The different theories of schizophrenia including: Biological: Neurochemical, Neuroanatomical, Genetics Cognitive: Abnormal Cognition, Abnormal Perceptions Social Cultural: Labelling Theory, Family Dysfunction, High Expresses Emotion (EE) Drug Treatment, Insight Therapy, Family Therapy, Community Care and Cognitive Behavioural Therapy (CBT)

2.  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

3.  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

4.  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

5.  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.

6.  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

7.  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

8.  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

9.  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

10.  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

11.  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

12.  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%

13.  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

14.  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.

15.  Two main theories:
› delusions are the result of abnormal
cognitions in reasoning, attention and
memory
› Delusions are the result of abnormal
perceptions

16.  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

17.  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.

18.  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

19.  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

20.  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

21.  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

22.  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

23.  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

24.  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

25. 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

26.  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

27.  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

28.  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

29.  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

30.  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

31.  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.

32.  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.

33.  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.