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

Introduction, cont.

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 modern society.

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.

Major Depressive Disorder, cont.

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.


Major Depressive Disorder, cont.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).


Major Depressive Disorder, cont.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.


Major Depressive Disorder, cont.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.


Major Depressive Disorder, cont.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.


Major Depressive Disorder, cont.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.


Manic Episode, cont.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.

Manic Episode, cont.Behavioural symptoms• 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).

Behavioural symptoms• 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.

Biological factors, cont. 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.

Biological factors, 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.

Biological factors, 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.

Biological factors, 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 factorsChildbirth• 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.

Psychosocial factors, 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. Psychosocial factors, 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)

Psychosocial factors, cont.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.

Psychosocial factors, 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.

Psychosocial factors, 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. Psychosocial factors, 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).

Psychosocial factors, cont. 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. Psychosocial factors, 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.

Psychosocial factors, cont. 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.

Psychosocial factors, 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.

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.

Integrative model, 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.

Integrative model, 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.

Integrative model, 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

Education

Chapter 5 (revised)