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Schizophrenia Flashcards

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1
Q

What is S and who is most commonly diagnosed?

A

A serious mental disorder found in 1% of the population, diagnosed more in men than women, in people who live in cities and people categorised as the working class

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2
Q

What are the 2 main classification systems for S?

A

ICD-10 believes 2 or more negative systems must be present for diagnosis
DSM-5 blives 1 positive symptoms is sufficient for diagnosis

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3
Q

What is impaired with patients with S?

A

Reality and insight, an example of psychosis

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4
Q

What does S not have?

A

A single defining characteristic, rather a cluster of unrelated symptoms

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5
Q

What are the 2 positive symptoms of S?

A

ADDITIONAL EXPERIENCES
Hallucinations - unusual sensory experiences, some relating to events in environment, can be experienced in relation to any sense (e.g hearing voices, see things that aren’t there)
Delusions - Paranoid, irrational beliefs, delusions of grandeur and persecution. may believe body is under external control, can lead to aggression, seems normal to them but bizarre to others

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6
Q

What are the 2 negative symptoms of S?

A

LOSS OF USUAL ABILITIES/EXPERIENCES
Avolition - ‘apathy’, finding it difficult to begin or keep up with any goal related activity, reduced motivation. ANDREASON 1982 - 3 signs of avolition; poor hygiene, lack of persistence, lack of energy
Speech poverty - changes in patterns of speech,ICD-10 says negative symptom as reduction in amount and quality of speech, delays too. DSM-5 says positive symptom is SPEECH DISORGANISATION as it adds things does not take away anything

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7
Q

What is reliability and inter-rater reliability?

A

Reliability is about consistency - if diagnosis is reliable then it is consistent over time by different Psychiatrists
Inter-rater reliability - when 2 or more psychiatrists agree on diagnosis of S

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8
Q

What is validity and criterion validity?

A

Validity is the extent to which we are measuring what we intend to measure
Criterion validity - 2 or more different measures to diagnose S arrive at the same diagnosis

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9
Q

What research indicates issues with the reliability of the diagnosis of S?

A

Cheniaux at al 2009 - poor inter-rater reliability
2 separate psychologists who both used DSM-5 and ICD-10 to diagnose 100 patients.
1 diagnosed 26 with DSM compared to the other with 13
1 diagnosed 44 with ICD compared to the other with 24
WEAKNESS AS ILLUSTRATES THAT S DIAGNOSIS CAN LACK RELIABILITY - obviously an issue

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10
Q

What research indicates issues with the validity of the diagnosis of S?

A

Study above (Cheniaux et al) shows poor criterion validity too as it shows more likely to be diagnosed with ICD than DSM. So ICD either overdiagnosis S or DSM underdiagnoses S

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11
Q

What are the 4 factors which cause problems with the diagnosis of S?

A

Co-morbidity
Symptom overlap
Gender
Cultural bias

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12
Q

Why is comorbidity a problem when diagnosing S?

A

Refers to how common a medical condition is. It is the idea that 2 or more conditions can occur together, which questions the validity of their diagnosis as could be a single condition
Buckley at al 2009 concluded that around 1/2 of S patients have been diagnosed also with depression, 47% wth substance abuse, 29% PTSD and 23% OCD
WEAKNESS AS SAYING DOCTORS ARE BAD AT TELLING THE DIFFERENCE OR THE CLASSIFICATION IS WEAK AS COULD BE 1 CONDITION

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13
Q

Why is symptom overlap a problem when diagnosing S?

A

Considerable symptom overlap, e.g. bipolar symptoms include delusions, hallucinations and avolition. Questions validity of diagnosis and classification, patient may be diagnosed under ICD with S and under DSM with bipolar, could suggest S and B are the same condition given the amount of symptom overlaps

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14
Q

Why is gender a problem when diagnosing S?

A

Longenecker at al 2010 reviewed studies and concluded since 198’s men are more commonly diagnosed than women when prior to this there was no difference, could be men have more vulnerability or could be gener bias.
Cotton et al 2009 said women typically function better than men so symptoms could be masked or the idea that they are functioning so well means the idea of them having S is too wild

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15
Q

Why is cultural bias a problem when diagnosing S?

A

African Americans and Afro-Caribbean English people are more likely to be diagnosed in the UK. Rates in Africa are not very high so cannot be genetic vulnerability but in fact cultural bias.
One issue is that positive symptoms are acceptable in some countries as is seen as communication with ancestors, when they report it in this country it is seen as bizarre.
Escobar 2012 said that predominantly white psychiatrists tend to over-interpret symptoms and distrust honestly of black people during diagnosis

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16
Q

What is one weakness straight away of the genetic basis of schizophrenia in the biological explanation?

A

It says it runs in families but families also share the same environment

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17
Q

Who can be used as support for the genetic basis of schizophrenia?

A

Gottesman 1991 - supports association between greater genetic similarity and likelihood of developing S
Large scale family study, pooled data from 40 EU studies between 1920-1987, meta analysis and found likelihood of getting S if identical twin has it is 48%, siblings 9%, parents 6% and general public 1%

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18
Q

What are candidate genes in the genetic basis of S?

A

The idea that not 1 single gene is responsible for S, there are a number of genes associated with S, it is polygenic
AETIOLOGICALLY HETEROGENEOUS - different combo’s of factors leading to same condition

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19
Q

What is some research to support S being polygenic? (Biological explanation for S…)

A

Ripke 2014 - large study combining previous data from genome-wide studies (not focusing on 1 particular gene). Genetic makeup of 37000 patients compared to 113000 controls, found 108 separate variations for risk of S

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20
Q

What is the dopamine hypothesis in the biological explanation of S?

A

Dopamine is a neurotransmitter associated with increased risk of S - it is important in the functioning of several brain systems that may be implicated in the symptoms of S

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21
Q

Where are the 2 explanations for the dopamine hypothesis found?

A

Cortex - hypodopaminergia
Goldman-Rakic et al 2004 found low levels of dopamine in pre-frontal cortex responsible for thinking and decision making - negative symptoms of S
Sub-cortex - Hyperdopaminergia
Original version of D.H focused on high levels of dopamine in sub-cortex, excess of D in Broca’s area associated with poverty of speech and auditory hallucinations

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22
Q

What may it be about the hyper and hypodopaminergia explanations?

A

That they are both correct and both high and low levels of dopamine in different brain regions are involved in the development of S

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23
Q

What are neural correlates?

A

Measurements of structure/function of the brain that correlate with an experience, in this case S. Both positive and negative symptoms have neural correlates

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24
Q

What are the negative symptoms neural correlates?

A

Avolition involves loss of motivation, motivation involves anticipation of a reward, certain brain areas such as VENTRAL STRIATUM are believed to be associated with this anticipation
Juckel at al 2006 - measured activity levels in VS in S patients and found lower levels of activity than control group, this correlation is between activity levels in VS and severity of overall negative symptoms

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25
Q

What are the positive symptoms neural correlates?

A

Allen et al 2007 - scanned brains of patients experiencing auditory hallucinations compared to control group as they tried to identify whether pre-recorded speech was theirs or others. S group made more errors and lower activation levels found in superior temporal gyrus and anterior cingulate gyrus - reduced activity in these areas is a neural correlate

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26
Q

What is one strength of the biological explanation of S?

A

Multiple sources of evidence - Gottesman 1991 shows genetic similarity and risk of S are very closely linked
Tienari 2004 - children of suffers of S are still at high risk even when adopted by non-s sufferers
Ripke 2014 - shows certain variations of molecular levels significantly increase risk of S

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27
Q

What is one strength and one weakness of the dopamine hypothesis? (Used as EVAL for biological explanation)

A

Support for number of sources for abnormal dopamine functioning in S - amphetamines that increase level of dopamine make S worse and can produce symptoms in non-sufferers - Curran et al 2004
HOWEVER
Does not provide a complete explanation for S. Some of the genes in Ripke’s study code for different neurotransmitters such as Glutamate which seems to be another important factor (Moghaddam and Javitt 2012)

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28
Q

What is one weakness of the biological explanation of S?

A

Correlation-causation problem of neural correlates
Does the unusual activity in a region of the brain CAUSE the symptom? Could it be that the negative symptoms mean less info is passed through the VS resulting in reduced activity?

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29
Q

What are the 2 main umbrella’s underneath the psychological explanations of S?

A

Family dysfunction - attempt to link S to childhood experiences in living in a dysfunctional family.
3 factors that increase risk of S - schizophrenogenic mother, double bind theory and expressed emotion
Cognitive explanation - focuses on role of mental processing saying cognitive processes are faulty

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30
Q

What is the schizophrenogenic mother?

A

SCHIZOPHRENIA CAUSING
Frieda Fromm-Reichmann proposed psychodynamic explanation, formed by talking to patients about their childhoods
Mothers were cold, rejecting and controlling, which created an atmosphere of tension and secrecy, which developed into paranoid delusions and then S

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31
Q

What is double bind theory?

A

Gregory Bateson et al believed communication is key
Children may find themselves trapped where they are afraid of doing wrong, but the wrong thing is not clearly communicated, punished with withdrawal of love, feeling the world is confusing and dangerous so patients are confused between what’s reality and whats not. Disorganised thinking and paranoid delusions are the result

32
Q

What is expressed emotion?

A

Level of negative emotion directed towards an individual, including; verbal criticism, sometimes violence, hostility, anger and rejection and emotional over-involvement and needless self-sacrifice
They are very stressful and may lead to relapse or trigger S in high risk individuals

33
Q

What are the 2 dysfunctional thought processes under the cognitive/psychological explanation of S identified by Frith et al 1992?

A

Metarepresentation

Central control

34
Q

What is metarepresentation in the cognitive explanation?

A

Our ability to reflect and understand upon our own thoughts and behaviour - if this fails we do not recognise our thoughts and behaviours as our own - e.g. thinking a tune in their head comes from an external radio, such as speech in a hallucination

35
Q

What is central control in the cognitive explanation?

A

Important cognitive ability to suppress responses, this seems to be malfunctioning in brains of people with S. End up with disorganised speech because they can no longer suppress every little thought as each word triggers new associations

36
Q

What is one strength for family dysfunction as an explanation of S?

A

Evidence to suggest that difficult relationships in childhood are associated with increased risk of S - Read et al 2005 reviewed 46 kids with child abuse and S and concluded 69% of women patients with S had a history of physical and sexual abuse as kids, 59% for men
ADULTS WITH INSECURE ATTACHMENTS WERE MORE LIKELY TO HAVE S - Berry 2008
PATIENTS COULD HAVE DISTORTED IDEAS ABOUT THEIR CHILDHOODS NOW WHICH COULD MEAN THEY HAVE POOR VALIDITY

37
Q

What is one weakness for family dysfunction as an explanation of S?

A

Almost no support for schizophrenic mother and double bind their. Earlier evidence involved assessing mothers personality for ‘crazy-making characteristics’ which is not modern - Harrington 2012
Another weakness is that it leads to parent-blaming which is highly socially sensitive - very subjective

38
Q

What is one strength for the cognitive approach as an explanation for S?

A

Support for the idea that info is processed differently in patients with S - Stirling et al 2006 compared 30 S patients to 18 controls including troop test, patients with S took over twice as long as control group, in line with Frith’s ideas

39
Q

What is one weakness for the cognitive approach as an explanation for S?

A

Links between symptoms and faulty cognition are clear however this does not tell us anything about the origins of the condition. May be that faulty processing is a symptom rather than a cause - cause and effect problem

40
Q

What are the biological treatments for S?

A

Drug therapy - antipsychotics

41
Q

What is the background for biological treatments for S?

A

Most common treatment for S, involving use of anti-psychotic drugs in the form of tablets, syrup and injections (every 2-4 weeks). Treatment may be required long-term or short-term, the 2 categories are typical and atypical

42
Q

What is the most common typical drug for treatment of S?

A

Chlorpromazine
Around since 1950’s, tablet, injection or syrup, max dosage of 1000mg, dosage declined over last 50 years
Strong association with use of typical antipsychotics and dopamine hypotheis

43
Q

How does the typical drug Chlorpromazine work?

A

Acts as an antagonist in the dopamine system - blocks dopamine receptors in the synapses of the brain reducing the action of dopamine.
It normalises neurotransmitters in key areas of the brain which reduces symptoms like hallucinations.
It is also an effective sedative - don’t know why, often used to calm patients with S and other conditions
SYRUP IS ABSORBED FASTER - WHEN THEY FIRST ENTER HOSPITAL NORMALLY GIVEN TO CALM

44
Q

What are the 2 atypical drug for treatment of S?

A

Clozapine and Risperidone

45
Q

What is the background into the drug clozapine?

A

Developed on 1960’s, 1st trialled in 1970’s, was withdrawn for a while due to a few patients dying from blood condition ARANGULOCYTOSIS (deficiency of granulocytes in the blood)
People taking it need to go for regular blood tests - not available as an injection due to side effects

46
Q

How does clozapine work?

A

Binds to dopamine receptors but also serotonin and glutamate receptors, helps to improve mood and reduce depression/anxiety. As it is a mood enhancer it is often prescribed when a patient has a high risk of suicide

47
Q

What is the background into the drug risperidone?

A

Around since 1990’s, developed to be as effective as Clozapine but without such serious side effects, tablet, injection or syrup. Small doses build up to a daily dosage of 4-8mg, 12mg is max dosage

48
Q

How does risperidone work?

A

Binds to dopamine and serotonin receptors but dopamine stronger so this is why you need a smaller dose, as you give a lower amount there are fewer side effects

49
Q

What is a strength to drug therapy to treat S?

A

Evidence of effectiveness -
Typical - Thornley et al 2003 compared C to a placebo and found in 13 trials, 1121 participants showed C was associated with better overall functioning and reduced symptoms & relapse rate was lower
Atypical - Meltser 2012 found C is more effective than typical antipsychotics as 30-50% of cases where typicals failed, atypicals worked
STUDIES COMPARING THE TYPES OF ATYPICAL HAVE BEEN INCONCLUSIVE, AS IT MAY BE THAT ONE PATIENT RESPONDS BETTER TO ONE THAN ANOTHER

50
Q

What is a weakness to drug therapy to treat S that all drugs hold?

A

Side effects, such as TARDIVE DYSKINESIA - involuntary facial movements and NEUROLEPTIC MALIGNANT SYNDROME (NMS) which can be fatal
Also with atypical drugs you still have to have regular blood tests

51
Q

What is a theoretical issue of drug treatment for S?

A

Our understanding of mechanism of antipsychotics comes from the dopamine hypothesis (too much dopamine in subcortex of brain) however evidence suggests there is too LITTLE and therefore how do antipsychotics help S if this is the case?

52
Q

What is a weakness of drug treatment for S?

A

Evidence that challenges usefulness of antipsychotics -
Healy 2012 suggested some successful trials have data published more than once and therefore exaggerates positive effects. Also suggested that antipsychotics have a powerful calming effect but this is not the same as reducing severity of psychosis

53
Q

The chemical cosh argument is a weakness of drug treatment for S. Why?

A

It is widely believed that antipsychotics have been used in hospitals to calm patients so they work well with staff rather than for patients benefits - this practise, approved by NICE, is seen by some as human rights abuse

54
Q

What are the 3 psychological therapies for treating S?

A

CBT - cognitive behaviour therapy. tends to be between 5-20 sessions individually or in small groups. Aims to help patients identify irrational thoughts and challenge them
Family therapy - involves family unit in therapeutic setting, designed to improve nature of interaction and communication within the unit. Reduce levels of expressed emotion too
Token economies - based on operant conditioning, involves use of positive reinforcement

55
Q

What is the main concept of CBT for S in the psychological therapy?

A

TARRIER - coping strategy enhancement
Builds on patients existing coping strategies for S. the 2 types are;
Positive self-talk and behavioural relaxation techniques
The 2 parts to the therapy are;
Develop rapport with client and identify psychotic symptoms and existing strategies
Target specific symptoms and find strategies to deal with them. e.g. loud music to block out voices
DELUSIONS ARE CHALLENGED TO SEE BELIEFS ARE NOT BASED ON REALITY

56
Q

What study supports CBT as a treatment for S?

A

Turkington 2004 - challenges a patients paranoid delusions about the mafia wanting to kill him

57
Q

What is one strength of CBT as a treatment for S?

A

Evidence for effectiveness - Jauhar et al 2014 reviewed results of 34 studies of CBT for S and found CBT had a significant but fairly small effect on positive and negative symptoms
Overall there is modest support for CBT but S remains one of the harder mental health disorders to treat

58
Q

What is one weakness of CBT as a treatment for S?

A

Improves quality of life but does not cure. Allows patients to make sense of and challenge their symptoms but failure to cure is a weakness

59
Q

According to Pharoah et al 2010 how does family therapy work?

A

Range of strategies to aim to improve functioning of a family with a member with S;
1) Forming a therapeutic alliance
2) reducing stress of caring with a relative with S
3)improves ability of family to anticipate and solve problems
4) reduction in anger and guilt of family members
5) helping balance caring for patient and maintaining own lives
6) improving families beliefs and feelings towards S
THIS REDUCES STRESS LEVELS AND EE LEVELS WHILST INCREASING PATIENTS CHANCES OF COMPLYING WITH MEDICINES AND REDUCES RELAPSE AND READMISSION TO HOSPITAL

60
Q

What does family therapy also consider?

A

Double bind theory - states S is caused by mixed messages from parents causing them to develop an incoherent version of reality - influences symptoms of S such as social withdrawal

61
Q

What is one strength of family therapy for S?

A

Evidence for effectiveness - Pharoah et al concluded there is moderate support to show family therapy significantly reduces hospital readmission over the course of a year and improves quality of life. However, they noted different studies were inconsistent and there were problems with some evidence, overall fairly weak evidence

62
Q

What is one weakness of family therapy for S?

A

Alternative therapy’s may be more effective for people who do not like to talk in regular therapy. Art therapy allows people to access and express feelings through a different medium, it is recommended by NICE providing there is a qualified art therapist who has worked with people with S
IT IS UNLIKELY 1 TYPE OF TREATMENT WILL ADDRESS ALL OF S’S SYMPTOMS

63
Q

How does token economy work as a psychological treatment for S?

A

Reward systems are used to manage a patients behaviour, according to individual behavioural issues. Helps those who have developed maladaptive behaviour from being institutionalised for a long time, therapy does not cure but modifies bad habits so they can live outside a hospital setting
Immediacy of a reward prevents ‘delay discounting’.

64
Q

What do tokens in token economy therapy not have?

A

Value themselves, they can be used to gain more tangible rewards. They are secondary reinforcers as they only have value once the patients learn they can be used to obtain rewards

65
Q

What study is there to support token economies?

A

Ayllon and Azrin 1968 - found the system worked to improve a wide range of prosocial behaviours in schizophrenics, but did not reduce the frequency or intensity of positive symptoms.
THEY STATED THE SYSTEM WORKED SUCCESSFULLY AS GOAL WAS NOT TO CURE BUT TO IMPROVE DAILY BEHAVIOUR WITHIN A HOSPITAL

66
Q

What is one weakness of token economies as a psychological treatment for S?

A

Ethical issues - Token economy requires patients to adhere to desired behaviours in order to gain the tokens. This proves much harder for those with more severe symptoms. This shows a clear discrimination for those with severe symptoms

67
Q

What does the diathesis stress model suggest about schizophrenia?

A

Diathesis (vulnerability) stress (negative psychological experience) model suggests there is a genetic vulnerability to S however a stress trigger is needed for the condition to be developed - 1 or more underlying factors make someone vulnerable

68
Q

What does the interactionist approach state about how S is developed?

A

Complex mix of 3 essential interacting factors. Biological - genes, neurochemical and neurological
Psychological - stress, poor interactions with family
Societal factors - drugs, alcohol, daily hassles

69
Q

What was the old interpretation of the interactionist model?

A

Meehl’s model (original) 1962
Stated vulnerability was entirely genetic as a result of the ‘schizogene’, led to development of schizotypic personality, where one factor was stress
If you do not have the schizogene, no amount of stress would lead to S.
However, having a schizophrenogenic mother could result in development of S

70
Q

What is the modern understanding of the diathesis stress model?

A

Clear now many genes increase genetic vulnerability - there is no schizogene (Ripke 2014).
View on psychological trauma becoming the diathesis rather than stress according to Ingram and Luxton 2005
Read et al 2001 proposed neurodevelopmental model where early trauma such as child abuse alters the brain so the hypothalamic-pituitary-adrenal (HPA) system becomes overactive, making you more vulnerable to later stress

71
Q

What treatment does the interactionist model say is correct?

A

Both biological and psychological treatments combined. Turkington et al 2006 said it is possible to believe in the biological causes of S but also believe psychological treatments will relieve symptoms - not possible with only 1 treatment
In the UK it is common to treat patients with both types of therapies which may have led to the fast adoption of the model unlike the US

72
Q

What treatment does the interactionist model state is unusual to use alone?

A

Psychological treatments, usually carried out whilst patients are taking anti-psychotics

73
Q

What is one weakness of the interactionist approach?

A

The original model holds a oversimplified view of S
Now seen that there is no 1 schizogene, multiple genes increase vulnerability to developing S.
Now believed vulnerability can be result of early trauma - Houston et al 2008 found childhood sexual trauma emerged as a vulnerability factor whilst cannabis use was the trigger
Shows old idea of diathesis as biological and stress as psychological is oversimple

74
Q

Combination therapies have been found to be useful in the interactionist approach. Explain Tarrier et al 2004’s findings…

A

315 patients were randomly allocated to a medication and CBT group, or to a medication and supportive counselling group or to the control group of just medication. He found patients in 2 combined groups showed lower symptom levels, although there was no difference in rates of hospital readmission. Shows a clear practical advantage to adopting interactionist approach and their idea of superior treatments

75
Q

The role of triggers was also found to be a strength of the interactionist approach. Why?

A

Tienari et al 2004 investigated combo of genetic vulnerability and parenting style with 19000 children adopted in Finland with schizophrenic mothers. Compared to a control group of adopted children with mothers with no genetic risk. Found child-rearing style was characterised by high criticism and conflict levels and low empathy levels but ONLY for those with the pre-existing genetic risk
Suggests both genetic vulnerability and family related-stress are important in the development of S

Psychology A2 (6 decks)

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