1 Nandini Pandey

INTRODUCTION

Most of us get depressed from time to time, failing in an exam, not getting into one’s first
choice of college, breaking up with a romantic partner, not getting a suitable job, etc., are all
examples of events that can precipitate a depressed mood in many people, however, mood
disorders involve much more severe alterations in mood and for much longer periods of
time. In such cases, the disturbances of mood are intense and persistent enough to be clearly
maladaptive and often lead to serious problems in relationships and work performance.

☆ Broadly speaking, the emotions can be described as of two main types

1. Affect-which is a short-lived emotional response to an idea or an event

2. Mood-which is a sustained and pervasive emotional response which colors the
whole psychic life.

☆ The two key moods involved in mood disorders are

1. MANIA- often characterised by intense and unrealistic feelings of excitement and

euphoria 2. DEPRESSION-which usually involves feelings of extra-ordinary
sadness and dejection.

Some people experience both of these kinds of moods at one time or another (both manic
and depressive episodes-bipolar disorders) and other people experience only depression
(only depressive episodes-unipolar disorders). This distinction is prominent in DSM-IV TR
and although, the unipolar and bipolar forms of mood disorder may not be wholly separate
and distinct, there are notable differences in symptoms, causal factors and treatment. It is
also important to differentiate mood disorders in terms of

☆-Severity- the no. of dysfunctions experienced and relative degree of impairment

evidenced in those areas.

☆-Duration- whether the disorder is acute, chronic and intermittent (with periods of
relatively normal functioning between the episodes of disorder)

OPTIONAL ((According to ICD-10, the mood disorders are classified as follows

1. Manic episode
2. Depressive episode
3. Bipolar mood disorder
4. Recurrent depressive disorder
5. Persistent mood disorder (including cyclothymia and dysthymia)
6. Other mood disorders ( mixed affective episode and recurrent brief depressive disorder)

Recurrent depressive disorder- This disorder is characterised by (at least 2) depressive

episodes (unipolar depression)
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Persistent mood disorder- These disorders are characterised by persistent mood

symptoms which last for more than 2 years (one year in children and adolescents) but
are not severe enough to be labelled as even hypomanic (symptoms listed are the same
for manic and hypomanic episodes, there is much less impairment in social and
occupational functioning in hypomania and hospitalisation is not required) or mild
depressive episode. If the symptoms consist of persistent mild depression, the disorder
is called as dysthymia (neurotic depression);
and if symptoms consist of persistent instability of mood between mild depression
and mild elation, the disorder is called as cyclothymia.

Other mood disorders- This category includes the diagnosis of mixed affective episode. In
this type, the full clinical picture of depression and mania is present (for at least one
week) either at the same time, intermixed, or alternates rapidly with each other (rapid
cycling) without a normal intervening period of euthymia. The person experiences
rapidly alternating moods such as sadness, euphoria, and irritability- all within the same
episode of illness.))

☆ According to DSM 4 TR, the mood disorders are classified as follows

1. UNIPOLAR DISORDERS- Dysthymia, adjustment disorder with depressed

mood, major depressive disorder
2. BIPOLAR DISORDERS- Bipolar I disorder and Bipolar II disorder

• Adjustment disorder with depressive mood- Basically, this disorder is behaviourally

indistinguishable. It differs in that it does not exceed six months in duration and it requires the
existence of an identifiable (presumably precipitating) psycho-social stressor in the client’s
life within 3 months with the onset of clinical depression. The justification for making a
clinical diagnosis is that the observed stressor would not normally be considered severe
enough to account for the client’s depression. There is a difficulty here because assessing the
severity of a stressor is a highly subjective matter. Also, the diagnosis assumes that the
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person’s problems will remit when the stressor ceases or when a new level of adjustment is
achieved.

•Bipolar I Disorder-characterised by episodes of severe mania and severe depression (at

least one episode of mania or a mixed episode)

•Bipolar II Disorder-characterised by episodes of hypomania (not requiring

hospitalisation) and severe depression.
Even though a patient may be exhibiting only manic symptoms, it is assumed that a bipolar
disorder exists and that a depressive episode will eventually occur. Although, some
researchers have noted the probable existence of a unipolar type of manic disorder (Kessler
et al., 1997, Solomon, Leon et al., 2003). Critics of this diagnosis argue that such patients
usually have bipolar relatives and may well have had mild depression that went
unrecognised (Winokur and Tsuang, 1996).

Diagnosing Unipolar or Bipolar disorder first requires diagnosing what kind of mood
episode the person presents with. The most common form of mood episode that people
present with is a major depressive episode.

(UNIPOLAR – ONLY DEPRESSION; BIPOLAR- BOTH

DEPRESSION AND MANIA) The diagnostic criteria for major
depressive episode-
•The typical depressive episode is characterised by the following features (which should
last for at least 2 weeks for a diagnosis to be made). DDPPBPSA

1.Depressed mood- The most important feature is the sadness of mood or loss of interest
and/or pleasure in almost all activities (pervasive sadness) present throughout the day
(persistent sadness). This sadness of mood is quantitatively as well as qualitatively different
from the sadness encountered in “normal” sadness or grief. The depressed mood varies little
from day to day and is often not responsive to the environmental stimuli. The loss of interest
in daily activities results in social withdrawal, decreased ability to function in occupational
and interpersonal areas and decreased involvement in previously pleasurable activity. In
severe depression, there maybe complete anhedonia (inability to experience pleasure).

2. Depressive ideation or cognition- Sadness of mood is usually associated with

pessimism which can result in 3 common types of depressive ideas

i) Hopelessness (no hope in the future)

ii) Helplessness (no help is possible now)

iii) Worthlessness (feeling of inadequacy and inferiority)

The ideas of worthlessness can lead to self reproach and guilt feelings. The other features are
difficulty in thinking, difficulty in concentration, indecisiveness, slowed thinking, subjective
poor memory, lack of initiative and energy. Often, there are ruminations (repetitive intrusive
thoughts) with pessimistic ideas. Thoughts of death and preoccupation with death are not
uncommon. Suicidal ideas may be present. In severe cases, delusions of nihilism (for eg-
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world is coming to an end, my brain is completely dead, my intestines have rotten away)
may occur

3.Psychomotor activity- In younger patients (less than 40 years of age) motor retardation
is more common and is characterised by slowed thinking and activity, decreased energy and
monotonous voice. In a severe form, the patient can become stuperous (depressive stupor-
a clinical syndrome akinesis and mutism with relative preservation of conscious awareness;
depressive stupor and
catatonic stupor differ, the former involves conscious awareness and in the latter, there is not
insight regarding the rigid posture). In the older patients, (for eg-post menopausal women)
agitation is common. It is often accompanied with marked anxiety, restlessness (inability to
sit still, hand wringling, picking body parts or other objects and a subjective feeling of
unease. Anxiety frequently occurs with depression. Irritability may be present as easy
annoyance and frustration in day-to-day activities, for e.g. unusual anger at the noise made
by children at the house.
4. Physical symptoms- Multiple physical symptoms (called general aches and pains) are
present in most patients. Hypochondriacal features may be present in upto a quarter of
depressives. These physical symptoms are almost always present in severe depressive
episode. Another common symptom is the complaints of reduced energy and easy
fatigueability.

5.Biological functions- Disturbance of biological functions is common with insomnia (or

sometimes hypersomnia) loss of appetite and weight (or sometimes hyperphagia) and weight
gain, and loss of sexual drive. There is disruption of normal menstrual cycle in women i.e.
usually lengthening of the cycle and the women may skip one or several periods. The volume
of menstrual flow may decrease.
Another physiological or somatic symptom frequently accompanying depression is
constipation- the person may not have bowel movements for days at a time.

6.Psychotic features- About 15-20% of depressed patients have psychotic symptoms such as
delusions, hallucinations, grossly inappropriate behaviour or stupor. The psychotic features
can be either mood congruent (for eg- nihilistic delusion, delusions of guilt, delusions of
poverty) which are understandably in the light of depressed mood or can be mood
incongruent (for eg- delusions of control) which are not directly related to depressive
mood.

7.Suicide- Suicidal ideas in depression should always be taken seriously. Although, there is
a risk of suicide in every depressed patient with suicidal ideation, presence of certain
factors increases the risk of suicide

i) presence of marked hopelessness

ii) the risk of suicide is more in males, in age greater than 40, in unmarried, divorced
or widowed iii) written or verbal communication of suicidal intent and/or planned.
iv) in early stages of depression
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v) While recovering from depression ( at the peak of depression, the patient is usually
either too depressed or too retarded in terms of psychomotor activity to commit suicide)

8.Absence of underlying organic cause- if depressive episode is secondary to an organic

cause, a diagnosis of organic mood disorder should be made.

MANIC EPISODE DIAGNOSTIC CRITERIA

A manic episode is typically characterised by the following features which should last for at
least one week and cause disruption in occupational and social activities: EPSGOA

1) Elevated, expansive, or irritable mood

The elevated mood can pass through following four stages depending on the severity of the
manic episode

- euphoria (mild elevation of mood): an increased sense of psychological wellbeing and

happiness not in keeping with ongoing events. This is usually seen in hypomania (stage I).

- elation (moderate elevation of mood): a feeling of confidence and enjoyment along

with an increased psychomotor activity. Elation is classically seen in mania (stage II).
- exaltation (severe elevation of mood): intense elation with delusions of grandeur; seen in
severe mania (stage III)

- ecstasy (very severe elevation of mood): intense sense of rapture or blissfulness; typically
seen in delirious or stuporous mania (stage IV)

Along with these variations in elevation of mood, expansive mood may also be present which
is an unceasing and unselective enthusiasm for interacting with people and surrounding
environment. At times, elevated mood may not be apparent and instead an irritable mood
may be predominant, especially when the person is stopped from doing what s/he wants.
There may be rapid, short lasting shifts from euphoria to depression or irritability.

2) Psychomotor activity

There is an increased psychomotor activity ranging from overactive-ness & restlessness to

manic excitement where the person is "on the toe, on the go", (involved in ceaseless
activity). The activity is usually goal oriented and is based on external environmental cues.
Rarely a manic patient can go into a stuporous state (manic stupor).

3) Speech, thought, and perception

The person is more talkative than usual; describes thoughts racing in his/her mind;
develops pressure of speech; uses playful language with punning, rhyming, joking, &
teasing; and speaks loudly.
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Later, there is flight of ideas (rapidly produced speech with abrupt shifts from topic to topic,
using external environmental cues. Typically, the connections between the shifts are
apparent). When the "flight" becomes severe, incoherence may occur. A less severe and a
more ordered "flight" in the absence of pressure of speech is called "prolixity".

There can be delusions (or ideas) of grandeur (grandiosity) with markedly inflated self
esteem. Delusions of persecution may sometimes develop, secondary to the delusions of
grandeur (for eg, I am so great that people are against me). Hallucinations (both auditory and
visual) often with religious content can occur (for eg, God appeared before me and spoke to
me). Since these psychotic symptoms are in keeping with the elevated mood state, these are
called "mood congruent psychotic features".

Destructibility is a common feature and results in rapid changes in speech and activity, in
response to even irrelevant external stimuli.

4) Goal directed activity

The person is unusually alert, trying to do many things at one time. In hypomania the ability
to function becomes much better and there is a marked increase in productivity and
creativity. Many artists and writers have contributed significantly in such periods. As past
history of hypomania and mild forms of mania is often difficult to elicit. It is really important
to take additional historical information from reliable informants ( family member). In
mania, there is marked increase in activity with excessive planning and at times execution of
multiple activities. Due to being involved in so many activities and distractibility, there is
often a decrease in the functioning ability in later stages. There is marked increase in
sociability even with previously unknown people. Gradually, this sociability leads to an
interfering behavior though the person does not recognise it as abnormal at that time. The
person becomes impulsive and disinhibited with sexual indiscretions and can later become
hypersexual and promiscuous.
Due to grandiose ideation, increased sociability, overactivity and poor judgement, the manic
person is often involved in the high risk activities such as buying sprees, reckless driving,
foolish business investments and distributing money and/or personal articles to unknown
persons. S/he is usually dressed up in gaudy and flamboyant clothes although, in severe
mania there may be pure self-care.

5) Other features- Sleep is usually reduced with decrease need for sleep. Appetite may be
increased but later there is usually decrease food intake due to marked overactivity. Insight
into the illness is absent, especially in severe mania.

Psychotic features such as delusions ( a false unshaken belief which is not amenable to
reasoning and is not in keeping with patient’s socio-cultural and educational background),
hallucinations (a perception that occurs in the absence of a stimulus) which are not
understandable in the context of mood disorder (called mood incongruent psychotic
features) for e.g.,- delusions of control (a person’s belief that other people, animals or
objects are trying to influence or take control of her/him) may be present in some cases.
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6) Absence of underlying organic cause- If manic episode is secondary to an organic

cause, a diagnosis of organic mood disorder should be made.

UNIPOLAR MOOD DISORDER

Specifiers for major depression- Some individuals who meet the basic criteria for diagnosis
of major depression also have additional patterns of symptoms or features that are important
to note when making a diagnosis because they have implications for understanding more
about the course of the disorder and/or its most effective treatment. These different patterns
of symptoms or features are called specifiers in DSM IV TR. MPADRS
SPECIFIERS CHARACTERISTIC SYMPTOMS

Major depression with melancholic Three of the following: early morning

features awakening, depression worse in the
morning, marked psychomotor agitation
or retardation, loss of appetite or weight,
excessive guilt, qualitatively different
depressed mood. This severe sub type is
associated with a higher genetic loading
than other forms of depression
(Kendler,1997)

M.D with psychotic features Delusions 1or hallucinations (usually

mood congruent), feelings of guilt and
worthlessness are common

M.D. with atypical features Mood reactivity- brightens to positive

events; two of the following symptoms-
weight gain or increase in appetite,
hypersomnia, leaden paralysis (heavy
feelings in arms or legs), being acutely
sensitive to interpersonal rejection

Double depression It is not uncommon that major depression

may co-exist with dysthymia in some
people.

M.D. with recurrent features When a diagnosis of major depression is

made it is usually also specified whether
this is a first and therefore single (initial)
episode or a
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recurrent episode (preceded by one or more

previous episodes) . This reflects that
depressive episodes are usually time
limited. According to DSM 4 TR, the
average duration of an untreated episode is
about 6 months. In a large untreated
sample of depressed women, certain
predictors pointed to a longer time to
spontaneous remission of symptoms:
having financial difficulties, severe
stressful life events and high genetic risk
(Kendler et al.,1997). In some cases major
depression does not remit for over 2 years,
in which case chronic major depression is
diagnosed. Although, most depressive
episodes remit (which is not set to occur
until symptoms have remitted for at least
two months), depressive episodes usually
recur at some future point. In recent years,
recurrence has been distinguished from
relapse, where the latter term refers to the
return of symptom within a fairly short
period of time and probably reflects the
fact that the underlying episode of
depression has not yet run its course.
Relapse may commonly occur for example
when pharmacotherapy is terminated
prematurely after symptoms have remitted
but before the underlying episode is rarely
over ( Hollon et al. 2005)

M.D. with seasonal pattern At least 2 or more episodes in past two

years that have occurred at the same
time (usually winter), and full
remission at the same time
(usually spring). No other non-
seasonal episodes in the same 2
year period

ETIOLOGY OF UNIPOLAR DEPRESSION

Following the multi-path approach, research seems to show that various biological,
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psychological, social, and socio-cultural factors interact in complex ways to cause

unipolar depression

BIOLOGICAL DIMENSIONS

•Genetic predisposition

•Dysfunction in neurotransmitters in the

brain

•Brain structure differences

•Abnormal cortisol levels

•REM Sleep disturbances

PSYCHOLOGICAL
SOCIO-CULTURAL DIMENSIONS
DIMENSION •Low SES
•Cultural differences •Inappropriate separation and
anger response
•Gender differences (more
•Inadequate/insufficient reinforcers
common in women)
•negative thoughts & specific
SOCIAL DIMENSION errors in thinking

•Stress •Learned helplessness and

attribution style
•Lack of social support /resources

Biological approaches to the causes of mood disorders generally focus on genetic

predisposition, physiological predisposition or the combination of the two.

1.ROLE OF HEREDITY- There is now overwhelming evidence that mood disorders carry
significant genetic components whose ultimate phenotypic expression is highly dependent on
environmental factors (Leonardo and Hen,2006). Compared with bipolar disorder, major
depression is much more heterogeneous (symptoms and causes seem to vary a great deal),
and the contribution of environmental factors is larger than that of genetic factors
(Kato, 2007). Depression tends to run in families and the same type of disorder is generally
found among the members of the same family (Goldberg, 2006).
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Studies of MZ and DZ twins revealed a significantly higher discordant rates for depressive
symptoms among MZ twins than among DZ twins (McGue and Christensen, 1997).
Interestingly, concordance is higher for female than male twins perhaps, indicating gender
differences in genetic heritability (Goldberg, 2006)

2.NEUROTRANSMITTERS AND MOOD DISORDERS-The evidence for the importance

of the level of neurotransmitters in depression comes from a variety of sources. For example,
it was discovered that drug reserpine was used in treating hypertension, many patients
became depressed. Reserpine depletes the level of neurotransmitters in the brain. More
recently, studies of the effects of anti depressant medication also implicated
neurotransmission. Anti-depressant medication appeared to increase the level of
neurotransmitters. One group, the mono-amine oxidase inhibitors (MAOIs), blocks the
effects of monoamine oxidase in breaking down the neurotransmitters. Another group, the
tricyclic drugs block the reuptake of certain transmitter substances. Fluoxetine (Prozac)
seems to block the reuptake of serotonin.

Several hypotheses have been proposed for problems in neurotransmission-

•Depression may be caused by a deficit of specific neurotransmitters at brain synapses

(Bunny et al., 1979)
•To travel from one neuron to another, an electrical impulse must release
neurotransmitters that stimulate the receiving neuron. The problem may not be amount
of neurotransmitters made available by the sending neuron, but rather a dysfunction in
reception of neurotransmitter by the receiving neuron (Sulser, 1979).

•Drugs that raise the level of neurotransmitters in the synapse trigger such increases
immediately yet the alleviation of the depressive symptoms may be delayed for several
weeks after this increase. This delay may indicate that other factors such as membrane
responses to neurotransmitters are also important in depression (Rivas-Vazquez and Blais,
1997).

•Transporter proteins regulate the concentration of neurotransmitters in synapses and

therefore, have effects on a receiving neurons receptor. Reduced serotonin transporter and
dopamine transporter proteins may decrease serotonin’s “feel good” effects (Hariri and
Brown,2006)

3.BRAIN STRUCTURES

In depression, abnormalities in activation of prefrontal regions have been frequently

reported. Recent reports have documented decreased activation in these brain areas in
patients with major depressive disorder. Reduction in activation appears to be at least
partially a function of a reduction or shrinking of grey matter in the brain as revealed by
MRI derived measures.

* It is also possible that depression disorders can be produced by abnormalities in many

different parts of the circuitry of the brain. In summary, major depression maybe caused by
deficiency in the production of neurotransmitter substances.
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* By a blunted receptor response

* By a more general dysregulation in neurotransmission.

* By other brain abnormalities.

4. Abnormal Cortisol Levels- considerable interest has also focused on possible

abnormalities in neuroendocrine regulation in depression. People experiencing depression
tend to have high levels of cortisol (a hormone secreted by the adrenal cortex). A somewhat
different hypothesis has been proposed by Gillespie & Nemeroff (2007). They observed that
many individuals with depression have had early life traumas or stressors such as child
abuse, neglect or loss of a parent. Their belief is that exposure to stress (such as child abuse,
neglect or loss of a parent) during1 early development affects the cortisol and the
hypothalamic-pituitary-adrenal (HPA) system. This makes one more prone to depression
in later life, especially among those who have genetic vulnerability.

5. REM Sleep Disturbance

Depression is linked with a relatively rapid onset and an increase in REM sleep. Moreover,
reducing REM sleep of person with depression. However, all these deviations may simply be
a bi-product or correlate of depression and not the cause of depression. With the ongoing
advances in research and technology, researchers are continuing to find more precisely the
biological contributors to depression.

PSYCHOLOGICAL DIMENSION

A number of psychological theories have been proposed to account for the life experiences
that lead to depression-
1. Psychodynamic explanations- Focuses mainly on 2 concepts: separation and anger.
Separation may occur when a spouse, lover, child, parent or significant other dies or
leaves for one reason or another. But depression can not always be correlated with
immediate loss of a loved one and for those instances, Freud used the construct of
symbolic loss i.e. the depressed person may perceive any form of rejection or
reproach as symbolic of an earlier loss. For eg-the withdrawal of affection or
support or a rejection can induce depression. Freud believed this was especially true
because depressed people are fixated at the oral stage and excessively dependent.
Freud also believed that a person in depression fails to follow through the normal
process of mourning which he called “grief or mourning work”. In this process, the
mourner consciously recall and expresses memories about the lost person in an
attempt to undue the loss. In addition, the mourner is flooded with 2 strong sets of
feelings: anger and guilt. The anger which arises from the sense of being deserted
can be very strong. The mourner may also be flooded with guilt feelings about real or
imagined sins committed against the lost person.
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Psychodynamic explanations of depression have strongly emphasised the dynamics of

anger. Many patients in depression have strong hostile or angry feelings and some
clinicians believe that getting clients to express their anger reduces their depression.
Such a belief have led some to speculate that depression is really anger turned
against the self. Freud suggested that when a person experiences a loss (symbolic or
otherwise) he or she may harbour feelings of resentment and hostility toward the lost
person in addition to feelings of love and affection.
However, stressors other than the loss of significant other may bring about
depression and the loss of significant other can lead to disorders other than
depression such as anxiety and substance abuse.

2. Behaviouristic explanation- Behaviourists also see the separation or loss of

significant other as important in depression. However, behaviourists tend to see
reduced reinforcement as the cause rather than fixation or symbolic grief which
they view as untestable concepts. When a loved one is lost, an accustomed level of
reinforcement (whether affection, companionship, pleasure, material goods or
services) is immediately withdrawn. The survivor can no longer obtain the support or
encouragement of the lost person and the survivor’s level of activity (talking,
expressing ideas, working, joking, engaging in sports) diminishes markedly in the
absence of this reinforcement. Thus many behaviourists view depression as a
product of inadequate or insufficient reinforcers in a person’s life leading to a
reduced frequency of behaviour that previously was positively reinforced.

Lewinsohn’s model of depression (1974, 1985)- This model is perhaps the most
comprehensive behavioural explanation of depression. Along with the reinforcement
view of depression, lewinsohn suggested 3 sets of variables that may enhance or
hinder a person’s access to positive reinforcement
a) The number of events and activities that are potentially reinforcing to the
person this depends very much on individual differences and varies with the
biological traits and experiential history of the person. For eg-age, gender or
physical attributes may determine the availability of reinforcements. For eg-
handsome people are more likely to receive positive attention.
b) The availability of reinforcements in the environment- harsh environments
such as regimented institutions or remote, isolated places reduce
reinforcements.
c) The instrumental behaviour of the individual-the number of social skills a
person can exercise to bring about reinforcement is important. People in
depression lack social behaviours that elicit positive reinforcements. They
interact with fewer people, respond less, have very few positive reactions
and initiate less
conversations. They also feel more uncomfortable in social situations
(Youngren & Lewinsohn, 1980) and they elicit depression in others
(Hammen and Peters, 1978). A low rate of positive reinforcements in any
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of these 3 situations can lead to depression.

The occurrence of stress also plays a strong role in theory. Lewinsohn et al.,
believed that an antecedent event such as stress disrupts the predictable and
well established behaviour patterns of people’s life. Such disruptions then
reduce the rate of positive reinforcements or increase aversive experiences. If
individuals are unable to reverse the impact of the stress, they begin to have a
heightened state of self- awareness (for eg self criticism, negative
expectancies, and loss of self confidence) and to experience depressed mood.
With depressed moods, persons then have a more difficult time functioning
appropriately which makes them further vulnerable to depression. Thus,
Lewinsohn’s model attempts to cover not only behavioural elements but also
cognitive and emotional consequences.

3. Existential explanations
Viktor Frankl (an Australian psychiatrist) believed that psychopathology, particularly
depression, occurs when a person has no purpose in living. From his concentration
camp experience, he developed psychotherapeutic approach called Logotherapy
(after the Greek word logos- meaning). The goal is to restore meaning to the client’s
life. This is accomplished first by accepting in an empathic way the subjective
experience of the client’s suffering rather than conveying the message that suffering
is sick and wrong and should therefore, not be regarded as normal. The logotherapist
then helps the client make some sense out of his/her suffering by placing it within a
larger context, a philosophy of life in which the individual assumes responsibility for
his/her existence and for living according to a set of values. As Nietzsche wrote “ He
who has a why to live for, can bear almost any harm”.

4. Cognitive explanations- Cognitive psychologists have proposed that the way people
think, rather than low rates of positive reinforcement, can cause depression. In their
view, depressed persons have negative thoughts and specific errors in thinking that
result in pessimism, negative views of themselves, feelings of hopelessness and
depression (Emmelkamp, 2004). Depressed people often perceive themselves as
inept, unworthy regardless of reality. If they do succeed at any thing, they are likely
to dismiss it as pure luck or to forecast eventual failure. Hence, a cognitive
interpretation of oneself as unworthy may lead to thinking patterns that reflect self
blame, self criticism, and exaggerated ideas of duty and responsibility. Such beliefs
are often exaggerated and irrational and are interpreted in a catastrophic manner
(Ellis, 1989).
Beck (1976) proposed one major cognitive theory that views depression as a primary
disturbance in thinking rather than a basic disturbance in mood. How persons
structure and interpret their experiences determines their affective state. If
individuals see a situation as unpleasant, they ‘ll feel an unpleasant mood. According
to beck, patients with depression have schemas (cognitive framework that help
organise and interpret information) that set them up for depression. Depression
14 Nandini Pandey

involves schemas that perpetuate negative outlooks and attention to negative

messages.
According to Beck’s theory, depressed people operate from a cognitive or primary
triad of negative self views, present experiences and future expectations. Four
characteristic errors in logic typify this negative schema
i) Arbitrary inference-the person with depression tends to draw conclusion
that are not supported by evidence. For eg-a woman may conclude that
“people
dislike me” just because no one speaks to her on the bus or in the elevator.
ii) Selected abstraction- the individual takes a minor incident or detail out
of context and focuses on it and these incidents tend to be trivial. A
person
corrected for a minor aspect of his/her work maintain the correction as s
sign of incompetence or inadequacy-even when the supervisor’s overall
feedback is
highly positive.
iii) Overgeneralisation-The individual tends to draw a sweeping conclusion
about his/her ability, performance or worth from a single experience or
incident. A
woman laid off from a job, because of budgetary cuts, may conclude that
she is worthless.
iv) Magnification and minimisation- the individual tends to exaggerate
(magnify) limitations and difficulties and play down (minimise)
accomplishments,
achievements and capabilities. Ask to evaluate personal strengths and
weaknesses, the person lists many shortcomings or unsuccessful efforts but
finds it almost impossible to name any achievements.

People with low self-esteem may have experienced much disapproval in the
past from significant others such as parents. Their parents or significant others
may have responded to them by punishing failures and not rewarding successes
or by holding unrealistically high expectations or standards.

Evidence of a link between cognition and depression comes from the studies of
memory bias. When people with depression are given lists of words that vary in
emotional content, they tend to recall more negative words than do their control
group. This may indicate a tendency to attend to and remember and negative and
depressing events (Mineka & Sutton,1992). Cognitive or perceptual bias was also
found when individuals were asked to identify happy faces from a movie that
varied in degrees of happiness (Joormann,2006). Those with major depression
compared with non-depressed controls required greater facial intensities to
identify happy faces.
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BECK’S COGNITIVE MODEL OF DEPRESSION

CRITICISM- At times, negative cognitions may be the result rather than the
cause of depressed moods as noted by Hammen (1985). Hammen also found
that a person schema tends to mediate the relationship between stress and
depression.

Cognitive-learning approaches (learned helplessness and attributional style)-

Martin Seligman (1975) and Nolen-Hoeksema et al., (1992) proposed a unique
view of depression based on cognitive learning theory. The basic assumption of
this approach is that both cognitions and feeling of helplessness are learned and
that depression is learned helplessness. An acquired belief that one is helpless
and unable to affect in one’s life. People who feel helpless make causal
attributions or speculations about why they are helpless. These attributions can
be external or internal, stable or unstable, and global or specific. Abramson et
al., (1978) believed that a person whose attributions for helplessness are internal,
stable, and global, is likely to have more pervasive feelings of depression than
someone whose attributions are external, unstable and specific.

Both theories propose a diathesis-stress process. The diathesis involves

vulnerability because of negative cognitions (Beck) or pessimistic attributional
styles (Seligman). This vulnerability in the presence of stress, negative life
events results in depression according to each theory.

In 1989, a further revision-known as the hopelessness theory (Abramson et al).

16 Nandini Pandey

These investigators proposed that having a pessimistic attributional style with

one or more negative life events was not sufficient to produce depression,
unless one experience a state of hopelessness. A hopelessness expectancy was
defined by the perception that one had no control over what was going to
happen and by absolute certainty that an important bad outcome was going to
occur or that a highly desired good outcome was not going to occur. Such
expectations may themselves be a sufficient condition for depression.

Criticism-Cognition and attribution may be important factor in depression but

the disorder is complex; current models tend to include or explain only
particular facets of depression. Helplessness theory and attribution may explain
only a certain type of depression (Abramson, 1989).

Critical Evaluation

Gotlib and Colby (1987) found that people who were formerly depressed are
actually no different from people who have never been depressed in terms of
their tendencies to view negative events with an attitude of helpless resignation.
This suggests that helplessness could be a symptom rather than a cause of
depression. Moreover, it may be that negative thinking generally is also an effect
rather than a cause of depression

SOCIAL DIMENSION

Some investigators such as Lewinsohn have found that stress significantly affects the
occurence of depressive disrderds. Because stress has been primarily associated with
interpersonal situations, we focus on stress from social situations.

•Stress and depression- the importance of stress especially stress that is interpersonal in
nature has been demonstrated for depression (Hammen, 2006). In a study of individual’s
stress report of daily stress and depressive moods, stressors such as dependency (i.e. having
to depend on others) and interpersonal problems (such as having an argument with
someone) tend to occur just before the onset of depressive symptoms (Stader & Hokanson,
17 Nandini Pandey

1998). Other studies have shown that severe psychosocial stress such as the death of a loved
one, a life threatening medical condition or frustration of major life goals often precedes the
onset of major depression (Mazure,1998). Stress also appears to be important in recurrence
of depression.

Brown & Harris (1989?) concluded that severity, chronicity, time of onset and particular
type of stress is important to consider. Experiences occurring during childhood may
affect depression in later life. Harsh discipline in childhood is associated with levels of
depression among people who experience a major depressive episode (Lara et al,2000).
Thus, vulnerability may arise from early experiences in the family. Stressors such as loss
and humiliation are associated with depression
whereas others such as exposure to dangerous events are more likely to be associated with
anxiety (Kendler et al.,2003). Also, people may differ in their degrees of vulnerability to
depression. The vulnerability may be caused by biological factors, psychosocial factors or
both. Hammen et al., (1992) argued that the relationship between stress and depression is
complex and interactive.

In a longitudinal study of people with unipolar depression, the investigators found evidence
that having dysfunctional parents who create stressful conditions in the family may
influence an individual’s vulnerability to stress. Individuals from such families may fail to
acquire adaptive skills and positive self images which in turn brings on more stress which
can trigger depression. Not only does stress cause depression, but depression can also
cause stress. Hammen (2006) has found that individuals who are depressed compared with
those who are not are more likely to have stressors that are within their control, initiating an
argument rather than outside of their control (for eg cancer occuring in a sibling). She
believes that depressed persons may create and generate stress from themselves. Thus, the
research suggests that stress and depression are bi-directional.
Adequate social support or resources may act as a buffer against depression when we are
exposed to stress. Holahan &Moos (1991)collected data on individuals at the beginning and
end of a 4 year period. Information was included on personality characteristics, family
support (such as helpfulness of fam members), stress and depression. At the end of the 4
year period, persons with positive personality traits and family support had less depression
than those without these characteristics, even when initial level of depression ( during one
year) was controlled. The researchers speculated that personal or family resources help
individuals cope and adjust to stress. A 10 year follow-up of clients with depression (Moos
et al., 1998) showed that social resources such as more helpful friends, fewer family
arguments and sharing activities with friends were important in remission.

Depressed people not only have interpersonal problems but their own behaviour also seems
to make these problems worse. For example, the behaviour of a depressed individual often
places others in the position of providing sympathy, support and care. However, such
positive reinforcement does not necessarily follow. Depressive behaviour can and over time
frequently does elicit negative feelings and rejection in other people. In fact, nearly being
around a depressed person may induced negative affect in others (Joiner and Metalsky,
1995), and may make a non-depressed person less willing to interact again with a depressed
18 Nandini Pandey

person.

If the other people with whom a depressed person interacts are prone to guilt feelings, a
depressed person may elicit considerable sympathy and support at least over the short term.
More commonly. The ultimate result is probably a downwardly spiralling relationship from
which others finally withdraw, making the depressed person feel worse. The high co-
occurrence of marital distress and depression may occur also because the depressed
partner’s behaviour triggers negative affect in their spouses. Parental depression puts
children at high risk for many problems. Most evidence points to the maternal interactional
style as playing the most decisive role in the negative outcomes on infants and children
(Murray & Cooper, 1997). For example, depressed mothers show more friction and have
less playful and less mutually rewarding interactions with their children. They are also less
sensitively attuned to their infants and less affirming of their infant’s experiences.

Sociocultural Dimension

Sociocultural factors found to be associated with depression include culture, race and
ethnicity, sexual orientation, and gender.

-Cultural influences on Depression A person’s cultural background may influence descriptions

of depressive symptoms, decisions about treatment, doctor–patient interactions, and the
likelihood of outcomes such as suicide (Kleinman, 2004). In some cultures, depression is
expressed in the form of somatic or bodily complaints, rather than as sadness. For example,
depression is often experienced as “nerves” and headaches in Latino and Mediterranean
cultures; weakness, tiredness, or “imbalance” in Chinese and other Asian cultures; problems
of the “heart” in Middle Eastern cultures; and being “heartbroken” among the Hopi (American
Psychiatric Association, 2000).

Analysis of everyday encounters with discrimination among African American women

revealed that those subjected to frequent discrimination were most likely to have depressive
symptoms (Schulz et al., 2006). Societal stressors such as prejudice and discrimination
related to having a gay, lesbian, or bisexual orientation can also result in depression.

Why do reactions and symptoms differ from culture to culture? In a study, investigators
(Greenberger et al., 2000) compared the correlates of depressed mood among adolescents in
China and US. In both cultures, “cultures general” stressors such as parent’s illness and
family economic
losses had similar effects on depressed mood. Cultural differences emerged for other
variables, for instance, the correlations between depressed mood and poor relationships
with parents, as well as poorer academic achievement were higher for Chinese than for
Americans, perhaps reflecting the Chinese cultural emphasis on family and achievements.

-Gender and Depressive Disorders evidence indicates that women do have higher rates of
depression than men and that the differences are real, rather than an artefacts of self reports
and biases (Rieker and Bird, 2005). The higher rates seem to occur regardless of age,
although the gender gap appears to be the greatest during reproductive years. Attempts to
19 Nandini Pandey

explain these differences have focused on physiological (hormonal changes may affect
systems associated with depression, i.e., neurotransporter system or hypothalamic-
pituitary-adrenal system) and social psychological factors (for example, women’s
traditional gender role).

☆ BIPOLAR DISORDER- One minute you’re up and the next you’re down

Etiology- Biological causal factors have been found to be clearly dominant in bipolar
disorder and the role of psychosocial causal factors have received significantly less
attention.

BIOLOGICAL CAUSAL FACTORS-

•Genetic Influences-There is a greater genetic contribution to bipolar disorder than to

unipolar disorder. A summary of studies suggests that about 8-9% of the first degree
relatives of a person with bipolar illness can be expected to have bipolar disorder relative to
the 1% in the general population (Plomin et al., 2001). The first degree relatives of the
person with bipolar disorder are also at elevated risk for unipolar major depression (esp.
atypical depression), although the reverse is not true (Akiskal & Benazzi, 2005).

Although, family studies cannot by themselves establish a genetic basis for the disorder,
results from early twin studies also point to a genetic basis because the concordance rates
for these disorders are much higher for MZ than for DZ twins. Studies suggest that genes
account for about 80-90%of the variants in the tendency to develop bipolar disorder
(McGuffel et al.,2003). Efforts to locate the chromosomal sites of the implicated genes in
this genetic transmission of bipolar disorder suggest that they are polygenic.

•Neurochemical factors- norepinephrine, serotonin and dopamine are all involved in

regulating our mood states (Southwick, et al.,2005). There is some evidence for increased
norepinephrine activity during manic episodes and for lower norepinephrine activity during
depressive episodes (Manji & Nenox,2000). However, serotonin activity appears to be low
in both depressive and manic phases. Evidence for the role of dopamine stems in part from
research showing that increased dopaminergic activity in several brain areas may be related
to manic symptoms of hyperactivity, grandiosity and euphoria (Howland &Thase, 1999).
High doses of drugs such as cocaine which are known to stimulate dopamine also produce
manic like behaviour. In depression, there appear to be decreases in both norepinephrine and
dopamine functioning (Manji & Lenox,2000). Thus disturbances in the balance of these
neurotransmitters seem to be one of the keys to understanding this debilitating illness.

Lithium is the most effective and widely prescribed drug used in treatment of bipolar
disorder. It can stabilise individuals from both depressive and manic episodes. Lithium is
closely related chemically to Sodium which plays a key role in passage of neural impulse
20 Nandini Pandey

down an axon, therefore, questions have been raised about whether bipolar patients have
abnormalities in the way ions (such as Na+) are transported across the neural membranes.
Research suggest that there is indeed some such
abnormality in bipolar disorder (Whybrow, 1997). One possibility is that Lithium may
substitute for sodium ions

•Other biological factors-

--Some neuro-hormonal research has focused on the abnormalities of the hypothalamic-

pituitary adrenal and HPT axis among bipolar patients

--With PET scans, it has even proved possible to visualise variation in brain glucose
metabolic rate in depressed and manic states. Several summaries of the evidence from
studies using PET and other neuroimaging techniques show that, whereas blood flow to the
left prefrontal cortex is reduced during depression and during mania, it is reduced in the right
frontal and temporal regions (Howland & Thase, 1999). During normal mood, blood flow
across 2 brain hemispheres is approx. equal. Structural imaging studies suggest that certain
sub-cortical structures including basal ganglia and amygdala are enlarged in bipolar
disorder (Malhi et al.,2004). Studies using fMRI also find increased activation in bipolar
patients in sub-cortical brain regions involved in emotional processing such as the thalamus
and amygdala relative to unipolar patients and normals (Malhi et al., 2004)

--There is considerable evidence regarding disturbances in biological rhythms such as

circadian rhythms even when symptoms have mostly remitted. Even between episodes,
people with bipolar disorder show substantial sleep difficulties including high rates of
insomnia. Bipolar disorder also sometimes show a seasonal pattern the way unipolar
disorder does, suggesting disturbances of seasonal biological rhythms although this may
be result of circadian abnormalities in which onset of sleep-wake cycle is set ahead of the
onset of the other circadian rhythms. Given the cyclic nature of bipolar disorder itself , this
focus on disturbances in biological rhythms holds promise. This is particularly true because
bipolar patients seem esp. sensitive to and easily disturbed by any changes in their daily
cycles that require a resetting of their biological clocks (Jones et al., 2005)

PSYCHOSOCIAL CAUSAL FACTORS-

•Stressful life events-early in the course of bipolar disorder, stressful life events preceding
manic or depressive episodes may be precipitants (just like Kraeplin had noted in his
clinical observations) in several good studies using the most sophisticated stress
measurement techniques ( Hammen, 1995). Followed patients with established bipolar
disorder for one to two years . They found a significant association between the occurrence of
high levels of stress and the experience of manic, hypomanic or depressive episodes. A study
even found that patients with more prior episodes were more likely to have episodes
following major stressors than patients with fewer prior episodes (Hammen & Gitlin, 1997).
A study found that patients who experienced severe negative events took an average three
times longer to recover than those without a severe negative event (Johnson & Miller, 1997).
Even minor negative events were found to increase recovery (Johnson et al., 1997). One
21 Nandini Pandey

hypothesised mechanism is through the destabilising effect that stressful life events may have
on critical biological events. Although, evidence in support of this idea is stile preliminary
though a promising hypothesis.

•Other Psychological factors

There is also some evidence that other social environmental variables may affect the course
of bipolar disorder. For e.g.-one study found that people with bipolar disorder who reported
low social support showed more depressive recurrences over a one year follow-up
independent of the effects of stressful life events which also predicted more
recurrences(Cohen et al.,2004). There is also some evidence that personality and cognitive
variables may interact with stressful life events in
determining the likelihood of relapse and recurrence. For e.g.2 studies found that the
personality variable, neuroticism predict increases in depressive symptoms in people with
bipolar disorder just as in unipolar disorder. Moreover, 2 personality variables associated
with high levels of achievement striving and increased sensitivity to rewards in the
environment predicted increases in manic symptoms (Meyer et al.,2001). Another study
found that students with a pessimistic attributional style who also had negative life events
showed an increase in depressive symptoms whether they were bipolar or unipolar
depressives. Interestingly, however, the bipolar students who had a pessimistic attributional
style and experienced negative life events also showed increases in manic symptoms at other
points in time (Reilly-Harrington et al., 1999).

•Psychodynamic perspective

According to psychodynamic theorists, manic reactions are an extreme defence against or

reaction to depression. A contemporary reformulation was presented by Neale (1988) who
argued that individuals with unstable self-esteem along with unrealistic standards for what
constitutes success are at risk for bipolar disorder. Neale argued that the grandiose ideas that
often occur during manic states may serve the purpose of defending against distressing
thoughts (fuelled by low self-esteem) by distracting the individual from them. Several
studies have provided some support for this view (Lyon et al.,1999 & Winters & Neale,
1985).

Although, this view may seem plausible up to a point the effectiveness of biological
treatment in alleviating severe manic and depressive episodes testifies to the importance
of biological causal factors. At the same time, the importance of psychological treatments
along with medication has been increasingly recognised in recent years.