Schizophrenia Flashcards
What are the positive symptoms of schizophrenia?
- Hallucinations
- Delusions/paranoia/grandeur
- Disorganised speech
- Disorganised/catatonic behaviours
What is meant by a positive symptom of schizophrenia?
They aren’t “positive” because they’re good
They’re thinsg that are ADDED & which “normal” people dont’ have
What are hallucinations?
Seeing/hearing things
What are Delusions/paranoia/grandeur?
Flase cognitions
What is disorganised speech
“word salad” - unable to form proper sentences
What is disorganized/catatonic behaviour?
Completion/motivation issues
Catatonic behaviour = freezing/ unable to move limbs or respond to speech
What is a negative symptom of schizophrenia?
Known as “defecits” if they’re present for at least a year
These are things that people have lost
What are the two types of drugs used to treat sz?
- Typical
- Atypical
Give an example of a typical antipsychotic
Chloropromazine
Give an example of an atypical antipsychotic
Clozapine
What are sz symptoms also known as?
Psychosis
What is the general name for drugs that are used to treat sz?
Antipsychotics
What are typical antipsychotics like?
- Developed in the 1950s
- Stop hallucinations/delusions
What are atypical antipsychotics like?
- More modern than typical (popular since 1980s)
- Treat +ive AND -ive symptoms
- Work on “ hard-to-treat” patients
What are typical antipsychotics also known as?
Known as dopamine antagonists
Why are typical antipsychotics also known as dopamine antagonists?
(What is the action of typical antipsychotics?)
They bind to D2 receptors but they don’t stimulate them
Block the action of dopamine
What was the conclusion of Kapur et al.’s study on typical antipsychotics?
In order for them to work, 60-75% of mesolimbic pathway D2 receptors must be blocked
These drugs don’t only work on that pathway so there are some pretty horrible side effects
What is the action of atypical antipsychotics?
Act on D2 receptors - help with +ive symptoms
Side effects are less severe too, since blockage doesn’t last as long (rapid dossociation)
What is rapid dissociation?
In atypical antipsychotics?
Doesn’t block D2 recpetors for too long
How are atypical antipsychotics different to typical antipsychotics?
They act on serotonin as well as dopamine
Why are atypical antipsychotics better than typical antipsychotics?
They don’t only reduce SZ symptoms - also reduce depression & anxiety
Great as 30-50% of SZ patients attempt suicide at some point
Which studies led to the development of family therapy?
Batedon et al. (1956) - Double-Bind Theory
Kuipers et al. (1983) - Expressed Emotion
How long does family therapy (for SZ) usually last?
3-12 months
At least 10 sessions
What is family therapy (for SZ)?
Family members educated about SZ & how to help relatives cope
Learn to support the patient through treatment & spot/discuss problems positively
How successful is family therapy for treating SZ?
- So successful that NICE recommends it for all SZ families
- It reduces the chance of relapse by up to 50% (Garety et al. 2008)
What sort of patient is family therapy used to treat?
A patient who suffers from SZ whose family is hostile/overly expressive
These sorts of families cause more relapses in SZ patients
What is used alongside family therapy to treat SZ?
It is commonly used in conjunction with drug therapy and outpatient clinical care
What happens in family therapy?
It is a range of interventions aimed at the family of someone with SZ
Should also involve the patient with SZ if practical
What is the aim of family therapy?
Aims to improve the quality of communication & intervention between family members & reduce the stress of living as a family & so reduce rehospitalsation
What happens during a family therapy session?
During sessions the individaul with SZ is encouraged to talk to their family & explain what sort of support they do & do not find helpful
How does family therapy improve family relationships for the patient with SZ?
It improves relationships within the household as the therapist encourages family members to listen to each other
Also to discuss problems & negotiate potential solutions together
What did Pharoah et al. (2010) suggest about the sucess of the strategies used in family therapy?
He suggested that the strategies reduce stress & expressed emotion
Also increasing the chances of patients complying with medication
It tends to result in a reduced liklihood of relapse & readmission to hospital
What are some strategies used in family therapy to treat SZ?
- Helping patient & family understand & be better able to deal with SZ
- Forming a theraputic alliance w family members
- Reducing stress of caring for relative with SZ & emotional climate in family
- Improving ability of family to anticipate & solve problems
- Reduction of anger & guilt in family members
- Helping family members achieve balance between caring for individual w SZ & maintaining own lives
- Improving families knowledge & beliefs on SZ
- Maintaining reasonable expectations among family members towards SZ
Give 3 evaluations of family therapy treating SZ?
- Ethical benefit to quality of life for patients
- Scientific & objective methodology in supporting research
- Reduces the need to prescribe dangerous drugs with side effects
What are the two pychological explanations for SZ?
- Dysfuncitonal families
- Cognitive explanations
Which pychological explanations for SZ does the Double bind theory come under?
Dysfuncitonal families
Who came up with the Double bind theory?
Bateson et al. (1956)
What is the double bind theory (give example too)?
A child receiving contradictory messages from parents is responsible for children becoming schizophrenic
e.g. mother tells he son she loves him while physically punishing you - child can get confused what reality is
What is the type of parenting called that leads to the Double bind theory?
Who came up with this?
“Schizophrenogenic mother”
Fromm-Reichmann - 1948
What did Fromm-Reichmann say about what a schizophrenogenic mother was like?
“A cold, rejecting and secretive mother creates a family environment that makes paranoia perfectly reasonable. The constant fear of persecution, if generalised, will be diagnosed with SZ”
Who came up with the Expressed Emotion theory for SZ?
Kuipers et al. (1983)
What was Kuipers et al.’s theory for SZ of Expressed Emotion?
- Families w high “emotional expression” can trigger SZ
- These families describe SZ relatives as hostile, critical terms
- EE level in family/friends is strongly correlated with relapse rates
What did Noll (2003) suggest about the Expressed Emotion theory?
Negative emotions can trigger SZ episodes in vulnerable people
Supportive environments may be protective
This is a diathesis stress model
What is the cognitive explanation for SZ’s process for delusions?
Inadequate info processing --> Egocentric bias --> Failure to contextualise events
What is the cognitive explanation for SZ’s process for hallucinations?
Hypervigilance
–>
Higher expectancy of voices
–>
Patients can’t distinguish between sensory info & internal images (Aleman 2001)
–>
Misattribute source of internal images to external sources (Baker & Morrison 1998)
–>
Don’t see disconfirming evidence as they don’t reality check
–>
Patients unable to perform “reality testing” (Beck & Rector, 2005)
What was Beck & Rector’s cognitive reason for why hallucinations occur overall?
Patients unable to perform “reality testing” (Beck & Rector, 2005)
Apply Beck and Rector’s stages for delusions occuring to the biological context that causes them
Cognitive processing biases = Hyperdopaminergia in/around mesolimbic pathway (MLP)
Misattribution of concequences to causes = Hyperdopaminergia in ACC and PFC
Failure to test reality with memory or logic = DLPFC - Hippocampus link atrophy or dysfunction
Link the cognitive process for delusions to the biological explanation for it:
- Cognitive processing biases = ?
Hyperdopaminergia in/around mesolimbic pathway (MLP)
Link the cognitive process for delusions to the biological explanation for it:
- Misattribution of concequences to causes = ?
Hyperdopaminergia in ACC and PFC
Link the cognitive process for delusions to the biological explanation for it:
- Failure to test reality with memory or logic = ?
DLPFC - Hippocampus link atrophy or dysfunction
What was Frith et al.’s study on?
A very influential cognitive study into SZ that described these deficits as the underlying cause of some symptoms
When can a token economy be used?
It is a system used for many psychological conditions
It’s been proven effective for SZ (Ayllon & Azrin, 1968)
What theory is the token economy based on and how is it used?
A behaviourist theory/learning theory
Patients learn to associate +ive behaviours with +ive outcomes
This, it is hoped, will lead to behavioural changes
How is a token economy used to help SZ?
A form of behavioural therapy used int he management of SZ
It is used to shape & manage behaviour so that patients in long stay hospitals are easir to manage
How does a token economy teach SZ patients desirable behaviours?
It involves these desirable behaviours being encourages through SELECTIVE REINFORCEMENT
When are rewards given to a SZ patient in a token economy?
They are given immediately as secondary reinforcers when patients engage in desirable behaviours
e.g. getting dressed in the morning, making a bed, taking medication etc
What is a secondary reinforcer in a token economy?
Reward tokens that are given immediately after the desirable behaviour
What is a primary reinforcer in a token economy?
These are tangible rewards that can be redeemed later
e.g. sweets, magazines or other privileges
How can tokens earned by SZ patients be used?
The tokens themselves have no actual value, they can however be swapped for more tangible rewardsw
(Primary reinforcers)
e.g. sweets, magazines and privileges etc
How does a token economy encourange positive behaviours in SZ patients?
It encourages desirable behaviours to be repeated becuase they have become associated with rewards & privileges
Is a token economy an effective way to deal with SZ?
Modifying these behaviours does not cure SZ, it does however improve patients’ quality of life
It makes it more likely that they can live outside a hospital setting
What is the cycle for a token economy?
- Tokens paired with rewarding stimuli & become secondary reinforcers
- Patient engages in ‘target’ behaviours/reduces inappropriate ones
- Patient given tokens for engaging in these target behaviours
- Patient trades these tokens for access to desirable items/other privileges
What did Kazdin (1977) find about the effectiveness of tokens in the token economy?
The quicker they’re exchanged, the more effective they are
What did Sran & Borrero, (2010) say about rewards in a token economy?
The more variety of rewards available, the better the reinforcers work
How is not knowing how/if the token economy works a limitation?
Researchers question its validity compared to evidence-based medical techniques like drugs or CBTp
However it is still used extensively in some developing countries - where successes are reported
Why is a lack of potential in a token economy a limitation?
Corrigan (1991) highlights the difficulty in monitoring & administering this procedure with anyone outside of hospital
However, used in conjunction with family therapy it can be effective
Why is CBTp used for conditions like SZ instead of regular CBT?
Normal CBT (e.g. for depression) is inappropriate for psychotic disorders (like SZ)
This is because SZ is largely biological & cannot yet be “cured”
How do CBT and CBTp differ?
CBT (for depression) –> We try to change behaviours in order to SOLVE the probelm
CBTp (for SZ) –> We try to change behaviours in order to COPE with the problem
What is the aim of CBTp?
Aims to help patients identify irrational thoughts & challange them (inc. origin of voices) & reality testing to reduce distress
How long does NICE reccommend that CBTp should take place for?
5-20 minute sessions, NICE reccommends around 16 sessions
What model does CBTp use?
The ABCDE model
What does the ABCDE model stand for that is used in CBTp?
A - identifying the ACTIVATING events
B - & resulting BELIEFS that
C - cause emotional & behavioural CONCEQUENCES
D - these beliefs can then be rationalised, DISPUTED & changed through critical collaborative analysis
E - leading tothe EFFECT of restructured beliefs
What is critical collaborative analysis?
The therapist uses gentle questioning to help the patient to understand & changeillogical deductions & conclusions
e.g. “if your voices are real, why can no one else hear them”
How does CBTp help SZ patients?
Rather that “getting rid” of SZ, CBTp helps patients to COPE better with their symptoms as it reduces distress
How do therapists use normalisation in CBTp?
The therapist shares with the patient that many people have unusual experiences such as hallucinations & delusions in many different circumstances
Reduces anxiety & sense of isolationby making patient feel less alienated & stigmatised
Makes posibility of recovery more likely
What are behavioural assignments in CBTp?
Pateints are set these behavioural assignments to improve their general level of functioning
e.g. to shower everyday or to go out & socialise with friends once between now and the next session
What are the stages in CBTp?
- Assessment
- Engagement
- The ABC model
- Normalisation
- Critical collaborative analysis
- Developing alternative explanations
Give 3 evaluation points on CBTp
1 - Lack of availability - NICE found only 1/10 affected people in the UK get it
2 - Good research backing - NICE (2014) better outcomes after 18 months
3 - CBTp may have become over-hyped - Jauhar et al. (2014) found it only had a small effect on SZ symptoms
What are the 4 types of negative symptoms?
- Avolition
- Speech poverty (Alogia)
- Affective flattening
- Anhedonia
What is Avolition?
Reduced motivation/goal-directed behaviour where options are present
What is speech poverty (alogia)?
Loss of fluency/productivity
They don’t know less - they just produce less in a given time
What is affective flattening?
Reduced range/intensity of emotions, even body language
What is anhedonia?
Loss of interest/pleasure, or reduced reaction to things that are pleasurable
Social aspect confused with depression - only physical anhedonia is reliable for SZ
What is reliability (in terms of SZ)?
How consistently clinicians coem to the same conclusion using the criteria (test-retest reliability) & agree with each other (inter-rater reliability)
What is validity (in terms of SZ)?
How far the DSM measures what it says it does & whether a diagnosis represents a clear, distinct “condition” (internal/external)
What are the probelms that occur when diagnosing SZ?
- Symptoms overlap wiht other disorders
- Gender bias in diagnostic criteria (aimed at men)
- Cultural differences (in some cultures you’d be revered if you saw things)
- Comorbidity (which disorder came first and/oris the main cause of illness
When and where did the “Being Sane in Insane Places” case study take place?
1973 - in 4 states
What happened in the “Being Sane in Insane Places” study?
- Covert ppt observation (1973)
- Students reported only “dull thud” - not actual symptom (DSM-II)
- All diagnosed with SZ & hospitalised
- All given meds/treatment & not allowed to leave until the university intervened - in some cases after 2 months
How reliable was the “Being Sane in Insane Places” study?
Inter-rater reliability good byt internal validity was poor
Who conducted the “Being Sane in Insane Places” case study?
Rosenhan - 1973
How did Rosenhan follow up his “Being Sane in Insane Places” study?
- Later phoned the hospitals & said he was sending more fake patients over soon. Over next 2 weeks , 21% patients were labelled as “pseudopatients” & released
- Rosenhan actually never sent any more people to the hospital
How can comorbidity occur?
- Depression, anxiety disorders, PTSD etc
- The symptoms can overlap - disassociative personality disorder especially
- Application issues, if treated with wrong drugs can make condition worse
Is SZ completely biological?
Not completely - thought to be partly biological & partly psychological
This means genes, hormones, brain structure, cog. styles & emotional factors all had good research support
How does SZ being partly biological & partly psychological affect the way we look at the condition?
We must consider all factors: biology & the environment interact to produce SZ
This is known as a diathesis-stress model
What are biological explanations?
Emphasise the role of inherited factors & dysfunction of brain activity int he development of a behaviour or mental disorder
What is the dopamine hypothesis?
Claims that an excess of the NT dopamine in certain regions of the brain is associated w +ive symptoms of SZ
What is genetics?
Inherited factors make certain individuals more likely to devlop a behaviour or mental disorder
Whatis neural correlates?
Changes in nueronal events & mechanisms that result in the characteristic symptoms of a behaviour or mental disorder
What are cognitive explations?
Cognitive explations of mental disorders propose that abnormalities in cog. function are a key component of SZ
What is dysfunctional though processing?
Cog. hobits pr beleifs that cause the individual to evaluate info inappropiately
What is family dysfunction?
The presence of problems within a family that contribue to relapse rates in recovering SZs, including lack of warmth between parents & child, dysfunctional communication patterns & parental overprotection
What are atypical antipsychotics?
Carry a lower risk of extrapyrimidal side effects, have a deneficial effect on -ive symptoms & cog. impairment & are suitable for treatment-resistan patients
What is drug therapy?
Involves treatment of mental disorders such as SZ through the use of antipsychotics to reduce the symptoms of the disorder
What are typical antipsychotics?
They’re dopamine antagonists in that they bind but do not stimulate sopamine receptors & so reduce the symptoms of SZ
What is family therapy?
The name given to a range of interventions aimed at the fmaily of someone with a mental disorder
What is a diathesis-stress model?
Explains mental disorders as the result of an interaction between biological (diathesis) & environmental (stress) influences
What are the two genes implicated in SZ?
- Dopamine receptor genes (D2, DRD2)
- Glutamate receptor genes (AMPA)
They’re both excitatory NTs (learning, mem, motivation & arousal)
What do dopamine receptor genes (D2) do?
Affect no. dopamine receptor sites & transpor proteins for dopamine
What do glutamate receptor genes (AMPA) ?
Affects no. glutamate receptor sites
Especially important in the basal ganglia
What were the 3 studies conducted on genetic factors contributing to SZ?
- Family (Gottesman - 1991)
- Twins (Joseph - 2004)
- Adoption (Tienari et al. 2000)
What happened in Gottesman’s (1991) study on genetic factors affecting SZ?
Study on families - studied concordance rates in children with SZ parent(s) or siblings
- 2x SZ parents –> 46% concordance
- 1x SZ parent –> 13%
- 1x SZ sibling –> 9%
What happened in Joseph’s (2004) study on genetic factors affecting SZ?
Twins - meta-analysis of data on MZ vs DZ twin concordance for SZ
- MZ concordance –> 40.4%
- DZ concordance - 7.4
What happened in Tienari et al.’s (2000) study on genetic factors affecting SZ?
Adoption - compared siblings raised together vs. apart
- 164 adoptees had SZ mothers. Of these, 6.7% also developed SZ
- 197 adoptees were in control grp. 2% developed SZ
Conclusion - genetic liability for SZ is “decisively confirmed”
How does the dopamine hypothesis cause SZ?
- They have too many D2 receptors
- Thier D2 receptors are too sensitive/fire too often
- They produce too much dopamine
What is dopaminergia?
What dopamine’s actions in the brain are known as
What is hyperdopaminergia?
If you have too much dopamine
What is hypodopaminergia?
If you have too little dopamine
What sort of symptoms are hyperdopaminergia assocaited with?
Positive symptoms
What sort of symptoms are hypordopaminergia assocaited with?
Negative symptoms
Give an example of hyperdopaminergia causing +ive symptoms?
Broca’s area produces speech - too much dopamine here leads to the speech & hearing-related symptoms
Give an example of hypordopaminergia causing -ive symptoms?
PFC is the sentral executive - too little dopamine here leads to avolition/catatonia
How do we know that it’s dopamine that causes SZ?
Drugs that decrease dopamine levels reduce SZ symptoms
e.g. chloprozamine or clozapine
What is the action of chloprozamine?
It acts on dopamine
What is the action of clozapine?
Act on dopamine & serotonin
What is the process of dopamine creating poitive symptoms?
Too much dopamine in MESOLIMBIC PATHWAY => positive symptoms
What is the process of dopamine creating negative symptoms?
Too little dopamine in PREFRONTAL CORTEX -> negative symptoms
What did Davis & Khan (1991) find about dopamine affecting SZ?
- Too much dopamine in MESOLIMBIC PATHWAY = positive symptoms
- Too little dopamine in PREFRONTAL CORTEX = negative symptoms
What is the DLPFC?
Dorsilater Prefrontal Cortex
What evidence is there for the dopamine hypothesis?
Patel et al. (2010) - PET scans
Wang & Deutch (2008) - rat study
What did Patel et al.’s (2010) study using PET scans show?
The scans showed lower dopamine levels in the PFC of SZ patients compared to controls
Supports the dopamine hypothesis
What did Wang & Deutch’s (2008) study on rats show?
They lowered rats’ levels of dopamine in their PFC - this impaired their cognition
They then gave them atypical antipsychotics (improve -ive symptoms) & this was reversed
Proved dopamine hypothesis
