Schizophrenia: Biological explanations for schizophrenia

Question 1

What are biological explanations?

Answer 1

Emphasise the role of inherited factors and dysfunction of brain activity in the development of the behaviour of mental disorder.

Question 2

What are the genetic factors of sz?

Answer 2

• Family studies
• Twin studies
• Adoption studies

Question 3

How do family studies play a part in explaining sz?

Answer 3

Gottesman, (1991) family studies find individuals who have schizophrenia and determine whether their biological relatives, are similarly affected more often than the non-biological parents. Many studies have established that schizophrenia is more common among biological relatives of a person with SZ, and that the closer the degree of genetic relatedness, the greater the risk. For example, in Gottesman’s study, children with two schizophrenic parents had a concordance rate of 46%, children with one schizophrenic parent rate of 13%, and siblings (where a brother or sister has schizophrenia) had a concordance rate of 9%

Question 4

How do twin studies play a part in explaining sz?

Answer 4

As always, twin studies are a useful way to determine whether or not a condition is inherited through genetics. If it is more common for both identical twins to suffer from schizophrenia than it is for both non-identical twins, this would suggest a genetic component to schizophrenia. The reason for this is that identical twins have 100% identical genetics whereas non-identical twins only share 50% of their genes and so any genetic condition would be equally common to both identical twins. Joseph (2004) calculated that the pool data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins.

Question 5

How do adoption studies play a part in explaining sz?

Answer 5

Tienari et al (2000) in Finland found of that 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis of schizophrenia, compared to just 4 (2%)of the 197 control adoptees (those born to non-schizophrenic mothers). The investigators concluded that these findings showed that the genetic liability to schizophrenia had been decisively confirmed.

Question 6

What is the neural explanation of sz?

Answer 6

The neural explanation of schizophrenia looks at correlations among the brain structures of people with schizophrenia.

Question 7

What is the dopamine hypothesis?

Answer 7

Claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with positive symptoms of schizophrenia. Messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions which are the characteristic positive symptoms of schizophrenia. Schizophrenics are thought to have abnormally high numbers of D2 receptors and receiving neurons, resulting in more dopamine binding and therefore more neurons firing.

Question 8

What are drugs that increase dopamine?

Answer 8

1. L-Dopa which raises DA, and has been given as a treatment for Parkinson’s, can produce sz-like side effects.
2. Amphetamine is a dopamine antagonist. It stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter. Normal individuals who are exposed to large doses of dopamine-releasing drugs such as amphetamines can develop the characteristic hallucinations and delusions of a specific episode.
3. Anti-psychotic drugs, which lower DA levels, have been found to reduce sz symptoms.

Question 9

What drugs decrease dopaminergic activity?

Answer 9

Although there are many different types of antipsychotic drugs, they will have one thing in common. They block the activity of dopamine in the brain. By reducing activity in the neural pathways of the brain that use dopamine as a neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions. The fact that these drugs alleviated many of the symptoms of schizophrenia known as dopamine antagonists strengthens the case for the important role of dopamine in this disorder.

Question 10

What is the revised dopamine hypothesis?

Answer 10

David and Kahn (1991) proposed that the positive symptoms of schizophrenia are caused by excessive dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway. The negative and cognitive symptoms of schizophrenia are thought to arise from a deficit of dopamine in areas of the pre-frontal cortex. Evidence for this revised hypothesis comes from various sources:

• Neural imaging: Patel et al (2010) used PET scans to assess dopamine levels and schizophrenic patients and normal individuals, and found lower levels of dopamine in the dorsolateral prefrontal cortex in schizophrenic patients compared to their normal controls.
• Animal studies: Wang and Deutch (2008) induced dopamine depletion in the pre-frontal cortex in rats. This resulted in cognitive impairment that the researchers were able to reverse using olanzapine, and atypical antipsychotic drugs thought to have beneficial effects on negative symptoms and humans.

Question 11

What is neural correlates?

Answer 11

Neural correlates refer to the changes in neuronal events and mechanisms that result in the symptoms of a specific behaviour.

• Prefrontal cortex- is the main area involved in executive control. Cognitive impairments of sz could be a consequence of PFC impairment
• Hippocampus- Heckers suggest heightened activity in the hippocampus may lead to many of the symptoms of SZ.
• Grey matter loss- SZ patients have less grey matter in the Temporal and frontal lobes. Less tissue, worse symptoms.
• White matter abnormalities- these were found in patients. White matter is never fibres covered in myelin sheaths.

Question 12

A03: Genetic factors

Answer 12

+ Common rearing patterns may explain family similarities.
- Reductionist

Question 13

A03: Dopamine hypothesis

Answer 13

+ Evidence from treatment
- Challenges to the dopamine hypothesis

Question 14

A03: Genetic factors: Reductionist

Answer 14

Although most studies suggest genetics play a part in the development of schizophrenia, it is clear that other factors are important too. If schizophrenia was 100% genetic, you would expect concordance rates between identical twins to be 100%. However, most studies find concordance rates among identical twins to be less than 50%, which suggests there is more to schizophrenia than just genetics such as Joseph was 40.4% for MZ twins. This suggests an interactionist approach is best for explaining schizophrenia.

Question 15

A03: Genetic factors: Common rearing patterns may explain family similarities.

Answer 15

Research has shown that schizophrenia appears to run in families, supporting the argument for a genetic basis for the disorder. However, many researchers now accept that the fact that schizophrenia appears to run in families maybe more to do with common rearing patterns or other factors that have nothing to do with heredity. For example, research on expressed emotion has shown that the negative emotional climate in some families may lead to stress beyond an individual’s coping mechanisms, that’s triggering a schizophrenic episode.

Question 16

A03: Dopamine hypothesis: Evidence from treatment

Answer 16

Much of the evidence from the dopamine hypothesis comes from the success of drug treatments that attempt to change levels of dopamine activity in the brain. The basic mechanism of antipsychotic drugs is to reduce the effects of dopamine and so reduce the symptoms of schizophrenia. For example, Leucht et al (2013) carried out a meta-analysis of 212 studies that analysed the effectiveness of different antipsychotic drugs compared with a placebo. They found that all the drugs tested were significantly more effective than placebo and the treatment of positive and negative symptoms was achieved through the normalisation of dopamine.

Question 17

A03: Dopamine hypothesis: Challenges to the dopamine hypothesis

Answer 17

Noll (2009) claims there is strong evidence against both original dopamine hypotheses in the revised dopamine hypothesis. He argues that antipsychotic drugs do not alleviate hillucinacions and delusions in about one-third of people experiencing the symptoms. Noll also points out that in some people, hallucinations and delusions are present despite levels of dopamine being normal. Blocking the D2 receptors of these individuals has little or no effect on their symptoms. They suggest that, rather than dopamine being the sole cause of positive symptoms, other neurotransmitter symptoms, acting independently of the dopaminergic system, may also produce the positive symptoms associated with SZ.