depression 4

Question 1

Depression neuroanatomical reasoning:

Answer 1

decreased activity, decreased volume, lesioned white matter integrity in prefrontal cortex areas

Question 2

Prefrontal regions role:

Answer 2

executive functioning, cognitive control of behavior

Question 3

Anterior cingulate cortex role in depressed people:

Answer 3

reward based learning, impulsivity, interface of decision making/attentions/emotion- higher activation, decreased volume

Question 4

Ventral tegmental area in depressed patients:

Answer 4

motivation, reward processing, prediction, dopamine center- deficits in activity

Question 5

Hippocampus in depressed people:

Answer 5

decreased volume

Question 6

Amygdala in depressed people:

Answer 6

increased activation and increases in anatomical changes

Question 7

Thalamus in depressed people:

Answer 7

relay stations sending sensory/ motor input to the cortex- decreased size in individuals with depression

Question 8

Dysfunction in brain may be due to:

Answer 8

networks or connectivity, people with depression show altered connectivity among multiple networks

Question 9

Default mode network:

Answer 9

involved in “wakeful rest,” brain regions that are active when you are not engaged in a task

Question 10

Affective network and increased or decreased activation?

Answer 10

processing emotional information, increased activation at rest and during an associative task

Question 11

Salience network and increased or decreased activation:

Answer 11

detection, and filtering of important stimuli. decreased activation in depressed people

Question 12

Cognitive control network and increased or decreased activation?

Answer 12

involved in attention-demanding tasks. decreased activation in task-related activity, but increased when at rest.

Question 13

Neuroplasticity hypothesis of depression:

Answer 13

dysfunctional neural plasticity leads to impairments seen in depression

Question 14

neuroplasticity:

Answer 14

ability of neurons and networks of neurons to change and adapt over time in response to stimuli

Question 15

Idea of neuroplasticity hypothesis:

Answer 15

alteration in structure and function of neurons impair functional networks that may lead to depressive symptomology

Question 16

Neurogenic hypothesis of depression:

Answer 16

impaired hippocampal neurogensis results in depression

Question 17

neurogenesis:

Answer 17

birth of new neurons

Question 18

Idea of neurogenic hypothesis:

Answer 18

new neurons in the hippocampus may restore hippocampal deficits to improve control of mood outcomes

Question 19

Idea of apoptosis hypothesis of depression:

Answer 19

neuronal loss may be responsible for the volumetric changes and symptomology seen in depression

Question 20

Monamine Theory of depression:

Answer 20

depression is due to norepinephrine and serotonin level depletion

Question 21

Norepinephrine and serotonin are important in:

Answer 21

mood, emotional expression, arousal, behavioral activity

Question 22

Dopamine:

Answer 22

involved in reward, motivational stimuli, punishment and motor control

Question 23

Why do people say dopamine is lacking in depressed people?

Answer 23

depressed people show diminshed interest/motivation and psychomotor dysfunction and dopamine is what gives you motivation and is in control of motor control

Question 24

Glutamate:

Answer 24

Main excitatory neurotrans, our “stop” and “go” switches

Question 25

Stepped care model:

Answer 25

most “effective” intervention is provided first, then if not effective, move on to next one

Question 26

Stepped care model order of administering:

Answer 26

1. behavioral therapy
2. SSRIs, NRIs, SNRI’s
3. tricyclic antidepressants
4. MAO irreversible inhibitors
5. then stuff like ECT

Question 27

All typical medications have what percentage of remission, what percent of response rates, and what percent relapse rate?

Answer 27

remission: 15-30 %
response: 45-75%
relapse: 70-90%

Question 28

When do you see alleviation of depressive symptoms after taking meds?

Answer 28

roughly 2-6 weeks, aka “therapeutic lag”

Question 29

All medications can PRODUCE:

Answer 29

discontinuation syndrome which is anxiety flu-like symptoms, or insomnia

Question 30

all medications can CAUSE:

Answer 30

Serotonin syndrome which is when switching antidepressants can build up serotonin levels and lead to minor side effects

Question 31

how do typical antidepressants work?

Answer 31

changes in neurotransmitter levels, typically increasing levels

Question 32

Tricyclic antidepressants:

Answer 32

suited better for depression with melancholic features and have to experiment with dose, blocks reuptake transporters which allows more neurotransmitters

Question 33

Monoamine oxidase inhibitors:

Answer 33

effective in atypical depression, efficacy in anxiety and panic disorders, binds to and inhibits enzyme that breaks down serotonin and dopamine

Question 34

SSRI’s, SNRIs, NRIs:

Answer 34

mild undesirable side effects, efficacy in anxiety and OCD, blocks reuptake transporters which means more neurotransmitter in synaptic cleft

Question 35

Ketamine:

Answer 35

Rapid, works in hours, no withdrawal symptoms after discontinuing

Question 36

Ketamine mechanism:

Answer 36

blocks glutamate at PCP binding site

Question 37

Electroconvulsive therapy:

Answer 37

brief electrical current passed through patients brain to endive a seizure

Question 38

ECT is reserved for patients with:

Answer 38

treatment resistant depression and with melancholic, psychotic, or catatonic depression

Question 39

ECT mechanisms:

Answer 39

direct/indirect effects of seizure which increases hippocampal and amygdala volumes

Question 40

Transcranial magnetic stimulation:

Answer 40

non-invasive neurostimulator that uses electromagnetic induction to cause electric flow in brain

Question 41

Issues of TMS:

Answer 41

targets superficial layers of brain, and difficult to test bc of placebo effect since subject knows they are receiving it.

Question 42

Leading brain targets in TMS:

Answer 42

left and right dorsolateral prefrontal cortex

Question 43

Mechanisms of TMS:

Answer 43

increases neurotransmitter activity and increases activity within neuronal circuits

Question 44

Transcranial direct current stimulation:

Answer 44

using constant low direct current delivery via electrodes to alter the resting membrane

Question 45

Deep brain stimulation:

Answer 45

neurosurgical procedure to implant electrodes into specific brain area

Question 46

Lesioning:

Answer 46

ablating certain parts of brain

Question 47

Amygdala role:

Answer 47

Threat center/ negative emotional regulation

Question 48

Hippocampus role:

Answer 48

emotional learning and memory