Schizophrenia (Paper 3) Flashcards
1
Q
Symptom overlap def + evaluation + implications
A
Def: When SZ shares symptoms of other disorders. e.g. SZ and BPD both have the symptoms of delusions and avolition
Evaluation:
Reliability:
- Different diagnosis systems have different criteria for diagnosis.
- eg DSM requires 1 positive symptom vs ICD needs 2 or more negative symptoms
- Therefore, different researchers using different systems results in low inter- rater reliability
Validity:
- Ophoff (2011) Found that of 7 genes associated with SZ, 3 were also associated with BPD
- Suggests underlying similarities between SZ and BPD, questioning whether they are 2 separate disorders?
Implications:
- Misdiagnosis due to symptom overlap = inappropriate treatment which = ineffective treatment
- This can lead to potential worsening of condition or exposure to side effects of unnecessary drugs
2
Q
Comorbidity def + Evaluation
A
Def: When a patient has SZ while having another disorder at the same time.
Evaluation:
Reliability:
- Comorbidity is common
- Buckley (2009) Found that of people who have SZ: 50% had depression, 47% had substance abuse, 23% had OCD, 29% had PTSD.
- Hard to reliably allocate symptoms to the right condition
Validity:
- Can impact a diagnosis as it’s hard to be sure which symptoms ‘belong’ to which condition
- eg avolition is due to depression or SZ?
- Evidence from Sim (2006) found 32% of SZ patients had comorbidity.
3
Q
Culture bias def + Evaluation
A
Def: Culture bias may occur when there is a mismatch of cultural background between the psychiatrist and the patient
e.g. Psychiatrists in western cultures are usually upper/middle class and white. If they had a afro-caribbean patient who reported hearing voices of deceased ancestors (which is normal in that culture), the psychiatrist may report this as a symptom of SZ, when it’s not.
Means people from these backgrounds living in western culture are more likely to get diagnosed with SZ.
Evaluation:
Reliability:
- Keith (1991) found 2.1% of African Americans were diagnosed with SZ compared to 1.4% of White Americans
- Suggests there’s a lack of consistency in diagnoses among races
Validity:
- Escobar found white psychiatrists tend to over-interpret symptoms and generally distrust black patients
- Therefore affects the accuracy of the diagnosis as they are more likely to diagnose them, even if they don’t have SZ.
4
Q
Gender bias def + evaluation
A
Def: Males are more likely to receive diagnosis than females due to the gender differences of:
- Males have earlier onset than females
- Males tend to suffer more negative symptoms then females
- More likely to suffer substance abuse in addition to SZ
Evaluation:
Reliability:
- Loring & Powell (1988) performed a study that had 290 researchers assess 2 cases. The cases were presented as ‘males’ or no gender identity
- Found when cases were presented as ‘Male’ or no gender identity, 56% diagnosed them with SZ
- But when they were presented as ‘female’ only 20% diagnosed them with SZ.
- Suggests lack of consistency of diagnosis’ between genders
Validity:
- Males + Females can have similar symptoms, but females hide it better due to them being more likely to work and/or maintain relationships.
- Therefore they seem to have better social functioning, masking the severity of their symptoms
- Therefore, male mental health may be used as the benchmark for assessing SZ, creating a gender bias in the application of the C & D assessment systems.
5
Q
Biological explanation of SZ: Genetic Factors
A
Says SZ is inherited and is polygenic (requires multiple genes to predispose an individual).
- Children of two parents with SZ: 46% chance of developing
- Children of one parent with SZ: 19% chance of developing
- Children with SZ sibling: 9%
Found first degree relatives of people with SZ are 18x more likely to develop it
6
Q
Evaluation of Genetic Factors of SZ (2 S + 1 L)
A
Strengths:
- Ripke et al (2014)
- Compared 37,000 patient’s genetic makeups with SZ to 113,000 in a control group
- Found 108 separate genetic variations in the patients arhat are associated with SZ
- Due to the highly scientific and large sample size, this has helped us understand SZ better, leading to better treatments and care
- Twin studies
- Found there is a 48% concordance rate for SZ in MZ twins and 17% in Dz twins
- As MZ twins share there genetic makeup, the higher concordance suggests a genetic basis
Limitation:
- Problem with twin studies: Reductionist
- It is hard to assess whether the twin studies results are due to nature or nurture as they grow up in the same environment
- Also, if SZ was solely biological, you would expect an 100% concordance rate (which there isn’t)
- This suggests there is a environmental/social factor that biology overlooks
- This makes it reductionist and therefore negatively affects its validity
7
Q
Dopamine Hypothesis
A
Claims that SZ is due to either too much or too little dopamine in the brain.
This is called:
-
Hyperdominergia: High level of dopamine activity in the subcortical regions (underneath) of the brain which leads to positive symptoms.
Eg higher dopamine in pathways between subcortical and broca’s area = auditory hallucinations -
Hypodominergia: Low level of dopamine in pre-frontal cortex which links to negative symptoms.
Eg frontal cortex does thinking, decision making etc so less dopamine = avolition and speech poverty
8
Q
Other neural correlates to SZ (Other than Dopamine Hypothesis)
A
Been found that schizophrenics have enlarged ventricles - cavities in the brain that supply nutrients and remove waste.
Enlarged ventricles are associated with damage to central brain areas and prefrontal cortex, resulting in negative symptoms.
Torey (2002) found that people with SZ have 15% bigger ventricles than normal people.
9
Q
Evaluation of The Dopamine Hypothesis (2 S + 1L)
A
Strengths:
- Supporting research: Falkai et al Post mortems
- Found in post mortems of SZ patients that there was an increased concentration of dopamine in the amygdala (subcortex)
- Supports the view that SZ is due to hyperdominergia in subcortical regions
- Practical applications: Treatments
- Research into neurotransmitters (dopamine) have helped develop anti-psychotic drugs) which work by reducing dopamine activity in the brain
- These have been shown to be effective and reduce positive symptoms
- Therefore increasing the wellbeing of SZ patients and credibility of the hypothesis
Limitation:
- Problem with research: Cause and effect
- Due to the examination being post mortum, the P would have already developed the disorder and received treatment
- Therefore, not able to compare to before they had the disorder
- This makes it unclear whether it’s the SZ that altered dopamine activity or the dopamine activity causing the disorder.
10
Q
Typical Anti-Psychotic Drugs: How they work and Overview + Examples
A
How they work:
- Block activity of of dopamine by binding to receptor sites (specifically D2 receptors) in the synapse, making dopamine unable to bind.
- Therefore, this reduces dopaminergic activity in the brain and then reduces symptoms.
This occurs within 48 hours, but symptoms take a few weeks to subside - because initially dopamine levels build up, but then its production is reduced and therefore its concentration.
Overview:
- Created in 1950s
- Can be taken orally (tablet/syrup) or via injection
- Use primarily for positive symptoms
- Example: Chloropromazine, Haldol
11
Q
Evaluation of Typical Anti-psychotic drugs (1 S + 2 L)
A
Strength:
- Supporting research: Davis et al (1980) Placebo study
- Davis performed a meta-analysis of 29 studies
- Found a 55% relapse rate when drugs were replaced with a placebo, but a 19% relapse late if patients were actually on the drug.
- Suggests treatment as effective and therefore supports them as a treatment.
Limitations:
- Birchwood & Jackson: (2001): Not effective in reducing negative symptoms
- Only effective in treating positive symptoms
- Suggests they cannot offer a full treatment for SZ, affects their reliability.
- Side effects
- There are many side effects. Such as urinary problems, constipation, dizziness, weight gain.
- These problems can create issues with the patients taking the drugs, as they want to stop the side effects. This can lead to their symptoms coming back
- Furthermore, life-threatening conditions can come from taking these drugs (such as NMS - involves unstable blood pressure), which raises ethical issues to whether people should
12
Q
Atypical Anti-Psychotics: How they work and Overview + Examples
A
How they work:
- Block dopamine receptors in the brain as well, but also block serotonin receptors
- Temporarily occupy/block the D2 receptors, then rapidly dissociate from them to allow more ‘normal’ levels of dopamine to flow
- This is thought to create fewer side effects
Overview:
- Emerged in 1990s
- Examples: Clozapine, Risperidone
Clozapine:
- Binds to dopamine receptors, but also acts on serotonin and glutamate receptors.
- This can enhance mood and have an effect on negative symptoms.
- Can’t be taken via injection as you may die, so taken orally instead.
Risperidone:
- Can be taken orally or via injection
13
Q
Evaluation of Atypical Anti-Psychotics (1S + 2 L)
A
Strength:
- Better than Typical Anti-Psychotics - More effective
- Because they can treat the positive and negative symptoms whereas typical can only treat positive.
- For example, Meltzer 2012) found Clozapine was effective in 30-50% of treatment-resistant cases (where typical drugs didn’t work)
- Suggests Atypical to be better than Typical
Limitations:
- Opposing evidence: Atypical are actually not ‘superior’
- Leucht (1999) in a meta-analysis found Atypical were only slightly better then typical
- Two drugs were better, two drugs were worse
- Also, only slightly better at reducing negative symptoms
- Suggests Meltzer’s finding to be ‘overtstated’ and Atypical are not ‘superior
- Serious side effects
- Clozapine: risk of diabetes, stroke and blood clots
- Must be careful when prescribing these drugs and people must be monitored to be sure their not being harmed by side effects
- This costs money (to monitor) and can cause ethical issues if prescribed wrong.
14
Q
Psychological Explanations of Schizophrenia: Family dysfunction - 3 Main points
A
All aspects of a dysfunctional family that cause SZ:
- Schizophrenic mother
- A mother that is cold, rejecting and controlling, causes high family emotional tension and conspiracies.
- Leads to distrust and eventual paranoid delusions/psychosis
- Double bind theory
- Suggests frequent contradictory messages from parents will lead a child to SZ
- For example, telling a child to play outside more but having a go at them when they do
- Child finds themselves trapped in a position where they are confused and fear making mistakes, cannot ask for clarification or protest about unfairness.
- This makes the child confused, leading to disorganised thinking and paranoid delusions.
- Expressed emotion
- Focuses on the course instead of the cause.
- Level of emotion expressed towards the patient.
- Consists of verbal criticism, hostility and over involvement in the patients life including unnecessary self-sacrifice.
- This is a serious source of stress, and therefore causes relapse often.
15
Q
Evaluation of Family Dysfunction (2 S + 1L)
A
Strengths:
- Supporting research: Adoptive parents
- Study follows children adopt from 19,000 Finnish mothers with SZ. Adoptive parents were assessed on their parenting style.
- A parenting style was implicated in the development of SZ (only for the children also with a genetic risk, not the control).
- These findings suggest the communication styles and relationships within families of those with and without SZ are quite different
- This validates the claim family communication may be a factor in the development of SZ
- Practical application: Family therapy treatment
- We can help families manage their levels of hostility or expressed emotion through family therapy
- Also offer guidance on how to help the schizophrenic
- Shown to be effective
- Therefore helps the patient not relapse, benefiting their health and the economy (NHS) as they don’t have to spend more money on them.
Limitation:
- Methodological problems with research
- Research is based on clinical observations and case studies of families which are often subjectively assessed (family members are asked to self-report/review the family)
- Therefore, lack of direct empirical evidence and their answers could be subject to social desirability.
- Therefore, validity is questioned
