Schizophrenia

Types Of Schizophrenia

Paranoid › Preoccupation with one or more delusions or

frequent auditory hallucinations. None of the following are prominent; disorganised speech, disorganised or catatonic behaviour, the flat or inappropriate effect

Catatonic› At least two of the following is present;

immobility including waxy flexibility, stupor, excessive motor activity, extreme negativism, mutism, posturing, prominent mannerisms, echolalia

Type Of Schizophrenia

Disorganised› Disorganised behaviour, disorganised speech and

the flat effect are all present Undifferentiated

› A mixture of other symptoms from other subtypes of the disorder

Residual› An absence of prominent delusions or

hallucinations, disorganised speech and catatonic behaviour. There are negative symptoms or 2 or more symptoms in criteria A in a less intense form

Symptoms

Positive symptoms – additional to reality› Auditory hallucinations› Delusions› Experiences of control› Disordered thinking

Negative symptoms- things the person is lacking› Flat effect› Alogia – poverty of speech› Avolition – lack of motivation

Biological – Dopamine Hypothesis

It was first thought that schizophrenia was caused by an increase in dopaminergic activity in the brain – neurons fire too easily and too often

Inconsistent evidence for the aforementioned theory led to the theory that it was heightened sensitivity of dopamine receptors was to blame for schizophrenia.

This led to an abundance of dopamine in the synaptic cleft.

Dopamine Hypothesis

Drugs that increase dopaminergic activity, when taken by health individuals cause schizophrenic like symptoms

These drugs were also found to exacerbate psychotic symptoms in those with schizophrenia

Neuroleptic drugs the block dopaminergic activity reduce psychotic symptoms

The theory was first amended was difficult to support due to inconsistent post mortem evidence

Dopamine Hypothesis

Ivernsen (1979) Post mortems of schizophrenia suffers show high levels of dopamine

Pearlson et al (1993) PET scans have reported a substantial increase of D2 receptors in those with schizophrenia

Seeman et al (1993) found a 6 times greater density of D4 receptors in the brains of those with schizophrenia

Biological – Neuroanatomical

Differences in structure and function Nasrallah et al (1986) found that the

gender difference in the thickening of the corpus callosum is the opposite in those with schizophrenia

Jernigan et al (1991) found significant cell loss in the limbic system – more specifically the amygdala and hippocampus

Neuroanatomical

Andreason (1990) found significantly larger ventricles in patients with the disorder

Liberman (2001) found the same results Weyandt (2006) linked them to negative

symptoms Liddle (1996) found that t rest, people

with schizophrenia show underactivity in temporo frontal areas. Particularly in chronic patients

Biological - Genetics

Gottesman (1991) suggested that schizophrenia is inherited through genes. Found concordance rates of 40% for MZ twins and 17% for DZ twins

Gottesman also found that is both parents suffer from schizophrenia then you have a 46% chance of being diagnosed also compared to a1% chance in someone selected at random

Biological - Genetics

Joseph et al (1991) found concordance rates of 40% for MZ twins and 7.4% for DZ twins

Cardno (2002) found concordance rates of 26.5% for MZ twins and 0% for DZ twins

Higher concordance rates for MZ twins could be due to greater environmental similarities

Genetics are only a risk factor and not a causal factor

Biological - Genetics

Tienari (1990) studied 155 adopted children whose biological mothers had schizophrenia. Concordance rate of 10% to 1% in the general public.

Heston (1966) study of 47 mothers with schizophrenia whose children were adopted within days by families without schizophrenia found the incidence of schizophrenia in those children to be 16%

Cognitive – Hallucinations

Bentall (1990) stated that hallucinations occur when people mistake their own internal, mental or private thoughts for external, publically observable events

Slade and Bentall (1988) suggested that hallucinations decrease anxiety

Close and Garety (1998) suggested that hallucinations actually increased anxiety

Cognitive – Hallucinations

Model suggests that sensory information from the environment triggers hallucinations

People only hallucinate what they believe already exists e.g. religious experiences

Slade and Bentall (1988) Five Factor Model for the onset of hallucinations

Stress induced arousal causes info to be processes incorrectly meaning they cannot decide what is real.

Cognitive - Delusions

Two main theories:

› delusions are the result of abnormal cognitions in reasoning, attention and memory

› Delusions are the result of abnormal perceptions

Abnormal Cognitions

Bentall (1991) suggested that paranoid and persecutory delusions are a defence mechanism against depression and low self esteem

Defences are maintained through attention and memory biases

Mainly external biases where negative outcomes are attributed to an external cause e.g. the person is fired, it is not their fault the management just hate them

Bentall argues that we attempt to explain discrepancies between our actual self and ideal self in order to maintain self esteem

Abnormal Perceptions

Delusions are a adaptive and rational response to abnormal internal events like hallucinations

Zimbardo (1981) stated that delusions happen to make sense of a situation

Maher (1974) proposed a model of how delusions occur. Some cognitions lead to normal and delusional beliefs, these act as mini theories that provide order. These theories are needed when events are not predictable. Delusional explanations for unpredictable events bring relief.

AO2 - Delusions

Manschreck (1979) Delusions occur in a wide range of disorders where no cognitive impairment is evident;

Zimbardo (1981) Normal people that undergo abnormal experiences can also experience delusions

Theories point to the importance of attribution and reasoning biases that may contribute to the maintenance of delusions but do not provide an explanation for how schizophrenia is developed

Social Cultural - Labelling

Scheff (1966) suggested that Schizophrenia is a learned social role that is learnt through labelling

Szasz (1962) once a person has been given a label they then begin to act accordingly and become a self-fulfilling prophecy. He also argued that labelling is a way to control those that break one or more residual rules

Rosenhan (1973) demonstrates how easy it is to receive a label. The label stuck with the participants forever. Their behaviour was a result of their label once given

Social Cultural – Family Dysfunction

Bateson et al (1956) stated that sometimes a child received conflicting messages from their parents e.g. asked for a hug and then being pushed away. This is referred to as a ‘double bind’

They learn that they cannot trust the messages that they receive from others, their own emotions and their perceptions.

This may cause them to withdraw socially and cause the flat effect in those diagnosed.

They may also grow to not trust any communications , this is shown in those with paranoid schizophrenia

Social Cultural – Family Dysfunction

Family Socialisation Theory – families do not always provide supportive or appropriate environments for their children

Schismatic families – conflict and division between the parents where one is competing for the love and affection of the family members

Skewed families – the balance of power is biased towards one dominant parent where the children are encourages to follow their direction

In both families the parent fail to act role-appropriate. This causes anxiety. Schizophrenia may be a way to handle conflict

Social Cultural – High EE

The over expression of hostility, critical comments (both verbal and tone of voice)and emotion (both positive and negative)

Brown et al (1958) found that those released into the care of a family fares worse than those that lived alone

Butzlaff and Hooley(1998) 70% chance of relapse within one year in a high EE environment compared to 30% in low EE families

Treatments - Biological

Conventional Antipsychotics (Neuroleptics)› Only work on positive symptoms› They block dopamine receptors› Have to be taken continuously or › Have terrible side effects › Cole et al (1964) – groups taking

Chlorpromazine showed significant improvement over placebo groups. 76% compared to 25%.

› Some patients fail to respond to treatment Loeble et al (1992) 16% failed to respond within a 12 month period

Treatments - Biological

Atypical Antipsychotics› Treat both positive and negative symptoms› Focus less on reducing dopamine and more

on changing the level of serotonin back to a normal level

› Tend to be affective I those patients that did not respond to conventional drugs

› Have bad side effects like weight gain, nausea, irregular heartbeat, excessive salivating

Treatments – Biological

Negatives of drug treatment

Drugs have to be taken continuously

Have undesired side effects

Really expensive to keep taking

People may stop taking them and their symptoms reappear

Positives of drug treatment

Addresses the patients symptoms

Gives them their lives back

Treatments – Insight Therapy

Focuses on the idea that people can be helped to understand their symptoms

It requires the individual to be able to think rationally and logically. This may not be possible with the presence of positive symptoms

Talking about their symptoms may cause them to relapse

Treatments – Family Therapy

Looks at changes in communication patterns in the families of schizophrenics, particularly with high EE

Main objectives are to :› Get families to be more tolerant and less critical› Help the family members feel less guilt

Tends to work well when conjoined with other treatment

Therapy needs to be ongoing or there is a chance of relapse

Treatments – Community Care

Aims to give the person continuous support without having them go into hospital.

Emphasises case management – it tailors the treatment for each individual so that they are being cared for in the way in which they need to be

The person is assigned a key worker – usually a community psychiatric nurses whose job it is to asses and co-ordinate appropriate care

Treatments – Community Care

Hospitals can be seen as very stressful and can exacerbate some symptoms

Hospitalisation does not equip the patients with the skills that they need to function and live in society

Community care gives the person their independence back

Some people may slip through they cracks in community care

Institutionalisation means that the person is in a stable environment

Mental health care is very expensive

Treatments - CBT

Requires thoughts and associated beliefs to be challenged

It was though that attempting to modify beliefs may strengthen them

Two important principals underpinning the present approach are:› Must start with the least important belief› Work with the evidence for the belief and

not the belief itself

Treatments - CBT

Usually involves verbal challenges i.e. questioning the delusional interpretation and puts forward a more reasonable one

By challenging evidence it leads to a decrease in conviction. Also the person become aware of the link between events, beliefs, effect and behaviour

Reality testing involves planning and performing activities that invalidates a belief.

Treatments - CBT

Chadwick et al (1996) – presented the case of Nigel that claimed to be able to tell what people were going to says before the said it. The challenge this belief video recorders were paused and Nigel had to say what they were going to say next. Out of 50 attempts Nigel didn’t get one correct and concluded that he did not have the power at all.

Treatments - CBT

Kupiers et al (1997) found a 40% reduction is the severity of psychotic symptoms found through research trials using cognitive therapy for delusions

Druary et al (1997) during a period of acute psychosis, CBT led to a faster response to treatment in a group of patients compared to drugs.