Mood Disorders, Treatments, and Exam Focus

Classification of Mood Disorders

  • Two broad categories
    • Unipolar (Depressive) Disorders
    • Mood range: “roughly normal” ⟶ depressed, then returns.
    • Recurrent episodes common unless effectively treated.
    • Sub-types to know:
      • Major Depressive Disorder (MDD) – “major depression.”
      • Dysthymia (Persistent Depressive Disorder)
      • Chronic (≥ 2 yrs), milder intensity.
      • Disruptive Mood Dysregulation Disorder (DMDD)
      • Pediatric diagnosis; severe temper outbursts + persistent irritability.
    • Bipolar Disorders
    • Alternating poles: depression ↔ mania/hypomania.
    • Sub-types to know:
      • Bipolar I – at least one full manic episode.
      • Bipolar II – hypomanic episodes + major depression (no full mania).
      • Cyclothymia – ≥ 2 yrs fluctuations between hypomanic-like symptoms & mild depressive symptoms (never meeting full criteria).

Psychological Treatment Highlight: CBT

  • Cognitive-Behavioral Therapy reduces risk of future, deeper depressions.
  • Targets:
    • Maladaptive coping styles.
    • Negative thinking loops / cognitive distortions.
  • Builds skills that buffer against relapse.

Pharmacological Treatments & Study Chart Advice

  • Instructor will devote ≈ 10 questions (≈\frac{10}{50}=0.20 or 20 %) on medication content; recommends a comparative chart:
    • Columns: Disorder | Drug Class | Prototypes | Mechanism (optional) | Side-effects.

Antidepressants (Primarily for Unipolar Depression)

  • SSRIs (Selective Serotonin Re-uptake Inhibitors)
    • Prototypes: Prozac, Lexapro, Zoloft, Paxil.
    • Common side-effects:
    • Nausea (≈ 2 weeks, dose titrated slowly).
    • Insomnia → may require adjunct sleep aid (risk: poly-pharmacy).
    • Sexual dysfunction: desire intact but anorgasmia.
    • Overall effect: elevate mood but also dampen extreme positive affect.

Mood-Stabilizing Agents (Primarily for Bipolar)

  • Lithium – “gold standard.”
  • Anticonvulsant mood stabilizers – e.g.
    • Carbamazepine.
    • (Atypical antipsychotic) Abilify.
  • Conceptual mechanism: flatten mood amplitude (reduce highs & lows).
  • Critical issue: non-compliance much higher in bipolar than in unipolar depression.
    • Reasons:
    1. Manic phase is pleasurable/“exhilarating” → patient misses the high.
    2. Disorder-related traits: impulsivity, poor self-regulation, disorganization.

Natural / Lifestyle Intervention

  • Aerobic exercise
    • Elevates heart & respiration rates for sustained periods.
    • Evidenced to trigger physiological changes overlapping with antidepressant effects (unknown exact mechanisms).
    • No medication side-effects.
    • Barrier: low motivation during depressive episodes → value of pre-existing habit.
    • Personal anecdote: instructor’s swim & dry-land workouts; post-exercise mood & body sensations markedly improved.

Neurobiology of Mood Disorders

  • Frontal Lobe Activity
    • Depression: Generally reduced activity, especially left frontal lobe.
    • Schizophrenia also shows frontal hypoactivity but more diffuse.
  • Amygdala Activity
    • Heightened in depression and anxiety disorders.
    • Supports link between emotional reactivity & mood dysregulation.

Genetics & Stress (Diathesis–Stress Model)

  • Shared genetic liability for major depression & anxiety disorders (twin studies).
  • Genes create vulnerability but significant stressors are required for expression.
    • Common life events, losses, chronic adversity, etc.
  • Pandemic example: population-wide stress elevates depression/anxiety rates, disproportionately affecting lower socioeconomic groups (job loss, unstable healthcare, etc.).
  • Family history as estimator: higher number of depressed/anxious relatives → higher personal genetic risk.

Twin-Study Graph (Explained)

  • Four strata (descending genetic risk):
    1. Identical twins with depressed co-twin (highest risk).
    2. Non-identical twins with depressed co-twin.
    3. Non-identical twins with no depression.
    4. Identical twins with no depression (lowest risk).
  • Findings:
    • When stressful events absent → all groups show low & similar depression rates.
    • When stressful events present → clear dose–response: higher genetic risk = higher depression prevalence.
    • Even “low-risk” individuals display increased depression under severe stress → genetics not the sole path.

Neurochemistry (Brief Mentions)

  • Monoamine / serotonin theory is an “incredible simplification.”
    • Real mechanisms more complex; deeper study in psychopharmacology.
  • Mania parallels pharmacological dopamine & norepinephrine surges (cocaine/amphetamine analogy).

Compliance & Self-Regulation Themes

  • Medication adherence crucial; noncompliance = relapse.
  • Organizational demands of daily dosing clash with impulsivity & executive deficits in bipolar patients.

Holistic View of Depression

  • Not purely “medical” – integrates biological, psychological, and environmental factors.
    • Example case: family breakup, child injury, violence → massive environmental stress fueling depression.
  • Medication helpful but only one component of multifaceted treatment plan.

Exam Preparation Reminders

  • Memorize:
    • Diagnostic distinctions (Bipolar I vs II, cyclothymia, dysthymia, DMDD).
    • Drug classes, prototypes, and side-effects.
    • Brain structures associated with each disorder.
  • Use charts & bullet notes; content is memorization heavy, not conceptually hard.