SCHIZOPHRENIA

A2 Clinical Psychology

Lesson aims

To identify symptoms of Schizophrenia in case studies

To check through how diagnoses can help reduce the chances of living with Schizophrenia for life

To Evaluate the key Biological study for Schizophrenia

Quiz time!

What is catatonic schizophrenia?What are type 1 and type 2

characteristics of schizophrenia? What is the DSM?What is the % lifetime risk of developing

schizophrenia? Give 2 examples of a positive symptom of

schizophreniaGive 2 examples of negative symptoms of

schizophrenia

3% of the population suffer from schizophrenia

The word schizophrenia means ‘split mind’The DVM is used to diagnose schizophreniaA delusion is a positive symptomThe symptoms must persist for one year in

order to be diagnosed as schizophrenic The flattening of emotion is a positive

symptom

True/False

Read through the case studies

Identify using the DSM and then the ICD symptoms of Schizophrenia within the case studies!

Biological V Psychological

Nature V Nurture

In your notes

Take 5 mins to outline the Nature nurture debate

Diathesis-Stress Model

A theory that explains behaviour as both a result of biological and genetic Factors ("nature"), and life experiences ("nurture").

This model thus assumes that a disposition towards a certain disorder mayresult from a combination of one's genetics and early learning.

The term "diathesis" is used to refer to a genetic predisposition toward anabnormal or diseased condition.

According to the model, this predisposition, in combination with certain kindsof environmental stress, results in abnormal behaviour.

This theory is often used to describe the pronunciation of mental disorders,like schizophrenia that are produced by the interaction of a vulnerable hereditary predisposition, with precipitating events in the environment.

Vulnerability

In the diathesis–stress model, a biological or genetic vulnerability or predisposition (diathesis) interacts with the environment and life events (stressors) to trigger behaviours or psychological disorders.

The greater the underlying vulnerability, the less stress is needed to trigger the behaviour or disorder.

Conversely, where there is a smaller genetic contribution greater life stress is required to produce the particular result.

Even so, someone with a diathesis towards a disorder does not necessarily mean they will ever develop the disorder.

Both the diathesis and the stress are required for this to happen.

This theory was created by Holmes & Rahe.

Here comes the Science!

DNA contains a set of instructions. It is the carrier of information.

Half of their genes come from their maternal line, and half from their paternal.

The DNA is composed of a series of genes, each of which ‘codes’ for a particular protein.

Minute differences in the DNA code create different shaped / functions in the proteins made.

As each persons DNA is different from anyone else’s, this is their specific Genotype.

This results in a completely unique Phenotype (the characteristic show, as a result of both the genes and the way in which it interacts with the environment).

Some genes always lead to certain characteristics; these are known as dominant genes. To produce a characteristic, dominant genes need to be on only one pair of chromosomes (one copy).

Some genes need more than one copy to produce a characteristic, there are known as recessive genes – if a Recessive gene is present on only one chromosome, the characteristic will not appear.

HOWEVER, they may be passed on and appear in a future generation.

Characteristics can be aspects of appearance, personality, physical health and behaviour.

Dizygotic twins (non-identical twins) share similar

characteristics, much like a siblings.

Monozygotic twins (identical twins) are the result of an

embryo viably splitting early on in development. They share

almost exactly the same Chromosomal DNA.

Genes and Schizophrenia

• R E S E A R C H E R S H AV E L O O K E D F O R A PA R T I C U L A R ‘ S C H I Z O P H R E N I A G E N E ’ W I T H O U T S U C C E S S.

• I T I S N O W T H O U G H T T H AT C O M B I N AT I O N S O F C E R TA I N G E N E S M I G H T M A K E P E O P L E M O R E V U L N E R A B L E T O S C H I Z O P H R E N I A , B U T T H I S D O E S N O T N E C E S S A R I LY M E A N T H AT T H E Y W I L L D E V E L O P T H E

S Y M P T O M S.• T H E E V I D E N C E S H O W S T H AT P E O P L E W H O H AV E A PA R E N T W I T H S C H I Z O P H R E N I A A R E M O R E L I K E LY T O D E V E L O P I T T H E M S E LV E S .

• B I O C H E M I C A L R E S E A R C H H A S B E E N C E N T R E D O N D O PA M I N E , W H I C H I S O N E O F T H E C H E M I C A L S T H AT C A R RY M E S S A G E S

B E T W E E N B R A I N C E L L S. • T H E T H E O RY I S T H AT A N E X C E SS O F D O PA M I N E , O R D O PA M I N E

R E C E P T O R S M AY B E I N V O LV E D I N T H E D E V E L O P M E N T O F S C H I Z O P H R E N I A .

•C O M P L E T E T H E G O TT E S M A N N A N D S H E I L D S R E S E A R C H W O R K S H E E T.

Evaluate

AO2• How do the findings compare to the probability of a

random member of the general population suffering from schizophrenia?

• What should concordance be for MZ twins if genetics was the only explanation?

• Is there another explanation for high concordance amongst family members, particularly identical twins?

• What about those people diagnosed with the disorder but who have no relatives suffering from it?

• Are the concordance rates for twin studies similar?• Why is concordance for MZ twins always higher than that

for DZ twins?• What is the problem with retrospective data?• If diagnostic criteria has changed over time how will it

affect the research findings?

AO2/AO3 PARAGRAPH

Exam questions

Complete the exam questions for the biological explanation for schizophrenia

Pass the Pen Activity

A Genetic Explanation – The Synapse

How does this explain the

Dopamine Hypothesis

DOPAMINE HYPOTHESIS

Lets remind ourselves how neurotransmitters work

Lets remind ourselves how neurotransmitters work

DOPAMINE HYPOTHESISThe Dopamine hypothesis states that

the brain of schizophrenic patients produces more dopamine than normal brains.–Evidence comes from

–studies with drugs –post mortems –pet scans

Disturbance in the Neurochemistry

The first discovery in the mid 1950s was that chronic usage of large daily doses of Amphetamines could produce a psychosis that was virtually indistinguishable from schizophrenia.

It was found that Amphetamine could enhance neurotransmission of Dopamine, Norepinephrine and (to a lesser extent) Serotonin Synapses.

The second discovery was that Chlorpromazine could improve symptoms for schizophrenia.

It was also discovered that Chlorpromazine could prevent Dopamine from activating it’s D2 receptor subtype.

The knowledge that Chlorpromazine improves symptoms of schizophrenia while blocking D2 receptors for Dopamine has led to the development of drugs that have similar pharmacological properties to chlorpromazine.

Normal Level of Dopamine In The

Human Brain

Elevated Level of Dopamine In The Brain of a Schizophrenic Patient

(specifically the D2 receptor)

Neurons that use the transmitter ‘dopamine’ fire too often and transmit too many messages or too often.

Certain D2 receptors are known to play a key role in guiding attention.

Lowering DA activity helps remove the symptoms of schizophrenia

ROLE OF DRUGS

–Amphetamines (agonists) lead to increase in DA levels

–Large quantities lead to delusions and hallucinations

– If drugs are given to schizophrenic patients their symptoms get worse

Parkinson’s disease

Parkinson’s sufferers have low levels of dopamine

L-dopa raises DA activity People with Parkinson's develop

schizophrenic symptoms if they take too much L-dopa

–Chlorphromazine (given to schizophrenics) reduces the symptoms by blocking D2 receptors

Falkai et al 1988Autopsies have found that people with

schizophrenia have a larger than usual number of dopamine receptors.

Increase of DA in brain structures and receptor density (left amygdala and caudate nucleus putamen)

Concluded that DA production is abnormal for schizophrenia

POST MORTEM

Lindstroem et al (1999)Radioactively labelled a chemical L-Dopa administered to 10 patients with

schizophrenia and 10 with no diagnosisL-Dopa taken up quicker with schizophrenic

patientsSuggests they were producing more DA than

the control group

PET SCANS

Schizophrenia or Faulty Chemicals?

Faulty chemicals cause schizophrenia but

schizophrenia may cause faulty chemicals

Chickens hatch from eggs, but

a mother chicken must keep an egg

warm in order for it to hatch

The Chicken or the Egg?Which Came First?

Drugs may influence other systems that impact on schizophrenia so cant be 100% sure about their effects

ACTIVITY

Use the evaluation points to write effective AO2 commentary for the studies on the handout

• You must comment on how the evidence you use supports or challenges the DA hypothesis. • You should comment on evidence both for and against the hypothesis. • You could use your own skills and knowledge to make additional critical and evaluative points.

EVALUATION POINTS

There is a lack of correspondence between taking the drugs and signs of clinical effectiveness. It takes 4 weeks to see any sign that the drugs are working when they begin to block dopamine immediately. We can not seem to explain this time difference.

It could be that the development of receptors in one part of the brain may inhibit the development in another.

Type 1 cases respond well to conventional anti-psychotic drugs. Drugs such as CHLOPROMAZINE: Only effective at relieving the Positive Symptoms of the Illness.

Not good at explaining negative symptoms. Therefore suggested that Type 2 is related to a different kind of abnormality such as brain structure.

PET scans have suggested that drugs did not reduce symptoms of patients diagnosed with disorder for 10 yrs or more

There may be other neurotransmitters involved. Possible that social and environmental factors trigger the condition.