Addiction Flashcards
voluntary motor behavior
BG
input stage of BG
caudate/putamen
caudate + putamen =?
corpus striatum
striatum –> pallidus –> thalamus
loop
planning, controlling impulsivity
PFC
early assessment of keys in env and linking to cues in emotional responses
amygdala
processing memory, general emotion regulation
hippocampus
circuit for translating emotion into action
CSPT:
PFC/Amygdala/Hippo –> nuc acc –> V pallidum –> MD thalamus –> cortical motor planning regions
nuclei that supply DA in the mesencephalon
SN, VTA
cells in striatum:accumbens that receive this input? what are they able to do w multiple inputs?
medium spiny neuron
receives GABA
INTEGRATORS!!! of glutamate from cortical regions with DA from VTA
lots of these are found in the striatum
opioids
DA+opioids involved in addiction
convey info
modulate info
DA
muOpioids
key site in brain to stimulate DA reward
VTA
can block D1 receptors to blunt this
destroying VTA blunts reward fxn
wanting chemical liking chemical (hedonic response: liking chocolate cake after eating)
DA
opioids
which pathway will amphetamines effect?
wanting/goal-pursuit
NOT “liking”
neurochemical most predictive in reward stimulai
DA
most active when cues to predict reward, or when we have to learn something new (when env changes)
opponent process theory
A process: euphoria (e.g.)
B process: counteradaptation initiated to oppose the A process; over time this gets stronger and stronger
When A is removed then strong B leads to dysphoria
w/d theory: constantly taking drug to stave off B process
cue-elicited cocaine craving elicits?
DA release in the striatum
low striatal D2 receptor binding correlates with diminished activity where?
PFC
impulsivity results from impaired fxn of what?
PFC inhibitory control
compulsivity results from shift in what?
PFC-accumbens motor circuits to emphasis on dorsal striatal control (habit-mediator)
incentive-sensitization hypothesis
drug use leads to sensitization of DA ability to produce drug wanting
reward-error prediction hypothesis
enhanced DA release during drug taking produces condition in which all stimuli encountered during this period are experienced as being better than expected
big addiction characteristics
loss of control of limiting intake
taking persists despite negative consequences
alternatives no longer pursues
potential for relapse throughout lifespan
def: a) tendency to choose immediate reinforcement over delayed gratification, even when smaller or less beneficial, and b) impairment of inhibiting a course of action once initiated
impulsive behavior
def: perseveration in a certain behavior even in the face of unsuccessful/adverse outcomes
compulsive behavior
a gradual decrease in the use of alcohol past 20 years of age or so
desistence: usually due to other reinforcers e.g. career/family etc
epi of substance use d/o’s
70% of drug abusers are unemployed
300% higher med costs
50% of domestic violence, major crimes assoc
17% of pregnant women smoke, 13% use alcohol
24% of suicides have BAC >0.1
genetic fx of alcohol abuse
low levels of what in CSF?
sons of fathers have 50% chance
inheritance of impulsivity as well as general addictive tendency
serotonin
other factors assoc in development of addiction
parental discouragement and monitoring
focus on academics
defense mechanisms (denial/rationalization)
early psychoactive substance use
almost all drugs of abuse elevate what neurochemical in the where?
DA in the nuc accumbens
locations of DA-producing neurons
SN –>
VTA –> Acb/amyg/hippo/PFC (MCL pathway)
how would you take away the “good” of food/drugs/other goal objects?
what projection plays role in wanting/seeking and reward-learning
block DA receptors
mesocorticolimbic projection
system involved in “wanting”
peptides involved in liking
DA (VTA-Acb)
opioids (endorph/enkeph)
3 components of the striatum
dorsal striatum?
ventral striatum?
caudate + putamen + nucleus accumbens
caudate + putamen
nuc accumbens
loops that direct conscious control of voluntary motor action; hijacked in substance use d/o
cortico-striato-pallidal-thalamic
inputs to Acb: motivation and emotion
amygdala and hippocampus
also PFC
drugs augment the transmission of what where?
DA in the nuc accumbens
hypothesis that states that DA codes for affective experience of reward
anhedonia
neither reward-based nor w/d-based theories describe what?
lifelong propensity to relapse
which theory does not require drug to cause subjective state of euphoria?
which theory describes increased wanting while decreased liking?
reward-learning
incentive-sensitiztion
this theory posits that individuals w/addiction acts compulsively due to diminishment in these 2 brain regions
PFC and anterior cingulate cortex
BAC levels: 50, 80, 200-300, 400-600
50 –> loss of cognition, judgment, coord
80 –> driving impaired
200 –> all faculties
400 –> coma/death
tx for alcohol w/d (w/in 72h)
tx: supportive
w/d: BZD taper + thiamine, Mg (incr glutamate to offset opponent-process of dec GABA and incr glutamate) and anticonvulsants (gabapentin) modulate Glu, diazepam, lorazepam
tx for opioid w/d
tx: naloxone
w/d: buprenorphine or methadone, clonidine/BZD regimen, suboxone, psychosocial support
tx for stimulant w/d
tx: BZD’s
w/d: support + antidepressants
wernicke’s encephalopathy
due to thiamine deficiency (give thiamine)
confusion, ataxia, ophthalmoplegia
meds and psychosocial tx (3) for alcohol
naltrexone, acamposate, disulfuram, buprenorphine + methadone for cocaine
CBT: relapse prevention, motivational enhancement (learn to avoid stimuli and chose positive habits), 12 step
timeline of w/d sx: alcohol BZD's opioids stimulants
sx subside in 72-96h; DT’s for 10+ days
depends on half-life (d-wks)
days (heroin/morphine) to wks (methadone)
cocaine shorter than methamphetamine
dangerous sx of: alcohol BZD's opioids stimulants
psychosis, delirium, seizures
seizures
dehydration (NVD), leave to get more
leave to get more
common sx of: alcohol BZD's opioids stimulants
anx, nausea, tremors, sleep, restlessness, sweating, headaches, pulse, HTN
same as above
NVD, craving, rhinorrhea, tearing, muscle aches/cramps, gooseflesh, dilated pupils
tired, prolonged sleeping, amotivational, depressed, overeating, craving
tx of BZD w/d
switch to long-acting BZD and taper
some now use anticonvulsants
goal of substance use tx
prevent relapse!
most common time is 1st month-1 yr
MOA naltrexone
acamprosate effects which two systems?
MOA disulfiram (induction of fear)
interferes with + reinforcement (blocks effects of opioids released during use/cravings)
GABA/Glutamate; may decrease DA in nuc accumbens
antagonizes aldehyde dehydrogenase
