‘madness’ and we probably think of schizophrenia. It is the ultimate
when it comes to psychological disorders and abnormality, strange then
that as a condition it is so loosely defined, to the point were some
question its very existence!
That is not to
question that some people (about 1% of the population) do suffer what we
would term ‘schizophrenic symptoms,’ but given that the symptoms are so
varied can we really group them all under on umbrella term of
is a massive health care issue. It is estimated that there are over half
a million schizophrenics and that 10% of all NHS beds contain a
schizophrenic. As a nation we spend an estimated £1.7 billion
(£1,700,000,000) on treating schizophrenia each year. That is more than
we spend on treating cancer!
Not an easy
question to answer, but one thing it certainly is not is ‘split
personality!’ This confusion probably arises due to the meaning of the
word itself ‘split mind,’ but in fact schizophrenia is not a disorder of
personality at all. It is probably best described as a detachment from
reality in which the sufferer experiences hallucinations, delusions and a
possible host of other symptoms.
History of the
(1898) first described a disorder that he called ‘dementia praecox’
or senility of youth. Typically the onset of what we now call
‘schizophrenia’ is in the late teens or early twenties in men and a little
later in women.
believed that mental disorders should be categorised as either:
become schizophrenia and
a term still
used today and sometimes referred to as ‘bipolar disorder (see notes on
categorisation led to the development of the DSM (Diagnostic and
Statistical Manual) still used today as a method of classifying mental
disorders (particularly in the USA). It is also used as a basis for the
ICD (International Classification of Diseases) used by the World Health
Organisation in classifying all disorders (mental and physical).
Note: you may
see during the course of your extensive background reading the terms
DSM-IV and ICD-10. These refer to the latest editions of the two
(1908) called the disorder ‘schizophrenia’ and described its symptoms as a
loosening of the threads that hold the mind together or as a loss of
connections between thoughts.
refers to a disorder of affect or mood, such as anxiety, panic,
phobias and depression. Generally people suffering form neurotic
disorders are treated with sympathy and understanding. We all know
how it feels to be stressed and down so can empathise with a person
who is suffering from these in an exaggerated or prolonged form.
on the other hand is outside of most people’s comprehension and refers
to a detachment from reality. Symptoms may include hallucinations
(auditory and visual), delusions (thinking you’re someone else for
example), thought disorders etc. Psychosis is a technical or informed
way of describing a person that the bloke down the pub would describe
as ‘mad’ or ‘a nutter!’
are so varied that it is useful to categorise them in one of a number of
(1959) described what he termed ‘first rank symptoms.’ To be diagnosed
with schizophrenia one or more of these needs to be present:
DSM-IV (categorisation system used by the American Psychiatric
Association) believe that a schizophrenic has to be suffering one or more
of the following symptoms:
states that schizophrenia can be diagnosed if one of these is
present OR two of the following:
persistent hallucinations, breaks in the train of thought, catatonic
behaviour, negative symptoms, change in personal behaviour.
section will look at some of these in more detail.
disturbance or control of thought
are being placed in the mind by external forces
are being removed from the mind by external forces
are being broadcast to others for example over the radio or through
common symptom of schizophrenia. Voices telling the person what to do
example touch or visual. The schizophrenic might see Elvis or feel
people touching them.
you’re Napolean really is quite common amongst schizophrenics.*
one in which they think people are out to get them. (Also common in
sleep deprivation studies).
believes that characters in a book, songs or in films are actually
referring to them.
You may be
familiar with the song ‘They’re coming to take me away ah ah!’ This was
sung by a bloke calling himself Napolean 14th who was quite
bizarre. The B side was the track played backwards. (This was in the
days of vinyl when the recording medium had two sides!).
of Schizophrenia (according to Slater and Roth 1969)
in which there are breaks in the train of thought and the person appears
to make illogical jumps from one topic to another (loose association).
Words may become confused and sentences incoherent (so called ‘word
(or catatonic behaviour) were the patient may adopt strange postures or
engage in repetitive movements such as pacing or rocking (which I
witnessed in one Victorian-style asylum I visited… as a student!).
Catatonic refers to the tendency of some patients to hold a particular
position for an extended length of time (in extreme cases several
in which a person becomes totally apathetic and sits around waiting for
things to happen. They engage in no self motivated behaviour. Their get
up and go has got up and gone!
were the patient may show little in the way of emotional response or in
some situations may exhibit inappropriate emotional responses:
Show few signs of emotional sensitivity (e.g. on the death of a friend)
affect: More general loss of emotional expression.
Inappropriate affect: Laugh at bad news or at a funeral (think of the
‘giggle-loop’ in Coupling)
symptoms appear to be describing the ‘core’ characteristics of
schizophrenia and the ones that most people find most concerning. Slater
& Roth on the other hand see these so called ‘first rank’ symptoms as
being secondary manifestations of other underlying processes.
essential to remember that there is no one characteristic that must
be present for a person to be diagnosed with schizophrenia!
There is one
other, particularly useful, way in which the symptoms can be broken down:
refer to the characteristics that appear in addition to existing
behaviours, for example hallucinations, delusions and thought
disturbances such as thought insertion.
those symptoms that an impairment of usual behaviours such as
psychomotor disturbances, lack of volition, disturbances of mood and
This is a
useful distinction to make since it appears that the dopamine
hypothesis (medical model) accounts for positive symptoms whereas
other explanations (serotonin or brain structure) are needed to
explain the negative symptoms. Note however, that Schneider’s first
rank symptoms all appear to be positive and most of Slater & Roth’s
of schizophrenia has a single disorder is questioned by many. This is a
useful point to emphasise in any essay on the disorder. The symptoms are
so diverse and the possible causes so varied that it seems likely that we
are in fact dealing with many different psychological disorders. One way
round this problem is to consider different types of schizophrenia. Below
are the main five subdivisions which just a brief description of each:
by type I or positive symptoms. Typically the paranoid schizophrenic
experiences delusions of persecution or grandeur that are very detailed
and complex. On average about 100 paranoid schizophrenics are arrested
outside the Whitehouse, and in Britain sufferers are drawn to Downing
Street or Buck House. Sometimes they are seeking money but often want to
give advice on how to run the country or on impending disaster. This
category is odd in that patients do not have any of the negative symptoms
and other than their strange beliefs show no outward signs of their
schizophrenia (formerly hebephrenic)
means ‘silly mind.’ The characteristics of this disorder are silly and
incoherent behaviour such as giggling and inane laughter and a tendency to
talk about meaningless topics for hours! Negative symptoms such as
disorganised behaviour and incoherent language are common. (Tune into the
Radio 1 breakfast show any morning for a fuller understanding).
by impairment of body movement. This may involve wild and uncontrolled
movements that put themselves or others in danger or may be simply holding
one particular posture for long periods of time. ‘Waxy flexibility’ may
also result, when someone attempts to move them they simply freeze in the
new position instead. The movements may coincide with hallucinations,
often about death and catastrophe.
by a withdrawal from reality resulting in declining academic performance,
loss of friends and extreme apathy or loss of volition. Note: simple
schizophrenia is not recognised by all categorisations of the disorder.
these categories of schizophrenia
exception of paranoid schizophrenia the others types are difficult to
distinguish in practice (even for psychiatrists specialising in the
condition). On top of this the symptoms may change over time so that a
patient displaying one set of symptoms may display a different set a few
schizophrenia (the rocking and strange movements seen in films about the
Victorian-style asylums) are very rare today. This could be due to much
improved drug therapy or it could be that this was a mis-diagnosis in the
first place. The film ‘Awakenings’ starring Robin Williams and Robert de
Niro looks at a case of sleeping sickness* that could have been
misinterpreted as catatonic schizophrenia.
types are of little use in helping treatment or suggesting prognosis
(unlike the Positive and Negative symptoms distinction).
* The precise
cause of sleeping sickness (an epidemic of which occurred in the 1920s) is
not known. It could be due to a viral infection or perhaps even an
auto-immune response triggered by a bacterium. The symptoms include very
high fever and in some cases coma (hence the name). They can also include
disturbances of movement and slowing of mental responses, hence the
confusion with schizophrenia.
The course of
Onset is usually late teens.
Patient becomes withdrawn, takes less interest in education and
shows flattened affect.
Symptoms are reduced and person returns to symptoms similar to
25% return to ‘normal.’
Main symptoms appear e.g. hallucinations, delusions. 10% remain in
this phase and show no further improvement.
question could ask you to describe the clinical characteristics of a
psychopathological disorder (be it schizophrenia, depression or phobias).
Schizophrenia, being an umbrella term has a wide variety of possible
symptoms and be classed as having a particular type of the disorder as a
result. You could mention the extent to which these types really are
different and the extent to which they really do exist. As we shall see
there are many issues related to diagnosis including social class and
cultural background making definitions even more blurred. There are also
some similarities between aspects of mania and schizophrenia.
characteristics (adapted from Gross & Rolls)
||FIRST RANK SYMPTOMS
||Disturbance of mood
Disorders of movement
Lack of volition
Subjective experiences of the patient
since they are in addition to expected behaviours
since they are expected behaviours that have become impaired
can be measured and assessed
Models of schizophrenia
Most likely questions are on the models or
explanations of the causes of the psychotic disorder. Think back to work
on eating disorders at AS. At A2 you will be expected to describe or
outline the various theories and then either evaluate them or compare them
to other approaches.
Important point to ponder: At the outset
of the course you looked at the psychodynamic and behaviourist
approaches. You are also familiar with the behaviourist, cognitive,
psychodynamic and medical explanations of eating disorders. Each of these
approaches to psychology has its own distinct, some would say entrenched,
view on explanations to everything regarding the human condition. As a
initially based on the work of Freud. Theories concentrate on experiences
in childhood, particularly during the various psychosexual stages of
development (oral, anal etc.). Conflict between id, ego and superego are
also central. Other ideas frequently cited include repression, regression
and other ego defence mechanisms.
ignores genetic factors and concentrates on learned behaviour. Three main
classical conditioning, learning by association
operant conditioning, learning by being reinforced or punished
Social learning (SLT), learning by the observation of others.
concentrates on faulty processing of
information or inappropriate perceptions of ourselves.
believes disorders have one of four
genetic, the disorder is inherited
biochemical, disorder is caused by disruption of the brains
neuro-developmental, the disorder is caused by damage to brain structures
infection by virus or bacterium
uses environmental and social factors to explain disorders, for example
role of family or social class.
Some of these approaches are better suited
or provide better explanations of certain disorders than others. As we
saw at AS, a combination of behaviourist and cognitive approaches seems to
offer a good account of eating disorders. The medical model seems to be
the favoured account of schizophrenia and depression but clearly does not
paint the whole picture.
Diathesis refers to a genetic predisposition to the disorder
refers to a triggering factor.
A simple example of this, though obviously
not psycho-pathological would be lung cancer. As you are doubtless aware
some people can smoke 30 a day and live to 98. Others die much younger.
The obvious conclusion being that some people, because of their genetic
make up, are more susceptible to the disorder, smoking then triggers the
Note: the specification requires that you
know biological (e.g. genetics, brain biochemistry) and psychological
(e.g. social and family relationships). So in theory you can get away
with knowing just one of each. However, in order to evaluate theories it
is advisable for you to learn a few examples of each. Genetics and
biochemistry are essential for the medical model. Family model is the
most useful of the psychological but try to learn one other as well (e.g.
psychodynamic). Make sure you learn the evidence on which they are based
The incidence of schizophrenia in the
general population is 1%. If the incidence within families is higher than
this then it suggests a genetic link. This section of the topic
shows considerable overlap with earlier work on intelligence with the main
body of evidence coming from twin studies, family studies and adoption
studies. As with intelligence it is vital to bare in mind that it is
very difficult to separate out the effects of inheritance and environment
(nature and nurture), even when monozygotic twins are reared apart.
Shields (1972) examined the records of 57 schizophrenics between 1948 and
1964. About 40% of the twins were determined to be MZ and about 60% DZ.
If the pair were discordant, that is one had schizophrenia and the other
did not then the none schizophrenic was followed (not literally James) for
at least 13 years to see if it developed later.
rates, (i.e. probability of a twin having schizophrenia if its twin has
the disorder) were as follows:
Monozygotic twins 42%
Dizygotic twins 9%
(1991) in a review of over 40 other studies found
Monozygotic twins 48% concordance
Dizygotic twins 17%
found that if one MZ twin has schizophrenia that there’s a 90% probability
that the other will have ‘some sort’ of mental disorder!
What this suggests:
a genetic link for schizophrenia
schizophrenia is not entirely genetic, otherwise the concordance for MZ
twins would be 100%
However, as with all studies of this sort
it is vital to consider the role of environmental factors. MZ twins are
more likely to be brought up in similar conditions, be treated similarly,
same class at school, have similar friends and experiences, even be
dressed and treated similarly. Therefore it is not surprising that the
concordance is so high.
The usual way around this problem is to
consider MZ twins reared apart. However, as Gottesman (1991) discovered
the concordance rates are similarly high. But, the same proviso still
applies. Twins that are adopted into different families still tend to be
reared similarly and are often adopted into members of the same family! (Kamin
One other evaluation point that is always
worth mentioning, particularly for early studies, is that until the advent
of sophisticated genetic testing it was very difficult to distinguish MZ
and DZ twins, especially at birth. Some of the statistics for MZ twins
may actually be DZ twins and vice versa.
Be sure to emphasise the possible role of
environmental factors to gain AO2 marks. Module 5 is testing all round
understanding of psychology. Nature-nurture debate is crucial to all
aspects of explaining human behaviour.
One other point you could make (providing
you follow what I’m about to say) is that we tend to assume that MZ twins
are treated more alike because they are MZ twins. Lytton (1977) turned
this on its head and suggested that the greater similarity of MZ twins
ensures that they elicit a more similar response from their parents. That
is the greater similarity of identical twins is a cause of their more
similar parenting rather than an effect of it!
Look at patterns of the disorder within
families. As already mentioned your chances of developing the disorder
are about 1%. Family studies examine the possibility of getting the
disorder if parents etc. have the disorder. Again if this is greater than
1% then this could be seen as possible support for the genetic cause,
however, the same provisos remain. Living with schizophrenics could
increase your chances of developing it yourself.
Gottesman (1991) in a review of other
studies published the following findings:
Probability of developing
‘Randomly’ chosen from population
Brother or sister has schizophrenia
One parent has schizophrenia
Both parents have schizophrenia
Perhaps the most powerful of all evidence
for a genetic link is the following. Note, this is not easy to get your
head round so read it a few times or draw a family tree to clarify. If
all else fails you could always ask!
Gottesman & Bertelsen (1989). If your
parent is an identical twin who has schizophrenia then you have a 17%
chance of getting it too, (compare with one parent in table). However, if
your parent does not have the disorder, but their identical twin does,
then your chance of getting the disorder is still 17%. This is good
evidence because it seems to minimise environmental causes since you are
not living with a schizophrenic. However, you are living with someone who
is predisposed to schizophrenia, (i.e. carries the genes for it), since
they have the same genetic code as their twin who has developed it.
(Richard) Uncle Robert (Richard’s MZ twin)
If Richard has schizophrenia then Ryan has
a 17% chance of getting it too. (No surprises there). But this could
obviously be due to environment rather than genetics since Ryan is living
with his father. However, supposing dad (Richard) has an
identical twin (Robert) who is genetically identical. Imagine a
situation where uncle Robert is diagnosed with the disorder, so obviously
has the genetic predisposition, but his brother Richard, (Ryan's dad)
doesn't. Richard must also have the genetic predisposition (he
shares his genes with Robert) but shows no outward signs of this. In
such cases, the son still has a 17% chance of developing schizophrenia.
This is very powerful evidence for a
genetic cause since it shows that Richard (the father) who must be
genetically predisposed to schizophrenia but has never shown the symptoms,
has passed on the genes for it to his son, who has developed the disorder
but without having been exposed to the behaviour. Bob's your
Remember: in studies where twins have been
separated at birth there is still one environment that they have shared
for nine months; the womb.
This may seem obvious and to some extent irrelevant but this is a vital
time for the child’s development and pre-natal factors may be crucial in
determining later functions.
See the section on viral theory of schizophrenia as an example.
One possible way of minimising
environmental effects is to look at schizophrenics that have been brought
up away from biological parents. Kety et al (1978) looked at adopted
children in Finland who had developed the disorder.
Their biological parents, whose genes they
possess, were more likely to have schizophrenia than the parents who had
adopted them and brought them up.
Genes appear to play a role in
schizophrenia although other factors must also be involved. The
chromosome or specific gene(s) responsible have not yet been identified.
The tips of chromosomes 5 and 22 have both been suggested as possible
sites for the faulty genes but now appear to have discounted.
Schizophrenics are often very heavy smokers. An area on chromosome 15,
known to be responsible for the brain area involved in filtering
information (implicated in some types of schizophrenia), is known to be
stimulated by nicotine. It is thought that faulty neurons in this area
may be causing the schizophrenia and nicotine may be acting as a
Heston (1947) followed 47 children born to
schizophrenic mothers but who were separated from them within the first
three days of life. They were adopted into families not related to the
biological mothers. Later in life (30s) they were compared with a control
group of children who had been separated in similar circumstances at
birth, but crucially, not born to schizophrenic mothers. Five of the 47
in the experimental group had gone on to develop schizophrenia (over 10%),
whereas none of those in the control group had developed the disorder!
MZ or DZ?
Many twin studies compare the concordance rates for schizophrenia in MZ twins
with those in DZ but can we always be sure whether twins are identical or not,
particularly at birth? Clearly DNA
testing has now solved this problem but prior to the 1980s this would not have
been so clear cut and many early twin studies may lack validity because of this.
A few past paper
questions for you to consider:
evaluate the possible contributions of genetic/neurological factors to
appears to be due to an abnormality in brain development that arises from
mainly genetic but also environmental factors.”
research into the causes of schizophrenia. (30)
evaluate the possible contributions of biological factors to
the clinical characteristics of schizophrenia.
one explanation of schizophrenia, and evaluate this explanation in terms
of research studies and/or alternative explanations.
are many different kinds of depression, e.g. unipolar and bipolar,
endogenous and reactive.’
(Is there a chemical cause for
Some hallucinogenic drugs such as LSD produce symptoms that are
indistinguishable from schizophrenia.
Cocaine and amphetamines can produce hallucinations and delusions of
persecution, again not dissimilar to those reported by schizophrenics.
Smyhies (1976) found traces of
hallucinogenic chemicals in the CSF (cerebro-spinal fluid) of
schizophrenics. One role of the CSF is to mop up excess chemicals in the
brain. Smythies findings therefore suggest that schizophrenics are
producing more of these chemicals than normal.
Hallucinogenic drugs are chemically
similar to the neurotransmitter dopamine. Researchers therefore believed
dopamine could be the cause. They concluded that the brains of
schizophrenics were more sensitive to dopamine than the brains of non-
schizophrenics. See your beautifully drawn diagrams of the dopamine
pathway for details.
Evidence for the dopamine hypothesis
Amphetamines and cocaine increase the effects of dopamine in the
(a chemical that increases the levels of dopamine) can produce
Chlorpromazine, (an anti-psychotic drug frequently used in the
treatment of schizophrenia), blocks dopamine receptor sites. This
makes the brain less sensitive to dopamine. Again see your diagram.
Post mortems carried out on schizophrenics, show that they have up
to six times the number of dopamine receptors than normal. Again
this suggests that their brains are more sensitive than usual to the
Chlorpromazine only reduces the positive symptoms of schizophrenia such as
hallucinations and delusions.
Neuroleptic drugs (such as chlorpromazine) have their effect on the brain
almost immediately, but they take weeks to affect the behaviour of the
patients. The dopamine hypothesis is unable to explain this delay.
Chlorpromazine makes little or no difference to 30% of schizophrenics.
The role of serotonin
Recently, Kane (1988) the drug clozapine
has been used in the treatment of the disorder. Clozapine is more
effective in reducing the negative symptoms of schizophrenia (e.g.
disturbances of speech and flattening of affect). Clozapine seems to work
by blocking serotonin sites in the brain.
Barlow & Durand (1995): both dopamine and
serotonin are probably involved, but the precise role played by each is
All the evidence provided is correlational.
It implies an association between schizophrenia and chemicals in the
brain. It does not prove cause and effect. It could be that
schizophrenia has caused the abnormal chemical levels rather than the
other way around.
(do the brains of
schizophrenics have an abnormal structure?)
Johnson (1989) reported that some
schizophrenics have a reduced blink reflex, evidence for neurological
damage. Others have reported that some schizophrenics have difficult
births which could have starved their brains of oxygen. This would also
explain why the incidence of schizophrenia is declining as monitoring
techniques at birth improve.
Chua & Mckenna (1995) reported the
following abnormalities in the brains of some schizophrenics:
grey matter in the temporal lobes
ventricles resulting in loss of brain tissue.
activity in the prefrontal cortex
However, none of these findings are
consistent amongst schizophrenics. The most common abnormality amongst
patients is the enlarged ventricles which would result in less brain
tissue, particularly in the medial temporal lobes of the brain. This has
been confirmed using techniques such as MRI scans.
It could be argued that this does not show
cause and effect. Perhaps the schizophrenia led to the abnormal brain
structure. However, Harrison (1995) believes that these differences occur
before the onset of schizophrenia, implying that they are more likely to
be a cause than an outcome of the disorder. Since the abnormalities in
brain structure do not increase over time, as is the case with diseases
like Alzheimer’s, then it appears that the problems are due to a failure
of the brain to develop normally in the first place.
damage associated with the negative symptoms such as inability to
concentrate and plan.
How does this tie in with the central executive of the working
Temporal lobe damage associated with
the positive symptoms such as delusions and hallucinations.
One criticism often aimed at the possible
relationship between brain damage and schizophrenia is that no one pattern
of damage seems to correlate with the disorder. Perhaps, however this
should not be surprising, given the variety of symptoms associated with
schizophrenia. It seems that certain damage is associated with certain
symptoms however. Damage to the temporal lobe is associated with some of
the positive symptoms whereas damage to the frontal lobe is associated
more with the negative symptoms.
Any such differences between the brain of
a ‘schizophrenic’ and ‘non-schizophrenic’ brain are so small that it is
not possible to detect them in the individual. They only become apparent
if groups of schizophrenics and non-schizophrenics are compared.
Significantly more schizophrenics are born
in late winter or early spring (figures suggest up to 8% more likely than
at other times of the year. Because various diseases such as colds,
influenza, chicken pox etc. also show such a seasonal variation it was
suggested that there might be a link.
Torrey (1988) proposed a link with a viral
infection in the mother during the second trimester of pregnancy (months 4
to 6). Barr et al (1990) found those in the fifth month of foetal
development during the influenza pandemic of 1957 grew up to have a
significantly higher risk of developing schizophrenia. This has been
questioned by others in particularly because the effects are not seen
worldwide. This increased risk was only evident in England, Wales and
Finland and was not apparent in Scotland or the USA.
Viral theory updated
However, more recently a new variation on
this old theory has arisen. The theory suggests that some of our genes
developed from viruses and became incorporated into our genetic make up.
Blomberg estimates that about 1% of the human genome is made up of these
retroviruses. These remain ‘dormant’ but can be activated by certain other
viral infections that we contract or perhaps by other factors during
foetal development or infancy.
Blood samples were taken from 53,000
pregnant women in the USA during the 1950s and subsequently frozen. Buka
(1999) checked the offspring of these women and found 27 schizophrenics in
the Boston area. Buka found that their mothers’ blood was significantly
more likely to contain antibodies (suggesting a viral infection during
pregnancy). The most common infection found was herpes.
Some of these quiescent genes are
responsible for making proteins and these can be detected in the CSF of
the brain. Karlsson found genetic material from these viruses in 29% of
recently diagnosed schizophrenics. There was no sign of such material in
Retroviruses are responsible for AIDS and
research is now ongoing to see if some of the drugs developed to treat
AIDS can help with schizophrenia.
The ventricles are hollow chambers within the brain filled with CSF
(cerebro-spinal fluid). The CSF
helps to cool the brain (like a car radiator), absorbs the waste products of the
brain and to some extent acts as a shock absorber.
However, it is also clear that the larger the ventricles the less space there is
for neurons and brain tissue.
Perhaps this is the problem with the brains of some schizophrenics.
No essay on the causes of schizophrenia
would be complete without a mention of this. It is particularly good
since it can be used in either a question asking for medical explanations
or one seeking information on the social and psychological explanations.
Diathesis is a person’s genetic
predisposition to a particular disorder. Because of the genes they've
inherited some people are more likely to develop schizophrenia than
others. However, this alone does not guarantee that they will. (Think of
MZ twins, one of whom has the disorder and the other who does not).
Stress refers to the environmental factors
that trigger it, for example high levels of expressed emotion, major life
events or a dysfunctional family.
Tienari (1987) found that in all cases of
schizophrenia that he studied one or other members of the sufferer's
family were disturbed.
Marcus (1987) Israeli study, all parents
of schizophrenics studied had poor parenting skills.
Social and psychological explanations of
Family Models of schizophrenia
Bateson (1956) described the situation
were families send out contradictory information to their children. For
example parents who say they care whilst appearing critical or who express
love whilst appearing angry. A classic example would be telling the child
you’d like a hug and then pulling away when they try! Bateson believed
that this caused confusion and self-doubt in the child leading to their
withdrawal as they lose confidence in their own ability to express
into this theory are retrospective (get the person to think back to
childhood), this makes them notoriously unreliable.
Wynne & Singer (1963) believined that the
communication in some families was 'fragmented and disjointed.' Sentences
show little continuity with Liverpool having a particularly good win at
Leeds yesterday! Conversations switch focus from one topic to that really
good curry we had last year in Bognor! To test their theory they counted
the 'deviance score' for conversations. They would record families
carrying out tasks and count the number of such defects in communication.
The deviance score for schizophrenic families were significantly higher.
& Waxler (1968) found that mothers do talk to their schizophrenic
daughters in an unresponsive way, but talk to their 'normal' daughters in
a 'normal' way, suggesting again that it is having a schizophrenic in the
family that causes the abnormal communication rather than vice versa.
Fromm-Reichman (1948) coined the term to
describe a mother likely to produce the disorder in her offspring.
Typically these are cold, domineering conflict inducing, rejecting and
very moralistic, particularly about sex. Her behaviour is often
contradictory (compare to double bind), so for example saying ‘yes’ when
her body language suggests ‘no.’ Fromm-Reichman believed that such a
mother in conjunction with a weak and ineffectual father could 'drive' a
child to schizophrenia. Little research evidence has found support for
Support for the
theory is limited although it is clear that the families of schizophrenics
are often in some way different, often showing high levels of conflict and
poor communication. However, we again come up against the problem of
cause and effect. To what extent is the schizophrenia a result of these
issues and to what extent may it be a cause?
Rodnick (1975) believed family problems were a cause rather than a
consequence. They found that often the family problems pre-dated the
onset of schizophrenia.
reported that children born to schizophrenic mothers and later adopted
were far more likely to develop schizophrenia if adopted into a disturbed
family. This provides good evidence for the diathesis-stress model;
genetic predisposition followed by an environmental (family) trigger.
Expressed emotion (EE)
High levels of expressed emotion are
typified by extremes of emotional content in conversations and daily life,
for example high levels of hostility and criticism and of over concern
with others. The researchers concluded that this is more important in
maintaining schizophrenia than in causing it in the first place, (Brown et
al 1958). Schizophrenics returning to such a family were more likely to
relapse into the disorder than those returning to a family low in EE. The
rate of relapse was particularly high if returning to a high EE family was
coupled with no medication.
This is now well established as a
'maintenance model' of schizophrenia. Treatment of schizophrenia often
involves education and training for other family members in reducing their
levels of EE.
Some schizophrenics have little or no
contact with their families when released back into the community, but
their relapse rate does not appear to be any lower as a result.
General evaluation of the family models
It is difficult to know with any certainty
whether the dysfunctional families reported in these studies have lead to
schizophrenia in some family members or whether simply having a
schizophrenic member in the family has lead to some degree of
dysfunction. Yes you guessed it folks that good old cause and effect
question yet again!
Perhaps the effect is two way. Rosenfarb*
et al (1995) observed recently diagnosed schizophrenic patients that have
been discharged back into family care. Before the arrival of the patient
the families had been classed as high in expressed emotion (support for EE
causing schizophrenia). On arrival EE comments by other family members
increased the schizophrenic symptoms (again). However, having the
schizophrenic back in the family also increased the level of expressed
emotion! *Did Rosenman marry Goldfarb?
included this (and the bit about Szasz) as an area of general interest
or extension piece for evaluating the medical model. Laing’s theories
are similar to the family systems models but take an anti-medical
Laing does not see schizophrenia has a disorder, rather as a way of
explaining away those people whose behaviour does not conform to
societal norms. Laing’s ‘family interaction model’ of 1961 is similar
to the theory proposed by Bateson. In his book ‘Self and Others,’
Laing proposes that schizophrenia is not something that happens inside a
person but between people. In a number of family case studies looked
at, Laing & Esterson conclude that schizophrenia did make sense in terms
of the family relationships involved.
take a more radical and controversial approach seeing schizophrenia as a
means of labelling and controlling. In the ‘conspiratorial model’ he
suggests psychiatrists label and imprison schizophrenics in order to
maintain their own definitions of normality. He takes this a stage
further in his ‘psychedelic model’ suggesting that the schizophrenic
just happens to be a particularly ‘eloquent critic of society.’
Schizophrenia is seen as a way of coping with the ‘disorder’ that is
normality within society. However, the schizophrenic is not usually
allowed to complete this healing process since psychiatrists intervene
and administer ‘treatment’ of their own!
Is a powerful
critic of the psychiatric model. Psychiatrists see ‘mental disorders’
as being of physical origin. To Szasz this is contradictory. If
illness has an organic (or physical cause) then it should be classed as
a disorder of the brain. Although there are various biological models
of disorders, such as schizophrenia, as yet none are proven. As Szasz
points out in the majority of cases of patients with ‘mental illness’
there is no obvious physical defect in brain structure or genetic make
up. (Exceptions are Alzheimers, Korsakoffs etc.).
‘mental illness’ is ‘a problem of living’ brought on by the bizarre
nature and structure of societies. As such they should be seen in an
ethical and social context and not simply treated by the administration
On being sane in
An all-time classic study in psychology
that breaks some of the unwritten rules in that the real participants are
the psychiatric establishment! This could be used as very clear evidence
for some aspects of Laing’s theory and of labelling theory in general:
Eight supposedly ‘normal’ stooges present
themselves at various psychiatric establishments in America. The texts
always emphasise their normality; they were in fact three psychologists, a
psychiatrist, a psychology student, a paediatrician, a decorator and a
housewife… (leave you to decide!).
Each complained of hearing same sex voices
which simply said ‘hollow’, ‘empty’ or ‘thud.’ All eight were admitted
predominantly with a diagnosis of schizophrenia and in one case with manic
or bipolar depression. On being admitted they stopped reporting the
voices. During their stay the patients kept written records in the form
of a diary. At first they tried to keep this from the staff until they
all realised that the staff really didn’t care or see it as odd. All
patients wanted to be released as soon as possible and apparently tried
their best to behave in as friendly, cooperative and ‘normal’ manner as
Their average stay in the institutions that
admitted them was 19 days with the shortest being 7 days the longest 52
days before they were able to convince staff that they were well enough to
be released. Each was released with a diagnosis of ‘schizophrenia in
remission’ meaning that although they were no longer displaying symptoms
they were still schizophrenic. Such a diagnosis would make future
employment difficult. Each patient had given a false name at the outset!
During their stay they were famously
administered (between them) a total of 2100 tablets, only two of which
were actually swallowed. The only people to suspect they were not
genuinely unwell were other patients (perhaps a case where the lunatics
should have been taking over the asylum!)
In a less well reported follow up study one
of the hospitals was told about the results of the first study and warned
that there may be other ‘pseudo-patients’ seeking admission in the coming
months. In that time 193 patients were admitted and many of these were
alleged to be stooges when in fact all were genuine.
One thing becomes very clear when the
medical records of the pseudo-patients during their stay are read.
Symptoms were not guiding diagnosis, rather diagnosis was influencing
perception of the symptoms. Once labelled as schizophrenic that label
sticks and determines how people view your case and your behaviour. The
patients reported that the most simple of their behaviours were seen as
being symptoms of their disorder. For example in three cases nurses had
found their writing symptomatic of their disorder, ‘patient engages in
writing behaviour’ appearing on their report. Another example reported by
example of such translation is found in the case of a pseudopatient who
had had a close relationship with his mother but was rather remote from
his father during his early childhood. During adolescence and beyond,
however, his father became a close friend, while his relationship with his
mother cooled. His present relationship with his wife was
characteristically close and warm. Apart from occasional angry exchanges,
friction was minimal. The children had rarely been spanked. Surely there
is nothing especially pathological about such a history. . . . Observe how
such a history was translated in the psychopathological context, this from
the case summary prepared after the patient was discharged.
39-year-old male . . . manifests a long history of considerable
ambivalence in close relationships, which began in early childhood. A warm
relationship with his mother cools during his adolescence. A distant
relationship to his father is described as becoming very intense.
Affective stability is absent. His attempts to control emotionality with
his wife and children are punctuated by angry outbursts and, in the case
of the children, spankings. And while he says that he has several good
friends, one senses considerable ambivalence embedded in those
points out, with physical illness it may be safer for the medical
profession to play safe and risk admitting someone who is really well
rather than risk missing someone who is ill. The danger with adopting the
same approach to mental illness is that a diagnosis then stays with you
for life and can adversely affect your relationships, job prospects and
Family and social theories are generally
recognised as the better non-medical explanations of schizophrenia. Other
theories you may want to accustom yourself with are the behaviourist,
cognitive and psychodynamic. These are predictable and generally not as
good (nor are they essential!).
Conditioning: Ullman & Krasner (1969):
believed that strange behaviour is inadvertently reinforced by others.
For example, the staff in psychiatric hospitals paying more attention to
those showing the worst symptoms.
1. Labelling theory: Scheff (1966).
Children who for whatever reason withdraw into an ‘inner world’ are
labelled because of their bizarre behaviour. This leads to attention,
such as sympathy, which acts to reinforce the behaviour and causes the
person to seek further attention by behaving even more strangely.
2. Social learning: Watching others being
rewarded for behaving strangely.
Some of the strange behaviour of
schizophrenics can be modified using behaviourist methods such as being
reinforced for more appropriate behaviour.
SLT does not explain how people can
develop schizophrenia when there has been no chance to observe
It is possible to see how observable
behaviours such as motor disturbances can be acquired in this way.
However it seems unlikely that hallucinations, delusions and disturbances
of thought could be acquired through reinforcement.
According to Freud psychotic behaviour was
due to inter-psychic conflict. Either the ego cannot cope with the
demands being made upon it by the id, or the guilt caused by an overly
Since the ego is too weak to resolve the
conflicts that arise between opposing elements of personality it retreats
(regresses in Freud-speak) to the oral stage of development, a stage at
which it felt safe and secure. At this age the child was unable to
distinguish between itself and the outside world (good evaluation marks
to be had here if you mention Piaget), and this, according to Freud
causes the schizophrenic symptoms.
The symptoms of schizophrenia bare little
resemblance to child-like behaviour.
Other comments on schizophrenia
Validity of the disorder
Is schizophrenia one disorder or a number
of related disorders? Evidence for the latter:
Many of the symptoms occur in other mental disorders, e.g.
thought disorder in mania
hallucinations in some forms of depression
The onset of the disorder can be sudden or insidious (person being unaware
of the early stages).
Its course can be continuous (no breaks), or episodic.
Prognosis (outcome of the disorder): 50% go on to develop moderate or
severe symptoms, 25% make a full recovery.
No one clear cause.
(1973) referred to depression as the ‘common cold’ of psychiatry because
of its frequency of diagnosis. According to BPS figures a staggering 9
million people in Britain reported feelings of depression to their GP in
1998! However to continue Seligman’s analogy, although this ‘cold’ may
have reached epidemic proportions in the West it is certainly not pandemic
since many cultures and areas of the World report little or no depression
Characteristics of depression
an affective disorder in that it is characterised by disturbances of
affect (or mood). During the course of any period of time it is not
unusual for a person’s mood to alter. However with affective disorders
this variation is more marked and is accompanied by other symptoms.
of depression do vary; the DSM-IV recognise three main types of
depression, only two of which will be mentioned here, and only one of
which will be covered in detail. A possible 6 mark question on the paper
could ask you to describe the symptoms or characteristics of depression.
Clearly ‘feeling sad’ is not going to earn you very much credit!
we most associate with depression, those feelings of sadness, loss of mood
and loss of pleasure from what were previously enjoyable activities. Mood
may also alter during the course of the day, typically being lowest in the
morning and gradually showing improvement as the day progresses. This may
be associated with circadian rhythms.
of sleep: patients sometimes report insomnia, but sleeping longer than
before is also common, perhaps as patients attempt to escape their
also decrease or it may increase in the form of comfort eating. Part of
this may be due to boredom since typically depressed people tend to have
lower activity levels.
loss of drive are common. Typically the depressed person will sit around
waiting for things to happen, making no attempt to initiate activity or
social contact. This could be because they don’t want people to see them
in a depressed state.
These can vary
from negative self thoughts, loss of self esteem and self confidence,
feelings of despair and hopelessness, inability to concentrate on tasks
for any length of time to feelings of inadequacy and blaming themselves
for their situation and on occasions and suicidal thoughts.
Famously Sir Winston Churchill suffered from manic depression and referred to
his low moods as his ‘Black dog.’
Bit of trivia for those of that persuasion: this particular photograph, perhaps
the most famous of Churchill was taken by the great *Karsh of Ottawa.
Legend has it that having problems getting the picture he wanted he
leaned forward and pulled the cigar from Churchill’s mouth.
This was the result!
although always referred to as ‘Karsh of Ottawa’ was actually born in
Categories of depression
(major or clinical depression)
This is what
we normally consider to be depression and can comprise a combination of
any of the symptoms mentioned above. Minor depression occurs when the
patient suffers the low mood but without any of the cognitive or other
of clinically depressed symptoms that alternate with periods of near
normal mood and/or elevated mood (mania).
between unipolar and bipolar disorder
between high and low mood
Up to 3
times more common in women
incidence in men and women
incidence in the general population
incidence in the general population
common in creative people (writers, actors, comedians etc).
studies about a 46% concordance rate between MZ twins
studies about a 72% concordance rate between MZ twins.
This is a
second way of distinguishing between depressions that relates more to
causes rather than symptoms.
depression (as the name suggests) comes from within and is thought to be
caused by chemical imbalance and is explained and treated best by the
depression on the other hand is caused by external factors such as loss of
job, death of relative etc. and is usually explained using psychological
approaches such as behaviourist or cognitive models.
also a major factor in a number of other related disorders such as
Seasonal Affective Disorder (SAD), Premenstrual syndrome (PMS) and
Postpartum depression (PPD). The latter was formerly known as post natal
Models of depression
This is the
most likely area to be examined and could ask you for the extent to which
physiological or psychological models are able to explain the onset of the
disorder. We shall look at medical explanations first, particularly the
permissive amine theory and genetic evidence, and then consider the
psychological models. It would be useful at some point during such an
essay to suggest the medical model is used to explain endogenous
depression and the psychological models used to explain reactive
which way the question is worded it is useful to mention psychological
models and medical models since each can be used to fill in the
gaps left by the other. If the question asks for description and
evaluation of the medical model, describe the medical model but use
psychological explanations to evaluate.
of genetic evidence and discussion of the permissive amine theory is
needed here. Remember too that the two approaches are not mutually
exclusive. A decreased sensitivity to a particular neurotransmitter is
likely to be caused by a genetic abnormality!
All the usual
points need to be borne in mind and spelt out to the examiner. Clearly
you will want to mention trends within families, twin studies (MZ and DZ),
adoption studies and gene research. These then need to be evaluated in
terms of environmental influences and the extent to which they can explain
patterns such as sex differences.
patterns and studies
does tend to ‘run in families.’ Gershon (1990) found that the incidence
of depression is up to three times higher in families with a history of
the disorder than it is within the general population as a whole. Others
have put this figure even higher. Weissman (1987) looked at the
prevalence of affective disorders in general and found that family members
with first degree relatives (parent, sibling) with a mood disorder were up
to ten times more likely to suffer from one too.
distinguish here between unipolar and bipolar disorders:
reported the following concordance rates:
MZ twins 40%
DZ twins 11%
genetic component to explain the difference between the two.
72% (This is the highest concordance rate for any psychological
DZ twins 14%
It is worth
mentioning that different studies have produced varying percentage figures
but the overall trend is usually the same.
You must point
out however the shortcomings of twin research:
Environmental factors cannot be ruled out. Clearly MZ twins share a
more similar environment than DZ twins so influences of events, family,
friends, education etc. are more likely to be similar on both.
research it wasn’t always possible to distinguish between MZ and DZ
twins so figures may be inaccurate.
Even in MZ
twins reared apart environments may not be that different etc.
is not entirely genetic since no studies have shown a 100% concordance
rate between MZ twins!
Wender et al
(1986) found that the biological parents of adopted children who had
developed depression, were eight times more likely to have the disorder
than the adoptive parents. As usual, adoption studies like this provide
some of the most powerful evidence for a genetic component.
specific genes for depression
attempt was by Egeland et al (1987) who researched 81 members of the Old
Order Amish Community of Pennsylvania. Four families within the community
showed a much higher than expected incidence of bipolar (manic)
depression. Of the 81 studied 14 were diagnosed with bipolar disorder and
all had abnormalities on the tip of chromosome 11. This caused particular
interest at the time since this location is adjacent to genes known to be
involved in the production of serotonin (see biochemical section below).
studies have failed to replicate the findings suggesting that either this
gene is not responsible or more likely; more than one gene is involved.
Nemeroff (1998) has implicated a gene on the X chromosome.
link between genetic and biochemical influences…
Ogilvie et al
(1996) found that people with depression were far more likely to have
abnormalities on a gene known as SERT that is used to make
serotonin-transporter protein. New drugs used to treat depression are
believed to act on serotonin-transporter protein.
and serotonin are the likely candidates. Both are classed as amines.
(1965) found that too high a level of noradrenalin led to mania and too
little to depression. The first finding should not come as a surprise if
you consider the chemical similarity between noradrenalin and adrenalin!
Schildkraut believed that serotonin behaved in the same way. We now know
that this is not the case.
(1997) found that drugs used to treat depression increased levels of both
noradrenalin and serotonin.
carbonate used to level out some of the mood swings of manic depressives
(such as Valerie in the video) decrease levels of noradrenalin and
How do these
two neurotransmitters work to create depression?
believed that fluctuations in noradrenalin levels affect our mood: high
levels of noradrenalin leading to heightened mood and eventually mania,
low levels to a lowering of mood and eventually to depression. But what
about the role of serotonin which is clearly playing an important role
that it is serotonin that controls the levels of noradrenalin by
restraining the fluctuations.
this sense refers to allowing or letting. One amine (serotonin) permits
the other (noradrenalin) to fluctuate.
the permissive amine theory.
*Teuting et al
(1981) examined the urine of depressed patients and found chemicals that
suggest lowered levels of both serotonin and noradrenalin.
Mr Teuting speaking to the careers adviser at school. ‘And what would you
like to do when you grow up master Teuting?’ ‘I’d like to collect urine
samples’ comes the reply. ‘You’re taking the **ss!!!’ exclaims the
found higher than expected levels of noradrenalin in manic patients.
Bunney et al
(1972) reported fluctuating levels of noradrenalin in bipolar disorder
against the permissive amine theory
Graeff (1991) report that even following recovery from depression the
deficits in serotonin and noradrenalin levels still remain which questions
the cause and effect relationship assumed by the model.
evidence for the other models of depression can be used to question the
the permissive amine theory
are problems of cause and effect (as always). We cannot be certain that
fluctuating levels of noradrenalin are causing altered mood states. It
could be altered mood states causing the fluctuation or a third variable
that is causing both.
anti-depressives such as MAOIs (monoamine oxidase inhibitors) increase the
levels of noradrenalin and serotonin within minutes. However, they have
no effect on mood for many weeks suggesting that they are not working
simply by increasing the levels of chemical in the brain. Kennett (1999)
believes drugs like Prozac are causing structural changes within the brain
such as making neurons more sensitive to amines. This would explain the
all depressives show reduced levels of these chemicals and similarly not
all patients benefit from anti-depressives that work by increasing
is the issue of ‘treatment aetiology fallacy.’ Just because increasing
the level of a chemical solves a problem it doesn’t necessarily follow
that it was lack of that chemical that caused the problem in the first
place. MacLeod (1998) cites the example of aspirin curing headache as a
more obvious example. Although taking aspirin cures our headache we would
not assume that it was lack of aspirin that caused it in the first place!
reduces the symptoms of depression probably by increasing levels of serotonin.
But can we
be certain that it was lack of serotonin that led to the depression in the first
For a fuller
account of this theory see the back two pages borrowed and adapted from
the ‘find the light’ mental health support group website.
another family of biochemicals that we need to consider. These seem to be
implicated in disorders such as PMS, PMD and possibly SAD. They may also
help us explain why women are far more prone to depression. More on
gender differences later when we briefly consider other, more feminist,
al (1983) found that 43% of women report depressive symptoms at some point
in their menstrual cycle.
al (1982) reported that 41% of women admitted to a psychiatric hospital
were admitted either on the first day of their monthly cycle or the day
20% of women
report feelings of depression after the birth of a child. Normally this
occurs within a few days but typically only lasts for about a week or so.
It is still
unclear whether this is due to levels of oestrogen or progesterone or to
lowered levels of cortisol which make it difficult to cope with stress.
PPD appears to
be more common in women from families with a history of clinical
depression suggesting that there may be a family predisposition to mood
disorders of this kind.
already familiar with this from the work we did on biological rhythms.
When I say that it may be linked to melatonin production does that ring
any bells? If you recall we also mentioned that there is a close link
between melatonin and serotonin…you see it all starts to fall into place
by the time it’s almost too late!
common form of SAD is experienced in the winter and is associated with
falling light levels. In the summer light levels suppress melatonin
production and darkness stimulates its production which is a factor in the
onset of sleep.
It is thought
that lack of natural light in the winter months desynchronises our daily
fluctuations of melatonin which in turn will affect serotonin production.
Summer SAD is
not so easy to explain. Kay (1994) suggests that changes within the
Earth’s magnetic field may cause the alternation between winter and summer
SAD. At first glance this does sound unlikely but there is surprisingly
increasing evidence to support it. I’m not sure where you could tie this
in but I’ll include it for general interest and in the hope (rather than
the expectation) that a question on external factors of depression may
geomagnetic storms admissions to psychiatric wards for summer SAD increase
(1996) found that pregnant women and new mothers are 60% more likely to
suffer from depression if they live near power cables that also disrupt
local magnetic fields.
just the mention of that name… reported significantly higher
suicide rates (six times higher than expected) in 15 to 24 year olds
living in the Alaskan hinterland. He put this down to the aurora
borealis (or northern lights) that create changes within the Earth’s
magnetic field. I will leave you to hypothesise about other possible
causes of depression in young people living in a freezing cold climate in
the back end of nowhere!
explanations of depression
here! The usual collection of explanations based on some all too familiar
approaches to the subject. As always I think it’s a useful exercise to
spend a few minutes attempting to predict how each approach will seek to
explain a given topic… useful since not only will it boost your confidence
but also be good practice for the approaches section of the synoptic
As always with
the approaches there is a mixture of the good, the bad and the downright
ugly! Work out which is which for yourselves but as always keep opinions
on the paper as objective as possible and always be sure to back up
arguments with research!
Freud was the first to offer possible explanations of depression and was
also the first to notice the similarity in feelings reported by patients
suffering from depression and those who had recently suffered bereavement.
has a number of interconnecting strands. What follows is only a brief
overview of what he saw as a complex process:
Loss could be
‘actual,’ as in the case of death of a close friend or relative, or it
could be ‘symbolic’, as in the case of a lost job etc. Either way loss in
adulthood causes us to relive childhood experiences of loss explaining the
clingy behaviour of some types of bereavement. In extreme cases
regression to childhood may occur, particularly if the child had suffered
bereavement during their own childhood.
aggression are also involved. Death causes feelings of anger at our loss
and this has to be displaced inwards towards ourselves since outward
expression of anger at such a sensitive time would not be acceptable to
the superego. Anger directed towards ourselves causes the feelings of
guilt and despair associated with many forms of depression.
assumed that in most cases we would have had fallings out with the
deceased which would also cause guilt on their death.
Freud’s ideas that early loss can make us more susceptible to depression
in later life is mixed. At AS we looked at Bowlby’s work on maternal
deprivation and separation. Bowlby suggested that early separation or
loss can cause problems in forming later attachments (his so called
‘internal working model’). This inability to form loving relationships
later in life may result in depression. Others, such as Parker (1992)
have failed to find any link between early loss and later depression.
Freud’s ideas on the workings of the unconscious mind are impossible to
confirm one way or t’other.
offered an explanation of bipolar disorder. The depressed phase is due to
the Superego gaining overall control of personality and creating an
overwhelming feeling of guilt and unworthiness. Eventually the Ego
strikes back and is able to regain control of personality, but in so doing
swings the balance too far the other way producing the manic backlash.
This then leads to a further counter attack by the Superego producing
alternating mood swings.
Look back at
your notes on schizophrenia and eating disorders (year 12) and you will
notice the tendency for the cognitive model to treat the symptoms of a
disorder as being the causes, for example faulty or distorted thinking or
explanations of depression can broadly be split into two:
explanations that combine cognitive and behavioural approaches
explanations that adopt a purely cognitive approach
We’ll look at
the first category for starters:
It should come
as no surprise that these are combined; i. We have seen them used in this
way before and ii. They do complement each other nicely, one concentrating
on events outside the person and the other considering only events within
Maier (1967) carried out their classic study in which dogs were given
electric shocks to the feet. In the control condition the dogs could jump
a small barrier and escape the shocks, but in the experimental condition
the barrier was higher and the foot shocks were therefore inescapable.
In the follow
up trial dogs that could not escape in the first part of the study made no
attempt to escape the shocks even when they were given the opportunity.
Past experience had taught them that they had no control over outcomes, in
effect they had learned to be helpless!
noticed the similarity between learned helplessness and some of the
symptoms of human depression in which patients become passive and
accepting of their situation and make little or no attempt to resolve
their problems. This similarity was reinforced by findings that showed a
reduction in serotonin and noradrenalin levels in rats that had become
helpless in this way.
Would humans placed in a similar situation behave in a similar way?
Hiroto (1974) got participants to endure inescapable loud noise.
In a follow up trial when they were provided with a handle that would
turn the sound off they sat back and endured it.
theory however, did not provide a full picture. Not everyone becomes
helpless in these situations and Seligman was unable to explain the
culture of self-blame or blaming others for their predicament. For
example, many depressed patients blame themselves for their failings which
does not tie in with Seligman’s idea that they see themselves as
of feeling out of control in one particular situation is an experience
common to most people at some time but very rarely does it lead to
seen as a link between behaviourist and cognitive explanations.
al’s theory (1978) can be seen as a logical extension of learned
helplessness theory. They combined the theory with attribution theory.
Basically any kind of experience we have in life we try and account for
using attributions. However, according to this theory the depressed
patient faced with an experience of failure, attributes the failure in a
particular way according to three variables. We shall consider each using
the unfamiliar experience of examination failure as an example:
blames themselves. In the case of exams, I failed to put in the necessary
work or I wasn’t up to the task.
blames others or look for external excuse. We had a crap teacher or there
was too much noise in the exam hall.
The idea that
things will always be this bad and won’t get better in future. I just
can’t do exams!
improve. Next time I’ll be prepared and will succeed
will apply in all other situations. There’s no point in sitting other
exams because I’m no good at them.
applies only to this examination. Maths and psychology will be fine.
helplessness would equate to an internal, stable and global outlook. It’s
all my fault, it will always be like this and regardless of the
Metalsky et al
(1987) questioned students who had just failed a psychology exam. Those
found to have an internal, stable, global outlook were still suffering
mild depression two days later.
As always we
have the problem of chicken or egg (cause and effect). Does this
particular attribution lead to depression (as the theory implies) or does
negative attribution arise from a depressed state of mind? Peterson &
Seligman (1978) believe that it is causal and suggested that this
internal, stable, global outlook is present in people prone to depression
and acts to trigger depression in those suffering negative life events.
The cause of
this depressed attributional style is thought to arise in childhood. Rose
et al (1994) attributed it (that word again) to abuse, parents being
overly protective, harsh discipline within the family and to very high
expectations from parents. In fact very similar to some of the possible
triggers for anorexia.
Much of the
research has been done on laboratory experiments of students (as most
university based research is). This clearly raises questions about
generalisation and about the ecological validity of the research.
Much of the
research is questionnaire based (Peterson & Seligman’s Attributional style
questionnaire), with all the problems that arise because of this… demand
characteristics, fibs etc…
perspective would not be complete without schemas! Remember memory? (no
joke intended), Piaget etc?
involves unrealistically negative views about self, the world
and the future. According to Beck this negative outlook would have
originated in childhood, perhaps due to bereavement, overly critical
parents or teachers etc.
Beck believes that a depressed person has developed a negative set of
schemas (schemata) upon which their expectations about life are based.
For example they may have developed a self-blame schema which
makes them feel responsible for all the things in their life that go wrong
or an ineptness schema that causes them to expect failure every
schemas are caused by cognitive biases (faulty perceptions if you
like): Some examples of cognitive biases suggested by Neck:
an overall negative conclusion about all situations based on one, perhaps
trivial event. For example a bad test result in a maths lesson convinces
the person that they are stupid and should not be going to University!
interference: an assumption arising from no evidence at all. For example
you arrange a barbecue and it rains. Person assumes they are useless!
Beck these three types of cognition: views, schemas and biases interact
and in doing so reinforce each other eventually leading to clinical
The very kindly looking Mr. Aaron Beck.
plenty of evidence to suggest that Beck’s views on negative thinking do
apply to depressed people. However, we still have the issue of what
causes what. Davison & Neale (1998) believe that the process is two way.
Depression leads to negative thinking which in turn worsens the effects of
the depressed mood.
A number of
successful techniques have built up based on the cognitive approach such
as Ellis’ Rational Emotive Therapy (RET) which encourage patients to
recognise their negative thoughts and replace them with more realistic
outlooks. Cognitive Behaviour Therapies in general have proved to be
effective in treating a variety of disorders including depression, eating
disorders and anxiety disorders. This also provides indirect evidence for
the validity of the theory on which the therapies are based.
society, gender and depression
Perhaps not a
likely topic for an entire essay, this could certainly be questioned as a
six-marker warm up question!
far more widely reported in Western society. Is this due to its higher
prevalence, its wider diagnosis or differences in diagnosis in other
In the West we
associate depression mostly with lowered mood, although as we saw at the
outset there are distinct physical symptoms too. In Asian culture
depression is very rarely reported or diagnosed. However, the physical
symptoms that we associate with depression do appear to be common, namely
apathy, tiredness, lack of volition (no attempt to initiate actions or
interactions), loss of appetite etc. This unwillingness to report
psychological symptoms may be due to the stigma some societies associate
with illnesses of the mind and the discrimination that families may face
as a result.
The Hopi of North America have no word for ‘depression.’
Does this mean it doesn’t exist in their culture?
Perhaps the social support in their culture alleviates the worst effects
of stress and depression.
Or could it be that they only report the physical symptoms so suffer from
increased incidence of lethargy, tiredness etc.?
provide another explanation of the apparent rarity in Asian culture.
Extended families provide social support that we know can alleviate
problems that are stress related (recall your AS). Stress and depression
are known to be closely correlated.
other cultures refer to ‘depression.’ Just as a matter of general
‘Exhaustion of the nerves’ and ‘Hearts being weighed down.’
crawling in parts of my brain.’ (Anatomically closer than the
More likely to
be examined since it does shed some light on the possible causes of
Hargreaves (1995) reported that women are up to three times more likely to
suffer depression than men. One theory for this discrepancy is that in
fact men do suffer just as much depression as women but they fail to
report it. Some of it may be hidden behind other behaviours such as
alcohol or drug abuse or behind aggression. Research, however, suggests
that men who do suffer depression were just as likely to report it as
explanations for sex differences:
cycle that results in cyclical changes in the body’s hormones. We have
already seen that PMS and PPD are associated with such fluctuations.
increasingly likely as a cause of the sex difference. Diksic et al
(1997) found that men make 52% more serotonin than women, which
according to the medical model would make men far less prone to
depression than women. Smith, in the same year attributed some of this
difference to dieting, particularly in the teenage years. Low calorie
diets reduce the amount of the essential amino acid tryptophan.
Tryptophan is a vital ingredient in the production of serotonin. (Meat,
milk and eggs are the most common sources of tryptophan).
factors alone seem unlikely as an explanation of the huge sex difference
that exists. Other, non-biological factors have been implicated:
sexual abuse in early years is known to be a contributory factor to
later depression. Girls are far more prone to these kinds of abuse.
role. Jessie Bernard (1976) said that ‘being a housewife makes women
sick.’ Unlike men who seem to fair better in a relationship, women
(particularly in the housewife role) are far more likely to suffer from
depression than unmarried women. The housewife has little control in
her life which can lead to stress, (stress and depression closely linked
remember!). The feeling of lack of control may also contribute to
learned helplessness. Staying at home, looking after children can also
be isolating, cutting the woman off from her network of social support,
which would normally act as a buffer against stress. Cochrane (1983)
goes further, suggesting that depression may actually be a coping
strategy for what they see as an intolerable situation.
economic status: women generally are lower paid than men and far more
likely to claim state benefits (particularly single parents who are
predominantly women). Again poverty and lack of control is a major
factor in stress and again we have the link between stress and
links between culture and gender and depression are complex, but in both
cases stress and social support appear important.
Behaviourist explanations of depression
do with culture or sex differences but instead a very weak explanation
of depression in general.
(1974) believed that death of a person close to you reduces the amount
of positive reinforcement you receive (because they can no longer say
or do nice things). As a response to a loss the person may become
withdrawn and avoid social contact. This causes concern from those
around, in the form of increased attention, which seeks to reinforce
the withdrawn behaviour making it more likely.
Eventually, as the depression continues, the interest by others begins
to decline reducing positive reinforcement and furthering the
(1993) did report fewer pleasurable experiences however, yet again we
have issues of cause and effect. Unfortunately, as always, the
behaviourist explanation offers little insight into individual
differences, is very reductionist in that it seeks to explain complex
issues in overly simplistic ways and is unable to explain the
subjective feelings of low mood.
those who want to know more!
Neurotransmitters are chemical messengers within the brain that facilitate
communication between nerve cells.
illustrate with serotonin. Figure 1 depicts the junction between two
nerve cells. Packets of serotonin molecules are released from the end of
the presynaptic cell (the axon) into the space between the two nerve cells
(the synapse). These molecules may then be taken up by serotonin
receptors of the postsynaptic nerve cell (the dendrite) and thus pass
along their chemical message. Excess molecules are taken back up by the
presynaptic cell and reprocessed.
things might potentially go wrong with this process and lead to a
serotonin deficit. Just to enumerate a few possibilities:
enough serotonin is produced,
are not enough receptor sites to receive serotonin,
Serotonin is being taken back up too quickly before it can reach receptor
Chemical precursors to serotonin (molecules that serotonin is manufactured
from) may be in short supply, or
Molecules that facilitate the production of serotonin may be in too short
As you can
see, if there is a breakdown anywhere along the path, neurotransmitter
supplies may not be adequate for your brain's needs. Inadequate supplies
lead to the symptoms that we know as depression.
1960s Schildkraut cast his vote with noadrenaline as the causative factor
for depression in the now classic "catecholamine" hypothesis of mood
disorders. He proposed that depression stems from a deficiency of
noradrenaline in certain brain circuits and that mania arises from too
much of this substance. There is indeed a large body of evidence that
supports this hypothesis, however, changes in noradrenaline levels do not
affect mood in everyone.
there must be some other factor that interacts with noradrenaline to cause
depression. Serotonin has been found to be this other factor. Serious
investigations into serotonin's role in mood disorders, however, have been
going on for almost 30 years, ever since Prange et al put forward the
so-called "permissive amine hypothesis". This view held that synaptic
depletion of serotonin was another cause of depression, one that worked by
promoting, or "permitting," a fall in noradrenaline levels.
although, noradrenaline still played a major role in depression, serotonin
levels could altered to indirectly raise noradrenaline levels. Newer
antidepressants like Effexor are actually targeted at both serotonin and
noradrenaline. Tricyclics (TCAs) also affect both noradreanline and
serotonin, however, they have the added effect of influencing histamine
and acetylcholine, which produces the side-effects that TCAs are known
for, such as dry mouth or eyes, peculiar taste in mouth, sensitivity to
light of the eyes, blurry vision, constipation, urinary hesitancy, and
others. SSRIs (selective serotonin reuptake inhibitors) do not affect
histamine and acetylcholine and thus do not have the same side-effects as
the older medications.
Anxiety disorders: Phobias
asks for any one anxiety disorder. There are a number of these:
post traumatic stress disorder (PTSD), panic disorder and obsessive
compulsive disorder (OCD). The one we do is phobias! When the paper
asks for ‘any one anxiety disorder’ that is your cue to talk about
It seems odd
that fear of spiders is seen as a psychological disorder. About 14% of
the population suffer from one phobia or another and most of these do not
interfere with a person’s normal style of life. However, some such as
social phobia and most notably agoraphobia do prevent people from leading
life to the full.
The one that
many of us are familiar with. Specific phobias are an irrational fear of
a specific object, situation or creature. Most common are specific
phobias of certain animals such as spiders (arachnophobia), snakes (ophidiophobia),
but they may also include situations such as heights, thunderstorms,
enclosed spaces (claustrophobia) and aerophobia (flying, not the fear of
chocolate with lots of holes!). Particularly common are those involving
blood and injections.
(diagnostic and statistical manual) that is used to categorise and define
mental illness describes the following characteristics:
fear of a specific object or situation
that the fear is irrational and excessive
to avoid the phobia inducing situation
interferes with the person’s life
an undue concern about your own behaviour and particularly the reaction of
others to your behaviour:
social phobia involves the person being shy in most social situations
social phobia involves shyness being triggered by certain social
situations such as public speaking.
Characteristics are very similar to specific phobias only related to
suffering social phobia is afraid that others will see them being
frightened or embarrassed, for example blushing or shaking. There are
well documented cases of people avoiding shops because they may have to
pay by credit card and are frightened that others will see their hand
On the face of
it this appears similar to social phobia in that both involve fear of
social situations. However, it is different in that agoraphobia involves
the fear of panic attack. The DSM-IV actually classes the disorder as
‘panic disorder with agoraphobia.’ Usually the fear is triggered by one
or a series of panic attacks in a public place. Symptoms include
sweating, very rapid increased heart rate leaving people fearful for their
lives and intense fear. In future this leaves people afraid to go out in
case the attack occurs again in front of others. Many agoraphobics are
confined to their houses for years.
be no surprises here! Just a re-working of the oh so familiar approaches!
Medical or biological model
noses) tend to run in families, for example if a person has blood and
injection phobia then there is a 64% chance that some other person in the
family will suffer the same. This compares to an incidence of about 4% in
the general population.
(1983) reported the following concordance rates for agoraphobia:
MZ twins: 31%
DZ twins: 0%
are the usual cases of nature or nurture! To what extent has the phobia
been inherited and to what extent learned? Clearly, sharing a house with
a mother that screams whenever she sees a spider may is likely to instil a
fear of spiders in her offspring.
are more easily aroused than others (tell me about it!). Since arousal is
controlled by activity in the sympathetic branch of the ANS it could be
that there is a biological predisposition to phobias. Lader & Mathews
(1968) did find that agoraphobics and social phobes have a higher level of
could be tied in with the genetic argument since a higher state of
physical arousal like this is probably inherited.
Biological preparedness (Seligman 1971)
A little bit
different to the usual medical explanations, this one takes an
evolutionary stance. Basically it suggests that it could be an
evolutionary advantage to have certain phobias meaning that we are more
likely to develop some phobias than others. Clearly being frightened of
snakes and spiders could help prolong our lives by ensuring that we stay
well clear of them!
Ohman et al
(1975) used classical conditioning to induce a fear of either snakes and
spiders or houses and flowers. They did this in the time honoured way of
pairing the stimulus with electric shocks (like my number 3). After a
shock-free period the fear for houses and flowers extinguished (died out)
very quickly, whereas the fear of snakes and spiders persisted. This
suggests that we may be predisposed to acquire phobias to situations or
objects that are life-threatening.
ease with which we acquire phobias of spiders and snakes could just as
well be explained by social conditioning. From an early age we are made
aware of the dangers of such creatures through stories, books and films
and simply by being warned.
At first this
seems out of place in a biological explanation. However social phobia may
be caused by the personality characteristic of excessive shyness or
introversion. Perhaps we inherit the personality type that then makes it
more likely that we will become a social phobic. The extent to which
personalities are determined by genes and environment is hotly debated!
medical model does not offer a very convincing explanation of phobias.
Many of their arguments can just as easily be explained using the
Psychological explanations of phobias
Have a guess!
The specific case of Little Hans is classic Freudian thinking and we’ll
consider that in a few moments. First let’s consider the broader picture:
between the id and the ego causes anxiety. The id is the source of your
selfish urges. These can be a source of anguish, embarrassment and stress
so they tend to be repressed into the unconscious mind by one of a variety
of defence mechanisms… stop me if this is not making sense.
One of the
defence mechanisms (check your list in ‘approaches’), is displacement.
Anxiety caused by an object may be displaced onto something else. A
classic case would be a woman’s fear of the male genitalia being displaced
onto snakes or perhaps neck ties.
was based on his case study of Little Hans which you should all know
backwards (it would probably make more sense that way). Briefly: Hans’
father was a friend of Freud who was concerned about Hans’ fear of
concluded that this had come about because of an unresolved Oedipus
complex. During the Phallic stage of development little boys develop an
unconscious desire of their mother and become fearful that the father will
find out. This fear is caused by castration anxiety, the worry that the
father will chop off their ‘wedding tackle.’
In the case of
Little Hans his unacceptable fear of his father had been displaced onto
horses who bore some striking resemblances to his father (not to be
quoted). Hans’ father wore glasses (similar to a horse’s blinkers), he
had a moustache (similar to a horse’s reigns) and he’d been ridden to
victory in the previous year’s Cheltenham Gold Cup (no not really!). Oh
yes and Hans used to ride on his dad’s back and his dad had once told him
to ‘trot away.’
To be fair
Hans did seem overly fascinated with his ‘widdler’ but what little boy
here. Some of Freud’s ideas are still well respected and many of his
theories were ground breaking, but to be fair this probably isn’t one of
his finer moments. There appears to be a far more logical explanation of
Hans’ fear as postulated by the behaviourists.
sheds a different light on this particular case. He believes that the
fear was not of the father but instead provides evidence for the fear
being of the mother. On catching Hans playing with his ‘widdler’ (or ‘wi-wi-maker),
his mother had threatened to take him to the doctors to have it chopped
off! It was also his mother who on a number of occasions had threatened
to leave Hans.
clearly other explanations for Hans’ fear of horses which we shall come to
with the behaviourist model. But for purposes of evaluation it would also
be worth mentioning that there appears to be some association of horses
and other events (behaviourist approach). Shortly before Hans’ problems
started, his friend Lizzi had gone away and not returned. Her luggage was
taken to the train station by a white horse, so we have an unhappy
association with horses. Similarly Hans’ condition appeared to worsen
after his tonsillectomy. Slap (not slap-head!) 1961, says that the fear
of a surgeon in a long white coat also became added to his fear of his
moustached father (again association), the white coat may have reminded
him of white horses.
reality! Obviously the stimulus-response lot are going to argue that
phobias are learned and provide plenty of evidence and treatments to back
up their claim.
briefly to Hans. We know that Hans had witnessed a horse falling over in
the street and being pinned down by the cart it was pulling. Clearly this
would have been distressing and frightening so an obvious explanation (for
the behaviourists) is an association between horses and fear
Just as Freud
has Little Hans, the behaviourists have their Little Albert!
Raynor (1920) classically condition a fear of white rats in an 11 month
old boy, Albert. Over a period of weeks each time he plays with a toy
white rat an iron bar is struck. At first this causes hesitation when
dealing with the rat and eventually after 10 days or so (the third trial)
he becomes distressed when the rat is seen. Worth mentioning is that the
fear was immediately generalised to a toy white rabbit (sufficiently
similar in appearance to the rat to illicit the response) whereas fear of
cotton wool and of a toy dog was not so pronounced (evidence of
ethics of the study can be questioned. Watson & Raynor were both doctors
so would have been aware of the long term effects their procedure may have
had. It is clear when reading their report that they did consider the
consequences in advance but went ahead on the grounds that this was no
more distressing than the experiences he was likely to encounter in the
It had been
their intention to treat Albert’s condition with a number of experimental
techniques, including reconditioning in which he would have been given
‘candy’ each time the rat was presented. His mother removed Albert from
the experiment before this could be done.
Conditioned, unconditioned and neutral stimuli (a brief explanation)
purposes of this explanation think of ‘conditioned’ as learned and
‘unconditioned’ as already present.
stimulus: the loud noise
outset this produces the
response: the fear reaction
unconditioned stimulus is paired with the
stimulus: white rat
after training the neutral stimulus becomes associated with the
conditioned response and now becomes the
stimulus: white rat (after training)
And this alone
can now elicit the
response: fear of white rat
situation or object that causes anxiety or fear is seen by behaviourists
as being rewarding in itself. If you suffer from arachnophobia then
avoiding spiders will result in you suffering less anxiety. As a result
you will behave in a way that keeps you clear of spiders. Unfortunately
this means that your fear will not be extinguished since the only way to
lose a behaviour, in behaviourist terms, is by unlearning the association
between fear and the stimulus that causes it.
sound familiar since we covered in year 12 with eating disorders. Mowrer
believed that both classical and operant conditioning are involved in
acquisition and maintenance of phobias.
As we have
seen with Little Albert and other studies, we initially learn fear by
association. Classical conditioning therefore explains how we acquire
fear-provoking stimulus then prevents us from unlearning the fear so as a
result the fear is not extinguished. Operant conditioning therefore
explains why a phobia is maintained.
a young age you’re out on a picnic with mum. A spider crawls over her
hand, she screams and this frightens you. You have learned to associate
spiders with being frightened.
this fear what you really need to do is relearn and associate spiders with
things pleasant. But this means having to encounter spiders. Instead
what you do is avoid them since this is reinforcing because it prevents
anxiety. As a result you remain frightened of spiders. Only when you
confront the fear and take positive steps to overcome it will you lose the
There is some
evidence to support the theory, particularly the case of Little Albert who
clearly did acquire a phobia via classical conditioning and who did
generalise it, as predicted by behaviourists, to similar objects such as
rabbits. Some successful treatments for phobias are based on behaviourist
Durand (1995) report that 50% of people with a phobia for driving could
remember a specific incident that had triggered the fear… again supporting
the theory that phobias are learned following some incident or incidents.
Mineka et al
(1984) provided evidence for the SLT or modelling approach when they
taught monkeys to fear snakes by getting them to watch video footage of
other monkeys being frightened of snakes!
50% of people with phobias cannot recall a specific event that triggered
DiNardo et al
(1988) reported that only about half of all people that have had
frightening experiences of dogs go on to develop a phobia of dogs.
Behaviourists are unable to explain this sort of individual difference
using stimulus response theory.
worth making: the behaviourist theory is unreliable since much of the
research is retrospective, relying as it does, on people thinking back to
early childhood experiences. As always the theory is reductionist
(explains a complex behaviour in very simple terms) and ignores biological
or genetic factors. It is unable to explain why it is easier to become
afraid of some things (snakes, spiders) than others such as flowers and
phobias in terms of cognitive biases that exaggerate the threat being
Tomarken et al
(1989) took participants that were frightened of snakes and/or spiders and
compared them to people not afraid of these creatures. They would show
them slides of snakes, spiders and non-fear provoking creatures. After
each slide there would either be a tone, silence or an electric shock.
The participants with phobias drastically overestimated the number of
times the snake, spider etc. would be followed by an electric shock.
have shown that phobics over-estimate the threat being posed. For example
they see spiders in a jar trying to jump towards them or over estimate the
size of the creature. People frightened of spiders, cockroaches etc.
often perceive that these creatures always run towards them when
and agoraphobia is explained in terms of the patient over-estimating the
threat from their bodily arousal. An increase in heart rate is seen as
potentially life threatening leading to even greater increase and
The theory is
descriptive but lacks explanatory power. It is able to describe the
symptoms of phobias but unable to explain how these have come about. Why
do some people over-estimate the threat from one particular creature and
happens with the cognitive theory of abnormal behaviour it is almost
impossible to separate out cause and effect since it treats symptoms and
causes as being alike. Does the warped perception cause the disorder or
does the disorder lead to an over-estimate of the threat?
of the behaviourist and cognitive could also be considered. We learn
phobias but because of the different ways in which different perceives the
world, some people are more likely to develop fears than others. Compare
this to the behaviourist-cognitive theories of eating disorders and
inherited, biologically prepared, learned, displacements of other fears or
caused by cognitive bias?
is synoptic so in your answers assume and create arguments for all of
Phobias is a
relatively short topic,
so nothing to be afraid of!