schizophrenia

Question 1

define schizophrenia

Answer 1

-schizophrenia is a serve mental disorder where contact with reality and insight are impaired. The sufferer may experience delusions or hallucinations

Question 2

concordance rates of schizophrenia

Answer 2

Concordance rate of schizophrenia is higher in men than it is women – onset = late adolescence and early adulthood

Question 3

5 types of schizphrenia

Answer 3

-Undifferentiated –> variation between symptoms and not fitting into a particular type

-Residual –> absence of prominent delusions. A presence of negative symptoms

-Paranoid –> preoccupied with false beliefs (delusions) about being persecuted or punished by someone. Their thinking, speech and emotions remain fairly normal

-Disorganized –> often are confused and incoherent with nonsensical speech. Their outward behaviour may be emotionless/falt etc. Disrupt their ability to perform normal daily activites like preparing meals etc

-Catatonic –> generally immobile physically and unresponsive to the world around them. Their bodies are often very rigid and stiff and unwilling to move. Increased risk of malnutrition etc

Question 4

factors in the development of schizophrenia

Answer 4

-genetics (hereditary) –> passed from parents to children

-Brain chemistry –> imbalance of certain chemicals in the brain e.g dopamine. Dopamine levels affects the way the brain reacts to certain stimuli

-brain abnormality

-environmental factors -> poor social interactions, highly stressful situations or hormonal changes between teen and adult years

-no lab tests to diagnose schizophrenia so x-rays, blood tests etc are used to rule out a physical illness

-early diagnosis of schizphrenia can help avoid or reduce frequent relapses

Question 5

positive vs negative symptoms

Answer 5

-positive symptoms = additions of something (delusions and hallcunations)

-negative symptoms = loss of something (speech poverty and avolition)

Question 6

delusions

Answer 6

Delusions –> beliefs that have no basis in reality e.g belief there are victim of conspiracy.

-Paranoid delusions = someone is attempting to hurt them

-belief they have an imaginary power

Question 7

hallucinations

Answer 7

Hallucinations –> experiencing sensations that arent caused by anything or anybody around the,. Most common is hearing voices. Feels very real to the person experiencing them. No basis is reality/distorted perceptions

Question 8

speech poverty

Answer 8

Speech poverty –> Social withdrawal + difficulty in starting a conversation

-involves reduced frequency and quality of speech

Question 9

avolition

Answer 9

Avolition –> loss of motivation to carry out tasks and lowered activity levels. No interest in socialising or hobbies

Question 10

treatments

Answer 10

CBT + antipsychotics

Question 11

DSM vs ICD

Answer 11

DSM-5 = 2 or more positive or negative symptoms of schizphrenia must be present for a diagnosis (American)

ICD-10 = range of subtypes for schizophrenia e.g paranoid (more international)

• Despite both requiring persistence of symptoms for at least 1 month, the DSM-V has more specific diagnostic criteria and so requires at least 2 or more of delusions, hallucinations, disorganized speech and catononic behaviour, whereas the ICD-10 takes a broader approach to diagnosis, simply stating that “the clinical picture is dominated by relatively stable, often paranoid delusions, usually accompanied by hallucinations

Question 12

Rosenhan (1973)

Answer 12

-experiment into how accurate psychiatrists are at diagnosing abnormality

-involved the use of pseudopatients who stated they kept hearing the word thud in an attempt to gain admission to psych hospital. These patients told the doctors they felt fine and hospital staff failed to detect a single pseudopatients

-41/193 identified as pseudopatients

Question 13

evaluating the reliability and validity of schizphrenia

Answer 13

-symptom overlap between symptoms

-co-morbidity

-gender bias = men more commonly diagnosed than women

-culture bias

Question 14

reductionist nature of clinical diagnosis

Answer 14

Reductionist nature of clinical diagnosis = despite evidence that schizophrenia and bipolar disorder overlap they continue to be treated as separate illnesses

Critics argue there is no diagnostic boundaries in diagnosis

DSM-5 = eurocentric

Question 15

strengths = validity and reliability

Answer 15

-classification = real life applications in treatment

Question 16

limitations = validity and reliability

Answer 16

• There is a significant co-morbidity (high frequency of diagnosis of two disorders together) between schizophrenia and other mental health disorders, such as OCD and post-traumatic stress disorder, as suggested by Buckley et al (2009). These researchers found that 29% of their SZ patients suffered from post-traumatic stress disorder, whilst 50% suffered depression. Particularly in the case of depression, this suggests that if schizophrenia is so frequently diagnosed with other psychiatric disorders, then these two disorders may actually be the same, and so a more accurate and valid method of diagnosis would be to combine these two. Therefore, there are issues of validity in the diagnosis of SZ and attempting to differentiate its symptoms from that of other disorders.

-— There may be gender bias in the diagnosis of schizophrenia, as suggested by Longenecker et al (2010), who could not find an explanation for the sudden increase in the number of male SZ diagnoses made after 1980s. Cotton et al (2009) suggests that because there are no differences in genetic susceptibility for men and women in terms of SZ, then gender bias must be to blame. Dispositional traits of most women, such as high interpersonal functioning and being able to work even when suffering, means that such traits may mask the symptoms of schizophrenia or distort their severity so that they are not serious enough to call for a diagnosis. This means that the current system of the diagnosis of SZ does not account for these biases or differences in functioning between men and women, increasing the likelihood of inaccurate diagnoses.

— A second type of bias which may reduce the validity of the diagnosis of SZ is the problem of cultural bias, as suggested by Escobar et al (2012). For example, African Americans are far more likely to be diagnosed with SZ compared to patients belonging to Western cultures, due to their increased openness about admitting to certain SZ symptoms which may appear normal in their respective cultures. For example, the phenomenon of hearing voices may be considered a desirable sign of increased spirituality and connectedness with ancestors, and so may even be encouraged. However, both classification systems would view this as a hallmark characteristic of SZ and, combined with the potential distrust in African Americans that white psychiatrists may have, could increase the likelihood of false diagnoses.

-poor reliablity = Cheniaux et al 2009 = two psychiatrists independently diagnose 100ppl using both DSM and ICD. Inter-rater reliability was poor = 26 for DSM but 44 for ICD compared to 13 DSM and 24 ICD

Question 17

biological explanations of schizphrenia

Answer 17

-genetic basis, dopamine hypothesis, neural correlates

Question 18

genetic factors

Answer 18

-genetic component that predisposes people to the illness

-schizophrenia runs in familes suggesting evidence for a genetic link because family members tend to share the same aspects of their environment as well as their genes

-adoption studies = Heston 1966 = compared 47 adopted children whose biological mother has schizophrenia = higher risk even when raised in non-schizophrenia families

-higher associations of genetic similarity = higher likelihood of developing schizophrenia

-candidate genes = individual genes are believed to be associated with a level of inheritance. Schizophrenia is polygenic and aetiologically heterogenous (different combinations of factors can lead to the condition)

-Stephen Ripole et al (2014) –> genome-wide studies = 108 genetic variations associated with an increased risk of schizophrenia comparing 37,000 diagnosed and 113,000 controls

-genes affecting functioning of neurotransmitters such as doapamine

-10-20% concodrance rates in DZ twins but 40-50% in MZ twins

-Tierni (2004) = 5.8% in functional families and 36.8% in disfunctional families

Question 19

Gottesman (1991)

Answer 19

Gottesman (1991) demonstrated a positive correlation between the increasing genetic similarity of family members and their increased risk of developing schizophrenia. The concordance rates are as follows = Monozygotic twins (48%), dizygotic twins (17%), siblings (9%) and parents (6%). This, particularly due to monozygotic twins sharing 100% of their genes, strongly suggests a genetic basis and the existence of candidate genes for schizophrenia. However, it is important to note that there are no 100% concordance rates, therefore demonstrating that there are environmental influences acting on the development of SZ e.g. the schizophrenogenic mother and dysfunctional thought processing.

Question 20

strengths = genetic explanation

Answer 20

-multiple sources of evidence for genetic predisoposition = Gottesman 1991, adoption studies. Evidence suggests genetic susceptibility is very important

Question 21

Limitations = genetic explanations

Answer 21

deteministic

diathesis stress

Question 22

dopamine hypothesis

Answer 22

-dopamine is a neurotransmitter, causes neurons to fire in the brain

-original dopamine hypothesis stated that schizophrenia sufferes had an excessive amount of dopamine = too many messages

-amphetamines increase the amount of dopamine = give paranoid behaviour similar to schizophrenia

-antipsychotic drugs block dopamine receptors

-hyperdopaminergia in the subcortex = role of high levels of dopamine in the subcortex e.g brocas area associated with speech poverty

-hypodopaminergia in the cortex = Rakic et al 2004 = role of low levels of dopamine in the pre-frontal cortex is reponsible for negative symptoms of schizophrenia

Goldman Rakic et al (2004) suggested that hypodopaminergia in the prefrontal cortex may be responsible for negative symptoms of SZ, such as speech poverty and avolition. This is because the prefrontal cortex is associated with logical thinking, so abnormally low dopamine levels in this area may impair an individual’s ability to construct grammatical sentences that are focused upon one topic (speech poverty) or the ability to make decisions about how to function in day to day living (avolition).

Question 23

strengths dopamine hypothesis

Answer 23

-practical application = antipsychotic drugs (Tausher et al 2014) –> important role of dopamine for schizophrenia. Genes that increase dopamine = Riker et al

Question 24

limitations dopamine hypothesis

Answer 24

-mixed evidence for dopamine hypothesis –> increase dopamine = schizophrenic like symptoms but not the disorder (Curran et al 2004)

-correlation doesn’t mean causation

Question 25

neural correlates

Answer 25

-patterns of structure or activity in the brain that occur in conjunction with an experience

-negative symptoms = avolition = ventrical striatum = involved in motivation and anticipation of a reward. Judel et al = lower levels o activity = severity of negative symptoms

-Allen et al (2007) concluded that “the mis-identification of self-generated speech in patients with 6 auditory verbal hallucinations is associated with functional abnormalities in the anterior cingulate and left temporal cortex”, as SZ patients’ brain activity was recorded using fMRI during auditory hallucinations, and compared to a control group who identified pre-recorded words as their own or not. Therefore, this suggests that speech poverty (a positive symptom) may be associated with this neural correlate, as shown by the SZ group also making more mistakes compared to the control group

Question 26

strengths neural correlates

Answer 26

-There is evidence supporting the biological and genetic basis of schizophrenia. For example, Brown et al (2002) found that the risk of having offspring with SZ increased by over 1.3% if the father was over 50 years old, compared to if the father was under the age of 25. Therefore, this suggests that mutations in the sections of DNA containing the candidate genes, such as those coding for serotonin and dopamine production specifically, means that SZ is likely to have a strong heritability coefficient and biological basis. This supports the use of family studies and neural correlates as ways of studying and explaining incidence rates of SZ.

Question 27

limitations = neural correlates

Answer 27

-— The main issue associated with the use of neural correlates as a means of explaining schizophrenia is that such evidence is correlational and so does not take into account the ‘third variable problem’, whereby a third unstudied factor could be affecting both outcomes. Taking the example of the link between lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus, and the experience of auditory hallucinations, one explanation would be the lowered activation levels causing the hallucinations, or the hallucinations themselves causing the lowered activation levels. A third possible explanation would be the third variable problem. Therefore, this demonstrates that correlational research cannot be used to reliably demonstrate a ‘cause and effect’ relationship between two variables.

-— The evidence for the dopamine hypothesis can be best described as ‘mixed’. On the one hand, support comes from Tauscher et al (2014) who found that antipsychotics, which act as dopamine antagonists and so reduce dopamine activity by binding to complementary receptors on the post-synaptic membrane, alleviated the symptoms of SZ, suggesting that dopamine has a key role in its development, in line with the predictions of the dopamine hypothesis. On the other hand, some researchers such as Moghaddam and Javitt (2012) have criticised the dopamine hypothesis and biological explanations of SZ as emphasising the role of dopamine too far. For example, the neurotransmitters glutamate and serotonin may also play a key role, as evidenced by the antipsychotic Clozapine acting upon both of these substances and being more effective than other atypical antipsychotics in reducing SZ symptoms, as suggested by Meltzer (2012).

Question 28

antipsychotic medication

Answer 28

-drugs are effective in treating the most disturbing forms of psychotic illness

-helps the person with the disorder function as well as increasing feelings of subjective wellveing

-example = chlorpromainze

-combat hallucinations and thought disturbances which are thought to be the products of overactive dopamine

-Antipsychotic medications are effective treatments for several mental health conditions. This group of medications is divided into two classes: typical and atypical antipsychotic medications. Typical antipsychotics tend to more strongly block dopamine. Atypical antipsychotics have greater effects on serotonin.

Question 29

psychological explanations to schizophrenia

Answer 29

-family dysfunction (poor family communication etc), cognitive explanations (mental processes), dysfunctional thought processing (informational processing is abnormal)

-role of internal mental processes and irrational cognitive thinking in the development of schizophrenia

Question 30

Stirling et al

Answer 30

Stirling et al (2006) –> studied the performance of people with schizophrenia and non-patient groups on the stroop test (neural psychological test to focus on cognitive stimulus). Epople with SZ are slower than control group in cognitive test. SZ patients had increased interference

Question 31

family dysfunction = schizophreogenic mother

Answer 31

-Fredia-Fromm-Reichman (1948) proposed a psychodynamic explanation for schizophrenia based on accounts she heard from her clients about their childhood. The schziophrenogenic mother = cold, rejecting and controlling and tends to create a fairly tense climate

-leads to distrust and paranoid delusions

Question 32

double bind theory

Answer 32

-Gregory Bateson et al (1972) –> agreed that family climate is important to the development of schizophrenia but emphasises the role of communication style within a family

-the developing child regularly finds themselves trapped in situations where they fear they are doing the wrong thing

-feel unable to comment on the unfairness of a situation or ask for clarification

-when getting something wrong the child is often punished by loss of love

Question 33

expressed emotions

Answer 33

-the level of emotion (particularly negative) expressed to a person with schizophrenia by their carers e.g hostility towards the person including anger and rejection.

-emotional over-involvement

-verbal criticism

Question 34

cognitive explanations

Answer 34

-focuses on the role of mental processes –> disruption to normal thought processing

-reduced processing in the ventral striatum is associated with negative symptoms whilst reduced processing of information in the temporal cingulate gyri are associated with hallucinations

-Frith et al (1992) –> 2 types of dysfunctional thought processing could underline some symptoms

-metarepresenation –> cognitive ability to reflect on feelings of thought and behaviour. Allows an insight into intentions and goals. Explains hallucinations as they cannot distinguish between reality

-central control –> cognitive ability to suppress automatic responses while we perform deliberate actions instead. Disorganized speech could result from the inability to repress automatic thoughts

Question 35

strengths of psychological explanations to schizophrenia

Answer 35

-support for family dysfunction as a risk factor –> difficulty in family relationships are associated with an increased risk of schizophrenia. Read et al (2005) reviewed 46 studies of child abuse and concluded that 69% o adult women inpatients with a diagnosis of SZ faced abuse. Barry et al = adults with insecure attachment style more likely to have SZ. However results have been inconsistent.

-strong evidence to support dysfunctional thought processing –> and that faulty central control skills may be responsible for some SZ symptoms, as demonstrated by Stirling et al (2006). The researchers found that SZ sufferers made significantly more mistakes and twice as long to complete the task, compared to a healthy neurotypical control group. However, it should be emphasised that dysfunctional thought processing can only offer explanations for the indirect, proximal causes of SZ, and not the distal causes, meaning that such theories can explain the symptoms but not the origin of SZ. This limits the utility of psychological explanations for schizophrenia.

Question 36

limitations of psychological explanations to schizophrenia

Answer 36

-critisised theory for parent blaming

-lack temporal validity

-little empirical research

-gender bias = focus on schizophrenogeic mother

-weak evidence for family based explanations –> lack of emprical evidence supporting double bind. Both theories are based on clinical observations

-evidence for biological factors is not adequatly considered e.g diathesis stress model

-cannot conclude cause and effect relationship

Question 37

psychological therapies for schizophrenia

Answer 37

CBT, family therapy, token economies

Question 38

family therapy + research

Answer 38

-aims to reduce stress within the family that might contribute to a persons risk of relapse

-reduce high levels of expressed emotions

-all family members share their experiences of schizophrenia

-develop practical coping skills that enable everyone to manage having schizophrenia in the family. Family may feel angry or impatient but are encouraged to express these in constructive ways

-lasts 3-12 months

-recognise signs of relapse and respond quickly

Pharoah et al 2010 = identified a range of strategies that aim to improve the functioning of a family. Reducing stress of caring fo a relative with schizophrenia. Reduction of anger and guilt.

Question 39

CBT + research

Answer 39

-cognitive explanations view the symptoms of schizophrenia as resulting from dysfunctional thought processes leading to fault interpretation of events. CBT assumes delusions influence a persons behaviour in a maladaptive way

-offering cognitive explanations for the existence of delusions and hallucinations can help reduce anxiety

-challenge irrational beliefs by reality testing to reduce distress

-Coping strategy enhancement = cognitive strategies to cope with their hallucinations

-Pilling et al 2002 = conduct meta-analysis of CBT that included a total of 392 ppts and concluded that CBT was effectve in improving the mental state of patients

Question 40

CSE

Answer 40

-specific form of CBT

-identify triggers for schizophrenia e.g people, being on their own etc

-develop strategies such as distraction or relaxation techniques or loud music to drown out voices etc

Question 41

token economies

Answer 41

-neutral rewards that encourage good/positive behaviour

-reward systems used to manage the behaviour of patients with schizophrenia

-for those who have been instiutionalised for a long period of time and who have developed bad habits

-based on the principles of operant conditioning

-staff give patients token when they perform desirable behaviours

-tokens are secondary reinforcers as they only have value when the patient recieves the reward

Question 42

strengths of psychological treatmemts to schizophrenia

Answer 42

-evidence for effectivness e.g Turkington et al (2004), who found that CBT could be used to challenge a patient’s paranoid beliefs about being targeted by the Mafia. More effective behaviours are put into place by questioning the reality of the patient’s beliefs and considering other, more reasonable alternatives. For example, beliefs about the Mafia can be rationalised as simply being based upon a single day where an individual was staring at the patient for an extended period of time, perhaps lost in thought.

-CBT gives patients autonomy in their own treatment = long-term strategies but not always appropriate for everyone

-no side effects = more likely for people to try = more inclusive

Question 43

limitations of psychological explanations to schizophrenia

Answer 43

-subjective = only useful for patients who have the motivation

— None of the three psychological therapies above actually treat the patient and ‘cure’ their schizophrenia. Instead, these therapies simply improve their quality of life through making the symptoms more manageable. For example, token economies increase the likelihood that the patients act in accordance with hospital rules and breaks disruptive patterns of behaviour, whilst family therapies reduce stress within a schizophrenic family and so increase the likelihood of the patient complying with their medical advice, whereas CBT improves the patient’s understanding of their symptoms. This suggests that an interactionist approach towards treatment is best adopted: biological therapies can treat the distal causes of SZ, whilst psychological therapies can treat the proximal symptoms!

• There are serious ethical issues associated with the use of psychological therapies, and specifically concerning token economies. For example, some may argue that the ‘privileges’ that patients receive upon displaying appropriate behaviours are actually rights. Preventing patients from calling home or exercising outside may increase their stress and so aggravate their condition further. In addition, patients with the most severe SZ may find it near impossible to comply with these rules, and so will bear the most negative consequences. Similarly, CBT raises ethical issues because the therapist essentially has control over the patient’s views. This means that by challenging the idea of a Mafia as a controlling government instead, for example, the therapy is infiltrating into the patient’s personal beliefs. These changes can be anything, and not always beneficial.

-alternative psychological therapies

-token economies only help with negative symptoms

Question 44

antipsychotics

Answer 44

Antipsychotics = drugs used to reduce the intensity of symptoms particularly positive symptoms

Question 45

typical antipsychotics

Answer 45

-first generation

-phenothiazines known as chloropromazine –> taken orally, injection or by syrup

-inhibitiory effect

-dopamine antagonists (Working against the action of dopamine)

-They block the action of D2 dopamine receptors on the post-synaptic neuron by binding to them but not simulating them. This reduces the activation of dopamine

-improvement in positive symptoms such as hallucinations (claming + sedative effect)

-strong association between chloropromazine and the dopamine hypothesis

Question 46

atypical antipsychotics

Answer 46

-second generation

-examples = clozapine (reduce negative symptoms) or risperidone (reduce positive)

-introduced to minimise side effects and address both positive and negative symptoms

-dopamine antagonist

-lower affinity = bind temporality to D2 receptors then rapidly dissociate for normal dopamine transmission

-allows endogenous dopamine to work

-reduces positive and negative symptoms

-also a serotonin antagonist = blocks 5-HT(2a) receptor = lead to reduction in negative symptoms like avolition

-The key advantage of Clozapine is the improvements in cognitive functioning and mood which patients experience when taking it. This is particularly useful considering that SZ has a 50% comorbidity rate with depression - however, these benefits may be offset by the serious side effect of agranulocyotis, which is a severe and dangerous leukopenia which has caused several deaths in the past.

Question 47

strengths of biological treatments

Answer 47

-evidence for its effectiveness –> Thornley et al (2003) –> reviewed studies comparing the effects of taking chloropromazine to control conditions who received a placebo. 1121 ppts thought chloroproamzine had association with better overall functioning and reduced symptom severity. Relapse rate was also lower in 512 participants

-Metzler (2012) –> Clozapine is effective 30-50% of treatment resistant cases where typical antipsychotics have failed

Question 48

limitations of biological treatments

Answer 48

-Serious side effects –> The short-term side effects of typical antipsychotics are relatively mild (e.g. agitation and weight gain), whilst the long-term risk include tardive dyskinesia (characterised by involuntary contraction and relaxation of the facial muscles) and neuroleptic malignant syndrome (NMS). NMS is 7 characterised by fever, altered mental states, muscle rigidity and autonomic dysfunction and is thought to be caused by dopamine receptor blockage or central nervous system infections. These side effects are not offset by atypical antipsychotics, where agranulocyotis remains a serious concern for those taking Clozapine, whose state must be continually monitored using blood tests. Therefore, a cost-benefit analysis should be carried out to consider whether the benefit of symptom reduction outweighs the cost of side effects for each specific patient.

-depends on the dopamine hypothesis and the patient themself –> higher than usual levels of activity of dopamine in the subcortex of the brain For example, if antipsychotics appear to alleviate symptoms by reducing the action of dopamine, this makes sense considering the original dopamine hypothesis i.e. hyperdopaminergia in the subcortex. However, this action is not in line with the revised version of the dopamine hypothesis, which suggests that abnormally low levels of dopamine in the cortex are responsible for symptoms. Therefore, a further reduction in dopamine levels should make symptoms worse, and not better. This paradox has caused some to question the validity of the use of antipsychotics, as well as the accuracy of the dopamine hypothesis as an explanation for schizophrenia.

-Despite there being a range of evidence supporting the use of typical (Thornley et al, 2003) and atypical antipsychotics (Meltzer, 2012), these studies still suffer from problems of validity, as suggested by Healy (2012). For example, since Chlorpromazine has particularly powerful sedative effects, then this suggests that studies reviewing the effectiveness of antipsychotics in terms of symptom reduction may actually be measuring how calm and functional the patient appears to be - simply suppressing the symptoms is not a way of controlling them, and so such studies may lack validity due to not accurately assessing the actual effectiveness of antipsychotics in treating the proximal cause of SZ. Secondly, drug companies are selective about what type of information they publish: many focus on the short-term benefits as opposed to the long-term risks, and use inappropriate control groups, such as patients suffering from withdrawal symptoms as they have stopped taking their medication. This distorted focus brings into question, yet again, the validity of research into the effectiveness of antipsychotics.

Question 49

benefit of questionnaries over interviews

Answer 49

anonymity when referncing sensitive topics

Question 50

side effects of typical antipsychotics

Answer 50

-typical antipsychotics = more liable to movement side effects

Question 51

interaction between nature and nurture

Answer 51

-interactionist = interaction between nature and nurture

Question 52

Meehs Original diathesis-stress model (1962):

Answer 52

-in the original diathesis-stress model, the vulnerability was entirely genetic, the results of a single schizogene

-this led to the development of a biologically based schizophrenic personality known as the schizotypic personality. One characteristics of this personality was a high sensitivity to stress

-Meehs argued that for a person without the schizogene, no amount of stress would trigger schizophrenia. However in carriers of the gene, chronic stress throughout childhood and adolescence could lead to the development of schizophrenia

Question 53

diathesis stress model

Answer 53

-theory about how stress and genetics play into the manifestation of different mental disorders and conditions

-high stress and high predisposition significantly increase your risk of developing the disorder

-even high stress but low disposition can increase your risk

-the model states that individuals have varying internal vulnerabilities for schizophrenia

-these the combine with external environmental stressors

-Prescence of schizogenic mother

Question 54

modern understanding of diathesis stress

Answer 54

-it is now clear that multiple genes increase the risk of schizophrenia slightly (polygenic) and there is no single schizogene (Ripke et al 2014)

-Read et al 2001 = proposed neurodevelopmental model in which early trauma alters the developing brain. Child abuse = overactive HPA = more vulnerable to later stress

Question 55

diathesis

Answer 55

-genes or biology (genetic/biochemical)

-cognitive factors

-trauma or environmental stressors in early life which may affect brain development

-situational factors e.g living with a parent with mental illness

Question 56

stress

Answer 56

-divorce

-death in family

-global pandemic

-breakdown of relationship

-academic pressure

-family dysfunction

-drug abuse –> cannabis = alters with dopamine system

Question 57

interactionist treatment

Answer 57

-combined biological and psychological treatments would be the most effective

-patient will be given antipsychotic drugs to rduce symptoms

-can engage with psychological treatments such as CBT or family therapy which enable them to cope with their symptoms

-drug treatment continues while their psychological therapy is in progress

-psychological therapies can also increase compliance with drug treatments

Question 58

Guo et al

Answer 58

Guo et al (2010) = studied patients in the early stages of schizophrenia and found that those who received both drug treatments and a psychological therapy have improved insight into their condition, improved quality of life and social functioning. Continued treatment = less likely to relapse compared to taking antipsychotic drugs alone

Question 59

Holism

Answer 59

Holism:

-interactionist approach takes a holistic approach to explaining and treating schizophrenia

-schizophrenia cannot be explained by reducing it down into simple elements

Question 60

strengths of interactionist approach

Answer 60

-The main evidence for the potential effectiveness of adopting an interactionist approach towards explaining SZ comes from Tienari et al’s 2004 adoption study. The researchers used data from 19,000 Finnish mothers and adoptees who suffered from SZ and compared these findings to a neurotypical group of children adopted across the same period (1960 to 1979). The researchers found that “in adoptees at high genetic risk of schizophrenia, but not in those at low genetic risk, adoptive-family ratings were a significant predictor of schizophrenia-spectrum disorders in adoptees at long-term follow-up”. Therefore, this provides strong support for the diathesis-stress model because the findings demonstrate that a single diathesis or stressor is not enough to trigger the development of SZ, but rather a combination of the two is required.

-There is significant evidence supporting the use of a combination of treatments and the interactionist approach to treating SZ, as suggested by Tarrier et al (2004). These researchers studied 315 patients who were randomly allocated to one of three conditions, where the last control group received no treatment and the first two groups received a combination of psychological and biological treatments. The researchers found that, after an 18 month follow-up, “there were significant 8 advantages for CBT and supportive counseling over TAU (treatment as usual) alone on symptom measures at 18 months but no group difference was seen for relapse or re-hospitalisation. Therefore, adjunctive psychological treatments can have a beneficial long-term effect on symptom reduction”. This suggests that there is a therapeutic advantage in adopting an interactionist approach, further supporting the validity of the diathesis-stress model as an explanation for SZ.

Question 61

limitations = interactionist approach

Answer 61

• The original diathesis-stress model can be considered as an over-simplified explanation of SZ and a reflection of the outdated understanding of that disorder in the mid-twentieth century. For example, Ripke et al (2014) demonstrated that there are over 108 candidate genes, each slightly increasing the risk of SZ, and so there is no single ‘schizogene’. Stress can come in many forms apart from the schizophrenogenic mother, such as high levels of expressed emotion, childhood trauma (Read et al, 2001) and the excessive use of cannabis (Houston et al, 2008). Therefore, the diathesis is not exclusively biological, nor is the stressor exclusively psychological. Hence, this may also be considered a strength in the sense that our current understanding of SZ is far more accurate than the original perspective.

-lack of empirical evidence