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symptoms nearly everyday for 2 weeks
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səhifə | 14/30 | tarix | 27.04.2018 | ölçüsü | 469 b. | | #49225 |
| 5 symptoms nearly everyday for 2 weeks 5 symptoms nearly everyday for 2 weeks Must have either sad, depressed mood or anhedonia Difficulties sleeping Shift in activity level Poor appetite with weight loss or increased appetite with weight gain Loss of energy or fatigue Negative self-concept Difficulty concentrating Lifetime prevalence—about 17 %, though some estimates are as low as 4-5% 90% recover in a year, but ¾ of cases will recur (average duration of an untreated episode is 8-10 months) Typical onset is age 24-29 Symptoms of anxiety are common (not factor analytically distinct in children)
Melancholic features—more severe type, loss of pleasure, more of a genetic loading Melancholic features—more severe type, loss of pleasure, more of a genetic loading Atypical features—mood reactivity (brightens at times in response to events). - May respond better to MAOIs than other subtypes
Seasonal pattern (AKA Seasonal affective disorder)
Genetic influences Genetic influences - 3x more common among blood relatives
- MZ concordance—46 %, DZ 20%
Biochemical factors - Low levels of norephinephrine and serotonin have been linked to depression
- Some theorists look to a balance of these two, dopamine and acetylcholine
- Hypothalamic-pituitary-adrenal axis
- --elevated levels of cortisol in 60-80% of severely depressed hospitalized pts
- Hypothalamic-pituitary-thyroid axis
- --20-30% of depressed with normal thyroid show dysregulation here. Increasing thyroid hormone levels may help
Sleep and other rhythms - Greater amounts of REM sleep, enter it earlier in night
- Circadian rhythms may be out of sync, particularly in SAD
Psychoanalytic Psychoanalytic Beck’s cognitive theory - Depressogenic schemas/Dysfunctional beliefs
- Beliefs predispose a person to depression
- Develop in childhood and adolescences as a function of negative experiences with parents and sig others
- Activated by current stressors or depressed mood—create a pattern of automatic negative thoughts
- Negative cognitive triad—self, world and future
- Negative cognitive biases—
- Arbitrary inferences
- Selective abstraction
- Overgeneralization—overall, sweeping conclusions
- Magnification and minimization
- Dichotomous or all-or-none thinking
- Support for Beck’s theory—strong support as a descriptive theory, mixed but positive support as a causal theory
Helplessness and Hopelessness theories of depression Helplessness and Hopelessness theories of depression - Learned helplessness—individual’s passivity and sense of being unable to act and control life is acquired through unpleasant experiences
- Revisions—attribution theory—Global, stable, internal
Hopelessness-expectation that desirable outcomes will not occur. Has generated a Interpersonal theory - Social support
- Depressed people elicit negative reactions
- Depressed people seek other depressed people and bring others down, too
Stressful life events - Severely stressful life events play a causal role in 20-50% of cases
- Risk and resilience
Personality risk factors
Cyclothymia—cycles between hypomania and depression Cyclothymia—cycles between hypomania and depression - Mild form of major bipolar disorder
Bipolar Disorders (I and II) - Kraepelin 1899—manic-depressive insanity
- Bipolar I
- One episode of mania or mixed episode
- Bipolar II
- Hypomania
- More common than bipolar I
Symptoms of depression are almost identical to that of major depression Suicide attempts may be more common in bipolar May be misdiagnosed (until first mania appears) Rapid cycling in 5-10% 24 % relapse in 6 mos, 77 % have a new episode in 4 yrs, 82 % by 7 yrs Onset typically in early 20s
Genetic influences Genetic influences - Account for 80-90% of the variance
- About 70% of heritability is distinct from unipolar
- Polygenic
Neurotransmitters - Increased levels of dopamine may be related to mania
- Abnormalities in how ions are transported across neural membranes (this is where lithium helps)
Some differences in brain structures—enlarged basal ganglia and amygdale
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