Mood Disorders

DSM-IV criteria for:
- MDD.
 Depressive symptoms: at least 2 weeks.
 Must include either loss of interest/pleasure & depressed mood.
 4 other symptoms must be present.
 Episodic.
 Every new episode experiences increases risk for another episode by
16%.
 Subclinical depression: can predict future occurrence of MDD.
 Can also cause troubles in functioning.
- Dysthymic disorder.
 Chronically depressed.
 More than ½ the time for 2+ years.
 Have 2 other depression symptoms.
 Not enough symptoms to qualify for MDD.
 Can worsen.
 95% develop MDD.
 Diff. btwn this & MDD: chronicity.
- Bipolar I disorder (B1).
 1+ episode of mania or 1+ mixed episode.
 Tend to recur.
 > 50% of ppl have 4+ episodes.
- Bipolar II disorder (B2).
 Milder form.
 At least 1 major episode of depression & at least 1 episode of hypomania.
- Cyclothymic disorder.
 Chronic.
 Symptoms for 2+ years.
 Frequent but mild symptoms of depression alternating with mild symptoms of
mania.
 At risk for developing episodes of mania & major depression.
Epidemiology & Consequences of:

- MDD:
 2x more common among women.
 3x more common among poor.
 Cross-cultural diff.:
 Asian symptoms: fatigue, weakness, inabilty to concentrate.
 Latinos: headaches, nerves.
 SAD (diff. in distance from equator).
 Prevalence of MDD increased.
 Age of onset decreased.
 Diff. in symptoms:
 Young: somatic complaints.
 Old: distractibility, memory loss.
 Often comorbid w/ anxiety disorders, substance-related disorders, sexual
dysfunctions, personality disorders.
 2/3 of ppl who have MDD have anxiety disorder at some point.
- Dysthymia:
 Comorbid w/ the same disorders as MDD.
 Avg. duration of symptoms: 5 years.
 More likely to require hospitalization, to attempt suicide, & to have impaired
functioning than ppl w/ MDD.
- Bipolar disorders:
 Mania:
 Flight of ideas.
 Mixed episodes: both mania & depression.
 Significant impairment.
 Symptoms last at least 1 week or requires hospitalization.
 Most ppl who experience mania will also experience depression at some
point.
 Hypomania:
 No significant impairment.
 Change in functioning that doesn’t cause problems.
 B1 is v. rare; only 1% of ppl meet the criteria for it.
 ~2% of ppl experience B2.
 ~4% of ppl experience cyclothymic disorder.
 Avg. onset: 20s.
 Decreasing.
 Equally often in men & women, but women experience more depressive
episodes.
 Comorbid w/ anxiety disorders.
 High suicide rates.
 High risk for other medical conditions (e.g., cardiovascular disease, etc.).
Subtypes of depressive disorders & bipolar disorders:

- Can be seasonal.
- B1 & B2 are rapid cycling if:
 Person experiences 4+ episodes within past year.
- Psychotic features: delusions, hallucinations.
- Catatonic features: extreme physical immobility, excessive peculiar physical movement.
- Postpartum onset: onset within 4 weeks postpartum.
- Melancholic: used only for episodes of depression.
 MDD w/ melancholic features might be a more severe type of depression.
Neurobiological factors:
Genetic influences:
- Heritability of MDD: 37%.
 Genes more important among women -> higher among women.
- BD is the most heritable of disorders.
 Can be as high as 93%.
Neurotransmitters:
- Original models:
 Depression: low levels of norepinephrine, dopamine, & serotonin.
 Mania: high levels of norepinephrine & dopamine, low levels of serotonin.
- Ppl w/ depression respond differently to drugs that increase dopamine levels.
 Functioning of dopamine is lowered in depression.
- In BD: dopamine receptors might be overly sensitive.
- Depression – Sensitivity to serotonin:
 Insensitive receptors: experience depression as serotonin levels drop.
 To lower serotonin, lower levels of tryptophan.
 Lowering levels tryptophan causes temporary depressive symptoms.
  ppl who’re vulnerable to depression might have less sensitive serotonin
receptors, so they respond more dramatically to lower serotonin levels.
Brain imaging studies:

- Structural studies: focus on whether there are fewer cells or connections within a given
region of the brain.
 Can show whether a person has lost connections btwn brain cells.
- Functional activation studies: can show whether there’s a change in the activity of a
brain region.
 Used to get info on how ppl use the brain cells they have.
- Amygdala: helps a person assess how emotionally important a stimulus is.
 Damage: fail to react to threatening stimuli.
- Hippocampus: retrieve memories of the stimulus.
- Prefrontal cortex, subgenual anterior cingulate: focus on the situation & execute
appropriate plans.
- In MDD – functional studies:
 Elevated activity in amygdala.
 Vulnerability to depression.
 Oversensitivity to emotional stimuli.
 Less active subgenual anterior cingulate, prefrontal cortex, & hippocampus
during exposure to emotional stimuli.
 Not able to plan as well.
- In MDD – structural studies:
 Smaller volume of subgenual anterior cingulate & prefrontal cortex.
 If the person has been depressed for a long time: smaller volume of
hippocampus.
- Changes in sensitivity in reward system:
 Less motivation to pursue rewards when depressed, overly focused on rewards
during mania (overactivity of basal ganglia).
- B1 – functional:
 Overactivity of amygdala.
 Decreased activity of hippocampus & prefrontal cortex.
- BD – structural:
 Loss of volume in prefrontal cortex.
- Ppl w/ BD have deficits in the membranes of their neurons (but this isn’t seen in MDD).
- Protein kinase C activity is abnormally high among ppl w/ mania.
 Protein kinase C is involved in how receptors function & how messages are sent
btwn neurons.
Neuroendocrine system:
- HPA axis: biological system that manages reactivity to stress.
 Overly active during episodes of MDD.
 Triggers release of cortisol.
 Depression: higher levels of cortisol.
 E.g., Cushing’s syndrome: oversecretion of cortisol. Ppl w/ this syndrome
experience depressive symptoms.
- Cortisol levels might be poorly regulated.
- Dex/CRH (dexamethasone suppression test):
 Used to measure cortisol regulation.
 In some ppl w/ mood disorders (esp. ones w/ psychotic features),
dexamethasone doesn’t suppress cortisol suppression like it normally does.
 In 80% of ppl w/ depression, there’s a deficit in cortisol regulation.
 Ppl who continue tos how elevated responses to the dex/CRH test are likely to
relapse within one year.
- Too much cortisol for a long period of time can damage the hippocampus (decrease its
volume).
- Ppl w/ BD might also have a poorly regulated cortisol system.
Social factors:
- Diathesis-stress model.
 Neurobiological factors may be diatheses, & life events are stressors.
 Life events may cause depression or depression may cause life events.
 Diatheses can be social, biological, or psychological.
- Some diatheses:
 Lack of social support.
 Expressed Emotion (EE):
 Family member’s critical/hostile comments toward or emotional
overinvolvement w/ the person w/ depression.
 High EE = strongly predicts relapse in depression.
 Marital discord.
Psychological factors:
Freud’s theory:
- Potential for depression created during oral period of childhood.
- Anger towards a lovedone gets directed inward.
Affect & neuroticism:

- 3 dimensions:
 Negative affect (distress & worry).
 Positive affect (happiness & contentment).
 Somatic arousal.
- Anxiety & depression expected to involve negative affect.
- Anxiety involves somatic arousal.
- Depression involves low levels of positive affect.
- Ppl who show high negative affect, low positive affect, & high somatic arousal are at risk
for comorbid anxiety & depression.
- Neuroticism predicts onset of depression.
- Low extraversion may predict onset of depression.
Cognitive theories:
- Beck’s theory:
 Ppl develop depression b/c their thinking is negative.
 Depression is assoc. with the negative triad:
 Self, the world, & the future.
 “world” = person’s own corner of the world.
 Ppl w/ depression acquire negative schemata.
 Negative schemata activate cognitive biases.
 Dysfunctional Attitudes Scale (DAS).
 High scores on DAS w/ neg. life events predict onset of MDD.
 High scores on DAS can predict relapse within next several years.
- Hopelessness theory:
 Seligman’s learned helplessness theory.
 Attributional style:
 Internal vs. external.
 Stable vs. unstable.
 Global vs. specific.
 Ppl who attribute negative life events to internal, stable, global causes
are likely to become depressed.
 Hopelessness theory: hopelessness is the most important trigger of depression.

Mood Disorders

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Mood Disorders

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DSM-IV criteria for:

Epidemiology & Consequences of:

Subtypes of depressive disorders & bipolar disorders:

Brain imaging studies:

Affect & neuroticism:

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