Mood (Affective) disorders

Department of psychology
The first affiliated hospital of ZZU
Huirong guo
Preface
 The affective disorders are so called because one
of their main features is abnormality of mood
 Nowadays the term is usually restricted to disorder
in which this mood is depression elation, but in the
past some authors have included states of anxiety
as well
 The symptom of depression is a component of
many psychiatric symptoms and is also found
commonly in certain physical diseases
Preface
 The central features of these syndromes are known
as mood, pessimistic thinking, lack of enjoyment,
reduced energy, and slowness. Of these,
depressive mood is usually, but not invariably, the
most prominent symptom
 Similar considerations apply to states of elation.
Elation can also occur as a symptom in several
psychiatric syndromes, though it is less widely
encountered than depression
Preface
 The central features are over-activity, self-
important ideas, and elation. Of these, elation
occurs least constantly, and irritability sometimes
occurs instead. This syndrome is called mania
 Depression
 Mania
Classification and Epidemiology
 mania and depression as a single entity
(Kraepelin )
 unipolar depression
 unipolar mania
 bipolar (Leonhard et al , 1962 )
 Nowadays it is standard practice not to use the
term unipolar mania, but to include all cases of
mania in the bipolar group
Classification and Epidemiology
 Depressive symptoms are common ,point prevalence of
between 13%-20% of the population , more frequent
among women, the lower socioeconomic groups, and
the divorced or separated
 Unipolar depressive disorders, the point prevalence is
about 3% for men and 5%-9% for women, annual
incidence vary from about 80 to 200 per 100000 among
men and from 250 to 7800 per 100000 for women
Classification and Epidemiology
 bipolar disorder is less than 1 per cent and the
annual incidence between 9 and 15 per 100000 for
men and between 7 and 30 per 100 000 for women
 the ratio of women to men differ, but it is generally
agreed to lie between 1.3:1 and 2:1
Etiology
 Geneticcauses
 Biochemical causes
 The amine hypothesis
 Endocrine abnormalities
 Psychosocial factors
 Pathogenesis

Biological Psychological Social

Depression Disorder
Genetic causes
 Most family studies have shown that parents, siblings,
and children of severely depressed patients have a
morbid risk of 10%-15% for affective disorder, as
against 1%-2% in the general population
 Twin studies suggest strongly that these high rates
within families are largely due to genetic factors
 There are conflicting theories about the mode of
inheritance because no simple genetic model fits the
frequencies of cases observed among family members
of different degrees of relationship to the proband
Biochemical causes
 The amine hypothesis
 this hypothesis is that depressive disorders are
due to depletion, and mania to excessive provision,
of a monoamine neurotransmitter at one or more
sites in the brain
 More recent elaborations suggest a change in
receptor sensitivity as well as a change in the
turnover or level of the amines (noradrenaline,
dopamine, and 5-hydroxytryptamine (5-HT) )
Biochemical causes
 The amine hypothesis
 The hypothesis has been tested by observations of three
kings of phenomena (1) antidepressant drugs, (2) the
metabolism of neurotransmitters in patients with affective
disorders, (3) the clinical effects of amine precursors and
anatomists
 monoamine oxidase inhibitors (MAOI)
 tricyclic antidepressants
 These actions suggest that the concentration of one of these
transmitters may be important in depressive disorders, but
they do not indicate which one is involved
Biochemical causes
 The amine hypothesis
 More direct evidence comes from studies of post-
mortem brain
 Some investigators have reported lowered
concentrations of 5-HT in the brain stem of
depressed patients, but other investigators have
not confirmed this
 No significant changes have been reported in
concentrations of noradrenaline or dopamine in
post-mortem brains of depressed patients
Biochemical causes
 Endocrine abnormalities
 These abnormalities are important in etiology for three
reasons:
(1) some disorders of endocrine function are followed by depressive
disorders more often than would be expected by chance ,
(2) endocrine abnormalities found in depressive disorder suggest that
there may be a disorder of the hypothalamic centers controlling the
endocrine system ,
(3) endocrine changes are regulated by hypothalamic mechanisms,
which in turn are partly controlled by monoamine systems
Biochemical causes
 Endocrine abnormalities
 Much research effort has been concerned with
abnormalities in the control of cortisol in
depressive disorders
 Attempts have been made to relate these findings
to changes in the neurotransmitters involved in the
central control of ACTH secretion (5HT and
acetylcholine may stimulate, and GABA and
noradrenaline inhibit )
Biochemical causes
 Endocrine abnormalities
 The evidence reviewed above suggests that 5HT
may be low rather than high depressive disorders,
so increased 5HT could not account for the high
output of cortisol
Biochemical causes
 Psychosocial factors
 Depressive disorders often follow stressful events,
However, several other possibilities must be
discounted before it can be concluded that
stressful events cause depressive disorders that
succeed them
 Firstly, the association might be coincidental
 Secondly, the association might be non-specific;
there might as many stressful events in the weeks
preceding other kinds of illness
Biochemical causes
 Psychosocial factors
 Thirdly, it might be spurious; the patient might have
regarded the events as stressful only in retrospect
when seeking an explanation for his illness, or he might
have experienced them as stressful only because he
was already depressed at the time
 It is less certain whether mania is provoked by life
events , mania was thought to arise entirely from
endogenous causes in the past
Biochemical causes
 Psychosocial factors
 However, clinical experience suggests that a
proportion of cases are precipitated, sometimes by
events that have been expected to induce
depression, for example bereavement
Manic episode and bipolar
affective disorder
 Manic episode is characterized by a predominantly
elevated, expansive, or irritable mood that presents as a
prominent or persistent part of the illness
 The bipolar affective disorder is characterized by two or
more episodes in which the patient’s mood and activity
levels are significantly disturbed
 This disturbance consists on some occasions of
an elevation of mood and increased energy and
activity and on others of a lowering of mood and
decreased energy activity (depression)
Manic episode and bipolar
affective disorder
 Clinical features :The central features of the
syndrome of mania are elevation of mood,
increased activity, and self-important ideas
 The patient’s clothing
 overactive
 speech is often rapid and copious
 Sleep is often reduced
 Appetite is increased
 Sexual desires are increased and behavior may be
uninhibited
Manic episode and bipolar
affective disorder
 Clinical features
 Expansive ideas are common
 grandiose delusions
 Hallucinations also occur
 Insight is invariably impaired
Diagnosis
 Criteria for manic episode (DSM-IV, CCMD-3) are as
follows:
 A distinct period of abnormally and persistently
elevated, expansive, or irritable mood, lasting at 1
week
 During the period of mood disturbance, three (or
more) of the following symptoms have persisted
(four if the mood is only irritable) and have been
present to a significant degree:
Diagnosis
 Inflated self-esteem or grandiosity
 Decreased need for sleep (feels rested after only 3
hours of sleep)
 More talkative than usual or pressure to keep
talking
 Flight of ideas or subjective experience that
thoughts are racing
 Distractibility (attention too easily drawn to
unimportant or irrelevant external stimuli)
Diagnosis
 Increased in goal-directed activity (either socially,
at work or school, or sexually) or psychomotor
agitation
 Excessive involvement in pleasurable activities
that have a high potential for pain all
consequences (engaging unrestrained buying
sprees, sexual indiscretions, or foolish business
investments)
Diagnosis
 The mood disturbance is sufficiently severe to
cause marked impairment in occupational
functioning or usual social activities or
relationships with other, or to necessitate
hospitalization to prevent harm to self or others, or
there are psychotic features.
 The symptoms are not due to the direct
physiological effects of substance (a drug of
abuse, a medication, or other treatment) or a
general medical condition
Treatment & Prevention
 Treatment of bipolar disorder depends on the
specific form of behavioral disorder at presentation
 Lithium carbonate is the treatment of choice for the
acute manic state
 Complications are relatively, infrequent, but a
transient "rebound" depression following
resolution of a manic state is not uncommon
Treatment & Prevention
 The degree of psychomotor activation and the
fragile structure of the treatment alliance in acute
mania require that supplemental treatment with
faster-acting neuroleptics be instituted in most
cases
 Chronic treatment with neuroleptics is to be
avoided, as the risk of tardive dyskinesia (TD) is
increased in mood disorders
 the anticonvulsant drugs carbamazepine and
valproate may be tried
Treatment & Prevention
 Some form of psychosocial intervention is almost
always indicated in the treatment of bipolar disorder
 Some patients with bipolar disorder have infrequent
recurrences, experience long symptoms-free
intervals, and are able to lead productive lives
 Others may have a particularly malignant form of
the syndrome or may exhibit pathological degrees
of denial and lead turbulent lives calling for active
psychosocial involvement by the therapist
Depressive Disorder
Depressive syndrome can occur only or in a
bipolar disorder. The clinical picture of depressive
syndromes is so varied that they can not be
described fully in a short space
Clinical Features
 The patient's appearance is characteristic
 Psychomotor retardation is frequent
 The mood of the patient is one of misery
 Agitation is state of restlessness that is
experienced by the patient as inability to relax, and
seen by an observer as restless activity
 Lack of interest and enjoyment is frequent, though
not always complained of spontaneously
Clinical Features
 Reduced energy is characteristic
 The patient feels lethargic, finds everything an
effort, and leaves tasks unfinished
 Sleep disturbance in depressive disorder is of
several kinds
 Most characteristic is early morning waking, but
delay in falling asleep and waking during the night
also occurs
Clinical Features
 Weight loss often seems greater than can be accounted for
merely by the patients’ lack of appetite
 Pessimistic thoughts are important symptoms
 concerned with the present
 The second group is concerned with the future
 The third group of thoughts is concerned with the past
 The delusions of severe depressive disorders are concerned
with the same themes as the non-delusional thinking of
moderate depressive disorders (worthlessness, guilt, ill
health, and poverty .Persecutory delusions )
Diagnosis
 DSM-IV CCMD-3 criteria for depression as follows:
 Major depressive episode
 Five (or more) of the following symptoms have
been present during the same 2-week period and
represent a change form previous functioning
 at least one of symptoms is either (1) depressed
mood or (2) loss of interest or pleasure
Diagnosis
 The symptoms do not meet criteria for a mixed
episode.
 The symptoms cause clinically significant distress
or impairment in social, occupational, or other
important areas of functioning.
 The symptoms are not due to the direct
physiological effects of substance (a drug of
abuse, a medication) or a general medical
condition (hypothyroidism)
Diagnosis
 The symptoms are not better accounted for by
bereavement, i.e. after the loss of a loved one, the
symptoms persist for longer than 2 months or are
characterized by marked functional impairment,
morbid preoccupation with worthlessness, suicidal
ideation, psychotic symptoms, or psychomotor
retardation
Diagnosis
 Major depressive disorder, single episode
 Presence of a single major depressive episode
 The major depressive episode is not better accounted for by
schizoaffective disorder and is not supperimposed on
schizophrenia, schizophreniform disorder, delusional
disorder, or psychotic disorder not otherwise specified.
 There has never been a manic episode, a mixed episode, or a
hypomanic episode
Diagnosis
 Major depressive disorder, recurrent
 Presence of two or more major depressive episodes;
 The major depressive episodes are not better accounted for
by schizoaffective disorder and are not superimposed on
schizophrenia, shchizophlreniform disorder, delusional
disorder, or psychotic disorder not otherwise specified.
 There has never been a manic episode, a mixed episode, or a
hypomanic episode
Differential Diagnosis
 Depression occurs concomitantly with a number of
different disease states :depression and dementia,
especially in the elderly, may be confused.
However, patients with dementia may develop
major depression as well
 Schizophrenia
 present with behavioral and physiological changes
identical to those observed in major depression
Treatment
 Biomedical therapies
 Psychosocial Therapies
Treatment :Biomedical therapies
 Antidepressant drugs have therapeutic effects in
depressive illness .Two groups of drugs :one consists of
the tricyclic antidepressants and related compounds ; The
second consists of the monoamine oxidase inhibitors ;
New generation antidepressants, such as selective
serotonin reuptake inhibitors (SSRIs)
 Drug selection should be based on the patient's general
medical condition, the drug's side effects, and a personal
or family history of therapeutic response to a specific
agent
Treatment :Biomedical therapies
 Clear therapeutic benefit usually is noticed 14-
21days after starting treatment
 MAO inhibitors
 It is not always clear how long maintenance
treatment should be continued after acute
symptoms have subsided
 Patients with very severe depressions and
prominent delusional features are relatively
refractory to traditional antidepressant treatment
Treatment :Biomedical therapies
 The response often can be enhanced by addition of
an antipsychotic agent. Electroconvulsive therapy
should be considered in such cases and in cases
of no delusional major depression resistant to drug
therapy
 There are few contraindications to the use of
electroconvulsive therapy
Treatment :Psychosocial therapies

 improving social functioning following remission

of acute symptoms
 the combination of psychotherapy and
antidepressant medication is more effective than
either used alone
 therapies focused on the depressed patient's
interpersonal functioning and cognitive distortions
appear to be the most productive
 Insight therapy
 Cognitive therapy (homework assignments )
Treatment :Psychosocial therapies

 Family and spouse involvement should not be

neglected in treatment planning
 education about the illness
 emotional support
 consideration of interpersonal issues
Some clinical cases
A 27-year-old male graduate student
 The patient was a surgeon referred by an
internist
A 34-year-old unmarried computer programmer
was referred for evaluation of chronic depression.
summary
It is difficult to conceive of an area in psychiatry in which
the clinician’s attitude, knowledge, and skills are more severely
tested than in the diagnosis and treatment of mood disorders.
 As reviewed in this chapter, there is considerable evidence
for a biological basis for most mood disorders. Data
supporting this hypothesis have come from genetic,
biochemical, psychopharmacological, and
neuroendocrinological （神经内分泌） investigations, and
the hope is that psychiatric diagnoses in this area will become
a more objective press as these research efforts continue.
summary
Although subgroups of mood disorders seem relatively
distinct from one another as described, in clinical practice
there is often considerable overlap between symptoms of
different disorders as well as ambiguity about the class in
which a given individual belongs.
With the present state of knowledge, predictions about
course of illness and response to treatment for patients with
mood disorders remain as much an art as a science
Use of the bio-psychosocial model in the understanding of
mood disorders illustrates the awesome complexity of central
nervous system regulation of affect but holds out promise of
successful methods of treatment on many different levels
Thank you

See you next time

Thank you

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