DISORDERS OF MOOD CHAPTER 6. 2 DISORDERS OF MOOD 2 KEY EMOTIONS: DEPRESSION: LOW, SAD STATE IN WHICH...

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DISORDERS OF MOOD CHAPTER 6

Transcript of DISORDERS OF MOOD CHAPTER 6. 2 DISORDERS OF MOOD 2 KEY EMOTIONS: DEPRESSION: LOW, SAD STATE IN WHICH...

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DISORDERS OF MOOD

CHAPTER 6

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DISORDERS OF MOOD

• 2 KEY EMOTIONS:

•DEPRESSION: LOW, SAD STATE IN WHICH LIFE SEEMS DARK; ITS CHALLENGES OVERWHELMING; NO HISTORY OF MANIA

•MANIA: STATE OF BREATHLESS EUPHORIA OR FRENZIED ENERGY

DEPRESSION N O R M A L M O O D MANIA

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UNIPOLAR DEPRESSION•“DEPRESSION” OFTEN USED TO DESCRIBE GENERAL

SADNESS OR UNHAPPINESS

•CLINICAL DEPRESSION CAN BRING SEVERE AND LONG-LASTING PSYCHOLOGICAL PAIN THAT MAY INTENSIFY AS TIME GOES BY

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HOW COMMON IS UNIPOLAR DEPRESSION?

•AROUND 8% OF ADULTS IN ANY GIVEN YEAR

•AS MANY AS 5% SUFFER FROM MILD FORMS

•AROUND 19% OF ALL ADULTS AT SOME TIME IN THEIR LIVES

•HIGHER AMONG POOR

•ONSET: ANY AGE

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HOW COMMON IS UNIPOLAR DEPRESSION?•WOMEN ARE AT LEAST TWICE AS LIKELY AS MEN TO

EXPERIENCE SEVERE UNIPOLAR DEPRESSION

•LIFETIME PREVALENCE: 26% OF WOMEN VS. 12% OF MEN

•AMONG CHILDREN, THE PREVALENCE IS SIMILAR AMONG BOYS AND GIRLS

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CRITERIA FOR A MAJOR DEPRESSIVE EPISODE

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DSM-5 LISTS SEVERAL TYPES OF DEPRESSIVE DISORDERS:

•MAJOR DEPRESSIVE DISORDER

•MAJOR DEPRESSIVE EPISODE WITH NO HISTORY OF MANIA

•PERSISTENT DEPRESSIVE DISORDER (DYSTHYMIC DISORDER)

• LONGER-LASTING (AT LEAST TWO YEARS) BUT LESS DISABLING PATTERN OF DEPRESSION

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DSM-5 LISTS SEVERAL TYPES OF DEPRESSIVE DISORDERS:

• PREMENSTRUAL DYSPHORIC DISORDER

•REPEATEDLY EXPERIENCE CLINICALLY SIGNIFICANT DEPRESSIVE SYMPTOMS DURING THE WEEK BEFORE MENSTRUATION

•DISRUPTIVE MOOD REGULATION DISORDER (CHILDREN)

•CHARACTERIZED BY A COMBINATION OF PERSISTENT DEPRESSIVE SYMPTOMS AND RECURRENT OUTBURSTS OF SEVERE TEMPER

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STRESS AND UNIPOLAR DEPRESSION

•STRESS: TRIGGER FOR DEPRESSION• THOSE DIAGNOSED EXPERIENCE A GREATER NUMBER OF

STRESSFUL LIFE EVENTS DURING THE MONTH JUST BEFORE THE ONSET OF SYMPTOMS

• LOSS OF A LOVED ONE, SERIOUS THREATS TO IMPORTANT RELATIONSHIPS OR ONE’S OCCUPATIONS, SEVERE ECONOMIC OR HEALTH PROBLEMS, EVENTS INVOLVING HUMILIATION.

• MINOR EVENTS MAY PLAY MORE OF A ROLE IN THE ONSET OF RECURRENT EPISODES THAN IN THE INITIAL EPISODE.

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GENETIC FACTORS• TWIN, ADOPTION, AND GENE STUDIES SUGGEST THAT SOME

PEOPLE INHERIT A BIOLOGICAL PREDISPOSITION

•AS MANY AS 20% OF RELATIVES ARE DEPRESSED, COMPARED WITH FEWER THAN 10% OF THE GENERAL POPULATION

•CONCORDANCE RATES FOR IDENTICAL (MZ) TWINS = 46%

•CONCORDANCE RATES FOR FRATERNAL (DZ) TWINS = 20%

•MAY BE TIED TO SPECIFIC GENES (SEROTONIN-TRANSPORTER GENE)

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BIOLOGICAL MODEL

•BIOCHEMICAL FACTORS

•SEROTONIN AND NOREPINEPHRINE

•DEPRESSION LIKELY INVOLVES NOT JUST SEROTONIN NOR NOREPINEPHRINE; A COMPLICATED INTERACTION IS AT WORK, AND OTHERS MAY BE INVOLVED

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BIOLOGICAL MODEL• ENDOCRINE SYSTEM / HORMONE RELEASE

•ABNORMAL LEVELS OF CORTISOL

•ABNORMAL MELATONIN SECRETION

•DEFICIENCIES OF IMPORTANT PROTEINS WITHIN NEURONS AS TIED TO DEPRESSION

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BIOLOGICAL MODEL· ANATOMY

· EMOTIONAL REACTIONS OF VARIOUS KINDS ARE TIED TO BRAIN CIRCUITS

· LIKELY INCLUDE PREFRONTAL CORTEX, HIPPOCAMPUS, AMYGDALA

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BIOLOGICAL MODEL•IMMUNE SYSTEM

•WHEN STRESSED, THE IMMUNE SYSTEM MAY BECOME DYSREGULATED, WHICH SOME BELIEVE MAY HELP PRODUCE DEPRESSION

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WHAT ARE THE BIOLOGICAL TREATMENTS FOR UNIPOLAR DEPRESSION?

• USUALLY BIOLOGICAL TREATMENT MEANS ANTIDEPRESSANT DRUGS:

•MONOAMINE OXIDASE INHIBITORS (MAO INHIBITORS)

• TRICYCLICS

• SECOND-GENERATION ANTIDEPRESSANTS

• SSRI’S- SELECTIVE SEROTONIN REUPTAKE INHIBITORS

• SSNRI’S - SELECTIVE SEROTONIN NOREPINEPHRINE REUPTAKE INHIBITORS

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WHAT ARE THE BIOLOGICAL TREATMENTS FOR UNIPOLAR DEPRESSION?

• ELECTROCONVULSIVE THERAPY (ECT)

•CONTROVERSIAL

• PROCEDURE CONSISTS OF TARGETED ELECTRICAL STIMULATION TO CAUSE A BRAIN SEIZURE

•~ 6 TO 12 SESSIONS SPACED OVER 2 - 4 WEEKS

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WHAT ARE THE BIOLOGICAL TREATMENTS FOR UNIPOLAR DEPRESSION?

•BRAIN STIMULATION

•VAGUS NERVE STIMULATION

•TRANSCRANIAL MAGNETIC STIMULATION

•DEEP BRAIN STIMULATION18

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PSYCHOLOGICAL MODELS

• THREE MAIN MODELS:

•PSYCHODYNAMIC MODEL

•NO STRONG RESEARCH SUPPORT

•BEHAVIORAL MODEL

•MODEST RESEARCH SUPPORT

•COGNITIVE VIEWS

•CONSIDERABLE RESEARCH SUPPORT19

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COGNITIVE MODEL•LEARNED HELPLESSNESS – (SELIGMAN) ASSERTS

PEOPLE BECOME DEPRESSED WHEN THEY THINK THAT:

•THEY NO LONGER HAVE CONTROL OVER THE REINFORCEMENTS (REWARDS AND PUNISHMENTS) IN THEIR LIVES

•THEY THEMSELVES ARE RESPONSIBLE FOR THIS HELPLESS STATE

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COGNITIVE MODEL· LEARNED HELPLESSNESS

•ATTRIBUTIONS: INTERNAL/EXTERNAL, GLOBAL/SPECIFIC, STABLE/UNSTABLE.

•PESSIMISTIC ATTRIBUTIONAL STYLE ASSOCIATED WITH DEPRESSION.

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COGNITIVE MODELOTHERS SUGGEST ATTRIBUTIONS LEAD TO DEPRESSION WHEN THEY PRODUCE A SENSE OF HOPELESSNESS

•ONE HAS NO CONTROL OVER WHAT WILL HAPPEN AND SOMETHING BAD WILL HAPPEN.

• INTERNAL/EXTERNAL DIMENSION NOT IMPORTANT.

• LIKELY NEGATIVE CONSEQUENCES WILL OCCUR AND NEGATIVE INFERENCES ABOUT THE IMPLICATION OF THE EVENT FOR THE SELF-CONCEPT.

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Beck: Negative thinking

BECK THEORIZES FOUR INTERRELATED COGNITIVE COMPONENTS COMBINE TO PRODUCE UNIPOLAR DEPRESSION:

1. MALADAPTIVE ATTITUDES

2. COGNITIVE TRIAD

3.COGNITIVE DISTORTIONS

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NEGATIVE COGNITIVE TRIAD

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COGNITIVE DISTORTIONS

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COGNITIVE MODELBECK: NEGATIVE THINKING

BECK’S COGNITIVE THERAPY–DESIGNED TO HELP CLIENTS RECOGNIZE AND CHANGE THEIR NEGATIVE COGNITIVE PROCESSES

1.INCREASING ACTIVITIES AND ELEVATING MOOD

2.CHALLENGING AUTOMATIC THOUGHTS

3.IDENTIFYING NEGATIVE THINKING AND BIASES

4.CHANGING PRIMARY ATTITUDES26

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SOCIOCULTURAL MODELPROPOSE THAT DEPRESSION GREATLY INFLUENCED BY SOCIAL CONTEXT

• FAMILY-SOCIAL PERSPECTIVE

•MULTICULTURAL PERSPECTIVE

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SOCIOCULTURAL MODELGENDER AND DEPRESSION

•ARTIFACT THEORY

•HORMONE EXPLANATION

•LIFE STRESS THEORY

•BODY DISSATISFACTION EXPLANATION

•LACK-OF-CONTROL THEORY

•RUMINATION THEORY

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BIPOLAR DISORDERS•PEOPLE WITH A BIPOLAR DISORDER EXPERIENCE BOTH

THE LOWS OF DEPRESSION AND THE HIGHS OF MANIA

•MANY DESCRIBE THEIR LIVES AS AN EMOTIONAL ROLLER COASTER

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CRITERIA FOR MANIA

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CRITERIA FOR HYPOMANIA

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BIPOLAR DISORDERS I AND II

Bipolar I disorder

• Includes at least one manic episode

• More severe• More dangerous• More impairments

socially/occupationally

Bipolar II disorder

• Includes hypomanic episodes & depression

• Less severe• Can be MORE

competent/social

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DIAGNOSING BIPOLAR DISORDERS

·~1% AND 2.6% ADULTS

·EQUALLY COMMON IN WOMEN AND MEN

·ONSET USUALLY OCCURS BETWEEN 15 AND 44 (~22 YEARS)

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CYCLOTHYMIC DISORDER

Cyclical mood swings

• Less severe than those of bipolar disorder

• Symptoms present for at least 2 years

• Lacking severe symptoms and psychotic features of bipolar disorder

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MANIC-DEPRESSIVE SPECTRUM

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WHAT CAUSES BIPOLAR DISORDERS?•NEUROTRANSMITTERS

•OVERACTIVITY OF NOREPINEPHRINE

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WHAT CAUSES BIPOLAR DISORDERS?•SEROTONIN: “PERMISSIVE THEORY”

•MAY BE LINKED TO LOW SEROTONIN ACTIVITY:

•LOW SEROTONIN MAY “OPEN THE DOOR” TO A MOOD DISORDER AND PERMIT NOREPINEPHRINE ACTIVITY TO DEFINE THE PARTICULAR FORM THE DISORDER WILL TAKE:

•LOW SEROTONIN + LOW NOREPINEPHRINE = DEPRESSION

•LOW SEROTONIN + HIGH NOREPINEPHRINE = MANIA

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WHAT CAUSES BIPOLAR DISORDERS?• ION ACTIVITY

•SOME THEORISTS BELIEVE THAT IRREGULARITIES IN THE TRANSPORT OF THESE IONS MAY CAUSE NEURONS TO FIRE TOO EASILY (MANIA) OR TO STUBBORNLY RESIST FIRING (DEPRESSION)

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WHAT CAUSES BIPOLAR DISORDERS?•BRAIN STRUCTURE

•BASAL GANGLIA AND CEREBELLUM

•NOT CLEAR WHAT STRUCTURAL ABNORMALITIES PLAY

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WHAT CAUSES BIPOLAR DISORDERS?•GENETIC FACTORS

•IDENTICAL (MZ) TWINS = 40% LIKELIHOOD

•FRATERNAL (DZ) TWINS AND SIBLINGS = 5% TO 10% LIKELIHOOD

•GENERAL POPULATION = 1 TO 2.6% LIKELIHOOD 40

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PHARMACOTHERAPY

Lithium

Anti seizure, antipsychotic

drugs

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TREATMENTS FOR BIPOLAR DISORDER:•DO NOT FULLY UNDERSTAND HOW MOOD

STABILIZING DRUGS OPERATE

·PSYCHOTHERAPY ALONE RARELY HELPFUL

·MOOD STABILIZING DRUGS ALONE ARE NOT ALWAYS SUFFICIENT

·30% OR MORE OF PATIENTS DON’T RESPOND, MAY NOT RECEIVE THE CORRECT DOSE, AND/OR MAY RELAPSE WHILE TAKING IT

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