Schizophrenia Flashcards
Schizophrenia
A mental illness where contact with reality is impaired.
Classification systems of mental disorders
International Classification of Disease edition 10 (ICD-10)
Recognises different types.
Requires two negative symptoms.
American Association’s Diagnostic and Statistical Manual edition 5 (DSM-5)
Dropped sub-types.
Requires one positive symptom to be present.
Positive symptoms definition
Additional experiences beyond those of ordinary existence.
Positive Symptoms
Hallucinations
Delusions
Hallucinations
Unusual sensory experiences.
Some bear no relation to real events in the environment.
Some are related to what the senses are picking up from the environment/an extension to what is going on.
e.g. Hearing voices, see distorted facial expressions
Delusions
Irrational beliefs that take a range of forms.
Involves, being important historical, political or religious figures.
Mire likely to be victims of violence but some delusions can lead to aggression.
e.g. Thinking you’re as important as Jesus
Negative symptoms definition
Involve the loss of usual abilities and experiences.
Negative symptoms
Avolition
Speech poverty
Avolition
Find it difficult to keep up with goal orientated activities.
Poor hygiene, grooming, lack of persistence in work or education, lack of energy.
E.g. Keeping up with revision.
Speech poverty
Changes in patterns of speech.
A reduction in amount/quality of speech.
No logical structure and may have delays.
E.g. Changing topic, whistling, speaking, writing.
Subtypes of schizophrenia
Disorganised Catatonic Paranoid Undifferentiated Residual
Disorganised schizophrenia
Behaviour: disorganised, not goal directed.
Symptoms: thought disturbances, absence of expressed emotion, incoherent speech, mood swings, social withdrawal/loss of interest in life.
Diagnosed in adolescence/young adulthood.
Catatonic schizophrenia
Symptoms: severe motor abnormalities (unusual gestures or use of body language).
Repeated gestures that have meaning to them.
This type involves doing the opposite of what is asked or repeating everything that is said.
Main feature: almost total immobility for hours at a time with patient staring blankly.
Paranoid schizophrenia
Symptoms: delusions, emotionally responsive, more alert, argumentative.
Least serious, most well known. Later onset.
Undifferentiated schizophrenia
A broad category. Includes those who do not clearly fit into one category.
Show symptoms but do not fit into other types.
Residual schizophrenia
Those that have had an episode in the last 6 months and still exhibit some symptoms. These are not strong enough to merit putting them into other categories.
Mild symptoms.
Evaluation of diagnosis of schizophrenia
- Culture bias
Javier Escobar 2012: mostly white psychiatrists tend to over-interpret symptoms and distrust the honesty of black people in diagnosis. - Gender bias
Julia Longenecker et al 2010: reviewed studies of prevalence of schizophrenia and concluded since the 1980s men have been diagnosed with schizophrenia more often than women.
Evaluation of classification and diagnosis
+ classification systems provide a common language for practitioners
- reliability
Cheniaux et al 2009: 2 psychiatrists independently diagnose 100 patients using DSM and ICD criteria. 1: DSM 26/ ICD 44
2: DSM 13/ ICD 24
- validity
Cheniaux found more likely to be diagnosed using ICD
- co-morbidity
Having 2 illnesses together, so which symptoms for which illness.
- symptom overlap
Between schizophrenia and other illnesses (bipolar disorder: delusions, avolition)
Biological explanation of schizophrenia
Gottesman
Gottesman 1991
The closer related you are to someone with schizophrenia, the more likely you are to also have it.
Biological Evidence for schizophrenia
Family studies: Gottesman 1991: - could’ve been how you’ve been raised, similar situation to someone with schizophrenia.
Twin studies: Joseph 2004: concordance rate 40.4% MZ and 7.4% DZ so inherited by genes : - MZ more similar environment? Share more nurture too, so high concordance rate due to nurture?
Adoption studies: Tienari 2000: 6.7% children’s mum who had it got it/ 2% who’s mother didn’t, got it: - individual differences, sime stay in similar situation i.e. Adopted by grandparents. Also age adopted?
Ripke 2014: huge study of data of genome = 108 genes implicated
The dopamine hypothesis
Hyperdopaminergia in subcortex: too much dopamine.
High levels or activity in central brain and mesolimbic pathway.
E.g. Too much dopamine D2 receptors in Broca’s area can lead to speech poverty/auditory hallucinations.
Hypodopaminegia in cortex: Goldman-Rakic et al 2004: found low levels or activity in prefrontal cortex (thinking and decision making) and mesocortical pathway in patients with negative symptoms of schizophrenia.
Evaluation of dopamine hypothesis
Dopamine agonists: inc level of dopamine and make symptoms worse. Curran et al 2004. E.g. Cocaine exaggerates positive symptoms in people who have schizophrenia.
Dopamine antagonists: anti-psychotic drugs reduce levels of dopamine and can eliminate hallucinations and delusions. Tauscher et al 2014.
- Ripke 2014: 108 genes implicated, not all connected to dopamine, other neurotransmitters.
Neural correlates
Measurements of the structure or function of the brain that correlate with an experience (schizophrenia).
Both positive and negative symptoms have correlates.
Neural correlates of negative symptoms
Activity in ventral striatum has been linked to development of avolition.
Ventral striatum has been linked to anticipation of rewards.
Therefore, abnormality in ventral striatum = lack of motivation (avolition).
Neural correlates of positive symptoms
Reduced activity in superior temporal gyrus and anterior cingulate gyrus have been linked to development of auditory hallucinations.
Allen et al 2007: patients experience auditory hallucinations showed lower activity levels in these areas then controls.
Therefore, neural correlates.
Evaluation of neural correlates
+ lots of neural correlates: useful in identifying brain systems not working correctly.
- correlation not causation.
Something else could have caused the symptoms of schizophrenia.
Therefore, neural correlates don’t determine exactly what causes the problem.
Biological explanation of schizophrenia Evaluation
- reductionist
Multi-faceted disorder has been reduced to cells, chemicals, genes. - good evidence for psychological theories (familt functioning during childhood).
Therefore, diathesis-stress relationship. (Have a gene that is triggered by environment).
Psychological Explanations of Schizophrenia
Family Dysfunction
Cognitive Explanation
Family Dysfunction Sections
Psych Expl
Schizophregenic mother
Double bind theory
High expressed emotion
Family Dysfunction
AO1
Schizophregenic mother
Fromm-Reichmann 1948
A psychodynamic expl based on patients accounts of their upbringing - a type of parent emerged.
Mothers: cold, rejecting, controlling created a tense, conflict and secrecy family
This leads to distrust = paranoid delusions + schizophrenia
Family Dysfunction
AO1
Double bind theory
Bateson et al 1972
Focus on communication
Child receives mixed messages about how to behave in diff situations or about parents emotions -love you then ignore
Child feels unable to comment on unfairness
Behave incorrectly: punished: withdrawal of love
Learn world is confusing and dangerous
Leads to paranoid delusions and disorganised feelings
Family Dysfunction
AO1
High expressed emption and schizophrenia
High EE is the level of emotion (often negative) that is expressed to the patient.
Family communication that involves:
- critical comments (tone, content, sometimes violence)
- hostility to patients (anger, rejection)
- emotional over-involvement in life of patient (self sacrifice)
Family Dysfunction
AO3
+ evidence for link between childhood and schiz
Read et al: 46 cases of child abuse 69% of women in-patients with schiz had history of sexual/physical abuse. Men was 59%. But did patients make up?
- retrospective research
Reads info based on memories, schiz have distorted memories
- lack of evidence for family expl and almost none for schiz mother.
Cognitive explanation
AO1
Psych expl
Mental processing:
Metarepresentation
Central control
Cognitive explanation
AO1
Mental processing
Sz associated with abnormal info processing.
E.g. Reduced processing parts of brain (ventral striatum) associated with negative symptoms.
This lower than usual processing suggests impaired cognition.
Frith et al 1992 identified two kinds of dysfunctional thought processing in sz: metarepresentation, central control.
Cognitive explanation
AO1
Metarepresentation
Ability to reflect on thoughts and behaviour, allowing instant insight into our intentions, goals and to understand actions of others.
Sz patients - dysfunction in this as fail to recognise own thoughts and actions as being carried out by themselves.
Cognitive explanation
AO1
Central control
Cognitive ability to suppress automatic responses while we perform deliberate actions instead.
Why sz have disorganised speech. Each word triggers and association.
Normal: suppress and continue conversation
Sz: cannot so speech incomprehensible
Cognitive explanation
AO3
+ strong evidence
Stirling et al 2006:
Compared 30 sz patients with 18 controls in a range of cognitive tasks e.g. Stroop test - say colour of ink.
Sz do poorly - took twice as long as controls.
However, this doesn’t tell us the origins of cognitions of sz.
- direction of causality?
Can’t determine cause and effect: cognitive issues cause or result of neural correlates and abnormal neurotransmitter levels seen in sz.
Issue of validity of both explanations.
Biological therapies
AO1
Chlorpromazine
Typical Antipsychotics
1950s
Start low 400-800mg
Chemical that reduces action of a neurotransmitter
Blocks dopamine receptors in brain- normalises neurotransmission in key areas of brain reducing symptoms like hallucinations
Also a sedative
Usually a syrup
Biological therapies
AO1
Clozapine
Atypical
1970s - more effective, fewer side effects
Death of patients = agranulocytosis
Relaunched in 1980s as more effective than typical (last resort)
Regular blood tests
300-450 mg
Binds to dopamine, serotonin, glutamate receptors (S&GR improve mood)
Prescribed if chance of suicide is high
Biological therapies
AO1
Risperidone
Atypical
1990s
As effective as clozapine, fewer side effects
Lasts two weeks
Small dose initially 4-8mg (max 12)
Binds to dopamine and serotonin receptors
Binds more strongly therefore, smaller dose
Biological therapies
AO3
+ evidence for effectiveness
Thornley et al 2003 reviewed studies comparing effectiveness of chlorpromazine to controls who received a placebo. 1121 patients showed chlor was associated with better overall functioning.
- side effects
Dizziness, sleepiness, tardive dyskinesia, agranulocytosis.
Drugs blocked dopamine in hypothalamus which is involved in many systems. NMS: delirium, coma, death.
Psychological therapies
CBT
Family therapy
Token economies
CBT
AO1
Challenging distorted beliefs Group or individual 5-20 sessions Links thoughts and feelings with symptoms which allows patients to consider alternative ways of explaining their behaviour. Reduces stress Improve functioning
CBT
AO3
+ NICE found CBT more effective in reducing relapse rates than meds 18 months after
But most studies patients on meds as well as CBT so hard to determine effectiveness independently
- lack of availability/access
UK= 1/10 access CBT (lower in some areas)
Haddock et al 2013: NW Eng: 187 patients only 13 offered CBT
Family therapy
AO1
10 sessions
Aimed to reduce EE
Provide family info of disorder
Improves relationships in house as therapist encourages listening
Family therapy
AO3
+ Pharoah et al 2010
53 studies from between 2002-2010
Investigate effectiveness of FT compared to meds
Europe, N America, Asia
Mental state: mixed
Compliance with meds: inc with FT
Social functioning: some general improvement but not key like living independently/employment
Relapse rate: dec in 24 months after
- worthwhile?
Garety et al 2008 found similar relapse rates of FT and meds
- most studies for FT had lack of blinding, observer bias, no random allocation
Token economies
AO1
Reward systems
Institutions
Not a cure - management, improves quality of life
Behaviours targeted for reinforcement, immediately
Swap discs for tangible rewards
Operant conditioning
Tokens are secondary reinforcers
Token economies
AO3
+ Dickerson et al 2005
13 studies using tokens
11/13 beneficial effects
Therefore, beneficial in increasing adaptive behaviours of sz
- hard to assess success
Comer et al 2013
Studies uncontrolled, no control group to compare to, so have to compare to past behaviour of patients
So improvements may not be due to tokens but other factors (inc staff attention instead)
The Interactionist Approach
The Diathesis-Stress Approach
Diathesis (vulnerability/gene) - Stress (trigger/situation)
The Traditional Diathesis-Stress Approach
Meehl:
Schiz is a result of a combination of the schizogene and stress in their childhood.
Gene leads to dev of schizotypic personality = vulnerable to effects of stress (schizophregenic mother).
stressful events in life trigger schiz in genetically vulnerable people.
The Modern Diathesis-Stress Approach
Diathesis not due to a single gene = suggests range of vulnerability factors including multiple genes, early trauma, stress which may be psychological (family dynamics) or biological (cannabis).
The Modern Diathesis-Stress Approach
Evidence - AO1 info
Read et al 2001:
proposed a neurodevelopmental model = early trauma alters the developing brain
e.g. child abuse can affect the hypothalamic-pituitary-adrenal (HPA) system to become overactive, making the person vulnerable to stress.
Some have also noted that living in a highly populated urban area can also be a stressor.
Treatment according to the interactionist approach
Combination treatments:
Biological (drugs) and psychological therapies.
This is standard practice in Britain.
Interactionist Approach AO3
+Evidence for role of vulnerability and triggers
Tienari et al:
Studied children adopted away from SZ mothers.
The adoptive parenting styles were compared to a control group of adoptees with no genetic risk.
SZ is more likely in children with genetic vulnerability and parents high in criticism/low empathy.
This shows how genetic vulnerability and parenting styles interacts in SZ.
Interactionist Approach AO3
-Original Diathesis-Stress model is overly simple
Psychologists thought vulnerability was purely biological and stress as psychological.
Now = know more complicated:
- early trauma (psychological) causes vulnerability
- Biological events (smoking cannabis) can be environmental stressors
So original approach not sufficient on its own.
Interactionist Approach AO3
+Support for effectiveness of combined treatments
Tarrier et al:
greater effectiveness for combined treatment (meds+CBT) over medication alone.
Matters as interactionist approach has application to treatments for positive outcomes.
Interactionist Approach AO3
-The treatment-causality fallacy
Just because a combination of treatments is effective doesn’t mean that the interactionist model is correct.
Therefore, we do not know how diathesis or stress works.
