Download Schizophrenia: THE BARE BONES File

SCHIZOPHRENIA: The Bare Bones
CLINICAL CHARACTERISTICS OF SCHIZOPHRENIA
BE SELECTIVE FROM THE FOLLOWING – THERE WILL PROBABLY ONLY BE A MAXIMUM OF 4 MARKS ON
OFFER FOR THIS.
Since 1994, the two main classification systems in use worldwide are DSM-IV and the ICD-10.
DSM-IV diagnostic criteria for schizophrenia.
Characteristic symptoms: two (or more) of the following, each present for a significant portion of time during
a 1-month period (or less if successfully treated):
1. Delusions
2. Hallucinations
3. Disorganised speech (e.g. frequent derailment or incoherence)
4. Grossly disorganised or catatonic behaviour
5. Negative symptoms affective flattening (lack of emotion), alogia (lack of communication) or avolition
(lack of motivation or desire to pursue goals).
Only one criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice
keeping up a running commentary on the person’s behaviour or thoughts, or two or more voices
conversing with each other.
Duration: continuous signs of the disturbance persist for at least 6 months.

The above symptoms must not be due to the physiological effects of a drug of abuse or medication.
ISSUES WITH CLASSIFICATION AND DIAGNOSIS OF SCHIZOPHRENIA
BE SELECTIVE – YOU WILL NOT BE ABLE TO WRITE ABOUT ALL OF THESE EFFECTIVELY EVEN IF THE QUESTION
IS FOR 24 MARKS. CHOOSE THE ONES YOU CAN COMPETENTLY DISCUSS.

Description of the following issues







The existence of different diagnostic criteria
The lack of objective tests
Cultural differences in diagnosis
The validity of the disorder
Problem of co-morbidity
The reliability of diagnosis
Anti-psychiatry perspective. The question of whether schizophrenia is a mental disorder at
all. Mental illness as dehumanising and a form of political control. 
 The existence of different diagnostic criteria and cultural differences in diagnosis
AO1 Schizophrenia is a difficult disorder to test for in the same way that one might diagnose a
physical disorder. The main diagnostic criteria for schizophrenia are the ICD and the DSM. The
diagnosis of schizophrenia has been very widely used in the past, and prior to the 1970s there was a
significant difference in the prevalence rates of schizophrenia in different countries. In America
particularly, the diagnosis was used a lot in comparison to other countries because their
classification systems used broader definitions. In the US 20 per cent of patients were diagnosed
with schizophrenia in the 1930s, but this rose to 80 per cent in the 1950s. In a hospital in London,
the diagnosis rate of 20 per cent remained constant through the same period (Cooper et al. 1972).
To address these differences the ICD and DSM are now very similar. The major difference now is
Page | 1
SCHIZOPHRENIA: The Bare Bones
that the DSM specifies that signs of disturbance must be present for at least six months, while the
ICD requires that important symptoms are present for only one month.
AO2/3 There are several diagnostic tools in addition to the DSM and ICD that have been created
specifically to help clinician diagnose schizophrenia (e.g. Schneider Criteria). The use of these
criteria can actually improve the reliability of diagnosis. For example, Farmer et al. (1988) found
high levels of reliability using the standard interviewing technique known as PSE (Present State
Examination). Reliability here means that different clinicians/psychiatrists using the same criteria
arrive at the same diagnosis.
AO2/3 However, the fact that different criteria have been used to diagnose schizophrenia makes it
difficult to research studies. For example, in outcome research (investigating the outcome of
treatment) it is hard to compare data based on individuals who have been diagnosed with
schizophrenia using different criteria.
AO2/3 The existence of different criteria also emphasise that the diagnosis of schizophrenia cannot
be fully objective and is vulnerable to change, over time and/or between cultures.
AO2/3 The classification systems, if valid, should be able to predict the outcome and response to
treatment. However, it has proved very difficult to predict this with accuracy and there are wide
individual variations.
 Problem of co-morbidity
AO1 Schizophrenia is often co-morbid with mood disorders, such as depression. Therefore in
practice, it is often difficult to define the boundaries between schizophrenia and other disorders.
AO2/3 The ICD and DSM have tried to address this problem by proposing mixed categories such as
schizoaffective disorders, but the validity of such categories has been questioned.

 Commentary: Labelling and the self-fulfilling prophecy
Students achieve AO2/AO3 credit by evaluating and offering commentary and offering commentary
on the issues they have identified for example considering the consequences arising from the issue.
You may discuss advantages of using classification systems in relation to effective treatment
programmes and support and /or problems associated with classification and diagnosis. For
example, diagnosis might lead to labelling and stigmatisation (Scheff 1996) causing long-term
problems of getting/keeping employment and leading to a self-fulfilling prophecy.
 Anti-psychiatry perspective. The question of whether schizophrenia is a mental disorder at
all. Mental illness as dehumanising and a form of political control. 

AO1 There are those, such as Thomas Szasz, who have questioned the whole concept of mental
illness and has suggested that the process of diagnosis is just a form of political control. He argues
that physical illness is different from mental illness.
Page | 2
SCHIZOPHRENIA: The Bare Bones
AO2/3 Szasz’s main objection to the concept of mental illnesses, such as schizophrenia, is that it
dehumanises people. To say that someone is ill is to remove responsibility from them for their
problems. Szasz mounted a strong and direct challenge to the medical model of mental disorders.
His work may have helped to give rise to the ‘patient power’ movement in the early 1960s.
 Conclusion: the benefit of early diagnosis. 
Page | 3
It is important to diagnose schizophrenia correctly in order to provide the most appropriate form of
treatment. Additionally, there is now evidence that early diagnosis and prompt assignment to
treatment is associated with a better long-term outcome for people with schizophrenia (Jackson and
Birchwood, 1996). This demonstrates how important it is to get the diagnosis right.
BIOLOGICAL EXPLANATIONS FOR
SCHIZOPHRENIA
Genetic explanations
It is highly likely that schizophrenia is transmitted from parents to children via their genes, since
research has consistently indicated that the risk of developing schizophrenia in families where there
is already someone with the disorder is greater than the 1% naturally occurring rate in the general
population. This fact is not sufficient in itself to prove that schizophrenia is genetic, as children of
schizophrenic parents don’t just share some of their genes, they usually share the same environment
too.
AO1
Two main methods have been used to investigate the relative importance of genetic and
environmental factors: Twin studies and adoption studies. I would suggest focussing on twin studies,
and just referring to the findings adoption studies (e.g. Tienari 1991) as a way of
supporting/evaluating the findings of twin studies.
Twin Studies
AO1 Gottesman (1991) reported on several twin studies carried out since 1966, and found that the
risk of a particular individual developing schizophrenia is proportional to the amount of genes they
share. For example, for monozygotic twins (who share 100% of their genes), the risk is 48%, whereas
for dizygotic twins (who share about 50% of their genes), the risk is 17%. This suggests that genetics
are a significant part of the picture when looking at the causes of schizophrenia, though they are not
the only factor, otherwise concordance rates for MZ twins would be 100%.
AO2/3 The findings of Gottesman’s report are supported by the findings of adoption studies, such
as Tienari (1991).
SCHIZOPHRENIA: The Bare Bones
There are some problems with the findings of this twin research. One issue is that MZ twins are
relatively rare in the population and, of these, only 1 per cent would be expected to have
schizophrenia, so sample sizes in these studies are usually small. Twin studies do not all use the
same diagnostic criteria, so this makes it difficult to compare the data of different studies. Different
definitions produce different concordance rates (McGuffin et al. 1984).
Page | 4
Many of the older studies used less sophisticated methods to determine zygosity, that is whether a
twin is identical (MZ) or non-identical. This reduces the validity of the studies reviewed by
Gottesman.
Concordance rate appears to be related to the scientific rigour of the studies. For example, studies
that have used ‘blind interviewers’ (people who are not aware of the diagnosis of the patients) have
found lower rates of concordance than other studies. Marshal (1990) has suggested that the better
the controlled the study, the lower the concordance rate.
AO2/3 Even though there is strong evidence for a genetic influence on the development of
schizophrenia, there has not yet been specific genes reliably identified that may increase the risk.
Until these have been reliably identified, it is difficult to understand the precise mechanism of
genetic transmission. It should be noted though, that genes combine and affect behaviour in a very
complex way, so it is perhaps too simplistic to expect a ‘schizophrenia gene’ to be identified.
Biochemical factors
AO1 Genetic factors may lead to differences in brain chemistry, so that it is the brain
chemistry that is the immediate causal factor. Biochemical abnormalities may be important
in the development and maintenance of schizophrenia. Neurotransmitters are the chemical
messengers that transmit impulses across synapses between neurons. There are several
neurotransmitters that have been linked to the development of schizophrenia, the main
focus being on dopamine.
According to the dopamine hypothesis, schizophrenia results from an excess of dopamine
activity or an over-sensitivity of dopamine receptors in the brain of sufferers. Support from
this hypothesis comes from the fact that drugs such as Phenothiazines act by blocking
dopamine receptor sites, and are effective in alleviating (lowering) some of the main
symptoms of schizophrenia. Additionally, L-dopa, which is taken to treat Parkinsons
disease, works by increasing levels of dopamine, and can bring about schizophrenic-type
symptoms in patients.
AO2/3
One issue with the dopamine hypothesis is that Phenothiazines do not work for everyone
diagnosed with schizophrenia. Additionally, they also tend to only treat the positive
symptoms and not the negative symptoms. This leads some such as Crow (1985) to the
conclusion that different types of schizophrenia have different causes
SCHIZOPHRENIA: The Bare Bones
PET scans have investigated the brains of live schizophrenic patients. Wong et al. (1986)
found a two fold increase in the density of dopamine receptor sites in schizophrenic patients
who had never been treated with drugs compared to patients who had been treated with
drugs and to a control group. This finding is supported by Post-mortem examination of
people with schizophrenia. For example, Seeman (1987) reviewed a number of studies
Page | 5
which found increases in dopamine receptor density between 60 and 110 per cent
compared to controls.
However, later studies have not replicated Wong’s results.
The dopamine hypothesis could also be criticized for being reductionist. It reduces a
complex and varied disorder to the action of one chemical operating in specific areas of the
brain.
Neuroanatomical factors (brain structures)
AO1 Several researchers have argued that brain abnormalities may be involved in
schizophrenia. There are several sophisticated techniques for studying the brain, some of
which have been used to study brain structure in schizophrenia.
For example, the frontal lobes, which are known to have an important role in intellectual
functioning and clear communication, are smaller than in controls. Also ventricles, which
are fluid-filled cavities in the brain, have been shown by numerous studies to be larger in
people with schizophrenia.
AO2/3 Buchsbaum (1990) used sophisticated PET scans to reveal reduced cerebral blood
flow in the frontal lobes of people with schizophrenia. Andreasen et al. (1990) conducted a
well-controlled CT scan study and found significant enlargement of the ventricles in
schizophrenic patients compared to controls.
Though these studies have provided scientific/empirical evidence to support the role of
brain structure in the development of schizophrenia, there have been contradictory
findings. Also, as the participants in these studies have been suffering from schizophrenia
for many years, and most likely taking medication, it is difficult to establish whether these
brain abnormalities are the cause or effect of schizophrenia.
Candidates might also use the diathesis-stress model as a way of
reconciling biological and psychological explanations.
Diathesis-Stress model
Due to the issues discussed, it is hard to pinpoint a single cause for such a complex and
varying disorder such as schizophrenia.. Zubin and Spring (1977) put forward the idea that
stressful life events could trigger psychotic symptoms in individuals with an underlying
SCHIZOPHRENIA: The Bare Bones
predisposition/vulnerability to schizophrenia. Genetic factors and prenatal insults (trauma
to the unborn child), could lead to a biological vulnerability, and this can take the form of
biochemical abnormalities. This could in turn lead to cognitive deficits, which could become
delusions and hallucination when exposed to environmental stress. This diathesis-stress
model attempts to integrate different potential causes, to give a more complete explanation
Page | 6
of schizophrenia.
PSYCHOLOGICAL EXPLANATIONS FOR
SCHIZOPHRENIA
If you are asked to outline ‘psychological explanations’ in a 24 marker, then
you have the choice on which theories to apply. You would be advised to focus
on more than one; this way it’ll give you better scope for your AO2/3
discussion.
The psychodynamic approach (including family systems theory)
Traditional psychodynamic approach
AO1 According to traditional psychodynamic explanations, schizophrenia is caused by a problem
with an ego defence mechanism called regression. Freud believed that if a child is raised by cold and
uncaring parents, their Ego will attempt to protect them from the trauma this causes. To do this it
employs the defence mechanism of regression, which is when a person psychologically reverts back
to a past stage in their development. The person in a cold and uncaring environment will have a
weak Ego, and so, in dealing with the huge demands placed on t by employing its defence
mechanisms, the Ego shatters, leaving the Id in charge of the sufferer’s personality. The person
becomes totally focused on themselves, to such an extent that they lose all touch with reality. This is
the cause of the visual and auditory hallucinations of schizophrenia.
AO2/3
The androcentric nature of Freud’s theories, heaping much of the blame on the mothers of
schizophrenics, has attracted considerable criticism. A great deal of research has found that the
parents of the vast majority of schizophrenic sufferers are not cold and uncaring as Freud described
them, but sensitive and caring individuals, scared and devastated by their child’s illness. Another
criticism that has been applied to the psychodynamic theory of schizophrenia relates to the
therapies that have been established to try and cure individuals. If Psychodynamic theory can
explain why schizophrenia has occurred, it can propose a way to cure it. So far, there have been no
real breakthroughs with sufferers of schizophrenia who have undergone psychodynamic therapy.
SCHIZOPHRENIA: The Bare Bones
Family systems theory
AO1 In another psychodynamic explanation, Fromm-Reichman (1948) proposed that schizophrenia
was caused by ‘schizophrenogenic families’ and in particular a schizophrenogenic mother (a mother
who causes schizophrenia). The mothers, she suggested, seem to convey conflicting messages to the
child. They are cold and distant but dominating and severe. They were often rejecting of the child,
Page | 7
but still demanded that the child show emotional expression and were dependent on the mother at
all times. Repeated exposure to such contradictory messages causes the child to resort to selfdeception and to develop a false concept of reality and an inability to communicate effectively. For
Fromm-Reichman, there also seemed to be a link between schizophrenogenic families and those
with high emotional tension, many secrets and plots. They had very high levels of conflict and
lacked the abilities to arrive at resolutions.
AO2/3
Brown et al (1966 and 1972) focused on one aspect of the theory proposed by Fromm-Reichman,
and that was the emotion expressed (e.g. criticism, hostility and over concern) within the family of a
schizophrenic sufferer. They conducted a nine-month follow-up study of schizophrenic patients who
had returned to their family homes after being discharged from hospitals. In the nine months
following their return home, 10% of the patients returning to low EE (expressed emotion) homes
had relapsed. In the high EE group of families, 58% had relapsed. However, the concept of
expressed emotion is more of a predictor of relapse, than an explanation of the initial development
of schizophrenia.
A problem with family systems theory is that we cannot infer a cause and effect relationship
between the behaviour of the family and the presence of a schizophrenic child. The data gathered
from research into this will almost always be retrospective [recording past events, usually by selfreport] and therefore it is difficult to draw conclusions relating to the accuracy and reliability of the
information. It may also be the case that the disturbed behaviour in the family is not the cause of a
child developing schizophrenia, but rather that the disturbed behaviour in the family is the result of
the family having a schizophrenic in their midst.
Cognitive explanation
AO1 Whilst a number of different cognitive explanations have been put forward, they all have in
common the idea that schizophrenia is caused by disorganised thinking.
One of the most important general cognitive theories of schizophrenia is the attention deficit
theory. According to Frith (1979), schizophrenia is the result of a faulty attention system.
Preconscious thought (i.e. thought that occurs without awareness contains huge quantities of
information from our senses that would normally be filtered, leaving only a small amount to enter
into conscious thought.
Schizophrenia may be the result of a breakdown of the filtering process, resulting in overload. It is
this that gives rise to cognitive abnormality. For example, thoughts that would usually be filtered out
as irrelevant or unimportant are now interpreted in conscious awareness as more significant than
SCHIZOPHRENIA: The Bare Bones
they really are. Because there is a problem with attention, schizophrenics have difficulty focussing
on anything for any period of time, giving the impression of disordered thought. For Frith, this
accounts for the positive symptoms of schizophrenia, such as delusions, auditory hallucinations and
disorganised speech.
Frith believed that this faulty filter is underpinned by an irregularity of the neuronal pathways
connecting the hippocampus to the pre-frontal cortex which is linked to faulty regulation of
dopamine in this part of the brain.
AO2/3 Frith showed that schizophrenics have reduced blood flow to these areas of the brain
(indicating reduced brain activity) during certain cognitive tasks.
AO2/3 If schizophrenics have an attentional problem then they would have difficulty doing tasks
that require focused attention. However, schizophrenics do not seem to be any easier to distract
than normal, when engaged on cognitive tasks (Mckenna, 1994). McKay et al (1996) point out that a
lack of experimental support has resulted in the attention deficit theory being abandoned by most
researchers. Most cognitive research now focuses on explaining specific symptoms of schizophrenia
rather than the disorder as a whole.
AO2/3 Schizophrenics clearly have disordered thoughts, but it is debatable whether this is a cause of
the disorder or a symptom of it. This means that it is not clear whether cognitive deficits cause
schizophrenia (and the associated biological changes), or whether the cognitive deficits are an effect
of other causes, such as neurochemical changes.
AO2/3 Whilst cognitive theories appear to explain many of the positive symptoms of schizophrenia
satisfactorily, they don’t adequately explain negative symptoms.
General evaluation and conclusion
AO2/3 A general criticism of psychological explanations is that they cannot account for the fact that
schizophrenia runs in families.
You could perhaps briefly outline the findings of Gottesman here as an elaboration of this point.
It is hard to pinpoint a single cause for such a complex and varying disorder such as
schizophrenia. An attempt to merge psychological and biological explanations of
schizophrenia is provided by the diathesis stress model. Zubin and Spring (1977) put
forward the idea that stressful life events could trigger psychotic symptoms in individuals
with an underlying predisposition/vulnerability to schizophrenia. Genetic factors and
prenatal insults (trauma to the unborn child), could lead to a biological vulnerability, and
this can take the form of biochemical abnormalities. This could in turn lead to cognitive
deficits, which could become delusions and hallucination when exposed to environmental
stress. This diathesis-stress model attempts to integrate different potential causes, to give a
more complete explanation of schizophrenia.
Page | 8
SCHIZOPHRENIA: The Bare Bones
THERAPIES FOR SCHIZOPHRENIA
Biological therapies
If you are asked to outline and evaluate one biological therapy, drug therapy counts as one
(in other words you could refer to both typical and atypical antipsychotics).
When discussing therapies (AO2/3), you’ll need to focus not only on the effectiveness (or
efficacy) of the treatment, but evaluate the relevant research and write about the
appropriateness of the therapy (this could include ethical considerations).
AO1 The major type of biological therapy for schizophrenia is antipsychotic drugs (also called
neuroleptics). There are broadly two groups of antipsychotics: ‘typical’ and ‘atypical’. These
essentially mean ‘older’ and ‘newer’ groups of drugs respectively. Both the typical and atypical
antipsychotics are ‘dopamine antagonists’ – they block dopamine receptors on the surface of
neurons. They reduce dopamine activity as they reduce overall dopamine signalling. By blocking
dopamine, the positive symptoms of schizophrenia seem to be controlled and there is a noticeable
cognitive and behavioural improvement as well.
Phenothiazines are a group of the traditional, ‘typical’ antipsychotics, which are widely regarded as
the most effective treatment for schizophrenia. A new range of atypical antipsychotics, e.g.
Clozopine have been introduced which avoid some of the problems associated with the older drugs.
AO2/3 The most widely used drugs do not seem effective against the negative symptoms (e.g.
apathy, social withdrawal, impaired personal hygiene).
AO2/3 They are not effective for everyone diagnosed with schizophrenia. About 30 per cent of
patients either do not respond to antipsychotic drugs or are intolerant to them. Clozapine can
sometimes be effective with these treatment-resistant patients, but only about half of such patients
respond favourably (Wahlbeck et al., 1999). This means that a minority of people with chronic
schizophrenia cannot be helped with antipsychotic medication.
AO2/3 Antipsychotics can produce some distressing and sometimes irreversible side effects.
Relatively minor side effects include drowsiness, visual disturbance, dryness of the mouth, changes
in weight and depression. More seriously, they can induce a disorder called tardive dyskinesia
which is irreversible and involves uncontrollable lip and tongue movements and facial tics.
Approximately 24 per cent of people develop this after taking antipsychotics for seven years.
AO2/3 Adverse effects sometimes cause patients to stop taking their medication. This leads to the
so-called ‘revolving door phenomenon’ whereby patients relapse and have to return to hospital. To
combat this, patients are sometimes given injections (depots) of long-lasting anti-psychotics which
Page | 9
SCHIZOPHRENIA: The Bare Bones
takes away their option to ‘stop taking the tablets’. However, there is an ethical issue here as it
removes control from the individual.
AO2/3 A new range of atypical neuroleptics has been introduced which avoid some of the problems
of the older drugs. Clozapine, for example, appears to be effective in controlling the positive
symptoms particularly in those who have proved resistant to other neuroleptics (Meltzer, 1999) and
does not give rise to the side effects discussed previously.
However, it can produce a condition in which the immune system is damaged. This can be
counteracted by the use of other drugs and by regular blood monitoring, making the treatment
expensive and time-consuming.
Psychological therapies
Social interventions
AO1 Social interventions often make use of behavioural techniques. They are based on research
from those such as Wing and Brown (1970) who found significant improvements in schizophrenic
patients when social changes were made in hospital wards to make them more ‘stimulating’.
Milieu therapy is based on the idea of promoting self-esteem and personal control. Social
learning programmes focus on improving self-care routines, conversational skills and jobrole skills. Milieu therapy can include a token economy system where schizophrenic
patients earn privileges by conforming to expected norms, e.g. staying out of bed in the day,
and stopping any bizarre behaviours.
AO2/3 Critics of this kind of therapy suggested that the training did not generalise to reallife situations. However, as the training programmes improved over time, this criticism was
less valid. Birchwood and Spencer (1999) have reviewed research into SST and found that
such programmes are generally beneficial in increasing the individual’s skill and
assertiveness in social situations. However, it appears that some kind of active intervention
needs to be maintained otherwise social skills will start to decline again.
Cognitive-behavioural therapy (CBT)
AO1 Coping Strategy Enhancement (CSE) is a form of CBT, based on research that has found
that people with schizophrenic can often identify triggers to the onset of their psychotic
symptoms and that they develop their own methods of coping with the distress caused by
hallucinations and delusions (e.g. Tarrier, 1987). CSE aims to teach individuals to develop
and apply effective coping strategies which will reduce the frequency, intensity and duration
of psychotic symptoms and ease the accompanying distress. The two components are
‘education and rapport training’, where the therapist and client work together to improve
the effectiveness of the client’s own coping strategies and develop new ones; and ‘symptom
Page | 10
SCHIZOPHRENIA: The Bare Bones
targeting’, where a specific symptom is selected for which a particular strategy can be
planned.
AO2/3 A controlled trial carried out on people diagnosed with schizophrenia by Tarrier et al.
(1993), found a significant easing of positive symptoms in a CSE group as opposed to a nontreatment group held on a waiting list, and a significant improvement in the effective use of Page | 11
coping skills. This kind of research study is encouraging and suggests that CSE provides an
effective way of helping people with the disorder to control their symptoms.
AO3 Tarrier’s (1993) study was well-controlled. However, out of an initial sample of 49
people, 45 per cent refused to cooperate or dropped out during this trial. This is a frequent
problem of outcome research in schizophrenia and causes the loss of valuable data. This
could mean that the remaining sample were individuals more likely to be more determined
in character, thus meaning a greater chance of success from psychological therapies.
Family intervention
AO1 Research on expressed emotion (EE) has shown that certain aspects of family life can
affect the course of schizophrenia. This has led to the development of various family
intervention programmes. Central to these programmes is the emphasis on inclusion and
sharing information. Session aim, at the beginning, to develop a cooperative and trusting
relationship with the family group and the contributions of all family members are valued.
The therapist provides information about the cause, course and symptoms of schizophrenia,
while family members, including the individual with schizophrenia, bring to the group their
own experiences of the disorder. The goal of the sessions is to provide the whole family
with practical coping skills that enable them to manage the everyday difficulties arising as
a consequence of having schizophrenia in the family.
AO2/3 Several studies have been conducted in the UK and other countries to compare high
EE families who are then randomly assigned either to family intervention, routine treatment
or a control treatment. There has been overwhelming support for the effects of family
intervention. It has been shown not only to reduce the rate of relapse significantly, but also
to improve compliance with medication and to reduce ratings for EE within the family.
Conclusion
Psychological therapies are used mainly to supplement medication and are not usually
effective on their own. While drugs tend to target the psychotic symptoms of schizophrenia,
psychological interventions are intended to help people with schizophrenia to cope with the
problems of everyday living. They often involve other family members as well because
schizophrenia can have devastating effects on the whole family.
SCHIZOPHRENIA: The Bare Bones
Page | 12