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Mood Disorder Categories (DSM-IV) • Depressive disorders – Major depressive disorder, clinical depression – Dysthymia – Depressive Disorder Not Otherwise Specified (NOS) • Bipolar disorder – – – – Bipolar I Bipolar II Cyclothymic Disorder Bipolar Disorder NOS Changes from DSM-IV-TR to DSM-5 • Depressive Disorders contains new categories – disruptive mood dysregulation disorder • children up to age 18 years • replaces bipolar disorder in children – premenstrual dysphoric disorder – persistent depressive disorder • chronic major depressive disorder • dysthymic disorder • Major Depressive Disorder: changes to the organization of categories – bereavement exclusion removed • Bipolar Disorders has more emphasis on changes in activity and energy – bipolar I disorder includes “with mixed features” http://www.nimh.nih.gov/health/statistics/prevalence/major-depression-among-adults.shtml http://www.nimh.nih.gov/health/statistics/prevalence/major-depression-among-adolescents.shtml Gender Differences in Depression • Major Depression – Women twice as likely as men – But girls and boys have equal rates – Power Theory • Higher levels of physical and psychological abuse • Living in poverty • Overburdened by family & work responsibilities – Coping Style • Women are more interpersonally oriented • Respond to interpersonal stressors with rumination • Men more likely to use alcohol to cover up symptoms – Reactivity to Stress • HPA response to stress dysregulated • HPA modulated by estrogen levels? • Postpartum depression Symptoms of Clinical Depression • Clinical symptoms common to depression include – – – – – – Pervasive unhappiness and despair Negative, pessimistic thoughts Anhedonia (inability to experience pleasure) Loss of self-esteem Impairment of normal functioning (home, social, work) Suicidal ideas • Vegetative symptoms that warrant medication treatment (when seen with symptoms above) – – – – Appetite disturbance Sleep disturbance (early am wakening, frequent awakenings) Diurnal mood variation (worse in morning) Marked anhedonia “inability to experience pleasure in normally pleasurable acts” Role of genetics in depression • High concordance rates: (60%) in monozygotic twins • High rates of mood disorder in family members • No evidence of a single gene – small associations between the polymorphism in the serotonin transporter promoter region – association of Major Depression Disorder with polymorphisms gene for brain-derived neurotrophic factor (BDNF). • BDNF is related to recovery from stress Treatments for depression • Drug Therapy • Monoamine Oxidase (MAO) Inhibitors • Tricyclic drugs • Selective serotonin reuptake inhibitors (SSRIs) • Ketamine and leptin • Brain stimulation • Deep brain stimulation (DBS) • Vagal nerve stimulation • Electroconvulsive shock therapy (ECT) • Transcranial magnetic stimulation (TMS) • Cognitive behavioral therapy (CBT) Table 16.3 Drugs Used to Treat Depression The most commonly prescribed antidepressants in the US retail market in 2010 were Drug name Commercial name Drug class Total prescriptions Sertraline Zoloft SSRI 33,409,838 Citalopram Celexa SSRI 27,993,635 Fluoxetine Prozac SSRI 24,473,994 Escitalopram Lexapro SSRI 23,000,456 Trazodone Desyrel SARI 18,786,495 Duloxetine Cymbalta SNRI 14,591,949 Paroxetine Paxil SSRI 12,979,366 Amitriptyline Elavil TCA 12,611,254 Venlafaxine XR Effexor XR SNRI 7,603,949 Bupropion XL Wellbutrin XL NDRI 7,317,814 Mirtazapine Remeron TeCA 6,308,288 Venlafaxine ER Effexor XR SNRI 5,526,132 Bupropion SR Wellbutrin SR NDRI 4,588,996 Desvenlafaxine Pristiq SNRI 3,412,354 Nortriptyline Sensoval TCA 3,210,476 Bupropion ER Wellbutrin XL NDRI 3,132,327 Venlafaxine Effexor SNRI 2,980,525 Bupropion Wellbutrin IR NDRI 753,516 Antidepressant From Wikipedia, the free encyclopedia https://en.wikipedia.org/wiki/Antidepressant Drugs Used To Treat Depression Amitriptyline Placebo Effect in Depression • Effectiveness of antidepressant drugs typically reported as – 50-60 % symptom free – 20-30 % some improvement – 20 % no improvement • However, placebo effect: 50 – 80 % show improvement • Blind trials are difficult because most patients know they are getting a drug • Patients at the very extreme end of depression severity, showed the most improvement over placebo • Drug therapy plus Psychotherapy is most effective treatment Amine Depression Hypotheses • Biogenic amine hypothesis suggests that depression reflects a suboptimal level of NE, DA, EPI, or 5-HT in brain • Evidence from – Reserpine depletes CNS catecholamines (leads to depression) – Depressed patients have low levels of 5-HIAA (metabolite) – Drugs used to treat depression elevate synaptic levels of NE and 5HT (e.g. imipramine, ) • Problems for the amine hypothesis – Some drugs used to treat depression (bupropion) do not block reuptake of amines – Why doesn’t Cocaine reduce depression? – Why doesn’t Ecstasy reduce depression? – Why is there a temporal delay between drug administration, onset of amine changes, and reduction in depression? Role of Glutamate in Depression • Too much glutamate can overstimulate neurons causing collapse of the branches by which they communicate with other cells • One effect of antidepressants is to reduce the sensitivity of receptors in the PFC for glutamate • Antidepressant-like actions of compounds which reduce transmission at N-methyl-D-aspartate (NMDA) receptors • Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders. (2012) Sanacora G, Treccani G, Popoli M Neuropharmacology. Jan;62(1):63-77. Role of Glutamate in Depression • Treating depression with Ketamine – Blocking NMDA type of glutamate receptors – A single dose of ketamine has rapid and lasting antidepressant effects in patients with major depression or bipolar disorder. – Zarate CA Jr. A randomized add-on trial of an N-methyl-Daspartate antagonist in treatment-resistant bipolar depression. Arch Gen Psychiatry. 2010 Aug;67(8):793-802. – Zarate CA Jr. Rapid resolution of suicidal ideation after a single ketamine infusion in patients with treatment-resistant major depression. J Clin Psychiatry, 71:1605-11, 2010. Role of Stress in Depression • Dysregulation of HPA : to much cortisol • Damages hippocampus – Changes the shape, size and number of neurons • Suppressed nerve cell growth in a part of the hippocampus • Damages prefrontal cortex and the amygdala – smaller in people with recurrent depression Brain Activity Patterns from PET scan in Depression Increased activity in Prefrontal Cortex and Amygdala Diathesis-Stress Model • Diathesis is vulnerability or susceptibility – Genetic influences • High concordance rate in twin studies • family history of mental disorder • hypothalamic-pituitary-adrenal responsivity – Developmental • maternal stressors • childhood maltreatment • Interaction of Diathesis and Stress – Individuals with more vulnerability are more likely to become ill when challenged by stressors The Hypothalamic-Pituitary-Adrenal Axis in Depression Sleep and Depression Light therapy for Seasonal affective disorder (SAD) Bipolar disorder • Characterized by periods of depression alternating with expansive mood, or mania. • The rate of cycling varies–rapid cycling consists of four or more cycles in one year. • Some individuals may cycle several times in one day. • In Cyclothymia–a milder form of bipolar disorder–patients cycle between dysthymia (mild depression) and hypomania (increased energy). • Lithium is a mood-stabilizing drug used to treat bipolar disorder. The Treadmill of Depression