Chapter 10- Schizophrenia Flashcards

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1
Q

Describe the clinical characteristics of SZ:

A

According to DSM-V 5, there are 2 main types of symptoms, positive (excess of normal functioning) and negative (loss of normal function)

  • Positive Symptoms:
    1. Delusions - irrational beliefs that seem real to SZ person, but in actualality are not real. 2 types of delusions: delusions of persecution (false belief that they are being attacked/followed, paranoid in nature) and delusions of grandeur (false belief that they are powerful/important/famous/have special abilities).
  1. Hallucinations - unusual and unreal perceptions of the environment that can be auditory (hearing), visual (seeing), olfactory (smell), tactile (touch). These feel real only to SZ person.
  • Negative Symptoms:
    1. Poverty of Speech (alogia) - reduction in amount and quality of speech, produce fewer words, difficulty spontaneously producing words.
    2. Avolition - reduction of interests and desires and inability to initiate + persist in goal directed behaviour. Reduction in self-initiated involvement in activities available to patient.

Under DSM-V 5 criteria, diagnosis of SZ needs 2 or more +ve or -ve symptoms to persist for at least 6 months.

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2
Q

What are some issues with validity of classification and diagnosis of SZ:

A

Validity = extent to which diagnosis of SZ is accurate diagnosis, and is distinct from other disorders, and the extent to which classification systems like ICD and DSM measure what they intend to measure.

A number of issues make it difficult for classification sys. and diagnosis to be valid:
1. Gender Bias - accuracy of SZ diagnosis dependent on individual’s gender; diagnostic criteria may be more biased towards one gender rather than the other; also, clinicians may base judgements on stereotypical beliefs held about gender (freud believed women had hysteria)
2. Symptom Overlap - symptoms of SZ found in other disorders like depression and BPD (BPD and SZ both have positive symptoms like delusions and negative symptoms like avolition). Therefore, difficult to distinguish accurately SZ from related disorders during diagnosis.
3. Co-morbidity - extent to which 2 or more conditions occur, e.g. people with SZ may also experience depression. This makes it difficult to separate different conditions and deciding which treatments to administer.

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3
Q

What are the evaluations for the issues of validity in the classification and diagnosis of SZ?

A
  • Evidence for gender bias in diagnosis, Loring + Powell ‘95: when group of randomly selected male and female psychiatrists were given a case described as male, 56% gave diagnosis of SZ, and when given a case described as female, ony 20% gave diagnosis of SZ. It was also found that the gender bias wasn’t evident amongst the female psychiatrists, this suggets that diagnosis of SZ is unfairly influenced by gender of patient and this is prevelant amongst male psychiatrists.
  • Evidence for Symptom Overlap issues in diagnosis, Ellason + Ross ‘95: found great amount of overlap between SZ and BPD, and also another disorder called Dissociative Identity Disorder (DID), with people with DID having more symptoms of SZ than people diagnosed with SZ. This is an issue as it questions whether SZ, BPD, DID are separate disorders or all part of the same spectrum.
  • Evidence for Co-morbidity, Buckley et al 2009: found comorbid depression occurs in 50% of SZ patients, which suggests that there is significant overlap between disorders making SZ diagnosis as a distinct disorder difficult.
  • HOWEVER: criterion validity is whether or not different diagnostic tools like DSM-V 5 and ICD 11 arrive at the same assessment of condition of individual. Cheniaux et al found lack of truth in these supposedly objective measures, as each diagnostic tool was found to diagnose different symptoms. BUT, nowadays, DSM-V 5 has been refined and has evolved with evidence, so diagnosis today is more consistent with ICD.
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4
Q

What are the issues with reliability of classification and diagnosis of SZ?

A

Reliability = consistency of diagnosis when two independent assessors use same classification system given same diagnosis (inter-observer reliability) or whether diagnostic tests are consistent of different occassions, (test-retest reliability).

There seems to be a **culture bias **- this may lead to problems with both reliability and validity of SZ diagnosis, as this is when psychiatrists are influenced by their own culture’s values and expectations when diagnosing patients. If what is seen as unusuale in one culture is not viewed as unusual in another culture, this leads to inconsistent therefore unreliable diagnosis.

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5
Q

Evaluate the issues with reliability of classification and diagnosis of SZ:

A
  • Evidence for cultural bias in diagnosis comes from Copeland 1971, found when UK and USA psychiatrists given description of patient and asked for diagnosis, 69% of USA psychiatrists diagnosed SZ, but only 2% of UK ones did. Suggests diagnosis has low inter-observer reliability between cultures.
  • Some patients are more likely to being diagnosed with SZ than others, suggesting reliability and validity issues; Harrison et al ‘97 reported that African-Caribbean groups were 8x more likely to be diagnosed with SZ than white groups in UK. This suggests psychiatrists may be misinterpreting cultural differences in behaviour as SZ symptoms when they are simply differences in culture. This ethnocentric bias reduces validity of diagnosis. HOWEVER, it could indeed be that genuine differences between cultures is caused by genetic inheritance of SZ. It could represent effects of poorer housing, more unemployment and social isolation commonly experienced by minority groups that may lead them to have SZ.
  • Cheniaux et al 2009 has 2 psychiatrists independently diagnose 100 patients using DSM and ICD. Using DSM, psychiatrist 1 diagnosed 26 people with SZ whereas psychiatrist 2 diagnosed 13. Using ICD, psychiatrist 1 diagnosed 44 people with SZ, whereas psychiatrist 2 diagnosed 24. There is a disparity between diagnosis, ICD diagnoses more people with SZ, and psychiatrist 1 had higher perception of diagnosis.
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6
Q

What is the genetic explanation for SZ?

A
  • Family Studies: confirmed risk of SZ is directly proportional to genetic similarity to relative with SZ. Gottesman ‘91 reviewed 40 twin studies and found 48% concordance for SZ in MZ twins, and 17% concordance for DZ twins. Gottesman also found found that if you have parents with SZ, you are at 47% risk, and if you have sibling with SZ, you are 8% risk. He found that if you have first degree relative with SZ, you are 18x more likely to have SZ. Problems with this research? MZ twins may be treated the same by environment, DZ twins may be treated differently. Also, if both parents have SZ, why not 100% risk? Shows there is some role of environment, maybe using SLT?
  • Candidate Genes: number of different genes trigger SZ, = polygenic. These genes likely code for NTs like dopamine. Ripke et al combined previous data from genome-wide studies of SZ, compared genome of 37,000 SZ poeple with 113,000 controls with no SZ, and found 108 genetic variations that were associated with increased risk of SZ. This also proves that SZ is **aetiologically heterogenous ** as different combinations of genes and factors lead to condition.
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7
Q

What is the Neural Correlates explanation of SZ?

A

Neural Correlate = brain function associated with SZ. Dopamine is related to symptoms of SZ.

The original dopamine hypothesis:
Based on discovery that antipsychotics caused symptoms similar to people with Parkinson’s disease, a condition associated with low dopamine levels (hypodopaminergia). Therefore, it was concluded that SZ is caused by high levels of dopamine (hyperdopaminergia) in subcortical regions of the brain. Excess of dopamine D2 receptors in pathways from subcortex to Broca’s area may explain SZ symptom of speech poverty.

Updated version of dopamine hypothesis:
Davis et al proposed addition of cortical hypodopamingeria (abnormally low dopamine in brain’s cortex) can also explain SZ symptoms, like cognitive problems. Cortical hypodopaminergia leads to subcortical hyperdopamingeria, both high and low levels of dopamine in different regions may lead to SZ.

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8
Q

Evaluate the genetic explanation for SZ:

A
  • Research Support: strong evidence base; family studies like Gottesman show increased risk with genetic similarity to family member with SZ. Adoption studies like Tienari et al show that biological children of parents with SZ have more SZ risk even if they grow up in adoptive family. This shows that some people are more vulnerable to SZ due to their genetic make-up.
  • LIMITATION: clear evidence for environmental factors increasing risk of SZ too; this includes biological and psychological influences, like birth complications and smoking THC rich cannabis in teen years, and childhood trauma, leaving people vulnerable to mental health problems, and perhaps SZ. Morkved at al found that 67% people with SZ had at least one childhood trauma, opposed to 38% to matched control group with no psychotic mental health issues. Therefore, genetic factors alone may not provide complete explanation for SZ.
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9
Q

Evaluate Neural Correlates explanation for SZ:

A
  • Evidence for dopamine: amohetamines increase dopamine and worsen symptoms in SZ people and induce symptoms in non-SZ people (Curran et al). Antipsychotic drugs reduce dopamine activity and reduce intensity of symptoms (Tauscher et al). This strongly suggests dopamine is involved in symptoms of SZ.
  • Limitation of dopamine hypothesis is that there is evidence for central role of glutamate; post-mortem and live-scanning show raised levels of NT glutamate in several regions of brain in people with SZ (McCutcheon et al). This means that many other NTs may also be involved in SZ symptoms, not just dopamine.
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10
Q

What is the biological therapy for SZ?

A

Drug Therapy:
Using ‘antipsychotic drugs’, either for short or long term basis. 2 types of antipsychotics:

  1. Typical Antipsychotics:
    Chlorpromazine, taken as tablets, syrup, injection.. Maximum dosage of 800mg. Positive symptoms of SZ thought to be products of overactive dopamine system, the typical antipsychotic drugs like chlorpromazine are dopamine antagonists, work directly on reducing effects of dopamine, by binding to D2 dopamine receptors. This reduces dopamine’s influence on thought, cognition, behaviour therefore reduces positive symptoms of SZ, like hallucinations.
    Chlorpromazine is an effective sedative as well.

**2. Atypical Antipsychotics: **
Clozapine have been developed with aim of more effective treatment of both positive and negative symptoms of SZ. Unlike typical antipsychotics, these drugs only temporarily block D2 receptors before dissociating to allow normal dopamine transmission. These drugs have lower risk of extreme side effects, have beneficial effect of negative + positive symptoms and suitable for treatment resistant patients.

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11
Q

Evaluate the biological therapy for SZ:

A
  • Evidence for effectiveness of Chlorpromazine comes from placebo research: Thornley et al reviewed studies comparing effects of Chlorpromazine to control groups where patients receieved a placebo. Found that chlorpromazine was associated with reduced symptom severity and reduced relapse rates. Suggests that typical antipsychotics are medically effective at preventing relapse.
  • Support for benefits of atypical antipsychotics; Meltzer concluded that Clozapine is more effective than typical antipsychotics and that it is effective in 30-50% pf treatment-resistant cases where typical antipsychotics failed. Suggests that atypical antipsychotics are much more effective than typical antipsychotics in treating SZ.
  • Criticism of typical antipsychotics is they are less appropriate for their worrying side effects, about 30% of people taking it develop ‘tardive dyskinesia’, whihc causes patient to suffer uncontrollable, repetitive movements like grimacing, blinking and jaw clenching. It makes the patient’s life more difficult and also may increase costs.
  • Issues with patient compliance, side effects may effect patient is willing to take drug, on average 50% of SZ patients stop taking their own medication after a year, 75% after 2 years. This causes something called ‘Revolving Door Syndrome’, where patient is reluctant to take their medication and regularly relapses before being admitted for care, treated with drugs again, and then only to avoid taking them when released. This raises doubts over how appropriate antipsychotic treatments are if they rarely lead to long term and stable recovery.
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12
Q

What is the Family Dysfunction explanation (psychological) for SZ?

A
  • The schizophrenogenic mother; Fromm-Reichmann proposed psychodynamic explanation for SZ based on accounts from her patients. She noted that many patients spoke of a particular type of parent which she called schizophrenogenic mother, which is a cold, rejecting and controlling person, who tends to create a family climate of tension and secrecy - this leads to distrust that later turns into paranoia delusions, and ultimately SZ.
  • Double-bind theory: Bateson et al agreed that family climate is important in development of SZ, but emphasised role of communication style within family, the developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed signals on what exactly is the wrong thing. They feel unable to comment on unfairness of situation or seek clarification. When they get things wrong, the child is punished by withdrawal of love. This leads them to understand the world as a confusing and dangerous place, and this is reflected in SZ symptoms like disorganised thinking, paranoid delusions. Bateson recognised that this was only a risk factor, not the only factor.
  • Expressed emotion, EE : is the level of emotion, particularly negative, expressed towards patient by their carers (family). EE contains several elements:
    1. Verbal Criticism of patient, with violence
    2. Hostility towards patient, anger + rejection
    3. Emotional overinvolvement in life of patient, including needless self-sacrifice

These high levels of EE directed towards patient are serious source of stress for patient, this is primarily explains relapse in patients with SZ. It has also been argued that EE may trigger onset of SZ in someone who is already vulnerable (diathesis-stress model).

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13
Q

What are is the cognitive explanations (psychological) for SZ:

A
  • Dysfunctional thinking: a cognitive explanation focusses on mental processes, SZ is associated with dysfunctional thought processing. SZ characterised by disruption to normal thought processing; reduced thought processing in ventral straitum is associated with negative SZ symptoms, whilst reduced processing of info in temporal + cingulate gyri are associated with positive SZ symptoms (Simon et al). This shows that decrease in cognitive processes in certain areas provokes SZ symptoms.
  • **Metarepresentation dysfunction: **Fritch et al identified two kinds of dysfunctional thought processes. Metarepresentation, the cognitive ability to reflect on thoughts and behaviour, allowing us to have insight into our own intentions and goals, and interpret other people’s actions. Dysfunction in metarepresentation disrupts our ability to recognise our own actions, thoughts as being a product of one’s own action, explaining hallucinations of hearing voices.
  • Central Control Dysfunction: Frith et al also identified issues with cognitive ability to suppress automatic responses while perforiming deliberate actions. Speech poverty + thought disorder could result from inability to suppress automatic thoughts and speech triggered by other thoughts. People with SZ cannot suppress automatic responses so when speaking, their words jumble due to associations of the words.
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14
Q

Evaluate Family Dysfunction explanation (psychological) for SZ:

A
  • Research Support: evidence linking family dysfunction to SZ; indicators of family dysfunction include insecure attachment and exposure to childhood trauma, like abuse. Read et al did a review and found that adults with SZ are disproportionately more likely to have insecure attachment, particularly type C or D. Read et al also reported 69% women and 59% men with SZ had history of physical and/or sexual abuse. This suggests that family dysfunction make people more vulnerable to SZ.
  • Limitation; poor evidence base of any explanaton. Despite there being evidence for idea of childhood family stress associating with adulthood SZ, almost no support for importance of traditional family theories like schizophrenogenic mother and double bind theory. Both these theories are based on clinical observations from patients and informal assessment of personality of mothers of patients, but no systematic evidence.
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15
Q

Evaluate the cognitive explanations (psychological) for SZ:

A
  • Research support; evidence for dysfunctional thought processing; Stirling et al compared performance on range of cognitive tasks in 30 people with SZ and control group of 30 people without SZ. Tasks included the Stroop task, where PPs had to name font colour of colour words and so had to suppress the tendency to read the words aloud. As predicted by Frith et al central control theory, SZ people took twice as long to name font colours. This shows that the cognitive processes of people with SZ is impaired.
  • Limitation of cognitive explanations is that they only explain proximal origins of symptoms, so what is happening now to produce symptoms. A distal explanation focusses on what initially caused the condition. It is uncelar how genetic variation or childhood trauma might lead to issues in metarepresentation or central control. Therefore cognitive theories on their own only provide partial explanations for SZ.
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16
Q

Explain CBT as a psychological therapy for SZ:

A

CBT for people with SZ takes between 5-20 sessions (longer than most conditions), it aims to tackle both thoughts and behaviour.
CBT helps client sense how their irrational cognitions (delusions) impact on their feelings and behaviour. Just understanding where symptoms come from can be helpful for people with symptoms like hallucinations. If therapis convinces them that voices are not in fact dangerous, and that the voices come from a malfunctioning centre in their own brain, it reassures the patient and allows them to better cope with it. Helps them function adequately.
Delusions can be challenged and CBT can help alleviate anxiety.

17
Q

Explain family therapy as a psychological treatment for SZ:

A

Family Therapy takes place with families as well as identified patient (the person who experiences the family’s conflicts). The therapy aims to improve quality of communication and interaction between family members.
Pharoah et al identified range of strategies that family therapists use to improve functioning of family that has member with SZ.
Reduces negative emotions - reduces level of negative emotion like anger, which leads to stress, reducing stress reduces likelihood of relapse.
Improves family’s ability help - therapist encourages family to form therapeutic alliance where they all agree on aims of therapy, and improve families’ beliefs about behaviour towards SZ.

Burbach proposed model for working with families with SZ.
Phase 1 is sharing basic info and provides emotional support
Phase 2 involves identifying resources including what different family members can/cannot offer
Phase 3 encourages mutual understanding
Phase 4 identifies unhelpful interactions
Phase 5 skills training, like stress management technqiues
Phase 6 is relapse prevention
Phase 7 is maintenance for da future.

18
Q

Evaluate CBT as a psychological treatment for SZ:

A
  • Evidence for strength of CBT; a psychologist reviewed 34 studies using CBT with SZ, concluded that there is clear evidence for small but significant effects on +ve and -ve symptoms of SZ. Other studies have found reductions in frequency and severity of auditory hallucinations. The NICE recommends CBT for SZ. Both research and clinical experience support benefits of CBT for SZ.
  • Limitation is wide range of techniques and symptoms inluded in studies. CBT technique and SZ symptoms vary widely from one case to another, Thomas (2015) found that different studies used different CBT techniques and SZ people with different combinations of +ve and -ve symptoms. Makes it hard to say how effective CBT will be for particular person with SZ.
  • NOT a cure for SZ. Only improves quality of life. Costly. Time consuming.
    *
19
Q

Evaluate Family therapy as a psychological treatment for SZ:

A
  • Evidence for effectiveness, a review of studies found that family therapy was most consistently effective treatments available for SZ, relapse rates reduced, by 50-60%. The NICE recommend family therapy for everyone with diagnosis of SZ. Therefore, family therapy is likely to benefit people with both early and chronic SZ.
  • Further strength: benefits the whole family of SZ person, not just them; therapy isnt just for benefit of identified patient, but also for families that provide bulk of care, by strengthening the functioning of whole family, family therapy lessens negative effect of SZ on other family members and strengthens ability of family to provide support to SZ person. Therefore, this form of therapy has wider benefits beyond obvious positive impact on identified patient.
20
Q

How are Token economies used in the management of SZ?

A
  • Token economy = reward system used to manage behaviour of people with SZ who have developed patterns of maladaptive behaviour through spending long periods in psychiatric wards.
  • Ayllon and Azrin demonstrated token economy, trialled the system in a ward of SZ women, and everytime they carried out a ‘good’ task, they were given a plastic token embossed with ‘one gifft’. These tokens could be swapped for ward priveleges, like being able to watch TV. They found that no. tasks beuing carried out increased.
  • Token economies for SZ was more common in the past when treating SZ was mainly long-term hospitalisation. Nowadays it has declined, due to closure of psychiatric wards and unethicalities raised by restricting rewards to people with mental disorders.
  • Institutionisation develops under prolonged hospitalisation, leading to people developing bad habits like not maintaing good hygeine, stopping socialising etc.
  • Matson et al identified three categories if institutional behaviour dealt by token economies: personal care, condition related behaviours, social behaviours. Modifying these behaviours doesn’t cure SZ, but instead:
    1. Improves QoL within hospital setting
    1. Normalises behaviour so it is easier to adapt back into life in community.
  • In a token economy, small coin-shaped tokens are given out when a desirable behaviour is done; target behaviours are decided on individual basis; tokens themselves have no value, but are swapped for more tangible rewards. Tokens must be administered right after target behaviour performed for best effect.
  • Token economies are a type of behaviour modification using operant conditioning techniques.
21
Q

Evaluate token economies as a management technique of SZ:

A
  • Strength: evidence for effectiveness of token economies for managing SZ; A psychologist 2016 identified seven high quality studies published betwen 1999 to 2013 that examined effectiveness of token economies for chronically ill people in hospital setting; found a reduction in negative symptoms of SZ, and decline in frequency of undesirable traits. Supports value of token economies
  • HOWEVER - 7 studies is small evidence to support effectiveness of technique. Issue with small number of studies is ‘file drawer problem’, leads to bias towards positive published findings because undesirable results have been ‘filed away’. This raises questions over the validity of the studies we have found, if the results are construed, cherry picked, not honest? Is there an honest basis of token economies?
  • Ethical Issues: gives professionals considerable power to control behaviours of patients who are vulnerable due to their SZ. Could possibly impose their own/institution’s own norms on them SZ person, especially if target behaviours are not identified sensitively (restricting pleasures to people who don’t behave as intended could worsen symptoms of SZ) Impacts on personal freedom and short-term reduction of QoL. Therefore, do the drawbacks outweigh benefits???
22
Q

Explain the interactionist approach to SZ:

A

Interactionist app also called ‘biosocial approach’.
This approach acknowledges biological, psychological and social factors in development of SZ. These include genetic vulnerability, neurochemical/neurological abnormality, stress from life, and violent interactions from family.
Diathesis-stress model:
Underlying biological factors may make person vulnerable to SZ, but stress triggers onset for SZ, both of these cause development of SZ according to this model.

Meehl’s Model:
original 1962 model, diathesis was entirely genetic, SZ was result of ‘schizogene’. This led to idea of biologically based ‘schizotypic personality’, characteristics that are sensitive to stress. According to Meehl, if person doesn’t have schizogene, no amount of stress would lead to SZ, but carriers of gene if they experience chronic stress throughout their life (through prescence of schizophrenogenic mother) could result in development of condition.

Modern day diathesis model:
With modern day evidence, diathesis model has evolved. Now it is clear that many SZ is polygenic, no single schizogene. Modern day diathesis involves other factors leading to SZ, like psychological trauma, which could also act as stressor other than stress itself. Read et al proposed neurodevelopmental idea where trauma alters developing brain, and early + severe trauma can affect brain development, leading to SZ.

Modern day understanding of stress:
Originally, stress was seen as psychological in nature, often related to parenting. Today, psychological stress from parenting is still considered important, but the modern definition of stress in relation to diathesis stress model includes any risk that triggers SZ. Recent research into triggers for SZ episode concerned substance abuse, in particular substances high in THC, and can actually make someone 7x more at risk to SZ, due to these chemicals interfering with dopamine system.

Treatment according to Interactionist model:
Since the model acknowledges both bio and psy explanations, both bio and psy treatments can be applied. This interactionist approach is more concerned with pairing the use of antipsychotics with psychological therapies, like CBT.

23
Q

Evaluate the Interactionist approach to SZ:

A
  • Evidence supporting both vulnerability and triggers; large scale study by Tienari et al investigated impact of both genetic vulnerability and psychological trigger, followed 19,000 Finnish children whose biological mothers has SZ. In adulthood this high risk group were compared to control group of adoptees without family history of SZ (low genetic risk), adoptive parents were assessed for child rearing style and found that high levels of criticism, hostility and low empathy were associated with development of SZ only in high risk group. Shows combination of genetic vulnerability and family stress lead to increased SZ risk.
  • Real world application; combination of drug treatment and psychological therapies has been used practically; studies show that combining these two treatments enhances their effectiveness. Tarrier et al randomly allocated 315 PPs to 1. medication + CBT, 2. medication + counselling, 3. control group, only meds. PPs in the two combination groups showed lower symptoms than control group. THEREFORE, clear practical advantage of adopting interactionist approach to SZ.