Schizophrenia Flashcards
1
Q
What is Schizophrenia?
A
-Psychotic disorder characterised by the loss of contact with reality.
-Shown as; lunacy, madness, insanity.
-Until 1908, known as dementia praecox.
-Symptoms: characteristics of disorder (emotional/behavioural/cognitive).
-Feature: the facts about schizophrenia (stats/who suffers).
-Occurs in 1% of the population.
-25% will recover fully, 25% improve with treatment, 25% relapse & 25% do not improve at all.
2
Q
How is it classified?
A
Positive symptoms: Type 1, Distortion of normal function - being added - (delusions, hallucinations, disorganised speech, grossly disorganised behaviour).
Negative symptoms: Type 2, Lack of normal function - taken away - (Alogia, affective flattening, avolition, anhedonia).
3
Q
Discussion of the symptoms
A
Positive:
-can be affected by cultural differences.
-tend to have greater weight when diagnosing.
-hard to measure objectively.
Negative:
-start before positive.
-less affected by cultural factors.
-more objectively measured.
4
Q
Positive symptoms: Hallucinations
A
-Bizarre sensory experiences & perceptions of the environment.
-Can be; visual, auditory, olfactory (smells), tactile (feelings).
-ie. Hearing voices criticising them.
5
Q
Positive symptoms: Delusions
A
-Irrational beliefs that seem real to the person but are not.
-Paranoia (belief of being followed/spied on etc).
-Delusions of grandeur - inflated beliefs of a person’s power & importance.
-Delusions of reference - messages directed to them.
-ie. Someone may think their phone is tapped into or they have superpowers etc.
6
Q
Positive symptoms: Disorganised speech
A
-Result of abnormal thought processes where the individual has problems organising thoughts which shows up in speech.
-Derailment - slip from one topic into another.
-Word salad - speech is incoherent & sounds like gibberish.
-ie. Replying in gibberish or jumbled words when asked a question.
7
Q
Positive symptoms: Grossly disorganised behaviour
A
-Inability or motivation to initiate a task or complete it once it’s started leading to difficulties in daily life.
-Catatonic behaviours - reduced reaction to immediate environment, rigid postures or aimless motor activity.
-Bad hygiene & decreased interest in appearance.
8
Q
Negative symptoms: Speech poverty (alogia)
A
-Lessening of speech fluency, productivity, reflecting slow/blocked thoughts.
-Producing fewer words in a given time on a task of verbal fluency.
-Less complex
9
Q
Negative symptoms: Avolition
A
-Sometimes called ‘apathy’.
-Reduction of interests & desires as well as an inability to initiate & persist in goal-directed behaviour.
-Physical inability to achieve goals.
-Lack of desire to persist in goal-directed behaviour (emotional inhibition).
-ie. Reduction in self-initiated involvement in activities that are available to them.
10
Q
Negative symptoms: Affective flattening
A
-Reduction in the range & intensity of emotional expression, including facial expression, voice tone, eye contact, body language.
-Fewer body & facial movements & smiles.
-Less co-verbal behaviour.
-Deficit in prosody (ie. tempo, pausing) - paralinguistic feature.
-ie. Not using movements of body when talking, no extra info provided via prosody*
*flow of speech
11
Q
Negative symptoms: Anhedonia
A
-Loss of interest or pleasure in almost all activities or a lack of reactivity to normally pleasurable stimuli.
-Pervasive call- embracing or confined to the aspect.
-Physical - inability to experience physical pleasures.
-Social - inability to experience pleasure from interacting, which normally overlaps with depression.
-ie. Not interested in talking to others, does not enjoy food etc.
12
Q
How is a person diagnosed with schizophrenia?
A
-Clinicians determine symptoms and compare it to the classification criteria within a diagnostic tool (ICD/DSM).
-If they fit the criteria, they’re diagnosed with it.
-DSM signposts to alternative disorders if they do not meet the criteria.
13
Q
Diagnostic tool: DSM-5
A
-American Psychiatric association’s Diagnostic & Statistical manual of Mental Disorders.
-Book outlining classification criteria.
-Doctors signpost relevant treatments.
-Used to help with correct diagnosis.
14
Q
Diagnostic tool: ICD-10 (1994)
A
-International classification of Diseases, 10th revision, Clinical Modification.
-Developed by the WHO.
-Subsection for mental & behavioural disorders.
-ICD-11 released in Jan 2022.
15
Q
DSM: Criteria
A
A. Characteristics of symptoms (TWO OR MORE) persistent significant period of time for a month: -Delusions, hallucinations, disorganised speech, catatonic behaviour, negative symptoms.
-only one “A” symptom required in extreme cases
B. Social/occupational Dysfunction: one or more major areas of functioning (ie. work), marked below the level achieved prior to onset.
C. Duration: continuous signs for at least 6 months, including a month of symptoms meeting criterion A.
Excluding: the symptoms are not better accounted for by another disorder; psychiatric, substance abuse or a general medical condition.
16
Q
ICD-10 criteria: 6A20 Schizophrenia
A
-Symptoms persisting for at least one month for diagnosis.
-Not a manifestation of another health condition or due to a substance or medication on the CNS.
-At least 2 of the following symptoms, 1 from item a-d to be qualified.
A. persistent delusions
B. Persistent hallucinations
C. Disorganised thinking
D. Experienced of influence, passivity or control
E. Negative symptoms
F. Grossly disorganised behaviour impeding goal-directed activity
G. Psychomotor disturbances
17
Q
Strength of diagnosis of schizophrenia: Reliability
A
-A psychiatric diagnosis is reliable when different diagnosing clinicians reach the same diagnosis for the same individual (inter-rater reliability).
-Also, when a clinician reached the same diagnosis for the same individual on 2 occasions (test-retest reliability).
-Osorio et al report excellent reliability for the diagnosis of sz in 180 individuals using DSM-5.
-Pairs of interviewers achieved inter-rated reliability of +0.97 & test-retest of +0.92.
Shows diagnosis of sz is consistently applied.
18
Q
Limitation of diagnosis of schizophrenia: Low validity
A
-Criterion validity is about how different assessment symptoms may not arrive at the same diagnosis for the same patient.
-Cheniaux et al had 2 psychiatrists independently assess the same 100 clients using ICD-10 & DSM-5 & found 68 diagnosed under ICD, but only 39 under DSM.
Suggests issues with diagnosis and low criterion validity.
Counter: in Osario’s study, there was excellent agreement between clinicians when using 2 measures from DSM, meaning criterion validity is good if it takes place within a single diagnostic system.
19
Q
Limitation of schizophrenia diagnosis: Co-morbidity
A
-If conditions occur at the same time, this question the validity of their diagnosis & classification since it might be a single condition.
-Sz is commonly diagnosed with other conditions.
-ie. 1 review found that half of those diagnosed with sz had a diagnosis of depression or substance abuse.
-Hard to establish cause and effect.
This is a problem for classification since it means sz may not exist as a distinct condition & poses an issue for diagnosis since some diagnosed with sz may have unusual cases of conditions like depression.
20
Q
Limitation of schizophrenia diagnosis: Gender bias
A
-Since the 80s, men have been diagnosed more commonly than women (1.4:1 ratio).
-Could be because women are less vulnerable than men because of genetic factors.
-However, it’s more likely because they have closer relationshios and get support so women with sz function better than men.
Under diagnosis is a gender bias and means some women may not receive beneficial services & treatment.
21
Q
Limitation of schizophrenia diagnosis: Culture bias
A
-Some symptoms, particularly hearing voices, have different meanings in different cultures.
-ie. In Haiti, they believe voices are from ancestors.
-African-Caribbean’s are 9X likelier to receive a diagnosis as White British people, though people living in African-Caribbean countries are not, ruling out a genetic vulnerability.
-Could be due to cultural bias by psychiatrists from different cultural backgrounds.
-Leads to over interpretation of symptoms in black British people.
Means African-Caribbean’s may be discriminated against by a culturally biased diagnostic system.
22
Q
Limitation of schizophrenia diagnosis: Symptom overlap
A
-Overlap between symptoms of sz and others.
-ie. Overlap between sz and bipolar disorder as they both involve positive symptoms (delusions) & negative (avolition)z
-As for classification, this means sz and bipolar disorder may not be 2 different conditions but variations of a single condition.
-Means sz is hard to distinguish from bipolar disorder.
-Read found most diagnosed with sz could be diagnosed with a diff disorder.
-Problematic and can lead to a lower standard of care of some medical conditions & unhelpful treatments.
As with co-morbidity, symptom overlap means that sz may not exist as a distinct condition & if it does, it may be hard to diagnose.
Both classification & diagnosis are flawed.
23
Q
Biological explanations of schizophrenia: The genetic basis - Family studies
A
-Sz is more common among biological relatives of a person with sz.
-ie. Someone with an aunt who had it has a 2% change, sibling 9%, identical twin 48%.
-Gottesman’s study found that as genetic similarity increases, so does the probability of sharing sz.
-Family members tend to share environmental aspects as well as genes so the correlation represent both - but family studies are still important for supporting genes explanation.
24
Q
Family studies: Twin studies
A
-If MZ twins are more concordant than DZ, then this suggests the greater similarity is due to genetic factors.
-Joseph (2004) found that studies showed a concordance rate for MZ twins of 40.4% and 7.4 for DZ twins.
-This shows that genetic similarity can increase chance of developing sz.
25
Family studies: Adoption studies
-Since it’s difficult to separate genetic and environmental influences, studies of genetically related individuals who were reared **apart** have been used.
-**Tienari et al** 11/164 (6.7%) adoptees whose mothers had sz, revived a diagnosis compared to 4/197 control adoptees (non sz).
-Shows that the genetic liability had been ‘decisively confirmed’.
26
The genetic basis of schizophrenia: Candidate genes
-Nucifora et al (2012) found a link between mutations in the NPAS3 gene & sz but there’s more.
-Sz is polygenic.
-108 separate genetic variations are associate with the increased risk of sz.
-As many different genes are involved, sz is seen to be aetiologcally heterogenous.
27
Candidate genes: Ripke et al
-Combined all previous data from genome-wide studies of sz.
-The genetic makeup of 37,000 people with a sz diagnosis was compared to control and 108 genetic variations were associated with slightly increased sz risk.
-Different studies identified different candidate genes and it appears sz is **aetiologically heterogeneous** (diff combo of factors can lead to condition).
28
Positive & negative consequence of Ripke’s findings
:) Identifying genetic variations that increase risk mean sz would be easier to detect for medical professionals and could help ensure correct diagnosis.
:( Socially sensitive as this data might act as a self-fulfilling prophecy, where parents with a variation could be convinced they are developing it and can cause anxiety/paranoia.
29
The genetic basis of schizophrenia: The role of mutation
-Can have a genetic origin in the absence of a family history of the disorder.
-An explanation is mutation in parental DNA which can be caused by radiation, poison or viral infection.
-Evidence comes from positive correlations between paternal age & risk of sz, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50.
(Brown et al 2002)
30
Strength of the genetic explanation: Research support (Tienari & Hilker)
Highlights links between genetics and sz.
-Tienari et al found 6.7% of 164 adoptees whose biological mothers had sz also diagnosed, whereas only 2% of 197 control group diagnosed.
-Hilker et al found a concordance rate of 33% for identical twins and 7% for non-identical twins.
More genetic similarity increases risk of vulnerability to schizophrenia.
31
Evaluation of the genetic explanation: Real-world application - Genetic counselling
-If 1 or more potential parents have a relative with sz, they risk having a child who has it (Gottesman).
-Involves informing potential parents of probabilities so they can make informed choices of whether to have children who risk having a poor quality of life if they develop sz.
-However, genetic counselling provides only an average risk estimate based on the whole population.
-But, this doesn't accurately predict whether a specific child will develop schizophrenia because their environment also plays a role.
-ie, a child's risk will be higher than their genetic likelihood suggests if they experience childhood trauma and use cannabis as a teenager.
-But, their risk will be lower if they avoid these environmental factors.
-Can lead to genetic modification to achieve ‘designer babies’ that suit preferences & suggests a person with sz is undesirable.
32
Limitation of the genetic explanation: Excludes environmental influences
Environmental factors increase risk of developing sz.
-Includes biological influences. Could include birth complications and smoking THC-rich cannabis in teenage years.
-Includes psychological factors. Trauma can lead to MH issues and vulnerability.
-Morkved et al found 67% of people with sz and related psychotic disorders reported at least 1 childhood trauma compared to 38% of a matched group with non-psychotic MH issues.
Genetic explanation alone is limited.
33
Biological explanation: Neural correlates explanation
-Focusses on important role of neurotransmitter dopamine and areas of the brain that are influential in the onset & development of sz.
34
Neural explanation: Discovering the dopamine link
-Chlorpromazine develops as an antihistamine to treat nausea & allergies to calm patients before surgery.
-Also found to be effective in reduction of symptoms in sz patients.
-Links to expkanation since scientists understood how it worked on CNS (reduced dopamine).
-Noticed peope taking it had similar symptoms to Parkinson’s (low dopamine)
Means dopamine plays a role in development!!!
**Dopamine**: neurotransmitter that has an okie in pleasure & reward seeking behaviour helps memory, focus, motivation & controls mood & emotions.
35
Neural explanation: The original dopamine hypothesis - Hyperdopaminergia
-Sz is result of high levels of dopamine in sub cortical regions of the brain which is associated with positive symptoms. Sz people have high no. of D2 receptors on receiving neurons so more dopamine binding & neurons firing.
-Drugs that increase dopamine activity, like amphetamines, flood synapses with dopamine. In high doses, they can cause schizophrenia-like symptoms in healthy individuals, which disappear once the drug is stopped. This supports the role of dopamine in schizophrenia.
-Antipsychotic drugs, known as dopamine antagonists, work by blocking dopamine activity in the brain. By reducing dopamine levels in neural pathways, they help remove schizophrenia symptoms such as hallucinations and delusions.
36
How would dopamine affect functioning?
-Too much dopamine receptors in pathways from the subcritical area to Broca’s may explain speech poverty/auditory hallucinations.
-More dopamine receptors on post-synaptic membrane means more neurotransmitters can bind.
-Increased probability of dopamine binding to post-synaptic receptions (excitatory -> summation) action potential.
37
The neural explanation: Updates dopamine hypothesis
-Sz is result of low levels in cortical areas of brain.
-Low dopamine in prefrontal cortex can link to changes in cognitive functioning and can present as negative symptoms.
-Davis & Kahn said positive symptoms are caused by an excess of dopamine, especially in mesolimbic pathway.
-Negative from deficit of dopamine, prefrontal cortex, mesocortical pathway.
38
What causes it?
-Howes (2017) - genetic variations & physical & environmental stressors = greater sensitivity to hypo & hyper dopaminergia.
39
The neural explanation: Specific brain areas involved in schizophrenia
-**The prefrontal cortex (PFC)** is responsible for executive functions like planning and reasoning, but research shows it is impaired in schizophrenia. Cognitive symptoms may result from deficits in the PFC and its connections, particularly with the hippocampus.
-**Hippocampus:** Studies have found anatomical changes in the hippocampus in schizophrenia patients, and weaker nerve connections between the hippocampus and PFC are linked to working memory impairments. Additionally, hippocampal dysfunction may influence dopamine release in the basal ganglia, further affecting PFC function.
-**Grey matter:** especially in the temporal and frontal lobes, and enlarged ventricles. Enlarged ventricles may result from improper brain development or damage. Individuals at high risk who develop schizophrenia show faster grey matter loss and greater ventricular expansion.
-**White matter:** linked to reduced myelination of white matter, particularly in pathways between the prefrontal cortex and hippocampus. This affects communication between brain regions and contributes to cognitive symptoms.
40
Strength of the genetic explanation: Supporting evidence (Leucht et al 2013)
-Meta-analysis of 212 studies & he concluded that all antipsychotic drugs tested in these were significantly more effective than placebo in treating positive & negative symptoms.
-This was achieved by reducing the effects of dopamine.
Reinforces idea that lower levels of dopamine reduce sz symptoms & influence it.
41
Limitation of the genetic explanation: Glutumate
Evidence for the central role of glutamate.
-Post-mortem & live scanning studies consistently found raised levels of neurotransmitter glutamate in people with sz.
-Also, several candidate genes for sz are believed to be involved in its production or processing.
Means there’s an equally strong case for role of other neurotransmitters.
42
Strength of the genetic expkanation: Real-world application - Early intervention
Early intervention may prevent development of later stages of disorder.
-This concept of ‘treatment of prevention’ is seen in NA longitudinal study using assessments like neuroimaging to predict who will develop psychoses such as sz.
-These people can be given early treatment to prevent it getting worse.
43
Biological treatment of schizophrenia: Drug therapy
-Most common treatment is **antipsychotics.**
-Some people take these over a short course and some for life, some have reoccurring sz when they stop.
-Work by blocking dopamine receptors and its re uptake.
-Can be taken as tablets, syrups, injections (long/short - term).
44
Drug therapy: Typical antipsychotics
-Schizophrenics produce too much dopamine.
-We cannot decrease the amount of dopamine or receptors so you block the receptors.
-They decrease the activity of dopamine & are seen as **dopamine antagonists.**
-They also have a sedative effect on those that take them (because of effect on histamine receptors).
-Most typical one is **chloropromazine.**
(Initially when they take it, dopamine will build up, then production will be reduced, which normalises neurotransmission in brain and reduces symptoms like hallucinations).
45
Drug therapy: Atypical Antipsychotics - Why?
1. They carry a lower risk of extrapyramidal side effects (involuntary movements).
2. They have a beneficial effect on negative symptoms and cognitive impairment.
3. They suitable for treatment-resistant patients as they can be administered through injection.
46
Drug therapy: Atypcial antipsychotics
-Only temporarily occupy D2 receptors and then rapidly dissociate to allow normal transmission.
-Because atypical antipsychotics like **clozopine** have little effect on dopamine systems, they tend to not cause movement problems like typical ones do.
-Have a stronger affinity for seratonin receptors and a lower for D2 receptors. Explains difference in effects of them.
47
Atypical antipsychotics: Clozapine & Risperidone
**Clozapine**
-Development and Usage: Introduced in the 1960s, clozapine is effective for treatment-resistant schizophrenia but carries a risk of agranulocytosis, necessitating regular blood monitoring.
-Efficacy: Studies suggest clozapine may be slightly more effective than risperidone, with fewer patients discontinuing due to ineffectiveness.
-Administration: Administered orally, with typical daily doses ranging from 300 to 450 mg.
**Risperidone**
-Development and Usage: Developed in the 1990s to provide efficacy similar to clozapine without its severe side effects.
-Efficacy: Effective against both positive and negative schizophrenia symptoms, with a low incidence of extrapyramidal side effects.
-Administration: Available in tablet, syrup, and bi-weekly injection forms, with typical daily doses ranging from 4-8 mg, up to a maximum of 12 mg.
48
Strength of the biological treatment: Supporting evidence
-Thornley et al reviewers studies comparing effects of chloropromaxine to controls. 13 trails found it was associated with better functioning & reduced symptom severity.
-Meltzer concluded clozapine is more effective than typical antipsychotics & atypical a that it’s effective in 30-50% of treatment-resistant cases where typical have failed.
Antipsychotics work
49
Limitation of the biological treatment: Flawed evidence
-Healy said most studies are of short-term effect only & some successful trials have had their data published multiple times.
-This exaggerates size of evidence base for positive effects.
-Also, as they have powerful calming effects, it’s easy to demonstrate that they have positive effect on symptoms, but this isn’t the same as saying they reduce the severity of the psychosis.
Evidence base for antipsychotic effectiveness isn’t as impressive.
50
Limitation of biological treatment: Side effects
-Typical associated with dizziness, agitation, sleepiness, weight gain, itching.
-Long term use can cause **tardive dyskinesia** such as grimacing & blinking.
-The most serious one is **neuroleptic malignant syndrome.** This happens when the drug blocks dopamine action in hypothalamus.
-NMS results in high temp, coma etc.
-Estimates of its frequency range from less than 0.1%-2%.
Means antipsychotics can do harm as well as good & people may avoid them.
51
Limitation of biological treatment: Unclear mechanism
We do not know why they work.
-Understanding of mechanism is tied with original dopamine hypothesis (idea that symptoms are linked to high activity in sub cortex).
-Some dopamine levels are too low than too high.
-If this is true, most antipsychotics shouldn’t work.
May be not be the best treatment (maybe another factor makes them successful).
52
Limitation of biological treatment: Treats symptoms
-Doesn’t treat underlying causes of psychotic disorders, since they primarily target neurotransmitter imbalances.
-Does not address environmental or psychological issues like trauma.
-Limits their effectiveness in promoting long-term recovery and can leave underlying issues unresolved.
53
Psychological explanation: Family dysfunction
Claims sz is caused by abnormal communication patterns in the family.
Focusses on:
1. Schizophrenogenic mother
2. Double-bind theory
3. Expressed emotion
54
Family dysfunction: Schizophrenogenic mother (Fromm-Reichmann)
-Belives the mother is cold, rejecting, fearful of intimacy, perfectionist & controlling.
-Creates tension and secrecy.
-Confusing for child as mother may be overprotective but then rejecting child.
-Leads to child being distrustful and can create paranoid delusions.
55
Supporting evidence for Sz mother: Mednick (1984)
-Identified 207 children to be at high risk of developing sz because of their dysfunctional families (with sz mothers).
-Comapred to control gopi of 107 people.
-Within 10 years, 17 of high risk diagnosed compared to 1 in control group.
Shows that children of mothers who display these temperamental & unstable mothers are more likely to develop sz.
56
Why is it socially sensitive?
-Blames mother for their child developing sz.
-Doesn’t take into account involvement of other family members (ie. father).
-As well as this, mother’s trauma can lead to them being cold based on their own parenting.
57
Family dysfunction: Double-bind theory (Bateson et al 1972)
-States sz is caused by mixed messages from parents that express care but also appear critical.
-Can relate to a contradiction between a persons verbal & non-verbal behaviour.
-Causes recipient to develop an incoherent perception of reality causing sz symptoms such as social withdrawal.
-Child feels trapped & is scared to do the wrong thing & is unsure of what that is.
-Child received invalidating & mixed messages from parents -> disorganised thinking & delusions.
-Prevent development of accurate perception of reality.
58
Evaluation of Double-bind theory
:( Reductionist -> blames mothers and ignores genetic basis.
:) Berger found that sz reported a higher recall of double-bind statements than non.
:( Weak evidence - based on **clinical observations** rather than systematic evidence. & uses self-reports.
:) Gibney claims it has value since it led to development of family therapy.
59
Family dysfunction: Expressed emotion
-Members of family talk about the patient in a critical or hostile manner or a way that indicates emotional over-involvement with patient.
-Focusses on level of negative EE expressed towards a person with sz.
-Contains several elements:
-> verbal criticism
-> anger and rejection
-> emotional over involvement
-High levels of EE are a serious source of stress for those with sz.
-Can trigger onset of sz of someone vulnerable to it.
-Can increase relapses in sz.
-Sz people have low tolerance for intense environmental stimuli & the negative emotions arouse patient leading to stress & sz episode.
60
Supporting research - Relapse
-Linszen et al found a patient returning to family with high EE is 4X likelier to relapse than a family with low EE.
-Kuipers et al found high levels of EE likely to influence relapse rates.
61
Limitation of expressed emotion: Individual differences
Not all patients who live in high EE families relapse & not all in low EE homes avoid relapse.
-Altorfer et al found 25% patients studied show no physiological response to high EE comments by relatives
-Lebell et al say how patients perceive the behaviour he is more important. When high EE behaviours arent perceived as negative, patients can do well regardless of the environment.
62
Strength of Family dysfunction: Research support (Read et al)
Links family dysfunction to sz.
-Indicators of this include insecure attachment and exposure to childhood trauma like abuse.
-Found adults with sz are disproportionately likely to have insecure attachment (type C/D).
-Reported 69% women & 59% sz men have history of physical and/or sexual abuse.
Family dysfunction increases people’s vulnerability to sz.
63
Psychological treatment: Family therapy
-During sessions, the identified patient is encouraged to talk to their family & explain the support they’d find helpful.
-Commonly used in conjunction with routine drug treatment & outpatient clinical care.
-Aims to support carers in an attempt to make family less stressful & reduce relapse, & improve communication.
64
What is family therapy (Pharoah 2010)
-Typically offered for period of 3-12 months with at least 10 sessions.
2 strategies:
1. Reduce negative emotions and EE to reduce chance of relapse.
2. Encourages family members to improve beliefs of sz and improve their ability to help.
-Garety et al estimates the relapse rate for individuals who receive family therapy as 25% compared to 50% who receive standard care alone.
65
NICE - therapy
-Recommend it should be offered to ‘all individuals diagnosed with sz in in contact with family.’
-Priority where there’s persistent symptoms or high relapse risk.
-Involves; comfy setting, positive psychology, strategies etc.
66
Strategies family therapy uses
-Psychoeducation to help both understand sz.
-Reducing emotional climate within the family (ie. anger)
-Enhancing relatives’ ability to anticipate & solve problems.
-Setting reasonable expectations among family members.
-Encouraging boundaries.
-Resolving practical issues.
67
Family therapy - A model of practice (Burbach 2018)
1. Sharing basic info & provide emotional and practical support.
2. Identifying resources including what family can and can’t offer.
3. Encourage mutual understanding creating safe space.
4. Identifying unhelpful patterns of interaction.
5. About skills training (ie. stress management)
6. Relapse prevention planning.
7. Maintenance for the future.
68
Strength of Family therapy: Benefits whole family
-Lobban et al analysed results of 50 studies that included family intervention.
-60% of thne reported a positive impact on at least 1 outcome category (ie. problem-solving).
-This reduces negative aspects of EE which reduced presence of an environmental stressor, reducing w of sz symptoms.
Helps patient AND relatives.
69
Strength of Family therapy: Cost-effective due to low relapse rates
-NICE review showed that family therapy is related to cost savings when offered to people with sz in addition to standard care.
-Large reduction in hospitalisation di to low relapse rates associated with this intervention, by 50-60% (McFarlene).
-Evidence that it reduces relapsed rates for a significant period after completing the intervention.
70
Limitation of Family therapy: Overestimated significance
-Found little difference between those given sessions of family therapy compared to those who had carers but no therapy.
-Both had low relapse rates.
-Researchers found carers displayed low rates of EE, which may reflect cultural changes in carers attitudes towards sz.
Profession of knowledge in sz means that a lack on understanding in a family is not as prevalent as it used to be.
71
Limitation of Family therapy: Pharoah et al
-Says it is mainly effective since it increases medication compliance.
-Does not itself help symptoms.
-Makes people fake medicine to improve mental state.
Counter: However, his research has issues. 10/53 studies in his meta-analysis didnt use any blinding and the ragers aware of the treatment they’re rating.
May lead to teacher bias affecting validity.
72
Psychological explanations for schizophrenia: Cognitive explanation - Dysfunctional thought processing
-Any abnormalities in thought and behaviour (output) is a result of dysfunctional thought processing.
-Therefore info that is inputted isn’t processed correctly, or it’s interpreted incorrectly.
-Dysfunctional thoguht processing could have biological causes.
-Reduced thought processing in ventral striatum associated with negative symptoms, while reduced processing of info in the temporal & cingulate gyri is associated with hallucinations. (Simon et al)
73
Cognitive explanation: Egocentric bias
-Characteristic of delusions is the degree to which the individual perceived themselves as the central component in events **(egocentric bias)** & jumps to conclusions about external events.
-Causes people with sz to interpret neutral events as centred around them, false conclusions.
74
Cognitive explanation: Metarepresentation (Frith 1992)
-Ability to reflect on our behaviours and thoughts.
-Dysfunction results in a person being unable to differentiate between thoughts and behaviours carried out by ourselves or others.
-Would explain hallucinations of hearing voices and delusions like thought insertion.
75
Cognitive explanation: Impairments in selective attention
-Normally able to process filter incoming info & process its meaning.
-Thought that these filtering mechanisms & processing symptoms are dysfunctional in sz people.
76
Cognitive explanation: Auditory selective attention
-Refers to process by which the brain selects the sounds it responds to.
-Our brain selects info to pay attnetion to & ifnored the rest.
-The negative symptoms of sz may be the result of cognitive strategies used by the individual to keep mental stimulation manageable.
-This happens when people experience over-whelming levels of info from the external world & their inner world.
-> could be due to auditory selective attention impairment.
77
Cognitive explanation: Central control dysfunction (Frith et al)
-Suggested there’s issues with ability to suppress automatic responses.
-While we do things, there’s multiple possible triggers & thoughts that can come to mind.
-A sz person is unable to suppress these automatic thoughts (ie. say words that trigger new thoughts)
-May explain symptoms like; delusions - speech derailment/disorganised speech, speech poverty.
78
Strength of the Cognitive explanation: Research support (Stirling et al)
-Evidence for dysfunctional thought processing.
-Sterling et al compared performance on a range of cognitive tasks in 30 sz people and a 30 control group.
-Used tasks like the **stroop task** where ppts name the font-colours of colour-words, so they have to suppress the tendency to read the words aloud.
-People with sz took longer - **twice** as long.
Means the cognitive processes of people with sz are impaired.
79
Limitation of Cognitive explanation: Proximal explanation
Only explain the proximal origins of symptoms.
-Expain what is happening *now* to produce symptoms - as distinct from distal explanations which focus on what initially caused the condition.
-Possible distal one are genetic & family dysfunction.
-What’s unclear is how genetic variation or dysfunction can lead to metarepresentation or CCD.
Cognitive theories only provide partial explanations for sz.
80
Evaluation of Cognitive explanation: Psychological or biological? (Toulovpoulou et al)
-Found cognitive deficits in both sz people and their non-sz relatives suggesting a genetic basis for cognitive dysfunction.
-Supports the cognitive explanation by highlighting deficits in memory, attention, and problem-solving, which may contribute to schizophrenia.
Counter: The presence of cognitive impairments in non-sz relatives suggests these deficits increase vulnerability rather than directly causing schizophrenia.
-Cognitive deficits could be a consequence of sz rather than a cause, meaning neurobiological factors might be responsible for these impairments.
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Psychological treatment: CBTp (for psychosis)
-A talking therapy lasting over 5-20 weeks & can be in groups or individually.
-Identified and changes ‘faulty cognitions’. Focus on addressing distorted thought patterns & how a patient responds to them. (ABC MODEL)
-NICE recommended.
-Sz patients encouraged to **reality-test** their hallucinations & delusions to reduce distress.
-Sz people may question & try to control the voices they hear.
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CBTp: Coping strategy enhancement (Tarrier)
Involved building upon existing strategies of people with sz.
-Noted individuals were able to identify triggers for episodes and devise own strategies.
-Examples of triggers:
-> people
-> stress
-Aim of CBTp is to develop coping strategies and the stress produced.
2 types of strategy developed:
1. **Cognitive** such as distraction, positive self-talk, concentration.
2. **Behavioural** such as relaxation, social withdrawal/increase, music etc.
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CBTp: Therapy method
2 parts to the therapy:
1. Develop a rapport with client and identify triggers of psychotic symptoms, & review existing coping strategies and develop new ones.
2. Target specific symptoms and find strategies to deal with them.
-Ppts have homework to consolidate strategies between sessions.
-Overall aim is to have **two** effective strategies for each negative symptom.
-Develop client-patient relationship, identify triggers, challenge then & cope.
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CBTp: 6 processes
1. **Assessment:** patient talks about their experienced & therapist helps them set goals.
2. **Engagement:** therapist emphasise with patient & says explanations of distress can be developed together.
3. **The ABC model:** patient beliefs are rationalised, disputed & changed to prevent consequences.
4. **Normalisation:** undertanding that others also have unusual experiences reducing anxiety & increases chance of recovery.
5. **Critical collaborative analysis:** therapist uses gentle questioning to help patient understand illogical deductions in a non-judgmental environment.
6. **Developing alternative explanations:** patient develops healthier explanations which can be made with therapist if they struggle with dysfunctional thinking patterns.
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Strength of CBTp: Evidence for effectiveness (Chadwick)
-Helped an individual with a delusion his thinking could influence the future.
-Patient failed to predict what would happen in 50 video clips shown to him which gave him evidence to show that his delusional beliefs were false.
Demonstrates that CBTp can help patients reality-test their delusions and reduce symptom severity.
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Explainining schizophrenia: The Interactionist approach
-The ‘bio social’ approach.
-Interaction of biological factors (genetic vulnerability/neurological/chemical), psychological (stress) and social (family).
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Interactionist approach: Diathesis stress model
-People have a predisposition (ie. genetic vulnerability) which is triggered by environmental stressors (ie. life events/abuse/trauma) and this can lead to sz.
-People can have high vulnerability and low stressors or even low vulnerability and high stressors.
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Interactionist approach: Meehl’s original diathesis stress model (1962)
-Diathesis (vulnerability) is entirely genetic - result of a single schizogene, which led to a biologically based schizotypic personality - extremely sensitive to stress.
-No amount of stress will lead to sz if there’s no gene.
-However, chronic stress in someone with the gene can lead to the development of the disorder since nature and nurture interact.
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Limitation of Meehl’s original stress model: Narrow
-Ripke et al found many genes (polygenic), not a single gene, increases vulnerability slightly. This casts doubt on a single schizogene.
-There are other factors other than psychological, that can trigger the disorder.
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Interactionist approach: Modern understanding of ‘diathesis’
-Understand multiple genes can increase vulnerability.
-Views of diathesis include a range of factors beyond the genetic, including psychological trauma, so trauma becomes the diathesis rather than the stressor.
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Modern understanding of ‘Diathesis’: The effect of psychological trauma (Read et al 2001)
-Created neurodevelopmental model where early truna affects developing brain.
-Can cause the HPA (hypothalamic-pituitary-adrenal) system to become overactive.
-HPA regulates body’s response to stress.
-Shows that it can cause the vulnerability, not be the stressor.
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Interactionist approach: Modern understanding of ‘stress’
-In the original model, stress was psychological, especially the influence of parenting.
-Now it’s seen as anything that triggers sz.
-Evidence shows that cannabis increases risk of sz by **7x**.
-Because it interfere with the dopamine system.
-But, most who smoke it still don’t develop sz bs side they lack the requisite vulnerability factors.
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Support from Varese et al & Vassos et al
-Varese found that children who experienced severe trauma before the age of 16 were 3 times more likely to develop schizophrenia.
-This supports the idea that environmental stress (trauma) interacts with a pre-existing vulnerability.
-Vassos found that schizophrenia risk in highly urbanised environments was 2.37 times higher than in rural areas.
-This suggests that environmental factors such as urban stress contribute to schizophrenia development.
Highlights that not everyone exposed to trauma or urban stress develops schizophrenia, implying that biological vulnerabilities (e.g., genetic predisposition) play a crucial role in whether stress leads to the disorder.
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Support for Interactionist approach: Tienari et al 2004
-Found that genetic risk (having a biological mother with sz) alone was not enough to cause schizophrenia; environmental factors also played a role.
-High-risk adoptees raised in healthy adoptive families (low OPAS ratings) were significantly less likely to develop schizophrenia, showing that a supportive environment can reduce the impact of genetic vulnerability.
-High-risk adoptees raised in dysfunctional families (high OPAS ratings) were more likely to develop schizophrenia, suggesting that family stress acts as an environmental trigger.
Demonstrates that schizophrenia results from an interaction between biological predisposition and environmental factors, rather than being caused by just one.
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Treatment according to interactionism (AO1)
-Believed that a combination therapy should be employed between antipsychotic drugs & psychological therapies such as CBT.
-Turkington et al said we can still believe that sz has a biological basis but use CBT to relieve the psychological symptoms.
-UK: acceptable to use combination of both therapies.
-USA: conflict between biological and psychological therapies which has led to slower adoption of interaction alone (only meds is common).
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Limitation of Interactionist approach: Diathesis & stress are complex
OG model was too simple.
-Multiple genesis infkuenve Diathesis.
-Stress also comes in many forms & isnt limited to dysfunctional parenting.
-Houston et al - childhood abuse emerged as the major influence on vulnerability. Cannabis use was the major trigger of stress.
Supports modern explanation & critiques OG model.
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Strength of Interactionist approach: Real-world application
Support for combo of psychological & biological treatments.
-Tarrier et al randomly allocated 315 ppts to (a) medication & CBT (b) medication & counselling (c) control group only meds.
-Ppts in combo groups showed lower symptoms than the only meds group, but no difference in hospital readmission.
Clear practical advantage to adopting Interactionist approach for superior treatment outcomes.
Counter: Just because a combo of treatments work, doesn’t mean that’s the cause of disorder. Jarvis & Okami refer to this as the treatment-causation fallacy. Use example of somebody who’s less shy when they drink alcohol & how it doesn’t mean the lack of alcohol causes shyness.
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Limitation of Interactionist approach: Urbanisation
Argument against urban triggers.
-People with sz may move to cities due to the better healthcare.
-Could me more likely that people in the cities are just more likely to seek help and be diagnosed.
Therefore, there’s not solid evidence of cause and effect, instead correlation.
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Limitation of Interactionist approach: Neural vulnerability explanation
-Increased risk can result from brain damage caused by environmental factors.
-Verdoux et al estimated the risk of developing sz later in life for individuals who have experienced obstetric complications at birth (ie. prolonged labour causing oxygen deprivation) is 4x larger than those who experience no complications.
Reductionist and is limited.
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Managing schizophrenia: Token economies
Behaviour modification is used to try change someone’s behaviour. It’s based on principles of **operant conditioning.**
1. Extinguishing undesirable behaviours (by removing reinforcer).
2. Replacing original behaviour with a desirable behaviour & reinforcing that instead Token Economy Programmes are a type of behaviour modification technique.
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Token economy programme
-Method of managing behaviour (encouraging positive behaviours).
-Used to manage symptoms (mainly negative) & used in institutions.
-TEP use positive reinforcement techniques.
-These are a form of behaviour modification and desired behaviour is identified and agreement before programme. Usually involve a reward.
**Primary reinforcer:** a reward wanted/needed by individual. Usually something to meet biological need (ie. food)
**Secondary reinforcer:** reward that can buy or be used to obtain what’s wanted. Symbolises you getting a reward.
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Developing token economies with schizophrenia (Avllon & Azrin 1968)
-Trialled a token economy system in a ward of women with a diagnosis of sz.
-Every time the participants carried out a task, such as making their bed or cleaning up, they were given a plastic token embossed with the words ‘one gift’.
-Tokens swapped for privileges (ie. watch a film)
No. of tasks carried out increased significantly.
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How does it treat schizophrenia?
-Institutionalisation develops under prolonged hospitalisation.
-Aims to manage behaviour of those who suffer & develop bad habits.
-Matson says there’s 3 categories of behaviours tackled; personal care, condition-related behaviours & social behaviour.
-Aims to improve the person’s quality of life within the hospital setting (ie. makeup for someone who takes pride in their appearance).
-Normalised behaviour & makes it easier for people who’ve spent time in hospital to adapt to community life (ie. making bed).
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How often are they used?
-Used a lot in 60-70s when norm was hospitalisation for sz.
-Use has declined in UK:
-> because of the growth of community-based care and the closure of many psychiatric hospitals.
-> because of the ethical issues raised by restricting rewards to people with mental disorders.
Still a standard approach to managing it in many parts of the world.
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What is involved in a token economy?
-Tokens given when individual carries out a desirable behaviour.
-Target behaviours decided on an individual basis & it’s good for the person to be known so appropriate ones are decided **(Cooper et al)**.
-Delayed rewards are less effective so tokens given immediatly for some satisfaction.
-Rewards can include: walk outside, sweets, magazines etc.
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Theoretical understanding of token economies
-Modify behaviours based on operant conditioning.
-Tokens are secondary reinforcers since they only have value when person knows they can be used to obtain meaningful rewards, which are primary reinforcers.
-Tokens that can be exchanged for primary reinforces are quite powerful secondary reinforcers, known as *generalised reinforcers.*
Becomes a token economy, when reinforced administered together.
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Strength of Token economies: Supporting evidence
-Dickerson et al reviewed 13 studies of token economy use.
-11/13 reported beneficial effects.
-Concluded that it is effective in increasing the adaptive behaviours of patients with sz.
-Glowacki examined 7 high quality studies and all the studies showed a reduction in negative symptoms & a decline in frequency of unwanted behaviours.
Supports value of token economies.
Counter: small amount of studies used has the issue of the file drawer problem. This leads to a bias towards positive published findings since undesirable results are filed away.
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Limitation of Token economies: Lack of control (Comer)
Problem with assessing effectiveness due to uncontrolled studies.
-Typically in a token economy system, all patients brought to progressed rather than having an experimental and contrl group.
-Means that patient’s improvements can only be compared to their past behaviours rather than to a control group.
-May be misleading as other factors (ie. increased staff attention) can cause improvements.
Reduces validity of token economies as there may be confounding variables acting as second, unintended IV.
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Limitation of Token economies: Ethical issues
-Gives professionals too much power to control behaviour of people in role of patient.
-Involves imposing one’s norms into another’s which can be problematic if target behaviours not sensitively identified.
-ie. Someone who wants to get up late might have this freedom restricted.
-Restricting availability of pleasures means that ill people who already experience distress, are having a worse time.
-Legal action by families seeing their relatives in this position has contributed to decline in usage.
Means benefits may be outweighed by the impact on personal freedom and short-term restriction in quality of life.
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Limitation of Token economies: Alternative approaches
-More pleasant & ethical alternatives.
-Chiang et al concluded that art therapy is a good alternative.
-Evidence base is small and has some methodological limitations but appears to show that art therapy is a high-gain low-risk approach.
-Pleasant experience without major side effects or ethical abuses and NICE guidelines recommend it.
