OCD patients had traumatic experiences in their past.

41
Q

Is it problematic that no single gene has been isolated for OCD?

A

Yes, the polygenic nature of the disease means that there are too many combinations of the candidate genes to scan for specifically.

42
Q

Twin studies tend to have a relatively small sample size, how does this limit the biological explanation of OCD?

A

Small sample sizes mean that anomalous values have higher significance and are represented in the data set.

43
Q

Concordance rates of 100% are never found, what does this suggest to us about the nature of OCD?

A

There is some environmental influence as genetics cannot fully explain it.

44
Q

Approximately 40% of OCD patients do not reply to SSRI treatment. What does this suggest about the causes of OCD?

A

It is not solely caused by low seratonin levels as treatment to increase the level does not help 40% of patients, therefore, other factors must be involved.

45
Q

Using the analogy that “taking a painkiller to relieve a headache does not mean that the cause of the headache was due to a lack of painkillers”, explain the limitation of the neurotransmitter explanation:

A

OCD might not be caused by low seratonin levels, these levels could simply be a result of the OCD. Therefore, SSRI’s could only be treating the symptom of the OCD rather than the cause.

46
Q

Explain why the reductionist approach of the neural explanation can be a strength:

A

It breaks down the explanation so that it is easy to understand and can be scientifically studied.

47
Q

Explain why the reductionist approach of the neural explanation can be a weakness:

A

It is too simplistic to explain complex mental disorders and doesn’t consider any environmental factors.

48
Q

It can be hard to establish a cause and effect relationship in many biological explanations of OCD. What is the cause and effect relationships and how does it apply to neural explanations?

A

It is the idea that correlation does not mean causation, the stimulus may not cause the response. In this case it is the idea that OCD could cause low seratonin not the other way around, or their could be a third factor involved in the levels.

49
Q

The ‘worry circuit’ consists of which three parts of the brain?

A
  • Orbito-frontal cortex,
  • Thalamus,
  • Caudate nucleus.
50
Q

Explain the ‘worry circuit’:

A

The caudate nucleus suppresses signals from the O-FC and when it is damaged it cannot suppress these minor worry signals. Therefore, these minor worries are sent to the thalamus, where they are confirmed and sent to the O-FC.

51
Q

The ‘worry circuit’ works with a loop of three brain structures, in an OCD sufferer, which of these structures would said to be damaged?

A

Caudate nucleus.

52
Q

Neurotransmitters are responsible for relaying information from one _________ to another _________.

A

Neurotransmitters are responsible for relaying information from one neuron to another neuron.

53
Q

If someone has low seratonin levels, what would this mean for them?

A

Then normal transmission of mood-relevant information does not take place and mental processes are often affected.

54
Q

AO3 - Supporting evidence. (genetic)

A

There is lots of evidence that suggests your genetic makeup can leave you with a certain vulnerability to OCD. Nestadt (2010) reviewed many twin studies and found that 68% of MZ twins shared OCD whilst only 31% of DZ twins shared OCD.

55
Q

AO3 - Candidate genes.

A

Although twin studies have shown there is a strong genetic element to OCD, it has been very difficult to find any definite genes involved. This is because it appears that there are many genes involved and each gene increases the vulnerability by only a fraction. This means that the explanation has little predictive value.

56
Q

AO3 - Environmental risk factors.

A

It seems environmental factors also have a role in the risk of developing OCD, Cromer (2007)found that over half of his patients had experienced a traumatic event, and that OCD was more severe in those with multiple traumas. This suggests OCD cannot be completely genetic as this number of traumatic events is too high to be a coincidence.

57
Q

AO3 - Supporting evidence. (neural)

A

There is evidence to support the idea of neural mechanisms affecting OCD, antidepressants work purely on the seratonin system, increasing neurotransmitter levels. These drugs are effective in reducing OCD symptoms which suggests the serotonin system is involved in it.

58
Q

AO3 - Unclear specifics.

A

Other studies have shown the same areas to be active in decision making as those said to function abnormally in OCD (Cavedini, 2010). Therefore we cannot really claim to understand the true role of the neural mechanisms involved in OCD.

59
Q

AO3 - Assumptions of cause.

A

Although there is evidence to show that various neurotransmitters and brain structures function abnormally in OCD patients. However, this is not the same as saying that this abnormal function is the cause, these biological abnormalities could simply be the result of OCD rather than the cause.

60
Q

AO3 - Co-morbidity as extraneous variable.

A

Many OCD sufferers become depressed (they are co-morbid). This is likely to involve disruption to the seratonin system. Meaning it is hard to establish the seratonin system as the cause of OCD because then all depression sufferers would have OCD.

61
Q

AO3 - Twin studies flawed.

A

Twin studies are a standard source of evidence for genetic influences, however, they make the assumption that MZ twins are only more similar than DZ twins in terms of genetics. Whilst they are more than likely to have shared environments aswell.

62
Q

AO3 - Co-morbidity with Biological Diseases.

A

OCD symptoms form part of a number of other conditions that are biological in origin such as Parkinson’s Disease (Nestasdt, 2010). This suggests biological processes that cause symptoms in these conditions may also be responsible for OCD rather than OCD being responsible.

Psych (1.5) Psychopathology (11 decks)

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