Lecture 7 - Major Depressive Disorder Flashcards
History
Melancholia
* MDD first described by Hippocrates
- Melancholia
* Four humors– yellow bile, black bile,
phlegm, and blood.
* Disease occurred when humors were out
of balance
* Melancholia resulted from the presence
of too much black bile
History of classification
* Emile Kraepelin
* Chief origin of psychiatric disease is biological and genetic
malfunction
-Kraepelin= not psychodynamic
-Very medical model as opposed to Freud
* Group diseases together based on classification of syndromes (cluster of symptoms that co-occur),
not similarity of symptoms
* Refined unitary concept of psychosis:
- Manic depression (now includes MDD and BP)
- Dementia Praecox
Kraepelin’s Theory of Psychosis
Two distinct syndromes:
* Dementia Praecox
- “rapid cognitive disintegration”
- Disruption in attention, memory, goal-directed behavior
- Eventually re-labeled “schizophrenia”
* Manic-Depressive Illness
- Primary mood disturbance
- Disruption in affective functioning
- Eventually split into multiple mood disorders
* Distinguishes radically different forms of functioning
- Still unitary view of mood disorders
Classification
* Kraepelinan view dominant until mid 1950’s
* Karl Leonhard proposes unipolar-bipolar distinction - and first to describe nosology
* If a patient experiences exclusively episodes of one pole (e.g., only depressed, or
only manic), unipolar.
* Episodes of both, bipolar
* Leonhard described these as different groups.
* This distinction (somewhat modified) holds true today.
* Very rare to have only manic episodes– generally classified as bipolar (according
to the DSM).
Major Depressive Disorder
* Introduced into the DSM in DSM-II as
“Depressive reaction,” or a response
to adverse life events
* Major Depressive Disorder
introduced in DSM-III
-Stripped out etiological
-Don’t need trauma/negative experience, but cluster of symptoms
DSM-5
* Same chapter, but separates into “Depressive and Related
Disorders” and “Bipolar and Related Disorders”
* Bipolar between Depressive and Schizophrenia Spectrum
and Related disorders
* Bipolar changes: More specific symptomology for
hypomanic and mixed manic states
* Depressive changes:
- Addition of disruptive mood dysregulation disorder
- Persistent Depressive Disorder (formerly Dysthymia)
- Premenstrual Dysphoric Disorder
- Bereavement Clause removed
MDD characteristics and diagnosis
DSM-5 diagnosis of MDD
* Diagnosed when a history of depressive
episodes, but no mania.
* Need five or more symptoms within the
same two-week period.
- All must be present simultaneously
during that 2-week period.
- Person must report experiencing marked
distress or a decrease in functioning
during these 2 weeks
* At least one must be one of two cardinal
symptoms (dysphoric mood and anhedonia)
* Dysphoric Mood
- (sad, empty, tearful)
* Markedly diminished interest or
pleasure in all or almost all activities
- ANHEDONIA.
-can also be to negative stimulus (don’t care if bad stuff happens)
* In addition to ONE of these two,
the person must also meet criteria
for at least four other symptoms
(three if both dysphoric mood and
anhedonia are present)
* Weight loss or weight gain
* Insomnia or Hypersomnia:
* Psychomotor agitation or retardation
* Fatigue or loss of energy
* Feelings of worthlessness or excessive or inappropriate
guilt.
* Diminished ability to think or concentrate, or
indecisiveness
* Recurrent thoughts of death; suicidal ideation or
attempts.
* Symptoms must cause serious distress or impairment
Because of how unspecific it is…
Heterogeneity : two people can have same diagnosis with completely different symptoms
Unipolar/bipolar distinction
*unipolar = MDD
* MDD 10-20 x more common than Bipolar.
* Differ in gender distribution:
- Bipolar: M≈F
- Unipolar: 2F = 1M
* Differ in course:
- Bipolar– earlier onset
- Bipolar– more episodes
- Bipolar– more pernicious course
Forms of Unipolar/specifiers
Psychotic MDD
-depressive episode with psychosis = loss of contact with reality (hallucinations, delusions)
Recurrent Depression
-multiple mdd episodes across lifetime
Melancholia
Profound anhedonia, lack of activity to usually pleasurable stimuli, empty void-like mood, worse in the morning, early awakening, excessive psychomotor agitation or retardation, anorexia (significant weight loss, not nervosa), guilt
Symptoms do tend to cluster together
Biological disorder?
- Do well w/ ECT, but less evidence for antidepressants
- Don’t respond to placebos
- Do respond to psychotherapy
No differences in family history
No difference in premorbid personality
Supposed to be endogenous, so fewer
precipitating factors– evidence for this is
mixed
NOT stable across episodes
Distinct form of depression? Mixed evidence
Atypical
*Most recent specifier
*Kind of the opposite of melancholia
*Majority women
*Intact mood reactivity (do feel better when things go well)… unlike in melancholia
*Sleeping too much (instead of insomnia)
*Marked increase in appetite
*Sense of limbs really heavy
*Rejection sensitivity
*Called atypical but not at all rare (15% of depressed people)
* Characterizes ~ 15% of depressed patients
* Earlier onset
* More comorbidity
* Strongly associated with specific treatment response
(main reason for subtyping):
- Responds preferentially to MAOIs, not tricyclics
- Many treated with SSRIs; less effective, but more
convenient and safer
Chronic Major Depression
*Long lasting recurrent episodes
*Episodes can last minimum 2 years
*Less responsive to treatment
*More severe
*More associated with familial depression
Seasonal Affective Disorder
*Recent subtype-specifier
*Episodes in fall and winter, improve or euphoria in summer and spring
*More women
*Milder
*Overlap with atypical
*Further from equator, more likely to experience
*Responds well to treatment (light therapy, antidepressants, psychotherapy)
-But non-seasonal depression also responds well to light…
Postpartum depressive disorder
-Hormones, identity change, sleep loss, conflict with partner or family….
Persistent Depressive Disorder (PDD;
formerly Dysthymic Disorder/Dysthymia)
*Lower level but more sustained
*2 years, marked change in low mood
*Doesn’t meet criteria for full mdd
Models of mood disorders
Lot of overlap in symptoms and also highly comorbid between depression and anxiety disorders
Dimensional/Hierarchical Models
Internalizing tendency
Tripartite model
What they (mdd and anxiety disorders) have in common and disorder specific factors
Anhedonia = general distress/negative affect
Physiological hyperarousal (anxiety)= general distress/negative affect
(idk what this really means)
Epidemiology of MDD
Lifetime prevalence 16-17%
- 20-25% for women, 9%-12% for men
Point prevalence rates: 6% for women, 3% for men
Persistent Depressive Disorder: 3-6%
Marked sex differences
Rates lower in Asia than Europe and North America
-Depression higher risk in industrialized countries than developing countries (esp. PDD)
Prevalence rates may differ according to racial or
ethnic groups, but data are mixed
- Some data showing Black/ African-American groups
have lower lifetime prevalence (~10%) than White
Americans (~18%) (Williams et al., Archives of General
Psychiatry)
–But black americans more depressive symptoms (and more chronic), but less diagnosed (that’s why seems like more white americans with depression)
- Prevalence rates may be higher among Black youth
than among White youth
Similarly mixed evidence for prevalence rates in
studies looking at First Nations groups, Asian-American groups relative to Caucasian-American/
White participants
* Expression of depression may
differ cross-culturally
- Frequently more somatic (physical)
presentation in Asian, Latin
American, and North African
cultures (e.g., Parker et al., Social
psychiatry and psychiatric epidemiology, 2001)
– Headaches, loss of energy,
sleeplessness; not depressed, sad,
feeling down
Course of MDD
- Age-of-onset– usually teens/ mid-20’s
- 25% of the time, MDD preceded by low-grade, chronic
PDD/depression - Duration of episodes typically 5-6 months
- Predictors of longer episodes:
- Personality disorder
- Non-mood comorbid disorders
- 20% of the time, episodes will > 2 years
- At least ½ of individuals who have one depressive
episode will have at least one more - 1/2 to 2/3 will relapse
- 4-6 episodes over lifetime is average
- Dysthymic disorder (Persistent Depressive
Disorder): Very chronic course - Over 10 year study, 75% recovered
- But risk for relapse is high
- Suicide
- Some estimate 15% of people with
mood disorders will commit suicide - More likely: 5-6% inpatients, 2%
outpatients - Much higher than general population
- Suicide most common in the 1st 6
months after recovery
Etiology of MDD
Rates of disorders in probands and relatives
(see chart slide 36)
Genetic Contributions: McGuffin Study
* Study of consecutive admissions to Maudsley
hospital in London
* Excellent twin registry
* Look at “index twin”
* Find their co-twins
* 67 index twins (probands) with Bipolar
* 177 index twins with MDD
- Some monozygotic, some dizygotic
Results:
* Of monozygotic Bipolar twins, 67% of co-twins had a mood disorder
* Of dizygotic Bipolar twins, 19% of co-twins had a mood disorder
- Suggests a 96% heritability!
* Of monozygotic Bipolar twins, 40% of co-twins had Bipolar
* Of dizygotic Bipolar twins, 5% of co-twins had Bipolar
- 70% heritability
* Of monozygotic MDD twins, 46% of co-twins have MDD
* Of dizygotic MDD twins, 20% of co-twins had MDD
- 52% heritability
* BUT, to date, no reliable/ specific genetic differences identified
KendlerTwin Study
* National twin registry in Sweden
* 15,000 complete twin pairs
* Diagnostic interviews
* MDD
* For male twins: r=.31 for Mz, .11 for Dz
* For female twins: r=.44 for Mz, .16 for
Dz
Adoption Studies
* Adoptee= proband
* Looked at rates of disorder in biological and
adopted families
* also Adopted controls
* ONLY biological families had elevated rates of
mood disorders
* Again supporting notion that genetic factors are
playing a role.
Stress and Adversity: Early Adversity
* Freud: Loss of a parent
* PBI (Parental bonding instrument) (Parker)
- Two dimensions of caregiving:
– Care, nurturance
– Overprotection, control
- Depressed patients frequently
report parents lower in care
- Less consistently: higher in
overprotection.
- This interaction poses a heightened
risk for depression
* Abuse associated with higher rates
of depression
* Chronicity (Early adversity can make it more chronic)
Third Variable Problem: Genes
* Depression in parents, leads to
poor parenting, leads to
depression in children
* OR may be that kids who will
become depressed elicit more
negative parenting
* BUT, control for parental hx of
depression, association still there.
* Twin Studies:
- 1 twin sexually abused, the other
not
– Rates of depression higher in
the abused twin.
Stress and Adversity
* In 6 months prior to onset of MDD,
increased rate of stressful life events
* 20% of women who experienced these
events became depressed
* 75% of depressed women studied had
experienced such an event in the 6 months
prior
* Not seen in non-depressed
* Most powerful stressors related to themes
of loss:
- Loss of a loved one
- Loss of a job
- Loss of a cherished ideal or goal
* Depressed people more sensitive to the
effects of stress (e.g., Harkness & Monroe,
2002, 2006)
- But also generate more stress in their lives
(e.g., Hammen, 2006)
- Particularly interpersonal stress
* Distinction between TYPES of stressors
- Dependent
- Independent
* Depression associated with higher number
of independent events as well
Depression causes stress AND stress causes depression
Psychological aspects of MDD
Behavioral models: Reward and Positive
Reinforcement
* Skinner, Ferster, Lewinsohn:
* Depression related to a reduction in
behaviors that are positively reinforced
* Receive less positive reinforcement, mood
declines
* Become less likely to engage in behaviors
that receive positive reinforcement
Aaron Beck: Cognitive Triad
Negative views about oneself… negative views about the world… negative views about the future
Martin Seligman: Learned Helplessness
Dog and electric shock
Eventually just give up
Revising Learned Helplessness
* Reformulated in late 1970s (Seligman &
Teasdale)
* Focused on 3 dimensions of attributions:
- external vs internal
- global vs specific
- Stable vs unstable
* Internal, global and stable attribution styles
associated with depression
Laboratory Studies
* Cognitive schemas not readily accessible by
self reports.
- latent and activated by stress.
- Therefore need experimental laboratory
studies.
* Memory biases
-Memory Biases: SRET (relisten cuz idgi)
* Attentional biases
-notice faster the snake (bias for negativity) (idk, relisten)
-Stroop task
(name colour of the ink of the word)
(rewatch)
-Dot-probe task
(rewatch)
-Dichotic listening task
Yellow= task relevant ear
White = distractor box
People with depression more errors repeating task relevant ear, distracted if distractor = negative words like death, misery…
Summary
* Evidence for attentional biases in depression not terribly strong.
* Mixed results in each case.
* What is “threatening”?
-What are the best stimuli for detecting ‘bias’?
* Words?
* Angry faces?
* Fearful faces?
* Ambiguity/Moderately threatening stimuli?
