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Schizophrenia Flashcards

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1
Q

overview of schizophrenia

A
  1. Diagnosis and Classification

2.Biological explanations
3.Psychological explanations

  1. Drug therapy
    5.Psychological treatments

6.Interactionist Approach

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2
Q

What is schizophrenia (classification and diagnosis)

A

Schizophrenia is a type of psychosis, a severe mental disorder in which thoughts and emotions are so impaired that contact is lost with external reality
(includes positive and negative symptoms)

-must be diagnosed by a “clinical interview” with a psychiatrist + assessment tests to see if symptoms match with those listed on classification index of mental illness (DSM-V)

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3
Q

What are examples positive symptoms of schizophrenia
- reflect excess or distortion of normal functioning

A

HALLUCINATIONS (a sensory experience in which a person can see, hear, smell, taste or feel something that is not there)
1. Auditory H (external voices commanding them to act/ commenting on one’s actions)
2. Visual H (perception of colours, shapes that are not present or of a person)

DELUSIONS (erroneous beliefs that involve misinterpretation of experiences)
-sufferer able to bring reason to support their delusion despite it being bizarre/ absurd
PERSECUTORY D (being spied upon)
DELUSIONS OF CONTROL (believe external forces control their thoughts etc supernatural)

  1. DISORGANISED SPEECH (incoherent speech, result of abnormal thought process)
  2. GROSSLY DISORGANISED (inability to initiate tasks resulting in difficulties in daily living) CATATONIC BEHAVIOUR (reduced reaction to immediate environment, rigid motor activities)
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4
Q

What are examples of negative symptoms of schizophrenia? ( reflect a reduction/ lossnof normal functions, persist even during low/ absent positive symptoms)

A
  1. SPEECH POVERTY (change in patterns of speech)
    -brief empty replies to questions, lessening of speech fluency, difficulty in spontaneously producing words
    - fewer clauses, shorter utterances, associated with long illness
  2. AVOLITION (inability to carry out normal daily activities, little interest in social activities)
    -sharply reduced motivation
    (a) poor hygiene
    (b)lack of persistence in education/work
    (c)lack of energy
    Affective flattening - reduction of intensity of emotional expression
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5
Q

Most common used classification systems are DSM and ICD (FOR DIAGNOSIS)

A

Diagnostic and Statistical Manual (2013)
Criteria A: two or more symptoms (only 1 when delusions are bizarre, inc voice commenting)
Criteria B: Social Dysfunction
(interpersonal and self-care below the level achieved prior to onset)
Criteria C: Duration (continuous signs of disturbance over 6 months inc those in Criteria A) non-active periods, limited to negative symptoms or symptoms in reduced form (odd beliefs)

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6
Q

Why is classification and diagnosis of schizophrenia so important?

A
  1. full understanding ensures that we know what symptoms are, accurately identify
  2. accurate identification leads to right people having treatment, inaccurate ones led to misdiagnosis
  3. common condition, full understanding enables them to try to live their lives normally
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7
Q

Diagnostic reliability refers to the consistency (a diagnosis of schizophrenia must be repeatable)

A

-must be able to reach the same conclusions at 2 different points in time (test-retest reliability) different clinicians must reach the same conclusions (inter-rater reliability)
which is assessed by the degree of positive correlation between scores

-however schizophrenia only has a score of 4 when it has to be 8

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8
Q

Validity (whether an observed effect is a genuine one)

A

-is the diagnosis of the patient as a schizophrenic accurate reflection of the disorder

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9
Q

How is the Rosenhan Study relevant to the diagnosis of SCHZ

A

-showed how flawed and poor the classification and diagnostic process was
-was supposed to be standardised but actually was open to interpretation, more subjective
-checked for inter-rater reliability, it was very poor

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10
Q

Reliability -> cultural differences in diagnoses

A

-African Americans living in UK more likely to be diagnosed, but no info showing it is a genetic trait
-is a result of different social norms

-in African cultures, hearing voices from ancestors is a normal phenomenon (different views on external influence and intervention)
-the experience of hearing voices are different. Interviewed 60 adults with schizophrenia (20 in Ghana, US, India)
-US ones violent and hateful
-Ghana India positive, “playful” or advice

-cultural variation may continue on outcome of condition
“ethnic culture hypothesis’” -> social structure in ethnic minority means individual experiences less stress and fewer symptoms
HAVING A FULL UNDERSTANDING OF VARIATIONS IN EXPERIENCE OF SCHZ MUST BE ESSENTIAL TO HELP ALL PATIENTS (have variations documented)

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11
Q

validity of the diagnosis of SCHZ
1. problem of symptom overlap
(can not identify symptoms belong to what)
2. co-morbidity
(patient has two identifiable conditions or more, make the decision to treat one that is more serious)

A
  1. positive and negative symptoms might also be found in other disorders (depression and BPD) ex. people with DID have more SCHZ symptom than schizophrenics

2.affect validity of diagnosis
2 or more conditions can occur at the same time. (substance abuse, anxiety and symptoms of depression) 50% of patients experience co-morbid depression (OCD)

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12
Q

Gender bias affecting the diagnosis (gender of individual influences chance if being accurately diagnosed)
-more men have been diagnosed

A

research testing gender bias
-patients described as male or no gender (56% diagnosed) labelled as female (20%diagnosed)
gender of clinician and gender of patient might impact diagnosis

-ICD and DSM criteria developed using “male norms” -> women might be mis-diagnosed

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13
Q

Biological explanations for SCHZ

A
  1. genetics
    2.dopamine hypothesis
    3.neural correlates
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14
Q
  1. Gottesman conducted family studies to show the prevalence of schizophrenia between family members
A

Monozygotic twins (100%DNA) compared to dizygotic twins (50%DNA) (higher concordance rates for MN shows greater support for genetics)

Findings:
MZ twins + children with both schz parents (46%)
DZ+ one parent schz (13%)

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15
Q

Briefly outline what typical antipsychotics do

REDUCES DOPAMINERGIC TRANSMISSION

A

dopamine antagonists in that they bind to but do not stimulate dopamine receptors (reducing symptoms of schizophrenia)
-combat positive symptoms of schizophrenia (hallucinations as products of overactive dopamine system)

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16
Q

Briefly outline what atypical antipsychotics do

A

carry low risk of extrapyramidal side effects, beneficial effect on negative symptoms and cognitive impairments

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17
Q

It would be useful to establish what the genetic influence is, but research did not show ONE SPECIFIC IS ENTIRELY RESPONSIBLE

A

-schz is polygenic (involves different gene) and is heterogenous (involves different combinations of genes)
-Human Genome Project -> a large sample was available to indicate link between particular genes and schz in the past
Findings:
108 separate genetic variations are implicated
-> long way from being to identify candidate genes

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18
Q

Evaluation of role of genetics in developing schz

ALL SUGGESTING THAT THERE IS A GENETIC VULNERABILITY TO SCHZ

A

strong evidence from Gottesman and Shields
-> alternative reason for development (environment they share) MZ likely share every aspect of their lives (nature vs nurture) reduces the validity of the genetic link
(uncommon to encounter twins with schz, the small sample size in research studied, inappropriate to generalise to a wider population)

-> try to gain greater clarity on whether genetics or environment is the main cause BY DOING ADOPTION STUDIES (controlling environment by not sharing with schz relative)
Tienari -> 164 adoptees with mother diagnosed with schz
6.7% of them diagnosed with schz
2% of control group (non-schz mother) diagnosed with schz

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19
Q

Dopamine hypothesis -> involves area of neurotransmitter function -> link between dopamine function and schizophrenia (neural correlate)

A

-schz is result of faulty functioning of neurotransmitter function

  1. Hyperdopaminergia
    excess of dopamine in the subcortex and Broca’s Area (associated with positive symptoms such as speech poverty and auditory hallucinations)
  2. Hypodopaminergia
    unusually low levels of dopamine in the prefrontal cortex (thinking decision-making)
    links to negative symptoms
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20
Q

evaluation: supported by evidence from drug treatments

A

A meta-analysis (systematic review identifying an aim and searching for research studies that addressed similar hypotheses) (improve estimates of an effect size of the association and increase observational power) 212 studies concluded all antipsychotic drugs tested in studies were more effective than placebo (positive and negative symptoms) by reducing the effects of dopamine.

But antipsychotic drugs do not alleviate hallucinations in about 1/3 of people
(H and D are present despite dopamine levels being normal) abnormal dopamine production does not explain schz in all patients

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21
Q

Ripke’s study of genetic variations linked to schz found genetic codes associated with function of other neurotransmitters

A

dopamine levels are a common variant BUT NOT THE ONLY NEUROTRASMITTER INVOLVED
other neurotransmitter systems might also produce positive symptoms associated with schizophrenia

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22
Q

the dopamine function theory is too reductionist (focus on explaining schz of 1 neurotransmitter in isolation)

A

dopamine interest with other nt such as serotonin
-better to adapt a holistic approach
-should study combined effects of several neurotransmitters, can be supported by evidence of effectiveness of drug treatments that act on several nt

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23
Q

Neural correlates of schizophrenia (variations in brain structure with intention of finding links between particular parts of brain and behaviours associated with =ve and -ve symptoms in schz)

A

Sis have low functioning of the prefrontal cortex (cognitive deficits linked with -ve symptoms) poor connections with other brain parts

there is a positive correlation between nerve connection between PFC and hippocampus in SZs -> poor memory and cognition, poor hippocampi function also -> dopamine release

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24
Q

neural correlates pt.2 prefrontal cortex grey and white matter

A

Grey matter:
SZs have less grey matter in temporal and frontal lobes

White matter:
SZs have reduced myelination (conduct nerve impulses faster) in white matter esp in connection of PFC to the hypothalamus

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25
Q

evaluation of neural correlates (meta-analysis) (relevance)

A

19 studies comparing SZs with healthy control group

findings
-high reduction in grey matter volume (frontal temporal lobes) active in first stages of the illness
-identifying variations in brain structure using scanning techniques might predict late development of SZ (treated more effectively)

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26
Q

general evaluation

A

biological explanations suggest an alternative way that schz is implicated through gene mutation (sperm cells)
-prevalence of schz when gene mutation occurs -> positive correlation between paternal age and risk of schz
(older parents have an increased risk of sperm mutation)

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27
Q

other factors may be influential

A

biology alone does not account for all variations of schz
(concordance rate for MZ is less than 50%, not entirely biologically controlled)
-> suggests that it provides genetic vulnerability that is triggered by PSYCHOLOGICAL FACTORS
-> DIATHESIS STRESS MODEL reflects on the interaction and influence of both biological and internal factor (interactionist approach)

28
Q

Psychological explanations for schizophrenia

A
  1. family dysfunction
  2. cognitive explanations (dysfunctional thought processing)
29
Q

family dysfunction

A

(a) schizophrenic mother (maternal overprotection and maternal rejection)
(b) DOUBLE BIND THEORY
(c) Expressed Emotions

30
Q

Outline the double bind theory

A

-based on family relationships mixed messages
-Bateson suggested that children who received contradictory messages tend to develop SCHZ (unable to respond effectively bc of contradictions between them + parents)
-For example mother telling son she loves him but looks away in disgust
-ability to respond undermined by contractions as one message invalidates the other
-> prevents development of internally coherent construction of reality, shows itself as typically schz symptoms

31
Q

Outline the theory of “Expressed Emotion”

A

-level of emotion (negative) expressed towards patients by their carers

(a) verbal criticism (physical violence)
(b)hostility (anger and rejection)
(c) emotional over-involvement (needless self-sacrifice)

-> trigger schz, main cause of relapse
-> people with schz have low tolerance of intense environmental stimuli, negative emotional encionrxetn trigger SZ episodes

-> also acts as the STRESSOR in the diathesis-stress model in the interactionist approach

32
Q

Evaluation: linking attachments to schizophrenia

A

69% of women patients diagnosed had history of physical abuse/ sexual abuse
-identified with insecure attachments to primary caregiver more likely to be schizophrenic

BUT IS CHALLENGED as reports of childhood experiments were gathered after symptoms developed (altered perception, inaccurately recalled)

33
Q

methodological problems in research of schizophrenia

A

RETROSPECTIVE studies does not enable monitoring of one’s advance in developing a condition (affects accuracy)
-evidence provided shows relevant evident of family dysfunction being a factor but results are inconsistent
-Tierni’s adoption study shows influence of environmental factors (some adopted children without schz parents developed schz -> adoptive families rated as disturbed)
shows environment as an influential factor n

34
Q

evaluation of expressed emotions

A

Kuipers found that high EE relatives talk more and listen less
(4x likely to relapse in a high EE family than low one)
-> family relatively supportive and emotionally undemanding reduce patients dependence on antipsychotics and relapse rate

35
Q

cognitive explanations for schizophrenia (faulty mental processing)

A
  1. for delusions “impaired insight”
    2.for hallucinations “hypervigilance”
36
Q

cognitive explanations for delusions “impaired insight”

A

poor interpretation of experience leads to delusional thinking (egocentric bias) and jumps to conclusions about external events (linking themselves to everything) -> example flashes of light= signal from God
-unwilling to consider they are wrong

37
Q

cognitive explanations for hallucinations “hypervigilance”

A

focus excessive attention on auditory stimuli (expects a voice)
more likely to misattribute a sound they made or imagined to an external source
can not distinguish between imagined and real stimuli

38
Q

positive evolution of cognitive explanation

A

-> positive symptoms of schizophrenia have their origins in faulty cognition, hallucination is a positive symptom of schizophrenia.

-Delusional patients were found to show various biases in information processing (jumping to conclusions)

  • patients have impaired self-monitoring and experience their own thoughts as voices
    !! supports hypervigilance as an explanation for delusions.
39
Q

strong evidence of dysfunctional information processing in schz

A

compared 30 schz with 18 non-schz on a range of cognitive tests (Stroop test)
(patients would have difficulty suppressing the impulse to read the word as only colour of ink should be identified not the words itself)

Finding:
people with schz took twice as long to name the ink colours compared to control group

40
Q

cognitive explanation -> success of cognitive therapies

A

CBTp -> patients are encouraged to evaluate the content of their delusions + ways to test the validity of faulty beliefs
-effectiveness shown in NICE review od treatments for schz
-compared to antipsychotic meds CBT is more effective in reducing symptoms and improving social functioning

41
Q

Integrated model of schz would be better

A

-vulnerability factors (genetic with exposure to social stressors densities dopamine system)
based cognitive processing of this increased dopamine activity -> paranoia + hallucinations -> development of psychosis
(contributes to stress experienced, leading to more dopamine release…)

42
Q

what are the similarities between typical and atypical antipsychotics and give an example of each

A

Both reduce symptoms of schizophrenia (!!positive)
recommended for initial treatment
They all work by controlling levels of the neurotransmitter dopamine.

Typical antipsychotics e.g. chlorpromazine

Atypical antipsychotics e.g.
clozapine

43
Q

Outline the nature of typical antipsychotics

-year developed
-mg dosage
-argument of brain activity
-brief function, how does it work

A

-developed in 1950s
-the oral dose is up to 100mg a day, but it usually starts at a low dose and increases gradually, 400-800 mg
- 65-75% of the D2 receptors in the brain need to be blocked in order
to reduce schizophrenic symptoms
-A dopamine antagonist (reduces the function of dopamine)
Bind to but do not stimulate the dopamine receptors in the brain, so less dopamine is available to trigger synaptic activity.
-> normalises dopamine levels and has the consequence of reducing positive symptoms such as hallucinations and delusions.

44
Q

Outline the nature of atypical antipsychotics

3 main differences

A

Available since the 1970s

  1. lower risk of extrapyramidal side effects
  2. beneficial effect on negative symptoms
  3. treatment-resistant patients

Rapid dissociation – rapidly released from the receptors to allow normal dopamine transmission

Have a stronger affinity for serotonin receptors and lower affinity for D2
receptors (explains the different effects compared to typical
antipsychotics.

45
Q

Evaluation of drug therapy for schizophrenia
Antipsychotics vs placebo relapse rate

A

comparing relapse rates for antipsychotics and placebos
meta-analysis of 65 studies (6000 patients)
some taken off antipsychotic medication and given a placebo, other remained on regular antipsychotic
-64% placebo relapsed 27% stayed on antipsychotic

HOWEVER use must be weighed against side effects

46
Q

Evaluation of typical antipsychotic drugs
Extrapyramidal side effects

A

-produce movement problems (affect area on brain which helps control motor activity)
ex. Parkinsonian symptoms (Parkinson disease)
more than half of patients experience
involuntary movements (tardive dyskinesia) can occur

47
Q

evaluation of antipsychotics pt.2

A

Antipsychotics are regarded as being effective, Less than 3% of the people with schizophrenia in the UK now
live permanently in hospital.

side effects are major issues -> 40% of schizophrenics have a relapse in the first year and 15% in later years
because they could not cope with the reduced quality of life the drugs caused.

-> Advantages of atypical over typical antipsychotics (more likely to continue their medication)

48
Q

Ethical issues raised typical antipsychotics

A

In the US recently, a large out of court settlement was awarded to a tardive dyskinesia sufferer on the basis of Article 3 of the Human Rights Act
-> no one shall be subjected to inhuman or degrading treatment or punishment.

a cost-benefit analysis of typical antipsychotics would be negative as side effects, deaths and psychosocial consequences were taken into account

49
Q

comparison between typical and atypical antipsychotics

A

meta-analysis of 15 studies to examine the efficiency and side effects of those two drugs
-no sig dif in efficiency but dif in side effects
(typical-> extrapyramidal side effects)
(atypical-> gained more weight)

50
Q

Psychological Therapies

A
  1. cognitive behavioural therapy
    (cognitive explanation: faulty thinking occurs with positive symptoms of disturbed language, thought and perception)
  2. family therapy
  3. token economy
51
Q

cognitive therapy
Aim: identify and correct faulty thinking

A

CBTp (for treating psychosis)

-5-20 therapy sessions
-reflect and identify the origin and change irrational thoughts
-therapists start by developing empathy (the ABC model is applicable: activating event belief and consequences) then challenges beliefs
-normalisation: how delusions impact feelings and behaviours
-critical collaborative analysis (develop alternatives to previous beliefs to let them know their beliefs are not based on reality, reduce anxiety)

52
Q

evaluation of CBTp

A

(a) advantages over standard drugs in terms of social functioning and reduced symptoms (but actually patients receive both at same time-> arguably combined treatment being effective)

(b) argues level of effectiveness is dependent on specific stages (effective after stabilisation of condition after medication) group therapies also preferred more useful)

(c) once they have reasonable experience -> respond more to individual CBTp (must have a thorough understanding of each patient)

53
Q

involves a lot of commitment from patient

A
  • also requires a lot of cooperation between the therapist and patient
    -those who suffer from positive symptoms might not be able to handle CBTp rationally, negative symptoms - are unable to organise and motivate themselves
    -evidence of poor take-up rate and high drop-out rate - makes it less useful
54
Q

the use of meta-analysis might not be able to properly test the effectiveness

A

-lack of random allocation or a single-blind trial was actioned (researcher bias)
-benefits of treatment might be over-stated

55
Q

Family therapy
Aim: to improve quality of communication and interaction between family members

A

-reduces stress within the family (lower chance of relapse) reducing levels of expressed emotions

-treat family members as well as patient with schz (reduced high EE)

(3+ 12 months at least 10 sessions)
-reducing stress of caring for a patient
-reduction of anger and guilt
-improve beliefs about the schz
-improve ability to solve problems

56
Q

evaluation of family therapy

A

-helpful for patients who lack insight
family members may assist (lots of useful info + provide insight of their mood and behaviours) and also educate them to manage the patient’s medication regime (making treatment more cost-effective as clinicians do not have to do it)

  • HOWEVER some family members may remain reluctant (can cause tensions) not admit their problems
57
Q

more evaluation for family therapy

A

-compared family therapy with routine outpatient care
(first 9 months more relapsed rate in routine care compared to family therapy) useful in short term

suggested as key element as family therapy results in reduced relapse rates, symptom reduction

BUT evidence and findings should be treated with caution as some problems might assist in quality of evidence

-must referenced and assessed the same, similar sample sizes
-methodological problems: reliance on self reports (retrospective)

!evidence is scientifically rigorous
- used to influence decisions about national healthcare plans
- If the original data is flawed ->wrong treatment programmes will be put in place

58
Q

Token economy based on behavioural therapy (in a institution often)

A

-based on operant conditioning where clinicians set “target behaviours” (improve patient’s engagement in daily activities)
-target behaviour is reinforced with tokens (secondary reinforcers) and then exchanged for rewards (primary reinforcers more valuable than secondary reinforcer in an institution)

59
Q

Research support

A

reviewed 13 studies of token economy
11 reported there is improvement due to token economy
-prove how token economy is able to increase adaptive behaviours
BUT consist of methodological shortcomings

60
Q

many studies did not have control group

A

success was measured before after comparisons of the behaviour of patients

other factors eg levels of staff attention might be the cause instead of toke economy
-few randomised trials have been completed, the inadequacy of evidence shows how they are less frequently used

61
Q

ethical concerns of token economy

A

Clinicians may exercise control over important primary reinforcers such as food and privacy ( basic human rights and freedom)

  • all human beings have certain basic rights that can not be violated regardless of the positive consequences that might be achieved by manipulating them within a token economy programme.

-other useful in an institutional hospital setting

62
Q

An interactionist approach

A

acknowledges the BIOLOGICAL, PSYCHOLOGICAL and SOCIETAL factors in developing schizophrenia

BIOLOGICAL (genetic vulnerability, neurochemical abnormality)
PSYCHOLOGICAL ( stress from daily activities, poor interaction within the family)

63
Q

Outline the Diathesis-Stress Model in terms of explaining the development of schizophrenia

A

DSM: explains mental disorders as a result of interaction between biological (diathesis) and environmental (stress) influences
-suggests an inherited genetic vulnerability to schizophrenia along with a stress trigger (level of stress they experience) when developing the illness (one or more underlying factors)

64
Q

Diathesis (twin and family studies shows the predisposition to schizophrenia in terms of genetic vulnerability)
Outline the study conducted by Tienari

A

Tienari conducted a study where there is a HIGH RISK and LOW-RISK group
HIGH RISK: children with biological SZ parents
LOW RISK: without genetic risk

Longitudinal study: assessed family functioning by scale, interviewing psychiatrists also kept blind to the status of the biological mother

FIndings: 11 out of 14 schizophrenic adoptees were in the high risk group
high genetic risk adoptees less likely to develop the illness in a healthy (lower rate of lacking empathy, conflict)
-> in high genetic risk -> adoptive family stress was a sig predictor

65
Q

stress

A

Varese ->those who ndergo severe trauma under 16 were 3 times more likely to develop schz
(positive correlation between previous trauma and developing schz in later life)
-> high level of urbanisation (urban vs rural environments) densely populated area (increases frustration and anger)
!!BUT is almost certainly underpinned by
genetic predisposition (most people in cities don’t get SZ)!!

General stress – particularly if you have a high genetic vulnerability to SZ and a high-stress level created by the environment.
->SZs are more sensitive to expressed emotion – they might
react more than the average person to stress.

66
Q

different combination of both nature

A

low vulnerability + major stressors in life
high vulnerability+ minor stressors in life

BOTH PRE-SUPPOSES ADDITIVITY (both add up together)

Psychology Paper 3 (11 decks)

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