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depression
cognitive symptoms → difficulty with concentration or making decisions
behavioural symptoms → social withdrawal or agitation
somatic symptoms → insomnia or hypersomnia
affective symptoms → depressed mood and feelings of worthlessness or guilt
-DSM-5 breaks down depression into separate disorders with different criteria for each one
reactive depression
-triggered by a negative experience
endogenous depression
-no apparent negative life event
unipolar affective disorder
-major depressive disorder or major depressive episodes
bipolar affective disorder
-depression with periods of mania
-mania is the opposite of the depressive symptoms → the two alternate in a cycle
genetics (causes of depression)
-ascertained that mental health has a genetic component by looking at identical and non-identical twins
-look at concordance rate between sets of twins
-MZ twins have 39% concordance rate for depression compared to 27% for DZ twins
Brown - environment (causes of depression)
-looked at people of lower socioeconomic status and amount of severe stress in the previous year
-subjects who were suffering from depression experienced much more severe stress than the controls
-but many people experienced severe stress but did not get diagnosed with depression
diathesis-stress model (causes of depression)
diathesis → internal, often a genetic component
stress → something in the environment
-must have a predisposition towards depression and stress from the environment must occur in order to trigger depression
heritability (behavioural genetics)
-an estimate of how much variance in some characteristic within some population is due to differences in heredity
bipolar disorder → 0.85
major depressive disorder → 0.4
mono amine oxidase inhibitors
-first drugs used to treat depression
-monamine agonists → increases levels of monamines (norepinephrine + serotonin)
mono amine neurotransmitters
-monamines are split into:
catecholamines → dopamine, adrenaline, noradrenaline
indolamines → serotonin
serotonergic projections
-triggers amygdala → impacts how we think of the world and respond to stimuli
-this then triggers prefrontal cortex
noradrenergic projections
-has both dorsal and ventral projections
-diffuse projections → all over head and brain
monamine synapse
-causes serotonin to be released from synaptic cleft before being taken back up
-MAO inhibitors means there is more neurotransmitter left in the neuron to be released
tricylic antidepressants
-block reuptake in norepinephrine or serotonin synapse
-leaves more transmitter at the synapse
SSRIs
-serotonin synapse only
-serotonin is deactivated in the synapse by reuptake into the presynaptic neuron
-SSRIs blocks the reuptake of serotonin, thus increasing the activation of serotonin receptors
lithium
-used to treat bipolar disorder
-interferes with the second messenger system → works as a mood stabiliser
monoamine theory of depression
-anti-depressants work on monamines
-so depression is caused by a deficit of monamine neurotransmission
-some evidence of elevated receptors in depressed patients → to compensate for low levels of transmission
monamine and brain regions
-monamine neurotransmitters could modulate brain regions involved in emotion and cognition
-an overreactive limbic system and amygdala are implicated in affective disorders
-orbital and medial prefrontal cortex → ruminating and cognitions about the world
Beck’s cognitive triad
negative views about the world
negative views about the future
negative views about oneself
learned helplessness
-dog is in a box with a barrier
-a tone indicates a shock
-dog must jump over barrier to avoid shock
-after dog has been in a condition where they cannot escape the shock → they no longer jump to the no shock zone
Seligman’s attributional model
-attributions of negative events
-three dimensions are:
internal vs external
global vs specific
stable vs unstable
-depressed people tend to attribute negative life events to internal, stable, global causes