depression 4 Flashcards
Depression neuroanatomical reasoning:
decreased activity, decreased volume, lesioned white matter integrity in prefrontal cortex areas
Prefrontal regions role:
executive functioning, cognitive control of behavior
Anterior cingulate cortex role in depressed people:
reward based learning, impulsivity, interface of decision making/attentions/emotion- higher activation, decreased volume
Ventral tegmental area in depressed patients:
motivation, reward processing, prediction, dopamine center- deficits in activity
Hippocampus in depressed people:
decreased volume
Amygdala in depressed people:
increased activation and increases in anatomical changes
Thalamus in depressed people:
relay stations sending sensory/ motor input to the cortex- decreased size in individuals with depression
Dysfunction in brain may be due to:
networks or connectivity, people with depression show altered connectivity among multiple networks
Default mode network:
involved in “wakeful rest,” brain regions that are active when you are not engaged in a task
Affective network and increased or decreased activation?
processing emotional information, increased activation at rest and during an associative task
Salience network and increased or decreased activation:
detection, and filtering of important stimuli. decreased activation in depressed people
Cognitive control network and increased or decreased activation?
involved in attention-demanding tasks. decreased activation in task-related activity, but increased when at rest.
Neuroplasticity hypothesis of depression:
dysfunctional neural plasticity leads to impairments seen in depression
neuroplasticity:
ability of neurons and networks of neurons to change and adapt over time in response to stimuli
Idea of neuroplasticity hypothesis:
alteration in structure and function of neurons impair functional networks that may lead to depressive symptomology
Neurogenic hypothesis of depression:
impaired hippocampal neurogensis results in depression
neurogenesis:
birth of new neurons
Idea of neurogenic hypothesis:
new neurons in the hippocampus may restore hippocampal deficits to improve control of mood outcomes
Idea of apoptosis hypothesis of depression:
neuronal loss may be responsible for the volumetric changes and symptomology seen in depression
Monamine Theory of depression:
depression is due to norepinephrine and serotonin level depletion
Norepinephrine and serotonin are important in:
mood, emotional expression, arousal, behavioral activity
Dopamine:
involved in reward, motivational stimuli, punishment and motor control
Why do people say dopamine is lacking in depressed people?
depressed people show diminshed interest/motivation and psychomotor dysfunction and dopamine is what gives you motivation and is in control of motor control
Glutamate:
Main excitatory neurotrans, our “stop” and “go” switches
Stepped care model:
most “effective” intervention is provided first, then if not effective, move on to next one
Stepped care model order of administering:
- behavioral therapy
- SSRIs, NRIs, SNRI’s
- tricyclic antidepressants
- MAO irreversible inhibitors
- then stuff like ECT
All typical medications have what percentage of remission, what percent of response rates, and what percent relapse rate?
remission: 15-30 %
response: 45-75%
relapse: 70-90%
When do you see alleviation of depressive symptoms after taking meds?
roughly 2-6 weeks, aka “therapeutic lag”
All medications can PRODUCE:
discontinuation syndrome which is anxiety flu-like symptoms, or insomnia
all medications can CAUSE:
Serotonin syndrome which is when switching antidepressants can build up serotonin levels and lead to minor side effects
how do typical antidepressants work?
changes in neurotransmitter levels, typically increasing levels
Tricyclic antidepressants:
suited better for depression with melancholic features and have to experiment with dose, blocks reuptake transporters which allows more neurotransmitters
Monoamine oxidase inhibitors:
effective in atypical depression, efficacy in anxiety and panic disorders, binds to and inhibits enzyme that breaks down serotonin and dopamine
SSRI’s, SNRIs, NRIs:
mild undesirable side effects, efficacy in anxiety and OCD, blocks reuptake transporters which means more neurotransmitter in synaptic cleft
Ketamine:
Rapid, works in hours, no withdrawal symptoms after discontinuing
Ketamine mechanism:
blocks glutamate at PCP binding site
Electroconvulsive therapy:
brief electrical current passed through patients brain to endive a seizure
ECT is reserved for patients with:
treatment resistant depression and with melancholic, psychotic, or catatonic depression
ECT mechanisms:
direct/indirect effects of seizure which increases hippocampal and amygdala volumes
Transcranial magnetic stimulation:
non-invasive neurostimulator that uses electromagnetic induction to cause electric flow in brain
Issues of TMS:
targets superficial layers of brain, and difficult to test bc of placebo effect since subject knows they are receiving it.
Leading brain targets in TMS:
left and right dorsolateral prefrontal cortex
Mechanisms of TMS:
increases neurotransmitter activity and increases activity within neuronal circuits
Transcranial direct current stimulation:
using constant low direct current delivery via electrodes to alter the resting membrane
Deep brain stimulation:
neurosurgical procedure to implant electrodes into specific brain area
Lesioning:
ablating certain parts of brain
Amygdala role:
Threat center/ negative emotional regulation
Hippocampus role:
emotional learning and memory
