Paper 3: Schizophrenia Flashcards
- Classification and diagnosis of Schizophernia
define schizophrenia and what aspects of
functioning are affected by schizophrenia?
-Schizophrenia is a severe mental disorder characterised by a profound disconnection from reality, involving a disruption of cognition and emotion
-It affects a person’s language, thought, perception and even their sense of self
- Classification and diagnosis of Schizophrenia
At what age is
schizophrenia typically diagnosed and who is more commonly affected?
- most often diagnosed between the ages of 15-35
- more commonly diagnosed in men, in cities and in the working class population
- Schizophrenia ranks among the top 10 causes of disability worldwide and affects about 1% of the population at some point in their lives (Mathers et al., 1996)
- Classification and diagnosis of Schizophernia
What is the difference between positive symptoms and negative symptoms?
- Positive = atypical symptoms experienced in addition to normal experiences e.g. hallucinations and delusions
delusions:
- delusions of grandeur
- paranoid/persecutory delusions
- delusions of reference
- Negative = atypical symptoms that represent a loss to normal experiences e.g. speech poverty (alogia) and avolition (apathy)
- Classification and diagnosis of Schizophernia
How is schizophrenia
diagnosed, and why is this problematic?
- it does not have one defining characteristic
- This is true of all psychiatric disorders: there are no reliable diagnostic biomarkers of differential diagnosis (comparing to other illnesses) or prognosis (response to treatment)
- Diagnosis is done through interview and observation and is therefore subjective - this differs from physical illness which is measured objectively e.g. blood tests, x-rays
- In addition the ICD-11 and DSM-5 differ in their diagnosis
- Classification and diagnosis of Schizophernia
Which symptoms are required for an ICD-10 based diagnosis of schizophrenia and for how long and what are positive symptoms required for ICD-10 diagnosis?
- two or more negative symptoms for one month (i.e. positive symptoms are not required).
The ICD-10 also recognised a range of subtypes of SZ:
- Paranoid (powerful delusions and hallucinations but few other symptoms)
- Hebrephrenic - involves primarily negative symptoms
- Catatonic - involves disturbance to movement
- Classification and diagnosis of Schizophernia
Which symptoms are required for a diagnosis of schizophrenia using DSM-V and for how long and what are the additional criteria?
Two or more of the following for at least a one-month (or longer) and at least one of them must be positive symptoms (1, 2, or 3):
1. Delusions
2. Hallucinations
3. Disorganized speech
4. Grossly disorganized or catatonic behavior
5. Negative symptoms, such as diminished emotional expression
- Classification and diagnosis of Schizophernia
What are the main
differences between ICD-
10 and DSM-V and what is the impact of the differences in the classification systems?
Similarities: Both classify schizophrenia as a psychotic disorder, consider cultural factors, and are widely used internationally.
Differences: They vary in subtypes, symptom duration, emphasis on negative symptoms, and the handling of schizoaffective disorder.
- Classification and diagnosis of Schizophernia
How do the terms reliability and validity apply to schizophrenia?
- Reliability refers to the consistency of the diagnostic instrument to assess the severity of the schizophrenic symptoms.
- Validity refers to the extent that a diagnosis represents something that is real and distinct from other disorders and the extent that a classification system such as ICD-10 or DSM-5 measures what it claims to measure.
- Reliability and validity are linked - a diagnosis cannot be valid if it is not reliable.
- Classification and diagnosis of Schizophernia
What issues are there with the reliability of the
diagnosis of schizophrena?
Describe a research study that has investigated reliability of diagnosis in schizophrenia, and what
were the findings/ implications?
Reliability: the extent to which the diagnosis of SZ is consistent - the level of agreement between psychiatrists and diagnostic tools over time.
- It is the extent to which psychiatrists can agree on the same diagnosis when independently assessing patients (inter-rater reliability). In order for a classification system to be reliable, the same diagnosis should be made each time. Therefore different psychiatrists should reach the same decision when assessing a patient.
- The same diagnostic tool should also assess patients with the same diagnosis over a period of time (test-retest reliability).
- Classification and diagnosis of Schizophernia
what’s co-morbidity
co-morbidity is where two conditions co-exist in the same individual at the same
time
* a person with sz might also at the same time be suffering from
another condition, e.g. personality disorder, depression, alcoholism
- Classification and diagnosis of Schizophernia
One strength
P: its high reliability when using standardized diagnostic instruments.
Eg: Osorio et al. (2019) found excellent inter-rater reliability using the DSM-5, with a kappa score of 0.97.
E: shows that when psychiatrists consistently apply standardized criteria, such as the DSM-5, they can reliably diagnose sz across different cases, ensuring appropriate treatment and improving prognosis.
C: high reliability does not guarantee validity; psychiatrists may agree on a diagnosis that does not accurately reflect the underlying condition, highlighting the need for more research into schizophrenia’s biological and psychological markers.
L: Overall, the use of standardised tools plays a critical role in improving diagnostic accuracy and consistency.
- Classification and diagnosis of Schizophernia
Two limitations
P: A limitation of schizophrenia diagnosis is its lack of inter-rater reliability.
E: Cheniaux et al. (2009) had two psychiatrists independently diagnose 100 patients using the ICD and DSM criteria. One diagnosed 26 with DSM and 44 with ICD, while the other diagnosed 13 with DSM and 24 with ICD.
E: This inconsistency shows that the diagnosis of schizophrenia can vary depending on the psychiatrist, reducing its reliability and potentially leading to misdiagnosis and inappropriate treatment.
L: This undermines the validity and reliability of the diagnostic process.
P: Another limitation is the issue of symptom overlap, which reduces diagnostic validity.
E: Lichtenstein et al. (2009) found that schizophrenia and bipolar disorder share genetic causes, suggesting biological similarities.
E: This overlap can lead to different diagnoses under different classification systems, such as schizophrenia under ICD and bipolar disorder under DSM, highlighting inconsistencies.
L: This reduces the validity of diagnosis and limits the reliability of classification systems in accurately differentiating between disorders.
- Biological explanations of SZ
Is schizophrenia an inherited disorder?
What were Gottesman’s
(1991) findings?
There is evidence that schizophrenia runs in families. But families share the same environment - so is it nature or nurture?
There is a strong relationship between the genetic similarity of family members and likelihood of both developing SZ (concordance rate).
People do not inherit schizophrenia, but they inherit a genetic predisposition (vulnerability) to the disorder.
Gottesman (1991) carried out a family study and found the concordance rates for SZ:
- MZ twins: 48%
- DZ twins: 17%
- siblings: 9%
The results show that the closer the degree of genetic relatedness, the greater the risk of developing sz.
- Biological explanations of SZ
What does it means to say that schizophrenia is polygenic?
What is the role of genetics in the aetiology of schizophrenia?
What were the findings by Ripke et al. (2014)
many genes are involved, and a polygenic risk factor is calculated. Each individual gene presents a small increased risk of SZ.
Different combinations of these genes can lead to SZ. It is therefore aetiologically (caused) heterogeneous (by different things).
Ripke et al. (2014) studied 37,000 patients and found 108 separate genetic variations associated with increased of Schizophrenia.
- Biological explanations of SZ
Why are adoption studies helpful in determining the aetiological role of genetics?
What were the findings of Tienari et al. (2000)?
Adoption studies are very useful for disentangling shared genes from the same environment.
Tienari et al (2000) carried out an adoption study in Finland. Of the 164 adoptees whose biological mothers had sz 6.7% also were diagnosed compared to 2% of the 197 control group (no sz mother).
This is support for a genetic explanation for sz, but only that it increases the likelihood of developing sz.
- Biological explanations of SZ
strength of the genetic arguments as explanations of SZ
P: A strength of the genetic argument for schizophrenia is the clear link between genetic relatedness and risk of developing the disorder.
E: Gottesman (1991) showed that the closer the genetic relatedness, the greater the risk. Adoption studies, like Tienari et al. (2004), show that children of schizophrenia sufferers are at higher risk, even in families with no history of the disorder.
E: This supports the idea that genetic factors increase susceptibility to schizophrenia, emphasizing the role of biological inheritance.
C: However, genetics alone may not account for all cases, as environmental factors, such as stress or family dynamics, may also contribute.
L: This supports genetics’ involvement but suggests a diathesis-stress model, where genetic predisposition interacts with environmental factors to trigger the disorder.
- Biological explanations of SZ
limitation of the genetic arguments as an explanation of SZ
P: A limitation of the genetic argument for schizophrenia is the difficulty in separating the effects of nature and nurture.
E: Family and twin studies often investigate individuals who share similar environments, potentially inflating concordance rates regardless of genetic influence.
E: For example, high concordance rates in MZ twins could be due to their similar treatment, not just shared genetics. Even MZ twins reared apart still share the same prenatal environment, which may further contribute to their similarities.
C: This shared environment acts as a confounding variable, making it difficult to determine the relative influence of genetics and environment on the development of schizophrenia.
L: Therefore, the inability to disentangle nature from nurture reduces the validity of genetic explanations, as environmental factors may play a larger role than initially thought.
- Biological explanations of SZ
What is the dopamine hypothesis of schizophrenia?
What is hyperdopaminergia, in where is thought to occur in the brain in patients with schizophrenia?
- The original dopamine hypothesis stated that schizophrenia was caused by excessive activity of dopamine in the subcortex.
- This causes the neurons that respond to dopamine to fire too often and transmit too many messages. This message ‘overload’ may produce many symptoms of schizophrenia
- hyperdopaminergia is high levels of dopamine in subcortical areas projecting to Broca’s area may be associated with the experience of auditory hallucinations and/or speech poverty
- It is now thought people with sz have high numbers of D2 receptors
- Biological explanations of SZ
What is the updated dopamine hypothesis
How does Goldman-Rakic’s
(2004) work revise the dopamine hypothesis?
The more recent version of the dopamine hypothesis focuses on abnormal dopamine systems in the cortex - also focuses on hypodopaminergia
- Goldman-Rakic et al (2004) have identified low levels of dopamine in the prefrontal cortex in the negative symptoms of sz such as avolition. The prefrontal cortex is responsible for thinking and decision making.
- Biological explanations of SZ
explain the main 2 dopamine pathways associated with SZ
- Mesolimbic Pathway:
- Originates in the ventral tegmental area (VTA) and projects to the nucleus accumbens (NAc), where dopamine drives pleasure and reward.
- Stimulation of the NAc is essential for maintaining daily activities, but overstimulation can increase dopaminergic activity, leading to euphoria, dependence, and cravings.
- Hyperactivity of dopamine in this pathway is linked to the positive symptoms of schizophrenia (hallucinations, delusions), which are alleviated by antipsychotics (D2 antagonists).
- Overstimulation leads to positive symptoms. - Mesocortical Pathway:
- Dopaminergic projections from the VTA to the prefrontal cortex (PFC), which is involved in cognition, working memory, and decision-making.
- Dysfunction in this pathway leads to cognitive issues like poor concentration and decision-making.
- Medications like amphetamines can increase dopamine in the mesocortical pathway, enhancing cognition and activity in the PFC (e.g., Ritalin for ADHD works through this mechanism).
- Low dopamine levels in this pathway are thought to underlie the negative symptoms of schizophrenia.
- Dysfunction leads to negative and cognitive symptoms.
- Biological explanations of SZ
How is hypo- and hyper-dopaminergia thought to
relate to different symptoms of schizophrenia?
It may be that both hyperdopaminergia and hypodopaminergia are correct explanations - both high and low levels of dopamine in different brain regions are involved in SZ.
- Biological explanations of SZ
a strength and limitation of the dopamine hypothesis as a biological explanation of SZ
P: A strength of the dopamine hypothesis is that it provides an explanatory framework for positive symptoms of schizophrenia.
Eg: Kapur (2000) proposed the salience hypothesis, suggesting that dopamine abnormalities cause patients to attribute abnormal significance to otherwise neutral events. Dopamine, which normally codes salient environmental events, fires chaotically in schizophrenia, leading to delusional ideation as an attempt to reconcile this.
Ex: This suggests that delusions result from aberrant learning signals caused by dopamine dysfunction.
L: Therefore, the salience hypothesis bridges biological and clinical observations, enhancing its validity.
P: A limitation of the dopamine hypothesis is that it is supported by mixed evidence.
Eg: Amphetamines, which increase dopamine, can worsen schizophrenia symptoms or induce similar symptoms in non-sufferers. Antipsychotics, which reduce dopamine, alleviate symptoms in patients.
Ex: However, Moncrieff (2009) argues that dopamine levels are influenced by factors like stress and smoking, and research by Ripke et al. suggests that other neurotransmitters, like glutamate, also play a significant role. Recent studies using ketamine (a glutamate blocker) and investigating THC support this view.
L: This suggests dopamine may contribute to schizophrenia but is not the sole factor. A more comprehensive understanding likely involves multiple interacting neurotransmitters, undermining the validity of a purely dopaminergic explanation.
- Biological explanations of SZ
What does the ‘neural correlates’ of something mean?
Give an example of the neural correlates of schizophrenia
neural correlates refers to measurements of the structure or function of the brain that correlate with an experience. Both positive and negative symptoms have neural correlates.
- Enlarged ventricles and negative symptoms
- Ventral striatal activity and negative symptoms
- Superior temporal activity and positive symptoms
- Biological explanations of SZ
Describe how the study by Juckel et al. (2006) on the neural correlates of negative symptoms
Juckel et al. (2006) found a negative correlation between ventral striatum activity and overall negative symptoms of SZ.
The ventral striatum is part of the brain that is involved in the reward pathway. Loss of motivation (avolition) may be explained by low activity levels in this part of the brain.
- Biological explanations of SZ
Describe the work by Allen et al. (2007) on the neural correlates of hallucinations
The superior temporal gyrus consists of the auditory cortex. Allen et al (2007) found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus. Therefore we can say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.
- Biological explanations of SZ
a limitation of the neural correlates as a biological explanation of SZ
P: A limitation of the neural correlates argument for schizophrenia is that the findings are only correlational.
Eg: Juckel et al. (2006) found that lower ventral striatum activity is associated with negative symptoms like avolition. However, this brain activity could be influenced by other factors such as trauma or environmental stress, rather than directly causing schizophrenia.
Ex: This means that correlational evidence cannot establish causation, as it does not account for intervening variables that might affect both brain activity and symptoms.
L: Therefore, while neural correlates offer insights into the biological basis of schizophrenia, they do not conclusively explain its origins. This limits the application of this approach in treatment until more research determines whether abnormal brain activity is a cause or consequence of the disorder, clarifying the relationship between neural structures and symptoms.
- biological treatments
What is the role of the following brain regions, and how are they implicated in schizophrenia:
- Prefrontal cortex
- biological treatments
What is the role of the following brain region, and how are they implicated in schizophrenia:
- Visual Cortex & Auditory Cortex
- biological treatments
What is the role of the following brain regions, and how are they implicated in schizophrenia:
- Basal ganglia
- biological treatments
What is the role of the following brain regions, and how are they implicated in schizophrenia:
- Amygdala
- biological treatments
What is the role of the following brain regions, and how are they implicated in schizophrenia:
- Dopaminergic circuits
- biological treatments
What is the most common treatment for schizophrenia?
antipsychotic drugs (syrup or tablets)
- biological treatments
How is medication administered to non-compliant patients?
they may receive slow-release depot injections every 2-4 weeks
- They can be prescribed acutely (short term) or chronically (long term) to reduce the positive symptoms (no effect on negative or cognitive symptoms)
- biological treatments
What are typical antipsychotics?
How are typical antipsychotics thought to work?
What is the name of a common typical anti-psychotic, and what effect does it have?
first generation antipsychotics like chlorpromazine have been around since 1950s
Their discovery was serendipitous, initially developed as an antihistamine, but side effects of calmness and indifference, led to trials in patients with schizophrenia
chlorpromazine’s mechanism of action was as a D2 antagonist, and as a result, this led to the dopamine hypothesis: if a dopamine-blocking agent reduced the symptoms, it was presumed that the initial problem in schizophrenia is too much dopamine
All subsequently developed medications that are effective as antipsychotics have high affinity (bind tightly) to dopamine D2 receptors, and work as antagonists
* Antagonists work by blocking dopamine receptors in the synapses in the brain, reducing the action of dopamine by reducing the likelihood of an action potential in the post-synaptic receptor
* According to the dopamine hypothesis, blocking hyperdopaminergia at D2 receptors should normalise neurotransmission in key areas of the brain, which in turn reduces positive symptoms, such as hallucinations/delusions.
- biological treatments
What is tardive dyskinesia and other side effects of typical antipsychotics
Typical antipsychotics are liable to produce movement side effects, called
extrapyramidal symptoms, including tardive dyskinesia (lip smacking, grimacing, tongue protrusion), and movements resembling
Parkinson’s disease
(dystonia, akathisia) due to too much reduction of dopaminergic transmission in the nigrostriatal pathway
- biological treatments
Why were atypical
antipsychotics developed?
include clozapine, olanzapine and risperidone.
developed in the 1970s to try to improve the effectiveness of treating negative symptoms and reduce the side effects of typical antipsychotics
However, they have mainly been effective against secondary (eg depression), not primary (core) negative symptoms (alogia, avolition, anhedonia)
- biological treatments
Name an atypical antipsychotic
In what way is the mechanism of atypical antipsychotics similar and dissimilar to typical antipsychotics?
Unlike typical antipsychotics, atypicals, such as clozapine, target a range of neurotransmitters:
1. It binds to and blocks dopamine receptors in the same way as typical antipsychotics e.g. chlorpromazine
2. Also acts on serotonin (could impact depression and anxiety)
3. Acts on glutamate receptors - (could impact cognitive functioning; evidence is weak).
4. They are ‘loosely bound’ to a variety of receptors.
- biological treatments
What are the possible side effects of atypical antipsychotics?
- Agranulocytosis (a blood disorder which can be fatal) *
- Weight gain
- Cardiovascular problems
- biological treatments
How is risperidone different to clozapine?
developed because clozapine was involved in the deaths of some patients from agranulocytosis and was initially withdrawn.
- Like clozapine, risperidone binds to dopamine and serotonin receptors.
- But, risperidone binds more strongly than clozapine, to dopamine receptors and is therefore more effective in smaller doses than most antipsychotics and has fewer side effects.
- biological treatments
strengths of anti-psychotics
P: A strength of antipsychotics is their moderate effectiveness.
Eg: Thornley et al. (2003) reviewed 13 trials (1121 participants) and found chlorpromazine improved functioning and reduced symptoms over placebo. Meltzer et al. (2012) showed clozapine was 30-50% more effective in treatment-resistant cases than typical antipsychotics.
Ex: This supports their role in symptom reduction and improving outcomes, especially for non-responders.
C: However, they do not work for all patients, and side effects can limit long-term use.
L: Despite this, evidence supports antipsychotics, particularly atypical ones, as valuable treatments for schizophrenia, improving patients’ quality of life.
P: Atypical antipsychotics have advantages over typical ones, reducing side effects and improving adherence.
Eg: They cause fewer extrapyramidal side effects, such as rigidity and involuntary movements. The CATIE study (2005), a double-blind trial with over 1400 patients, found olanzapine had the longest time to discontinuation, suggesting better adherence.
C: However, only 26% completed the 18-month study, showing poor tolerance overall, and olanzapine caused significant weight gain and metabolic issues.
L: Reduced side effects make atypical antipsychotics more ethical and reliable for some patients, though not universally well-tolerated.
- biological treatments
limitation of anti-psychotics
P: A limitation of antipsychotics is that their effectiveness has been challenged.
Eg: Healy (2012) argues that many studies are short-term and published multiple times, exaggerating the evidence base. While antipsychotics have strong short-term calming effects, their long-term efficacy is uncertain. Prolonged use also causes side effects like weight gain, tardive dyskinesia, and cardiovascular issues, reducing compliance.
Ex: This questions the reliability of research, as it often overlooks long-term risks and benefits.
L: Thus, the evidence for antipsychotics may be weaker than it seems, highlighting the need for independent, long-term studies to assess their true effectiveness and risk-benefit balance.
4a. psychological explanations of SZ - the family
define Schizophernogenic mother
a negative stereotype coined by Frieda Fromm-Reichmann, that refers to mothers of individuals who develop schizophrenia, the implication being that the mother has induced the illness.
A schizophrenogenic mother is believed to cause SZ by being cold, rejecting and controlling (“the refrigerator mother”).
* They create a family climate of tension and secrecy.
* This leads to distrust that later develops into paranoid delusions (i.e. the belief that you are persecuted) and develops into schizophrenia.
4a. psychological explanations of SZ - the family
define double-blind hypothesis
A double bind is an emotionally distressing dilemma in communication in which an individual receives two or more conflicting messages, and one message goes against the other.
For example, the mother says ‘I love you’ but turns her head away in disgust.
4a. psychological explanations of SZ - the family
define expressed emotion
The expressed emotion explanation is where families persistently exhibit criticism, hostility and a general negative influence upon recovering schizophrenics, who when returning to their families react to the expressed emotion by relapsing and experiencing positive symptoms, such as delusions.
4a. psychological explanations of SZ - the family
Explain the family dysfunction view of schizophrenia
What symptoms is it linked to and why?
claim that sz is caused by abnormal patterns of communication within the family and conflict within the family.
those who advocate the family perspective would look to family therapy as the most effective approach to treatment.
- schizophrenogenic mother
- double-blind theory
-expressed emotion
4a. psychological explanations of SZ - the family
What is the double-bind theory of schizophrenia?
What symptoms is it linked to and why?
- Bateson (1972) emphasised the role of communication style within a family, as a risk of developing schizophrenia.
- He described how a child may be regularly trapped in situations where they fear doing the wrong thing, but receive conflicting messages about what counts as wrong. They cannot express their feelings about the unfairness of the situation.
- When they get it wrong (often) the child is punished by withdrawal of love - they learn the world is confusing and dangerous, leading to disorganised thinking and delusions.
4a. psychological explanations of SZ - the family
How is high expressed emotion thought to be linked to symptom expression?
High EE creates stress, increasing relapse risk in schizophrenia. It may also trigger onset in genetically vulnerable individuals (diathesis-stress model).
Expressed emotion (EE) refers to a negative family climate marked by criticism, hostility, and emotional over-involvement.
High EE families often have a rigid moralistic stance.
Returning to such families post-treatment raises relapse risk.
Stress from EE can trigger schizophrenic episodes.
Secret alliances within the family may reinforce paranoia and delusions of persecution.
4a. psychological explanations of SZ - the family
Give 3 aspects of
communication styles that characterise interactions in families with high expressed emotion
Elements of Expressed Emotion
* Verbal criticism of the patient - occasionally with violence
* Hostility towards the patient - including anger and rejection
* Emotional over-involvement - including needless self-sacrifice
4a. psychological explanations of SZ - the family
give an overview of symptom relationships
Schizophrenogenic mother: Paranoid delusions
Double-bind theory: Disorganised thinking and delusions
Expressed emotion:
Paranoia and delusions of persecution
4a. psychological explanations of SZ - the family
strength of psychological explanations of SZ
P: strong evidence linking family dysfunction to its development and relapse.
Eg: Butzlaff and Hooley (1998) found that high expressed emotion (EE) in families significantly increases relapse risk. Tienari et al. (2004) supported this by showing that only 5.8% of children of schizophrenic mothers developed schizophrenia when adopted into healthy families, compared to 36.8% in dysfunctional families.
Eg: This suggests that while genetics contribute, family environment plays a crucial role in triggering and maintaining schizophrenia.
L: These findings strengthen the validity of psychological explanations, supporting the diathesis-stress model by demonstrating how biological and environmental factors interact.
4a. psychological explanations of SZ - the family
limitations of psychological explanations of SZ
P: A limitation of family-based psychological explanations for schizophrenia is their lack of strong scientific evidence.
Eg: Many rely on case studies and clinical observations rather than rigorous empirical research. Harrington (2012) notes that modern psychiatrists largely reject these theories due to their anecdotal nature.
Ex: Case studies are subjective, small-scale, and difficult to generalize, reducing the validity of family dysfunction theories. Additionally, blaming families for schizophrenia raises ethical concerns and may harm relationships.
L: While family dynamics may contribute, the lack of scientific credibility weakens the reliability of psychological explanations, highlighting the need for stronger, evidence-based research.
P: family dysfunction theories overlook biological factors, which are well-supported by research.
Eg: These theories focus on environmental stressors but ignore genetic and neurobiological vulnerabilities that may predispose individuals to schizophrenia.
Ex: This raises doubts about whether schizophrenia caused by family dysfunction is truly the same as biologically driven cases. The diathesis-stress model suggests an interaction between genetic predisposition and environmental triggers, making family dysfunction an incomplete explanation.
L: By neglecting biological influences, the family dysfunction model oversimplifies schizophrenia, reducing its validity as a standalone explanation.
4b. psychological explanations of SZ - cognition
What biological evidence have we already covered that would suggest cognition is impaired in schizophrenia?
- reduced processing in the ventral striatum is associated with negative symptoms, whereas reduced processing of information in the temporal and cingulate gyri are associated with hallucinations.
- This lower than usual level of information processing suggests that cognition is likely to be impaired.
4b. psychological explanations of SZ - cognition
How does Frith suggest that attention plays a role in cognitive deficits in schizophrenia?
Cognitive explanations for schizophrenia are based on the assumption that the ability to process thoughts is dysfunctional.
- Frith’s (1979) “attention deficit theory” suggests schizophrenia is due to a faulty attention system unable to filter preconscious thought and gives too much significance to the information that would usually be filtered, therefore overloading the mind.
- This accounts for positive symptoms like hallucinations/ delusions and cognitive abnormalities
4b. psychological explanations of SZ - cognition
What does Frith suggest is the role of meta-
representation and central control, and how does it relate to symptoms?
Frith et al (1992) identified two kinds of dysfunctional thought processing that could underlie some symptoms:
- Meta-representation
- The cognitive ability to recognise own thoughts and behaviour. This is our ability to recognise our thoughts as our own
- Dysfunction of this process could lead to hearing voices (hallucinations), whereby our own inner speech is not recognised, as so mis-attributed to an external source
- This could also lead to thought insertion, where the patient feels thoughts have been projected into their mind by others - Central control
- The cognitive ability to suppress automatic responses while performing deliberate actions)
- Dysfunction could result in thought disorder: people with schizophrenia experience derailment of thoughts and spoken sentences because each word triggers automatic associations that they cannot suppress.
- Failure of central control could also explain speech poverty: patients become overwhelmed by thoughts and so begin to reduce speech
4b. psychological explanations of SZ - cognition
What evidence did Frith provide to support his theory of dysfunctional thought processing?
Frith (1992) supported these ideas with cognitive neuroscience studies:
* 30 schizophrenia patients with various symptoms had PET scans.
* These scans indicated a reduction in blood flow in the frontal cortex with patients with negative symptoms like avolition and the inability to suppress automatic thoughts.
* Those experiencing positive symptoms showed increased activity in temporal lobe regions associated with memory retrieval.
* These results suggest distinct biological differences in brain regions corresponding to specific cognitive processes implicated in schizophrenia
4b. psychological explanations of SZ - cognition
strength of the cognitive explanation for SZ
P: evidence supporting dysfunctional thought processing.
Eg: Stirling et al. (2006) used the Stroop test on 30 schizophrenia patients and 18 controls, finding patients took twice as long, indicating impaired suppression of automatic responses.
Ex: This supports the idea of faulty central control, a cognitive deficit linked to schizophrenia.
L: These findings strengthen cognitive models by demonstrating measurable impairments in executive function, highlighting potential areas for interventions like CBT.
P: its support from the success of cognitive behavioural therapy for psychosis (CBTp).
Eg: CBTp challenges delusions and hallucinations, targeting faulty cognition. NICE (2014) found it more effective than antipsychotics in reducing symptom severity and improving social functioning.
Ex: The effectiveness of CBTp suggests cognitive dysfunction plays a key role in schizophrenia. If cognition weren’t a factor, CBTp wouldn’t work.
L: This reinforces the cognitive explanation’s validity and practical importance in treatment.
4b. psychological explanations of SZ - cognition
limitations
P: A limitation of psychological explanations for schizophrenia is that they focus on cognitive impairment while overlooking biological factors.
Eg: Howes and Murray (2014) proposed an integrative model where genetic vulnerability and stress sensitise the dopamine system, increasing dopamine release. This dysregulation then triggers biased cognitive processing, leading to symptoms like paranoia and hallucinations.
Ex: This model shows how psychological and biological factors interact, creating a cycle of stress, dopamine release, and worsening symptoms.
L: While cognitive explanations are useful, they are incomplete without considering biological influences. The integrative model supports the diathesis-stress approach, offering a more comprehensive understanding of schizophrenia.
5a. psychological treatments of SZ - CBTp
How many sessions of CBTp does NICE recommened?
NICE (The National Institute for Health and Care Excellence) recommend that all patients with sz should receive СВТр.
CBT is now commonly used to treat SZ and takes place over 5-20 sessions. NICE recommend at least 16 sessions.
5a. psychological treatments of SZ - CBTp
What is the aim of CBTp?
- Targeting Distorted Thinking: CBT helps individuals with psychosis
Identity and challenge distorted thoughts and bellets, such as delusions and hallucinations, by developing alternative, more realistic interpretations and coping strategies. - Symptom Management and Coping Skills: The therapy focuses on equipping patients with practical skills to manage distressing symptoms, reduce emotional distress, and improve daily functioning without relying solely on medication.
- Adjunct to Medication: CBT is often used alongside antipsychotic medication to enhance treatment outcomes, particularly in cases where medication alone is insufficient or where individuals struggle with side effects or adherence.
5a. psychological treatments of SZ - CBTp
How does CBTp work?
Normalisation:
CBT helps patients to make sense of how their delusions and hallucinations impact on their feelings and behaviour. Offering explanations for symptoms helps to reduce anxiety and for the patient to realise their beliefs are not based on reality.
* Understanding that the voice the patient is hearing is not that of a demonic persecutor, but a mistiring in their brain that registers their own inner speech, can be a much less frightening and debilitating experience
* СВТ will not cure symptoms. The voice will remain, but knowing it’s origins can help patients to cope with them through disputing and restructuring beliefs (ABCDE)
* This process is called ‘Normalisation’, as they come to realise that hearing voices is an extension of ordinary experience of thinking in words.
Reality testing:
Delusions can also be challenged, by examining with the therapist the likelihood that their beliefs are true. Such as if the patient believes they can see into the future, then the clinician may as them to predict cards drawn from a deck.
* Delusions may be too entrenched to succumb to this process, but CBT can still be useful to reduce anxiety and depression associated with living with schizophrenia
5a. psychological treatments of SZ - CBTp
What is the ABCDE approaches to cognitive restructuring?
ABC (DE) model by Ellis is used to understand the source of the faulty cognition, and provide a process to cognitively restructure irrational beliefs (delusions).
A (Activating event) - Drug treatment causes side effects
B (Beliefs) - Hospital staff are trying to kill them
C (Consequences) - Refusing treatment
D (Disputing irrational beliefs (logical) - The staff have no reason to kill them
E (restructured belief (Effect)) - The drugs are necessary.
5a. psychological treatments of SZ - CBTp
strengths
P: A strength of CBTp is evidence supporting its effectiveness, particularly over standard care.
Eg: The NICE review found it reduces hospitalisation rates, symptom severity, and improves social functioning.
Ex: However, most studies involve patients also taking antipsychotics, creating a confounding variable that makes it difficult to isolate CBTp’s effects.
L: While CBTp is effective, its success may depend on being combined with biological treatments, raising concerns about internal validity.
P: CBTp can help where drug therapies fail.
Eg: Sensky et al. (2000) found that resistant patients showed long-term symptom reduction after 19 CBT sessions. Unlike medication, CBTp has no side effects.
Ex: However, engagement can be difficult for patients with severe symptoms like paranoia or avolition, and high costs limit accessibility.
L: While CBTp is valuable, it is not universally suitable. Combining it with antipsychotics may enhance its applicability by first reducing severe symptoms.
5a. psychological treatments of SZ - CBTp
limitation
P: A limitation of using psychological therapies alone is that research supports an interactionist approach.
Eg: Tarrier et al. (2004) found that combining drug therapy with CBT led to greater symptom reduction than either treatment alone.
Ex: Relying solely on psychological therapies overlooks biological factors like dopamine dysfunction, limiting effectiveness.
L: The diathesis-stress model provides a more comprehensive approach, as combining biological and psychological treatments leads to better patient outcomes.
5b. psychological treatments for SZ - family therapy
What is the overall aim of family therapy in schizophrenia?
What are some of the specific aims?
- Overall, family therapy aims to improve communication and interaction in the family
- In keeping with psychological explanations such as the double bind and schizophrenogenic mother, some therapists see the family as the root cause of the condition.
Nowadays family therapy aims to specifically:
* reduce levels of stress caused by expressed emotion (EE)
* reduces the risk of relapse
* increases the chance of the patient complying with medication
* Help families balance care of the individual, and maintain their own lives
5b. psychological treatments for SZ - family therapy
Where does family therapy typically take place?
What is the typical duration/frequency of sessions?
How many sessions does
NICE recommend?
Takes place in the people’s homes and typically two family therapists will work with the relatives and patient. It lasts between 3-12 months with sessions every 2-4 weeks. A minimum of 10 sessions are recommended by NICE.
5b. psychological treatments for SZ - family therapy
Give a brief overview of what happens during family therapy sessions
- Takes place in the people’s homes and typically two family therapists will work with the relatives and patient. It lasts between 3-12 months with sessions every 2-4 weeks. A minimum of 10 sessions are recommended by NICE.
- The therapists work with the family and the patient to develop strategies to cope better with the mental disorder and its symptoms. This hopefully leads to a more supportive and warm atmosphere.
- The relatives are made more aware of the information regarding psychosis and the diagnosis.
- The therapist encourages the relatives to ask questions and learn more about the disorder
- The patient is seen as the expert.
- The goal is also to provide the whole family with practical coping skills which enables them to manage the everyday difficulties.
- Family members learn more constructive ways of communicating and are encouraged to concentrate on any good things that happen rather than negative events.
- The relatives and the patient are also told that it is normal to feel angry and impatient towards each other but that they need to find ways of coping with these feelings without resorting back to high EE patterns of behaviour (which increase relapse)
- Lastly, the family and the patient are trained to recognise the early signs of relapse so that they can respond rapidly to reduce the severity of it.
5b. psychological treatments for SZ - family therapy
What phases does
Burbach’s model of Family therapy comprise?
Burbach’s (2018) Model:
- Phase 1-2: share information and identify resources family can offer
- Phase 3-4: learn mutual understanding, and look at unhelpful patterns of interaction
- Phase 5-7: skills training (eg stress management techniques), relapse prevention and maintenance
5b. psychological treatments for SZ - family therapy
strengths of family therapy
A strength of family therapy as a treatment for schizophrenia is its demonstrated ability to reduce relapse rates, particularly in the short term.
Leff (1985) investigated aftercare in patients with schizophrenia and found that 50% of those receiving
standard outpatient care relapsed within 9 months, compared to just 8% who received family therapy.
However, by two years, relapse rates increased to 50% for family therapy and 75% for standard care.
This suggests that family therapy is highly effective at
reducing hospital readmissions initially, as it promotes positive communication and reduces expressed emotion within families.
However, the long-term benefits may decline as families struggle to maintain these behavioural improvements over time.
This highlights the importance of addressing the reliability of family therapy’s long-term outcomes and suggests it should be used alongside other treatments to ensure sustained effectiveness and greater
generalisability across different families and care settings.
An strength of family therapy is its significant economic benefits when used alongside standard treatment for schizophrenia.
The NICE review of family therapy studies (NCCMH,
2009) found that while family therapy incurs additional costs, these are offset by a reduction in hospitalisation expenses due to lower relapse rates.
This is particularly important as patients are less likely to require frequent and costly readmissions, alleviating
pressure on healthcare systems while improving patient outcomes. Furthermore, the ability to remain at home allows individuals with schizophrenia to experience a more stable and supportive environment, enhancing their quality of life.
However, the effectiveness of family therapy can depend on the long-term engagement of families, which may not always be feasible.
Despite this, the cost-effectiveness and practical benefits of family therapy make it a valuable treatment approach, particularly when combined with other therapies for broader applicability and sustainabilitv.
5b. psychological treatments for SZ - family therapy
limitation of family therapy
A limitation of family therapy is that, while it improves the management of symptoms and supports family dynamics, it does not provide a cure for schizophrenia.
Family therapy primarily focuses on reducing stress, improving communication within the family, and preventing hospital admissions by alleviating expressed emotion.
However, the core symptoms of schizophrenia, such as delusions or hallucinations, often remain, albeit more manageable. This means that while family therapy improves day-to-day functioning and reduces relapse rates, it does not address the root cause of the disorder.
As a result, family therapy should be considered a supplementary treatment rather than a standalone intervention. Its limited impact on symptom elimination highlights the need for a combined approach, often involving biological treatments like antipsychotic medication, to ensure a more comprehensive and sustainable improvement. This raises questions about the validity of family therapy as a sole treatment and its generalisability across all patients with schizophrenia.
5b. psychological treatments for SZ - family therapy
token economies:
Explain how a token economy works
Token economies are a behavioural therapy technique based on Skinners operant conditioning. This is learning through re-enforcement of desired behaviours.
Tokens are used as positive re-enforcement. They are an immediate reward for when the patient shows pre defined target behaviour (such as washing). Tokens are then exchanged for something else that they want. (activities, chocolate)
5b. psychological treatments for SZ - family therapy
token economies:
what is behaviour shaping
Behaviours are progressively changed, with tokens first given for small changes in behaviour towards the ideal.
5b. psychological treatments for SZ - family therapy
token economies:
Where are token
economies implemented?
Psychiatric institutions: Treatment is designed to produce easier to manage behaviour within the hospital, or to prepare long stay patients for transfer into the community.
5b. psychological treatments for SZ - family therapy
token economies:
What sorts of symptoms respond best to token economies?
Mild negative symptoms: Treatment can be used for patients with mild symptoms, but more profoundly ill patients are less able or willing to engage.
5b. psychological treatments for SZ - family therapy
token economies:
What is the main limitation of token economies?
modifying these habits eg: bad hygiene, does not cure SZ but the therapy aims to improve the patient’s quality of life and makes it more likely they can live outside a hospital setting.
5b. psychological treatments for SZ - family therapy
token economies:
Tokens reduce delay discounting - how does this help the approach?
Tokens (e.g. coloured discs) are given to patients who carry out desirable behaviours (e.g. getting dressed, making a bed etc.) This token reinforces the desirable behaviour. The immediacy of the reward is important as it prevents
‘delay discounting’ — the reduced effort of a delayed
5b. psychological treatments for SZ - family therapy
token economies:
Explain how primary and secondary reinforces work in token economies
primary reinforcer: actual reward of what the patient wants eg: sweets or a walk outside
secondary reinforcer: the token, only has value once its paired with the primary reinforcer
5b. psychological treatments for SZ - family therapy
token economies:
describe how the cycle works
- tokens are paired with rewarding stimuli and become primary reinforcers
- patients engage in ‘target’ behaviour or reduces negative ones
- patients are given a token for engaging in these target behaviours
- patients trade these tokens for desirable items or privileges
5b. psychological treatments for SZ - family therapy
strength of token economies
P: A strength of token economies is research support for their effectiveness in treating schizophrenia.
Eg: Dickerson et al. (2005) found that 11 out of 13 studies showed positive effects.
Ex: However, methodological flaws, like lack of control groups and unclear outcome measures, undermine the reliability and validity of the findings.
L: While token economies may improve behavior and functioning, the evidence’s limitations question their overall effectiveness, highlighting the need for more rigorous research.
5b. psychological treatments for SZ - family therapy
limitation of token economies
P: A limitation of token economies is their effectiveness being limited to hospital settings.
Eg: Corrigan (1991) notes that in hospital wards, staff can consistently reward behaviors, but in community settings, limited treatment time makes reinforcement difficult.
Ex: This reduces the system’s real-world applicability and raises ethical concerns, as it benefits only hospitalized patients and excludes those in community care.
L: Therefore, token economies have limited ecological validity and may not offer equitable treatment options for all patients.
- interactionist approach
What does the diathesis stress model suggest in explaining sz?
The diathesis-stress model says both vulnerability/diathesis and a stress trigger are needed to develop SZ
diathesis:
-genetic factors
-physical trauma prenatally or during birth which leads to structural abnormalities of the brain and abnormalities in the neurotransmitter systems
stressors:
- chronic psychology and social stressors
-family environment with high expressed emotion
- drug use
- interactionist approach
What does the original diathesis-stress model suggest?
The original diathesis-stress model (Meehl,
1962)
Vulnerability - entirely genetic ‘single schizogene’
Meehl argued that someone without this gene should never develop SZ, no matter how much stress they are exposed to.
But a person who does have the gene is vulnerable to sz when exposed to chronic stress (e.g. schizophrenogenic mother)
- interactionist approach
What does the updated model suggest about the diathesis?
What does the updated model suggest about the stress?
It is now believed that diathesis is not due to a single schizogene. Instead it is thought that many genes increase vulnerability - SZ is polygenic, and that individuals vary in their polygenic risk factor
* Also, diathesis does not have to be genetic. It could be early psychological trauma that affects brain development.
* For example, child abuse affects the hypothalamic-pituitary adenal (HPA system), making a child vulnerable to stress.
- interactionist approach
What treatment would be offered using the
interactionist approach?
the model is associated with combining antipsychotic medication and psychological therapies, usually
CBT
Turkington et al (2006) suggest it is possible to see value in biological causes of SZ and still practise CBT to relieve psychological symptoms - perhaps this helps to manage symptoms rather than targeting any cause.
- interactionist approach
strengths
P: A strength of the interactionist approach is the supporting research showing the importance of both genetic and environmental factors in schizophrenia.
Eg: Gottesman (1991) found a higher concordance rate for schizophrenia in monozygotic (48%) compared to dizygotic twins (17%), which is much higher than the general population rate of 1%.
Ex: This suggests genetics play a key role, but environmental or psychological factors are also crucial, supporting the diathesis-stress model. However, twin studies may overestimate genetic influence due to shared environments.
L: Therefore, this research validates the interactionist approach by demonstrating that both genetic and environmental factors contribute to schizophrenia.
P: A strength of the interactionist approach in treatment is the evidence supporting combined medication and psychological therapy.
Eg: Tarrier et al. (2004) found patients receiving both drug therapy and CBT showed lower symptom levels than those receiving either treatment alone.
Ex: This suggests the interactionist approach offers a more comprehensive treatment by addressing both biological and psychological factors. However, practical limitations such as increased costs and the need for multidisciplinary teams may affect its accessibility.
L: Despite these limitations, the interactionist approach improves treatment outcomes, offering a holistic solution and enhancing the approach’s generalisability.
- interactionist approach
limitation
P: A limitation of the interactionist approach is that the original diathesis-stress model is overly simplistic.
Eg: The model suggests a single “schizogene” causes vulnerability, but research shows that multiple genes, each with a small effect, contribute to schizophrenia. Additionally, stress can come from various sources, including biological factors.
Ex: For example, Houston et al. (2008) found that childhood sexual trauma acted as a diathesis, while cannabis use triggered schizophrenia.
L: This highlights the reductionist nature of the original model, which viewed diathesis as purely biological and stress as purely psychological. The revised model is more comprehensive but still requires further refinement to fully explain the complexity of schizophrenia’s development.
