Schizophrenia Flashcards
Facts on SZ (A02)
- schizophrenia - a severe mental disorder where contact with reality and insights are impaired e.g psychosis
- Experienced about 1% of the world’s population
- commonly diagnosed in men, city dwellers and lower socio-economic groups
- the symptoms of schizophrenia can interfere severely with everyday tasks, so many people with schizophrenia end up homeless or hospitalised.
- Each patient has different symptoms
- 15-35
- people with a family x10 more likely to get SZ (genetic)
- Drugs, the environment may increase the development if they’re vulnerable to developing it (nurture)
antipsychotic drugs target neurotransmitters
- most effective when combined with CBT + EBT
Classification of SZ
DSM
one positive symptom must be present for a diagnosis of SZ.
No subtypes
Classification of SZ
2 or more negative symptoms of SZ
7 subtypes
Positive symptoms
- symptoms which have been added due to SP, that the general population don’t have
symptoms shouldn’t be there
Hallucinations - unusual sensory experiences.
Some hallucinations are related to events in the environment whereas others bear no relationship to what the senses are picking up from the environment. e.g. voices heard either talking to or commenting on a person often criticising them. They may see distorted facial expressions, people or animals that aren’t there.
Delusions - are irrational beliefs. They involve beliefs that have no basis in reality. e.g a person believes that they are someone else or that they are the victim of a conspiracy. A person may believe that they are under external control. Delusions can make a person behave in ways that make sense to them but bizarre to others.
- coherent/irrelevant speech
Negative symptoms
symptoms which have been removed due to SP, that the population have. Symptoms that should be there that aren’t (missing)
- Anhedonia
- Flatness of effect
Speech poverty is seen as a negative symptom because the emphasis is on the reduction in the amount quality of speech in schizophrenia. This is sometimes accompanied by a delay in the person’s verbal responses during a conversation.
Speech disorganization - speech becomes incoherent or the speaker changes topic mid-sentence. This classified in DSM-5 as a positive symptom in SZ.
Avolitation- finding it difficult t begin or keep up with goal-directed activity. People with SZ often have sharply reduced motivation to carry out a range of activities.
Nancy Andersen 1982 - identified 3 signs of abolition : poor hygiene and grooming/ lack of persistence in work or education and lack of energy
Classification of SZ - ICD 10 subtypes of SZ
- Paranoid Schizophrenia - Delusions and hallucinations. Do not usually have an absence of feelings and emotions of disorganised speech.
- Hebephrenic Schizophrenia (called disorganised SZ in DSM-IV) - often begins early age, with incoherent and disorganised speech, and lack of feelings or emotion (known as the flat affect). Sometimes hallucinations and delusions.
- Catatonic schizophrenia - Unusual motor activity (either agitation or immobility) often extreme negativism and strange posturing - very rare disorder
- Undifferentiated schizophrenia - Diagnosed when showing clear schizophrenic symptoms that do not fit into the other categories.
- Post-schizophrenic depression (not in the DSM-IV) - Criteria for schizophrenia have not been met for 12 months but are currently present. Depressive symptoms are prolonged and severe.
- Residual schizophrenia - At least one episode of SZ but no longer showing obvious signs of the disorder.
- Simple schizophrenia (not in DSM-IV) Slow but progressive development of social withdrawal, apathy, poverty of speech, and decline in scholastic or occupational performance.
Copeland et al 1971
described a patient to 134 US psychiatrists and 194 British psychiatrists. 69% of US psychiatrists diagnosed SZ, but only 2% of British psychiatrists gave the same diagnosis.
Issues with diagnosis and classification of SZ
Validity
A pathognomic symptom - unique to a particular disorder.
There are no pathognomic symptoms for SZ.
Brain tumours can also produce schizophrenic-like symptoms.
Rosenhan - symptoms can be faked
Blever’s - No predictive validity
This proves how schizophrenia develops cannot be predicted as the figures are not accurate - which is difficult to predict.
33-37% of people don’t respond to treatment.
However, schizophrenia overlaps with bipolar disorder. Depending on your mood and what’s going on in your life when you speak to a mental health professional. They might find it difficult to understand which diagnosis best fits their experiences.
Limited time and resources may explain low inter-rater reliability in the diagnosis of SZ. Diagnosis can be made by professionals, that are rushed and preoccupied with only admitting the most serious case in order to safeguard the resources of the institutions.
Co-mobility symptoms of different disorders overlap. High co-mobility rates question the validity and reliability of diagnosis and classification diagnosis - a single condition.
Reliability
Issues with diagnosis and classification of SZ
2 diagnostic manuals
No biological/diagnostic test
Co - mobility - the overlap of symptoms
Low - interrater - reliability
Wider applications - labelling, economic applications
Issues with diagnosis and classification of SZ
Gender bias
Fischer and Buchanan 2017 - Since the 1980s men have been diagnosed with schizophrenia more commonly than women (1.4:1)
Issues with diagnosis and classification of SZ
Cultural bias
In Haiti, Some people believe that voices actually are communications from ancestors.
Pinto and Jones 2008, African Caribbean origin are 9x likely to receive a diagnosis as white British people.
Biological explanation of Schizophrenia - The genetic hypothesis
Twin studies
Cardno et al - 40% concordance rate in MZ twins, compared with 5.3% in DZ twins
candidate may be inherited
SZ is polygenic
SZ is aetiologically heterogeneous - different combinations of the factor s may lead to SZ
There is no schizophrenic gene
Ripkeet al - 108 separate genetic variations
Rosenthal 1963 studied quadruplets in which all 4 girls were identical to each other. All 4 of them developed SZ, although they did differ in age of onset and the precise symptoms. It is worth noting that they had a dreadful and aberrant childhood, so the conclusion of this investigation is not clear out.
Biological explanation of Schizophrenia - The genetic hypothesis
Family studies
The general population have a 1% risk of getting schizophrenia
1st degree relative - 50%
2nd degree - 25%
3rd degree - 12.5%
Gottesman - the more genes you have with someone with schizophrenia the risk increases.
1st degree - 6-9%
2nd degree - 2-4%
3rd degree - 2%
Biological explanation of Schizophrenia - The genetic hypothesis
adoption studies
Tienari et al 2004 - children of SZ parents have a heightened risk of developing SZ even if the adopted family has no history of SZ.
genes associated with increased risk include those coding the functioning of a number of neurotransmitters including dopamine.
Biological explanation of Schizophrenia - Dopamine hypothesis
Hyperdopaminegia in the subcortex
SZ patients have excessive amounts/levels/activity of dopamine in the subcortex (central area of the brain)
What symptoms would be present if there is excessive dopamine in a broca area?
- Positive symptoms
- Poverty of speech
- Auditory hallucinations
Hypodopaminergia in the cortex
Low levels of dopamine in the prefrontal cortex (Goldman-Rakic et al 2004)
Prefrontal cortex - Thinking and decision making
What symptoms of SZ would be present ?
Negative symptoms
Both hyper and hypodopaminergia are correct explanations - both involved in the onset of SZ
Supporting evidence
1. the use of antipsychotic drugs
Supporting evidence Dopamine hypothesis
Drug therapy (practical application)
SZ is usually treated with chlorpromazine. Chlorpromazine is a drug that binds to dopamine (DA)
receptors without stimulating them, rendering them unavailable for activation by DA.
Barlow & Durand 1995 report that chlorpromazine is effective in reducing schizophrenic symptoms in about 60% of cases. It appears to have the most impact on the positive symptoms (hallucinations,delusions) and treated patients may still suffer from severe negative symptoms.
Supporting evidence for dopamine hypothesis
Post Mortems and PET scans
Wise & Stein 1973 found that schizophrenia patients who died in accidents showed abnormally low levels of Dopamine Beta Hydroxylase (DBH) in the brain fluid. DBH is an enzyme whose function is to break down the neurotransmitter Dopamine after release.
Autopsies have found that there are generally a large number of dopamine receptors (Owen et al 1987) and there was an increase in the amount of dopamine in the left amygdale (falkai et al 1988) and increased dopamine in the caudate nucleus and putamen (Owen et al, 1978).
Opposing evidence for Dopamine hypothesis
Kasper et al 1999
- Antipsychotic drugs are effective for only positive symptoms. Therefore, excessive dopamine can at best explain only some types of schizophrenia.
Newer atypical antipsychotic drugs e.g. clozapine have proved more effective than traditional ones in successfully treating the symptoms of schizophrenia despite blocking fewer dopamine receptors.
Biological explanation of Schizophrenia - Neural correlates
Certain structures and functions of brain structures with displaying symptoms of SZ :
Positive symptoms - Allen et al 2007 found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus.
Negative symptoms
- loss of motivation (anoiton)
- verbal stratum is involved in this abnormality in this area and may be involved in the development (avolition)
Jackel et al measured the activity of verbal stratum in SZ participants.
- lower levels of activity than control groups
- they also observed a negative correlation between activity levels in the verbal stratum and the severity of overall negative symptoms.
Neural correlates are…
Both positive and negative symptoms have…
Measurements of the structure or function of the brain that correlate with an experience.
Neural correlates
A03 - Neural Correlates
Supporting evidence
Buchsbaum 1990 - abnormalities in the frontal and pre-frontal cortex, the basil ganglia, the hippocampus and amygdale
Torrey 2002 - The ventricles (cavities in the brain) that supply nutrients and remove the waste of joy in a person with schizophrenia are on average about 15% bigger than normal.
Suddath et al 1990 - He used MRI (magnetic resonance imaging) to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic. The schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the schizophrenic twin could be easily identified from the brain images in 12 out of 15 pairs.
Methodological ‘issues’ of supporting evidence
Research is carried out in highly controlled environments, with specialist, high-tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the basil ganglia, the hippocampus and the amygdale. This suggests that if this research was tested and retested the same results would be achieved.
Biological therapies for schizophrenia: Drug therapy
Typical antipsychotic drugs
It can be in the form of Tablet, Syrup and Injection
Chlorpromazine (antagonists)- linked with the dopamine hypothesis.
It reduces the action of dopamine by blocking the dopamine receptors. This reduces symptoms like hallucinations.
Typical antipsychotics - The first generation of drugs for schizophrenia and other psychotic disorders having been used since the 1950s. They work as dopamine antagonists and include chlorpromazine.
Dopamine antagonists
Antagonists are chemicals which reduce the action of the neurotransmitter. Dopamine antagonists work by blocking dopamine receptors in the synapses of the brain, reducing the action of dopamine. This dopamine antagonist effect normalises neurotransmission in key areas of the brain, reducing symptoms like hallucinations.
Sedation effect - chlorpromazine is also an effective sedative. Chlorpromazine is often used to calm individuals not only those with schizophrenia but also with other conditions. Syrup is absorbed faster than tablets so it tends to be given when chlorpromazine is used for its sedative properties.
Windgassen 1992 Findings =
- about half of SZ patients taking neuroleptics (conventional drugs) reported grogginess or sedation
- 18% reported problems with concentration
- 16% had problems with salivation
- 16% had blurred vision
- 20% who had taken the drug for over a year developed the symptoms of tardive dyskinesia - these symptoms include voluntary sucking and chewing, jerky movements of the limbs and writhing movements of the mouth or face and the effects can be permanent.
