The different affective disorders include major depressive illness
(clinical depression) and mania, minor depressive states, and mood disorders
associated with childbirth. The most prevalent of the affective disorders is
depression, which refers to both a mood and a psychopathological syndrome. Large
random population surveys commonly report that between 10-15 per cent of adults
describe themselves as currently feeling at least somewhat depressed
but a if the label depression includes only severe emotional disturbances,
the number of cases decreases dramatically, but even major depression is relatively
common, affecting 15% of people at some time in their life. (Charney and Weismann,
1988). During the 1980s depression accounted for about one-quarter of all psychiatric
hospital admissions in the UK. (Department of Health, 1990).
Seasonal affective disorder
is the experience of a mild winter blue is now recognised by the
DSM. The symptoms associated with this condition include low mood, extreme lethargy
and sleepiness, and an increased appetite for food. Women are especially vulnerable,
the ratio of women to men diagnosed as suffering from SAD being in the region
of 4:1. One aetiological hypothesis suggests that the seasonal depression is
owing to high levels of the hormone melatonin,
which is secreted by the pineal gland. Environmental light suppresses the secretion
of the hormone, but in the winter, the level of natural light is low and the
level of melatonin then build op, leading to drowsiness and lethargy (Rosenthal
et al. 1984). The light-deprivation hypothesis is supported by the fact that
most people diagnosed as suffering from SAD show a substantial improvement after
several days of light therapy in which they remain for a number
of hours each day in artificial daylight. In some cases this seem to restore
the persons energy and to bring about a significant increase in emotional
well-being. When the light therapy is stopped, there may be a sudden relapse.
(Lewy et al. 1987) Travels to places with more light have tends to lift the
depression, whereas travels to places with less light tends to deepen the depression.
(Rosenthal et al. 1986)
Clinical depression: Unipolar disorder and bipolar disorder
Unipolar
disorder is defined by depression alone, whereas bipolar
disorder is defined as depression alternating with mania. The bipolar disorder
was formerly labelled manic-depressive disorder. The depression
found here is indistinguishable from that found in cases of unipolar depression.
The distinction between unipolar and bipolar forms of affective disorder therefore
rests on the occurrence or non-occurrence of manic episodes. In the bipolar
disorder, depressed and manic states may follow one another immediately, or
they may be separated by periods of normal functioning.
Bipolar disorder:
symptoms
In the bipolar disorder, depressed and manic states may follow one another immediately, or they may be separated by periods of normal functioning. Symptoms are the same as for mania and unipolar depression.
Symptoms of unipolar disorder:
Mania is a highly agitated state of mind, often experienced by the individual as euphoria. It is accompanied by hyperactivity, verbosity, and sleeplessness. In many respects, the symptoms of mania are the reverse of those associated with depression. The manic person may display elevated self-confidence, may lack sense of guilt and responsibility, and may find it difficult to stop laughing and giggling. Other symptoms, including delusions and disturbances in sleep patterns, overlap with those of depression, although they usually take very different forms in the two affective states. It is rare for someone to experience manic episodes without also experiencing alternating depressive episodes, but cases of pure mania do occur. In practice cases like this may be labelled unipolar mania, but the term used in the DSM system is all the same bipolar affective disorder on the grounds that there is little difference between cases of persistent mania and those of alternating state disorder in terms of their course and treatment.
Mania symptoms
Aetiology: Causes of depression
The aetiological subclassification differentiates cases in which
depression is a response to an environmental event (exogenous/reactive depression)
and those in which the disorder is not associated with such an event, and is
therefore assumed to result from internal (perhaps biological) processes (endogenous
depression). It is now accepted that in the majority of cases both endogenous
and exogenous factors play a significant aetiological role.
Many people who are depressed are physically run-down, perform poorly on cognitive
tasks, are pessimistic and have relationship problems. It is very often difficult
to distinguish between the causes of the depression and the effects of the disorder.
A depression that has arisen primarily as a reaction to life circumstances may
produce physiological changes, which serve to maintain the depression. The existence
of such causal relationships between biological and environmental factors reinforces
the view that it is often inappropriate to try to make a sharp differentiation
between endogenous and exogenous depression.
Whereas some cases appear to be primarily biological in origin, others appear
to be triggered by an adverse social or environmental change. In the majority
of cases, however, the development and course of the disorder will reflect complex
interactions between several biological and psychological factors. There is
now clear evidence that changes in the level of certain key neurochemicals can
precipitate a depressive episode, and it is equally clear that many cases of
clinical depression are triggered by negative events in the persons life.
Family bereavement, divorce, an accident and redundancy from work, for example,
all render the individual susceptible to clinical depression. In other cases
the depression appears to be a response not to a particular event but to long-term
circumstances, which are a continuing source of stress and disappointment.
Despite the general association between stress and depression, many people who
are subjected to high stress do not develop a depressive disorder. There are
important individual differences in vulnerability, and the risk of becoming
depressed is related to a number of biological factors, to the individuals
personality and early history, to cognitive style and coping skills and to the
level of available social support.
Biological accounts of depression (aetiology)
The genetic theory
This theory argues that genes are involved
in the cause of depression and one of the main ways to investigate this is twin
studies. Nurnberger and Gershon (1982) reviewed the results of 7 twin
studies and found that the concordance rate for unipolar depression was consistently
higher for MZ twins than for DZ twins, thus supporting the hypothesis that genetic
factors might predispose people to depression. Across the seven studies reviewed,
the average concordance rate for MZ twins was 65 %, whereas for DZ twins it
was 14 %. evaluation: The fact that the concordance rate for MZ twins is far
below 100 % indicates that depression is not genetically pre-programmed.
The evidence from the genetic studies does nothing to contradict the view that
environmental events and acquired psychological characteristics play a crucial
role.
Biochemical theories
Much of the current research interest focuses on the idea that depression is
caused by a deficiency in certain neurotransmitters, where high levels of neurotransmitter
substances lead to the symptoms of mania. Particular attention is now focused
on noradrenaline and serotonin. Low levels of these substances
could account for many of the symptoms commonly associated with depression.
Brain functioning is profoundly affected by neurochemical changes, and a number
of animal studies have shown that intense stress reduces levels of noradrenaline.
Evidence could also be that drugs known to decrease the level of noradrenaline
tend to produce depression in people.
Janowsky et al. (1972) demonstrated that experimental subjects within
minutes after having taken a drug called physostigmine became profoundly
depressed and experienced feelings of self-hate and suicidal wishes. The fact
that a depressed mood can be artificially induced by certain drugs suggests
that some cases of natural depression might stem from a disturbance
in the normal metabolic processes. Furthermore, drugs that increase the available
noradrenaline tend to be effective in reducing the symptoms of depression. Such
anti-depressants are monoamine oxidase inhibitors and the tricyclics.
The diathesis-stress model
This model is also called the stress-diathesis model and is a development towards
an interactionist model of explaining dysfunctional behaviour and it can be
a useful tool for integrating the evidence. Factors that appear to affect vulnerability
to depression include biological predisposing factors, cognitive style, personality
characteristics, and personal history. The stressors which precipitate depression
may be rather specific.
Psychological theories of depression (aetiology)
Psychodynamic
Freud suggested that adult vulnerability to depression has its roots
in early childhood experiences, and most especially in early experiences of
real or imagined loss. The idea that childhood experiences of separation and
loss may leave a lifetime vulnerability to sadness, anger and anxiety has remained
influential. In his theory of attachment, for example, John Bowlby 1980
places great emphasis on the relevance of loss and rejection in the early years
(The attachment Theory). Beck (1967) found support for the theory of
loss when he assessed depression in a mixed group of 300 psychiatric patients
and found that 27% of those who were highly depressed had lost a parent before
the age of 16, and a similar loss had occurred for only 12% of those who were
not significantly depressed. Brown and Harris (1978) Childhood loss was
found to be an important vulnerability factor in a study concerning the social
origins of depression in women. The researchers found that 29 out of 32 women
who became depressed had experienced a severe event but 78 percent of those
who did experience a severe event did NOT become depressed. He also found that
events that matched prior difficulties were more likely to lead to depression
and that events that matched prior commitments also more likely to lead to depression.
On the basis of this Brown suggested a Vulnerability model
with the following factors involved that would increase the likelyhood of depression
in that 1 out of 5 women who had reported a similar severe event had become
depressed. However, vulnerability factors are assumed to increase the probability
of depression only if a woman had experienced one of these severe life events:
Behaviourist and behaviourist-cognitive
approaches
Skinner (1953). Behaviours which are
not positively reinforced (by food, money, social attention etc) tend to disappear
form the persons behaviour repertoire and said to be extinguished. He
suggested that the behavioural pattern found in depression might be the result
of the extinction of positive reinforcement.
Lewinshohn (1974) Later conditioning
models of depression placed a special emphasis on the roles played by self-reinforcement
and social reinforcement. Social reinforcement may lift the recipients
mood, making the person feel valued and respected, and those who lack such reinforcements
are liable to feel ignored and unloved. Withdrawal from social contact (negative
reinforcement) will further reduce the opportunity for receiving social reinforcement,
and the vicious circle might therefore develop.
Other learning theory explanations suggest
that depression is maintained because of positive reinforcement (the person
only gets attention when being depressed).
Seligman (1975) Learned helplessness theory. People are likely to give up trying to exert influence on the physical and social environment when they find that important aspects of their lives are uncontrollable. When people feel helpless, they are likely to be drained of motivation
Cognitive psychology
It has long been recognised that people who feel depressed tend to think depressed thoughts. It is commonly assumed that the depressed mood is primary, and somehow leads to the cognitive symptoms. Cognitive theories of depression, however, suggests that depressed cognitions are primary and produce the disturbances of mood. The revised learned helplessness model is one of several cognitive models of depression and it emphasises the importance of the perceived uncontrollability of events. Other cognitive models emphasise the role of cognitive distortions and irrational beliefs.
Albert Ellis (1962)Cognitive style theory suggests that psychological
disturbances often come from irrational and illogical thinking. On the basis
of dubious evidence or faulty inferences about the meaning of an event, people
may draw false conclusions, which then lead to feelings of anger, anxiety or
depression. Ellis contends that irrational beliefs (such as I must be
competent in everything I do) together with certain observations (I
have not performed well on this task), can easily lead to disheartening
conclusions (Therefore I am stupid and worthless).
Rational-emotive behaviour therapy (RET). Ellis believed that the emotionally damaging consequences of illogical internalised statements led him to develop a particular approach to therapy (rational-emotive therapy, recently renamed rational-emotive behaviour therapy. Clients are taught to distinguish between rational and irrational beliefs, and to avoid continual negative, unrealistic, illogical self-defeating thoughts and self-statements.
Research evidence that confirms a close association between negative cognitions and depression:
According to Beck, negative cognitive schemata are activated by stressful events and the person over-reacts. In a way, it has to do with the way a person appraises situations, i.e. the attributional style. A person may have negative expectations about the future and may have a tendency to explain these in terms of internal, stable and global factors. The depression may be maintained in a vicious circle. The model has been criticized for claiming that the cognitive triad is a stable trait that develops with depression. However, research has shown that attributions fluctuate with mood. Beck sidesteps this problem by saying that the schemas are latent, but this is not an adequate solution. Furthermore, according to some, Beck has no explanation of how the schemas are activated in the first place, but Beck does in fact agree with Seligman that there are usually one or more precipitating events which triggers the development of depression. However, Beck posits that it is these negative life events in combination with a person's vulnerability factor, which determines whether he or she will develop depression. Those people who have a low level of vulnerability may experience stressful life events but may not become depressed; however, if someone with a high vulnerability to depression were to experience the same events, he or she may be more likely to develop depression.
A number of studies have supported Becks hypothesis. Joiner et al (1999)
measured college students dysfunctional attitudes, depressive and anxious
cognitions, and depressive symptoms before and after midterm exams. They found
that students who had high levels of dysfunctional attitudes and received poor
grades on the exams but were not highly vulnerable did not increase in depressive
symptoms. The study indicates that attitudes or vulnerability level play an
interactive role in determining whether negative life events result in depression.
However, the sample were college students (biased) so generalisations may be
problematic.
Cross-cultural issues concerning depression
An international study sponsored by WHO points at a common foundation of depressive experience in very different cultural settings. WHO (1983) identified common elements in four different countries: Iran, Japan, Canada and Switzerland. The symptoms were sad affect, loss of enjoyment, anxiety, tension, lack of energy, loss of interest, inability to concentrate, and ideas of insufficiency, inadequacy and worthlessness. These findings are compatible with an earlier study by psychiatrists covering 30 countries Murphy, Wittkower and Chance (1967). This study also found loss of sexual interest, loss of appetite, weight reduction, fatigue, self-accusatory ideas but it did not come up with a clear-cut pattern of universals.
Prince 1968. Earlier reports claimed that there was no depression in Africa and various regions of Asia, but this study found that rates of reported depression rise with Westernisation in the former colonial countries. Depression in non-modernised settings tend to be expressed differently and may escape the attention of a person who is of another culture (Diop, 1967). The negetative symptoms of depression (loss of appetite, insomnia, inability to experience sexual pleasure, fatigue etc.) are present but in most non-Western cultures the experience of guilt is mostly absent
Kleinman (1982) showed that in China somatization served as a typical channel of expression and as a basic component of depressive experience. (somatization=reporting of psychological problems in terms of bodily symptoms such as headaches, back problems etc.) . The Chinese rarely complain of feeling sad or depressed, rather they refer in these communications to the body as the medium of their distress.
De Hoyos and De Hoyos (1965) also showed that middle-class clinicians had problems recognising depression in their Black clients but they were quick to diagnose schizophrenia because of strange behaviour (which they did not know of or understand).
Evaluation: Cross-cultural research has demonstrated that the two most
serious psychological disorders exist in all regions of the world and in very
different cultures. There is a virtually identical core of symptoms present
in both depression and schizophrenia at widely different sites and diverse cultures.
However, around this core, there are manifestations that can be meaningfully
traced to the characteristics of the milieus in which they occur. These conclusions
do not support the extreme positions of universalism and cultural relativism
because schizophrenia and depression are not exactly the same the world over.
Each culture does not create its own distinct patterns of abnormal behaviour,
and the clinician working with a culturally diverse clientele is to combine
personal sensitivity with cross-cultural competence and to develop the ability
to adapt quickly and realistically to new and different cultural settings.
Depression and gender- a controversial issue:
This deals both with the issue of prevalence
(Is it actually true there is a higher rate of women than men who are diagnosed
with depression?), the problem of reliability of diagnosis (are the women diagnosed
as depressive actually suffering from depression or are there other problems
at stake?), and gender stereotyping (also including reliability) (will the doctor
be more likely to diagnose a woman as depressed?) In GB a woman is about 40%
more likely to be admitted to a psychiatric hospital than a man. Rates of hospitalisation
rise rapidly among the elderly, and women outnumber men by 2:1. Depression contributes
most to the high overall rate of treated mental illness among women (Cochrane,
1992). Women are 2-3 times more likely to become clinically depressed than men
(Williams and Hargreaves, 1995), and they are more likely to experience several
episodes of depression.
Are women naturally disposed towards depression?
It is a widely held belief that women are naturally
more emotional than men and therefore more vulnerable to emotional upsets because
of hormonal fluctuations etc. Williams and Hargreaves (1995) argue that
hormonal changes of the menstrual cycle may have an effect in change of mood
even though it cannot be said to directly cause depression. Callaghan and
OCarrol (1993) argue that there is some evidence that one in ten women
experience post-partum depression but no specific hormonal abnormality has been
identified and it is believed that social factors may be important to (adjustment
to mother role etc.). Hormonal changes cannot explain discrepancy in female/male
rates of depression. If women who have just become mothers are compared to a
sample of non-pregnant women of the same age, depression rates are similar (Cooper
et al, 1988). Cochrane (1995) claims there is no evidence that physiological
changes affect psychological functioning. Cochrane identifies a number of non-biological
explanations of womens greater susceptibility to depression:
Empirical research on gender and depression.
Key study: Brown and Harris (1978) Social
origins of depression theory
Many of the aetiological models discussed above, including the psychoanalytic model and the reinforcement model, assign an important role to interpersonal relationships. Several other models focus more specifically on the role of personal relationships in the development and maintenance of depression. Some suggest that problems in childhood may leave an individual particularly vulnerable to depression. In this way these theories address the diathesis element of the diathesis-stress model. But many relationship theories also focus on the stress element and suggest that relationship problems (especially those involving loss, loneliness and conflict) often precipitate the onset of a depressive disorder.
An impressive and highly influential study of social origins of depression was
done by Brown and Harris in their book The Social Origins of Depression (1978).
They examined the relationship between social factors and depression in a group
of women from Camberwell in London. They studied women who had received hospital
treatment for depression and women who had visited their physician seeking help
for depression. They also studied a general population sample of 458 women aged
between 18 and 65 years.
Important: The study found that stressful events often preceded the onset
of depression and that it was actually these events that triggered the depression
rather than simply bringing forward the onset of a disorder already developing.
The critical importance of severe life events and longstanding severe
difficulties in the aetiology of depression has been confirmed by the
results of nine subsequent studied which have attempted to replicate the original
research of Brown and Harris. These studies show that, on average, 82% of those
who become depressed have recently experienced at least one severe life event
or major difficulty, compared to only 33% of those in non-depressed comparison
groups. (Brown and Harris, 1989). The original Brown and Harris study found
evidence of a pronounced social class effect, at least for married women. Here
are listed some of the other findings in the study:
Evaluation: This study and others
following the same line have established that social stress plays a decisive
role in triggering many depressive episodes, but it has also demonstrated the
fact that social factors may increase an individuals vulnerability to
depression. It also confirms that social support may offer protection against
the effects of potentially stressful events. The work described here focuses
on objective social events and lifestyle characteristics, but it is also clear
that the affective impact of life events is mediated by cognitions (including
the persons evaluation of events) and how the individual try to cope with
stress. The cognitive account may help to explain how various vulnerability
factors actually operate to increase the risk of depression. Thus the early
loss of a mother might engender a general pessimism, so that a stressful event
occurring later in life will be perceived as highly threatening. The focus on
a diathesis is important.
Efficiency of therapy in depression
Elkin et al,
1989 One of the best-controlled comparative studies was conducted by the National
Institutes of Mental Health. This study included 28 clinicians who worked with
280 patients diagnosed as having major depression. Individuals were randomly
assigned to treatment using either an antidepressant drug (imipramine), psychodynamic
therapy (not psychoanalysis) or cognitive therapy. In addition, a control group
was given a placebo pill, together with weekly therapy sessions. The placebo/drug
group was conducted as a double-blind design, so that neither the patient nor
the doctor knew which was which. All individual were assessed at the start,
after 1 weeks of treatment, and after 18 months. The results do not point at
a clear-cut result. All three types of treatment produced better improvement
than did the placebo, drug therapy gave faster improvements than did insight
therapies, but also had higher rates of relapse of symptoms. In the placebo
group, some of the individuals with only moderate showed some improvements.