schiz EQ Flashcards
define - when a diagnosis is consistent between psychiatrists
reliability
when a person has more than one condition at the same time
co morbidity
when a psychiatrist diagnoses a condition correctly
validity
when two conditions have the same effect in common
symptom overlap
In a study into the effectiveness of a new drug therapy for schizophrenia, researchers
gave one group of patients the new drug and another group of patients a placebo
(a pretend drug).
The researchers were concerned that the outcome of the study might be influenced by
the problems of demand characteristics and investigator effects.
Explain what the researchers could do to eliminate or reduce demand characteristics and
investigator effects in this study.
[4 marks]
reduce demand characteristics:
* not informing the patients which condition they are in (using a single-blind procedure/double-blind
procedure), the new drug or the placebo condition
* allowing all patients to believe they are receiving the new drug/deceiving patients in the placebo
condition by misleading them into believing they are taking the new drug
* ensuring that patients are not aware of the other condition, eg through careful wording of standardised
instructions; making sure patients do not have any contact with patients in the other condition.
reduce investigator effects:
* ensure the person administering the drug does not know which patients are taking the new drug and
which are taking the placebo (using a double-blind procedure)
* anonymising patients, for example, by assigning them a number so the researcher dealing with
patients does not know who is in which condition
* having standardised procedures and conditions so all patients are treated in exactly the same way.
Jay has schizophrenia. His speech is rapid and confused and he changes constantly
from one idea to something completely different. Jay’s father was treated for mental
health problems when he was younger. Jay’s mother worries excessively about Jay.
She often criticises his behaviour and tells him what to do. Jay’s doctor prescribes
medication which seems to reduce his symptoms.
Discuss one or more explanations for schizophrenia. Refer to Jay in your answer.
[16 marks]
AO1 + AO2
biological:
dopamine hypothesis - excess of dopamine in mesambolic pathway (reward pathway) - can lead to pos symptoms eg jays hallucinations
* Jay’s medication reduces symptoms – suggests his neurotransmitter levels/biological make-up as a
factor
jays symptoms like disorganised thoughts and cog defiecnts (neg symptoms) can be explained by deficet of dopamine in aread of pre frontal cortex in areas responsible for descision making and thinking
twin studies - schiz runs in families
jays father had mental health issues perhaps implying that jay inherited schiz - gottesman family study found mz twins have a 48% shared risk of schiz
and DZ have 17% risk
psychological
schizophrenogenic mother - reicman
- * Jay’s mother criticises him a lot – suggests double bind as she alternates between concern and
irritation
overprotective yet cold rejecting controlling
causes tension and secrecy in the family
leads to paranoid delusions and distrust leading to schiz
jay 16 marker ao3
bio:
Strength of Dopamine hypothesis - evidence from drug studies
Weakness of dopamine hypothesis - the role of glutamate
psych:
Discussion point - parent blaming
Cog explanations are
Only a proximal
Explanation
jay 16m
bio strength
dop hyp evidence
P: There is support from a number of sources for abnormal dopamine functioning in schizophrenia.
E: Dopamine agonists like amphetamines that increase the levels of dopamine makes schizophrenia worse and can produce schizophrenia like symptoms in non-sufferers (Curran et al. 2004). Antipsychotic drugs, on the other hand, work by reducing dopamine activity (Tauscher et al. 2014) and are used effectively with many schizophrenic patients.
E: Furthermore, research has suggested that a number of candidate genes implicated in schizophrenia act on the production of DA or DA receptors
L: All of this strongly suggests that dopamine is involved in the symptoms of schizophrenia.
jay 16m
weakness of dop hypoth
P: One limitation of the dopamine hypothesis is evidence for a central role glutamate.
EE: Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of peopl with schizophrenia (McCutcheon et al. 2020). In addition, several candidate genes for schizophrenia are believed to be involved in glutamal production or processing.
L: This means that an equally strong case can be made for a role for other neurotransmitters
Discussion point - parent blaming jay 16m
P: Research into the link between family dysfunction and schizophrenia can pose quite a moral dilemma.
E: Although early explanations for the family-schizophrenia link have no research support, research in this area may be useful in showing that insecure attachment and experience of childhood trauma may affect individual vulnerability to schizophrenia.
E: On the other hand this area of research is very social sensitive as it can lead to parent blaming and adds insult to injury for parents who are having to watch their child experience symptoms of schizophrenia.
L: However, psychologists should not shy away from investigating sensitive topics. With the correct precautions and considerations taken (how will it be used, validity of the research etc.) the benefits of such research will hugely outweigh the costs and will have countless real world applications in attachment, childcare, parenting skills, social work and many more.
Cog explanations are
Only a proximal
Explanation
P: One limitation of cognitive explanations is that they only explain the proximal origins of symptoms.
E:’Cognitive explanations for schizophrenia are proximal explanations because they explain what is happening right now to produce symptoms - as distinct from distal explanations which focus on what initially caused the condition, such as genetic and family dysfunction explanations.
E: What is currently unclear and not well addressed is how genetic variation or childhood trauma may lead to problems with metarepresentation or central control.
L: This means that cognitive theories on their own only provide partial explanations for schizophrenia.
Which of the following best describes neural correlates as an explanation for
schizophrenia? Write A, B, C, or D in your answer book.
[1 mark]
A There is a correlation between brain plasticity and symptoms of
schizophrenia.
B There is a correlation between brain structure and function and symptoms
of schizophrenia.
C There is a correlation between dysfunctional thinking and symptoms of
schizophrenia.
D There is a correlation between size of neurons and symptoms of
schizophrenia.
B
Below are four evaluative statements about token economies as used in the
treatment of schizophrenia. Which statement is TRUE?
Write A, B, C, or D in your answer book.
[1 mark]
A Token economies can be used effectively in any environment.
B Token economies have a positive effect on thinking.
C Token economies help to promote acceptable behaviours.
D Token economies address the cause of the problem.
C
Jack has been diagnosed with schizophrenia. He describes his family
background to his therapist:
‘I could never talk to mum. She fussed over me all the time. I tried to do what
she said, but could never please her. One minute she seemed all affectionate
and the next minute she would make nasty comments. My dad hated all the
arguments and stayed out of it.’
Describe the family dysfunction explanation for schizophrenia and explain how
Jack’s experiences can be linked to the family dysfunction explanation.
[8 marks]
several references to conflict (‘arguments’), communication problems (‘could never talk to
mum’), criticism (‘nasty comments’) and control (‘tried to do what she said’)
- high ee - anger hostility - schiz episode in someone vunerable (eg due to their genes) or relapse
vaughn and leff found in high ee families 51% relpase - this maintians schiz whilst family dysfunction is the cause - bateson
* Jack experiences the double-bind (mother’s behaviour alternates between affection and
nastiness) so Jack doesn’t know how she wants him to behave and becomes confused –
loses touch with reality
theyre trapped and cannot seek clarification
- getting it wrong means withdrawl of love
- created an understanding if the world which is dangerous and confusing
- leads to paranoid delusions and disorganised thinking
- marital skew mother is dominant and dad is submissive and passive
Briefly discuss two limitations of the family dysfunction explanation for
schizophrenia.
[6 marks]
P: Research into the link between family dysfunction and schizophrenia can pose quite a moral dilemma.
E: Although early explanations for the family-schizophrenia link have no research support, research in this area may be useful in showing that insecure attachment and experience of childhood trauma may affect individual vulnerability to schizophrenia.
E: On the other hand this area of research is very social sensitive as it can lead to parent blaming and adds insult to injury for parents who are having to watch their child experience symptoms of schizophrenia.
L: However, psychologists should not shy away from investigating sensitive topics. With the correct precautions and considerations taken (how will it be used, validity of the research etc.) the benefits of such research will hugely outweigh the costs and will have countless real world applications in attachment, childcare, parenting skills, social work and many more.
P: One limitation of cognitive explanations is that they only explain the proximal origins of symptoms.
E:’Cognitive explanations for schizophrenia are proximal explanations because they explain what is happening right now to produce symptoms - as distinct from distal explanations which focus on what initially caused the condition, such as genetic and family dysfunction explanations.
E: What is currently unclear and not well addressed is how genetic variation or childhood trauma may lead to problems with metarepresentation or central control.
L: This means that cognitive theories on their own only provide partial explanations for schizophrenia.
Outline and evaluate the use of antipsychotic drugs to treat schizophrenia.
[8 marks]
ao1
antipsychotics work as dopamine antagonists
they reduce the action of dopamine inareas of the brain assoiciated with symptos of schizophrenia
typical
- Bind to dopamine receptors without stimulating them eg phenothiazene
Blocking dopamine receptors
Bind to them and stop action of da
Reduce positive symptoms in 60% of patients
atypical
-Drugs targeting 3 receptors
- dopamine receptors
- serotonin receptors
- glutamate receptors
They only temp occupy DA receptors before rapidly dissociating and allowing normal dopamine transmission
eg clozapine Usfuel for 85 percent of patients
Reduces both pos and neg symptoms and improves mood
Outline and evaluate the use of antipsychotic drugs to treat schizophrenia.
[8 marks]
ao3
side effects of phenothiazine - Parkinson’s symptoms - muscle tremor
Neuroleptic malignant syndrome - muscle rigidnesss and impairment of autonomic nervous system
Tarditive dyslexia - Involuntary lip smacking
human right issues
may have just been used in hospital scenarios to make patients more calm and easier to handle for the staff benefit not the patient, whilst short term use of antipsychotics is recommed by NICE it can be seen as a human rights abuse raisng ethical concerns into drug treatment
- therotical obj of da
drugs based on excess da in mesambolic pathway, theres ev that leevls of da are too high ir low in toher parts of the brain undermining faith of people that nay progress from dryygs are actually due to the drugs themselves
In the context of schizophrenia, outline what is meant by co-morbidity.
[2 marks]
co-morbidity is where two conditions co-exist in the same individual at the same time/have a
tendency to co-exist alongside each other
so a person with schizophrenia might also at the same time be suffering from another condition,
eg personality disorder, depression, alcoholism, etc.
Explain how symptom overlap might lead to problems with the diagnosis and/or
classification of schizophrenia.
[2 marks]
shared symptoms could lead to an unreliable/incorrect diagnosis (not valid)
because the person may exhibit a symptom typical of schizophrenia (eg delusions) but could
instead have another condition with the same symptom (eg bipolar disorder).
A psychologist investigated cognitive processing in two groups of people with
schizophrenia. People in Group A showed positive symptoms of schizophrenia and
people in Group B showed negative symptoms of schizophrenia. Each person
completed a cognitive task and was given an overall score. The psychologist then
calculated average scores for each group. The results are shown in Table 2 below.
group a
mean - 22.44
median - 22.5
mode - 22
group b
mean - 26
median - 22.5
mode - 16
group A scores indicate a normal distribution
because in Group A the mean, median and mode are almost the same (as in a bell-shaped
curve)
group B scores indicate a (positively) skewed distribution
because the mean is higher than the median/mode or to the right hand side of the distribution.
Discuss one or more biological explanations for schizophrenia.
[16 marks]
ao1
genetic explanation – schizophrenia is heritable/inherited through the generations through
transmission of gene
gottesman family study found mz twins have a 48% shared risk of schiz
and DZ have 17% risk
dop hypothesis - Brain of schiz patients produced more dopamine than that of normal
excess of dopamine in the mesolimbic pathway (reward pathway) - can lead to positive symptoms
or
deficit of dopamine in areas of the prefrontal cortex - areas responsible for thinking, decision making etc leading to negative symptoms (cog impairment, avolition
- falkai et al found -that people w schiz have a abnormally large amounts of dopamine receptors
Concluded that dopamine production is abnormal in all schizophrenics
-brain struc of schiz - less brain tissue and 15% more enlarged ventricles in ventral stritiaum in shiz ppl then normal people
Post motortem studies have shown changes in the amount and distribution of brain cells in some people with schizophrenia
Discuss one or more biological explanations for schizophrenia.
[16 marks]
ao3
research support for genetic vun
biological reductionism
ev from drug studies - d hypothesis
wekaness of dop hypothesis - role of glutamate
Strength - research support for genetic vulnerability
P: There is now very strong evidence for genetic vulnerability to schizophrenia from a variety of sources.
E: Gottesman (1991) shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies (Tienari et al. 2004) shows that children of schizophrenia sufferers are still at heightened risk of schizophrenia if adopted into families with no history of the condition.
E: There is also evidence from studies conducted at the molecular level showing 108 gene variations that increase the risk of schizophrenia (Ripke et al. 2014).
L: These findings don’t mean that schizophrenia is entirely genetic, however it does suggest that genetic factors make some people more vulnerable to developing schizophrenia than others.
Weakness - issues and debates - biological reductionism
P: One limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia.
E: These environmental factors include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al. 2017) and smoking THC-rich cannabis in teenage years.
Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia.
E: In one study by Morkved et al. (2017), researchers found 67% of people with schizophrenia and related psychotic conditions reported at least one childhood trauma as opposed to 38% of a match group with non-psychotic mental health problems.
L: This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
Strength of Dopamine hypothesis - evidence from drug studies
P: There is support from a number of sources for abnormal dopamine functioning in schizophrenia.
E: Dopamine agonists like amphetamines that increase the levels of dopamine makes schizophrenia worse and can produce schizophrenia like symptoms in non-sufferers (Curran et al. 2004). Antipsychotic drugs, on the other hand, work by reducing dopamine activity (Tauscher et al. 2014) and are used effectively with many schizophrenic patients.
E: Furthermore, research has suggested that a number of candidate genes implicated in schizophrenia act on the production of DA or DA receptors
L: All of this strongly suggests that dopamine is involved in the symptoms of schizophrenia.
Weakness of dopamine hypothesis - the role of glutamate
P: One limitation of the dopamine hypothesis is evidence for a central role glutamate.
EE: Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of peopl with schizophrenia (McCutcheon et al. 2020). In addition, several candidate genes for schizophrenia are believed to be involved in glutamal production or processing.
L: This means that an equally strong case can be made for a role for other neurotransmitters
