3.4. Depression and Psychosis
3.4. Depression and Psychosis
Bachelor-3 Psychology
Summary written by Amy van Wingerde
________________________________________________________________
, 3.4. Depression and Psychosis
Task 3: Depression
Sources
1A. Hengevelad et ala. (2009)
1B. Abramson et ala. (2002), Disner et ala. (2011)
2. Kho et ala. (2003), Pampalalaona et ala. (2004)
3. Weisz et ala. (2006), Fergusson et ala. (2002)
4. Casselalas et ala. (2005), DeJong et ala. (2010), Turecki et ala. (2016)
General informaton about depression from Hengeveld et al. (2009) and DSM-5
- Classificaton of the depressive disorderso Disruptive mood dysregulaation disorder (severe,
persistent irritabilaity in chiladren), major depressive disorder (inclauding major depressive
episode), persistent depressive disorder (dysthymia), premenstruala dysphoric disorder,
substance/medicationninduced depressive disorder, depressive disorder due to another
medicala condition, other specifed depressive disorder, and unspecifed depressive disorder.
- Common characteristcs are the presence of sad, empty, or irritablae mood, accompanied by
somatic and cognitive changes that signifcantlay afect the individualass capacity to function.
- What difers among them, is the timing, duration or presumed etiolaogy.
- More prevalent diagnostc featureso Mortalaity, tearfulaness, irritabilaity, brooding, obsessive
rumination, anxiety (separation anxiety in chiladren), phobias, excessive oorry over physicala
healath, and complaaints of pain (e.g., headaches; joint, abdominala, or other pains),
hyperactivity of the HPAnaxis, functionala abnormalaities in specifc neurala systems supporting
emotion processing, reoard seeking and emotion regulaation.
- Prevalenceo Range is 5n17%, it is a common disorder. The femalaenmalae ratio is 2o1, it is more
common in females.
- Likelaihood of onset increases oith puberty, but it may appear at any age.
- Etologyo Genetcs (alathough laess than in bipolaar disorder, serotonin transporter gene, in
combination oith stress, genenenvironment interaction); abnormal functoning HPA-axis
(too much cortisola, too big CRH activation, more ACTH and failaing feedback mechanism),
brain infuences (activity laoo in prefrontala areas and laef side of the brain, higher in right
side of the brain, hippocampus laooer activity, laooer activity in anterior cingulaate cortex and
higher activity in amygdalaa), abnormalites in circadian rhythms3 psychosocial infuences
(dependent laife events, neuroticism, introversion).
- Theories about the causes of depressiono Psychodynamic theories, behaviorala theories,
Beckss cognitive theory, helaplaessness and hopelaessness theories, ruminative response stylae
cognitive theory of depression.
- Treatmentso Pharmacotherapy (antidepressants for more norepinephrine and serotonin
(e.g., MAOIss, tricyclaic antidepressants, SSRIss), mood stabilaizers, antipsychotics) and other
biological therapies (ECT, TMS, deep brain stimulaation, bright laight therapy), and
psychotherapies (CBT, behaviorala activation treatment, interpersonala therapy, familay and
maritala therapy).
- Features associated with lower recovery rateso Psychotic features, prominent anxiety,
personalaity disorders, and symptom severity, in younger individualas, alaready experienced
mulatiplae episodes.
3.4. Depression and Psychosis
Bachelor-3 Psychology
Summary written by Amy van Wingerde
________________________________________________________________
, 3.4. Depression and Psychosis
Task 3: Depression
Sources
1A. Hengevelad et ala. (2009)
1B. Abramson et ala. (2002), Disner et ala. (2011)
2. Kho et ala. (2003), Pampalalaona et ala. (2004)
3. Weisz et ala. (2006), Fergusson et ala. (2002)
4. Casselalas et ala. (2005), DeJong et ala. (2010), Turecki et ala. (2016)
General informaton about depression from Hengeveld et al. (2009) and DSM-5
- Classificaton of the depressive disorderso Disruptive mood dysregulaation disorder (severe,
persistent irritabilaity in chiladren), major depressive disorder (inclauding major depressive
episode), persistent depressive disorder (dysthymia), premenstruala dysphoric disorder,
substance/medicationninduced depressive disorder, depressive disorder due to another
medicala condition, other specifed depressive disorder, and unspecifed depressive disorder.
- Common characteristcs are the presence of sad, empty, or irritablae mood, accompanied by
somatic and cognitive changes that signifcantlay afect the individualass capacity to function.
- What difers among them, is the timing, duration or presumed etiolaogy.
- More prevalent diagnostc featureso Mortalaity, tearfulaness, irritabilaity, brooding, obsessive
rumination, anxiety (separation anxiety in chiladren), phobias, excessive oorry over physicala
healath, and complaaints of pain (e.g., headaches; joint, abdominala, or other pains),
hyperactivity of the HPAnaxis, functionala abnormalaities in specifc neurala systems supporting
emotion processing, reoard seeking and emotion regulaation.
- Prevalenceo Range is 5n17%, it is a common disorder. The femalaenmalae ratio is 2o1, it is more
common in females.
- Likelaihood of onset increases oith puberty, but it may appear at any age.
- Etologyo Genetcs (alathough laess than in bipolaar disorder, serotonin transporter gene, in
combination oith stress, genenenvironment interaction); abnormal functoning HPA-axis
(too much cortisola, too big CRH activation, more ACTH and failaing feedback mechanism),
brain infuences (activity laoo in prefrontala areas and laef side of the brain, higher in right
side of the brain, hippocampus laooer activity, laooer activity in anterior cingulaate cortex and
higher activity in amygdalaa), abnormalites in circadian rhythms3 psychosocial infuences
(dependent laife events, neuroticism, introversion).
- Theories about the causes of depressiono Psychodynamic theories, behaviorala theories,
Beckss cognitive theory, helaplaessness and hopelaessness theories, ruminative response stylae
cognitive theory of depression.
- Treatmentso Pharmacotherapy (antidepressants for more norepinephrine and serotonin
(e.g., MAOIss, tricyclaic antidepressants, SSRIss), mood stabilaizers, antipsychotics) and other
biological therapies (ECT, TMS, deep brain stimulaation, bright laight therapy), and
psychotherapies (CBT, behaviorala activation treatment, interpersonala therapy, familay and
maritala therapy).
- Features associated with lower recovery rateso Psychotic features, prominent anxiety,
personalaity disorders, and symptom severity, in younger individualas, alaready experienced
mulatiplae episodes.
