Depression Flashcards
DSM-5 Depressive Disorders
- Disruptive Mood Dysregulation Disorder
- Major Depressive Disorder
- Persistent Depressive Disorder (Dysthymia)
- Premenstrual Dysphoric Disorder
DSM-4 Mood Disorders
- DSM-4 Depressive (Unipolar) Disorders o Major depressive disorder o Dysthymic disorder - DSM-4 Bipolar Disorders o Bipolar I and II - Extremes in normal mood
DSM-5 Major Depression
- Major Depressive Disorder:
o A single or recurrent depressive episode - Major Depressive Episode:
o Depressed mood most of the day, nearly every day
o Markedly diminished pleasure/interest in activities
o Significant weight loss or gain
o Insomnia or hypersomnia nearly every day
o Psychomotor agitation or retardation nearly every day
o Fatigue/loss of energy nearly every day
o Feelings of worthlessness, excessive guilt nearly every day
o Diminished ability to concentrate nearly every day
o Recurrent thoughts of death, suicide, suicide attempts
• 5 or more is needed, (including 1/ or 2/) in a 2-week period
• There has never been a manic episode or a hypomanic episode
Differences between DSM-4 and DSM-5 Major Depression
DSM-4 included bereavement period: persist longer than 2 months, DSM5 does not have this
DSM-5 Persistent Depressive Disorder (= DSM4 Dysthymia)
- Milder symptoms but more long running
- Depressed mood most of the day, more days that not
- Presence, while depressed, of 2 (or more) of the following:
o Poor appetite or overeating
o Insomnia or hypersomnia
o Low energy or fatigue
o Low self-esteem
o Poor concentration or difficulty making decisions
o Feelings of hopelessness
o No more than 2 months ‘normal’ mood in 2-years
o No manic features
o Symptoms are milder than major depression
o May also develop Major Depressive episodes
o Symptoms can persist unchanged over long periods (e.g., 20 years or more)
DSM-5 Disruptive Mood Dysregulation Disorder
- Severe recurrent tempter outbursts (verbal rages, physical aggression) that are grossly out of proportion in intensity or duration to the situation or provocation
- The mood between temper outbursts is persistently irritable or angry, and is observable by others (e.g. parents, teachers, peers)
- Childhood disorder → The diagnosis should not be made for the first time before age 6 or after the age of 18
DSM-5 Premenstrual Dysphoric Disorder
- In majority of menstrual cycles, at least 5 symptoms must be present in final week before onset of menses, start to improve within a few days after onset of menses and become minimal or absent in week post menses
- Symptoms include marked affective lability, irritability, anger, depressed mood, anxiety, decreased interest in usual activities, difficulty in concentration etc.
Summary of DSM Changes
- DSM-IV Mood Disorders –> DSM-5 ‘Depressive disorders’ vs ‘Bipolar and Related Disorders’
- DSM-IV Dysthymia –> DSM-5 ‘Persistent Depressive Disorder’
- Removed Grief exclusion from diagnosis of Major Depressive Disorder
- Added ‘Disruptive Mood Dysregulation Disorder’ in DSM-5
- Added ‘Premenstrual Dysphoric Disorder’ in DSM-5
DSM-5 Major Depression
- Subtypes/specifiers: MD with…
o Anxious distress
o Seasonal pattern (Seasonal Affective Disorder)
o Peripartum onset (Postnatal Depression)
o Atypical features (Weight gain, oversleep, rejection sensitivity)
o Psychotic features
o Melancholic features → do not respond to positive events, unable to experience positive affect, feel a distinct quality of depressed mood
Alternative Subtyping (Parker, 2000)
- Melancholic, psychotic, non-melancholic subtypes
o Assumes different symptoms, causation and treatment
o Melancholic depression: Lack of reactivity/total loss of pleasure, Distinct quality of mood, Mood worse in morning, Early morning awakening (sleep disturbance), Excessive/overwhelming guilt, Weight/appetite loss, Marked psychomotor agitation - Melancholic and psychotic subtypes are seen as ‘endogenous depression’ (biological)
o Best treated with biological treatments
o Melancholic less likely to respond to placebo
-Non-melancholic usually triggered by major life event - Evidence: difference in severity, rather than in cause
Prevalence of MDD
- 16.4% lifetime prevalence (Kessler et al, 2003)
- 3-5% one-year prevalence in Australia (3% of men, 5% of women)
o Steady increase in prevalence since 1950s
o Steady decrease in age of onset (younger onset)
• Increase speed of change/stress
• Decreased social support/family support
• More acceptable to report symptoms –> Overdiagnosis - Gender imbalance (2:1) → Twice as many women than men –> Emerges during adolescence, evens out after 65
Biological Influences of MDD
- Genetic:
o Family studies: High rate in relatives of probands
o Twin studies: Concordance rates higher in identical twins than in fraternal twins
o Adoption studies: Data is mixed - Neurochemistry:
o Low levels of Nonadrenalin, Dopamine, Serotonin → know they are effected but no good evidence for how mechanism, absolute levels are unlikely to be the cause
o Most studies are correlational, don’t know if chemical imbalance causes depression, if depression causes imbalance or how it is effected - Brain structures
o Amygdala, hippocampus, prefrontal cortex, anterior cingulated → differences between people with current or history of depression vs. no depression - Neuroendocrine system (hormonal)
o Over activity in the Hypothalamic-pituitary-adrenocortical axis (HPA Axis)
o Involved in regulating response to stress, excess cortisol (stress hormone) → related to damage to hippocampus? Lower density of serotonin receptors?
o Implicates role of (early) stress in depression
Importance of genetic influences?
- Just having biological factors does not determine if individual will definitely get depression, not mutually exclusive but interactive
- Respond to negative life events differently
- Interaction between genetic vulnerability and negative life events
Psychological Influences - Learned Helplessness Theory
- Learned Helplessness Theory (Seligman, 1975)
o Lack of control over life events
o Monkey receiving shocks, one can control the other can’t
Psychological Influences - Attribution Theory (Abramson, Seligman & Teasdale, 1978)
o Internal vs. external attributions
o Stable vs. unstable attributions
o Global vs. specific attributions
o Individuals with depression do the opposite, positive events due to external features, not themselves
• Interaction between cognitive style and life events
Psychological Influences - Hopelessness Theory (Abramson, Metalsky & Alloy, 1989)
o Helplessness expectancy plus
o Negative outcome expectancy
o Hopelessness is sufficient cause of depression
Psychological Influences- Schema Theory (Beck, 1976)
o Observed people with certain disorders tend to think differently than those without disorders or with other disorders
o Pre-existing negative schema, knowledge structures in long-term memory, effects behaviour, thoughts, feelings
o Developed during childhood (especially if vulnerable)
o If you have pre-existing belief, you look for things that are consistent with this belief → avoid cognitive dissonance
o This strengthens underlying belief
o 3 main schemas related to depression: the self, the world in general, and other people in general
o Negative schemas activated by stress, especially if stressful event is related to schema
• Results in cognitive biases (memory, attention, interpretation) → arbitrary interference, over-generalisation, magnification
o Depression cognitive triad:
• Negative thoughts about the self, the world, the future becomes dominant in consciousness
Psychological Influences - Response style theory (Nolen-Hoeksema, 2002)
o Dealing with content of thinking and process of thinking → what causes them to think of things in this way
o Rumination vs. distraction, problem solving, etc
• Women found to ruminate more than males, males tend to distract themselves more → suggests gender difference in prevalence
Psychological Influences - Create Depressive Circumstances?
- Depressed people cause more negative life events in their own lives, strong heritability factor of tendency to think to create these negative events → dependent negative events
o Interpersonal approaches → causal factors more important
o Interpersonal relations are negatively altered as a result of depression
o Depressed people have limited social support networks, elicit rejection and seek excessive reassurance from others, have/display limited social skills
o Stress-generation hypothesis → Depressogenic cognitions and behaviours generate negative life events and self-generated negative life events may partly explain depression recurrence
o 16% increase, each episode increases likelihood of having another depressive episode, trigger is easier as more practice
Psychological Influences
Learned Helplessness Theory Attribution Theory Hopelessness Theory Schema Theory Response style theory
Biological Treatments - Electroconvulsive Therapy (ECT)
o First introduced in 1938 to treat schizophrenia
o Only effective treatment for MD prior to 1950s → still very effective for severe depression despite negative reputation (85+%)
o Applying brief electrical current to the brain
o Results in temporary seizures
o A course of 6 to 10 sessions over 2-3 weeks
o Modern day very rare, only used for individuals who do not response to other treatment, put to sleep and muscle relaxant is used
o Relapse is common, few side effects (short-term memory loss)
o Uncertain why/how ECT works, what it changes in the brain
Pharmacological Treatment - Monoamine Oxidase Inhibitors (MAOIs)
o Introduced in 1856 first MAOI: iproniazide
o Originally used to treat tuberculosis
o Takes 14-21 days to take effect
o Break down monoamines → especially serotonin/norepinephrine
o Inhibitors block Monoamine Oxidase (A and B)
o Serious side effect → can cause hypertension, stroke if not on strict diet, must avoid Tyramine (beer, red wine, cheeses), ideally MAOI
o Tricyclic Medications
o Introduced early 1960s: Imipramine, originally for psychosis
o Increased suicide risk between 10th-14th day
o Negative side effects are common
Pharmacological Treatment - Tricylic Medications
o Introduced early 1960s: Imipramine
• Originally tried to treat psychosis
o Block presynaptic reuptake of Serotonin and Noradrenaline (Norepinephrine)
o 14-21 days to take effect
o Still widely used (Tofranil, Tryptanol)
o Vegetative symptoms often lift first
o Increased suicide risk between 10th-14th day
o Negative side effects are common:
• Anti-cholinergic: dry mouth, blurred vision, tremor
• Cardiotoxicity
Pharmacological Treatment - Selective Serotonin Reuptake Inhibitors (SSRIs)
o Introduced in 1980’s: Fluoxetine (Prozac)
o Drugs of choice at present
• Seltraline (Zoloft), Paroxetine (Aropax)
o Specifically block reuptake of Serotonin
o Negative side effects are fewer, less serious
• Insomnia, agitation, nausea, sexual dysfunction
o BUT: Possible risk of suicide, especially in children/adolescents (Paxil/Aropax)
• ‘off label’ use has been common until recently
• FDA, TGA now recommends warning labels
Biological Treatment - Drug Problems
- Extrapolate from treatment effectiveness to
o Neurochemical causes of Mood Disorders
• “Depression is caused by low levels of serotonin” (?) - Problems:
o Drug effects also on non-depressed people
o Non-specificity of treatment effects
o Timing of action not in sync with effect
• Uncertain how/why antidepressants work
• Possibly slow changes reversing stress-induced hippocampal damage? (Duman, Heninger & Nestler, 1994; Sapolsky, 2000)
Psychological Treatments - Brief Psychodynamic Therapy
o Some evidence for effectiveness
Psychological Treatments - CBT
o Addresses cognitive errors in thinking
• NOT positive thinking
• A.T. Beck , A. Ellis
o Includes behavioral components
• Behavioral activation, Behavioural experiments
o Outcomes are comparable to drug therapy
• Lower relapse rates vs. drug treatment alone
• Meta-analysis: 29 vs 60% (Gloaguen et al, 1998)
Mindfulness-Based Therapies (MBCT, MBSR)
Psychological Treatments - Interpersonal Psychotherapy (IPT)
o Beginning / exacerbation of depression:
o Interpersonal/role disputes
• Communication analysis, role expectations
o Role transitions
• Loss of relationship, marriage, job change, illness
• Forming new relationships, expanding old ones
o Interpersonal deficits
• Limited social support network
• Social skills training
o Outcomes are comparable to CBT
Which Treatment?
- Drugs or psychotherapy?
o Recommendations: drugs as first choice
• no research-based evidence (Seaman, 1999) - Drugs for ‘endogenous/organic/biological’ (melancholic) depression, psychotherapy for ‘reactive’ (non-melancholic) depression
o No good evidence (Zimmermann & Spitzer, 1989) - Client characteristics for CBT success:
o Introspective, abstract thinker, less rigid, more organised, conscientious
