3/1/2012

A2 EDEXCEL
PSYCHOLOGY
UNIT 3: CLINICAL PSYCHOLOGY

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Clinical psychology
3.1 An introduction to clinical psychology

What is clinical psychology?

Clinical psychology is about the study of mental health and mental disorders. This application of psychology focuses on
diagnosing, explaining and treating mental illness. As part of this course, areas of clinical psychology which you will cover
include methods of mental disorder diagnosis (and the reliability and validity of such diagnosis tools) and definitions of
what it means to be ‘abnormal’.

For this module, you are also required to study two mental disorders. One of these disorders must be schizophrenia, and
you are presented with a list of options for the second choice. For both of your disorders, you must learn the key features
and symptoms of the disorder, how it is diagnoses, two explanations from different AS approaches and two treatments.

Course outline: clinical psychology

This unit is separated out into the following sections. Tick the boxes as you go through them

Methodology
 Primary data and secondary data: methods used to collect primary and secondary data, and strengths and
weaknesses of each type of data
 Features of reliability and validity
 Research methods into studying schizophrenia (your course specifies interviewing and twin studies)

Content
 What is clinical psychology?
 Describe and evaluate two definitions of abnormality: the statistical and social norms definitions
 Use at least one other definition of abnormality, in brief, to evaluate the other two definitions
 Describe the DSM as a mental diagnosis tool, and with the use of studies for support and evaluation identify issues
of reliability, issues of validity and issues of culture with regards to diagnoses with the DSM
 Discuss two mental disorders, including schizophrenia and one other disorder from: unipolar depression, bipolar
depression, phobia, obsessive-compulsive disorders, anorexia nervosa and bulimia nervosa
 For schizophrenia, you must be able to:
 Describe key features and symptoms of schizophrenia
 Explain and evaluate two explanations for schizophrenia, including a biological explanation and one other
explanation from a different AS approach
 Describe and evaluate two treatments for schizophrenia from two different AS approaches
 For your other chosen disorder from the above list, you must be able to:
 Describe key features and symptoms of your chosen disorder
 Explain and evaluate two explanations from any two AS approaches for your chosen disorder
 Describe and evaluate two treatments from any two AS approaches for your chosen disorder
 Describe and evaluate five other treatments for mental illness (one from each of the five AS approaches)

Studies in detail
You must be able to describe and evaluate three studies:
 Rosenhan (1973), a study ‘on being sane in insane places’
 any one study into schizophrenia, from Gottesman and Shields (1966) and Goldstein (1988)
 any one study of your choice into your other chosen mental disorder

Key Issue
Describe one key issue from the following and conduct a practical which covers the key issue:
 the issue of understanding mental disorder (focusing on one of your chosen disorders)
 the issue of caring for someone at home who suffers from a mental disorder
 the issue of the portrayal of mental illness in the media

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Definitions of abnormality
3.2 The statistical and social norms definitions of abnormality

Normality and abnormality

It has been hard to describe exactly what is meant by ‘abnormal’ for a number of reasons. First of all, there is no clear
definition of what is ‘normal’ making it difficult to identify what is not normal. Also, there is no one shared characteristic
between everything that is described as abnormal, making it difficult to operationalise. Different cultures also interpret
behaviours differently, so whereas Westernised countries may see something as abnormal, others may see this as
perfectly normal, but you will come across cultural issues later on.

Therefore, there are a range of definitions of abnormality used by different psychologists. There are two discussed in
detail as part of this application, and two others (‘abnormality as dysfunction and distress’ and ‘deviation from ideal
mental health’) may also be looked at for evaluative purposes.

Deviation from statistical norms

Under this definition of abnormality, a person’s trait, thinking or behaviour is classified as abnormal if it is rare or
statistically infrequent. What is regarded as statistically unusual all depends on normal distribution. A distribution curve
can be drawn to show what proportions of people share the traits, characteristics or behaviours in question.

The graph shows the distribution of

IQ scores. 34.1% of people either side
of the mean score (100 in this case)
lie within 1 standard deviation of that
frequency

mean, either higher or lower, and

34.1% 34.1% 13.6% of the population either side of
2.1% 2.1% that sit within 2 standard deviations.
0.1% 0.1%
13.6% 13.6% Anything further than two standard
deviations is said to be statistically
-3SD -2SD -1SD mean +1SD +2SD +3SD infrequent.

Therefore, a very small subset of the population (2.2% in total) have an IQ which is more than two standard deviations
from the statistical norm, and are said to have an abnormally low IQ (this means less than 70). Similarly, anyone with an
IQ above 130 is said to have an abnormal IQ score, and these people site within the 2.2% above 2 standard deviations
from the mean. Normal distributions are calculated by mathematicians based on formulae which are designed to give
standard distributions.

A normal distribution curve has 95.4% of scores either side of the mean which are within two standard deviations, and
since this is a high percentage, it is considered statistically frequent. The more a person deviates from that mean, the
more they are considered to be abnormal, although anyone within that centre 95.4% is considered t be normal. Anyone
outside that percentage group is considered to be abnormal, approximately 2.2% at either end.

 The statistical definition gives a quantitative measure which is objective, and is more likely to be reliable because the
scores come from tests or studies which can be repeated
 Some measures of abnormality under this definition highlight ‘a lack of normal functioning’ and therefore this is a
scientific measure of whether or not someone is entitled to assistance, support and funding
 What is considered abnormal from a statistical sense may actually not be undesirable, for example people within the
top 2.2% of the population with high IQs (above 130) are considered abnormal, but this is actually seen as a good
trait and they are not treated as though they have mental health disorders
 Single cut-off points present difficulties, for example, saying that anyone with an IQ below 70 is abnormal makes it
difficult to justify someone having an IQ of 69 being abnormal and then someone else of 70 being normal
 Abnormal behaviour itself is not actually rare, most people are likely to show atypical behaviour at some point in
their lives, and mental disorders such as depression are actually very statistically common, so may not be as valid

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Deviation from social norms
The deviation from social norms definition of abnormality suggests that all behaviour which is socially unusual is
abnormal. Behaviour should conform to social norms in order to be considered ‘normal’. These norms are social rules
that people abide by, and are more often than not specific to one culture. There are a number of influences on social
norms that need to be taken into account when considering the social norms definition:

different cultures and subcultures are going to have different social norms
culture  for example, hearing voices in one culture may be seen as abnormal behaviour and signs of
mental illness, whereas in other cultures it may be a sign of being connected with spirits

at any one time, a type of behaviour might be considered normal whereas another time the
same behaviour could be abnormal, depending on both context and situation
context and situation  for example, wearing a chicken suit in the street for a charity event would seem normal, but
wearing a chicken suit for everyday activities such as shopping or going to church, it would
be socially abnormal

time must also be taken into account, as what is considered abnormal at one time in one
culture may be normal another time, even in the same culture
historical context
 for example, one hundred years ago, pregnancy outside of marriage was considered a sign
of mental illness and some women were institutionalised, whereas now this is not the case

different people can behave in the same way and for some will be normal and others abnormal,
depending on age and gender (and sometimes other factors)
age and gender
 for example, a man wearing a dress and high heels may be considered socially abnormal as
society would not expect it, whereas this is expected of women

Behaviour which goes against social norms may be incomprehensible to others, and it can make others feel threatened
and uncomfortable, or at the least surprised and confused.

 What this definition states is abnormal matches with what society normally means when it uses the term ‘abnormal’
as we normally mean odd behaviour, so traits such as having high IQs are not considered abnormal by this definition
 This definition helps to explain why different cultures have different ideas about what is normal, and the definition
itself takes into account that there is no universal rule about what abnormality is
 When culture, context, situation, historical context, age and gender have to be taken into account for a proper
understanding of abnormality, it makes it difficult to have a reliable idea of what is abnormal, so diagnosis using this
definition is difficult
 Some people might be mentally ill, perhaps suffering from extreme anxiety disorders, but not breaking any social
norms and therefore would not be considered abnormal and ill by this definition
 Criminals, for example, break social norms, and are seldom considered mentally ill

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DSM
3.3 The Diagnostic and Statistical Manual [of Mental Disorder] and an evaluation of the DSM

Diagnostic classification systems

There is no one manual for diagnosing mental illness. There are two classification systems which are most widely-used in
western cultures:
 the APA’s (American Psychiatric Association) Diagnostic and Statistical Manual of Mental Disorder (known as the
DSM) which is the most commonly-used manual, and is now in its fourth edition, the latest being the text-revised
version, called DSM IV-TR
 the WHO’s (World Health Organisation) International Statistical Classification of Diseases and Related Health
Problems (known as the ICD), which is similar to the DSM although not quite as widely-used, but it shares the same
sort of strengths and weakness – the ICD is now in its tenth edition, ICD-10

The DSM provides criteria from which mental health disorders can be diagnosed. The content of the DSM has changed
significantly since the publication of DSM-I in 1952, and there are to be many more updates and amendments in the
upcoming fifth version, DSM-5 (previously DSM-V) which is due to be published May 2013.

With each new version of the DSM, definitions have become more precise (for example, by including the duration of
symptoms needed for a diagnosis), and also changed have been made in line with changing social norms (for example,
homosexuality in DSM-I and DSM-II was considered a mental illness). New disorders are also outlined in each edition.

The multi-axial system

The DSM is used as a diagnostic manual, and the DSM’s system of diagnosis uses a five-axes model. Each axis measures a
different aspect in relation to the disorder. Axes 1-3 are compulsory, whereas axes 4 and 5 are optional, although are
usually included as well for a more reliable diagnosis. Having multiple axes allows a patient to be assessed by more than
one criterion, so a patient is put into a category on each axis using their symptoms and a diagnosis can be made from this.
 Axis I measures the clinical disorder, this gives the major diagnostic category arrived at by the diagnostician, so
disorders such as schizophrenia, depression, bulimia , sleep disorders, etc would be described under this axis (axis I
will also include anything which requires immediate intervention, such as history of sexual abuse or stress-related
physical symptoms which need quick attention)
 Axis II measures personality disorders and mental retardation (based on a ratings scale), and these chronic
conditions often go alongside the axis I disorders, and help understand these disorders – these are clinical syndromes
that are a permanent part of the patient and may affect treatment, such as OCR or paranoid personality disorder
 Axis III assesses general medical conditions, these are physical problems that are of relevance to the condition or
treatment – for example, if the patient has diabetes, this could contraindicate the use of certain drugs – and these
conditions may contribute to the patient’s ability to cope and their self-image
 Axis IV measures psychosocial and environmental problems (life problems that influence the psychological wellbeing
of the patient) – examples include homelessness, family issues and unemployment
 Axis V gives a score for the global assessment of functioning, whereby a score from 1 to 100 is used to classify the
patient based on an evaluation of how well the individual functions socially, occupationally and psychologically where
a score of 1 means ‘severe danger of harm to self or others’ and 100 shows the individual has superior functioning in a
wide range of activities (generally, a score of 50 or below indicates severe symptoms)

Strengths and weaknesses of the DSM

The main strength of the DSM is that it is in such wide use and is commonly agreed upon. This allows for a common and
universal diagnosis. Through its many revisions, the DSM has stood the test of time. Having a diagnostic companion such
as the DSM or ICD allows, theoretically, for two doctors to make the same diagnosis on the same patient – if the
symptoms are the same, a more agreeable diagnosis is likely using the DSM.

However, some criticise the DSM because it serves as confirmation that sufferers of these conditions are ‘sufferers’ who
need ‘treatment’, although some suggest mental illness is often just another way of living, who’s to say they’re actually
suffering a mental disorder? Laing (1960) suggested that schizophrenia is just another way of living and not a condition.

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Issues of reliability, validity and culture with diagnosis
3.4 Evaluating the DSM with regards to reliability and validity, and culture affecting diagnosis

Reliability and validity in clinical psychology

To be reliable as a diagnostic classification system, there would have to be consistency with the DSM. This means that the
DSM is reliable if the clinicians using it consistently arrive at the same diagnoses as each other. The term inter-rater
reliability is used to describe the extent to which different clinicians agree on the same diagnosis for the same patient.

Traditionally, reliability is calculated mathematically, often using a measure known as positive predictive value (PPV). The
PPV of a disorder shows the reliability, taking the example of depression, of the DSM with that disorder; so if depression
had a PPV value of 80, this means that 80% of diagnosed depression patients will have the same subsequent diagnosis
when re-assessed. However, there may also be a cultural element to reliability, for example with Cooper et al. (1972) who
showed the same patient interview tapes to various American and British psychiatrists, and American clinicians diagnosed
schizophrenia twice as often as the British, and the British clinicians diagnosed depression twice as often as the American.

Validity is the extent to which a measure of a psychological variable measures what it sets out to measure. Essentially this
means the correct variable (in clinical psychology, this variable will be a mental disorder) is measured, by arriving at the
correct diagnosis. Needless to say, if the DSM were not reliable, it would not be valid either. This is because if it is
unreliable it means inconsistent diagnoses are made, and so it must not be valid either as surely the correct diagnosis is
being made.

 construct validity refers to whether or not a classified disorder is actually a good indicator of what you’re really trying
to measure, for example, in operationalising (see below) a disorder such as depression by drawing a list of symptoms
and features, you begin to lose some understanding of the real nature of the disorder so the DSM becomes invalid
 concurrent validity is when the results of a study matches the result of another study done at the same time, so this
would mean that if a diagnosis made using the DSM arrives at the same mental disorder that another diagnosis has, it
is likely to have concurrent validity
 predictive validity, on the other hand, is when the results of a test or study match the result of another done at a
different time, so instead of looking at two diagnoses to see if they back each other up, the comparison is made over
two different time periods, for example the DSM could be used for a diagnosis, then some time later another measure
(perhaps a doctor’s view or observations by mental health personnel) would agree with the diagnosis to be valid
 convergent validity is when a test result converges (gets close to) the result of another test measuring the same thing
– a correlational test would be carried out to see the convergence (the difference between convergent validity and
concurrent/predictive is that convergent validity must be measuring the same thing, it can be different measures in
concurrent and predictive validity)

Operationalising mental disorders

Mental health disorders need to be operationalised is they are to be definable within the DSM. This would mean arriving
at lists of symptoms and behaviours to make the disorder measurable. It has been argued, however, that in
operationalising a concept such as depression, something is lost from the understanding of the nature of the whole
experience of depression, which means that the DSM is not a valid tool in that is lacks construct validity, in that the
constructs which are drawn up may not actually be sufficient to represent the disorder.

A further possible problem with validity and the DSM is that although taking into account axes IV and V in the later
versions of the DSM (personal and social factors and how well the patient is functioning in society), taking such factors
into account when diagnosing can actually lead to an invalid diagnosis. For example, someone diagnosed with depression
may not be functioning well in society at all, but this might not be due to their diagnosed disorder but actually for another
reason, possibly unemployment (for example), and so such a diagnosis would not be valid.

It has also been argued that since there has been significant change in the content of the DSM with regards to
categorising certain disorders that the manual is invalid. For example, homosexuality and epilepsy have both been
considered mental disorders and been included in the DSM at one stage, but are no longer, which might suggest that the
DSM has low validity.

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Studies evaluating the DSM in terms of reliability
The course requires that you know studies to evaluate the use of the DSM as a classification system in terms of reliability
and validity. Outlined here are three studies supporting the DSM in terms of reliability, and one criticising the DSM.

Goldstein (1988)
[For the full study by Goldstein, see 3.9 Goldstein (1988) in this section] Goldstein tested the DSM for reliability using the
at-the-time current version, DSM-III. One of the aims of her study was to test the DSM-III, comparing the results of the
re-diagnoses of 199 patients who had been originally diagnosed with schizophrenia using DSM-II. Experts carried out a
re-diagnosis of a random sample of eight patients using a single-blind technique (not allowing the experts to know the
hypothesis, so their answers are not biased, whereas Goldstein herself was aware of the hypothesis).

She found that 169 of the 199 patients diagnosed according to DSM-II as having some form of schizophrenia met the
DSM-III criteria too, so reliability was seen as good with the DSM. Of the patients assessed by the clinical experts as well,
she found high levels of inter-rater reliability.

Brown et al. (2001)

In 2001, Brown et al. studied anxiety and mood disorders in 362 outpatients in Boston, to test reliability of the DSM-IV
and patients underwent two independent interviews using anxiety disorder interview schedules for DSM-IV, known as
the life-time version.

Brown found good-to-excellent reliability for most of the DSM-IV categories (most of the disagreements tended not be on
what the symptoms were, but simply if there were enough of them). However, they found some boundary problems with
certain disorders, which made it hard to diagnose patients with disorders if they were at boundary level. Overall, the
study highlights some problems with the DSM but generally proves it to be a reliable tool.

Stinchfield (2003)
Stinchfield studied both reliability and validity by looking at the diagnosis of pathological (behaviour which is considered
abnormal due to its extreme or excessive nature) gambling. 803 people were studied from the general population, and
259 people on a gambling treatment programme, all from Minnesota, and they were assessed using a questionnaire of 19
items used to measure the DSM-IV diagnostic criteria for pathological gambling.

The DSM criteria were used to sort those linked to pathological gambling and those who were not. There were other
validity measures as well. It was found that the DSM-IV criteria were both reliable and valid.

Kirk and Kutchins (1992)

In a review paper, Kirk and Kutchins argued that methodological problems with studies conducted to test the reliability of
the DSM up until 1992 had limited the generalisability of their findings. For example, they argued that there had been
insufficient training and supervision of interviewers, and studies tended to take place in specialised research settings, and
so could lack validity as well as reliability.
Assessment of Kirk and Kutchins’ points
 Due to the specialised settings the findings may not be valid as they may not relate to the conclusions of real clinicians
 Their review paper was published in 1992, before the studies of Brown and Stinchfield, who showed the DSM-III and
DSM-IV to be reliable, so it is suggested that reliability of the DSM has improved since then
 The accuracy of their criticisms is debatable, as the above three studies all found the DSM to be a reliable tool
 Some of the points about interviewing – such as that different interviewers may affect the situation and lead to
different data – might be important, when considering generalising findings from studies; Goldstein, however, did not
use interviewing to test reliability, she used re-diagnosis using secondary data and still found reliability

Another study you could use for evaluation is Nicholls et al. (2000), which showed that using the DSM-IV there was not
good inter-rater reliability for the diagnosis of eating disorders in children.

Studies evaluating the DSM in terms of validity

The studies on the following page have evaluated the use of the DSM in terms of validity. It is recommended that you
learn at least two studies from this selection.

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In order to be valid, the diagnoses must identify a distinct condition that has different symptoms from other conditions
and that is likely to progress in a certain way and respond to one treatment over another. A valid diagnosis for a mental
disorder is more difficult than for a physical disorder because of a lack of objective physical signs. To be valid, the DSM
also has to be reliable.

Kim-Cohen et al. (2005)

In 2005, Kim-Cohen et al. undertook a longitudinal study of conduct disorder in five year olds, to test the concurrent,
convergent and predictive validity of the DSM-IV. There were 2,232 children involved in another, existing, longitudinal
study which was used as a focus. The children’s mothers were interviewed and teachers received postal questionnaires
asking about conduct disorder symptoms over the previous six months.

They found that 6% were diagnosed as having conduct disorder (displaying three or more symptoms), and 2% of the
children with severe conduct disorder (five or more symptoms). Children diagnosed with conduct disorder were more
likely to describe themselves are having antisocial behaviours than comparison children. Also, during observational
assessments these children were more likely to behave disruptively. Different measures were said to show the diagnoses
had validity, as different data sources were used to check validity.

Hoffmann (2002)
Hoffmann studied prison inmates to look at diagnoses of alcohol abuse, alcohol dependency and cocaine dependency, to
see if differences would occur in a computer-prompted structured interview, compared to the DSM-IV-TR criteria. It was
found that the DSM-IV-TR diagnosis was valid and that the interview data supported the idea that dependence was more
a severe syndrome than abuse. The symptoms from the automated interview matched those of the DSM criteria.

Lee (2006)
Lee studied the DSM-IV-TR diagnosis of ADHD to see if it would be suitable for Korean children, and looked at gender
differences in the features of ADHD in the DSM. The DSM lists eighteen criteria for ADHD linked to children’s behaviour.
In total, 48 primary school teachers rated the behaviour of 1,663 children (904 of which were boys, the remaining girls)
using a questionnaire. Lee looked for concurrent validity by comparing the DSM-IV-TR criteria with criteria arising from
the questionnaire, and compared DSM behavioural and psychological characteristics with those found in an ADHD test.

Previous studies had showed that ADHD children had oppositional deficit disorder, ODD, as well, having problems with
peers and discipline. Lee decided that finding the same correlation would support the diagnosis and show the DSM to be
a valid tool. The same relationship was observed, and so it was said that the DSM-IV-TR had concurrent validity. Also
found it to be reliable, as the correlation could check for similar diagnoses.

However, the study found that for girls, the DSM-IV-TR symptoms and diagnoses were less compatible than they were for
boys, which was a weakness found with the DSM as a diagnostic tool.

Culture affecting diagnosis

Whilst all of these above studies show the DSM to be a reliable and valid tool, the area it receives most criticism is in its
usefulness across different cultures. There are two schools of thought, outlined below:
Culture doesn’t affect diagnosis: mental disorders are ‘scientific’
 The DSM was developed in the USA and is used widely across many other cultures – this is a valid use if mental
disorders are clearly defined with specific features and symptoms
 In other words, this school of thought suggests mental disorders are scientifically defined illnesses that are explained
in a scientific way and therefore culture does not affect diagnosis as it should be the same cross-culturally
 The study of Lee (2006) can be used to support this, as the DSM-IV-TR was used deliberately in a non-western culture
to see if ADHD diagnoses were valid in Korea
Culture does affect diagnosis: a spiritual model
 There have been studies which have shown that culture can affect diagnosis, for example, hearing voices in western
cultures is normally an abnormal sign of, for example, schizophrenia, whereas in other countries this may be seen as a
positive characteristic, such as a sign of being connected to spirits
 Depending on cultural interpretations of what is being measured, the DSM is not always shown to be valid

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Cultural differences in the symptoms of schizophrenia
You are required to know how culture affects the symptoms of schizophrenia, the required mental disorder you should
know about for your course. It has been reported that catatonic schizophrenia (see 3.5 Schizophrenia) is on the decline,
and this could be because of health measures that prevent the development of this type of schizophrenia.

Auditory hallucinations were reported to doctors by patients more in Mexican-born Americans than in non-Mexican-born
Americans. Burnham et al. (1987) looked at this using self-reports and interviewing, and checked the evidence and found
that there was a difference. No other explanation could be found except that culture had led to the difference.

White Americans were reported, using patients’ records, as showing more grandiosity as a symptom compared with
Americans of Mexican origin, again showing cultural differences.

However, it should be noted that schizophrenia in all countries has more similarities than differences.

Culture-bound syndromes
A culture-bound syndrome (CBS) is a disorder which is isolated to one culture, usually only diagnoses exclusively in one
region or country. Psychiatrists tend to reject culture-bound syndromes, although some are listed in the DSM-IV. Two
examples of culture-bound syndrome are described below:
 one example is hikikomori (literally meaning ‘to be pulled away’ and translated to English as ‘complete social
withdrawal’), a condition which has attracted concern in Japan recently, affecting mainly male teens who are
otherwise perfectly healthy. The condition makes them withdraw completely, locking themselves in their rooms
sometimes for up to twenty years, in extreme cases leaving only occasionally to commit violent crimes, although must
sufferers are not violent, just depressive. The Japanese government have described hikikomori as a social disorder
rather than a mental disorder, and say it is representative of the economic downturn the country is going through
 a second syndrome is amok which comes from the Malay people, first described in the fifteenth century as an
‘understandable’ reaction to frustration, but now recognised as a mental disorder requiring treatment. Although the
disorder has been described elsewhere, it is most often found in Malay males, beginning with depressive brooding
and often following violent outbursts using weapons, commonly homicidal. The turn of phrase ‘running amok’ or
‘running amuck’ came from this, describing the sensation of rage leading to a killing spree

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Schizophrenia
3.5 Schizophrenia as a mental disorder: symptoms, features, two explanations and two treatments
Your course requires that you study two mental disorders: one being schizophrenia, and the other your choice from a list
provided by the board. The latter disorder is covered in the next section, and for this series of notes the chosen disorder
is unipolar depression, although other choices are available. This document covers the compulsory disorder, schizophrenia
and what you have to know: key features, key symptoms, two explanations and two treatments (both from different
approaches to psychology).

Symptoms and features of schizophrenia

Schizophrenia is a chronic mental health condition that causes a range of different psychological symptoms. Common
symptoms include:
 hallucinations – hearing and seeing things that do not exist
 delusions – believing things that are not true
and so schizophrenia is therefore a psychosis, not a neurosis, as the patient does not realise they have a condition.

The exact cause of schizophrenia is unknown as of yet, although there are a number of possible explanations. Two are
covered in this unit. The NHS suggests that as many as 1 of every 100 people will suffer at least one episode of acute
schizophrenia in their lifetime, although Jablensky (2000) suggested that the disorder is found in about 1.4 to 4.6 people
in every one thousand for any nation, on average. Men and women appear equally affected by schizophrenia, although in
men it is typically active between the ages of 15 and 30, whereas in women it usually becomes active between 20 and 30.

It is commonly thought that schizophrenics have a split personality, acting perfectly normal one minute, and then
irrationally the next. However, this is not the case, and though ‘schizophrenia’ derives from Greek and German words
meaning ‘split mind’, it is not a split personality disorder. Sufferers are said to suffer episodes of dysfunction, however.

Most studies confirm that there is some link between schizophrenia and violence, although the media tends to
exaggerate this. In reality, a sufferer is actually more likely to be the victim of violence than the initiator of a violent
attack. Experts at the RCP estimate that less than 1% of UK violent crime is committed by schizophrenics.

When discussing mental disorders, symptoms are what characterise the disorder, describing ways in which sufferers
think, feel and behave. Symptoms of schizophrenia are broken down into positive symptoms and negative symptoms.
Positive symptoms are additions or changes to the behaviour of a patient, whereas negative symptoms are removals from
the character or personality of the patient:
 first-rank symptoms include hearing voices and believing that others are guiding you, for example – these are positive
symptoms such as hallucinations and delusions, they are added to the patient’s behaviour as they were not there
before the disorder became active
 second-rank symptoms include flattened emotions and other negative symptoms, such as lack of energy, sex drive,
etc (so these are all removals from the personality) – these often start well before the positive symptoms and any
diagnosis, in what is known as the prodromal period

POSITIVE SYMPTOMS NEGATIVE SYMPTOMS

 delusions – firmly held erroneous beliefs due to distortions or
exaggerations of reasoning
 delusions of grandeur – one specific type of delusion, where
the patient believes they are more powerful than they are
 hallucinations – auditory and visual distortions, the hearing
voices can be critical, providing a commentary on what the
person is doing, controlling or telling them what to do
 disorganised thinking/speech – or ‘thought disorder’ this is
usually noticed through confusing speech and incoherency
 grossly disorganised behaviour – may include unpredictable
agitation, social disinhibition and other bizarre behaviour
 affective flattening – a reduction in range and intensity of
emotional expression, including eye contact, voice tone, body
language and facial expression
 alogia – (lack of speech) lessening of speech fluency
 avolition – (lack of energy) reduction or difficulty to
undertake normal daily tasks (sometimes mistaken for lack of
interest – apathy)
 anhedonia – (lack of pleasure) inability to experience
pleasure from previously-enjoyable activities/experiences,
including hobbies, social interaction, exercise and sex
 social withdrawal – avoidance of interaction with others

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The features of a disorder are aspects about how a disorder develops and consider the disorder on a wider scale, often
include facts and statistics. The key features of schizophrenia include:
 schizophrenia appears to be a universal disorder (the condition can affect anyone in any place, males and females)
 the profile of sufferers seems to be as follows:
- ¼ of patients will have one episode of schizophrenia and then fully recover
- ¼ of patients will suffer chronic schizophrenia, having continuous schizophrenic episodes
- ½ of patients will have occasional schizophrenic episodes but do not have a chronic disorder
 positive symptoms (those added to the sufferer’s being) can be overcome (e.g. hallucinations, delusions), whereas the
negative symptoms (those lacking in sufferers) tend to remain
 male sufferers tend to experience a more severe course of the disorder than females (Goldstein, 1988)
 there are five categories which psychiatrists and diagnosticians use to describe different types of schizophrenia

Types of schizophrenia
One feature of the disorder is that there are different types. The five types are described below:
 paranoid schizophrenia is when the patient is suspicious of others (delusions of being watched or followed are
common, and thinking that messages in TV and radio programmes or newspapers are aimed directly at them) and
common symptoms are delusions of grandeur and hallucinations
 disorganised schizophrenia is when the patient’s speech is hard to follow and behaviour may be bizarre, acting with
inappropriate moods for certain situations, although there are no delusions or hallucinations
 catatonic schizophrenia is when the patient becomes very withdrawn and isolated and has little physical movement,
they appear to be in a trance-like state, with very little speech or activity
 residual schizophrenia is when there are low-level positive symptoms but there are psychotic symptoms present
 undifferentiated schizophrenia is when the patient does not fit any of the four above types

The dopamine hypothesis: a biological explanation

The dopamine hypothesis is a theory that argues a biological explanation of schizophrenia. It suggests that the unusual
behaviour and experiences of schizophrenia can be explained by changes in dopamine function in the brain. Dopamine is
one of many chemical neurotransmitters which send messages of neuronal synapses.

The hypothesis suggests that there are an excess number of dopamine receptors at the post-synaptic membrane
(receiving end of the dopamine) of neurones in schizophrenic patients.

This is partly based on a number of studies that look

calcium voltage-
at the effects of drugs on dopamine receptors and gated channel
behaviour. It is also suggested that positive symptoms 2+
Ca
of schizophrenia might be due to an increase in
dopamine in one part of the brain, and negative
symptoms due to an increase in another part. Both electrical
PET scanning and animal studies have been used to calcium
impulse
binds to
look at excess dopamine receptors. dopamine passed on
vesicles
released
One suggestion is that development of receptors in into gap
one area of the brain might lead to the inhibition of dopamine
synap
their development in another area, so explaining why Ca vesicles binds to
tic
there are different numbers of dopamine receptors in 2+ containing receptors
knob
different parts of the brain. There also seems to be dopamine
links between damage to the prefrontal cortex and
schizophrenia. This area finishes developing in adolescence which is when the onset of schizophrenia may be observed.
Much support for the dopamine hypothesis comes from drugs studies, in particular those involving amphetamines
(speed), which are dopamine agonists and so prevent the breakdown of dopamine, leading to high levels. When
amphetamines are given in large quantities, they lead to delusions and hallucinations, similar to those in schizophrenic
patients, and symptoms get even worse when given to patients of schizophrenia.

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The table below shows pieces of evidence for and against the hypothesis. These also serve as an evaluation of the
dopamine hypothesis for schizophrenia.

Evidence for the dopamine hypothesis Evidence against the dopamine hypothesis

Amphetamines give similar symptoms Amphetamines only produce positive symptoms

HOWEVER
When given amphetamines, which in effect increase the
levels of dopamine, delusions and hallucinations are
common effects, which suggest that excess dopamine
neurotransmitter action produces positive symptoms
The effects of amphetamines are only those similar to
positive symptoms of schizophrenia, which suggests
that the dopamine hypothesis is not a completed
explanation

Schizophrenics are more sensitive to dopamine uptake Other neurotransmitters might be involved

HOWEVER
PET scanning has shown that when given amphetamines,
schizophrenics show greater release of dopamine than
non-schizophrenics, suggesting those with schizophrenia
are more sensitive to excess dopamine
Whilst this research shows schizophrenics to be more
sensitive to dopamine, other chemicals such as
glutamate have been shown to have similar psychotic
effects, so perhaps dopamine is not the full explanation

Biological factors influence dopamine sensitivity Social and environmental factors are also involved

HOWEVER
Brain differences have an effect, as the brains of those
with schizophrenia seem to be different, such as
differences in volume of grey matter, and such changes at
an early age are linked with sensitivity to dopamine
It cannot be said that the explanation is exclusively
biological, as environmental and social factors seem
also to be able to trigger schizophrenia – perhaps
stressful events trigger excess dopamine production

Blocking dopamine receptors reduces symptoms Blocking receptors does not take immediate effect
HOWEVER

When given phenothiazines, drugs which block dopamine However, it is interesting that whilst a patient who
receptors, the positive symptoms of schizophrenic takes anti-schizophrenic drugs has their dopamine
patients are alleviated, and since less dopamine is being receptor blocked immediately, the reduction in positive
taken up, this seems to support the hypothesis symptoms is not effective for at least a couple of days

Much of the evidence for the dopamine hypothesis comes from animal studies and PET scanning, but there is also
incidental evidence from cases of those on drug treatment for conditions such as Parkinson’s disease and the use of
recreational drugs on behaviour. All of these research methods give the methodology triangulation which improves
validity, another strength of the hypothesis. The methodology can also be said to be reliable, as there have been many
repeated studies into dopamine levels and its effects.

However, because so many animal studies are used in this evidence, the methodology can be criticised somewhat as the
findings of animal research might not always be generalisable to humans. Whilst we are fairly certain schizophrenia is a
disorder unique to humans, however, animals share many similarities in terms of nervous systems and biological models,
and so the research is most likely appropriate. Another possible weakness of the hypothesis is that it may be something
else to do with schizophrenia which causes the difference in levels of dopamine receptors, rather than having too many
dopamine receptors results in the development of schizophrenia.

The environmental breeder hypothesis: a social explanation

Statistics show that the majority of schizophrenics in the UK come from lower classes, or from groups such as immigrants.
Research suggests that social class is either a cause of schizophrenia, or at least somehow involved in its development,
according to a second possible, explanation: the environmental breeder hypothesis. This comes from the social approach.
In one meta-analysis of 17 studies, Eaton et al. (1988) showed that statistically there are more lower class schizophrenics
and the disorder is more common proportionately in lower classes.

Sufferers of a lower class also experience a different course of the illness and are treated differently. It was found that
they are more likely to be taken by the police or social services for treatment than those of upper classes, and also more
likely to become mandatorily committed or become long-term sufferers. Thus in the 1960s it was thought that being in a
lower class was a causal factor of schizophrenia. This was known as the social causation hypothesis, or environmental
breeder hypothesis. The ideas of social drift and social adversity offer two social explanations for schizophrenia, which are
both outlined on the following page.

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Social drift
It has been suggested that sufferers of schizophrenia actually become lower class because of the difficulties that arise
from having the disorder. One study took a sample of schizophrenic men and their fathers, and compared their social
classes. It was found that the sufferers were all in the lower classes, whereas their fathers typically were not, providing
evidence for social selection theory, which suggests just that. The theory argues social class isn’t the causal factor but
that schizophrenics drift downwards in terms of social class (this is known as social drift). Whilst social selection theory is
now widely accepted by most, recently studies have suggested that there are actually environmental and social factors
which can cause schizophrenia (or at least are involved in its development). Whilst social disadvantage may not be the
main cause of such a disorder, it certainly appears to be a contributing factor to the development of schizophrenia.
Social adversity
Schizophrenia is certainly more common in urban communities (large towns and cities) rather than rural areas, so it is
perhaps something about city life which leads to schizophrenia. In fact, schizophrenia tends to be almost exclusively
found in cities, but there are many lower class people in rural places – so the social drift hypothesis doesn’t seem to fit
here. Harrison et al. (2001) suggests being brought up in declining inner-city areas could lead to schizophrenia, as this is
where the bulk of sufferers lie.

Hjem et al. (2004) showed that social adversity (adverse being the opposite of favourable) in childhood has a correlation
link with schizophrenia. The areas identified by Harrison et al. as where clusters of schizophrenics live support Hjem’s
ideas, as the inner-city areas tend to be where the population groups of the lowest socioeconomic class are. It is
therefore suggested that city life must have something which leads to development of schizophrenia. The sociogenic
hypothesis (contrasting the social selection theory) suggests that it is stress factors which contribute to the disorder
developing. These include the stress from poor education, unemployment, low rewards, low income and few
opportunities, which have been suggested can lead to the disorder.

Below is an evaluation of the environmental breeder hypothesis, suggesting social class is linked to schizophrenia:
 The ideas support the facts that there are more
schizophrenics in inner-city areas and in lower classes,
and both the social drift and social adversity ideas
explain a possible link between the disorder and class
 Although not everyone who lives in environmental
conditions suggested by these explanations develops
schizophrenia, it is still highly likely that there are these
environmental triggers (rather than strict causes), it is
possible that there is a biological explanation also,
which requires some environmental activation for the
disorder to develop
 Since those in a lower socioeconomic group, with no
jobs and living alone are more likely to be diagnosed, it
suggests maybe a diagnosis problem, not an
environmental problem
 It is hard to separate those factors which might be
causing schizophrenia with those that are being caused
by schizophrenia, it may be that lower social class,
economic status and the lack of a job are all
consequences of the disorder, not the other way
around, as the social drift hypothesis suggests

Drug therapy: a biological treatment

Whilst there is no cure for schizophrenia, it is considered to be a highly treatable disorder. One treatment comes from the
biological approach: drug therapy. Drug treatment, according to the NAMH of the USA, for schizophrenia is comparable
to the success rate for drug treatment of heart disease. Drug therapy was an important step forward in the 1950s,
allowing the movement of sufferers out of mental institutions by helping them to function normally.

One of the biological explanations for schizophrenia suggests that the symptoms, such as hallucinations and delusions,
are due to excess levels of dopamine receptors, leading to increased dopamine activity in the brain. Therefore, it only
makes sense that drug treatment uses drugs which act to reduce dopamine action by blocking its receptors. For example,
drugs such as phenothiazines can be used (e.g. chlorpromazine) which removes excess dopamine by blocking its
receptors. This came about from French neurosurgeon Henri Laborit, who tried using anti-histamines to relax his patients
before surgery, and when he saw the calming effects chlorpromazine had on his patients, he thought they might be useful
in calming schizophrenic patients too. The results was spectacularly successful, and later it was discovered that the reason
for this was that chlorpromazine blocked dopamine receptors.

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Drugs which are used to treat schizophrenia are called antipsychotic drugs. They work to suppress hallucinations and
delusions, by correcting these chemical imbalances in the brain. Antipsychotic drugs are separated into two categories:
typical drugs (which are older, and already well-established – these have been in use for a long time) and atypical drugs
(which are much more modern and in less use, although they are more experimental they do have fewer side effects, but
act differently to typical antipsychotics).

Common side effects of antipsychotic drugs include sleepiness and tiredness, shaking and muscle spasms, low blood
pressure, problems with sex drive and weight gain. Other symptoms include dry mouth, constipation and blurred vision. A
particularly nasty side effect, Tardive Dyskinesia affects older patients on the chemotherapy for schizophrenia, which
causes involuntary spasms of the face and other areas of the body. These side effects are seen as a weakness.
Meltzer et al. (2004)
In 2004, Meltzer et al. conducted a study into the effectiveness of drug treatment for schizophrenia. He used 481 patients
randomly assigned into groups, where some were given a placebo, some given a new investigative drug, and others an
already established antipsychotic drug (haloperidol). They found that haloperidol and two of the new investigative drugs
were effective at reducing the schizophrenics’ symptoms, more so than the placebo. This was seen as strong evidence
that drug treatment works, at least to an extent.

 Drug therapy for schizophrenia is seen as much more
ethical, and certainly more effective, than some of the
pre-1950s treatments that there were, including
lobotomies which would not be allowed nowadays
 The treatment is supported by strong evidence (such as
Meltzer et al. 2004) and is based on a scientifically-
sound explanation of the disorder
 Drug treatment is a fairly easy and quick treatment, the
drugs are easily prescribed and all patients have access
to it, and it is also far cheaper than a person-based
therapy, such as psychodynamic therapy, and so is the
NHS therapy of choice for schizophrenia
 The drugs have many possible side effects which can be
a problem, including damaging effects on the central
nervous system and synaptic junctions becoming
blocked, which are serious issues
 It is often criticised for only masking the problem, as
drug therapy is by no means a cure for the illness, it is
just alleviating the symptoms, possibly for the doctors’
convenience more than anything else?
 Patients often forget or purposefully stop taking their
medication (if the latter, probably because they are
worried about the side effects), possibly due to their
disorder leading to problems with functioning

Cognitive-behavioural therapy: a cognitive treatment

This is currently the most popular form of psychological therapy for schizophrenia (drug treatment is chemotherapy, not
psychotherapy, but drug treatment is the most commonly used), and it comes from the cognitive approach. It provides
coping mechanisms, as it does not directly alleviate the symptoms of the disorder themselves. Cognitive-behavioural
therapy (CBT) involves accepting the patient’s view of reality, and using that to help them learn to cope.

A full course of cognitive-behavioural therapy lasts over a series of regular sessions, around 50 minutes to an hour in
length each, with between five and twenty weeks’ worth of sessions (usually at one per week). Progress will normally be
assessed at this stage of twenty weeks to see if further treatment is needed. An agreed agenda is established with the
patient and the therapist tries to uncover their core beliefs (this is very much a person-centred therapy). This means not
telling the patient their beliefs are ‘wrong’, but suggesting alternative thought patterns. The therapy may help the patient
to normalise their experience of the disorder, allowing them to understand that it’s not just them, and that others have
hallucinations and delusions too.

The eventual aim is to improve the self-esteem of the patient and to develop their self-concept (getting them to see
beyond their disorder, and see their positive features to focus on – for example a particular area they are interested in or
talented in, which they can build upon).
Bradshaw (1998)
An example of cognitive-behavioural therapy for schizophrenia in use comes from Bradshaw (1998). The aim was to look
at how the therapy was used to treat a woman with schizophrenia (this was a case study), including its effectiveness. Until
the time of the patient’s therapy, drug therapy had been the preferred treatment – there was little done of this therapy.

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The patient was Carol, who was educated up until her first year of college. She had a perfectly normal life and seemed
otherwise healthy, when during her first year at college she had auditory hallucinations and delusions and felt she was
“no good”. She began acting in a bizarre manner, and was subsequently hospitalised. There had been no family history of
psychiatric illness, and Carol was diagnosed with undifferentiated schizophrenia.

The therapy began and it took about three months for a rapport to be built up. Self-disclosure was used to promote
discussion of difficulties and to help build the rapport. Carol controlled a lot of the treatment: how often they met, how
long the sessions were and roughly what they spoke about – a common feature of CBT. A further two months were used
to get Carol to understand the therapy. The course of the therapy was as follows:
 the first phase lasted a year and focused on managing stress and anxiety
 behavioural activities were worked out during the second phase with further stress control training, with another
sixteen months of building cognitive strategies to cope with stressful situations
 finally, an ending phase of around three months where thoughts about the end of the treatment were focused on and
plans to maintain the treatment without the therapist’s input were developed (e.g. strategies written on cue cards)

It was shown that there was an improvement of psychosocial functioning after the treatment, as well as improvements in
achievement of goals, and a reduction in symptoms and far fewer hospitalisations. Further analyses one year on showed
more improvement as Carol’s social functioning improved yet again. There were considerable improvements in
functioning in four measures after the three year course of therapy. It was therefore concluded that cognitive-
behavioural therapy can be useful in the treatment of schizophrenia.

Below is an evaluation for cognitive-behavioural therapy as a treatment for schizophrenia:

 There is a wide range of evidence to support the
therapy for the disorder, such as Pfammater (2006) who
did a meta-analysis finding CBT often reduced positive
symptoms; Gould et al. (2004) who found a large
reduction in symptoms and fewer dropout rates of drug
treatment when patients also had CBT; and a study by
NICE (2004) who, backed by government funding,
studied courses of CBT finding a reduction overall in
positive symptoms and negative symptoms, and
concluded it should be made available publically for all
schizophrenic sufferers
 The therapy uses cognitive shaping to develop
strategies for stress management which has been
shown to be effective in improving the daily lives of
schizophrenics as they have new coping mechanisms
 Turkington et al. (2002) found that CBT was effective in
increasing patients’ insights and awareness of the
importance of taking medication, but with insights into
themselves, their rates of depression increased,
suggesting a link between CBT and depression
 CBT seems to be mainly effective when used alongside
drug treatment, as it does not directly tackle to
symptoms of the disorder, so drug treatment is usually
required as well as a psychotherapy such as CBT
 Certain studies have actually shown other person-
centred therapies to be more successful than CBT,
although the government uses CBT as its therapy of
choice for patients, presumably because it is cheaper
and has been in use longer, although this may not be
the best for patients

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D
Unipolar depression
3.6 Symptoms and features, two explanations and two treatments of unipolar depression

Symptoms and features of unipolar depression

Also known as clinical depression, or major depressive disorder, unipolar depression is a mood disorder, characterised by
varying degrees of sadness, disappointment, loneliness, hopelessness and guilt. It is a relatively common mental health
disorder, with an estimated 3.5 million sufferers in the UK.

Unipolar disorder should be distinguished from bipolar disorder. Whereas unipolar depression is a mood disorder which is
seen as a constant disturbance to mood, bipolar disorder involves fluctuations between moods of manic depression and
mania, which is not the case with unipolar depression.

Other than the depressive emotions listed above, common symptoms of unipolar depression are lethargy (lack of will or
energy), permanent anxiety issues and problems with sleep (including waking early or continually through the night and
difficulty getting to sleep). Some of the features of unipolar depression are listed below:
 Depression is twice as common in women as in men, although men are more likely to commit suicide
 Different people have different courses of the disorder, some are only affected once, for others it is chronic
 The peak time for depression is between the ages of 50 and 60, although it typically occurs between 30 and 40
 People who suffer any form of depression usually live shorter lives, possibly due to a link between depression and
heart disease and other stress-related illnesses
 There are as many as 3.5 million UK sufferers and 20 million American sufferers of unipolar depression

One specific subtype of unipolar depression is postpartum depression, for which there is
usually no obvious reason. This is a temporary form of unipolar depression which occurs,
almost exclusively in women, but also sometimes in men, where distressed mothers
suffer severe mood disorders. This is especially distressing for the mother when they have
looked forward to having the baby for months.

Feelings include guilt, and feeling unable to cope and as though you are a bad parent.
Some women can go weeks or months without seeking treatment, and in some cases,
even years! It is a very common disorder affecting as many as 1 in 10 new mothers.

The monoamine hypothesis: a biological explanation

One biological explanation for unipolar depression is the monoamine hypothesis. The monoamines are a group of
neurotransmitters which include serotonin, noradrenaline and dopamine. You will recognise the latter, dopamine, from
the biological offering of an explanation for schizophrenia. The monoamines are believed to regulate mood.

One of the functions of serotonin is to regulate the other neurotransmitters. Without the regulation provided by
serotonin, erratic brain functioning and thinking patterns occur. Low levels of serotonin produces low levels of
noradrenaline (a neurotransmitter needed for alertness, energy, anxiety and attention to life). Evidence suggests that low
levels of noradrenaline cause depression, and high levels cause mania, which suggests it is involved both in unipolar and
bipolar depression. Dopamine is also related to feelings of alertness, motivation and attention, and so it is suggested low
levels of dopamine similarly are linked to depression.

Essentially the monoamine hypothesis suggests that low levels of dopamine and low levels of noradrenaline result in
depressive moods, and low levels of serotonin mean low levels of noradrenaline. It can therefore be low levels of
dopamine or noradrenaline that result in depression, or a mixture of both. The hypothesis is used to work with drug
treatment, so that the correct drugs (antidepressants) can be prescribed based on the particular monoamine in question.
In other words, when a clinician is presented with a patient, they will choose the correct drug that alleviates the
presented symptoms of depression. Most antidepressants work by increasing levels of serotonin.

It cannot be concluded that the explanation for depression is strictly biological. The diathesis-stress model explains how
some mental disorders can have a biological underlying cause but require an environmental trigger to become active.

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Studies have indicated that there may be a genetic link for depression. Although ‘the role of genes in depression’ is an
alternative biological explanation, they share some similarities, and the genetic explanation also offers a diathesis-stress
model. McGuffin (1996) studied 214 pairs of twins, where at least one of each twin pair was being treated for unipolar
depression. It was found that 46% of the identical twins shared the disorder, and only 20% of fraternal non-identical twins
shared the disorder. This indicates a genetic link. Whilst genetic makeup may predispose somebody to develop
depression, a stressful life event might be needed to act as a trigger for that depression (diathesis-stress).

An evaluation for the monoamine hypothesis for depression is shown below:

 There is much sound evidence to support the theory,
particularly in treatment – if the hypothesis suggests
the symptoms are due to monoamine deficiencies and
drugs which replace those monoamines alleviate the
symptoms, there is evidence for the hypothesis
 Further evidence is seen from studies involving
monoamine oxidase inhibitor enzymes, which prevent
the inhibition of monoamines, so they can function
properly – which alleviates depression
 However, it could be argued that some drugs such as
opipramol help relieve depression yet do not adjust
monoamine imbalances, reducing the validity of the
explanation
 Furthermore, in some studies, levels of monoamines
have been deliberately depleted, which does not seem
to reproduce the symptoms of depression
 Much of the research comes from animal studies, and
we must take care when generalising from such data

Beck’s model of depression: a cognitive explanation

A different explanation for unipolar depression comes from the cognitive approach, from Aaron Beck, who is considered
the father of cognitive therapy. There are three aspects to Beck’s cognitive model of depression:
 the cognitive triad – three areas Beck considered suffered negative automatic thoughts
 the individual’s cognitive errors – faulty thought patterns and negative or unrealistic tasks
 the schemata – patterns of maladaptive thoughts and beliefs
The cognitive triad
Negative view
of the self The first part of Beck’s cognitive model of depression is the cognitive triad.
This suggests three areas where there are negative automatic thoughts.
The thoughts consist of negative views of the self (feeling inadequate and
unworthy), negative views of the world (feeling defeated or deprived) and
negative views of the future (believing that your suffering will continue). A
Negative view Negative view
sufferer of depression tends to think life will always be that way for them,
of the world of the future
and that nothing can improve: this comes from the ‘future’ aspect.
The cognitive errors
Cognitive errors mean that an individual gives selective attention to the negative side of a situation, and always ignore the
positive aspects. Beck described this as the faulty thought patterns. The ‘downside’ is overestimated so that the most
negative conclusion possible is reached when in a situation.
Schemata
Schemata are built up through experiences of the world, and involve developing positive and negative beliefs and
attitudes to interpret the world. A generalised negative belief pattern makes someone vulnerable to depression. A new
situation is interpreted through the use of a person’s relevant existing schemata, including a self-schemata (for example,
if someone is regularly criticised by their parents, they are going to develop a negative set of beliefs about themselves).

The way to overcome depression according to the cognitive model by Beck is to change the maladaptive thought
interpretations by considering alternative thoughts and interpretations of events. If evidence is presented that there are
other interpretations, an individual can change their cognitions. The likely schemata of a depressed person include:
 cognitive schemata – lead a person to seeing actual or threatened loss
 affective schemata – lead a person to feelings of sadness, loneliness and guilt
 physiological schemata – (biological schemata) lead to feelings of tiredness, lack of energy and activity
 motivational schemata – lead to helplessness and a lack of direction
 behavioural schemata – lead to social withdrawal and inactivity

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The cognitive model is shown in the flow diagram to the right.
There is some evidence which supports the cognitive model of Early experiences and
depression. interactions with the real world

Koster et al. (2005) examined the role of attention to negative

stimuli in depression. There were 15 depressed students and 15 Core beliefs
non-depressed students in the participant sample, and they were
each given a selective attention test on a computer screen, where
they were presented with positive (e.g. powerful, successful), Rules and assumptions (if… then…)
negative (e.g. loser, failure) and neutral (e.g. paper) words for one
and a half seconds each. Half a second after the word
Trigger
disappeared, a square would appear onscreen on either the left-
hand or right-hand side, and participants had to press q when it
appeared on the left, and p when on the right. Thoughts
The time for them to react and press the right key was
measured, and it was found that depressed people
Consequences Feelings
took an average of 12ms to disengage from negative
words, compared to non-depressed students who only
took 2ms. This supports Beck’s cognitive model as it Behaviour
shows depressed people respond to negative stimuli.

Strengths of Beck’s cognitive explanation of depression:

 Research has shown that depressed people have negative thoughts and that the cognitive model is backed up both by
self-report data and other test measures. The model is evidence-based, with many studies supporting Beck’s ideas,
including Ingram (2001) who found that those with adverse childhood experiences had depression later in life, as the
model suggests
 The theory takes into account other aspects, such as genes, development and early experiences and acknowledges
that such developmental issues can lead to certain thinking patterns and core beliefs which lead to depression
 After treatment for depression, patients biased negative thought patterns seem to disappear, which seems to be
evidence for the cognitive model for depression

Weaknesses of Beck’s cognitive explanation of depression:

 Strict evidence that shows negative thinking precisely causes depression is hard to find – whilst you could argue that
since faulty thinking stops when depression disappears this must be in favour of the model, it might also be seen that
perhaps faulty thinking and negative beliefs come with depression, rather than are the cause of depression
 It is difficult from a methodological point of view to distinguish between thinking which causes depression and
thinking that is caused by depression, so objective measure is difficult
 Some studies, such as Dykman et al. (1991) have not shown the cognitive biases Beck suggests, observing that
depressed people do not seem to have a distorted perception of their own abilities, and whilst perhaps still focusing
on the negative parts of events, they do in fact understand the events accurately, against what the model suggests

Drug therapy: a biological treatment

Just as with schizophrenia, depression is treatable with the use of drug treatment, from the biological approach. Drug
treatment for depression tends to happen in the community: rarely are depressed people hospitalised, unless they are at
risk of endangering themselves or others. Antidepressants are used to treat depression, and these drugs usually work by
increasing the levels of serotonin in the brain, since some of the symptoms of depression come about due to low levels of
serotonin (leading to low levels of noradrenaline). This is how the well-known drug Prozac works, although this is not to
say this is strict proof that the monoamine hypothesis is correct, it does provide some sound evidence.

Such drugs used to treat depression are called SSRIs (selective serotonin reuptake inhibitors). The SSRIs include drugs like
Prozac, and others such as Fluvoxamine and Citalopram, as well as some more modern and less-in-use atypical
antidepressants (drugs which target individual monoamines, such as specifically noradrenaline).

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Another group of drug used to treat depression is the MAOIs (monoamine oxidase inhibitors), which work to prevent the
breakdown of the monoamines (serotonin, noradrenaline and dopamine), so in effect achieving the same results:
increased levels of the monoamines in the brain.

As you would expect, no drug treatment comes without its potential side effects. Side effects of the SSRIs include nausea,
insomnia, anxiety, dizziness, weight fluctuations, headaches, fatigue and blurred vision, and the MAOIs have more severe
side effects and so are only used as a last resort if other drugs don’t work; similarly, another group of drugs, the tricyclic
antidepressants, are a subtype of SSRIs which are nowadays outdated, and also have more severe side effects.

Treatment of depression with antidepressants has to be withdrawn

gradually in order to avoid suffering withdrawal symptoms, which
develop with what is known as ‘antidepressant discontinuation syndrome’
and involve crying spells, insomnia, aches and pains and muscle spasms.
Kuyken et al. (2008)
In this study, Kuyken et al. compared drug treatment and a form of
cognitive-behavioural therapy, finding that a group version of CBT was at
least as successful as drug therapy. They divided 123 people with
depression into two groups: one continued with their medication, and the
other had the psychotherapy (with the option to remain on or come off of
their drug treatment). Over 8 weeks, the therapy group met and carried out group exercises, such as how to focus on the
present and not the past. About 47% of the CBT participants had a relapse rate over the 15 months after the course had
ended, whilst those who had drug therapy alone had a relapse rate of 60% and so it was thought that the person-centred
therapy gave the patients skills for life that drug therapy could not. This study showed that whilst drug treatment for
depression can be effective, it is not as effective as it could be without having another type of therapy used as well.

 Antidepressants can be used to boost mood so that
other therapies, such as CBT, can take place: without
drug therapy these other treatments cannot happen
 Research is constantly undergoing to find more
effective drugs with bigger success rates and fewer side
effects (atypical antidepressants, for example, have far
fewer side effects than the old tricyclic drugs)
 Drugs are easy, quick and cheap to prescribe and are
the favoured treatment for the NHS
 The use of antidepressants is based on a scientific
hypothesis, generally accepted by psychiatrists
 Although drugs are cheap and quick to prescribe and
are readily available, it may be the case sometimes that
doctors prescribe them over other treatments for their
own convenience, rather than the good of the patient
 Drugs are often criticised for only masking the problem,
they do not cure the disorder
 A common effect of discontinuation of drugs, especially
with antidepressants, is withdrawal symptoms, which
can prove troublesome and may need more drugs to
treat the withdrawal symptoms, which is not ideal
 Patients may forget to take their drugs or purposefully
choose not to take them to avoid the side effects

Cognitive-behavioural therapy: a cognitive treatment

A therapy from the cognitive approach, actually based around the work of Beck, cognitive-behavioural therapy (CBT) –
which you may have met from schizophrenia also – is a person-centred form of psychotherapy used to work with the
patient to try and overcome the symptoms of depression, rather than (or as well as) using chemotherapy.

Usually it takes place once a week and consists of at least five-to-twenty sessions, progress is reviewed at around 20
sessions. The therapy works to try and help the patient identify negative and unhelpful thoughts and to try and change
them. This may involve drawing diagrams for the patients to try and show them the links between their thinking,
behaviour and emotions. The rationale of CBT is that our thoughts affect our feelings and behaviour, and so by changing
our thoughts, we can make ourselves feel better. Some forms of CBT also focus directly on changing behaviour.

The therapy is collaborative, the therapist and the patient will agree on what the patient wants to change. The therapist
may then ask the patient to express their negative belief, for example, in relation to their social life. A depressed patient
might believe that there is no point in going out as they won’t enjoy it: the therapist will try and respond by convincing
them that they should try it and will in fact enjoy going out.

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Stiles et al. (2006)
This study looked at cognitive-behavioural therapy and other therapies (one person-centred therapy and psychodynamic
therapy) over a three-year period, in 58 NHS settings around the UK. They found that no therapy stood out as being more
successful than any of the others, but they were all very effective: there were reductions in relapse rates and
improvements according to self-report data. Whilst this study did not show CBT to be any more effective than other
psychotherapies, it did prove the therapy to be effective at treating depression.

Below is an evaluation for the use of cognitive-behavioural therapy for treating unipolar depression:
 The individual is helped to recognise any problems and
taught how to overcome difficulties, so solutions will be
more lasting than therapies outside the patient’s
control, such as token economy programmes
 Cognitive restructuring has been used successfully, for
example in stress management – by having a sense of
control and coping mechanisms, a person is better able
to deal with stressful situations in real life
 Studies such as Seligman et al. (1998) and Kuyken et al.
(2008) have shown CBT to be particularly effective,
especially when used alongside drug treatment
 The therapy relies on the assumption that the
individual can change their own thought patterns and
control their beliefs, so this isn’t a treatment which
everyone will get results from
 Whilst most studies support CBT as a treatment for
depression, many studies have suggested a mix of
therapies is more effective
 A weakness of Beck’s cognitive model is that it may be
depression which causes negative thoughts, not the
other way around – and if this is the case, the therapy
(based on the rationale changing thoughts changes
behaviour) is not going to be effective

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D
Treatments and therapies
3.7 How to describe and evaluate one treatment from each of the five AS approaches
This unit requires that you know one treatment or therapy for each one of the five AS approaches. For both schizophrenia
and depression, drug treatment (from the biological approach) and cognitive-behavioural therapy (from the cognitive
approach) were used. This means you still need to know one treatment from the social approach, psychodynamic
approach and learning approach. Although there are alternatives available, this document will discuss care in the
community programmes (social), dream analysis (psychodynamic) and systematic desensitisation (learning), and will also
cover drug therapy and CBT for comparison.

The social approach: care in the community programmes

This type of treatment arose during the social psychiatry movement, fronted by psychiatrist R. D. Laing who refuted the
medical model of mental disorders, suggesting symptoms were treated first, patients second. He advocated a more
humane method of treating those diagnosed with mental disorders, which treated them supposedly more so like human
beings, much to the disdain of the medical community.

Care in the community programmes (a treatment from the social approach)

Care in the community programmes bear in mind that a mental disorder is not just biological,
Rationale behind
there are social aspects to the disorder too – and the explanation works around the idea that
the treatment
there are environmental and social triggers and not just biological causes to mental illness
Nowadays when these programmes are used, the NHS aims to provide a ‘spectrum of care’:
 sheltered accommodation with 24-hour care for those who cannot live by themselves
 employment opportunities in sheltered social firms and cooperative businesses
Process of the
 specialist mental health outreach teams to provide long-term care and support
treatment
 in-patient hospital care if the patient’s condition worsens (those who do not need
hospitalisation are administered to psychiatric wards, but the aim of the programme is to get
the patients back out into the community as soon as possible)
Programmes are aimed at a wide variety of mental disorders, including depression and
Disorders treated
schizophrenia, most people are eligible so long as they do not need institutionalisation
 By shutting down the old, large institutions to allow for community care, funds will be
released which can be used to improve in-patient care and to fund the programme
 Research has shown that care in the community programmes can work, and have undoubted
potential, but only when they are properly funded
Strengths
 Care in the community programmes come from the social psychiatry movement and are a
much more person-centred treatment – they consider that patients are human beings and
treat them accordingly, which is advantageous over other treatments, such as drug therapy,
which can be just for the doctor’s convenience of reducing the symptoms of an individual

 Whilst regarded a much more ethical and person-friendly treatment, the monetary and time
investment required for care in the community programmes is significant, and the NHS finds it
Weaknesses difficult to sustain such programmes, especially given current budget cuts
 Care in the community programmes tend to be unsuccessful unless they are properly funded
and the carers are expertly trained individuals – it is difficult to provide out-patient care

 Leff (1997) showed that patients suffering from schizophrenia cared for in the community in
long-term sheltered accommodation showed much lower symptom severity than hospitalised
patients, especially for negative symptoms
 however, Leshner (1992) found that often communication was poor between different
Evidence and
agencies, with no overall strategy for coordinating patient care
studies
 and Shepherd (1998) saw that most care in the community programmes in this country are
severely under-funded – although Margaret Thatcher’s closure of the large psychiatric
hospitals saved £2,000m for her deinstitutionalisation scheme, none of this money was
reinvested in community care

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The cognitive approach: cognitive-behavioural therapy
Cognitive-behavioural therapy stemmed from the ideas of psychologist Beck, who put forward his cognitive model for
depression, and it remains one of the most popular forms of psychotherapy as a treatment for disorders today. It can be
used for a variety of disorders, and is often praised as it works with the patient, allowing them to move at their own pace.

Cognitive-behavioural therapy (a treatment from the cognitive approach)

This treatment is based around the idea that people develop maladaptive thoughts, emotions and
Rationale behind
behaviours, and suggests that by training the individual to change those maladaptive thoughts,
the treatment
their negative feelings, emotions and in turn, behaviours, too, will be changed respectively
 agree the agenda – agree with the client what the aims and the agenda are
 build a rapport – CBT cannot work if the client and therapist do not build a rapport, and this
part alone can take a few months before any real work can begin
Process of the
 assess core beliefs – discover the patient’s core beliefs, and rather than telling them “they’re
treatment
wrong” and “this is what you should think”, suggest alternative thinking patterns
 self-esteem – as the patient is trained to rethink differently, build their self-esteem: their view
of themselves and their view of the world around them
CBT can be used to treat a variety of disorders, it is most commonly used for treating non-severe
Disorders treated unipolar depression, but can be used to treat bipolar depression, some other anxiety disorders
and certain mental health disorders, including schizophrenia
 Unlike drug therapy, CBT does not just mask the symptoms, it attempts to address the cause
of the problem and treat accordingly, also possibly looking at the environmental and social
causes (which not all therapies do)
Strengths  There is a strong evidence base for CBT, including for schizophrenia and unipolar depression
as you will have seen
 The therapy is funded healthily by the government and is the NHS’ preferred choice of
psychotherapy, it is seen as successful and relatively cheap, and made available to many

 When used as a treatment for depression, increasing the patient’s insights into their disorder
can actually make them more depressed
Weaknesses  It is difficult to distinguish between what is causing the depression and what the depression is
causing, which makes treatment difficult
 The therapy can not usually be used without drug treatment as well (e.g. schizophrenia)

 Pfammater (2006) conducted a meta-analysis and found CBT to be effective in reducing the
positive symptoms of schizophrenia
 also, case studies such as Bradshaw (1998) have shown CBT to be successful
Evidence and
 although Turkington et al. (2002) suggested the link between CBT and depression, as the
studies
therapy course made patients more aware of their disorder and importance of medication
 and whilst Stiles et al. (2006) showed the treatment to be successful, it was not found to be
any more successful than other therapies, so perhaps a cheaper therapy should be used

The psychodynamic approach: dream analysis

Freud is considered the father of the psychodynamic approach, and one of the founders of psychoanalysis, another type
of psychotherapy still in use today, although the treatment has changed radically since its introduction to society. The
rationale, theory and method behind psychoanalysis remains questionable still, and dream analysis (one of Freud’s
original therapies which spawned from psychoanalysis) is one of those controversial treatments: both its success and
rationale are considered debatable.

Dream analysis (a treatment from the psychodynamic approach)

Freud’s personality theory suggests that our actions are governed by the thoughts of our
Rationale behind
unconscious, which are not normally accessible, but dream analysis aims to uncover the
the treatment
unconscious wishes by analysing the content of our dreams

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 The therapy involves frequent visits to a psychoanalyst, which can be expensive as lasts usually a
number of years. Traditionally, the psychoanalyst sits behind the analysand to allow them to fully
concentrate, and so that the focus is on them. The material for discussion is the consciously-
Process of the remembered dream: the manifest content is the actual content of the dream produced, which is
treatment analysed to discover the latent content (the underlying meaning of the dream). Patient’s defence
mechanisms are confronted, and transference (when the analysand transfers feelings onto the
analyst, such as love or hate – to be expected as part of the release of the unconscious wishes and
fears) is dealt with

Disorders treated Dream analysis can be used to treat non-severe depression and some anxiety disorders

 Dream analysis seems to be an effective way of uncovering unconscious thoughts, and

although the theory cannot be objectively tested, Freud questioned whether a strictly
scientific approach should be used to try and understand human individuals anyway
Strengths
 Freud’s work on dream analysis (and other psychoanalytical therapies) has led to the
development and use of other therapies, such as cognitive-behavioural therapy, humanistic-
centred therapy and conflict resolution

 Freud’s work is based on case studies of unique individuals such as Little Hans and himself, so
it is not necessarily a generalisable theory
 Research has shown dream analysis is not a hugely successful treatment
Weaknesses  Ethical issues may be raised regarding dream analysis
 It is frequently suggested that the therapy is highly subjective, and the success of the
treatment is questioned, seeing as if the same patient were to visit two different psycho-
analysts they would receive entirely different interpretations

 Shapiro (1991) suggests that psychodynamic therapies are only occasionally successful for
depression, possible as depressed people are not motivated enough to participate in this slow
process involving a great deal of concentration and personal-analysis
Evidence and
 Storr (1987) also criticised the psychoanalysts as they use much subjectivity: the therapy relies
studies
heavily on personal interpretation and so cannot be described as scientific
 famously, Masson (1989) argued against psychodynamic therapies, claiming psychoanalysts
have too much power over their analysand clients (e.g. case study of Beth Rutherford)

The biological approach: drug therapy

Biological psychology is a very much scientific approach to psychology: it considers the biological root causes of problems,
such as those to do with gender development and mental disorders. Drug therapies come about from scientific research
into biological causes for medical disorders: the drugs prescribed try and reverse the suggested issues.

Drug therapy (a treatment from the biological approach)

Rationale behind The rationale behind drug therapy is that disorders have biological causes, and a
the treatment chemotherapeutic approach is able to correct the biochemical problem, alleviating symptoms

The process is operationalised and always follows the same staged routine:
1 – diagnosis: the disorder in question is identified and its cause discovered
Process of the
2 – prescription: decide on the drugs to use (for example, to correct the chemical imbalance)
treatment
3 – course: let the patient take the prescribed drugs over a period of time
4 – amend dosage: over time the drug will be removed (phased out to reduce withdrawal)

Any disorder which has a biochemical cause which is reversible or treatable with the use of drugs,
Disorders treated
for example, due to a chemical imbalance or improper functioning of a neurotransmitter

 Very scientific approach, based on a biological explanation and evidence

 Biological treatment is constantly undergoing further research to discover more effective
Strengths drugs, with higher treatment rates and fewer side effects, which is an advantage
 Patients who are on drug therapy are able to participate in other, more personal, therapies,
such as cognitive-behavioural therapy, which certain patients would not otherwise be able to

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  Patients may forget to take their drugs, or choose not to so they can avoid the side effects
 People can become drug-dependent, or suffer withdrawal symptoms when drugs are stopped
Weaknesses
 The therapy is often criticised for not addressing the root cause and curing the disorder, it
simply corrects chemical imbalances to remove the symptoms of the disorder

 Meltzer et al. (2004) gave schizophrenic patients either haloperidol (an established anti-
psychotic), one of three new investigative atypical drugs, or a placebo, and found that two of
the new drugs and haloperidol were successful in reducing symptoms, the placebo was not
Evidence and
 however, Kane et al. (1988) found that between 10% and 20% of patients on chemotherapy
studies
for schizophrenia do not improve
 Kuyken et al. (2008) saw that whilst drugs do improve patients generally, they are less
effective than when they are used as well as a person-centred therapy, such as CBT

The learning approach: systematic desensitisation

The learning approach uses the principles of classical conditioning, operant conditioning and social learning theory to
address treatment. One is systematic desensitisation, which is based on the principles of classical conditioning, and can be
used to help individuals overcome fears in a way which is seen as more ethical than others, such as flooding.

Systematic desensitisation (a treatment from the learning approach)

Rationale behind The treatment is based on the “principle of incompatible responses” using the principles of
the treatment classical conditioning: it suggests one response can be replaced with another after treatment

 functional analysis: the therapist decides on the triggers and the strength of the phobia
 anxiety hierarchy: a series of ‘steps’ is decided, from the least-to-most stressful, based on a
Process of the hierarchy of fears, which the patient can work their way up as the therapy progresses
treatment  relaxation training: choosing methods of relaxation whilst coping (e.g. listening to music,
meditation, hypnosis, and sometimes – but less often – drugs, such as valium)
 graduated exposure: slowly introduce the phobia and work your way up the hierarchy

Disorders treated Effective for phobias and some anxiety disorders, but not used at all for other mental disorders

 It has been shown as very effective for treating phobias such as those of a particular species,
such as spiders
 The therapy is ethical as the individual is involved throughout, as they devise the hierarchy
Strengths and learn to relax in their own way
 As the goals are clearly specified, the therapeutic outcomes are easy to measure: this means
that data on the effectiveness of the treatment is easily compiled, providing scientific measure
for the therapy
 To work, the individual has to be able to relax and get involved in the whole process, which is
more difficult for some than others
 Although it may be useful for treating phobias and anxiety disorders, it is not useful for a large
number of other clinical disorders, such as psychoses
Weaknesses
 The treatment only focuses on observable symptoms, rather than any underlying issues and as
such makes little or no attempt to address the root cause of the problem
 Classical conditioning principles come mainly from animal studies, so there may be problems
with generalisability to humans as a treatment

 McGrath et al. (1990) found that 75% of patients with specific phobias showed clinically
significant improvements with their phobias following treatment
 similarly, Brosnan and Thorpe (2006) used a ten week desensitisation programme to help 16
Evidence and students who were technophobic, on an ICT course, and compared to a control group, their
studies anxiety levels were considerably lower by the end of the course
 on the other hand, some studies have shown it to be less successful, one where between 60%
and 80% of patients showed slight improvement following treatment, but the difference was
minimal and many completely relapsed after six months – Craske and Barlow (1993)

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D
Rosenhan (1973)
3.8 Study in detail: Rosenhan’s 1973 study ‘On being sane in insane places’

Aims
David Rosenhan was interested in the difficulty of defining abnormality. The aim of his study was to illustrate
experimentally the problems involved in determining normality and abnormality, in particular, the poor reliability of the
diagnostic classification system for mental disorder at the time (as well as general doubts over its validity); and the
negative consequences of being diagnosed as ‘abnormal’ and the effects of institutionalisation.

Procedure
The sample involve eight pseudo-patients (three women and five men), who were clinically sane, but were sent by
Rosenhan to a mental health institution (twelve hospitals in total were used, Rosenhan wanted different settings to
generalise the findings) with fake names and occupations, reporting one symptom: they were hearing voices – each
patient would report hearing one word repeatedly, either “empty”, “hollow” or “thud”. Apart from this one pseudo-
symptom and the fake names and jobs, each pseudo-patient did not change the rest of their behaviour.

The pseudo-patients called the hospitals to arrange appointments, and arrived at the admissions offices saying that they
were hearing this voice. It was unclear and always of the same sex as the patient. One of the pseudo-patients was
Rosenhan himself (where his research was conducted, the hospital administrator and chief psychologist knew about his
research, but the other seven patients were secret).

After being admitted, the pseudo-patients stopped simulating any symptoms immediately, and responded normally to all
instructions – except they did not swallow the medications they were given. They all reported they were fine and told
staff their symptoms had gone. Their tasks then were to:
 seek release from the psychiatric hospital by convincing the members of staff that they were sane, and all but one of
the pseudo-patients were very motivated to do this
 observe and record the experience of the institutionalised mentally disordered patient – each was to record notes
about patient life and how they were treated, based on their experience, and at first they recorded their experiences
covertly (although this was not specified as necessary by Rosenhan)

Findings
Admission
All of the pseudo-patients except for one were admitted to the wards with a diagnosis of schizophrenia in remission, but
all eight were admitted with some diagnosis to every hospital. None of the staff were doubtful of the pseudo-patients, in
fact Rosenhan stated that once given the label of ‘schizophrenia’ it seemed very hard to shake. He noted that more of the
actual patients on the ward, 35 of the 118 from the first three hospitalisations, were suspicious of the pseudo-patients,
suggesting things like “You’re not crazy, you’re a journalist or a professor” (due to the note-taking).

It should be noted that the hospitals were considered good or excellent and were not to blame for the failure to recognise
the patients’ sanity, and also that prior to admission, the pseudo-patients were not carefully observed: so it was not full
observation of their behaviour which led to the label of ‘schizophrenia’.
Release
The length of stay ranged from 7 days to 52 days (with an average stay of 19 days). All except the one had the diagnosis of
schizophrenia in remission (meaning schizophrenia, but being able to be discharged, so non-severe), supporting the view
that they had never been detected as sane. There were no records of any suspicion among the staff members.
Observations of pseudo-patients
 lack of monitoring – there was very little contact with doctors, and a strong sense of segregation between the staff
and the patients was noted
 powerlessness and depersonalisation – the pseudo-patients noted that powerlessness and depersonalisation was
produced in the institution through the lack of rights, constructive activity and privacy, plus there were frequent
verbal and even physical abuse from the attendants

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 distortion of behaviour – all normal behaviour become interpreted in the light of the schizophrenic label the pseudo-
patients were given, for example:
a note-taking – pseudo-patients were never asked why they were taking notes, but it was recorded by nurses as
“patient engages in writing behaviour” implying that it was a symptom of their disorder
b pacing the corridors – this was done out of boredom, and was noted by the nurses as a sign of nervousness,
again implying that this was a symptom of their supposed disorder
c waiting outside the cafeteria before lunchtime – this was interpreted as showing the “oral-acquisitive nature of
the syndrome” by a psychiatrist, rather than just waiting outside in preparation for lunch
 lack of normal interaction – for example, pseudo-patients courteously asked a staff member “Pardon me, doctor,
could you tell me when I will be presented at the staff meeting?” or “When am I likely to be discharged?” and they
found mostly a brief and not always relevant answer was given, on the move, without even a normal turn of the head
or any eye contact (psychiatrists were recorded as stopping to answer the questions a mere 4% of the time)

Follow-up
After Rosenhan published the results of his study, ‘On being sane in insane places’, to check the poor reliability of
diagnosis, and to see if the insane could be distinguished from the sane, a later study was conducted where a teaching
hospital, who had been informed of Rosenhan’s initial studies, was told to expect at least one more pseudo-patient over a
three month period. During that time, the teaching hospital rated 193 incoming patients for how likely they were
suspected to be pseudo-patients, and in total 41 patients were suspected of being pseudo-patients (19 of whom had
been suspected as so by both a psychiatrist and another staff member). Rosenhan had in fact sent no more pseudo-
patients, and so the 41 patients identified by the teaching hospital as fake were in fact real (as far as Rosenhan knew).

Analysis
Rosenhan claims that the study demonstrates that psychiatrists cannot reliably tell the difference between people who
are sane and those who are insane. The main experiment illustrated a failure to detect sanity, and the follow-up study
(above) demonstrated a failure to detect insanity.

Rosenhan explains that psychiatric labels tend to stick in a way that medical labels do not, and that everything a patient
does once admitted is interpreted in accordance with the diagnostic label once it has been applied. He suggested that
instead of labelling a person as insane, we should focus on the individual’s specific problems and behaviours.

The study demonstrates both the limitations of diagnostic classification and importantly the appalling conditions in many
psychiatric hospitals. This has stimulated much further research and has led to many institutions improving their
philosophy of care. Rosenhan, like other anti-psychiatrists, is arguing that mental illness is a social phenomenon. It is
simply a consequence of labelling. This is a very persuasive argument, although many people who suffer from a mental
illness might disagree and say that mental illness is a very real problem.

Evaluation
Strengths
 The hospitals used were varied (new and old, private and public, and different locations) allowing for generalisation,
and since twelve hospitals were used this strengthens the findings further again allowing for generalisation
 There was validity to the study in that the pseudo-patients behaved as themselves except for the voices which were
only mentioned in the admissions stage: this validity could be seen in that other patients questioned their diagnosis
 Using eight people in twelve hospitals meant that the study was replicated and, as the same results were found, this
gives the study reliability

Weaknesses
 The study involved telling the staff that they were hearing voices, which was a classic symptom of schizophrenia, so
perhaps it was hardly surprising they were diagnosed accordingly, similarly it might not be surprising that the teaching
hospital identified some people they thought to be pseudo-patients: the validity is compromised
 Since the study was carried out 30 years ago, methods of care and diagnosis has improved, and there is more
emphasis on care in the community, and so it might be wrong to say that there is still a problem with diagnosis

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D
Goldstein (1988)
3.9 Study in detail: Schizophrenia in women and men, and the reliability of the DSM
Goldstein (1988) is a study which comprises a number of parts. Primarily, Goldstein was interested in comparing the
experiences of schizophrenia in men and women. However, her study also used two measures which looked at the
reliability of the DSM in diagnosing schizophrenia.

Procedure
This was a longitudinal study, the main part of which followed 90 patients who had been hospitalised, and were followed
for ten years. They were chosen based on being diagnosed with schizophrenia using DSM-II, being aged between 18 and
45 and having no other mental health issues (or general conditions such as drug or alcohol abuse). They had all been
hospitalised for less than six months before returning to their families.

Rediagnosis and testing reliability of the rediagnosis

Firstly, in order to test for reliability of the DSM, Goldstein re-diagnosed 199 patients who had been diagnosed with
schizophrenia using DSM-II. The criteria for the disorder from DSM-III were used, and it was found that 169 of the
patients were re-diagnosed with schizophrenia. Such a proportion of the 199 sample suggests that the DSM is a reliable
tool for diagnosis of schizophrenia. In order to test the reliability of Goldstein’s re-diagnoses, she used a small sample of
these patients and asked an independent expert to diagnose the patients again to see if the diagnoses matched (below)

One of the parts of the study involved choosing 8 of the participants at random to be re-diagnosed using DSM-III to test
for reliability. Four males and four females were chosen to be diagnosed by experts (including Goldstein). The experts
were given case studies, including the patients’ names, but no other details: it was a single-blind technique as only
Goldstein knew the hypothesis, the experts did not. There was a 0.80 agreement, and only one case where they disagreed
with Goldstein’s diagnosis (she diagnosed schizoaffective disorder and the experts diagnosed schizophrenia). Overall, it
was thought that the diagnoses were reliable, even though there was this one disagreement

Information about the patients in terms of symptoms, premorbid functioning (how the patients functioned before the
onset of the disorder), social functioning (how the patients function post-diagnosis) and the course of the illness:
 information about symptoms was gathered by trained interviewers using specially-developed questions, focusing on
hallucinations, formal thought disorders, paranoia, isolation, withdrawal and anxiety, as well as depression
 information about premorbid functioning was measured by a questionnaire dealing with isolation, peer relationships
and interests the patients had when younger, also taking into account marital status and employment
 information about social functioning was measured using details about the patients after they received their
diagnosis, including marital status and employment
 information about course of the illness was operationalised in two ways: counting the number of re-hospitalisations
experienced and the duration of stay in the hospitals, data for which was taken from hospital records both five years
after diagnosis and ten years after diagnosis

Findings Mean
Goldstein was interested to see if men experienced a more severe 0 to 5 years
course of schizophrenia than women, and this was measured by seeing if Male 1.40
they had longer stays when admitted to hospitals, and also more Female 0.59
Number of re-
frequent hospitalisations. It turned out men did. Women had a hospitalisations
significantly lower average number of admissions and lengths of stay 0 to 10 years
than men when comparing the two over a ten year period (as the results Male 2.24
Female 1.12
table shows). The findings were found to be statistically significant in all
cases. Further statistical testing was carried out to explain the gender
0 to 5 years
differences in the courses of the disorder. Researchers could use these Male 267
tests to look at other factors (including premorbid functioning, social Length of stay Female 130
functioning and the diagnosis) to see how they affected findings. in hospital
(days) 0 to 10 years
Male 418
Female 207
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It was found that 13% of gender effect on re-hospitalisations was due to premorbid functioning, but only 4.3% was down
to social functioning. It was also found that 11.3% of gender effect on length of stay was due to social functioning and
only 4.2% was due to premorbid functioning.

Goldstein therefore concluded that the number of re-hospitalisations was largely affected by premorbid functioning,
whereas the length of stay was affected more by social functioning.

Conclusions
Goldstein concluded that her study had reinforced what other studies had found, supporting her hypothesis that women
had a less severe experience with schizophrenia than men. This was backed up in her study by the fact that men had
more hospitalisations and longer stays on average.

She also found that the DSM-III was a reliable tool for diagnosis, but noted that there were some diagnostic differences
(169 of the 199 patients were re-diagnosed with the same disorder). She concluded that premorbid functioning and social
functioning are important factors in the development of schizophrenia.

Evaluation
Strengths
 The secondary data (based on number of re-hospitalisations and average length of stay) are quantifiable and so
scientific conclusions can be drawn (and are also both valid as they come from real hospital records, and objective
because they require no individual interpretation)
 Goldstein could show that her schizophrenia diagnoses were reliable, as they were supported by two experts who
found the same diagnoses as her (despite one small disagreement of the eight cases)
 By using interviews, she was able to gather rich and detailed qualitative data (as well as the quantitative data), so all
the information about premorbid history and social functioning – among other factors – was detailed to enhance the
conclusions and ensure validity

Weaknesses
 Of women who are diagnosed with schizophrenia in the country, only 9% are over the age of 45, and yet no women
aged 45 or above were included in the sample, which may have affected the results (and conclusions) because women
over 45 tend to experience a more severe course of the disorder than those under 45 (so the findings may not be as
valid as previously thought, as the statistics for men cannot be applied to women)
 Goldstein used mainly white, middle-class people from one area within the USA, and the sample size of 90 was fairly
small, so the findings may not be generalisable to all populations and all schizophrenics
 There may have been interviewer bias when Goldstein conducted the interviews

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Gottesman and Shields (1966)
3.10 Study in detail: To test if there is a genetic basis to schizophrenia

Aims
The main aim of this study was to see if whether schizophrenia had a genetic basis. Using a twin study methodology,
Gottesman and Shields planned to test different twin pairs to investigate the concordance rates of schizophrenia in twins.
They also wanted to replicate other studies that had indicated a genetic basis to the disorder, to find if their findings
would be similar (to test for reliability).

Procedure
Researchers looked at patient records from a short-stay psychiatric hospital with a large outpatients department. The
records covered a sixteen year history from 1948 to 1964. Over that time, 392 patients were seen who said that they had
a twin of the same sex, and of those 68 had a diagnoses of schizophrenia or a related psychosis – although six patients
were discounted either because their twin counterparts were overseas or it was unclear whether they were monozygotic
(MZ) or dizygotic (DZ) twins. This left 62 patients: and 5 twin pairs were both on the register, leaving 57 study pairs. The
other 52 patients’ twin counterparts were tracked down to participate in the study.

Of the 62 patients in the participant sample, exactly half were

Monozygotic Dizygotic Total
male, and half were female. Their ages ranged from 19 to 64
Female 11 16 27 when they were last assessed, with the average patient age
being 32. Zygocity was determined using three methods:
Male 13 17 30
fingerprint testing, blood testing and resemblance
Total 24 33 57 assessments (this was done before DNA testing was around).

Multiple data collection methods were used, involving both primary and secondary resources. These included:
 hospital notes
 case histories based on self-report questionnaires and interviews with the twins and their parents
 tape-recorded 30 minute samples of verbal behaviour from semi-structured interviews
 personality testing
 testing to measure disordered thinking, conducted both on the twin sets and their respective parents
The researchers wanted to look at concordance rates. If the one twin had been diagnosed with schizophrenia, they
wanted to know how often their counterpart twin would also be diagnosed with schizophrenia, or a related psychosis.
The patient who had been admitted to the psychiatric hospital initially first coming to attention was called the proband.
The data was analysed between each proband and their twin, with twin pairs being categorised in four ways.

Findings
The tables below display the main results from Gottesman and Shields’ study. The four categories were:
 category 1 – both the proband and co-twin had been hospitalised and diagnosed with schizophrenia
 category 2 – both had hospitalisation, but the co-twin had been given another diagnosis related to schizophrenia
 category 3 – the co-twin had some psychiatric abnormality, but nothing related to schizophrenia
 category 4 – proband had schizophrenia, but the co-twin was diagnosed as clinically normal
It is recommended
Monozygotic twins Dizygotic twins Categories 1, 2 & 3: MZ DZ that you learn those
Category: Number %age Number %age Males 69% 29% figures highlighted
in red, as learning
1 10 42 3 9
Females 91% 62% them all is not
1 and 2 13 54 6 18 realistic
1, 2 and 3 19 79 15 45 Concordance rates: MZ DZ Note: severe means
4 5 21 18 55 having longer than
Severe schizophrenia 75% 22% two years’
Total: 24 100 33 100 hospitalisation, mild
Mild schizophrenia 17% 0%
means less than two
years
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In summary, the results showed:
 There was a significant difference found between MZ and DZ twins in all measures
 MZ twins were always more similar in diagnosis than DZ twins in each case where the co-twin had some diagnosis
 Similarity was greater between female twins compared to male twins (for both MZ and DZ twins)
 Concordance rates were higher for both MZ and DZ twins for severe schizophrenia compared to mild schizophrenia

Conclusions
The findings suggested that the closer the genetic relationship between two people, the greater the likelihood that if one
of them is diagnosed with schizophrenia , the co-twin is also going to develop schizophrenia or a related psychotic
disorder. The study also suggested that this relationship was more prevalent among females than males.

However, as twins in the monozygotic twin pairs did not have 100% concordance rates, the implication is that
schizophrenia is not caused entirely by genes. Instead, the results led Gottesman and Shields to believe that genetic
factors do predispose someone to schizophrenia, by lowering their threshold for coping with stress, but environmental
triggers may also be needed to actually start the development of the disorder. They said the diathesis-stress model best
fit this explanation, taking on board a biological and environmental explanation.

Gottesman and Shields also looked at 11 other studies, and concluded that their results did support each other, although
they thought there were some methodological issues, such as with the sampling techniques. This is how they concluded
their results were reliable, and that there is a genetic element to schizophrenia.

Evaluation
Strengths
 The results are supported and backed up by other studies which have produced similar findings, such as Inouye (1961)
who found a 74% concordance rate of twins with a progressive chronic schizophrenia disorder, and a 39%
concordance rate for mild schizophrenia
 One of the findings of their analysis of the other studies was that the sampling techniques were questionable, but a
strength of Gottesman and Shields’ study is that the sampling was carefully controlled using multiple measures to
make sure that twins were correctly allocated either MZ or DZ twin status, and a lot of data was gathered using
multiple research methods to check the diagnoses were correct

Weaknesses
 It would have been useful to know more about what ‘related psychosis’ meant when describing the schizophrenia
scale to take into account the related disorders, as they failed to make this clear
 Gottesman and Shields suggested that there are different types of schizophrenia and some might be caused by life
events (so environmental stimuli), such as being a prisoner of war, and it was hard to distinguish between such types
in the results of the study

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Brown et al. (1986)
3.11 Study in detail: Brown’s 1986 study on ‘Social support, self-esteem and depression’

Aims
Brown et al. looked at factors involved in depression, and considered only women. They used interviewing techniques to
find out how self-esteem and social support factors affected the development of depression. The aims were:
 to see whether crisis support protects against the onset of depression, even if there is low self-esteem and a lack of
general support
 to see if a lack of support and low self-esteem are vulnerability factors for depression
 to see if support from a husband, partner or close relationship reduces the risk of depression

Procedure
The study took place in Islington, North London. The study used a prospective design – this means that it was a
longitudinal study that started when the participants were not affected by the condition of interest, in this case
depression. This allows risk factors to be studied. If someone with depression is interviewed once they are depressed,
then the depression may affect answers given concerning events that led up to the depression. This would make it
difficult to investigate the causation factors.

Women whose husbands worked in manual occupations, had at least one child aged 18 or under living at home, and were
themselves aged between 18 and 50, were sent a letter by their GP asking if they were willing to take part. Women who
fit the criteria and all single mothers (since depression is frequent among single mothers) were put into the sample. In
total, 435 women were found, and a number of them were randomly selected to participate: 91% of the initial response
(so 395 women in total) were used in the first stage of the study.

The study had two phases:

 at first contact measures of self-esteem and personal ties were measured, and psychiatric history collected
 the second phase, one year later, collected data about any onset of psychiatric disorder in the twelve months
following first contact, and measures of live-event stress and social support were also taken
 the measures were carried out carefully and by experienced interviewers; there were tests for reliability, with 60
women being interviewed intensively and 21 used in a reliability study: of these 21, eleven were seen by two
interviewers and ten were rated by a second person using tapes of the original interviews, and satisfactory inter-rater
reliability was found

In this study, fifty participants who were found to be depressed when first contacted were excluded from the follow-up
study one year later, as the researchers were only interested in new cases of depression to find causation factors.

Findings
In all, 353 women agreed to the follow-up interview one year on (89% of the original sample interviewed), although 50 of
those were the initially depressed, and so the study excluded their data and analysed the cases of 303 women. About half
of those women (150) had experienced a severe event or major difficulty at some point in the twelve months between
first contact and the follow-up, and 32 of the women had the onset of depression.
Life events and onset of depression
Of the women who had developed depression in those twelve months, 29 of the 32 had experienced some major life
event (involving a loss, failure or disappointment) six months prior to developing depression – that’s 91% of all those who
were depressed. This compared to only 23% of the women without depression who had experienced such an event.
Self-esteem and the onset of depression

Of those who had a life event, Did they have negative Did the women have a provoking agent?
33% of those who developed evaluation of self? Yes (% of those with onset) No (% of those with onset)
depression had negative Yes 33% (18 out of 54) 4% (1 out of 27)
evaluation of the self and 13% No 13% (12 out of 96) 1% (1 out of 126)
did not. The table shows the relationship between provoking agents (life events) and negative self-esteem.

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Social support
The majority of women with core crisis support (85 of 92) saw it as helpful, and there was no difference in their
perception of support being helpful whether they had developed depression or not. It is interesting that where a woman
had said she had confided in a close tie (core support) at first contact, but not at crisis support and so felt let down, 42%
developed depression. Of those who had no support either at first contact or at crisis, 44% (or 4 of the 9) developed
depression.

Note: core support refers to the support of a husband, partner or other close relation, whereas crisis support refers to
(professional) support at the time of a provoking agent (life event) – which may possibly lead to depression

Conclusions
- In general, those who had a husband or other close tie had a lower chance of the onset of depression
- However, those women who were married and confided in their husbands (core support) but were let down by a lack
of such support at crisis (crisis support) had an increased risk of developing depression
- Low self-esteem is implicated in the onset of depression after a provoking agent
- A provoking agent seemed to be necessary for the development of depression in most cases

Evaluation
Strengths
 Both the first contact and follow-up interviews gave the in-depth and detailed data that were required for the analysis
of such complex inter-related concepts such as self-esteem, core social support and major life events
 There was strong inter-rater reliability, which strengthens the findings which come from the data
 The data were likely to be valid as they were gathered carefully by trained and experienced interviewers using a semi-
structured interview technique, allowing detailed information to be gathered and explored
 Sampling was carefully carried out by contacting all eligible women and then carrying out random sampling – this
meant that all the women had equal chances of being chosen, which removes a source of bias

Weaknesses
 It was hard to separate out the concepts that were scored as numbers and then percentages because qualitative data
were in some cases reduced to quantitative data – for example, the presence or lack of support from a husband or
partner at crisis point seemed easy to access, but then it was shown that such lack of support meant, at least in some
cases, that the husband was part of the situation, rather than a bystander
 This was a study of working-class women with at least one child still at home – the sample was quite precise, and
therefore generalising the findings to all women might not be possible

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