V. 기분장애(Mood Disorders)

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Transcript V. 기분장애(Mood Disorders)

V. Mood Disorders
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It was called as a "depressive disorders" or as an
"affective disorders“ or as "depressive neuroses”.
In DSM-III-R, changed as "Mood Disorders"
most common diagnosis
-> major depressive episode
 Diagnosis criteria
extreme depressive symptoms at least two weeks
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Cognitive symptoms (feeling of worthlessness,
difficulty in decision making)
Bodily symptoms (change of sleep pattern, appetite,
weight, reduced energy)
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Body symptom is most important component
General loss of interest in things
Inability to experience any pleasure from life,
including interaction with family or friends or
accomplishments at work or at a school
Lasts in average 9 months, if not treated
Second most common disorder
-> manic episode
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Diagnosis criteria ->
Symptom lasts at least 1 week
Require less, if symptoms are severe enough to
require hospitalization
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Elated mood, extreme excitement, euphoria
Excessive activities, reduced need of sleep
develop grandiose plan believing they can
accomplish anything they desire
flight of ideas : speech is typically rapid and may
become incoherent, because the individual is
attempting to express so many exciting ideas at
once
Often accompanies anxiety, especially in the
ending phase
Lasts 6 months, if not treated
hypomanic episode
=> not severe manic
no difficulties in adjusting to daily life or work
Characteristics of mood disorder
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Unipolar mood disorder
experience either depressive or manic symptom,
although it is rare that only manic symptoms are
present
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bipolar mood disorder
-> experience both
symptoms alternately
depressive
and
manic
depression and elation are relative independent ->
an individual can experience manic symptoms but
feel somewhat depressed or anxious at the same
time -> mixed manic episode
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feeling of out of control or dangerous
Manic
patients
experience
often
depression and anxiety
Course of disease
Individual difference in terms of frequency,
severity, and of symptoms
Unipolarity, bipolarity
Different intervention according to course
Most depression eventually remit on their
own within 6 months
10% last longer than 2 years
1. Depressive Disorders
< clinical description >
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major depressive disorder, single episode
- Pure depression without manic or
hypomanic episodes before or during the
disorder
- An occurrence of just one isolated
depressive episode in a lifetime is rare
major depressive disorder, recurrent
- If two or more major depressive episodes
were occurred and were separated by at
least two months during which the
individual was not depressed
- repeats recovering and relapse lifelong
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Relapse in average 4 times in a life
and lasts 5 months
High heredity
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85% of major depression, single episode
-> later becomes major depression, recurrent type
(Solomon et al, 2000)
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Feeling
of
worthlessness,
difficulty
in
concentration
 Repeated suicidal ideation, sleep difficulties, and
loss of energy
 Abraham Lincoln
severe depression
=> postponed his marriage for 3 days
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< dysthymic disorder >
Similar to major depression
 Symptom is weaker
 Duration is far longer (20, 30 years)
 Lasts at least 2 years
+ should not be without symptoms longer
than 2 months
 If major depression and dysthymic disorder are
present at the same time
-> double depression
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In most cases, it begins as dysthymic
disorder
-> later develops a major depression
in which case the prognosis is not good
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After recovery of major depression
-> dysthymic disorder
-> major depression
(Akiskal & Kassano, 1997)
< onset and duration >
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Average onset of the major depression
-> general group : 25 age
-> clinical group : 29 age
Recently earlier onset
Higher prevalence
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Born before 1905
-> less than 1 % at the age of 75
Born after 1955
-> 6% at the age of 24
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Confirmed in Puerto Rico, Canada, Italy, Germany,
France, Taiwan, Lebanon, New Zealand that this
trend
toward
developing
depression
at
increasingly earlier ages is occurring worldwide
(Cross National Collaborative group, 1992)
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Dysthymic disorder with onset before age 21
-> more chronic, poor prognosis
-> higher heredity
-> more often comorbid with a personality disorder
According to recent research
 High
prevalence of children dysthymic
disorder
-> 76% of these children develop later a major
depression
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Patients with dysthymia are more likely to
attempt suicide than major depression
patients
It is relatively common for major depressive
episodes and dysthymic disorder to co-occur
(double depression) (McCullough et al., 2000)
2. Bipolar Disorders
Alternation of manic episodes with major
depressive episodes
-> bipolar I disorder
 Alternation of hypomanic episodes with major
depressive episodes
-> bipolar II disorder
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Similar to major depression
only manic or hypomanic symptoms are added
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cyclothymic disorder
-> milder form of bipolar disorder
similar to dysthymic disorder
1/3 of them develop later a bipolar disorder
onset 12-14세
< onset and duration >
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bipolar I disorder -> average 18 age
bipolar II disorder -> average 22 age
Both can begin in childhood
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Rarely begins later than 40 age
Earlier onset than major depression
More abrupt onset
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1/3 of them begin in adolescence
Mostly begins as a mild cyclothymic mood swing
10-13% of bipolar II disorder
-> leads to bipolar I disorder
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Unipolar disorder and bipolar disorder are two
independent disorder
381 patients were observed for 10years
-> only 5.2% of unipolar depression patients
experience
manic episode (Coryell, Endicott, et
al., 1995)
Frequent suicidal attempt (19%; Jamison, 1986)
Mostly takes place during major depressive
episodes
symptom specifiers
1. atypical features specifier (type)
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specific features of depression
excessive sleep, intake of foods
gain weight during depressive episode
Partial interest in specific object
2. melancholic features specifiers (type)
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In case of major depression
Severe body symptoms
Wake up early, loss of weight, loss of libido
Excessive and inappropriate guilty feeling
Anhedonia
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Respond well to physical treatment (ECT)
Respond well to drug
(tricyclic antidepressant)
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Occur independent of stress
Can find more among the elderly
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3. Chronic features specifiers
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Continuous symptoms of major depression in
last 2 years
4. Catatonic features specifiers
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Rare, but in major depression or manic
disorder
Immobility, waxy posture
Excessive aimless movements
5. Psychotic features specifiers
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major depression or manic disorder
can have hallucination or delusion
bodily delusion (example: part of body
decay)
mood congruent hallucination
mood incongruent hallucination
(depression -> delusion of grandeur)
more severe -> likely to develop a schizophrenia
5-15% of depressive disorder patients experience
hallucination
poor premorbid adjustment -> more likely to
experience psychotic symptoms
need to be treated with neuroleptics
6. postpartum onset specifier
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severe major depression or manic episode
Within 4 weeks after delivery (typically within
2-3 days)
Experiences psychotic symptoms
Could be a beginning sign of a bipolar
disorder
1 out of every 1,000 women after a delivery
50% of those who had already experienced
one episode experience again
In some case, kills their baby
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Mild depression after delivery excluded
Physical exhaustion through labor
A new task to fulfill
Change of the identity
Change of the environment
Burden of child rearing
Relationship between childbirth and depression
-> comparative study
no difference found between the group with childbirth
and the group with no childbirth (Whiffen & Gotlib,
1993)
postpartum blues
tearful, temporary mood swing
50-80% of mother show this symptom 1-5 days after
childbirth -> disappears within a few days
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Specifiers describing course of Mood disorders
3 characteristics that distinguish between
recurrent depression and manic disorder
- longitudinal course
- rapid cycling,
- seasonal pattern
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They differ in the course and time pattern
-- needs different intervention strategies
1. Longitudinal course specifiers
It is important to know whether the individual had a
major depressive episode or manic episode
 Whether he/she recovered fully from it
 Whether a major depressive patient had in the
past a dysthymia
-> if yes, double depression
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Whether a bipolar disorder patient had in the past a
dysthymia or cyclothymia
-> if yes, low chance of full inter-episode recovery
In case of major depression, bipolar I, bipolar II
disorder, it is important to know the course
2. Rapid-cycling specifier
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It pertains to bipolar I, bipolar II disorder
Whether it has a slow or rapid cycling
In case of rapid cycling
-> more than 4 times per year
-> traditional therapy not effective
Tricyclic antidepressant -> there is a risk to evoke
a rapid cycling
3. Seasonal pattern specifier
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It pertains to bipolar disorder and recurrent major
depressive disorder
Changes according to season
Mostly begins at late fall and ends early spring
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During the winter depression, summer manic
episode
-> seasonal affective disorder (SAD)
In most cases depression during winter
-> 5% of American are afflicted -> excessive sleep
and eating -> gaining weight
diminishing sun light in winter -> increase of the
pineal gland hormone melatonin
Phototherapy
-> exposing to bright light in early morning 2 am
effects show up within 3-4 days
within 1-2 weeks SAD remit
side effect : 19% experience headache
17% eyestrain (Levitt et al., 1993)
< Prevalence of mood disorders >
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Life time prevalence in US 19% (Kessler, 1994)
Female have higher prevalence than men 2 : 1
In case of bipolar disorder, no difference
Black people show lower rate compared to whites or
hispanics
disease
last year
lifelong
-------------------------------------------------major depr
6.5%
16.1%
dysthymia
3.3%
3.6%
bipolar
1.1%
1.3%
< Depression of children and adolescence >
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3 month old infants can have also depression
Related to mother’s depression
(by way of genetics and interaction)
Child depression and adults depression are similar in
their character
There are no difference in regard to developmental
stages
But ‘look’ of depression changes with age
child-> facial expression, eating, sleep disorder
adolescence -> low self-esteem
frequent suicidal attempt
Prevalence rate of childhood lower than adult
During adolescence, it increases dramatically
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In childhood-> dysthymia is more frequent
In adolescence -> major depression is more
frequent
Bipolar disorder very rare in childhood
During adolescence -> dramatic increase of bipolar
disorder
Adolescence major depression occurs in most cases
to girls
Childhood major depression
-> irritability, mood swing
-> easily misdiagnosed as a hyperactivity
Childhood depression accompanies aggressive
behavior, especially for boys
-> easily misdiagnosed as a hyperactivity or conduct
disorder
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Quite often conduct disorder and childhood
depression occurs together (comorbid)
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32% of ADHD children -> major depression
comorbid (Biederman et al., 1987)
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Adolescence bipolar disorder
-> aggressive, impulsive, excessive sexual behavior,
traffic accidents
< Depression among the elderly >
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18-20% of nursing home residents experience major
depressive episodes
after age 60 mostly become chronic
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In case of late onset, sleep disorder
hypochondriasis
Physical illness, dementia, decrease of social
support -> depression
prevalence rate in the elderly -> similar to that of
general population
Physical illness with depression
-> needs longer treatment than pure physical illness
No sexual difference in terms of prevalence after age
65
< cultural differences >
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Differences among different cultures
Individualistic cultures
-> "I feel blue" or "I am depressed"
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Collectivistic cultures
-> "my heart is broken"
"our life has lost its meaning"
American Indian
Prevalence rate
men 19.4% ; women 36.7% (Kinzie et al., 1992)
< creativity >
Relationship between Mood disorder and creativity
In the New Oxford Book of American Verse
of the 36 poet enlisted, 8 were bipolar disorder ( 5
committed suicide )
Virginia Wolf was also bipolar disorder and
committed suicide
< Anxiety and depression >
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Anxiety and depression are closely related to each
other
Most of the depressive patients experience anxiety
But not all the anxiety disorder patients experience
depression
Pure depression component
-> anhedonia
 Lowered cognitive and motor functioning
most depression begins with anxiety
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cause
It is very complex
biological, psychological
interacting with each other
and
social
factors
1. Biological dimensions
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Family research
Family members of mood disorder patients have
higher prevalence rate
-> 2-3 times higher than general population
Family members of bipolar disorder
-> higher only in major depressive symptoms
Family members of the major disorder patients
-> higher prevalence only in major depressive
symptoms
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Is bipolar disorder -> an extension of unipolar
disorder ? (Blehar et al., 1988)
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Adoption study
Parents prevalence of the adopted mood disorder
children
- compared with the parents of the adopted
children without mood disorder symptom :
Mendlewicz & Rainer(1977)
-> higher prevalence
Von Knorring et al(1983)
-> no difference
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Twin research
Identical twin are likely to present 3 or more times
with mood disorder than fraternal twins, if the first
twin shows a mood disorder.
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If the first twin has a bipolar disorder, then even
higher concordance rate
-> if he /she is a bipolar I disorder
-> then the rate that the other twin shows a mood
disorder (not bipolar) is over 80%
in case of severe mood disorder
if the first twin is severe major depression
-> identical twin : 59%
-> fraternal twin : 30% concordant
In case of not severe major depression
-> identical twin : 33%
-> fraternal twin : 14% concordant
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Neurotransmitter systems
Close relationship between mood disorder and
neurotransmitter
serotonin’s function of emotion regulation
- by way of norepinephrine and dopamin
if serotonin level diminishes => get impulsive and
fluctuation of emotions
Absolute quantity of a single neurotransmitter is
not so much important as the balance with other
neurotransmitters
The importance of dopamine in the etiology of the
mood disorder gets attention
The relationship between L-dopa and hypomania
(Van Praag & Korf, 1975)
The endocrine system
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Mood disorder-> related to endocrine system
hypothyroidism (Cushing’s disease)
-> excessive secretion of cortisol -> depression
HPA axis (brain circuit)
hypothalamic-pituitary-adrenalcortical axis
DST (dexamethasone suppression test)
dexamethasone is a glucocorticoid that suppresses
cortisol secretion in normal subjects.
-> however, when this substance was given to
depressive patients, much less suppression was
noticed
=> 50% of depressive patients showed reduced
suppression
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In depressive patients the adrenal cortex
secreted enough cortisol to overwhelm the
suppressive effects of dexamethasone
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In recent study anxiety disorder patients
demonstrated also non-suppression on DST
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Sleep and circadian rhythms
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Sleep patterns of depressive patients
sleep time before REM phase is shorter than
the normal (90min)
Lack of deep sleep (slower wave sleep)
More intensive REM sleep than the normal
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More often awake in the middle of night
If being waked up in the later phase of the
sleep
-> improves depressive symptoms
-> relationship between depression and
biorhythm (Wehr & Sack, 1988)
Depression which came after stressful
event
-> didn’t show REM sleep disorder
-> better responded to psycho-social
treatment
2. Psychological dimensions
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Stressful life events
Stress events prior to onset of mood disorder
context and meaning of the stress is more
important than stress event itself
In most research was proven :
The relationship between mood disorder and
stressful event
Mood disorder following a severe stress
event => takes longer time for treatment
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Etiology of mood disorder
-> related to stressful events
-> its own dynamic after outbreak
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Only 20 - 50% of the normal population who
experienced a severe stress event develop a
mood disorder
-> interaction between stressful event, biological
and psychological vulnerability
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Learned
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attitude
helplessness
and
Seligman’s(1975) rat experiment
dysfunctional
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If electric shocks are not avoidable
-> develops a depression
First reacts with anxiety
-> learns that it is uncontrolable
-> depression
The depressive attributional styles
a) internal (“it is all my fault”)
b) stable (“additional bad things will always
be my fault”)
c) global (“the bad situations is
all my fault”)
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The causality of depressive attributional
style
Is that the cause or the result ?
Child study of Nolen-Hoeksema, Girgus &
Seligman (1992)
Life stress events explained more variance
than attributional style
- but childhood attributional style
explained much of the variance
in adult depression
- childhood stress event influences
children’s attributional style
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Negative attributional style is to be found not only
in depression but also in anxiety disorder
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Abramson, Metalsky and Alloy
-> revised the importance of the attributional style
in the etiology of depression
-> the sense of hopelessness is more important
Both anxiety disorder patients
and depressive disorder patients
experience helplessness,
but, only depressive patients give up
-> hopelessness about regaining the control
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Beck’s cognitive theory of depression (1967)
cognitive errors of the depressive patients
1) Arbitrary inference
-> fails to see various aspects of things (A high
school teacher infers that he is a terrible teacher,
because one student out of 20 students fell
asleep)
2) Over-generalization
-> when a professor makes a critical remark on
your paper, you then assume you will fail the class
despite a long string of positive comments and good
grades on other papers
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The depressed always makes thinking errors
-> they think negatively about themselves, their
immediate world, and their future => depressive
cognitive triad
Negative cognitive schema of the
depressive patients
1) self-blame schema
individuals feel personally responsible for
every bad thing that happens.
2) negative self-evaluation schema
individuals believe they can never do
anything correctly.
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These cognitive errors and schemas are automatic,
that is, not necessarily conscious. Beck’s cognitive
theory of depression (1967)
=> automatic thoughts
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Dysfunctional attitude and hopelessness
attribution (negative outlook)
-> high risk for depression
(M. Seligman)
Temple-Wisconsin study of cognitive
vulnerability of depression
Student group longitudinal study
(2.5year)
-> high risk group -> 17%
low risk group -> 1%
developed a major depression
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High risk group -> 39%
Low risk group -> 6%
developed a minor depression
(Gotlib & Abramson, 1999)
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Psychological vulnerability + biological
vulnerability
-> slippery path to depression
social and cultural dimension
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Influence of divorce on depression
study of Bruce and Kim(1992)
695 women and 530 men were re-interviewed
1 year after divorce
21% of divorced women showed severe depression
-> 3 times as much as women who were not
divorced
17% of divorced men showed severe depression
-> 9 times as much as men who were not divorced
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Marital support have a significant impact on
developing a depression
- high marital conflict + low marital support
-> susceptibility of depression
(Gotlib & Beach, 1995)
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Depression -> endangers marital
relationship ( in men )
Marital problem -> depression (in women)
=> treatment of marital problem is important
for treating depression (Fincham et al., 1997)
Mood disorders in women
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Bipolar disorder -> no gender difference in
terms of prevalence
Major depression-> 70% are women
similar distribution worldwide
the same with anxiety disorders
Low controllability of women
Men are expected to be independent, self
assertive, whereas women to more passive, to
be sensitive to other people, and perhaps to
rely on others more than males do
(Hammen et al., 1985)
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Men are at greater risk in the process of
divorce
Women are more disadvantaged in the
society
More
discrimination,
poverty,
sexual
harassment, and abuse
Full time working women
-> no difference compared to control
men group
Men group
-> higher rate on the problem related with
aggressivity, hyperactivity, drug abuse
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Social support
Existence of social support has great influence
on the development of depression
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Severe life stress
When there is social support
-> 10% developed a depression
when there is no social support
-> 37% developed a depression
(Brown et al., 1978)
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Social support have also influence on
the recovery of a depression (Keitner et al.,
1995)
Integrative theory
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Anxiety and depression may share a common
genetically determined biological vulnerability
-> excessive neurophysiological response to
stress
Stress event-> stress hormon-> influence on
neurotransmitter, especially on serotonin and
norepinephrine
New theory
stress hormone "turn on" certain genes
-> atrophy of neurons in the hippocampus
that help regulate emotions.
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Childhood stress experience
-> cognitive vulnerability
-> influences on adult stress response
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Problem
:
cannot
explain
specific
psychological disorders
- need a theory that differentially explains
between anxiety, depression, bipolar and
unipolar disorder
Treatment of mood disorders
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Drug therapy
Change in the level of neurotransmitters
or in neuro-chemical structures
- inhibition of reuptake of specific
neurotransmitters in the synapses
- down regulation of specific
neurotransmitters
Tricyclic antidepressants
Imipramine (Tofranil)
 Amitriptyline (Elavil)
-> down-regulate norepinephrine
-> down-regulating process take 2-8
weeks
 Side effects
- blurred vision, dry mouth, constipation
difficulty urinating, drowsiness, weight gain
(at least 13 pounds on average)
sexual dysfunction
-> 40% of patients drop out
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50% of the patients benefit
Placebo effect -> 25-30%
For patients who stayed to the end of the
treatment
-> 65-70% benefit
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Excessive use of tricyclic antidepressants
-> danger of death
-> needs attention when prescribed to a
suicidal patients
MAO inhibitors
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Block the MAO enzyme that break down such
neurotransmitters as norepinephrine and
serotonin
-> down-regulate the two neurotransmitters
-> have less side effects than tricyclics
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More effective to the atypical feature
depression
Interacts with foods that contain tyramine
(cheese, red wine, beer )
-> might induce high blood pressure
-> interact with other drugs and risk of fatal
side effects
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SSRIs (selective serotonergic reuptake inhibitors)
Inhibit reuptake of serotonin
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Enhance serotonin level in the receptor site
- exact mechanism is still not clear
- most well known SSRI -> fluoxetine (Prozac).
was regarded as a break through
(newsweek 3/26/90 cover story)
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side effect become known to public
physical agitation, sexual dysfunction or low desire
(75%), insomnia, and gastrointestinal upset
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But less side effects compared to those of tricyclic
antidepressants
< Two new antidepressants >
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Venlafaxine -> related to tricyclic
antidepressants, but less side effects
and less damage to the cardiovascular
system
Nefazodone -> similar to SSRIs
improve sleep efficiency
Great deal of interest in the antidepressant
properties of the natural herb
-> St. John's Wort (hypericum)
alters serotonin function
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Drug therapy of childhood depression
-> difference between children and adults
-> side effects of tricyclic antidepressants
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Risk of death due to cardiac side effects
(Tingelstad, 1991)
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Drug therapy of depression of the elderly
- side effects such as memory impairment,
physical agitation
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Prevention and delay of the next depressive
episode are more important than treatment
of depression itself
Because most of the depression remit after
some time
Need medication further 6-12 month after the
recovery
Women who are going to plan to have a
baby needs caution when considering drug
therapy, because the fetus can be affected
40-50% of the patients didn’t benefit from drug
therapy
Lithium
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In treatment of depression and bipolar
symptoms
More side effect than other antidepressants
- toxicity, lowered thyroid functioning
- intensify lethargy associated with depression
- substantial weight gain
Advantageous to treat manic symptoms
 Tricyclic antidepressants
-> can induce manic symptoms
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Can be prescribed to patients without
bipolar disorder
Mechanism are not known
probably influences the level of dopamine
and norepinephrine
Influences the production and availability of
sodium and potassium, which is electrolytes
found in body fluids
30-60% of bipolar patients respond (Prien &
Potter, 1993)
Prevents relapse for 66% of the patients
Manic symptoms
-> euphoric
-> compliance problem
Electroconvulsive Therapy(ECT)
In the past, immature ECT technique
-> recently improved
 For the patients who don’t respond to drugs
well and those who have psychotic
depression or are at risk of suicidal attempt
-> 50-70% benefit from ECT
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After anesthesia -> electric shock to brain
- shocks last shorter than 1 second each
time
- once every two days
6-10 times per day
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Side effects
relatively small
temporary memory disturbance
-> recover within 1-2 weeks
Mechanisms
-> not known
functional and structural change
in brain
< psychotherapy of major depression >
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A.T. Beck’s cognitive behavior therapy
Once a week and 10-20 sessions
monitoring thought process while
depressive symptoms come up
-> find out "depresssive errors in thinking"
-> replace with a more realistic thinking
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Negative cognitive schemas
-> find out them with the therapist as a team
-> test them as a home work

Hypothesis testing (as to responses of other people)

Reactivating the patients
-> compensate the patients through activity
-> improve self concept

Peter Lewinsohn, Gotlib & Clarke
Focused on reactivating patients in the beginning
Recently they deal with cognitions too


Interpersonal Psychotherapy; IPT




Klerman, Weissman, Rounsaville, Chevron,
Markovitz et al
A structured therapy like that of CBT
brief therapy with 15-20 sessions
Mainly focuses on the interpersonal
relationship and coping style
Focuses on one of the following 4
problems





Interpersonal disputes
The loss of a relationship
Acquiring new relationships
Identifying and correcting deficits in social
skills
Similar effects as medication, CBT (Elkin et
al., 1989)
Preventing relapse


Medication -> rapid response
Psychotherapy -> improve social functioning
and relapse prevention





medication + psychotherapy
-> combined effects
After medication offer a psychotherapy
For the bipolar disorder, combined therapy
of psychotherapy and family therapy are
effective
Family conflict -> related to relapse
When treated with psycho-social therapy
relapse rate decreased up to 50% compared
to drug therapy alone (Miller et al., 1991)


5-6 graders of elementary school
social skill training
teaching cognitive strategies
- was effective in the prevention of depression
(Gilham et al., 1995)
50% of depression patients
relapsed within 4 months, if medication was
stopped (Hollon et al., 1990)
after 24months
------------------------------------medication stop group
50% relapsed
medication cont. group
CBT group
CBT + drug therapy
32%
21%
15%




psychotherapy -> biophysiological change
Medication
-> pcychological change
Both of them lead to the DST change after
treatment
The level of tyroid hormone
thus, psychotherapy and medication
combined brings an integrative change
(Joffe, segal & Singer, 1996)
VI. Schizophrenia and Related Psychotic
Disorders





Complex disorder
Disorders in perception, thought, emotion,
language, movement, behavior
16-19 billion dollars annually spent for the
treatment in US
2.5% of total medical costs (Rupp & Keith,
1993)
1801, Pinel, 1809, John Haslam
1899, German psychiatrist Emil Kraepelin
combined three symptoms
“catatonia”, “hebephrenia” and “paranoia” that
were regarded at that time as independent
conditions into one category
=> dementia praecox



Catatonia (alternating immobility and excited
agitation)
Hebephrenia (silly and immature
emotionality)
Paranoia (delusions of grandeur
or persecution)



These three symptoms shared similar
underlying features
Early onset is at the heart of the three
symptoms
that will eventually lead to “mental weakness”
-> a diagnostic system that was focusing on
the onset and course of a disease
He pointed out that dementia praecox is
different form manic depressive illness in their
onset and course


In 1908, swiss psychiatrist Eugen Bleuler
introduced the term schizophrenia
The core problem of schizophrenia is according to
him
-> associative splitting of the basic functions
of the personality
-> breaking of associative threads
< Clinical description >

positive symptoms
-> more active manifestations of abnormal behavior
or an excess or distortion of normal behavior
-> delusions or hallucinations

Negative symptoms
Deficits in normal behavior like in speech and motivation

Disorganized symptoms
Rambling speech, erratic behavior, inappropriate affect

At least two of three symptoms must be present
at least longer than a month to be diagnosed as
a schizophrenia
Positive symptoms
Delusions






Unrealistic thoughts
“squirrels are aliens sent to Earth on a
reconnaissance mission"
“I can end starvation for all of the world’s children.”
“I will set up a base in the moon and evacuate
children there."
“My opponent will spray my bicycle with chemicals
that would take my strength away.”
Individuals with delusion
- different emotion from depression
- less depressive but less wise
Hallucinations



The experience of sensory events without input from the
surrounding environment
Can involve any of the senses
But auditory hallucination is most common
“It’s too damn loud. Turn it down."
“Good day for fishing. Got to go fishing.”
“You are strange. You are out.”

People tend to experience hallucinations more
frequently, when they are unoccupied or restricted
from sensory input

SPECT (single photon emission computed
tomography)
Cerebral blood flow of men with schizophrenia
 Were tested when they are hearing auditory
hallucination
-> Broca's area was being activated



Broca’s area is in charge of speech
production
The area that involves language
comprehension is Wernicke's area

This is a surprising discovery, because it
means that auditory hallucination is not
hearing the voices of others but are
listening to their own thoughts or their own
voices (Hoffman, Rapoport, Maure, &
Quinlan, 1999)
Negative symptoms




Absence or insufficiency of normal behavior
Emotional and social withdrawal
Apathy
Poverty of thought or speech
Avolition




Volition means act of willing, choosing or decision
Avolition means inability to initiate and persist in
activities.
Show no interest in carrying out basic life
functioning
Neglects personal hygiene
Alogia


Relative absence of speech
Respond to questions with brief replies that have
little content and appear uninterested in the
conversation

Reflect a negative thought disorder rather than
inadequate communication skills

Have trouble finding the right word to formulate
their thoughts

Delayed comments or slow response to questions
Anhedonia


Lack of pleasure
Not interested in the activities that bring pleasure
-> sex, food, social activity
Affective flattening






Flat affect
2/3 of the patients show this symptom
As if one has a mask on
Looks pointlessly
Speaks monotonously
Uninterested
surrounding
in
what
happens
in
the

Have feelings inside
-> difficulty expressing emotions, not a lack of
feeling (Berenbaum & Oltmanns, 1992)
-> emotional responses through physiological
recordings
Facial
expressions
of
schizophrenic
patients in childhood displayed
-> less positive and more negative affects

Disorganized symptoms

Disorganized speech
- difficult to get informations when talking
- lack of insight about one’s illness
- associative splitting
- cognitive slippage
- inconsistent in speaking
- illogical language

Tangentiality
-> cogintive slippage
Dr: why are you here in the hospital ?
Pt: I don’t want to stay here. I’ve got other things
to do. The time is right, and you know,
when opportunity knocks.

Loose association, Derailment
Dr: I was sorry to hear that your uncle Bill died a few
years ago. How are you feeling about him these
days ?

Pt: Yes, he died. He was sick, and now he’s
gone. He likes to fish with me, down at the river.
He’s going to take me hunting. I have guns. I
can shoot you and you’d be dead in a minute.
< Inappropriate affect and disorganized >





Emotional expression not fitting in the situation
Bizzare actions like hoarding objects
or acting strangely in public
catatonia
-> wild agitation or immobility
pace excitedly or move finger or arms
in stereotyped ways

Hold unusual postures
waxy flexibility
-> tendency to keep the body and limbs in the
position they are put in by someone else
Schizophrenia subtypes

Three divisions have persisted as subtypes of
schizophrenia

catatonic, hebephrenic, paranoid type

DSM-IV-TR
1. Paranoid type
- Delusion, hallucination being main
symptom
- Cognitive skills and affects are
relatively intact
- Better prognosis
- Delusions and hallucinations usually
have a theme such as grandeur or
persecution
2. Disorganized type

Flat or inappropriate affect
such as laughing in a silly way at the
wrong time

Delusion or hallucination
not organized around a central theme
as in the paranoid type, but are more
fragmented

Early onset, chronic
lacking the remissions

3. Catatonic type







Waxy flexibility
Excessive movement
Defiant attitude
Odd mannerism
stereotypical body movement, grimacing
Echolalia
Echopraxia
Relatively rare, because of recent
success of neuroleptic medications
4. Undifferentiated type

People who have the major symptoms of
schizophrenia but who do not meet the criteria
for paranoid, disorganized, or catatonic types
5. Residual type

People who have had at least one episode of
schizophrenia but who no longer manifest major
symptoms are diagnosed as residual type of
schizophrenia


They may display residual or “left over” symptoms
Such as negative beliefs, or they may still have
unusual ideas that are not fully delusional
Residual symptoms can include social withdrawal,
bizarre thoughts, inactivity, and flat affect
< Other psychotic disorders >
There are other psychotic disorders that don’t fit under the
hading of schizophrenia

Schizophreniform Disorder

Symptoms of schizophrenia for a few months only
Good premorbid social and occupational
functioning
absence of blunted or flat affect

Schizoaffective Disorder


People who have both schizophrenia and mood
disorder at the same time.
Mood disorder + delusion or hallucination longer than
2 weeks
Delusional Disorder

A persistent belief that is contrary to reality in
the absence of other characteristics of
schizophrenia
-Different
from
schizophrenia,
the
delusions of delusional disorder are
theoretically possible

Not organically caused delusion
Not caused by drugs or alcohol either
There are no negative symptoms such as flat
affect, anhedonia





Late onset (age 40-49)
subtypes =>
erotomanic, grandiose, jealous, persecutory,
somatic
Brief Psychotic Disorder


Characterized by the presence of one or more positive
symptoms such as delusions, hallucinations, or disorganized
speech or behavior lasting 1 month or less
Often precipitated by extremely stressful situations
Shared Psychotic Disorder
- An individual develops delusions simply as a result of a
close relationship with a delusional individual
1. Statistics




Lifelong prevalence 0.2% - 1.5%
Similar prevalence world wide, and
no gender difference
Onset of male begins earlier than
that of female
More men before age 36, more
women after age 36
< Development >

Children show some abnormal signs before they
display the characteristic sympotoms

(cf: 조승희, Virginia College of Technology. Massacre in April 17. 2007 killing
32 students and injuring 15 students)

Negative affects domineering
Bad adjustment
40 years follow up study of 52 schizophrenic
patients
Symptoms decreased as getting old
(Winokur et al., 1987)




Most of the patients kept their symptoms lifelong,
(moderate to sever symptoms)




Group1 (22%) -> one episode only, no
impairment
Group2 (35%) -> several episodes with no
or minimal impairment
Group3 (8%) -> impairment after the first
episode with subsequent exacerbation and
no return to normality
Group4 (35%) -> impairment increasing
with each of several episodes and no
return to normality





Schizophrenia found in all cultures
Differed in terms of prevalence rate or
recovery rate
In US more African Americans receive the
diagnosis of schizophrenia than whites.
People from devalued minority groups maybe
victims of bias and stereotyping.
Blacks were more likely to be detained
against their will, brought to the hospital by
police, and given emergency injections
(Goater et al., 1999)
2. Cause
< Genetic influences >




1938 Franz Kallmann
Examined family members of more than 1,000
people diagnosed with schizophrenia in a Berlin
Psychiatric Hospital
The severe the symptoms, the higher concordance
rate of family members
Various subtypes found in the same family
-> general predisposition for schizophrenia,
not specific predisposition







The
closer
genetically
concordance rate
Identical twin 49%
Fraternal twin 17%
Sibling
6%
Cousin
2%
(Gottesman, 1991)
the
higher
Quadruplets schizophrenia observed over
the years and all 4 sisters developed
schizophrenia
But they showed all very different courses
the same parents and family-> individually
different experiences (Rosenthal, 1963)
Adoption studies
1. adopted child research
first, identify schizophrenic patients
next, find their children given
to other families
2. Relatives studies
first, schizophrenic patients who were adopted are
identified
next, find their parents and siblings



Research in Finland (Tienari, 1992)
Adoption studies
Of the 20,000 female schizophrenic patients
164 were identified who gave their children
away for adoption
=> 155 children of these patients were
identified who were brought up in foster home
185 children of the normal parents were
compared as a control group who were
also brought up in foster home



Of the patients’ children,
16 were diagnosed either schizophrenia
or other psychosis -> 10.3%
Of the normal parents’ children,
2 were diagnosed as psychosis -> 1.1%
Gottesmann’s research (1989)
Children of identical twin patients
-> 16%
Children of identical twin patient’s
sibling who are not patients -> 17%


Children of fraternal twin patients -> 16%
Children of fraternal twin patient’s sibling
who are not patients -> 1.7%

The fact that the probability of outbreak of
schizophrenia in children of patient twin and
in normal twin are the same proves high
heredity

But it is only 17% -> the rest can be
attributed to other causes

Defects of not a single but several genes
combined together -> severe pathology


Search for markers
Characteristics common to schizophrenic
patients => will lead to a discovery of related
genes
One of them is :
Smooth-pursuit eye movement or eye tracking
The ability to track objects with eye movement
keeping head still.
schizophrenic patients lack in this ability
And this independent of drug
or hospitalization (Liebermann et al., 1993)
< Neurobiological factors >


Dopamine over-activity hypothesis
It is still controversial, but long lived
hypothesis
Evidences that support dopamine hypothesis
1.
Antipsychotic drugs that are often
effective in treating people with
schizophrenia are dopamine antagonists
2. These drugs can produce negative side
effects similar to those in Parkinson’s
disease, a disorder known to be caused by
insufficient dopamine.
3. The drug L-dopa, a dopamine agonist used
to treat people with Parkinson’s disease,
produces schizophrenia-like symptoms in
some people
4. Amphetamines, which also activate
dopamine, can make psychotic symptoms
worse in some people with schizophrenia
In other words, when drugs are
administered that are known to increase
dopamine (agonist), there is an increase
in schizophrenic behavior;
when drugs that are known to decrease
dopamine activity (antagonists) are used,
schizophrenic symptoms tend to diminish.
(mostly drugs that block the activity of D2
receptor)
< Evidences that contradict the dopamine
theory >
1.
A significant number of people with
schizophrenia are not helped by the use of
dopamine antagonists
2. Although the neuroleptics block the reception
of dopamine quickly, the relevant
symptoms subside only after several days
or weeks, much more slowly than
researchers would expect
3. These drugs are only partly helpful in reducing
the negative symptoms (e.g., flat affect,
anhedonia) of schizophrenia
4. There is no evidence that schizophrenic patients
have more D2 receptors than normals.
5. The research haven’t proved yet that there is
abnormality in D2 receptors of schizophrenic
patients.
6. Clozapine is effective to those patients who
don’t respond well to the traditional drugs.
But this drug is very weak in blocking D2
receptors.

Dopamine is related to schizophrenia, but its
role is very complex

Dopamine has a different effect in combination
with serotonin

Appropriate proportion of dopamine and
serotonin is important in regulating positive
symptoms such as hallucination or delusion

Clozapine plays a role in mediating these two
neurotransmitters.

Blocking only dopamine isn’t effective

Dopamine and serotonin must be blocked
simultaneously to be effective (more dopamine
should be blocked)
< Psychological and social influence >







Even the identical twins show different
prevalence rate
Environmental and experiential influences
Research with high risk children
In 1960, longitudinal researches of Danish
researchers Mednick & Schulsinger
207 children of schizophrenic mothers were
observed
104 control group children
The research is still being done




Most of the researches are retrospective
studies, the effects of which are limited
Ventura et al (1989)
30 patients were observed for one year
Interviewed every two weeks
Relapse often after stress events
But 55% of the relapsed hadn’t had a
considerable stress, which means there are
factors other than stress that impact relapse
< The influence of the family and culture on the
relapse >





Schizophrenogenic mother
(Fromm-Reichmann, 1948)
double bind (Bateson, 1958)
induces guilty feelings of the parents
-> which has negative impact on family
Recent research
The influence of the interaction among the
family members on the relapse
Brown et al (1959)





Expressed emotion (EE)
Patients who were restricted in their contact with
family members showed lower relapse rate
Criticism, hostility and emotional intrusiveness of the
family members had impact on relapse
(Brown et al., 1962)
High expressed emotion in family
-> a good predictor of relapse
(Bebbington et al., 1995)
Patients who lived in high EE family showed 3.7
times higher relapse rate than those who lived in
low EE family (Hooley, 1985)
2. Treatment
< Biological intervention >



In 1930s
injection of massive doses of insulin
-> insulin coma therapy
serious side effects, risk of death
psychosurgery
-> prefrontal lobotomies
In the late 1930s
Introduction of ECT
Today it is known to have no effect

Dramatic change after inventing neuroleptics in 1950
=> control delusion and hallucinations (mainly positive symptom)
class
example
degree of extrapyramidal effects
(side effects)
----------------------------------------------------------------------------------Conventional
antipsychotics
phenothiazines
Fluphenazine / Prolixin
high
Trifuluoperazine / Stelazine
high
Perphenazine / Trilafon
high
Mesoridazine / Serentil
low
Chlorpomazine / Thorazine
moderate
Thioridazine / Mellaril
low
Butyrophenone
haloperidol / Haldol
high
others
Thiothixene / Navane
Molindone / Moban
Loxapine / Loxitane
high
low
high
New Antipsychotics
Clozapine / Clozaril
Risperidone / Risperidal
Olanzapine / Zyprexa
Serindole / Serlect
low
low
low
Quetiapine / Seroquel
low
low

These drugs influence mainly dopamine
but also have influence on serotonin
system
It is only recently that we come to
understand better the mechanism of drugs
- Drugs are effective for some patients, but
not for other patients.

Clinicians and patients often must go
through a trial and error process to find
the medication that works best

Conventional antipsychotics are effective for
approximately 60% of people who try them
(APA, 2000)

Mostly many side effects
Some people respond well to newer
medications
The most common are clozapine, risperidone,
and olanzapine
These medications tend to have fewer serious
side effects than the conventional antipsychotics
(Davis, Chen, & Glick, 2003)







Noncompliance of the patients is a
significant problem
Approximately 7% of the patients refuse to
take medication
3 out of 4 patients refused to take the
antipsychotic medication for at least 1 week
(Weiden et al., 1991)
Negative side effects are a major factor in
patient refusal
grogginess
Deterioration in the ability to concentrate
(18%)
Dry mouth (16%)
Blurred vision (16%)

Akinesia
- one of the common side effect
it includes an expressionless face, slow motor
activity, and monotonous speech

Tardive dyskinesia
- involuntary movements of the tongue,
face, mouth or jaw
- results from long-term use of high doses of
antipsychotic medication
- often irreversible and may occur in as many
as 20% of people who take the medications
over long periods

The new antipsychotics such as
clozapine produce fewer side effects,
but even clozapine brings undesirable
effects and must be monitored closely

The compliance problem is serious
Psychosocial intervention can help to
increase compliance by helping patients
communicate better with professionals
about their concerns

< Psychosocial intervention >






Psychological intervention could be
combined with medications
Improving patient’s socialization
Participation in group sessions
self care such as bed making
Token economy, in which residents could earn access
to meals and small luxuries by behaving appropriately
Deinstitutionalization
- growth of human rights, integration
into community
- ill conceived policy produced many
homeless people
< Social skill training >







Basic conversation
Assertiveness
Relationship building
Maintaining eye contact while talking
to another person
Making friends
Relapse prevention
Utilizing social support system
< Family education >






Educating the family about the symptoms of
schizophrenia
Educating about the cause of the illness
Teaching the family members to communicate
more effectively
(learn more constructive way to express negative
emotions, listening more empathically)
Teaching practical facts about antipsychotics
(effects, side effects etc)
Teaching about support system
Teaching about problem solving strategies
< Vocational rehabilitation >
Enhancing the vocational ability
 Supportive rehabilitation
 Multilevel treatment
-> contribute to reducing relapse rate


Relapse rate of schizophrenia (after 2 year)
1. drugs + support or education -> 62%
2. drugs + social skills training -> 35%
3. drugs + famil stress management -> 38%
(Falloon, Brooker & Graham-Hole, 1992)
< Self help groups >



Recently change from large mental
hospitals to family homes in local
communities
Self help groups of former patients
Fountain House in New York City (Beard et al.,
1982)
Most of the Psychosocial club have differing
models, but all are "person centered“ and
focus on obtaining positive experiences
through employment opportunities, friendship,
and empowerment.

25,000 New Yorkers have participated in club-houses
sponsored by New York Association of Psychiatric
Rehabilitation Services.

Participation in club houses may help reduce relapse
(Beard, Malamud & Rossman, 1978)
But it is difficult to interpret the improvement,
because it is possible that those who have
participated may belong to a special group of
individuals (Mueser et al., 1990).

You’ve done a great job !
I appreciate very much your efforts to come along !
Have a good time during vacation !!