Schizophrenia Flashcards

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1
Q

What is schizophrenia?

When is the typical onset?

How common is it?

A

-psychotic mental illness characterized by a loss of reality, often with a breakdown of personality
-usually appears in late adolescence or early adulthood, with a peak onset between 25-30 years
-often appears earlier in men than in women, with twice as many men diagnosed between ages 15-24
-affects approximately 1% of the population

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2
Q

Outline positive and negative symptoms and schizophrenia

A

-positive symptoms involve an excess or distortion of normal functions, including hallucinations and delusions

Hallucinations:
-false perceptions
-most common example is auditory hallucinations, where one or more voices instruct the person to do certain things or make negative comments

Delusions:
-false beliefs, including:
Delusions of persecution: Belief that others want to harm, threaten, or manipulate them (e.g., thinking they’re being spied on).
Delusions of grandeur: Belief in having extraordinary powers or importance (e.g., thinking they’re Jesus Christ).
Delusions of control:Belief that their thoughts or actions are controlled by an external force, often attributed to spirits or radio transmitters.

-negative symptoms involve a loss of normal function
-e.g. speech poverty (reduced speech fluency) and avolition (lack of motivation)
-impacts daily life and social interaction

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3
Q

Outline reliability and validity in terms of schizophrenia

A

Reliability:
-consistency of a diagnosis
-consistency across different psychiatrists = inter-rater reliability
-a diagnosis is reliable if psychiatrists reach the same conclusion independently

Validity:
-accurately measuring what is intended
-for schizophrenia, it questions if diagnostic tools provide the correct diagnosis

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4
Q

Outline Rosenhan’s (1973) study

A

-aimed to see how situational factors affect schizophrenia diagnoses
-8 pseudopatients pretended to have auditory hallucinations, claiming to hear voices saying “empty,” “hollow,” and “thud”
-were admitted to 12 different psychiatric hospitals, where the staff never recognized their sanity
-average stay of 19 days before they were released once they had proven their sanity
-reveals a lack of reliability and validity in psychiatric diagnosis
-staff interpreted normal behaviours as symptoms of mental illness
-highlights influence of situational factors and questions the DSM’s effectiveness

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5
Q

Outline and evaluate comorbidity in the context of schizophrenia

A

-refers to the presence of more than one disorder alongside a primary diagnosis
-e.g. having both schizophrenia and a personality disorder
-overlapping symptoms might lead to misdiagnosis
-so raises questions about the validity of classifying both conditions

Strength - research support
-Buckley et al. (2009) found that approximately 50% of patients with schizophrenia also have depression
-47% have schizophrenia and substance abuse issues
-29% have schizophrenia and post-traumatic stress disorder
-23% have schizophrenia and obsessive-compulsive disorder
-shows that schizophrenia often coexists with other mental illnesses

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6
Q

Outline and evaluate culture in the context of schizophrenia

A

-research indicates significant variation in diagnosing schizophrenia across countries
-Harrison et al. (1984) found that individuals of West Indian origin were over-diagnosed by white doctors in Bristol due to ethnic bias
- Copeland et al. (1971) found that when patients were described to psychiatrists, 69% of US psychiatrists diagnosed them with schizophrenia, whereas only 2% of British ones did
-suggests symptoms of ethnic minorities may be misinterpreted
-raises concerns about the reliability of schizophrenia diagnoses, as ethnicity can influence diagnostic outcomes
-additionally, positive symptoms like hallucinations may be culturally acceptable in some African cultures
-may lead to potential misinterpretation by psychiatrists from different backgrounds
-Escobar (2012) noted that White psychiatrists might over-interpret symptoms in Black patients due to cultural differences in language and mannerisms, as well as stereotypes about mental health in Black communities
-therefore, greater attention to cultural factors in psychiatric diagnosis is essential

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7
Q

Outline and evaluate gender bias in the context of schizophrenia

A

-it is argued that DSM diagnostic categories often diagnoses one gender more than the other

Strength - research support
-Broverman et al. (1970) found that US clinicians associated mentally healthy ‘adult’ behavior with ‘male’ behavior
-leads to women being perceived as less mentally healthy if they didn’t conform to these standards
-suggests androcentrism
-Loring and Powell (1988) showed that 56% of psychiatrists diagnosed male patients with schizophrenia, compared to only 20% for female patients
-however, this bias was not evident among female psychiatrists
-indicates that both patient and clinician gender influence diagnosis

Limitation - clinicians may overlook that males often exhibit more negative symptoms and substance abuse
-in contrast, females have better recovery rates and lower relapse rates
-further affects diagnostic validity
-furthermore, differences in predisposing risk factors between genders can impact vulnerability levels
-explains disparities in the onset of schizophrenia

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8
Q

Outline and evaluate symptom overlap in the context of schizophrenia

A

-considerable overlap between the symptoms of schizophrenia and other conditions, like bipolar disorder
-shares positive symptoms (e.g., delusions) and negative symptoms (e.g., avolition)

Strength - research support for the influence of symptom overlap on reliability and validity of diagnosis
-Ellason and Ross (1995) noted that individuals with dissociative identity disorder (DID) exhibit more schizophrenic symptoms than those diagnosed with schizophrenia
-lowers validity of schizophrenia’s classification and diagnosis
-furthermore, a patient may be diagnosed with schizophrenia according to the ICD, while the DSM might classify them as bipolar
-suggests schizophrenia and bipolar disorder may not be distinct but potentially one condition

Limitation - research contradicts influence of symptom overlap on reliability and validity of diagnosis
-Serper et al. (1999) found that despite significant symptom overlap between schizophrenia and cocaine abuse, accurate diagnoses were still possible
-suggests that symptom overlap doesn’t always undermine diagnostic validity

Limitation - symptom overlap can delay appropriate treatment
-Ketter (2005) highlighted that this is due to the confusion caused by symptom overlap leading to misdiagnosis
-results in increased suffering and higher suicide rates

Strength - useful real world applications
-Ophoff et al. (2011) identified genetic overlap
-found that three of seven genes located on chromosomes associated with schizophrenia were also linked to bipolar disorder
-suggests the potential for developing gene therapies that could treat multiple disorders simultaneously

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9
Q

Outline and evaluate the genetic explanation of schizophrenia, including:
-specific genes

A

-schizophrenia appears to be polygenic
-requires several genes to work in combination
-aetiologically heterogeneous, as different studies have identified various candidate genes that may be involved in its development
-one study found that individuals affected by schizophrenia were more likely to have a defective version of a gene called PPP3CC
-this is associated with the production of calcineurin, a regulator of the immune system
-in contrast, another study identified a gene located on chromosome 5 linked to the disorder in a small number of extended families
-suggests that multiple genes may be implicated in the condition
-remains unclear whether it is one single gene or several working together that contribute to the illness

Limitation - genetic factors cannot be the sole explanation
-concordance rates for identical twins (MZ twins), range from 40% to 60%
-as these rates are not 100%, it indicates that genes cannot wholly explain the disorder
-an individual may be predisposed to schizophrenia
-increases their risk without it being the only cause
-suggests that the genetic account does not provide a full explanation of the disorder
-furthermore, it is biologically reductionist
-focuses solely on genetic factors and overlooks other biological or psychological influences, such as biochemistry or family dynamics

Limitation - difficult to separate the impact of nature and nurture
-both family and twin studies often involve individuals who share the same environment
-may inflate concordance rates, regardless of genetic factors
-possible that the high concordance rates among MZ twins arise due to more similar treatment than dizygotic (DZ) twins or ordinary siblings
-not solely due to genetic influences
-furthermore, even MZ twins who are raised apart share the same prenatal environment
-could also serve as a confounding variable
-makes it challenging to differentiate between genetic and environmental influences

Limitation - family studies often rely on retrospective data when comparing individuals who have already been diagnosed with schizophrenia
-can be unreliable due to potential issues with memory and record accuracy
-however, prospective studies provide more reliable data as they follow individuals over time
-can make comparisons before and after the onset of their condition

Limitation - not everyone with the disorder has a genetic predisposition
-two-thirds of people with schizophrenia do not have a relative with a similar diagnosis
-may be due to possibility of mutations in parental DNA, particularly in paternal sperm cells
-these mutations can be triggered by factors like radiation, poison, or viral infection
-evidence supporting the role of mutations comes from a study that shows a positive correlation between paternal age and the risk of schizophrenia, with risk increasing from around 0.7% for fathers under 25 to over 2% for fathers over 50

Limitation - research into the location of specific genes related to schizophrenia has not produced definitive results
-makes it impossible to understand the underlying mechanisms that connect genetic risk to the disorder

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10
Q

Outline and evaluate the genetic explanation of schizophrenia, including:
-inheritance

A

-evidence suggests that schizophrenia runs in families and is partly genetic
-comes from family studies
-indicate that the closer the genetic relationship to someone with schizophrenia, the greater the chance of developing the disorder

Strength- research support for genetic link from family studies
-Gottesman (1978) reports that while the rate of schizophrenia in the general population is 1%, the chances of first-degree relatives (e.g. parent or sibling) developing the disorder is 12%
-furthermore, if both parents have schizophrenia, there is a 40% likelihood that their child will develop the disorder
-Tsuang et al. (1990) estimated that a first-degree relative of a schizophrenic has a 5-20 times higher risk of developing the illness
-shows that the closer the genetic relationship to someone with schizophrenia, the greater the chance of developing the disorder

Strength - research has found a much higher concordance rate in MZ twins in comparison to DZ twins
-Gottesman and Shields (1972) found a concordance rate of 42% for MZ twins and 9% for DZ twins
-furthermore, a study in London using the Maudley Twin Register by Cardno et al. (1999) found a 40% concordance rate in MZ twins, compared to 5.3% in DZ twins
-shows that MZ twins have an increased risk of developing schizophrenia in comparison to DZ twins, who only share half of their genes
-suggests a degree of heritability

Strength- research support from adoption studies
-Heston (1966) compared 47 children of schizophrenic mothers who had been fostered or adopted during the first month of their life with a control group of 50 children who had been raised in the same homes as these children
-none of the control group developed schizophrenia, but 17% of the children with schizophrenic biological mothers did
-these 47 children were far more likely to have been diagnosed with other psychological abnormalities and to be involved in criminal activities than the control group
-shows that sharing genetic material with a schizophrenic mother increased a child’s chances of having schizophrenia and other mental illnesses
-even when not being raised by her or sharing the same environment

Strength - adoption studies are more effective than family or twin studies
-adoption studies isolate the effects of environmental and genetic factors to look at levels of schizophrenia in adopted children
-can compare them with their biological and adoptive parents

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11
Q

Outline the dopamine hypothesis explanation of schizophrenia

A

-dopamine is an excitatory neurotransmitter in the brain
-original dopamine hypothesis stated that schizophrenia was caused by excessive activity of dopamine
-causes the neurons that respond to dopamine to fire too often and transmit too many messages
-may produce many symptoms of schizophrenia
-hypothesis suggests that schizophrenia is caused by a high density of dopamine receptors and by a high level of sensitivity in these receptors, leading to messages from neurons that transmit dopamine firing too easily or too often
-Snyder (1976) suggests that too much dopamine released into the synapse leads to the onset of schizophrenia

-original version of the hypothesis focuses on the possible role of high levels or activity of dopamine in the subcortex
-e.g. an excess of dopamine receptors in Broca’s area might be associated with poverty of speech and/or the experience of auditory hallucinations (Broca’s area is responsible for speech production)

-updated dopamine hypothesis emphasizes abnormal dopamine systems in the brain’s cortex, particularly the prefrontal cortex (responsible for thinking and decision-making)
-could explain the negative symptoms of schizophrenia
-more probable that both hyperdopaminergia and hypodopaminergia are correct explanations, as high and low levels of dopamine in different regions are implicated in schizophrenia.

-Davis et al. (1991) updated the theory as high levels of dopamine are not found in all schizophrenics
-the modern anti-schizophrenic drug clozapine, which has very little dopamine-blocking activity, works effectively against the illness
-suggests that high levels of dopamine in the mesolimbic dopamine system are associated with positive symptoms
-whereas high levels in the mesocortical dopamine system are associated with negative symptoms

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12
Q

Evaluate the dopamine hypothesis explanation of schizophrenia

A

Limitation - newer drugs such as clozapine are more effective than traditional ones
-they affect dopamine as well as other neurotransmitters, such as serotonin
-appears that several neurotransmitters may be involved in the development of schizophrenia
-therefore, the hypothesis is too simplistic
-furthermore, alongside dopamine and serotonin, some research has implicated glutamate

Strength - practical applications using research
-led to the development of effective treatment options, e.g. clozapine
-much more effective than neuroleptics at relieving schizophrenic behaviour
-suggests that psychiatrists understand the role of neurotransmitters when treating different types of schizophrenia
-improves the patient’s quality of life.

Strength - research shows that schizophrenics have more dopamine receptors
-more neurons firing may lead to an overproduction of messages
-autopsies show that schizophrenics generally have a larger number of dopamine receptors
-Owen et al.: have increased dopamine in the caudate nucleus and putamen in the left amygdala
-Falkai et al. (1988): increased amount of dopamine in the left amygdala
-supports presence of dopamine abnormalities in the brains of schizophrenics
-however, not all schizophrenics, especially those with negative symptoms, have dopamine abnormalities
-dopamine abnormalities seem to be associated more with positive symptoms
-suggests that it may only explain certain aspects or types of the illness
-Davis et al. (1991) argue that the diversity of types and symptoms in schizophrenia implies that other neurotransmitters involved

Limitation - difficulty establishing cause and effect
-uncertain whether high dopamine levels lead to schizophrenia, or whether schizophrenia increases dopamine levels the result of schizophrenia
-Lloyd et al. believe that if dopamine is a causative factor, it may be an indirect one mediated through environmental factors
-may be due to abnormal family circumstances can lead to high levels of dopamine, which triggers the schizophrenia symptoms
-suggests the differences in the biochemistry of schizophrenics could just as easily be an effect rather than a cause of the disorder, so conclusions about factors affecting schizophrenia must be drawn with caution

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13
Q

Outline the neural correlate explanation of schizophrenia

A

-suggests schizophrenia develops due to structural and functional brain abnormalities
-specific brain areas are associated with development of schizophrenia
-evidence was originally limited to post-mortems on brains of schizophrenics
-but research now utilises non-invasive scanning techniques, such as fMRi
-provides a picture of the brain in action through magnetic fields and radio waves
-allows for a comparison of the functioning of the brains of individuals with schizophrenia with that of non-sufferers
-typically achieved by giving tasks to participants associated with types of functioning known to be abnormal in schizophrenia, e.g. social cognition and thought processing

-proposes that schizophrenia is caused by enlarged ventricles (fluid-filled gaps between brain areas)
-enlarged ventricles are especially associated with damage to central brain areas and the prefrontal cortex
-often linked to negative symptoms
-Johnstone et al. (1976) found that schizophrenics had enlarged ventricles, while non-sufferers did not
-implies schizophrenia is related to a loss of brain tissue

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14
Q

Evaluate the neural correlate explanation of schizophrenia

A

Limitation - enlarged ventricles may only explain certain symptoms of schizophrenia
-Weyandt (2006) reported that enlarged ventricles are specifically associated with negative symptoms
-implies that this explanation cannot account for all symptoms and types of the illness
-furthermore, research into the role of enlarged ventricles remains inconclusive
-some non-schizophrenics have enlarged ventricles, and some schizophrenics that don’t
-challenges notion that schizophrenia is solely linked to loss of brain tissue
-as not every person with enlarged ventricles would suffer from the illness

Limitation - difficult to establish cause and effect relationship
-evidence suggests that schizophrenics who do not respond to medication are those with enlarged ventricles
-raises the possibility that enlarged ventricles may be an effect of long-term suffering from schizophrenia rather than a cause
-hence the enlarged ventricles could be a consequence of the illness rather than a contributing factor to its development

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15
Q

Outline what antipsychotics are
Compare typical and atypical antipsychotics

A

-chemical treatment usually prescribed in the form of tablets, intravenous means, or both
-based on the dopamine hypothesis, which assumes that dopamine activity is linked to schizophrenia
-aims to treat psychotic illnesses, such as schizophrenia
-helps individuals improve their functioning and well-being
-however, they do not cure the illness
-can only reduce the symptoms to enable a degree of normal functioning to occur

Differences:
1. Atypicals have less of a risk of extrapyramidal (an area of the brain-particularly the motor function) side effects, such as tardive dyskinesia.
2. Research has indicated that atypicals have a beneficial effect on negative
symptoms.
3. Atypicals are suitable for a treatment-resistant schizophrenic patient, that is they are more likely to work when typicals have failed.

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16
Q

Outline how typical antipsychotics treat schizophrenia

A

-primarily used to combat the positive symptoms of schizophrenia, such as delusions and hallucinations
-e.g. chlorpromazine
-reduces or blocks the effects and actions of dopamine
-hence reducing the symptoms of schizophrenia

-drugs like chlorpromazine are classified as dopamine antagonists
-because they bind to dopamine receptors, particularly the D2 receptors
-reduce their action without stimulating the dopamine system of the brain
-hence antipsychotic drugs can eliminate the hallucinations and delusions experienced by individuals with schizophrenia
-therefore, antipsychotic drugs like chlorpromazine work by blocking dopamine production through blocking the receptors in synapses that absorb dopamine
-ultimately normalise neurotransmission by ensuring that the postsynaptic cells receive less dopamine and cannot be affected by it

Summary:
- They are dopamine antagonists.
- They bind to the dopamine receptors, particularly the D2 receptors.
- In binding to the receptors, they block the stimulation of these receptors, preventing them from absorbing dopamine.
- This normalizes neurotransmission as the postsynaptic cells receive less dopamine

17
Q

Outline how atypical antipsychotics treat schizophrenia

A

-atypical antipsychotics combat the positive symptoms of schizophrenia, and claimed to have beneficial effects on negative symptoms too
-e.g. clozapine
-these drugs work on the dopamine system, but they also block serotonin and glutamate receptors
-drugs like clozapine function by temporarily occupying the D2 receptors and then rapidly dissociating to allow normal dopamine distribution
-means the receptors still receive dopamine, but only in smaller amounts

-atypical antipsychotics are associated with lower levels of side effects, such as tardive dyskinesia, when compared to typical antipsychotics
-tardive dyskinesia is linked to various involuntary, repetitive movements caused by long-term or high-dose use of typical antipsychotics.

Summary:
- They work on dopamine receptors as well as serotonin and glutamate receptors.
- They occupy the D2 receptors.
- By doing so, they dissociate dopamine, allowing receptors to receive it in smaller amounts.

18
Q

Evaluate the use of drugs to treat schizophrenia

A

Limitation - possible side effects with typical antipsychotics
-Kapur et al. (2000) estimate that between 60-70% of D2 receptors in the mesolimbic dopamine pathway must be blocked for typical antipsychotics to be effective
-unfortunately, this also means that a similar number of D2 receptors in other areas of the brain are blocked
-one of the side effects caused is tardive dyskinesia
-often results in patients discontinuing their medication
-furthermore, there are several dopamine pathways in the brain
-although blocking dopamine receptors in one of them can be beneficial, blocking receptors in other pathways may be harmful to the individual

Strength - atypical antipsychotics generally do not cause the movement issues often associated with typical antipsychotics
-e.g. atypical antipsychotics lower the chances of tardive dyskinesia
-Jeste et al. (1999) found that 30% of patients on typical antipsychotics for nine months experienced tardive dyskinesia, compared to only 5% of those on atypical antipsychotics
-furthermore, atypical antipsychotics may ultimately be more appropriate for treating schizophrenia due to fewer side effects
-can make patients more likely to continue with their medications
-allows them to experience greater benefits, and can treat wider range of symptoms
-however, atypicals are not completely free of side effects
-they are associated with risks like diabetes and cardiac arrest, which can be fatal

Limitation - research about which antipsychotics are more effective at treating schizophrenia is inconclusive
-meta-analysis by Leucht et al. (1999) found that two atypical drugs were only slightly more effective than typical drugs
-furthermore, the claim that atypical drugs effectively treat negative symptoms has received limited support
-suggests that atypicals may not necessarily be a superior treatment

Strength - drug therapy has proven effective in reducing the symptoms of schizophrenia, especially positive symptoms
-these drugs are relatively inexpensive to produce
-makes them cost-effective and easy to administer
-have had positive effects on many sufferers, enabling them to live relatively normal lives outside of institutional settings
-furthermore, estimated that fewer than 3% of people with schizophrenia in the UK live permanently in hospitals, largely due to medication

Antipsychotic drugs have also been shown to be more effective than placebos. Leucht et al. (2012) found that patients who continued their antipsychotic medication were only 27% likely to relapse, compared to a 64% relapse rate for those given a placebo. This demonstrates that drugs are successful in preventing relapse. However, these medications are only palliative, meaning they treat the symptoms of schizophrenia rather than providing a cure. If a patient stops taking their medication, their symptoms often return. From a psychodynamic perspective, critics argue that drugs address only the symptoms, not the underlying cause of the illness. This can lead to a “revolving door” phenomenon, where patients are discharged and re-admitted to the hospital repeatedly. Patients may take their medication, feel better, then mistakenly assume they are cured, stop their medication, and subsequently become ill again.

There are ethical concerns surrounding the use of antipsychotic drugs. When considering side effects, potential fatalities, and social consequences, a cost-benefit analysis may lean toward a negative outcome. In the USA, there was a significant out-of-court settlement awarded to a tardive dyskinesia sufferer under the Human Rights Act 1988. Additionally, some in the psychiatric community believe that the widespread use of antipsychotics is heavily influenced by the powerful interests of pharmaceutical companies, which profit substantially from their ongoing use.

19
Q

Outline the schizophrenogenic mother as part of the family dysfunction explanation of schizophrenia

A

-proposed by Fromm-Reichmann (1948)
-suggests that schizophrenia arises from being reared by a cold and dominant mother
-both overprotective and rejecting
-although she may appear self-sacrificing, she uses the child to satisfy her own emotional needs
-hence individuals raised with this mothering style develop schizophrenia due to the confusion stemming from their mother’s contradictory behaviour

-modern day psychologists don’t take this hypothesis seriously
-Roff and Knight (1981) found a link between mothering style and schizophrenia
-but has also been found that this mothering style is implicated in many other disorders
-another reason why the hypothesis has largely been abandoned

20
Q

Outline the double-bind hypothesis as part of the family dysfunction explanation of schizophrenia

A

-proposed by Bateson (1956)
-suggests schizophrenia is a reaction to a parent presenting the child with a no-win situation, created by contradictory communication between tone of voice and content
-leads to social withdrawal in order to escape double-bind situations
-prolonged exposure to such interactions prevents the development of an internally coherent construction of reality
-this later manifests as typical schizophrenic symptoms, e.g. delusions and hallucinations, incoherent thoughts and speech, and paranoia

-e.g. a mother may say, “Come and give mummy a cuddle,” but then freezes when the child approaches and subsequently tells the child off for not being affectionate

21
Q

Outline the expressed emotion as part of the family dysfunction explanation of schizophrenia

A

-families persistently exhibit criticism and hostility towards recovering schizophrenics

-when these individuals return to their families, they may react by relapsing and experiencing positive symptoms, such as delusions

-Kuipers et al. (1983) found that high EE relatives tend to talk more and listen less

-high levels of EE are most likely to influence relapse rates

-a patient returning to a family with high EE is about four times more likely to relapse than a patient whose family is low in EE

-suggests that schizophrenics have a lower tolerance for intense emotional situations, critical comments and family dynamics

-causes stress beyond the patient’s coping mechanisms and triggers an episode

22
Q

Evaluate the family dysfunction explanation of schizophrenia

A

Double bind:
Limitation - little evidence of double-bind communication being associated with schizophrenia
-even when it occurs, it may be due to having a schizophrenic in the family rather than being the sole cause of the disorder
-lowers internal validity of theory
-however, Berger (1965) found that schizophrenics reported a higher recall of double-bind statements by their mothers than non-schizophrenics
-although it may not be reliable, as patients’ recall may be affected by their illness

Strength - research support
-Bateson (1956) reported case study in which a recovering schizophrenic was visited in the hospital by his mother
-he embraced her warmly, but she stiffened, and when he withdrew his arms, she said, “Don’t you love me anymore?”
-supports the idea of double-bind communication
-however, critics argue that this is weak evidence, as it is a case study
-lacks population validity and cannot be generalised

Limitation - contradictory research
-e.g. Liem (1974) found no difference in parental communication patterns in families with a schizophrenic child compared to normal families
-furthermore, Hall and Levin (1980) found no difference between families with and without a schizophrenic member in the degree to which verbal and non-verbal communication were in agreement

Expressed emotion:
Strength - research support
-Hooley et al. (1998) conducted a meta-analysis of 26 studies
-found schizophrenics returning to a family environment with high EE experienced more than twice the average rate of relapse
-supports claim that EE could be responsible for a patient’s relapse
-furthermore, Kavanagh (1992) also conducted a meta-analysis
-found that the relapse rate for schizophrenics living with high EE families was 48%, compared to 21% for those who returned to low EE families

Limitation - overlooks role of individual differences
-not all patients in high EE homes relapse
-not all patients in low EE homes avoid relapse
-Altorfer et al. (1988) found that one-quarter of the patients they studied showed no physiological responses to stressful comments from their relatives
-hence vulnerability to the influence of high EE may be psychologically based
-furthermore, if not all patients are equally vulnerable to high levels of expressed emotion, then other factors must be involved
-suggests a more holistic approach would be better suited to explaining different factors affecting response to high EE

Family dysfunction:
Limitation - research in this area is correlational
-many studies show a link between family dysfunction and schizophrenia
-uncertain if family dysfunctions causes schizophrenia, or if having a family member with schizophrenia leads to these dysfunctions
-cause and effect cannot be established
-lowers internal validity
-furthermore, there is limited research support for family dysfunction as a direct cause of schizophrenia
-suggests it is more likely to be a maintenance factor

Limitation - these theories do not explain why some children in dysfunctional families do not develop schizophrenia
-if family dynamics were the sole cause, then all children raised in such environments would develop the disorder
-implies family dysfunction cannot be considered the only cause
-weakens validity of theories
-furthermore, it is more likely that individuals have a biological predisposition to schizophrenia
-diathesis-stress model suggests biological vulnerability combined with a harmful family environment may trigger the illness
-a single element of nurture alone is likely insufficient to cause the disorder

23
Q

Outline cognitive deficits

A

-includes issues with attention, communication, and processing information
-affects perception of thoughts as inner speech
-schizophrenics often struggle to interpret others’ behaviour, which impacts social interactions
-difficulties in processing visual and auditory information may contribute to symptoms like reduced emotional expression, disorganized speech, and delusions

24
Q

Outline cognitive biases

A

-involves selective attention
-Bentall (1990) found that individuals experiencing auditory hallucinations may misinterpret their inner voice as speech from an external source
-these individuals often see themselves as powerless in comparison to others in their social network
-leads to feelings of worthlessness and incompetence
-most people experience an inner voice when thinking, such as when making decisions or solving problems
-but those who feel powerless may hear voices that reinforce their negative self-view
-the perceived power imbalance between themselves and others mirrors their relationship with the voice they hear
-the greater the perceived gap, the more powerful and controlling the voice becomes

25
Q

Dysfunctional thought processing

A

-metarepresentation: ability to reflect on our thoughts and behaviours
-helps us identify goals, intentions, and interpret others’ actions
-dysfunction in this area can cause us to confuse our own actions with someone else’s
-may explain hallucinations, as the inner voice is mistakenly experienced as coming from an external source

-central control: ability to suppress automatic responses in favor of deliberate actions
-disorganised speech in schizophrenia may result from an inability to suppress automatic thoughts and speech triggered by other thoughts
-many schizophrenics experience derailment in their thoughts and speech because each word triggers associations
-they struggle to suppress automatic responses to these associations

26
Q

Evaluate the cognitive explanation of schizophrenia

A

Strength - research to support that information processing differs in schizophrenics
-Stirling et al. (2006) compared 30 schizophrenia patients with 18 controls on cognitive tasks, including the Stroop Test
-participants named ink colors of color words, suppressing the impulse to read the word itself
-schizophrenic patients took twice as long as controls to complete this task
-implies difficulties with central control and suppressing automatic associations

Strength - further research support
-Sarin and Wallin (2014) found evidence that faulty cognition causes positive symptoms of schizophrenia
-delusional patients showed biases in information processing, e.g. jumping to conclusions and lack of reality testing
-patients with hallucinations displayed impaired self-monitoring, often perceiving their own thoughts as external voices
-demonstrates that cognitive biases are present in schizophrenia but not in typical controls

Limitation - cannot establish cause and effect
-cognitive approaches do not clarify the origin of cognitive deficits
-unclear whether these deficits cause schizophrenic behavior or whether schizophrenia causes cognitive deficits
-lowers internal validity of explanation
-however, links between symptoms and faulty cognition are evident

27
Q

CBT and CBTp as a treatment for schizophrenia

A

-primary psychological treatment for schizophrenia
-NICE (2014) recommends it for all patients with this condition
-operates on the belief that individuals with schizophrenia can be aided by identifying and altering faulty cognitions

-based on the assumption that individuals with schizophrenia hold distorted beliefs that influence their behaviour
-delusions are thought to stem from faulty interpretations of events
-CBT helps patients recognise and correct these irrational beliefs
-hence, CBT aims to improve symptoms by addressing maladaptive thinking and distorted perceptions underlying the disorder

-specific type of CBT used for schizophrenia is Cognitive Behavioral Therapy for Psychosis (CBTp)
-originally developed to address persistent symptoms that remain despite antipsychotic medication

28
Q

Process of CBTp

A

Note: Antipsychotic drugs are usually given first to reduce psychotic thoughts, making the CBT more effective

  1. CBTp usually takes place once every ten days for 12-16 sessions (NICE recommends 16)
  2. It can be delivered in groups, but is typically delivered on a one-to-one basis.
  3. The aim of CBTp is to establish links between the sufferer’s thoughts, feelings, actions and their symptoms and general level of functioning. By monitoring their thoughts, feelings and actions in relation to their symptoms, patients can consider alternative ways of explaining why they feel and behave the way they do. Patients are also taught to recognise the signs of relapse.
  4. Drawings are often used to display links between the sufferer’s thoughts, actions and emotions.
  5. Cognitive techniques are developed between patient and therapist such as distractions from intrusive thoughts, challenging intrusive thoughts, increasing/decreasing social activity to distract them from the thoughts, or using relaxation techniques
  6. This therapy relies on the patient taking an active part, and they are given ‘homework’ between sessions, like keeping a diary of the contents of their delusions, or trying out coping mechanisms
  7. During the therapy the therapist lets the patient develop alternatives to any previous maladaptive explanations, ideally looking for alternative explanations and coping strategies that are already present in the patient’s mind
29
Q

Evaluate CBT as a cognitive treatment for schizophrenia

A

Strength - research support
-patients who receive CBTp experience fewer hallucinations and delusions
-recover more effectively than those on antipsychotic drugs alone
-furthermore, Drury et al. (1996) found a 25-50% reduction in recovery time when CBT was combined with antipsychotic medication
-shows that patients make faster progress with both treatments together

Strength - beneficial when CBTp combined with drug therapy
-Tarrier et al. (2000) found patients receiving 20 one-to-one CBT sessions with drug therapy, followed by four booster sessions over a year, improved more significantly than those receiving drug therapy or supportive counseling alone
-Kuipers et al. (1997) also found that combining CBTp with medication resulted in lower dropout rates and higher patient satisfaction
-however, as CBTp was administered alongside drugs, it is difficult to conclude whether the effectiveness was due to CBT alone or the combination of treatments

Strength - effective for patients unresponsive to other treatments
-Sensky et al. (2000) found that CBT was beneficial for schizophrenics who hadn’t responded to drug therapy
-improvements continuing nine months after treatment ended
-suggests that CBT has long-lasting positive effects for drug-resistant patients

Strength - fewer side effects than drug therapy
-avoids physical issues like tardive dyskinesia or diabetes
-however, limited availability, due to budget constraints in healthcare
-only 1 in 10 patients in the UK are offered CBT
-Haddock et al. (2013) found that 6.9% of their sample of 187 sufferers received CBT

Limitation - CBT is more costly than medications
-may mean it is not accessible for many people
-however, although initially more expensive, CBT could save healthcare systems money long-term
-as it reduces the need for additional interventions associated with antipsychotic side effects

Limitation - not suitable for all schizophrenia patients
-Kingdon et al. (2006) studied 142 patients in Hampshire
-found many were not suitable for CBT, often due to an inability to fully engage with the therapy
-older patients were found to be less suitable than younger ones
-CBT may be inappropriate for those too disoriented, agitated, or paranoid to build trusting relationships with therapists
-however, it may benefit those refusing drug treatments

Limitation - questionable effectiveness
-Jauhar et al. (2014) conducted meta-analysis of 50 studies
-found only a small therapeutic effect on symptoms, including positive symptoms like delusions and hallucinations, which CBT aims to target
-small effect disappeared in studies using blind testing, where researchers were unaware of which patients received CBT
-however blind-testing is much less common than meta-analyses when studying treatments for schizophrenia
-Wykes et al. (2008) found that the more rigorous the study, the weaker the observed effect of CBT on schizophrenia

30
Q

Outline family therapy as a treatment for schizophrenia

A

-form of psychotherapy is that alters relationship and communication patterns within families
-commonly used alongside medication and outpatient clinical care
-NICE (2014) recommends that family therapy be offered to all schizophrenics who are in contact with family members, prioritising cases with persistent symptoms or a high risk of relapse

Main aims:
-improve positive and decrease negative forms of communication
-increase tolerance levels and reduce criticism among family members
-decrease feelings of guilt and responsibility for causing the illness within the family
-reduce the burden and stress of care for family members
-enhance relatives’ ability to anticipate and solve problems

How it works:

  1. The therapist meets regularly with the patient and close family members, who are encouraged to talk openly about the patient’s symptoms, behaviour and progress.
  2. They are taught to support each other and be caregivers, with each person given a specific role in the rehabilitation process.
  3. There is an emphasis on openness, with no details remaining confidential, although boundaries of what is and is not acceptable are drawn up in advance.
  4. Like CBT it is given for a set amount of time, usually between 3 months to a year, and at least ten sessions.
  5. This type of treatment is aimed at reducing the level of expressed emotion (EE) within the family, as EE has been demonstrated to increase the likelihood of relapse.
  6. It typically involves providing family members with information about schizophrenia, finding ways to support the individual and resolving any practical problems, like ensuring the sufferer keeps medical appointments and takes their medication.
31
Q

Evaluate family therapy as a treatment for schizophrenia

A

Strength - research support
-Pharoah et al. (2010) conducted meta-analysis of 53 studies from Europe, Asia, and the USA
-found that family therapy increased a patient’s compliance with medication
-reduced risk of relapse and hospital admission during and up to 24 months after treatment
-hence family therapy effective in the long term
-however, these findings may be due more to improved medication compliance, as patients benefit more from drugs when they stick to their treatment routine
-hence, the results may not be solely due to family therapy

Strength - further research support
-McFarlane et al. (2003) conducted meta-analysis
-confirmed that family therapy reduces relapse rates, lessens symptom
-also improves family relationships and enhances patient well-being
-reinforces effectiveness

Limitation - the focus on ‘openness’ may make family members hesitant to share information
-could cause or reopen tensions
-some may avoid confronting issues
-reduces effectiveness, as honest engagement is necessary to address faulty family communication

Strength - helpful for patients who lack insight into their illness or have difficulty speaking coherently
-family members can assist by providing information to the therapist
-they often have valuable insight into a patient’s behavior and moods, which the patient may not always be aware of

Strength - cost-effective
-by reducing relapse rates and decreasing the need for hospitalization, it can educate family members to help manage a patient’s medication regimen
-hence reduces the need for additional medical intervention
-furthermore, combining drugs with family therapy is ideal
-but budget constraints often prevent this approach
-the Schizophrenia Commission (2012) estimates that family therapy costs £1,004 less per patient than standard care (drugs alone) over three years
-suggests it can save money

32
Q

Outline token economies as a behaviourist approach to schizophrenia

A

Token economies are a behaviourist approach to the management of schizophrenia, where tokens are awarded for desired behavioural change.
When it was introduced in the 1970s, it was mainly used with long-term hospitalised patients to enable them to leave the hospital and live relatively independently in the community. It is particularly aimed at changing negative symptoms of schizophrenia, such as low motivation, poor attention and social withdrawal.

How it works:

  1. Clinicians set target behaviours that they believe will improve the patient’s engagement in their daily activities. For example, these target behaviours might be something as simple as the patient brushing their hair, or a more socially orientated behaviour such as persevering with a task.
  2. Tokens then are awarded whenever the patient engages in one of the target behaviours, and these tokens can be exchanged for various rewards at a later date.
  3. The idea behind token economy is that the patient will engage more often with
    desirable behaviours because the behaviours become associated with these rewards and privileges.
  4. With the token economy, the tokens in themselves are neutral. However, to give the neutral token value it needs to be repeatedly presented alongside or. immediately before the reinforcing stimuli (e.g. the reward). By pairing the neutral tokens with the reward, the neutral token acquires the same reinforcing properties. As a result of this process of classical conditioning, these neutral tokens become secondary reinforcers and so can be used to modify the behaviour in people with schizophrenia.
  5. During the early stages of the treatment, frequent exchange periods mean that the patients can be quickly reinforced and target behaviours can then increase in frequency.
  6. The effectiveness of the token economy may decrease if more time passes between the presentation of the token and exchange for the reward
33
Q

Evaluate token economies as a behaviourist approach to schizophrenia

A

Some research suggests that token economy is effective in managing schizophrenia. Ayllon and Azrin (1968) applied a token economy on a ward of female patients with schizophrenia, many of whom had been hospitalized for years. Patients received plastic tokens, each embossed with the words “one gift,” for behaviors like making their beds, which they could later exchange for rewards such as watching a film. This approach led to a dramatic increase in the number of desirable behaviors the patients displayed each day. Additionally, Dickerson et al. (2015) reviewed 13 studies and found the technique effective in increasing adaptive behavior in people with schizophrenia, particularly when used in combination with drugs, though the specific benefits of combining the two were not identified. This evidence suggests that token economies should not be seen as standalone treatments for schizophrenia.

There are issues with the research methodology used to study token economy in schizophrenia. Comer (2013) points out that studies on token economies tend to be uncontrolled. When a token economy is introduced into a ward, typically all patients participate rather than having an experimental group and a control group. Consequently, improvements in patients’ behaviors can only be compared with their own past behaviors instead of a control group. This comparison may be misleading, as factors like increased staff attention could contribute to patient improvement rather than the token economy itself.

One advantage of token economy is that it encourages patients to become more independent and active, which often leads to nurses showing increased respect for the patients. This, in turn, motivates patients and helps them develop positive self-esteem. Token economies are therefore effective in addressing the effects of institutionalization in long-term hospital patients. Additionally, when token economies are used in hospital wards, they help create a healthier, safer, and more stable environment, reducing staff and patient injuries and decreasing staff absenteeism and emergency incidents.

However, the positive effects of token economies are generally short-lived. This treatment does not seem to work long-term, as patients’ desirable behavior becomes dependent on reinforcement. Once patients are released into the community, the reinforcement ends, often resulting in high readmission rates. Without professionals to provide constant reinforcement, people with schizophrenia may struggle to maintain target behaviors outside the hospital setting, suggesting that token economies are ineffective outside of the hospital environment.

There are also ethical concerns regarding token economies, as some argue the approach can be humiliating for people with schizophrenia. To make reinforcement effective, clinicians may control access to primary reinforcers, such as food or privacy, which patients can earn by displaying target behaviors. However, it is generally accepted that all human beings have certain basic rights that should not be violated, regardless of the positive outcomes that may result from manipulating these needs.

34
Q

Outline the importance of an interactionist approach in explaining schizophrenia, including the diathesis-stress model

A

-considers both biological and psychological factors in the development of schizophrenia
-acknowledges that multiple factors contribute to the illness

-diathesis-stress model proposes that schizophrenia is triggered when environmental stress interacts with an existing biological vulnerability.
-suggests that both a vulnerability to schizophrenia (such as genetics) and a stress trigger (like dysfunctional family dynamics) are necessary for the illness to develop
-factors like genetics or biochemistry may increase a person’s vulnerability
-but schizophrenia will not manifest without an environmental stressor

-studies show that schizophrenia has a biological component, potentially linked to genetics or biochemistry
-certain genes are associated with increased vulnerability, and having a relative with schizophrenia raises an individual’s risk
-genetic factors are thought to be linked to abnormalities in dopaminergic systems and potentially other neurotransmitters
-however, the diathesis-stress model argues that biology alone does not cause schizophrenia; -instead, biological vulnerability increases the likelihood that environmental stressors will trigger the illness

-Read et al. (2001) suggest that diathesis encompasses various factors, including child abuse
-early psychological trauma may alter an infant’s brain development
-makes them more vulnerable to stress by causing the hypothalamic-pituitary-adrenal (HPA) system to become overactive

-stress can include any factor that could potentially trigger schizophrenia
-e.g. Houston et al (2008): cannabis use is considered a stressor because it disrupts the body’s dopamine system

35
Q

Evaluate the importance of an interactionist approach in explaining schizophrenia, including the diathesis-stress model

A

Strength - research support
-Barlow and Durand (2009) found that a family history of schizophrenia indicated a genetic link
-when combined with a dysfunctional family environment, the risk of developing schizophrenia increased
-supports the diathesis-stress model, as the heightened risk was due to the interaction between genetics and family-induced stress
-furthermore, Cannon et al. (2002) identified positive correlation between birth complications and a later risk of schizophrenia
-this was attributed to damage to the hormone and neurotransmitter systems
-reinforces idea of an interaction between biological vulnerabilities and later environmental stressors

Limitation - not entirely understood how various risk factors contribute to the diathesis-stress interaction
-e.g. biological, environmental, psychological, and social
-these causes may vary among individuals with schizophrenia
-lack of a full understanding of the mechanisms through which vulnerability and stress interact to produce the illness
-weakens internal validity of model

Limitation - original diathesis-stress model is criticised for being overly simplistic
-e.g. notion that a single gene, combined with a specific parenting style, leads to schizophrenia
-several genes have been linked to an increased risk of developing the disorder
-suggests that no single “schizogene” exists
-furthermore, stress is not limited to parenting styles or family dynamics
-Houston et al. (2008) found that vulnerability is not purely biological
-e.g. childhood sexual trauma heightened the risk of developing schizophrenia when paired with later cannabis use
-hence, the original model’s assumption that vulnerability is purely biological and stress is solely environmental is outdated

36
Q

Outline the importance of an interactionist approach in treating schizophrenia

A

-extensive research has examined the effectiveness of different treatments for schizophrenia
-Guo et al. (2010) found that combining both biological and psychological treatments is more effective
-however, determining the best combination of treatments can be challenging
-as it often depends on individual patient needs and circumstances
-e.g. combining drugs with family therapy may be less beneficial for patients who have limited family contact
-In Britain, antipsychotic drugs are typically prescribed first to reduce symptoms
-makes it easier for patients to engage with psychological treatments like CBT
-uncommon for patients with schizophrenia to receive psychological therapy without medication
-in the USA, treatment often focuses on medication alone, with psychological treatments being less frequently offered
-rare in both countries to offer a psychological treatment, such as CBT, without any accompanying medication

-Turkington et al. (2006) argue that it is possible to view schizophrenia as having a biological basis while still providing psychological treatment
-hence adopts an interactionist approach by addressing both biological and psychological symptoms
-however, it would be inconsistent to claim that schizophrenia is solely biological in nature, devoid of psychological aspects, while simultaneously offering psychological therapy
-using an interactionist approach to treat schizophrenia implies recognising the role of both diathesis (vulnerability) and stress in the development of the disorder

37
Q

Evaluate the importance of an interactionist approach in treating schizophrenia

A

Strength - combining antipsychotic medication and psychological therapies for schizophrenia can be cost-effective
-schizophrenia has both biological and psychological components
-so a combined treatment approach is more beneficial as it simultaneously targets both elements
-furthermore, although it initially appears costly, patients are achieving better and longer-lasting outcomes
-suggests increased effectiveness in the long term

Strength - research support
-e.g. Guo et al. (2010) found that patients in the early stages of schizophrenia who received both antipsychotics and psychological therapy showed improvements in insight and social functioning
-also had lower relapse rates compared to those on antipsychotics alone
-highlights the effectiveness of combining biological and psychological treatments
-however, combining treatments does not always yield positive results
-some patients undergoing CBT have misinterpreted the side effects of antipsychotics in a delusional way
-led to mistrust and resistance toward further treatment
-suggests that, in certain cases, combining treatments could introduce additional complications

Limitation - interactionist approach’s logic in treating schizophrenia is criticised
-Turkington et al. (2006) argue that while studies show that combined treatments are more effective than standalone approaches, this does not inherently validate the interactionist perspective
-referred to as the treatment-causation fallacy
-means that we cannot definitively conclude that it is the interaction of the treatments that enhances effectiveness