General knowledge

what is the difference between diagnosis and classification

classification is organising symptoms into categories based on which symptoms cluster together in sufferers, diagnoses use the classifications to decide if someone has a mental illness

what are the major systems for the classification of mental disroder

ICD-11 and DSM-5

what are the categories of symptoms for schizophrenia

positive and negative

what is a positive symptom

additional experiences beyond those of ordinary existence- adding something

what is a negative symptom

the loss of usual abilities and experiences

what are the positive symptoms of schizophrenia

hallucinations and delusions

what are hallucinations

positive symptom, unusual experiences of any sense, they can be related to events in the environment or bear no relationship to what senses are picking up e.g. distorted faces or hearing voices

what are delusions

positive symptom, irrational beliefs that have no basis on reality

what are the types of delusions

delusions of persecution, delusions of grandeur, delusions of control, delusions of reference

what are delusions of persecution

the belief others want to harm, threaten or manipulate you e.g.government/aliens

what are delusions of grandeur

the belief that you are an important individual, even God-like, have extraordinary powers

what are delusions of control

the belief that your body is under external control e.g. the government controlling you through an implant

what are delusions of reference

the belief that events in the environment appear to be directly related to you e.g. special personal messages through the TV/ animals

what are the negative symptoms of schizophrenia

speech poverty and avolition

what is speech poverty

negative symptom, reduced frequency and quality of speech, often repetitive or with delays

what is avolition

negative symptom, lack of purposeful, willed behaviour, reduction, difficulty or inability to start and continue with goal-directed behaviour

what are biological explanations for schizophrenia

genetic and neural

what does the genetic basis of schizophrenia state

• biological cause

• increased risk of schizophrenia in line with genetic similarity to a relative with the disorder

• due to candidate genes

• polygenic

• aetiologically heterogeneous

• can have no family history but due to mutations in DNA

what are the example candidate genes for the genetic explanation and what do they cause

• C4- plays role in synaptic pruning, excessive pruning can lead to symptoms of schizophrenia

• COMT- excessive dopamine, lead to positive symptoms including hallucinations and delusions

what are used to support the importance of genes in schizophrenia

family studies- twin studies, adoption studies

what are the aspects of the neural explanation for schizophrenia

dopamine hypothesis, neural correlates

what is the dopamine hypothesis

the brain of schizophrenia patients produces more dopamine than a normal brain, further research now shows low levels of dopamine may also explain schizophrenia

what are the names for the increased/decreased levels of dopamine

hyperdopaminergia, hypodopaminergia

what is hyperdopaminergia

high levels of dopamine

where is hyperdopaminergia in the brain

subcortex

what type of receptors are effected by hyperdopaminergia

D2

what type of symptoms are affected by hyperdopaminergia

positivewhat

is hypodopaminergia

low levels of dopamine

where does hypodopaminergia effect in the brain

prefrontal cortex

what type of receptors are effected by hypodopaminergia

D1 receptors

which symptoms are affected by hypodopaminergia

negative

what is a neural correlate

a pattern of brain activity or structural change that is regularly linked to a specific mental state, behaviour or cognitive process (correlation not causation)

what are the neural correlates of positive symptoms

lower activation levels in the superior temporal gyrus and anterior cingulate gyrus have been found in those experiencing auditory hallucinations

what are the neural correlates for negative symptoms

lower activation levels in the ventral striatum have been found in those experiencing avolition

what are the psychological explanations for schizophrenia

family dysfunction and cognitive explanations

what are the aspects of family dysfunction as an explanation for schizophrenia

the schizophrenogenic mother, double-bind theory, expressed emotion

what is the family dysfunction general explanation

linked schizophrenia to childhood and adult experiences living in a dysfunctional family

how does the schizophrenic mother theory describe the family

mother is cold, controlling and rejecting, creates a family climate that is tense with secrecy, father is often passive

who did research into the schizophrenogenic mother

Fromm-Reichmann

what impacts do the family characteristics of a schizophrenogenic mother have on the individual

leads to excessive stress and distrust as the family is characterised by tension and secrecy

what symptoms of schizophrenia are associated with the schizophrenogenic mother

triggers psychotic thinking and paranoid delusion, and ultimately schizophrenia

who did research on the double-bind theory

Bateson et al.

what is the double-bind theory as part of family dysfunction

the child receives mixed messages and cannot do the right thing, they get punished by withdrawal of love when they get it wrong, feel unable to comment on unfairness of situation

what is the impact of the double-bind theory on the individual

leads to understanding the world as confusing and dangerous

how does the double-bind theory cause schizophrenia

triggers disorganised thinking and paranoid delusions, and ultimately schizophrenia

what is the expressed emotion section of family dysfunction

the family shows exaggerated emotional overinvolvement in the life of the patient with needless self-sacrifice, verbal criticism of patient and occasionally physical, hostility towards patient including anger and rejection

how does expressed emotion impact the individual

leads to excessive stress beyond impaired coping mechanisms

how does expressed emotion impact schizophrenia

triggers relapse in patients with schizophrenia, may trigger the onset in a person who is already vulnerable due to genetic make-up (diathesis-stress model)

what is the general cognitive explanation for schizophrenia

dysfunctional thought processing

what is dysfunctional thought processing as a cognitive explanation for schizophrenia

cognitive habits or beliefs that cause an individual to evaluate information inappropriately and produces undesirable consequences

what are the types of dysfunctional thought processing

metarepresentation and central control dysfunction

who identified the different types of dysfunctional thought processing

Frith et al

what is metarepresentation as a type of dysfunctional thought processing

it is the cognitive ability to reflect on thoughts and behaviour which allows us insight into our own intentions and goals, allows interpretation of others actions, dysfunction in this disrupts the ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else, explains auditory hallucinations and delusions like thought insertion

what is the word for the cognitive ability to reflect on thoughts and behaviours and know them as our own

metarepresentation

what is central control dysfunction

the cognitive ability to suppress automatic responses while performing deliberate actions instead, dysfunction leads to disorganised speech and thought disorder, unable to suppress automatic thoughts and speech triggered by other thoughts, e.g. schizophrenic tend to experience derailment of thoughts and spoken sentences because each word triggers associations and they can’t suppress automatic responses to them

what is the word for the ability to suppress automatic responses to things

central control

what does the diagnosis of schizophrenia require

at least 2 symptoms

what is the interactionist approach also known as

the biosocial approach

what does the interactionist approach believe

suggests a range of factors including biological, psychological and social are involved in the development of schizophrenia

what is the key part of the interactionist explanation

the diathesis-stress model

what is the diathesis-stress model

diathesis- vulnerability, stress- trigger, states both vulnerability to schizophrenia and a stress-trigger are necessary in order to develop the disorder

what was the original diathesis-stress model

Meehl’s model: stated the diathesis was purely genetic as a result of singular gene called the schizogene, led to the idea of a schizotypic personality e.g. sensitive to stress, the stress was caused by a schizophrenogenic mother

how has the diathesis-stress model evolved

rom Meehl’s model to the modern understanding

what is the modern understanding of diathesis in the diathesis-stress model

diathesis is any early predisposing factor that occurred before the age of 3, many genes each increase genetic vulnerability a bit, not just the singular schizogene, include factors beyond genetics including psychological trauma (trauma is the diathesis not the stress), can be neurodevelopmental factors where early trauma alters the developing brain e.g. child abuse can affect many aspects of brain development such as hypothalamic-pituitary-adrenal system can become overactive making a person more vulnerable to stress

what is the modern understanding of stress in the diathesis stress model

anything that risks triggering schizophrenia including psychological stress, dysfunctional parenting and cannabis use which interferes with the dopamine system

what is the interactionist model treatment for schizophrenia

acknowledges both biological and psychological factors so combines antipsychotic medication and psychological therapies, mainly CBT

what are the geographic differences with the interactionist approach of treatment

in Britain it is standard practice to treat people with both antipsychotic drugs and CBT, in the US there is more of a history of conflict between psychological and biological models leading to slower adoption of interactionist approach and less combined treatment

what is the biological therapy for schizophrenia

drug therapy

what is the most common treatment for schizophrenia

antipsychotics

how can antipsychotics vary between schizophrenics

may be required short or long term, some people can take a short course and then stop their use without the return of symptoms, others may require antipsychotics for life or face the likelihood of a recurrence of schizophrenia

what are the types of antipsychotics

typical and atypical

when have typical antipsychotics been used since

1950s

when have atypical antipsychotics been used since

1970s

how can typical antipsychotics be taken

tablets, syrup or injections

how can atypical antipsychotics be taken

tablets

what is an example of a typical antipsychotic

chlorpromazine

what is an example of an atypical antipsychotic

risperidone and clozapine

what is the dosage of a typical antipsychotic- chlorpromazine

1000mg daily max

what is the dosage of atypical antipsychotics- risperidone and clozapine

risperidone- 4mg-8mg tablets, max 12 a day

clozapine- 300mg-450mg max

how do typical antipsychotics work

dopamine hypothesis: hyperdopaminergia causes positive symptoms (high dopamine at D2 receptors in sub-cortex, act as dopamine antagonists, block dopamine (D2) receptors in synapses of subcortex of the brain, reducing action of dopamine, reduces positive symptoms such as hallucinations

work as a sedative to effect histamine receptors, block D2 receptors in all areas of the brain

what is a summary of typical antipsychotics

• reduce positive symptoms as they block D2 receptors

• based on assumptions from biological approach

• lower dopamine levels

• bad side effects- more than atypical

• helps only 60% of people

• doesn’t impact serotonin levels so doesn’t help negative symptoms

what are the side effects of typical antipsychotics

tardive dyskinesia (movement disorder that causes sudden, uncontrollable movements in the face and body), dizziness

how do atypical antipsychotics work at helping positive symptoms

same as typical antipsychotics, block dopamine (D2) receptors in subcortex to reduce positive symptoms, dopamine hypothesis: hyperdopaminergia causes positive symptoms (high dopamine at D2 receptors in sub cortex), bind less tightly to D2 receptors which reduces side effects

how do atypical antipsychotics work at reducing negative symptoms

dopamine hypothesis: hypodopaminergia causes negative symptoms (low dopamine at D1 receptors in prefrontal cortex), atypical antipsychotics don’t directly increase dopamine at D1 receptors, act as serotonin antagonists, reduce serotonin in pre-frontal cortex, this increases dopamine at D1 receptors, reduces negative symptoms, reduces side effects by roughly balancing dopamine levels

side effects of atypical antipsychotics

cardiomyopathy,

what is a summary of atypical antipsychotics

• reduce positive symptoms as block D2 receptors

• based on assumptions from biological approach

• lower dopamine levels at D2 receptors

• some side effects

• helps 40% of the 40% who don’t benefit from typical antipsychotics (16%)

• reduces serotonin levels that will increase dopamine at D1 receptors to reduce negative symptoms