MOOD DISORDERS

Depression and
Mania
videos
 Depression
 https://www.youtube.com/watch?v=8jGdbwHYrHYArea
25 and MDD
https://www.youtube.com/watch?v=9-S7WAgVRcM
Behavioral activation
https://www.youtube.com/watch?v=O1dxNCiU92U
Judith Beck
https://www.youtube.com/watch?v=45U1F7cDH5k
Exam grades

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North Korean Defector Talk 7/19
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Overview for Mood Disorders
 Unipolar mood disorders
 Symptoms /Classification
 Epidemiology & Treatments

 Bipolar/cycling mood disorders

 Symptoms /Classification
 Epidemiology & Treatments
 To understand mood disorders, we must
understand the differences between:

 Emotion - Subjective states of feeling

 E.g., sadness, anger, disgust

 Affect - Observable behavior that goes with emotion

 E.g., facial expression

 Mood - Pervasive and sustained emotional response

 E.g., depression and elation
 What distinguishes normal sadness
from clinical depression?
 Pervasiveness across situation and time

 Absence of situational cues that you would

expect

 Additional signs and symptoms beyond sadness

 Subjective quality - doesn’t feel like ‘normal

sadness’
 Mood Disorders
 Usually characterized by moods that last a long time
 Depression and mania are the key emotions
 Depression
 Low, sad state in which life seems dark and its challenges
overwhelming
 Mania
 State of euphoria or at least frenzied energy in which people
may have an exaggerated belief that the world is theirs for
the taking.
 Can be characterized by anger/irritability/aggression instead
 DSM-5: Major Depressive Episode
A. 5 + of following during same 2 wks & change from previous
functioning
(1) depressed mood most of day, nearly every day (in kids can be irritable)
(2) anhedonia most of day, nearly every day
**at least one of these is required***
(3) Significant wt ↓ (not dieting) or wt ↑, or ↓ or ↑ in appetite nearly every day
(4) insomnia or hypersomnia nearly every day
(5) psychomotor agitation or retardation nearly every day (observable by others)
(6) fatigue or loss of energy nearly every day
(7) worthlessness or excessive or inappropriate guilt nearly every day
(8) difficulty concentrating, or indecisiveness nearly every day
(9) recurrent thoughts of death, suicidal ideation without a specific plan, or a suicide
attempt or specific plan for committing suicide

B. Sxs cause clinically significant distress or impairment in

functioning
DSM criteria for Major Depressive Disorder (aka
Unipolar Depression)

 Must have had one or more major depressive episodes

 No manic or hypomanic episodes
 Causes significant distress or impairment
 Specifiers:
 Mild, moderate, severe, with psychotic features

 https://www.youtube.com/watch?v=sDXIu8IL1rM
Domains of Impact & Variants
 Emotional  Recurrent  multiple episodes
 Motivational  Catatonic  immobility &
extreme inactivity
 Behavioral  Melancholic  early morning
 Cognitive wakening, weight loss, not reactive to fun
things
 Physical / somatic
 Atypical  will brighten to fun things;
over-eat and over-sleep; not rare
 Psychotic  w/ delusions or
hallucinations
 Major Depressive Disorder

 Prevalence
 Current/Point: 5-10% of U.S. adults, similar to other countries
 Lifetime: 16% Major depressive episode in lifetime
 Gender differences
 Women 2X as likely as men to have severe unipolar
depression (26% vs. 12%)
 …But in kids, prevalence is similar B = G
 Few differences among ethnic groups**
 Commonly comorbid with anxiety (~40%)
 & substance disorders (~18%)
 DSM-5 Persistent Depressive Disorder (Dysthymia)

A. Depressed mood for most of the day, for more days than not, for at
least 2 years (In kids, can be irritable and must last 1 yr)
B. Presence (while depressed) of 2 or more:
Poor appetite or overeating
Insomnia or hypersomnia
Low energy or fatigue
Low self-esteem
Difficulty concentrating/making decisions
Hopelessness
C. During 2 yr period, person has never been without symptoms for
>2 mos.
D. No history of manic or hypomanic episode
E. Significant distress or impairment in functioning
Dysthymia: Prevalence & Course
 Current/Point prevalence : 3%
 Lifetime prevalence: 6%
 Often early onset (childhood, adolescence or young
adulthood)
 Chronic course and usually does not spontaneously
remit without treatment
Other Depressive Disorders
 Seasonal affective disorder  mood ↓ in winter/fall,
improves in brighter months, for at least 2 cycles

 Post-partum depression  <4wks post giving birth

 Premenstrual dysphoric disorder  tied to menstrual cycle

 Disruptive mood dysregulation disorder  childhood

disorder of depression / outbursts
Theory-Based Etiology and Treatment
Approaches
to Major Depression
MOOD DISORDERS PART 2
Overview
 Biological perspective

 Psychodynamic theory

 Behavioral & Cognitive theories

 Gender/sex & risk of depression

 Sociocultural / Multicultural perspective

 Treatments
Biological Perspective - Genetics
 Concordance rates and heritability

Unipolar (MDD) Bipolar

MZ 50% 70%
DZ 25% 20%
Heritability 50% 80%

*Bipolar Disorder is more strongly heritable than

Depression
Heritability summarized
 Genetic factors are clearly involved in the transmission of mood disorders
 Studies that support this conclusion also suggest that bipolar disorders are
much more heritable than unipolar disorders
 Several twin studies of mood disorders have reported higher concordance
rates among MZ than among DZ twins (supporting genetic component)
 These analyses indicate that genetic factors are particularly influential in
bipolar mood disorders, for which the overall heritability estimate is 80
percent
 Genes and environment contribute about equally to the etiology of major
depressive disorder, in which the heritability estimate is 52 percent
MDD risk: genes and environment
• The onset of a mood disorders is determined by a
combination of genetic and environmental risk
factors

• The combined effects of genetic and environmental

factors have been evaluated by incorporating the
measurement of stressful life events into a standard
twin design
• One such study employed a large sample of female
same-sex twins in a study of unipolar mood
disorder:
• The negative impact of severe events was much
higher among those women who were also at
greater genetic risk for unipolar depression
• Therefore the effects of the environment and
genetic factors are not independent; it is a
combination of the two

• Genetic factors apparently control the person’s

sensitivity to environmental events

• Stress increases likelihood even in low genetic risk

Biological Perspective

Neurochemical theory:
 Decreased neurotramitters norepinephrine or

serotonin (or their interaction) in the limbic system

 Abnormal sensitivity or number of receptors*

Neuroendocrine theory:
 Dysregulation of the HPA axis leads to elevated

cortisol (stress hormone)

 Thyroid dysfunction can mirror MDD sxs
Biological Perspective

 Brain imaging studies indicate severe

depression associated with abnormal patterns
of activity and structural changes:

 Abnormal patterns of activation of prefrontal

cortex (PFC)

 Increased activity in limbic system, particularly

the amygdala

 Reduced size /overactivity of Brodmann’s

Area 25
 https://www.youtube.com/watch?v=9-
S7WAgVRcM
Biological Perspective

 Mood disorders are also thought to be

related to dysregulation in circadian
rhythms (guide sleep and wake cycles)
 Melatonin-related problems (hormone
related to activity level and sleep)
 Seasonal Affective Disorder (SAD)
 Mania
 Sleep cycle reversal with MDD
 Depression (REM starts sooner,
is shorter, less deep sleep)
 Psychodynamic View
 Childhood experience prevented
development of positive sense of self
 As adults, constantly seek
approval & security
 Fears of abandonment, separation, rejection
 Strive to be perfect, and therefore loveable

 “Imperfection”  depression
 Self-hatred & self-punishment
 Introjected Hostility – too afraid to express anger
toward others, so they turn it inward on themselves
STOP here
 Behavioral Perspective
Peter Lewinsohn’s Behavioral Theory

Stressor leads to reduction in reinforcers

Person withdraws
Peter
Lewinsohn
Reinforcers further reduced

More withdrawal and depression

• Positive rewards related to presence/absence of depression
• Person likely lacks skills to obtain reinforcement/reward or
cope with punishment
 Behavioral Perspective
 Consider role of
Negative Life Events
 3x more likely to have
experienced an negative
life event in the year prior
to onset of depressive
episode (Shrout et al.,
1989)
Behavioral Activation
 Aims to increase positive reinforcement/reward and
decrease disengagement

 https://www.youtube.com/watch?v=O1dxNCiU92U
Cognitive-Behavioral Perspectives

 Seligman’s Learned Helplessness Theory

 Beck’s Cognitive Theory

 Nolen-Hoeksema’s Response Style Theory

 Cognitive - Behavioral Perspective
Seligman’s Learned Helplessness

 Dogs placed in controllable and

uncontrollable shock cages
 Dogs who were unable to avoid shock just
gave up
 Could not learn how to avoid the shock when
an escape was possible
 People may learn to be “helpless” and
believe they cannot control events in
their environment
 e.g. spousal abuse
Cognitive - Behavioral Perspective
Reformulated Learned Helplessness
(Attribution-Helplessness Theory)
 However, many people who are depressed
blame themselves for their problems—how
can this be if they belief they are helpless and
don’t have an impact on the world? This lead
to the revised learned helplessness theory

 Believe that positive events unlikely to occur

and nothing you can do to control negative
events happening in the future (hopelessness)

 Added cognitive piece: causal attributions

(how we explain events)
 In depression, attributional style is: Internal,
Global, Stable
Cognitive - Behavioral Perspective
Reformulated Learned Helplessness
(Attribution-Helplessness Theory)
People with MDD more likely to make stable, global, internal
attributions for negative events.

Example Event: You fail your Abnormal Psychology exam.

Stability/Permanence: Temporary vs. Permanent

“I had a rough day.” vs. “I’ll never get good grades.”

Global/Pervasiveness: Specific vs. Universal

“This woman is unfair.” vs. “Professors are all unfair.”

Internal/Personalization: External vs. Internal

“The test was difficult.” vs. “I’m stupid.”
 Beck’s Cognitive Model of Depression

 Cognitive theories concerning the origins of unipolar

depression are based on the recognition that the ways in
which people think about and perceive their world
have an important influence on the way that they feel
 Cognitive theories about vulnerability to depression have
typically focused on the ways in which people respond
to negative experiences involving loss, failure, and
disappointment
 Negative thoughts influence how we feel and act.

 Depression characterized by the cognitive triad: A.T. Beck

 Negative thinking about the self, the world, and the future

 hopelessness - the person’s negative expectations about

future events and the associated belief that these events cannot
Beck’s Cognitive Model

 Depression is associated with errors in thinking or

cognitive biases
 Overgeneralization
 My relationship failed, this proves I am a failure
 Arbitrary inferences
I know my professors will think I am dumb
 Minimizing/magnifying
 Magnify the bad – ignore the good!
 The exam was easy, that’s why I did well

Judith Beck about CT:

 https://www.youtube.com/watch?v=45U1F7cDH5k
Beck’s Cognitive Model

 Automatic Thoughts: negative thoughts that

occur automatically in response to a situation

 Schemas: enduring,
patterns - organized representations
of prior experience that
guides the way people
perceive and interpret
environmental events
 Beck’s Cognitive Model

Formation of dysfunctional schemas:

Early Form errors Form

experience in thinking schemas
He left because he I am unlovable
Father leaves family does not love me
when client is a kid
 Beck’s Cognitive Model

Another
experience Activation Negative
of negative automatic
“Schema
schemas thoughts
relevant”
Significant other I am unlovable He left because he
breaks up with didn’t love me,
person nobody could love
me

Distress Negative
Mood verbalizations
Depressed Both covert (self-talk)
and overt (to others)
Nolen-Hoeksema’s
Response Style Theory

 How you respond to depressed mood determines its severity and

duration
 A ruminative response style is relatively stable over time and tends

to be associated with longer and more severely depressed mood

 Furthermore, women are more likely than men to exhibit a

ruminative coping style in response to the onset of a depressed mood

 Ruminative style = inward attention

 Longer, more severely depressed moods

 Distracting style = diverted attention

 Shorter, less depressed moods

Susan Nolen-Hoeksema
Sociocultural & Multicultural
 Social Support / Contacts
 Strong social supports decrease odds of MDD
 Depressed people exact social cost on contacts (e.g.,
friends, loved ones)
 Marriage reduces risk of depression, but marital conflict
linked to sadness

 Non-western MDD = ↑somatic, ↓cognitive

 In US, no differences in rates but Hispanics & African
Americans have more recurrence
 May be due to different / non-treatment (pp.272)
Gender Differences
 Some theories:
 Artifact  truly =, men less likely to admit it
 Hormone  cortisol, melatonin, and serotonin

 Life stress  W > M

 Body dissatisfaction

 Lack-of-control  see: LH

 Distraction vs. rumination

 Why don’t we see

F >> M in kids?
TREATMENTS
 Psychodynamic Tx
 Object Relations Therapy
 Identify patterns in relationships from past and how same
patterns played out in current relationships
 Identify how client communicates through actions rather
than words (e.g. a suicide attempt)
 Determine whether client has well-formed & balanced
sense of self & others (can see good & bad aspects of self
& others)
 Improve ways of relating to others.
 Uses relationship between client & therapist as a proxy
for other relationships
Behavioral Therapy
 Behavioral Activation
 Increase positive reinforcers & decrease

aversive experiences
by changing behavior
 Decrease oversleeping

 Increase pleasurable activities (activity

scheduling)
 Get client to engage in activities instead

of isolating
 Improve social skills
Cognitive Tx
Beck’s Cognitive Therapy for Depression
• Based on the assumption that, depression will be relieved if
maladaptive schemas are changed

• Cognitive therapists focus on helping their patients replace

self-defeating thoughts with more rational self-statements

• Primary Aim: to attend to and correct (negatively) distorted

thinking

• Therapy utilizes:
• Collaborative Empiricism (testing thoughts)
• Thought Records
• Behavioral Experiments
 Thought Record
Date / Time Situation Emotions Automatic Thought(s) Alternative Response Outcome

She's being She may have been busy

5-May Friend didn't Angry rude! all day. She usually returns Angry 15%
return my call 60% my calls promptly.
all day.
Sad She doesn't She calls me regularly to Sad 10%
80% want to be my friend. hang out. She seems to
have fun with me.
Traditional Cognitive Tx
 Self-monitoring to ↑ activity, mood
 Cognitive restructuring (challenge and change
unhelpful/maladaptive thoughts)
 Targeting schemas (e.g., “I’m unloveable” “I’ll
never succeed)
 Usually brief (10-14 sessions)
 Efficacious treatment w/ long-term benefits
 Variants of Cognitive & Behavioral Tx

 Mindfulness-Based Cognitive Therapy (MBCT)

Teasdale et al. (2001)
 Seems to reduce relapse rates in patients with recurrent depression

 Acceptance and Commitment Therapy

(ACT)

 Rational-Emotive Behavior Therapy

(REBT)
Sociocultural Tx

 Interpersonal Psychotherapy (IPT)

 The availability of social support reduces likelihood of
depression
 Lack social support remain depressed longer than those
who have a supportive spouse or warm friendships
 IPT Focused on problems in current relationships
 Focused on challenges in four areas:
 Interpersonal loss (grief)
 Role dispute (different expectations re: relationships)
 Role transition (major life changes like going off to college or birth of
child)
 Interpersonal deficits) (e.g., extreme shyness or social awkwardness)
 Biological Tx – Older Medications

Tricyclics (TCAs) Monoamine oxidase inhibitors

 Mechanism: reduces MAO, an
 Mechanism: likely
enzyme that breaks down NTs
prevents reuptake of (especially DA, 5HT)
 = effective but side effects potentially
norepinephrine (NA)
more dangerous vs. TCAs
and serotonin (5HT)  must avoid foods rich in tyramine
in synapse or by (e.g. beer, red wine, cheese, choco)
changing receptors’ d/t risk of ↑blood pressure
responsiveness  Can also cause liver damage, wt gain

 e.g. and interact with antihypertension

imipramine drugs and antihistamines
 Effective, but many
side effects. Also
fatal in overdose. 4-
Biological Tx – Modern Medications
 Selective serotonin reuptake inhibitors (SSRIs) e.g.
Prozac, Celexa, Paxil, Zoloft
 Mechanism: Similar in structure to tricyclics but works
more directly on serotonin
 Biological assumption is depression is caused by LOW
levels of seratonin!
 Also help anxiety and other issues
 Typically 2-4 weeks to experience effect
 Side effects: Less severe than others, lower risk of fatal
overdose but many experience problems if off “cold
turkey”
 See also SNRIs (NA only) and S-NRIs (5HT + NA)
Biological Tx – Augmentation
 Augmenting medications given to patients to help
with residual symptoms, commonly including:

 Sleep aids (e.g., Lunesta)

 Mood stabilizers (e.g., lithium)
 Attention meds (e.g., Ritalin)
 Atypical anti-psychotics (e.g., Abilify)
Biological Tx – Rx in General
 Rx for anti-depressants in US often given by
general practitioners (not specialists) w/o much
follow-up

 Strategies for non-response vary

 Increase dose / change medication / augment

 Many patients treated til responding, then stay on

indefinitely on medication (maintenance)
Biological Tx - ECT
 Electroconvulsive Therapy (ECT)
 Introduced in early 20th century for

treatment of schizophrenia
 Not effective for SZ but was effective for depression

 Anesthetized, muscle relaxant, electrodes on head, 70-130 volts

passed thru one side of brain for about .5 second. Pts go into
seizure, which lasts about 1 min.
 Typically 6-12 sessions

 Typically used with treatment resistant depression, not a 1st line

intervention
 Mechanism of effect: unclear

 Side effects (for some): memory loss, difficulties in learning

new information, but often lessens w/ time

Biological Tx – Other Brain Interventions
 Vagus Nerve Stimulation
 Pulseson main brain/body nerve link mimic ECT effect, tx
option for chronic/refractory depression

 Transcranial Magnetic Stimulation (TMS)

 Mimics ECT w/o side effects, magnets activate areas of PFC

 Deep Brain Stimulation (DBS)

 Brodmann’s area 25 “pacemaker”
Biological Tx – Lights!
 Light therapy:
 Used for seasonal affective
(depressive sx sthat crop up when
not exposed to enough light)
 Sit under specific kind of light,
helps to reset circadian rhythms
So…what works?
 General Tx Outcomes for MDD
 CBT ≈ IPT ≈ Medication in acute tx
 Non-response to any given tx is common
 CBT may protect against relapse
 Relapse post-tx is common (up to 30%)
 ECT = faster, + effective vs. medication but
medication most commonly used
 Combo medication and therapy = only modestly
better than either alone
WOW, that was a lot of material!!
 Aim for the major details
 Clear knowledge of the dx & sxs
 Good understanding of theories and interventions
 Links between a theory’s etiological explanation and
the putative treatment mechanism
 Tx outcomes, comparisons and
considerations/concerns