Schizophrenia

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THE DIAGNOSIS AND CLASSIFICATION OF SCHIZOPHRENIA

Classification of schizophrenia

The classification of a mental disorder is the process of organising symptoms into categories based on symptoms

2 major systems of classification: The World Health Organisation's International Classification of Disease edition 10 (ICD) and the American Psychiatric Associations Diagnostic and Statistical Manual Edition 5 (DSM)

Positive Symptoms: (added to behaviour)

Hallucinations: sensory experiences of stimuli that have either no basis in reality or are distorted perceptions of things that are there. eg - voices talking to the sufferer

Delusions: Involve beliefs that have no basis in reality - irrational. eg - believing to be an important historical, political or religious figure such as the queen

Negative Symptoms: (taken away from behaviour)

Avolition: involves the loss of motivation to carry out tasks, lowered activity levels. Anderson identified 3 signs of avolition: poor hygeine and grooming, lack of persistence in work/education and lack of education

Speech Poverty: reduction in quality and frequency of verbal output, speech disorganisation involves disorganised and inconherent speech (this is classified as a positive symptom)

Evaluation:

Reliability - in the case of diagnosis, inter-rater reliability is to what extent two or more mental health professionals arrive at the same diagnosis

Validity - to what extent to which we are measuring what we are intending to measure, one standard way of assessing validity of diagnosis is criterion validity

Co-morbidity - the occurance of two illnesses or conditions together , eg if a person has both schizophrenia and personality disorder. When 2 conditions are frequently diagnosed together it calls to question the validity of classifying the two disorders separatly

symptom overlap- occurs when two or more conditions share symptoms - calls into question the validity of classifying the two disorders separately

Gender Bias - Longenecker - since the 1980's men have had more diagnosis of Sz than women - suggests a gender bias with women being underdiagnosed due to good interpersonal functioning

Culture Bias - cultural bias due to cultural norms varying between cultures, distrust of black patients, westernised classifications of abnormality

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THE BIOLOGICAL EXPLANATIONS:

The Genetic Explanation:

·

Schizophrenia runs in families- this on

its own is weak evidence of a genetic link

·

Identical twins share 100% of genetic

materials

·

Non-identical twins and siblings share

only 50% of genetic material

·

Gottesmann’s study – the concordance

rate for identical twins to both have Sz is 48% versus 17% for non-identical

twins and 9% for siblings

·

Shows a relationship between the degree

of genetic similarity and shared risk of Sz

·

However it also shows that environmental

factors MUST have a role- identical twins normally share environment and are

treated the same due to looking the same, non-identical twins are more likely

to share environment than siblings explaining higher %

·

The brain is the source of all mental

states, Sz is a disorder of the mental state, if genes determine brain

structure/ neurochemistry then these determine our thought processing and

behaviours then we can inherit psychological traits and therefore Schizophrenia

·

Polygenic – schizophrenia requires a

number of factors to work in combination – a number of genes increase risk

·

Aetiologically heterogeneous – different

combinations of these genes can lead to the condition (Ripke et al: genetic

makeup of 37,000 patient’s vs 113,000 controls – 108 separate genetic

variations associated with risk of Sz)

The Dopamine Hypothesis:

·

Neurotransmitters: the chemical

messengers work differently in the brain of a patient with schizophrenia – in particular

DOPAMINE. It is important in the functioning of several brain systems that may

be implicated in the symptoms of schizophrenia

·

Hyperdopaminergia in the SUBCORTEX – the

original focus of the dopamine hypothesis was high levels of dopamine in the sub

cortex (central areas of the brain) – eg. Broca’s area which may be associated

with speech poverty

·

Hyperdopamingergia in the CORTEX – most recent

version of the hypothesis focus instead on abnormal dopamine systems in the

cortex. Goldman-Rakic identified role of low levels of dopamine in the

prefrontal cortex in negative symptoms

Neural Correlates:

·

Measurements of the structure or

function of the brain that correlate with experience – i.e schizophrenia. Both

positive and negative symptoms have neural correlates.

·

Neural correlates of negative symptoms: THE

VENTRAL STRIATUM involved in avolition/lack of motivation – abnormality in the

ventral striatum. Juckel et al : negative correlation between activity levels

in the ventral striatum and the severity of negative symptoms

·

Neural correlates with positive

symtpoms: Lower activation levels in the SUPERIOR TEMPORAL GYRUS and ANTERIOR

CINGULATE GYRUS were found with people with hallucinations – reduced activity

in these areas neural correlate with auditory hallucination

Evaluation:

·

Gottesmann study

·

Tienari et a : adoption study – children

of Sz sufferers are still at heightened risk if adopted into low risk families

·

Ripke et al

·

Mixed evidence for dopamine hypothesis

·

Correlation or causation ?????

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THE PSYCHOLOGICAL EXPLANATIONS

Family Dysfunction:

·

The schizophrenic mother – Fromm-Reichmann’s

psychodynamic explanation for schizophrenia, based on accounts of patients on

their child hood. Particular type of parent = schizophrenogenic mother = cold,

rejecting and controlling, which creates tension and secrecy. Leads to distrust

which develops into paranoid delusions

·

Double-blind theory – Bateson et al-

family climate is important, and emphasis on communication. Child receives mixed

messages about what they’re doing wrong. When they get it wrong they are

punished by the withdrawal of love, causes disorganised thinking and delusions

·

Expressed emotion (the accepted point) –

the level of emotion (in particular negative emotion) expressed towards patient

by carer. Contains the elements: verbal criticism, hostility and emotional over

involvement. Serious source of stress which can trigger the onset of Sz in

someone already vulnerable

Cognitive Explanations:

·

Focuses on the role of mental processes

·

Ventral striatum associated with

negative symptoms

·

Reduced info in the temporal and

cingulate gyrus associated with hallucinations

·

Frith et al identified two kinds of

dysfunctional thought processing that could underlie symptoms:

1. Metarepresentation:

the cognitive ability to allow us to reflect on thoughts and behaviour – dysfunction

would disrupt ability to recognise our own thoughts as being carried out by ourselves

explaining hallucinations

2. Central

control – the cognitive ability to supress automatic response, dysfunction

could result in disorganised speech and thought disorder

Evaluation:

·

Information gathered as a child may be distorted

by the symptoms and therefore reducing validity of their recall

·

Almost no evidence to support

schizophrenic mother or double blind

·

Leads to parent blaming

·

Stirling et al – 30 patients with 18

controls, range of tasks including stroop test – patients took over twice as

long as controls – supporting dysfunction

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DRUG THERAPIES

Two Kinds:

1. Typical Antipsychotics

2. Atypical Antipsychotics

Typical

antipsychotics:

-Have been around

since the 1950’s

-Example is

chlorpromazine

-taken as tablets,

syrup or injection

-Strong association to

the dopamine hypothesis

-Work as a dopamine ANTAGONIST as blocks the dopamine receptors in the

synapse and reduce the activity of dopamine, in particular D2 receptor

-Antagonists reduce the action of the neurotransmitters

-Works only on

positive symptoms

-Also a sedative –

related to its effect on histamine receptors

Atypical

antipsychotics:

-Have been used since

the 1970’s

-Example is clozapine

-not available as an

injection due to its fatal side effect

-Also a dopamine ANTAGONIST but also works on serotonin and glutamate

receptors – helps to improve mood and reduce depression and anxiety as well as

cognitive functioning

-often prescribed to

suicidal patients as mood enhancing effects- 30-50% of Sz patients want to

commit suicide

Evaluation:

Effectiveness:

-Thornley et al:

compared chlorpromazine with a placebo control group – from 13 trials 1121 ppts

showed that chlorpromazine was associated with better overall functioning,

reduction in symptoms severity and relapse rate

-Meltzer: Clozapine is

more effective than typical antipsychotics, effective in 30-50% of resistant cases

where typical antipsychotics failed

Side effects:

-Tardive dyskinesia:

caused by dopamine super sensitivity and is involuntary facial movements –

worse with typical antipsychotics

-Neuroleptic malignant

syndrome: most serious side effect for typical antipsychotics, caused when drug

blocks dopamine action in the hypothalamus – results in high temperature,

delirium and coma and can be fatal

-Agranulocytosis:

fatal, patients on clozapine need regular blood tests

Dependence on the

dopamine hypothesis:

-original dopamine

hypothesis not the complete explanation for Sz

-dopamine levels in

the brain apart from the sub cortex are actually too low rather than too high

-If this is true, not

clear how antipsychotics work as antagonists of dopamine – reducing dopamine

-the dopamine

hypothesis suggests then that antipsychotics shouldn’t work

-undermined by the

theory they rely on

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PSYCHOLOGICAL

THERAPIES

CBT:

-A method for treating

disorders based on both cognitive and behavioural techniques

-From cognitive

viewpoint the therapy aims to deal with thinking, such as challenging negative

thoughts

-involves up to 20

sessions, only 1-2-1 therapy the NHS offers

-Uses Ellis’s ABC

model

-The aim in general is

to help patients identify irrational thoughts and trying to change them

-How it helps: Helps

to make sense of HOW their delusions and hallucinations impact their feelings

and behaviour – just understanding where symptoms come from can be very

helpful.

-Offering psychological

explanations for the existence of hallucinations (for example) can help reduce

anxiety, psychologists also challenge irrational beliefs and provide

alternative explanations for them, use Normalisation techniques, give homework

Studies:

- Jauhaur et al – meta

analyses on the effectiveness of CBT and also investigated publication bias.

Results = overall symptoms (CBT vs no CBT) -0.62 v -0.15 with no consistent

evidence of publication bias across analyses. Conclusions = therapeutic effect

on symptoms in the ‘small range’, reduced further when sources of bias are

controlled

-Jones et al – Cochrane

review, all randomised controlled trials for CBT, 31 papers for 20 trials, no

difference in overall effectiveness was found between CBT and other talking

therapies, relapses and rehospitalisation was not reduced

-Evaluative point =

the ceiling effect – drugs already improved Sz as much as possible

FAMILY THERAPY:

-Takes place with the

family to improve quality of communication and interaction, to reduce stress

and expressed emotion and ensure compliance with drugs

-The therapy works

closely with the theory of expressed emotion

-Pharoah et al

identified a range of strategies which aim to improve functioning of a family,

eg. Reduction of anger and guilt in family members and improving behaviour and beliefs

towards Sz

Studies:

Pharoah et al –

randomised and quasi randomised studies on families with Sz and compared it to

standard care. Results = decrease in the frequency of relapse (RR = 0.55),

reduce hospital admission (RR = 0.78) and compliance to medication (RR = 0.6).

BUT methodological issues – problem of randomisation (majority of studies from

china which stated they used randomisation when they didn’t) and the lack of

blinding (observer bias)

McCreadie et al – 52 families

were offered family therapy, only 31 agreed and 14/30 didn’t attend – do people

actually want family therapy?

TOKEN ECONOMY:

-a reward system to

manage patients in psychiatric hospitals / modify bad habits or maladaptive

behaviour

-based on operant

conditioning to reinforce positive and desirable behaviour

-Tokens = secondary reinforcers

(no value until reward is obtained), given immediately for desirable behaviour,

this immediacy is important because it prevents delay discounting

-Rewards = the

positive reinforcement

Studies:

McMonagle and Sultana-

meta analysis of randomised studies comparing token economy to standard care.

Results = Only 3 trials could be included, there was no usable data on target

or non-target behaviour, one small study found an improvement in negative symptoms.

Conclusions – token economy may have an effect on negative symptoms, but it

still remains worthy of careful evaluation

Evaluation :

-improve quality of

live but do not cure

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THE INTERACTIONIST

APPROACH

THE DIATHESIS MODEL:

-means vulnerability,

in this context stress means a negative psyshcological experience

-The diathesis stress model

states that both a vulnerability to Sz and a stress trigger are necessary in

order to develop the condition

-One or more

underlying factors make a person particularly vulnerable to developing Sz but

the onset of the condition is caused by stress

-Meehl’s model – the original

diathesis stress model, entirely genetic, the result of a single ‘schizogene’ –

leading to the development of a biologically based schizotype personality. If a

person does not have the schizogene then no amount of stress would lead to Sz,

however in carriers of the gene, chronic stress through childhoods could result

in the condition

-The modern model – many

genes appear to increase genetic vulnerability, no single ‘schizogene’ (Ripke

et al). Modern model views a range of factors beyond the genetics- including

psychological trauma (Ingram and Luxton) so trauma becomes the diathesis rather

than the stressor. Read et al said that early trauma alters the brain – may affect

the brain development, eg. The hypothalamic-pituitary-adrenal can become over

active making a person more vulnerable to stress

-Modern understanding

of stress – in original model, stress was seen as psychological in nature, the

modern definition includes anything that risks triggering Sz (Houston et al).

The factor of cannabis – interferes with the dopamine system

-Interactionist

treatment – as the interactionist approach acknowledges both biological and

psychological factors it is compatible with both biological and psychological

treatment. The model is associated with combining drugs with psychological

therapies, most commonly CBT.

Study: Turkington et

al – points out it is possible to believe in biological causes and use CBT to

relieve psychological symptoms, but you have to adopt the interactionist

approach- not possible to adopt a purely biological approach

Evaluation:

-Tienari et al –

children adopted from Finish Sz mother, their adoptive parents assessed for

child-rearing style and rates of Sz were compared to a control group of

adoptees with no genetic risk. Results = child rearing styles of criticism,

conflict and low levels of empathy implicated development of Sz in HIGH genetic

risk children and not the control group. Suggests that genetic vulnerability and

family stress are important in developing Sz

-Houston et al –

childhood sexual trauma emerged as a vulnerability factor whilst cannabis use

was the trigger – shows the old idea that diathesis was biological and stress psychological

was overly simple

-Tarrier et al – 315 randomly

allocated to a medication + CBT group, medication + counselling or a control

group. Patients in the two combination groups showed lower symptoms levels than

those who just had medication (controls)