Schizophrenia - The biological explanation of schizophrenia and drug therapy Flashcards
The biological explanation of schizophrenia
- Biological explanations emphasise the role of inherited factors and dysfunction of brain activity in the development of schizophrenia.
- Most modern psychologists believe that schizophrenia is at least partly biological.
There are three main biological explanations:
1) Genetics
2) The dopamine hypothesis (role of neurotransmitters)
3) Neural correlates
- These explanations are inter-related, because if schizophrenia is genetic, those genes lead to biological differences such as abnormal levels of dopamine and/or abnormal structures of the brain.
1) Genetics
- There is considerable evidence that schizophrenia runs in families and is in part genetic (inherited as genes are transmitted from parent to child).
- Evidence: Gottesman (1991) conducted a large-scale study and found much higher concordance rates in MZ twins (48%) in comparison to DZ twins (17%).
- This supports that individuals with identical genetic make-up (MZ twins) have an increased risk of developing schizophrenia compared to those who share fewer genes, supporting the genetic explanation of schizophrenia as there is an association between the degree of genetic similarity and shared risks of schizophrenia.
- Schizophrenia is thought to be polygenic (it requires a number of different factors to work in combination) and so different combinations of genes can lead to the condition. Research suggests that there are 108 genetic variations associated with increased risk of schizophrenia.
1) Genetics - cont.
- The genetic explanation for schizophrenia suggests that schizophrenia is inherited and results from a biological process driven by the activity of certain genes, such as for brain structure development and neurotransmitter levels.
- There is no one “ schizophrenia gene”, however a collection of gene locations have been located that are associated with a higher risk of developing schizophrenia.
=>This means schizophrenia is thought to be a polygenic disorder. - If scizohpneia is genetic then we expect to see the more closely related two people are, if one person has the disorder the more likely the other person is to have the disorder (concordance rate)
- If one MZ twin is schizophrenic, there is a 48% chance of the other twin also being schizophrenic
1) Studies to support the genetic explanation
1) Ripke et al (2014) conducted genetic analysis of over 36 thousand schizophrenia cases, this identified 108 genetic loci associated with development of schizophrenia.This suggests a range of genes are responsible for schizophrenia, but also suggest the disorder is aetiologically heterogeneous as different combinations are games are correlated with having the disorder.
- Twin studies are particularly interesting for psychologists studying the genetic basis of schizophrenia as monozygotic twins are genetically identical and share environments
2) Gottesman (1991) reviewed cases of schixohenia in families and found a concordance rate of 48% for identical twins (MZ) and 17% for non identical twins (DZ).This compares to the general population rate of 1%.
=> This suggest schizophrenia has a genetic aspect as there is such a large difference between the two sets of twins
- Both DZ and MZ twins should share similar environments
- However concordance is not 100% in MZ so not fully genetic.
3) Tienari (2004) studied the biological children of schizophrenic mothers who had been adopted.It was found that 5.8% of children adopted into psychologically healthy families developed schizophrenia compared to 35.8% of children raised in dysfunctional families.
=> As the risk of both groups far above the 1% risk level of the general population,this suggests that schizophrenia has a genetic basis,however the difference between groups also suggests a role to play for psychological (environmental) factors.
2) The dopamine hypothesis
- The brain’s chemical messengers (neurotransmitters) appear to work differently in the brain of a patient with schizophrenia.
- Dopamine is a neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure.
- Unusually high levels are associated with schizophrenia, particularly the positive symptoms.
- Neurons that transmit dopamine fire too easily or too often in those with schizophrenia.
- Schizophrenics are also thought to have abnormally high levels of D2 receptors on post-synaptic neurons, resulting in more dopamine binding and therefore more neurons firing.
- This is thought to lead to hallucinations and delusions.
2) Revised dopamine hypothesis
- Davis and Khan (1991) proposed a revised dopamine hypothesis.
- They suggested that the positive symptoms of schizophrenia are caused by higher levels or activity of dopamine in the subcortex. E.g. An excess of dopamine receptors in Broca’s area may be associated with speech poverty and/or auditory hallucinations.
- The negative symptoms of schizophrenia are thought to arise from lower levels of dopamine in the prefrontal cortex.
- It may be that both high and low levels of dopamine in different brain regions are involved in schizophrenia.
2) Revised dopamine hypothesis - the prefrontal cortex
- The prefrontal cortex (PFC) is the cerebral cortex covering the front part of the frontal lobe.
- This brain region has been implicated in planning complex cognitive behavior, personality expression, decision making, and moderating social behaviour.
- The basic activity of this brain region is considered to be orchestration of thoughts and actions in accordance with internal goals.
3) Neural correlates
- Neural correlates are measurements of the structure or function of the brain that occur in conjunction with (correlate with) the characteristic symptoms of schizophrenia, and so may be implicated in the origins of schizophrenia.
- There are thought to be neural correlates of positive symptoms and negative symptoms.
- Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus have been found in those experiencing auditory hallucinations. Therefore, reduced activity in these two areas is a neural correlate of one positive symptom.
- Activity in the ventral striatum is a neural correlate of the negative symptoms of schizophrenia.
3) Neural correlates - research evidence
Juckel et al. (2006) found these results in their study
- Found negative correlation between the ventral striatum whilst thinking of a reward and avolition (inactivity and loss of motivation)
- Moderately strong negative correlation between avolition and activity in ventral striatum; therefore as the activity in ventral striatum decreases, avolition increases.
3) Neural correlates - negative symptoms
- The ventral striatum is thought to be involved in the anticipation of reward
- Juckel et al’s (2006) study found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms (loss of motivation etc).
- Therefore, activity in the ventral striatum is a neural correlate of the negative symptoms of schizophrenia.
Evaluating the biological explanation of schizophrenia - strengths
1) There is now strong evidence for genetic vulnerability to schizophrenia from a variety of sources, such as Gottesman’s and Tienari et al’s study into how adopted children of schizophrenia sufferers were still at heightened risk for the disorder is adopted into families with no history of it
- There is therefore a large amount of research evidence, providing external validity for the genetic explanation
2) Much of the evidence supporting the dopamine hypothesis comes from the success of drug therapies that attempt to change dopamine activity and levels (use of antipsychotics) - Leucht et al’s study found antipsychotics to be significantly more effective than a placebo in treating positive and negative symptoms - dopamine agonists that increase levels of dopamine make schizophrenia worse and can produce mimicked symptoms in non-sufferers (Curran et al 2014)
- External validity for the dopamine hypothesis explanation which then has real-world applications to the development of treatments by identifying the source of the symptoms
Evaluation of the biological explanation for schizophrenia - Weaknesses
1) The assumption that the greater concordance for schizophrenia between MZ twins is a genetic similarity rather than greater environmental similarity; however, MZ twins are treated more similarly, encounter more similar environments and are frequently treated as twins rather than two distinct individuals like DZ twins
- This is a weakness of twin studies, impacting their internal validity as it may be more due to rearing than genetics
2) Noll (2009) argues that antipsychotic drugs do not alleviate hallucinations and delusions in about 1/3 of people experiencing these symptoms and in some people, hallucinations and delusions are present despite dopamine levels being normal - blocking D2 receptors has little or no effect on their symptoms
- They have limited impact on all schizophrenic treatments, and so the explanation lacks generalisability of the dopamine hypothesis and so lacks external validity
Evaluation of the biological explanation of schizophrenia - Weaknesses cont.
3) Although studies of neural correlates are useful in flagging up particular brain systems that may not be working properly, this kind of evidence does not prove that the activity in the brain region causes the symptom. For example, whilst it may be that something wrong in the ventral striatum causes the negative symptoms, it is possible these symptoms themselves mean that less information passes through the striatum resulting in its reduced activity and it’s also possible that another factor influences both
- Therefore, the explanation is not good at establishing cause and effect for schizophrenia symptoms, a weakness of the explanation
4) Many researchers now accept that the fact the schizophrenia appears to run in families may be more to do with common rearing patterns or other factors that have nothing to do with heredity. For example, a negative emotional climate in some families may lead to stress beyond an individual’s coping mechanisms, thus triggering a schizophrenic episode. The genetic probability of having schizophrenia is less than 50% even for MZ twins.
- This suggests that schizophrenia is not solely caused by biological factors, a weakness of all the explanations for being biologically reductionist.
Drug therapy as a treatment for schizophrenia
- Drug therapy involves the treatment of schizophrenia through the use of antipsychotic medication to reduce the symptoms of the disorder.
- These can be taken as tablets, syrup or injections if necessary.
- They help the person with schizophrenia to function as well as possible whilst also increasing their feelings of subjective wellbeing.
- All antipsychotics work by reducing dopaminergic transmission i.e. reducing the actions of the neurotransmitter dopamine in areas of the brain associated with the symptoms of schizophrenia.
There are types of antipsychotics:
- Typical (traditional) antipsychotics
- Atypical (newer) antipsychotics
Typical antipsychotics
- Developed in the 1950s, drugs such as chlorpromazine
- The basic mechanism of typical antipsychotic drugs is to reduce the effects of dopamine and so reduce the symptoms of schizophrenia - typical antipsychotics are dopamine antagonists in that they bind to but do not stimulate dopamine receptors (particularly D2) receptors in the mesolimbic pathway thus blocking their action
- By reducing stimulation of the dopamine system in the mesolimbic pathway, antipsychotic drugs eliminate the hallucinations and delusions experienced by people with schizophrenia
- Hallucinations and delusions usually diminish in a few days and other symptoms can take a few weeks, before a significant improvement is noted
- Kapur et al (2000) estimated that between 60% and 75% of D2 receptors in the mesolimbic dopamine pathway must be blocked for the drugs to be effective
- Unfortunately, in order to do this, a similar number of D3 receptors in other areas of the brain must also be blocked leading to undesirable side effects; this problem has been addressed by development of the atypical antipsychotic drugs
- Side effects include dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin, and long-term use can cause tardive dyskinesia (involuntary muscle movements of the jaw, tongue and face)
