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43 Cards in this Set

  • Front
  • Back
1. James-Lange
emotion=a particular physiological state
2. Cannon-Bard
body reacts to a threat, while cortex assigns appropriate emotion
3. Schachter-Singer:
emotion is a cognitive label based on interpretation of situation
2. Papez Circuit
hypothalamus, mammilary bodies, anterior thalamus, amygdala, parahippocampal gyros, olfactory bulb, basal forebrain nuclei, and cingulate cortex
3. Kluver-Bucy Syndrome
flattened affect, odd oral behaviors, hypersexuality) demonstrates impact of temporal limbic structures
1. Fear
amygdala
2. Disgust
insula and putamen
3. Seeking/expectancy
reward areas
4. Panic
anterior cingulated, dorsomedial thalamus, periaqueductal gray
5. Happiness/play
dorsomedial thalamus, periaqueductal gray
2. Right hemisphere produces
"withdrawal" types of responses
3. Left hemisphere processes
emotional meaning of verbal material
left produces
"approach" types of responses
right processes
nonverbal, both visual and auditory emotional cues
Depression brain
Hypothalamic-pituitary-adrenal axis
Depression sleep changes
a. Far less stage 3 and 4, far more 1 and 2, shortened REM onset
b. Shortened REM latency is the one change with highest correlation with depression
selective REM deprivation makes depression remit
explain symptoms of depression
NE and 5HT
C. Best current theory of how antidepressants work:
C. down-regulation of key receptors S 6-1 to 6-6
D. All antidepressants metabolized by
CYP 450 system
1. Classical MAO inhibitors
phenelzine (Nardi])
tranylcipromine (Parnate)
isocarboxazip (Marplan)
2. Newer MAO inhibitors
moclobemide (Arorix)
deprenyl (Selegiline, Eldepryl)
3. Tricyclic Antidepressants: impact
5HT, NE, and sometimes DA by blocking reuptake pumps
SSRI's
block reuptake of serotonin
blocks both NE and 5HT reuptake, and also is anti-anxiety
F. Venlafaxin
block 5HT 2A receptors as well as reuptake; used mostly in practice in conjunction with SSRI's
G. Phenylpiperazines (nefazadone, trazadon
classic Mood stabilizing drug
Lithium
Lithium
1. Treats acute episodes, but also prevents recurrence
2. Works on only 40 to 50% of patients
3. Lots of gastrointestinal, cognitive and motor side effects are a problem
Anticonvulsants as mood stabilizers
1. Valproic acid (Depakote) appears to inhibit Na+ or Ca+2 channels and thus boost GABA's inhibitory action; also inhibits excitatory glutamate --mechanism may be either on enzymes or on the channels themselves
1. Valproic acid (Depakote)
appears to inhibit Na+ or Ca+2 channels and thus boost GABA's inhibitory action; also inhibits excitatory glutamate --mechanism may be either on enzymes or on the channels themselves
2. Carbamazepam (Tegretol)
may have similar effects on GABA, but not on glutamate
Gabapentin (Neurontin)
increases GABA, probably by affecting transporter, and decreases glutamate
4. Topiramate (Topamax)
enhances GABA and reduces glutamate by interfering with both Na+ and Ca++ channels
—side effect of weight loss is unique (most cause weight gain)
5. Lamotrigine (Lamictal)
5. inhibits Na+ channels and inhibits release of glutamate—may be effective for the depressive phase as well as mania
TRICYCLICS
amitriptyline*
imipramine*
doxepin
HE'I EROCYCLICS
trazodone*
Serzone*
SSRI
Prozac* Zoloft* Paxil*
Celexa* Lexapro* Luvox*
fluoxetine* sertraline* paroxetine* citalopram*
Norepinephrine/Dopamine reuptake inhibitor
Wellbutrin*
Noradrenergic and specific serotonergic
Remeron*
SNRI' s
Effexor* venlafaxine
Cymbalta*
MAO Inhibitors I
Nardil*
Parnate*
phenelzine* tranylcypromine*
MAO Inhibitors R
Arorix*
Eldepryl*
MOOD STABILIZERS
Lithobid* lithium* Neurontin* gabapentin*
Depakote* divalproic acid* Topamax* topiramate
Tegretol* carbamazepine* Lamictal* lamotrigine
Trileptal* oxcarbazepine