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Antidepressants and Treatment of Mood Disorders Anita S. Kablinger M.D. Associate Professor Departments of Psychiatry and Pharmacology Outline of Lecture • • • • • • Definitions DSM-IV diagnoses and criteria Epidemiology Neurobiology Psychosocial theories Treatments Definitions • Depression can refer to many things and mean different things to different people • Symptom versus syndrome • However, for a clinical depression consistent with DSM-IV, this must lead to functional impairment DSM-IV Diagnostic Categories • Major Depression • Dysthymia • Depressive Disorder NOS • Bipolar Disorder, Type I or II • Cyclothymia • Bipolar Disorder NOS • Mood Disorder secondary to GMC • Substance-Induced Mood Disorder • Adjustment Disorder (separate classification) Epidemiology • Depression is the most common cause of disability in the world • U.S. costs approximate 43$ billion per year for mood disorders • Lifetime prevalence rates: (according to NCS), 21-24% for women and 12-15% for men Major Depressive Disorder (MDD) • >2 week period of change in behavior with 5 of the following: – – – – – *depressed mood *anhedonia appetite disturbance sleep disturbance psychomotor disturbance – fatigue or loss of energy – worthlessness or guilt – impaired concentration – suicidal thoughts • * 1/5 symptoms must be these • Rule out physical cause Time Course of MDD • Often lasts for a year without treatment • Chances increase by 50% for another episode after current episode (i.e. high relapse and recurrence rates) • Many go on to experience chronic depression (but may be a result of inadequate treatment) Heritability of Mood Disorders • Genetic factors very important • RR of MDD is 2-5x greater in relatives of depressed patients than controls • First degree relatives of Bipolar patients are 24x more likely to develop BAD than general population • Twin and adoption studies help to understand and define this illness Psychosocial Theories of Depression • Risk factors include: – – – – – – recent stressors poor social support system history of early parental loss gender family history of depression negative cognitive style Theories of Depression • NE and DA broken down to variety of products through MAO and COMT • 5HT is broken down by MAO to 5-HIAA • Major mechanism for terminating signal is neuronal reuptake • Monoaminergic Theories – Reserpine (early antihypertensive) – Iproniazid (used to treat TB) – Imipramine (originally studied as an antipsychotic) – Drugs enhancing noradrenergic functioning were antidepressants (eg. stimulants) Indoleamine Hypothesis of Depression • Serotonin is functionally deficient in depression – Decreased brain 5-HT and CSF 5-HIAA in many depressed patients – Antidepressants tend to increase central serotonin transmission – Depressed patients show reduction in 5-HT reuptake sites – Blunted neuroendocrine challenges Neurotransmitter Hypothesis of Mood Disorders • Led to catecholamine hypothesis – NE ↓ in depression and in mania – 5-HT ↓ production or reuptake in depression • Flaws: depression or mania not reliably produced and clinical response exceeds mechanism of action of drug Neurobiology of Mood Disorders • Neuroendocrine abnormalities: reflect central neurotransmitter dysfunction – hyperactivity of HPA: increased cortisol, nonsuppression of cortisol in DST – blunting of TSH release following TRH infusion – blunting of GH release with alpha-2 adrenergic agonism and serotonin-mediated increases in prolactin Other Alterations in Depression – – – – CRH acetylcholine activity GABA levels Excessive glucocorticoid activity in psychotic depression – Hippocampal volume loss Neurobiology of Mood Disorders • Sleep abnormalities: usually found in endogenous depression – – – – – – prolonged sleep latency shortened REM latency and change in timing increased wakefulness decreased arousal threshold early morning awakening reduced stage 3 and 4 sleep Kindling-Sensitization Hypothesis of Mood Disorders • Suggests that repeated exposure to stress and/or neurochemical changes during depressed episode sensitize brain regions responsible for affect • Repeated episodes may permanently alter systems within the CNS • Leads to shorter well periods, increased frequency and severity of illness Treatments • • • • • • Pharmacotherapy Psychotherapy Social interventions ECT TMS VNS Which Medication? • • • • • Safety Tolerability Efficacy Payment Simplicity Available Types of Pharmacotherapy • • • • • • • Tricyclic antidepressants (TCA) MAOI’s SSRI’s SNRI’s Atypical antidepressants Mood stabilizers Antipsychotics General Treatment Rules • Often takes 4-6 weeks for response • Monitor for response versus remission • Vegetative symptoms tend to improve first, cognitive symptoms take longer • SSRI’s are the first line of treatment for most MDD’s • Address biopsychosocial needs and maintain meds for 6-12 months Tricyclic Antidepressants • Available for more than 30 years • Cheap but not clean • Act by NE and/or 5 HT presynaptic reuptake inhibition • Side effects include anticholinergic effects, orthostasis, slowing of cardiac conduction • Secondary better than tertiary compounds Selective Serotonin Reuptake Inhibitors • • • • • Produce response rates close to 70% Safer and better tolerated than TCA’s Given once daily Starting and therapeutic doses often similar Most common side effects include GI symptoms, HA, insomnia, anxiety, and sexual dysfunction • Five available in the U.S. Novel or Atypical Antidepressants • Bupropion (NE and DA reuptake inhibition) • Trazodone (5 HT2 alpha-ANT) • Venlafaxine and Duloxetine (NE and 5 HT reuptake blockers – SNRI’s) • Mirtazapine (presynaptic alpha 2 ANT and 5 HT2 and 5 HT3 ANT) Psychotherapy in Depression • • • • • • Supportive Insight-oriented Interpersonal Cognitive-behavioral Psychodynamic Individual, group or family