Schizophrenia: Biological Explanations And Drug Therapy Flashcards
Why might someone with SZ have a family member with SZ?
Whether a person develops SZ is at least partly down to their genes, this could explain why patients often have other family members with SZ
What was the family study which found a genetic link with SZ and other family members with SZ?
A very large scale family study carried out by researchers, findings have shown that the greater the degree of genetic relatedness, the greater the risk of developing SZ (concordance rate not 100% with M twins (48%) so could be due to other factors although % is still high, 17% for DZ)
What were the two adoption studies which compared SZ patients with SZ mothers?
Researchers compared 47 adopted children whose biological mother has SZ with a control group of adopted children with no SZ in their biological family, none of the control group ere diagnosed with SZ; 16% of the offspring of mothers with SZ were diagnosed. Also another study, 11% of 164 adoptees whose mothers have SZ developed SZ
What was the candidate gene with SZ risk study?
SZ is thought to be polygenic (large number of genes which can increase risk of SZ) and aetiologically heterogeneous (different combinations which can cause SZ in different people) researchers completed a study combining all data from a genome wide study of SZ, 37,000 patients were compared to 113,000 controls; 108 separate genetic variations were associated with increased risk of SZ ,
What is the dopamine hypothesis concerning a lower level of dopamine?
An excess of the neurotransmitter dopamine has been implicated in the symptoms of SZ, hypodaminergia in the cortex (meaning lower levels), Researchers identified role of low levels in PF cortex, thinking and decision making were both effected (negative)
What is the dopamine hypothesis concerning a higher level of dopamine (older hypothesis)?
Higher dopamine levels in the subcortex, excess levels of dopamine receptors in Broca’s area, poverty of speech, experience of auditory hallucinations effected (both negative and positive symptoms of SZ). Dopamine hypothesis states that messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic symptoms of SZ. People with SZ are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing
Supporting evidence for dopamine hypothesis
Amphetamines: dopamine antagonists, stimulate nerve cells containing dopamine causing the synapse to be ‘flooded’ - large doses of the drug can cause hallucinations and delusions (positive symptoms).
Cocaine: also increases the levels of dopamine in the brain and can cause the positive symptoms of SZ and exaggerate them in people who already have SZ
What is an antagonist?
An antagonist blocks or reduces the effect of a neurotransmitter
What is an agonist?
An agonist is a chemical that binds to a receptor of a cell and triggers a response by that cell
What are neural correlates?
Measurements of the structure or function of the brain that occur in conjunction with with an experience, in this case SZ
What is the neural correlates link with people with SZ?
There is growing evidence that SZ is down to structural abnormalities in the brain, brain scanning techniques have made it possible to investigate living brain images, both positive and negative symptoms have neural correlates.
What is the link between neural correlates and SZ negative symptoms?
Activity in the ventral striatum has been linked to the development of avolition (loss of motivation). The ventral striatum are believed to be particularly involved in the anticipation of a reward for certain actions. Researchers have identified lower levels of activity in VS for SZ patients compared to controls. Patients who exhibit lower ventral striatal activity show higher negative symptom severity
What is the link between neural correlates and SZ positive symptoms?
Reduced activity in the superior temporal gyrus and anterior cingulate gyrus have been linked to the development of auditory hallucinations. Patients experiencing auditory hallucinations showed lower activation levels in these areas than controls. Therefore, reduced activity in these areas of the brain is a neural correlate of auditory hallucinations. Researchers conducted EEG scans, testing errors made by people with SZ compared to controls during a memory task, SZ made more errors with the tasks which suggests auditory ability impacted their memory.
What is the link between correlates of SZ with brain ventricles?
Some people with SZ have abnormally large ventricles in the brain. Ventricles are fluid filled cavities, meaning that the brains of people with SZ are lighter than normal
Supporting evaluation for biological approach to schizophrenia
There is evidence for genetic link (family studies (however do not always emphasise environment importance and small sample sizes and concordance rate not 100%), adoption studies (however conducted in Finland so not generalisable), candidate gene study).
Evidence of mutations in parental DNA, parental sperm, caused by radiation, poison or viral infection mutating DNA and leading to higher risk of developing SZ.
Researchers found a correlation between paternal age and risk of SZ, increasing from around 0.7% for fathers under 25 and 2% in fathers over 50 (suggests age and other confounding factors)
Evaluations against the biological approach to schizophrenia
Mixed evidence, (Researchers found that dopamine antagonists increase the levels of dopamine and can make the symptoms of SZ worse. Other researchers found that antipsychotic drugs reduce the levels of dopamine, which contrasts this so evidence is mixed).
Neural correlates tell us very little about causes of SZ.
The correlation between ventral striatum and negative symptoms suggests that there is something wrong in the VS which is causing negative symptoms or that the negative symptoms, mean less info passes through the striatum.
Findings of neural correlates inconsistent, therefore inconclusive and cause and effect issues.
What is a typical antipsychotic?
The first generation of antipsychotics (developed during the 1950s) they work as dopamine antagonists (e.g. Chlorpromazine)
What is an atypical antipsychotic?
The second generation of antipsychotics (developed during the 1990s) antagonists which typically target a range of neurotransmitters such as dopamine and serotonin (e.g. Clozapine and Risperidone)
What is the dosage of Chlorpromazine?
Up to 1000mg daily, typical doses are 400-800mg but this has decreased over the last 50 years
What does Chlorpromazine (Typical) do?
(Typical) Initially it builds up dopamine in the brain, then reduces production. According to the dopamine hypothesis, this dopamine antagonist effect normalises neurotransmission, reducing symptoms such as hallucinations. Chlorpromazine is a sedative and is used to calm patients especially when admitted to hospital
What is the dosage of Clozapine?
300-450mg daily, lower than Chlorpromazine due to its fatal side effects. Can only be used in tablet form due to risks
What does Clozapine (Atypical) do and when was it developed?
Developed in 1960s and trialled in early 70s, it’s used when other treatments fail to work, binds to dopamine receptors similarly to Chlorpromazine, however it also acts on serotonin and glutamate receptors, helps mood and reduces depression and anxiety.
What is the dosage of Risperidone?
Smaller doses given, 4-8mg up to 12mg daily
What does Risperidone (Atypical) do and when was it developed?
Developed in 1990s as an attempt to reduce side effects of clozapine, binds to dopamine and serotonin receptors. It has a stronger binding effect on dopamine than clozapine and is effective in lower doses
