TASK 6 - MOOD DISORDER (DEPRESSION) Flashcards
depression
= sadness, apathy, hopelessness, low energy
- anhedonia
- psychomotor retardation: slowed down, talk more quietly, report feeling chronically fatigued + do not react quickly enough
- psychomotor agitation: exhibit physical agitation, cannot sit still, move around and fidget aimlessly
anhedonia
= diminished interest/pleasure in almost all activities most of the day, nearly every day
DSM-5 (MDD)
A.
five or more of the following symptoms have been present during the same2-WEEK PERIOD and represent a change from previous functioning; one of the symptoms is 1 or 2
- depressed mood most of the day, nearly every day (objective/subjective)
- anhedonia (subjective/objective)
- significant weight loss/gain (5% of the body weight in a month)
- insomnia/ hypersomnia nearly every day
- psychomotor agitation/ retardation nearly every day (must be observable by others)
- fatigue/ loss of energy nearly every day
- feelings of worthlessness or excessive/inappropriate guilt (may be delusional) nearly every day
- diminished ability to think or concentrate, or indecisiveness, nearly every day (subjective/objective)
- recurrent thoughts of death, suicidal ideation without a specific plan or a suicide attempt or a specific plan for committing suicide
DSM-5 (MDD)
B.
symptoms cause clinically significant distress/impairment in social/occupational/ other important areas of functioning
- impairment
DSM-5 (MDD)
C.
not attributable to other substances or medical condition
- medical exclusion
DSM-5 (MDD)
D.
not better explained by another disorder
- psychopathological exclusion
DSM-5 (MDD)
E.
there has never been a manic or hypomanic episode (this exclusion doesn’t apply if all the manic/hypomanic-like episodes are substance induced or attributable to another medical condition)
- bipolar exclusion
subtypes (MDD)
- persistent depressive disorder (dysthymic disorder): symptoms for at least 2 years (for children it’s 1 year)
- requires 2 or more: poor appetite, insomnia/hypersomnia, low energy/fatigue, low self-esteem, poor concentration, hopelessness
- must never have been without symptoms for more than 2 months - anxious distress: prominent anxious symptoms
- mixed features: at least 3 symptoms for mania
- melancholic features: physiological symptoms of depression are particularly prominent
- psychotic features: presence of mood-congruent or mood-incongruent delusions or hallucinations (schizo-affective)
- catatonic features – show strange behaviours (= catatonia) ranging from complete lack of movement to excited agitation
- seasonal pattern: seasonal affective disorder (SAD); 2 years of experiencing and fully recovering from major depressive episodes (recover when daylight hours are long)
- peripartum onset: onset of major depressive episode during pregnancy or in the 4 weeks following delivery
prevalence (MDD)
- increasing
- large differences across genders + cultures: women are 2x as likely
causes
- genetics
- moderate heritability (30-40%)
- 1st degree relatives 2 to 3 times more likely
- stronger genetic base for early onset depression
- serotonin transporter gene
causes
- biological/molecular
- reduction of the amount of neurotransmitter in the synapses
- monoamine neurotransmitters: norepinephrine, serotonin, dopamine (limbic system)
causes
- biological/structural
- PFC: reduced activity + grey matter (esp. left side: involved in goal-orientation)
- anterior cingulate: less active (response to stress; also emotion regulation)
- hippocampus: smaller volume + lower activity
- -> result of chronic arousal of body’s stress response (has many receptors for cortisol which is chronically elevated –> ruins the old neurones)
- amygdala: large + increased activity (emotion, fear)
theories
- HPA axis
- normal response to stressor: hypothalamus releases CRH (corticotropin-releasing hormone) onto receptors of anterior pituitary –> releases corticotropin into bloodstream –> stimulates adrenal cortex –> releases cortisol into bloodstream –> helps body fight the stressor or flee from it
- when stress over: hypothalamus has cortisol receptors that detect increased levels -_> decreases CRH
DEPRESSION: chronic hyperactivity of HPA axis –> elevated levels of CRH + cortisol –> inhibits receptors for monoamine neurotransmitters + hippocampal neurogenesis –> volume reduction in several brain areas (e.g. hippocampal atrophy)
–> neurogenesis is inhibited by excessive cortisol secretion - early traumatic stress can lead to some of these abnormalities (predispose people to depression)
- trait-level rather than state level –> vulnerability marker
- substantial heritability
- declarative memory impairment also between episodes + in non-depressed
behavioural theories
- life stress
= life stress reduces positive reinforcers in a person’s life
- life stress –> withdrawal –> further reduction of positive reinforcers –> more withdrawal
- esp. likely for people with poor social skills
- might be reinforced by sympathy + attention it engenders in others
behavioural theories
- learned helplessness theory
= uncontrollable negative event is most likely to lead to depression as it leads people to think that the situation isn’t controllable
cognitive theories
- negative cognitive triad
= negative views of themselves, the world & the future
- Beck
cognitive theories
- reformulated learned helplessness theory
= people habitually explain negative events by causes that are internal, stable + global
- experience long-term learned helplessness deficits + loss of self-esteem
cognitive theories
- hopelessness depression
= people make pessimistic attributions for the most important events in their lives & think they have no way of coping with the consequences (more likely to develop major depression + relapse)
cognitive theories
- ruminative response style theory
= focus on how they feel + identify many possible causes without doing anything about them + continue to ruminate about their depression
(Emma Ruminating Trinker)
theories
- cognitive processes + emotion regulation
= key symptoms of depression: sustained negative affect, deficiencies in emotion regulation
- through underlying processes
1. negative attention bias
2. negative interpretation bias
3. memory bias
4. deficits in cognitive control
underlying mechanisms
1. biased attention to negative events
= difficulties in not paying attention to negative emotions/stimuli
- important role in vulnerability to depression
- difficulties in disengaging from negative stimuli (not more likely to shift attention to negative events)
- don’t use effective emotion regulation strategies like distraction –> difficulties to see positive aspects –> hindering more balanced appraisal of event
underlying mechanisms
2. negative interpretation bias
= interpret stimuli negatively
- could result in mood-congruent interpretations of events
- make it more difficult to see situation from different perspective
underlying mechanisms
3. memory bias
= enhanced memory for negative relative to positive information
- leads to difficulties in accessing mood-incongruent material
- biased memory may also affect interpretation of situations
- over-general memory = associated with difficulties in problem solving, imagining future events; less emotionally charged
- -> inhibitory dysfunction may underlie
- -> rumination may maintain over-general memory (difficult to focus on goal of retrieving specific event)
underlying mechanisms
4. deficits in cognitive control
= can’t inhibit negative material from entering WM + cant remove previous negative material (difficulties keeping irrelevant emotional info from entering + removing info from WM)
- differential directed forgetting effect
- may interfere with ability to override biased attention
- leads to maladaptive ER-strategies –> increased tendency for rumination
- -> rumination = reduced ability to update WM
theories
- interpersonal
= chronic conflict in their relationships
- heightened need for approval + expression of support from others (annoy others)
- rejection sensitivity + don’t believe affirmations
theories
- sociocultural
- more recent generations at higher risk
- due to rapid changes in social values + disintegration of family unit + high expectations on themselves
- cultures with more poverty, unemployment + discrimination have higher rates
dysregulated pathways
- neurotransmitters
- serotonin, dopamine not at normal level
dysregulated pathways
- HPA axis
- cortisol
- chronic hyperactivity of HPA axis –> elevated levels of CRH + cortisol –> inhibits receptors for monoamine neurotransmitters + hippocampal neurogenesis –> volume reduction in several brain areas (e.g. hippocampal atrophy)
- -> neurogenesis is inhibited by excessive cortisol secretion
- early traumatic stress can lead to some of these abnormalities (predispose people to depression)
- trait-level rather than state level –> vulnerability marker
- substantial heritability
- declarative memory impairment also between episodes + in non-depressed
dysregulated pathways
- oxidative stress
= oxidation = cells oxidise
- we have mechanisms protecting us from too much oxidation
depression: less anti-oxidation –> more oxidative stress –> damage to DNA (lead to cancer)
dysregulated pathways
- nueroprogression
= neuroplasticity not enhanced anymore
- BDNF (= too low in depression) helps neuroprogression
- hippocampus
dysregulated pathways
- mitochondrial disturbances
= mitochondria = little machines that make you breath
- connected to oxidative stress
dysregulated pathways
- immuno-inflammation
= inflammation = attack via bacteria
- release inflammation factors to fight inflammation
depression: lower anti-inflammation factors
influence of lifestyle factors
- diet
GOOD = good fats, Meditterean diet BAD = fat + sweets
influence of lifestyle factors
- sleep
BAD = persistent insomnia = increased risk of developing a depressive episode & higher risk of relapse (90% have it during episode, 40% of episodes are preceded by sleep symptoms)
influence of lifestyle factors
- physical activity
GOOD = constant exercise
- enhances neuroprogression
- -> relations are bidirectional
- if you don’t sleep, eat, exercise well –> negative effects of pathways –> cause depression –> depression makes you less attentive to good sleep… –> lifestyle worsens
bipolar disorder
= depression + mania
DSM-5 (BD)
A.
distinct period of abnormally + persistently elevated, expansive or irritable mood
AND abnormally + persistently increased goal-directed activity/energy, lasting AT LEAST 1 WEEK and present most of the day, nearly every day (or any duration if hospitalisation is necessary)
DSM-5 (BD)
B.
during the period, three or more of the following symptoms (four if the mood is only irritable) are present to a significant degree + represent a noticeable change from usual behaviour
- inflated self-esteem/grandiosity
- decreased need for sleep
- more talkative than usual, pressure to keep talking
- subjective experience that thoughts are racing
- distractibility (reported or observed)
- increase in goal-directed activity or psychomotor agitation (= purposeless non-goal-directed activity)
- excessive involvement in activities that have a high potential for painful consequences
- change from usual behaviour
DSM-5 (BD)
C.
impair social/ occupational functioning OR necessitate hospitalisation to prevent harm to self or others OR there are psychotic features
- impairment
DSM-5 (BD)
D.
not due to substances or another medical condition
- medical exclusion
bipolar I
= not that severe depression + mania, possibly hypomania
- major depressive episodes: can occur but are not necessary
- mania is necessary
- hypomania can occur between episodes of severe mania or major depression but aren’t necessary
bipolar II
= depression + no mania, BUT hypomania
- major depressive episodes: necessary
- mania cannot be present
- hypomanic episodes: necessary
subtypes (BD)
- hypomania = not severe enough to interfere with daily functioning, don’t involve hallucinations or delusions
- last at least 4 consecutive days - cyclothymic disorder = less severe but more chronic form of bipolar disorder
- alternates between hypomanic symptoms and periods of mild depressive symptoms for at least 2 years
- both don’t meet the criteria
- dysthymia (depression) - rapid cycling bipolar I/II disorder = four or more mood episodes of mania/hypomania/ major depressive episode within 1 year
- disruptive mood dysregulation disorder = for youth age 6 and older
- must have severe temper outbursts, between outbursts, their mood is persistently + obviously irritable + angry
- must have at least 3 temper outbursts per week for at least 1 year in at least 2 settings
prevalence (BD)
- bipolar I: 0.6%
- bipolar II: 0.4%
- onset usually in late adolescence/ early adulthood
- likelihood equal across cultures + genders: biological factor must be more responsible than for major depressive disorders
treatment (MDD)
- biological/ medication
- slow-emerging effects on intracellular processes in the neurotransmitter system + on action of genes that regulate neurotransmission, the limbic system + stress response
- better for treating severe + persisting depression
- SSRIs, SSNRIs (affect serotonin AND norepinephrine)
- bupropion: norepinephrine-dopamine re-uptake inhibitor
- tricyclic antidepressants
- MAO-inhibitors (severe side effects)
- CRH-receptor antagonist for HPA axis (only an idea)
treatment (BD)
- biological
= relieve/prevent symptoms of mania
- lithium = effective in preventing both depression and mania + highly effective in reducing suicide risk
BUT small window for effectiveness because too much = toxic
- increase levels of serotonin (depression); decrease levels of norepinephrine (mania)
- atypical antipsychotic medications = reduce functional levels of dopamine (psychotic maniacs)
treatment
- electroconvulsive therapy
= induced brain seizures by passing electrical current through the patient’s head
- decreases metabolic activity in several regions of the brain, incl. PFC & anterior cingulate
- mostly right side because less involved in learning + memory
treatment
- brain stimulation
- rTMS: on left PFC which tends to show abnormally low activity
- vagus nerve stimulation (VNS): increases activity in hypothalamus + amygdala
- deep brain stimulation: not much researched
treatment (SAD)
- light therapy
= expose to bright light for a few hours each day during the winter months
- resets circadian rhythms –> normalises production of hormones + neurotransmitters
treatment
- behavioural
- analysis of connections between circumstances + level of depression
= change interactions with environment to increase positive and decrease negative experiences + reinforcers
treatment
- CBT
= change negative thinking patterns AND develop skills for concrete problems in daily life
√ decreases attention biases & changes memory biases
- increased skill use predicts treatment outcome (if use skills, decreased symptoms)
√ recognise deeper beliefs they hold that are fuelling their depression
- works for even very severely depressed people
treatment
- cognitive control/ Attention-training paradigm
- cognitive control: retrain people’s cognitive processing; enable them to more effectively responding to situations
- attention: learn to attend to neutral stimuli and away from threat/sad stimuli; reduced reactivity to stressful events
- memory: reduction in depressive symptoms + rumination
- interpretation: modify interpretations; changes in emotion regulation
