Chapter 5 (revised)

Chapter 5Chapter 5
Mood Disorders

Chapter outline
• Introduction
• History of mood disorders
• Epidemiology
• Life course
• Clinical picture
• SECTION I: BIPOLAR AND RELATED
DISORDERS
• SECTION 2: DEPRESSIVE DISORDERS
• Cross-cultural and African perspectives
• Aetiology of mood disorders

Introduction
• Traditionally depressive and bipolar disorders were seen to
be variations of mood, and were categorised together in
DSM-IV-TR as Mood Disorders.
• In the DSM-5, however, Bipolar and Depressive Disorders
have been split into two distinct categories.
• For the purposes of this chapter the two categories of
disorders will be discussed collectively as mood disorders,
as they share the component of mood.
• Distinctions between the two categories will however be
made in the discussion of the clinical pictures.

• Mood disorders = most common disorders; often under-treated
(esp. in developing countries).
• Suffering & suicide risk makes accurate diagnosis NB to ensure
effective Rx
• Mood disorder:
- person feels depressed and/or elated
- shows signs (affect) of depression and/or mania for a
significant period of time
- severe enough to impair normal functioning
- occurs in absence of clearly identifiable trigger
• More complex picture of mood disorders emerged from clinical
and biological research  changes in classification of mood
disorders in both DSM-IV-TR and ICD-10.
• Disorders include Major Depression, Bipolar Mood Disorder,
Dysthymia, and Cyclothymia.
Introduction

Introduction
• Complex in classification and aetiology.
• Affect: describes person’s mood as
displayed by behavioural responses.
• Mood: subjective

Key factors in mood disorders
Two extreme poles
• On one end, extreme dysphoria (Major Depressive
Episode); on other, extreme euphoria (Manic
Episode).
• Depression only = unipolar mood disorders.
• Episode of depression and mania = bipolar mood
disorders.
• Episodes of mania always linked to depressive
episodes and never exist on their own.
Introduction, cont.

Introduction, cont.
• Symptoms must be severe for disorder diagnosis; problem of
vague cut-off points (Parker, 2006).
• Duration of symptoms also used as criterion for diagnosis.

Introduction, cont.
The severity of the symptoms
•Normal human existence  many people
experience sadness, unhappiness, or disappointment.
•Emotions may be result of setbacks in life (e.g.
academic failure, relationship difficulties, loss, etc.).
•Normal functions (e.g. appetite, sleep) may be
affected; usually back to normal fairly quickly.
•If feelings are abnormally prolonged or a person’s
daily functioning is impaired, diagnosis of a mood
disorder is made.
•Abnormal sadness is not necessarily triggered by
clearly identifiable events

The duration of the symptoms
• Duration of symptoms differs between mood
disorders:
- Major Depression: Symptoms present for
two-week period.
- Dysthymic Disorder: Less severe
symptoms for two years.
- Bipolar Disorder: Symptoms of mania
present for period of one week.
- Cyclothymia: Less severe symptoms
(hypomania) for two years.
Introduction, cont.

Introduction, cont.
DSM-5
Bipolar and Related Disorder Depressive Disorders
Bipolar I
Bipolar II
Disruptive Mood Dysregualtion Disorder
Major Depressive Disorder
Persistent Depressive Disorder (Dysthymia)
Premenstrual Dysphoric Disorder

• Long history; mood disorders can be traced back to
ancient times.
• Written records in ancient civilisations; early Greeks
coined terms melancholia and mania.
• History characterised by various theories about
causes and classification.
• Theories include:
- biological humours
- religious and spiritual failings
- early loss
- unconscious conflicts
- irrational cognitions
- genetics
- neurotransmitters
- neuropsychological abnormalities
History of mood disorders

• Historically, descriptions of mood disorders
relatively consistent over time.
• Term ‘depression’ first used in early 1600s; only
replaced ‘melancholia’ in mid-1800s.
• Bipolar disorders first identified in 1850s;
initially called manic-depressive disorder.
• Karl Leonhard (1957) proposed
subclassification of bipolar disorder.
History of mood disorders, cont.

• DSM system provides operational definitions,
symptoms, and clinical severity of mood disorders.
• World Health Organisation (WHO) uses own
classification system (International Classification of
Diseases) (ICD).
• Significant congruence between the two systems.
• Goldney (2006): Classification debate will never
really be resolved; next advance will be move away
from ‘clinical phenomenological descriptions’ to
‘biological markers’.
• DSM-5: Divides mood disorders into two separate
chapters (‘Depressive Disorders’ & ‘Bipolar and
Related Disorders’).
History of mood disorders, cont.

Life course
• Moore & McLaughlin (2003): Increasing risk of
depression in children, adolescents, and elderly.
• DSM-5: Different manifestation of symptoms for
depressed children (e.g. irritable, rather than
depressed, mood).
• Depression in the elderly characterised by
cognitive symptoms (e.g. memory impairments)
 often difficult to distinguish from symptoms
of cognitive/other disorders.
• Physical, physiological, psychological &
social changes all contribute (e.g. social support
network declines due to loss of
friends/family/spouses).
• Also related to how elderly are treated in

BIPOLAR AND RELATED
DISORDERS
SECTION I

Introduction
• As far as Bipolar Disorders are concerned, DSM-5 makes
distinction between Bipolar I, Bipolar II and Cyclothymic
Disorders.
• For Bipolar I disorder, patients need to meet the criteria for
a fully syndromal manic episode, and possible major
depressive episodes, thereby placing more emphasis on
mania than depression (See Table 5.3).
• Bipolar II is different to Bipolar I in that there must be at
least one episode of Major Depression, and that instead of
a full manic episode, there is at least one episode of
hypomania (See Table 5.4).

Introduction cont.
• The ICD-10 does not distinguish between Bipolar I and II, but
distinguishes between different types of Bipolar based on manic vs.
hypomanic episodes.
• Another, interesting difference between the DSM-5 and ICD-10 is that
the ICD-10 makes a distinction between manic episodes with or without
psychotic symptoms (See Table 5.5).
• A distinction is made between mania and hypomania.
• This is because there are variations in the severity of manic episodes,
which may range from mania (during which a person may become
psychotic) to hypomania.
• A hypomanic episode, which is a subsyndromal counterpart of mania, is
characterised by a distinct period of persistently elevated, expansive, or
irritable mood, lasting throughout at least four days.
• It is also clearly different from the person’s usual mood but is not as
severe as mania in that the person is not psychotic, and judgement and
social and work performance are not impaired.

• Many patients suffering from bipolar disorders become
addicted to the heightened productivity and creativity
that they experience during a hypomanic phase.
• Hypomania can be seen as a separate and unique state,
or it could be an earlier and transitional state in an
episode of mania, as only 50% of those patients in a
hypomanic episode develop a full-blown manic episode
(Goodwin & Jamison, 1990).
Introduction cont.

Comparison of Bipolar Disorders between
DSM-5 and ICD-10
DSM-5 ICD-10: Bipolar affective disorder
Bipolar I Disorder
• Current or most recent episode manic
• Current or most recent episode hypomanic
• Current or most recent episode depressed
• Current or most recent episode unspecified
Bipolar II Disorder
Cyclothymic Disorder
Specifiers for Bipolar and Related Disorders
• With anxious distress
• With mixed features
o Manic or hypomanic episode
o Depressive episode
• With rapid cycling
• With melancholic features
• With atypical features
• With psychotic features
• With catatonia
• With seasonal pattern
Bipolar affective disorder, current episode hypomanic
Bipolar affective disorder, current episode manic
without psychotic symptoms
Bipolar affective disorder, current episode manic with
psychotic symptoms
• With mood-congruent psychotic symptoms
• With mood-incongruent psychotic symptoms
Bipolar affective disorder, current episode mild or
moderate depression
• Without somatic syndrome
• With somatic syndrome
Bipolar affective disorder, current episode severe
depression without psychotic symptoms
Bipolar affective disorder, current episode severe
depression with psychotic symptoms
• With mood-congruent psychotic symptoms
• With mood-incongruent psychotic symptoms
Persistent mood [affective] disorders
• Cyclothymia

Clinical picture
Major Depressive Episode
• Major Depressive Disorder not = temporary
sadness or ‘the blues’.
• Clinical syndrome including symptoms of
depression (as a mood), as well as cognitive,
physical (somatic), behavioural, emotional, and
perceptual symptoms (Sweeney & Maas, 1978).
• Episodic - minimum duration of unipolar disorder is
two weeks, but can last much longer.
• Heterogenous: not all people display the same Sx
but Core clinical features stable across cultures
and time (Ohaeri & Otote, 2002).

Clinical picture, cont.
Major Depressive Disorder, cont.
Cognitive symptoms
• Depressed patients usually have negative view of self,
the world, and the future.
• Manifests in extreme beliefs that they are worthless,
unimportant, and ineffectual.
• Circular thinking - components tend to reinforce each
other (i.e. low self-esteem  low mood  negative
view of the world and self  reinforces low self-esteem).
• People feel trapped  helplessness and hopelessness
(Beck et al., 1990).
• Thought content often revolves around loss, guilt,
suicide, and death.

Cognitive symptoms, cont.
• Kaplan et al. (1994): About 60% of depressed patients have
suicidal ideation (10% to 15% commit suicide).
• Other cognitive symptoms of depression include:
•thought-blocking
•poverty of content
•impaired concentration
•forgetfulness.
• Severe cases may display mood-congruent delusions.
• Include themes of guilt, failure, worthlessness, etc.

Somatic symptoms
• Physical manifestations of depression = vegetative
states. These include:
- fatigue and lethargy (a constant feeling of being ‘slowed
down’)
- aches and pains (e.g. headaches, lower back pain, etc.)
- changes in appetite
- significant changes in weight
- change in sleep patterns (insomnia, early-morning
awakening, and oversleeping),
- loss of pleasure in life (anhedonia)
- loss of libido (sexual desire).

Somatic symptoms, cont.
• Typical sign of depression is an overwhelming loss of
energy.
• Can limit person’s activities, including social
interaction.
• Compounds other effects of depression  work and
family obligations may be compromised.
• Patterns differ between people.
• Symptoms may  loss of intimacy and decline in
sexual activity  relationship difficulties  reinforces
feelings of worthlessness and inadequacy 
exacerbates symptoms of depression.

Somatic symptoms, cont.
• Two patterns of sleep disturbance - sleeping more
(hypersomnia) or less than normal (insomnia).
• Insomnia more common.
• Changes in EEG sleep patterns (Halgin &
Whitbourne, 2003).
• Intermittent awakening or early-morning awakening
(terminal insomnia).
• Exacerbates symptoms due to rumination and
fatigue.
• Increased duration of rapid eye movement (REM)
sleep.

Behavioural symptoms
• Two presentations:
- psychomotor retardation (e.g. stooped posture,
little spontaneous movement, poor eye contact, etc.)
- psychomotor agitation (e.g. generalised
restlessness).
• Also social withdrawal; includes marked reduction
in interpersonal contact with family, friends, and
colleagues.
• The severity of this symptom varies.
• Verbal communication: Decreased rate/volume of
speech and delayed responses to questions.

Emotional symptoms
• Dysphoric mood that exceeds ordinary feelings of
disappointment and occasional sadness.
• This dysphoria may appear as extreme dejection or
significant loss of interest in previously pleasurable
activities.
• Also sadness, feelings of guilt, and worthlessness.
Perceptual symptoms
• Hallucinations may be present (severe depression).
• Differ from those in other psychotic disorders in that
they are usually mood congruent.

Manic Episode
• Severity ranges from mania (during which a person
may become psychotic) to hypomania.
• Hypomanic episode:
- distinct period of persistently elevated, expansive, or
irritable mood
- lasting throughout at least four days
- clearly different from the person’s usual mood
- person is not psychotic
- judgment and performance not impaired
• Bipolar patients may  addicted to heightened
productivity and creativity of hypomanic phase.
• Hypomania could be transitional state in episode of
mania.

Manic Episode, cont.
Cognitive symptoms
• Thought content - manic patients’ thoughts include
themes of exaggerated self-confidence and
personal power.
• May reach delusional proportions (e.g. delusions
of grandeur).
• Thought processes - unrestrained and accelerated
flow of ideas are common.
• Other cognitive functions (e.g. memory and
orientation) usually remain intact; may be
concentration difficulties.

Somatic symptoms
•Decreased need for sleep; person in a manic
phase may need only a few hours of sleep a night, or
go for days without sleep.
Emotional symptoms
•Characteristic mood in manic episode is euphoria;
person may display endless optimism and
enthusiasm. Can quickly turn to irritability due to
low frustration tolerance.
•Emotionally labile.

• Obvious symptoms include over-activity and
endless energy.
• In hypomania, energy may be productive.
• Increased activity often involves pleasurable,
impulsive, and reckless activities (e.g. gambling,
dangerous driving, promiscuity, etc.); often results in
negative consequences.
• Risk to self and others - may attempt suicide or
homicide.
• Accelerated thought patterns  very fast speech;
speech may also be loud and difficult to interrupt.

Cyclothymic Disorder
• This disorder could be regarded as a less severe
disorder than either the Bipolar I or Bipolar II
disorders.
• The essential feature of this disorder is a chronic,
fluctuating mood disturbance which manifests in
symptoms of hypomania (but not a fully syndromal
hypomanic episode) and depression (but not a fully
syndromal major depressive episode) (APA, 2013).

DEPRESSIVE DISORDERS
SECTION 2

Introduction
• The common feature of these disorders
is primarily the presence of a sad, empty
or irritable mood.
• There are a number of associated
physical and cognitive symptoms, and
together these symptoms impair the
functioning of a person with one of these
disorders (APA, 2013).

Disruptive Mood Dysregulation
Disorder
• In the past there has been growing concern that children may be mis- or
overdiagnosed with Bipolar Disorder.
• This may, in part, be the result of clinicians attributing nonepisodic irritability
to a manifestation of paediatric mania (APA, 2013).
• The problem with this is that the DSM-5 reserves the diagnosis of bipolar for
episodic presentation of bipolar symptoms (APA 2013), and that the
presence of only nonepisodic irritability does not meet the criteria for this
disorder.
• In order to address this problem, a diagnostic category for children that
display nonepisodic irritability, namely Disruptive Mood Dysregulation
Disorder (DMDD), was created in the DSM-5, was created.
• This disorder is limited to children between the ages of 6 and 18 years, but
typically the age of onset is before the age of 10 years (APA, 2013).
• The core feature of this disorder is chronic, severe and persistent irritability
that manifests in two ways, i.e. frequent temper outbursts and persistent
irritable or angry mood in-between temper outbursts (APA, 2013).

Major Depressive Disorder
• Major Depressive Disorder, also called ‘clinical depression’, is a
serious psychiatric illness that should not be confused with
temporary sadness or ‘the blues’.
• Major Depressive Disorder is a clinical syndrome that includes
symptoms of depression (as a mood), as well as a variety of
cognitive, physical (somatic), behavioural, emotional, and perceptual
symptoms
• Major Depressive Disorder should be thought of as episodic. The
minimum duration of unipolar disorder is two weeks, but it can last
much longer.
• Although depression is heterogeneous (i.e. not all people who are
diagnosed with depression necessarily display the same symptoms),
there are core clinical features which are stable across cultures and
time (Ohaeri & Otote, 2002).
• These core features are either a depressed mood or the loss of
interest or pleasure in nearly all activities.

Cognitive symptoms
• Depressed patients usually have a negative view of themselves,
the world, and the future
• This usually manifests in extreme beliefs that they are worthless,
unimportant, and ineffectual, which could be described as an
extremely low self-esteem.
• The cognition of people with depression cannot be described in a
linear way as all the components of their cognitions tend to
reinforce each other in a circular way (i.e. low self-esteem
intensifies a low mood, which in turn creates a negative view of the
world and self, which in turn reinforces the low self-esteem).
• This circular reasoning often traps people in a situation which they
feel they cannot escape, thereby creating a sense of helplessness
and hopelessness (Beck, Brown, Berchick, Stewart, & Steer,
1990).
• Kaplan et al. (1994) state that, in depression, thought content often
revolves around thoughts of loss, guilt, suicide, and death.

Somatic symptoms
Somatic symptoms are those that result in physical
problems, such as:
•fatigue,
•lethargy (a constant feeling of being ‘slowed down’),
•aches and pains (e.g. headaches, lower back pain,
gastro-intestinal pain, etc.),
•changes in appetite,
•significant changes in weight (either weight loss or weight
gain)
•sleep patterns (insomnia, early-morning awakening, and
oversleeping),
•anhedonia (loss of pleasure in life), and
•a loss of libido (sexual desire).

• These symptoms are typically the observable manifestation of a disorder.
• In the case of depression we may have two, opposite, sets of behaviour,
depending on the type of depression that the person is suffering from:
• Psychomotor retardation, which is typically characterised by stooped
posture, very little spontaneous movement, poor eye contact, impaired
coordination, slow speech, and difficulties with articulation, or
• Psychomotor agitation, which is usually characterised by generalised
restlessness.
• A behavioural symptom that is seen often is social withdrawal.
• This includes a marked reduction in interpersonal contact with family,
friends, and colleagues.
• The severity of this symptom may vary from irritability with others to total
social withdrawal.
• In terms of verbal communication, Kaplan et al. (1994) state that depressed
patients may display a decreased rate and volume of speech and often give
only monosyllabic and delayed responses to questions.

Emotional symptoms
• Kaplan et al. (1994) state that, although depression is the
primary symptom of mood disorders, many patients deny
any feelings of depression, and may not even seem to be
depressed.
• Generally, the emotional symptoms of depression involve
a dysphoric mood that exceeds ordinary feelings of
disappointment and occasional sadness.
• This dysphoria may appear as extreme dejection or
significant loss of interest in previously pleasurable
activities (Halgin & Whitbourne, 2003).
• Other symptoms may include sadness, feelings of guilt,
and worthlessness.

Perceptual symptoms
• Although uncommon, hallucinations may
be present in severe cases of depression.
• These hallucinations differ from those that
one would find in other psychotic
disorders, such as Schizophrenia, in that
they are usually mood congruent
(consistent with the depressed mood)
(Kaplan et al., 1994).

Persistent Depressive Disorder
(Dysthymia)
• The essential feature of this disorder is a depressed mood that
occurs for most of the day, for more days than not for a period
of at least two years.
• Other symptoms of the disorder include changes in eating and
sleeping patterns, low energy, low self-esteem, concentration
difficulties and feelings of hopelessness.
• It is not uncommon for major depressive episodes to precede
this disorder, nor is the occurrence of these episodes
uncommon during this disorder (APA, 2013).
• People with this disorder are at high risk for other comorbid
conditions, specifically for anxiety disorders and substance
abuse (APA, 2013).

Premenstrual Dysphoric Disorder
• This disorder manifests mainly in mood lability, irritability,
dysphoria and anxiety symptoms.
• These symptoms occur repeatedly during the premenstrual cycle
and typically peak at the onset of menses and remit shortly
thereafter (APA, 2013).
• In addition to the alteration in mood, there are also other
symptoms such as decreased interest in usual activities,
concentration difficulties, lack of energy, increase in eating,
changes in sleeping pattern and a number of physical symptoms
(APA, 2013).
• These symptoms have an adverse effect on work and social
functioning.
• Of note is that this does seem to be a culture-bound syndrome
and that women who use oral contraceptives have a lower risk
for this disorder (APA, 2013).

Cross-cultural and African
perspectives
• Wide variations in ideas about depression, both within
and among cultures.
• Colonial period - widely assumed that depression was
rare amongst African people.
• Due to apartheid, this assumption endured  racially
skewed diagnoses.
• South African study (Freeman, 1992):
- Black patients predominantly diagnosed with
Schizophrenia (68%; 19% of white patients).
- White patients predominantly with a mood
disorder (41%; 9% of black patients).
• South African community – critical and negative view
of person with mood disorder.

Cross-cultural & African
perspectives, cont.
• German (1987) - mood disorders are common in
Africa.
• Different symptomatology:
- somatic symptoms more common in African
populations (Coleman et al., 2006)
- guilt and suicide more common in the European
populations.
• Critique of this research  need to focus on how
some population groups emphasise certain
symptoms to indicate a particular state of illness.

• Contextual factors also NB (e.g. levels of conflict in a
country).
• Need to focus on local cultural factors.
• Historically skewed diagnosis of mental disorder in
South Africa due to cultural insensitivity (rather than
different prevalence).
• Western societies typically ascribe causes of mood
disorders to internal states (i.e. biological or
psychological).
• Non-Western societies tend to ascribe the causes to
external forces (e.g. social conflict, envy, witchcraft,
or sorcery).
Cross-cultural & African
perspectives, cont.

Aetiology
• No single cause for any of the mood disorders.
• Interactions between causal variables still unclear.
• Cannot see mood disorders as a single entity.
• Both DSM and ICD describe variety of unipolar
and bipolar disorders.
• Ideally, need to identify aetiological factors for
each subcategory.
• Little conclusive evidence for the causes of
bipolar disorders (esp. in African countries).
• This creates problems for treatment, as treatment
is often based on aetiology of a particular
disorder.

Aetiology, cont.
Biological factors
Genetics
• Mood disorders consist of a cluster of symptoms (i.e.
a syndrome).
• One-dimensional aetiological perspective (e.g.
genetics) unhelpful.
• Family, adoption, and twin studies.
• Greater genetic risk for developing mood disorder also
associated with vulnerability to stressful life events.
• Integrative view – vulnerability to changes in certain
neurotransmitters (e.g. serotonin and dopamine) 
mood disorder when interacting with adverse life
events.

Biological factors, cont.
Brain structures
• MRI scans reveal differences in brain structure in
mood disorders:
- increased volumes of the lateral ventricles (implying
increased cortical atrophy) and the adrenal gland
- decreased volumes of the basal ganglia, thalamus,
hippocampus, and frontal lobe
• Knowledge of links between brain structures and
function  greater understanding of specific
aetiology.
Aetiology, cont.

Why? We mostly know which areas of
the brain are responsible for which
functions, so we can almost always trace
the affected brain structures back from
the observable symptoms, e.g., person
has memory problems, we can assume
the hippocampus is implicated.

Brain structures, cont.
• Link between depression and neurogenesis of the
hippocampus.
• Neurogenesis slowed by stress; increased by
serotonin.
• Same applies to the anterior cingulate?
(responsible for modulation of emotional behaviour)
• Posner & Raichle (1994): Prefrontal cortex,
thalamus, amygdala, and anterior cingulate are
joined by a neural pathway  activity in one of
these  activity in another.
Aetiology, cont.

Medical illness
• Physical factors may cause mood disorders
(as opposed to vegetative symptoms being
the result of depression).
• Depression may also arise from treatment of
a physical illness (e.g. chronic Hepatitis C
Virus) (HCV).
Aetiology, cont.

Neurochemicals
• Better understanding of neurotransmitters,
peptides, etc.  changed hypotheses about role
of neurotransmitters in depression.
• Prevailing hypothesis = depression caused by
depletion of monoamine neurotransmitters
(norepinephrine, dopamine, and serotonin). Does
not fully explain cause of depression though.
• But, many other neurotransmitter systems (e.g.
GABA & acetylcholine) may be altered by
depression.
Aetiology, cont.

Neurochemicals, cont.
• NB neurotransmitters in depression:
- Noradrenalin/norepinephrine: Works with serotonin in
pathophysiology of depression. When noradrenergic
receptors are destroyed, drugs that affect serotonin lose
normal potency and vice versa.
- Serotonin: Primary role in pathophysiology of mood
disorders (low serotonin  depression; high serotonin 
mania). Also, interaction effects between serotonin and
norepinephrine. Low serotonin leads to high norepinephrine
or mania.
- Dopamine: Reduced dopamine associated with depressive
symptoms (and vice versa).
- Gamma Amino Butyric Acid (GABA): Interacts with other
neurotransmitters (i.e. acts indirectly in development of
depression).
Aetiology, cont.

Neurochemicals, cont.
• Winters and Neal (1985) - bipolar disorders have
more of a biological cause (cf unipolar depression)
but exact mechanisms unclear.
• Norepinephrine plays NB role in bipolar disorders:
- low levels during depressed phase
- elevated during a manic phase
• Recently, move away from norepinephrine
hypothesis.
Aetiology, cont.

Endocrine system
• Overactive hypothalamic-pituitary-adrenal axis (HPA axis)
could  depression.
• Increased levels of cortisol and enlarged pituitary and
adrenal glands. (suggesting disturbances in endocrine system
may play role in mood and other disorders)
• Linked to over-secretion of corticotrophin-releasing hormone
from the hypothalamus. (implicated in cognitive and arousal Sx)
• Role of oestrogen:
- increased risk after puberty, during pregnancy; reduced
rates after menopause
- periods of low or fluctuating oestrogen associated with
increased risk
Aetiology, cont.

Aetiology, cont.
Stress
• Stress = NB mind-body link.
• Stress has emotional, cognitive, physical and
physiological effects.
• Stress is complex; may play a role in various
disorders (e.g. anxiety disorders, Schizophrenia).
• Long-term stressors deplete physical, emotional
and cognitive resources.
• Person feels unable to control stressor  feelings
of helplessness and hopelessness.
• Unpredictable stressors are most stressful.

Aetiology, cont.
Stress, cont.
• Physical/physiological aspects related to central nervous
system (i.e. hypothalamus, hippocampus, & neurotransmitters)
and the endocrine system (HPA axis). (link btwn stress and
alteration in neurotransmitters can be traced back to this axis
and hippocampus)
• Stress not only alters brain function, but in extreme cases, it
may even cause structural changes in the brain.
• Heightened HPA axis activity in depressed people may 
ongoing stress response  excessive secretion of the
corticotropin-releasing hormone (CRH)  decreased appetite,
weight loss, decreased sex drive, and hypersomnia.

Stress, cont.
• Depressed people tend to have a smaller
hippocampus.
• Duman et al. (1997) - this is important because:
- smaller hippocampus unable to inhibit
hypothalamus?
- depressed people likely to show longer stress
response than others.
• Also, smaller hippocampus may  under-
production of essential neurotransmitters
(monoamines like serotonin).
Aetiology, cont.

Psychosocial factors
Childbirth
• Birth of a baby requires major psychosocial
adjustment.
• Strong link between childbirth and depression 
separate diagnostic category, Post-Partum
Depression (PPD).
• Symptoms include sadness, emotional lability,
insomnia, confusion, anxiety, guilt, dependency.
• Disorder may be result of:
- biological factors (e.g. rapid changes in hormonal levels,
physical stress of childbirth, etc.)
- psychological factors (e.g. awareness of the increased
responsibility of motherhood)
Aetiology, cont.

Psychosocial factors, cont.
Childbirth, cont.
• Rates of pre- and post-natal depression in
developing countries are generally high (affects
10% to 34% of new mothers in South Africa every
year).
• Do not seem to be cross-cultural variations in PPD.
• Socio-economic status not a strong predictor for
PPD.
• Other variables are NB (e.g. history of depression,
personality traits, stressful life events, lack of support,
negative attitude from father).
• Maternal depression may  negative impact on the
infant’s development.
Aetiology, cont.

Loss and rejection
• Object loss = loss of loved one, through death or
separation.
• Link between childhood object loss and adult
depression?
• Not a direct causal link (?) but could predispose
person to depression with subsequent losses.
• Psychoanalytic theory (Freud, 1917) - loss, rejection,
and repressed anger are linked.
- Symptoms of grief and depression are very similar.
- Loss of affection  excessive, irrational grief 
depression and anger  unacceptable, so repressed
and turned inward  guilt.
Aetiology, cont.

Aetiology, cont.
Social support
• Social support = physical and emotional comfort we
receive from people around us.
• People are social beings  form complex network
of relationships.
• Network NB for moderating stress.
• Hause (1984) - four types of social support:
- emotional concern (e.g. caring, empathy, etc.)
- instrumental aid (e.g. money, transport, etc.)
- information (e.g. guidance, advice, facts, etc.)
- appraisal (e.g. feedback from others that is
relevant to our own self-evaluation)

Social support, cont.
• Adverse life events may  depression (and anxiety),
NB in the absence of family support.
• Not enough to simply have people available, they need
to be supportive too.
• Ross & Mirowsky (1989) - the more people talk to
others as a coping strategy, the more depressed they
tended to become.
• Inferential feedback NB for depression; addresses
cause, meaning, and consequences of negative life
events.
• Too much instrumental support may  negative
outcomes (promotes passivity and dependence).
Aetiology, cont.

Social support, cont.
• Combinations of control and support (Walker, 2001):
- High control, low support: Strengthens self-efficacy
and an internal locus of control.
- Low control, high support: Reinforces dependency
on others and an external locus of control.
- High control, high support: Fosters belief in own
capabilities and confidence in support from others.
- Low control, low support: Perceived lack of
resources  helplessness and hopelessness.
- Uncertain control, uncertain support: Results in
anxiety and helplessness, and strengthens an external
locus of control.
Aetiology, cont.

Aetiology, cont.
Behaviour
• Role of classical and/or operant conditioning to
explain the acquisition of abnormal behaviour:
- Negative responses are positively reinforced.
- Positive responses are not reinforced or they
are punished.
• Frude (1998):
- Depressed behaviour is result of behaviour
repertoires extinguished over time.
- Depressive behaviour is often positively
reinforced.

Aetiology, cont.
Behaviour, cont.
• Also, role of self- and social reinforcement as
contributors to depression.
• Social reinforcement improves mood by making
person feel valued/respected.
• No social reinforcement  feel ignored and
undervalued.
• But, depressed people may withdraw from others,
reducing opportunity for social reinforcement.
• Reinforcement may affect course (not be causal?).
• Note circular causal pattern (recursive feedback
loop).

Cognition
• How do depressed people perceive their world?
• Rotter (1966): Locus of control (belief in how one
can affect outcomes of a situation).
• Internal (perceived high personal control over
outcome) or external (perception of little or no
control).
• External locus of control  low self-efficacy and
self-esteem.
Aetiology, cont.

Aetiology, cont.
Cognition, cont.
• Theory of Learned Helplessness (Abramson et al.,
1978) - three basic attributional structures:
- Global vs. Specific: Person feels unable to deal with a
certain event (specific) or any event (global).
- Internal vs. External: internal attributional style
(ascribe failure to self) or external attributional style
(ascribe failure to causes out of their control).
- Stable vs. Unstable: If the person sees problem as
stable, expect it to be long term; unstable problems are
seen as being short term.
• This theory: Depressed people have a global-
internal-stable attributional style.

Cognition, cont.
• Beck (1967): Theory of Hopelessness similar to
Theory of Helplessness (both attribute depression to
faulty perceptions & thought processing).
• According to Beck, depressed people typically display
three basic negative thoughts (‘negative cognitive
triad’); they have negative views of:
- themselves (‘I am a failure.’)
- the world (‘All of my attempts to cope with life
result in failures.’)
- the future (‘Because I’m a failure and I cannot
cope, the future is hopeless.’).
Aetiology, cont.

Cognition, cont.
• Ellis (2004) - depressed people focus on negative
information then over-generalise to other situations.
• Faulty thought content (‘irrational beliefs’) further
perpetuates the problem.
• Thoughts are often expressed in absolute
statements.
• Three typical irrational beliefs that depressed people
display (Ellis, 2004):
- ‘I must always perform well, regardless of the conditions
under which I have to work’
- Others must always treat me fairly, and with respect’
- ‘My living conditions must always be perfect’.
Aetiology, cont.

Stimulus
Organism
Response
PhysiologicalBehaviouralEmotionalCognitive
S
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INTEGRATIVE MODEL

Integrative model
• Many aetiological factors:
- broader socio-economic system (e.g. poverty,
unemployment),
- social system (e.g. family)
- intrapersonal system which includes different
subsystems:
• the physiological,
• the neurological,
• perception,
• cognition, etc.
• NB to try and integrate all of these aetiological factors
 a coherent understanding of findings and theories.
Aetiology, cont.

Integrative model, cont.
• Genetic component: Inherited predisposition to
pathology in general.
• People also inherit specific ‘weaknesses’ which
then predisposes them to a disorder (diathesis-
stress model).
• How is this triggered? May be stress.
• First episode of depression often closely preceded by
stressful life events, more so than recurrent episodes
of depression.
• Increasing sensitivity to life stress over successive
episodes of depression.
Aetiology, cont.

• Biological factors also relate to person’s tendency to negative
emotions, as well as exposure to previous negative life
events, such as loss or rejection, which are stored in long term
memory.
• Poverty, child abuse (physical, sexual, and emotional), as well
as social isolation, are associated with increased risk of
developing depressive disorders later in life. (makes sense since
we learn during childhood how to become social beings.)
• Perceptual style:
- typical inflexible and negative perception of self and world
- maintained by the anterior cingulate  people struggle to
break cycle of negativity. AC plays role in regulating blood
pressure, heart rate and rational cognitive functions, such as
reward anticipation, decision making, empathy, impulse
control and emotion.
Aetiology, cont.

• How people make meaning of themselves and their
world  certain behavioural responses  affects
people’s responses to them.
• Depressed people may initially gain support, but
behaviour may ultimately  rejection by others 
reinforces how they see themselves and others.
• Role of socio-economic and social systems.
• Factors like unemployment, poverty, and childbirth
may directly or indirectly trigger a mood disorder.
- Note: Factors include both adverse life events and
‘normal’ life events (e.g. childbirth, loss, etc.).
Aetiology, cont.

• If person unable to cope effectively with the
demand, may trigger a mood disorder.
• Coping also influenced by how person makes
meaning of the event.
• Also NB role of social support (how much and
what types).
• Lack of social support may lead directly or
indirectly to depression
• Role of neighbourhood social disorder.
(crime/drugs = risk factors).
Aetiology, cont.

• Clearly still not full consensus about classification
and causes of mood disorders.
• Needs broader explanatory model ranging from
basic cellular processes to brain pathways and links
with psychological constructs.
• Need to treat each mood disorder as a separate and
unique entity, as causal factors vary from one
disorder to the other.
• Also, individuals differ in terms of their own unique
causal patterns; some are mostly biological, others
psychogenic.
• Likely that true aetiological picture for each disorder is
highly complex (on all levels) and involves many
different factors.
Conclusion

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