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variously included a level of severity that leads to distortion of reality, melancholic depression,
endogenous depression, or the opposite of neurotic depression (defined in this context as depression
with a psychosocial etiology) [8]. All of these classifications considered psychotic depression to be a
severe subtype of major depressive disorder (MDD). In DSM-IV [9], psychotic depression became a
severe subtype of MDD characterized by delusions or hallucinations [4]. In DSM-5 [10], psychotic
depression is still a subtype of MDD rather than a separate disorder, but the psychosis specifier is
independent of severity, so that depression does not have to be severe to justify a diagnosis of psychotic
depression [4]. In fact, DSM-5 permits psychotic features with dysthymia as well as major depression,
acknowledging the idea that psychotic features are not just a function of severity of depression [11].
This change reflects an understanding that many depressive disorders can occur with or without
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Depressive Disorders
MAJOR DEPRESSIVE DISORDER
DSM-5 DIAGNOSTIC CRITERIA FOR MAJOR DEPRESSIVE DISORDER (MDD)
Reprinted with permission from the Diagnostic and Statistical Manual of Mental
Disorders, 5th ed. 2013. American Psychiatric Association
A. presence of a single MDE (vs. recurrent, which requires presence of two or more
MDEs; to be
considered separate episodes, there must be an interval of at least 2 consecutive
mo in which criteria
are not met for a MDE)
B. the MDE is not better accounted for by schizoaffective disorder and is not
superimposed on
schizophrenia, schizophreniform disorder, delusional disorder, or psychotic
disorder NOS
C. there has never been a manic episode or a hypomanic episode
• Note: This exclusion does not apply if all of the manic-like, or hypomanic-like
episodes are substance or
treatment-induced or are due to the direct physiological effects of another
medical condition

• specifiers: with anxious distress, mixed features, melancholic features, atypical

features, mood-
congruent psychotic features, mood-incongruent psychotic features, catatonia,
peripartum onset,

seasonal pattern
Epidemiology
• lifetime prevalence: 12%
• peak prevalence age 15-25 yr (M:F=1:2)
Etiology
• biological
■ genetic: 65-75% MZ twins; 14-19% DZ twins, 2-4 fold increased risk in first-
degree relatives
■ neurotransmitter dysfunction: decreased activity of 5-HT, NE, and DA at
neuronal synapse; changes
in GABA and glutamate; various changes detectable by fMRI
■ neuroendocrine dysfunction: abnormal HPA axis activity
■ neuroanatomy and neurophysiology: decreased hippocampal volume, increased size
of ventricles;
decreased REM latency and slow-wave sleep; increased REM length
■ immunologic: increased pro-inflammatory cytokines IL-6 and TNF
■ secondary to medical condition, medication, substance use disorder
• psychosocial
■ cognitive (i.e. distorted schemata, Beck’s cognitive triad: negative views of the
self, the world, and
the future)
■ environmental factors (i.e. job loss, bereavement, history of abuse or neglect,
early life adversity)
■ comorbid psychiatric diagnoses (i.e. anxiety, substance use disorder,
developmental disability,
dementia, eating disorder)
Risk Factors
• sex: F:M=2:1
• family history: depression, alcohol use disorder, suicide attempt or completion
• childhood experiences: loss of parent before age 11, negative home environment
(abuse, neglect)
• personality: neuroticism, insecure, dependent, obsessional
• recent stressors: illness, financial, legal, relational, academic
• lack of intimate, confiding relationships or social isolation
• low socioeconomic status
Clinically-Significant Depressive Symptoms in the Elderly
• affects about 15% of community residents >65 y/o; up to 50% in nursing homes
• high suicide risk due to social isolation, chronic medical illness, decreased
independence
• suicide peak: males ages 80-90; females ages 50-65
• low mood or dysphoria may not be a reliable indicator of depression in those >70
y/o
• often present with somatic complaints (i.e. changes in weight, sleep, energy;
chronic pain) or anxiety
symptoms
• may have prominent cognitive changes after onset of mood symptoms (dementia
syndrome of
depression)
• see Table 3, for a comparison of delirium and dementia
Treatment
• lifestyle: increased aerobic exercise, mindfulness-based stress reduction
• biological: SSRIs, SNRIs, other antidepressants, somatic therapies (see
Pharmacotherapy, PS49 and
Somatic Therapies, PS57)
■ 1st line pharmacotherapy: sertraline, escitalopram, venlafaxine, mirtazapine
■ for partial response, optimize the dose or add augmenting agent (bupropion,
quetiapine-XR,
aripiprazole, lithium)
■ for non-response, change class of antidepressant
■ typical response to antidepressant treatment: physical symptoms improve at 2
wk, mood/cognition
by 4 wk; if no improvement after 4 wk at the highest tolerated therapeutic dosage,
alter regimen
■ ECT: currently fastest and most effective treatment for MDD. Consider in
severe, psychotic or
treatment-resistant cases
■ rTMS: current data support efficacy equivalent to medications (but not to ECT)
with good safety
and tolerability
■ phototherapy: especially if seasonal component, shift work, sleep dysregulation
• psychological
■ individual therapy (CBT, interpersonal, supportive), group therapy, family therapy
• social: vocational rehabilitation, social skills training
• experimental: magnetic seizure therapy, deep brain stimulation, ketamine
Prognosis
• 1 yr after diagnosis of MDD without treatment: 40% of individuals still have
symptoms that are
sufficiently severe to meet criteria for MDD, 20% continue to have some
symptoms that no longer meet
criteria for MDD, 40% have no symptoms

Mood Disorders in Children and Adolescents

MAJOR DEPRESSIVE DISORDER
Epidemiology
• lifetime prevalence for pre-pubertal 1-2% (F:M=1:1); adolescents 4-18% (F:M=2:1)
Clinical Features
• only difference in diagnostic criteria for children and adolescents is that
irritable mood may replace
depressed mood
• physical features: insomnia (children), hypersomnia (adolescents), somatic
complaints, substance
misuse, decreased hygiene
• psychological features: irritability, boredom, anhedonia, low self-esteem,
deterioration in academic
performance, social withdrawal, lack of motivation, listlessness
• common comorbid diagnoses: anxiety, ADHD, ODD, conduct disorder, eating
disorders, and substanc
misuse
Treatment
• majority never seek treatment
• supportive therapy including psychoeducation, active listening, and lifestyle
advice helpful in mild
depressive episode
• CBT or IPT, internet-based therapy if in-person options unavailable
• 1st line SSRI: fluoxetine
• 2nd line SSRIs: escitalopram, sertraline, citalopram
• close follow-up for adolescents starting SSRIs to monitor for increased suicidal
ideation or behaviour
• in severe depression, best evidence for combined pharmacotherapy and
psychotherapy
• ECT or rTMS: limited evidence in this population, only for use in adolescents ≥12
y/o with severe
illness, psychotic features, catatonic features, persistently suicidal
• light therapy, self-help books, and applications can be used as adjuncts
Prognosis
• prolonged episodes, up to 1-2 yr = poor prognosis
• prognosis variable; adolescents with depression more likely to have depression in
adulthood than
adolescents without
• approximately 2% of adolescents with depression will develop bipolar disorder
within 4 yr
• complications: negative impact on family and peer relationships, school failure,
significantly increased
risk of suicide attempt or completion (however, suicide risk low for pre-pubertal
children), substance
use disorder

at glance
clinical features:
 Pemikiran sering kali negatif, pesimis tentang

 Simptom biologis : menurun tidur, nafsu makan, dan libido may be particularly
prominent in older people, who less often complain of disturbed mood. There
is often a sleep pattern of early waking (more than two hours before usual)
and maximal lowering of mood in the morning (diurnal variation). Poor
appetite is often associated with weight loss; in severe cases, food and
fluids may be refused.
 Motor activity is often altered, with psychomotor agitation, retardation (of
speech and/or movement), or both.
 Cognition may be impaired, with reduced attention, concentration and
decisiveness.
 Depressive symptoms can be masked by severe anxiety, alcohol,
hypochondriacal preoccupations or irritability.
  Anhedonia is usually accompanied by loss of motivation and emotional
reactivity.
 Psychotic features may occur and are usually mood-congruent. Delusions are
usually nihilistic (e.g. a belief that one is dead, has lost all one’s assets or
one’s body is rotting), delusional or hypochondriacal, concerning illness or
death. Where hallucinations occur they are usually auditory, in the second
person and accusing, condemning or urging the individual to commit suicide.
 Atypical depression is characterised by initial anxiety-related insomnia,
subsequent oversleeping, increased appetite and a relatively bright, reactive
mood. It is more common in adolescence.
 Depression is often also comorbid with anxiety disorders, eating disorders,
personality disorders and substance misuse.
DD
• Normal sadness, particularly in the context of bereavement
(Chapter 10) or severe physical illness. The diagnosis depends on
finding a pattern of characteristic features and on the degree and
duration of associated disability. Predominant negative, guilty
or suicidal thoughts support a diagnosis of depression, but such
symptoms may be difficult to elicit if depression is severe.

• Psychotic depression should be differentiated from schizo-

phrenia (Chapter 6) on the basis of thought content (mood-con-
gruent psychotic features) and the temporal sequence in which the symptoms
developed.

• Depressive retardation may be difficult to distinguish from the

flat (unreactive) affect of chronic schizophrenia (Chapter 6).
• Alcohol or drug withdrawal may mimic depression.

Epidemiology
• The lifetime risk of depression is about 10–20%, with rates
almost doubled in women.
• First onset is typically in the third decade (earlier for bipolar
disorder).

• Depression is strongly associated with socioeconomic depriva-

tion.
Aetiology
• A genetic contribution is evident in both twin and adoption
studies but less markedly for unipolar than bipolar depression.
Current theories implicate gene-environment interactions – i.e.
a genetic predisposition to depression if exposed to adverse life
events.
• Monoamine neurotransmitter availability (particularly
noradrenaline and serotonin) in the synaptic cleft is reduced in
depressed patients, and antidepressants increase monoamine

availability. It is now thought that this results in secondary neu-

roplastic changes that bring about the antidepressant effect. One

suggested mechanism is that the greater monoamine availability

leads to increased production of Brain Derived Neurotrophic
Factor (BDNF) that promotes neurogenesis.
• Hypercortisolaemia has been reported in severe depres-
sion, while in atypical depression hypocortisolaemia has been
reported.
• The limbic system and related areas such as the prefrontal
cortex regulate emotion, reward and executive function, and
dysfunctional changes have been implicated in depression.
Deep brain stimulation of the subgenual cingulate cortex or the
nucleus accumbens has an antidepressant effect.
• Psychosocial factors implicated are recent adverse life events
(e.g. bereavement or deteriorating physical health) and adverse
current social circumstances, especially unemployment and
lack of a confiding relationship. Parental loss and major child-
hood stress or abuse appear to increase vulnerability to depres-
sion in adulthood. Stress leads to increased cortisol levels,
which may cause depressed mood through decreasing expres-
sion of BDNF.

• Cytokines are also important modulators of mood. Interleu-

kin 1 (IL-1) produces ‘sickness behaviour’ in rodents. A third of

those treated with recombinant interferons develop depression.

• Several physical illnesses (most endocrine disorders, many
cancers, some viral infections) and some medications (including
steroids, isotretinoin (for acne)) are specifically associated with
depression.
• Women are particularly vulnerable to episodes of depression
in the weeks following childbirth.

Management
• Most depressive illnesses can be managed in primary care,
although many are undetected. Psychiatric referral is indicated if
suicide risk is high or if the depression is severe, unresponsive to
initial treatment, bipolar or recurrent.
• Depressed patients often present with other conditions.
• Always assess risk of self-neglect and suicide.

• Treat comorbid physical illnesses or substance misuse prob-

lems.
• For mild depression, self-help groups, structured physi-
cal activity groups, guided self-help or computerised cognitive

behavioural therapy (CBT) are often helpful (Chapter 33).

• If these less intensive therapies do not help, individual CBT or
interpersonal therapy (IPT) may be recommended. Behavioural
activation or, where appropriate, behavioural couples therapy
can also be of use.

• Psychological therapy should be given together with antide-

pressants (Chapter 35) for moderate or severe depression. These

can have a 60–70% response rate but often fail because of inad-
equate dosage, duration or adherence.

• Continuing antidepressants for at least six months reduces

relapse; in recurrent depression, prophylactic effects have been

demonstrated for up to five years. When discontinuing antide-

pressants, taper slowly to avoid withdrawal symptoms. In bipo-
lar depression, mood stabilisers (e.g. lithium – Chapter 36) are

preferable. CBT or mindfulness-based cognitive therapy can also

help prevent relapse.

• Resistant depression may respond to combining an antide-

pressant (augmenting) with lithium, an atypical antipsychotic

(aripiprazole, olanzapine, risperidone, quetiapine) or another

antidepressant (e.g. mirtazipine).
• Electroconvulsive therapy (ECT) is very effective in severe
cases, particularly where psychosis or stupor is present, and can
be lifesaving if fluids and food are being refused.z
• Single episodes of depression usually last three to eight
months. About 20% of patients remain depressed for two years
or more and 50% have recurrences; this rises to 80% in severe
cases. Recurrent episodes tend to become increasingly severe

with shortening of disease-free periods, emphasising the impor-

tance of prophylactic treatment.

• Lifetime suicide risk is 15% in severe depression but much lower

in milder illness. There is an association between major depressive

disorder/bipolar disorder and increased cardiovascular morbid-

ity and mortality. Predictors of poor outcome include early onset,

greater symptom severity and psychiatric or physical comorbidity.

SIGN of Depression
1. veraguth fold
 triangular fold at nasal side of upper eyelid
2. omega sign
-> seen on forehead, due abnormal tone of facial muscles, see in old age
(tp no diagnostic value & not dependant on severity)
 Criteria for depression fulfilled