Download Emo7onal decision‐making systems and their role in addic7on

Emo$onal
decision‐making
systems
and
their
role
in
addic$on
Antoine
Bechara
Objec&ves:
1.
Habit
(Impulsive)
system:
Dopamine
mediated
(striatal).
2.
Inhibitory
control
(Reflec$ve)
system:
Prefrontal
cortex
dependent—
a.
Decision‐making
b.
Simple
inhibitory
control.
3.
Insular
cortex
system:
responsive
to
homeosta$c
imbalance
(depriva$on
states),
which
ac$vity:
a.
Exacerbates
the
ac$vity
of
the
habit/impulsive
system.
b.
Disable
(or
“hijack”)
ac$vity
of
the
prefrontal
(control/
reflec$ve)
system.
1.
The
habit
(impulsive)
system—reward
seeking
A.
The
Nature
of
reward:
The
term
“reward”
describes
the
positive
value
an
individual
ascribes
to
an
object,
behavioral
act
or
an
internal
physical
state.
There
are
two
kinds
of
rewards
that
can
establish
addictive
behaviors:
(1)
Natural
rewards
are
those
that
reach
the
brain
circuitry
of
motivation
via
the
Bive
senses.
The
rewards
of
food
for
a
hungry
person,
water
for
a
thirsty
person,
or
copulation
for
sexually
receptive
individual
reach
the
brain
via
peripheral
sensory
pathways
(e.g.,
vision,
taste,
olfaction,
sensation,
and
audition).
(2)
“Unsensed”
rewards
denote
those
with
the
capacity
to
activate
the
brain
substrates
of
motivation
directly,
bypassing
the
peripheral
sensory
pathways.
Drugs
taken
orally,
inhaled,
or
injected,
do
not
have
a
particular
taste,
or
smell,
that
makes
them
rewarding.
They
act
directly
on
the
brain
to
produce
reward.
(3)
“Money”
is
a
reward
too:
Through
learning,
money
becomes
strongly
associated
with
natural
rewards,
like
food,
water,
sex,
and
shelter.
Because
learning
about
money
is
so
extensive
and
spans
our
entire
life,
these
learning
associations
with
natural
rewards
become
powerful,
automatic,
and
non‐conscious.
Although
there
are
obvious
differences
between
how
natural
(e.g.,
sex)
and
unsensed
(e.g.,
drugs),
or
money
rewards
reach
the
reward
systems
within
the
brain,
a
large
volume
of
studies,
dating
back
to
the
1980’s,
have
implicated
the
“mesolimbic”
dopamine
system,
and
several
of
its
afferents
(inputs)
and
efferents
(outputs),
in
mediating
the
motivational
functions
of
both
types
of
reward.
Both
animal
and
human
studies
have
linked
natural
rewards
to
the
same
mesolimbic
dopamine
system.
Thus
drugs
are
rewarding
because
they
have
the
capacity
to
activate
directly
in
the
brain
the
endogenous
reward
mechanisms
subserving
natural
or
biological
rewards,
which
existed
before
the
invention
of
drugs.
B.
The
dopamine
system
and
reward:
There
are
several
systems
of
dopaminergic
neurons
or
systems
(5
in
total).
However,
the
three
most
important
of
these
originate
in
the
midbrain,
speciBically:
(1)
The
substantia
nigra,
which
projects
to
the
dorsal
striatum
or
neostriatum=
mesostriatal
(or
nigrostriatal)
dopamine
system‐‐‐Parkinson
Disease.
Medications:
predominantly
D2
receptors—Parkinson
DA
agonist
therapies
target
these
receptors.
(2)
The
ventral
tegmental
area,
which
projects
to
the
nucleus
accumbens=
mesolimbic
dopamine
system‐‐‐‐reward.
Medications:
predominantly
D3
receptors—Parkinson
medications
that
are
D3
agonists
(e.g.,
Mirapex)
have
high
likelihood
of
inducing
addictive
behaviors
(e.g.,
pathological
gambling)
in
individuals
whom
otherwise
never
gambled
before.
(3)
Another
one
from
the
ventral
tegmental
area,
which
projects
to
the
prefrontal
cortex=
mesocortical
dopamine
system—decision‐making
and
inhibitory
control.
C.
The
history
of
research
on
dopamine
and
reward.
Research
on
the
difference
between
the
nigrostriatal
and
mesolimbic
systems
in
terms
of
their
contribution
to
movement
versus
reward
is
old
and
dates
back
to
at
least
the
early
1980’s
(it
started
in
the
late
70’s):
1.
The
Birst
proposal
of
a
unique
relationship
between
dopamine
and
reward
was
provided
by
R.
Wise:
Wise,
R.A.,
Catecholamine
Theories
of
Reward
­
Critical­Review.
Brain
Research,
1978.
152(2):
p.
215­247.
Wise,
R.A.
and
M.A.
Bozarth,
A
psychomotor
stimulant
theory
of
addiction.
Psychological
Review,
1987.
94:
p.
469­492.
The
literature
from
that
era
(the
80’s)
clearly
demonstrates
that
the
dopaminergic
projection
to
the
nucleus
accumbens
(the
mesolimbic
dopamine
system),
but
not
the
dorsal
striatum
(the
dorsal
part
of
the
neostriatum,
which
excludes
the
ventral
striatum,
where
the
nucleus
accumbens
is
located),
is
the
one
that
plays
the
most
signiBicant
role
in
the
reward
derived
from
drugs
of
abuse
(e.g.,
psychostimulants).
1.a.
It
was
also
recognized
in
the
late
1980’s
and
early
1990’s
that
the
abuse
potential
of
drugs
of
abuse
(e.g.,
opiates,
alcohol,
nicotine,
caffeine,
barbiturates,
benzodiazepines,
cannabis,
and
phencyclidine)
all
are
linked,
one
way
or
another,
to
this
mesolimbic
dopamine
system.
While
these
different
drugs
may
act
initially
on
different
receptor
sites
in
the
brain,
ultimately
they
all
act
(directly
or
indirectly)
on
the
mesolimbic
dopamine
system
to
exert
reward:
Wise,
R.A.,
The
neurobiology
of
craving:
Implications
for
the
understanding
and
treatment
of
addiction.
Journal
of
Abnormal
Psychology,
1988.
97:
p.
118­132.
1.b.
It
was
also
well
accepted
in
the
late
1980’s
and
early
1990’s
that
manipulations
of
the
same
mesolimbic
dopamine
system
(with
pharmacological
blockade
of
dopamine
or
with
selective
lesions
of
the
dopamine
neurons
using
6‐hydroxydopamine
or
6‐OHDA)
exert
an
impact
on
natural
rewards,
such
as
food,
sweet
drinks,
and
sex.
Most
of
these
experiments
showed
that
during
dopamine
blockade,
animals
would
not
be
motivated
to
eat,
for
example,
even
though
food
may
be
readily
available,
and
even
when
their
motor
capacity
to
walk,
chew,
swallow
and
perform
other
movements
are
preserved.
It
was
also
recognized
that
dopamine
stimulation
in
the
accumbens
increases
the
motivation
for
food.
Microinjections
of
dopamine
agonists
directly
into
the
nucleus
accumbens
do
increase
the
motivation
for
natural
rewards,
such
as
food:
Wise,
R.A.
and
P.P.
Rompre,
Brain
dopamine
and
reward.
Annual
Reviews
of
Psychology,
1989.
40:
p.
191­225.
1.c.
More
than
25
years
has
passed,
and
the
original
conclusion
that
manipulations
of
the
mesolimbic
dopamine
system
inBluences
the
motivation
to
seek
rewards
remains
valid:
‐When
brain
dopamine
levels
are
low,
the
motivation
to
seek
reward
becomes
halted.
It
is
the
stimulation
of
the
dopamine
system,
or
the
presence
of
a
drug
that
activates
the
dopamine
system,
not
the
absence
of
dopamine,
that
energizes
and
motivates
behaviors
towards
the
seeking
of
rewards.
‐Cellular
physiology
and
pharmacology
demonstrates
that
the
action
of
dopamine
in
the
nucleus
accumbens
is
to
inhibit
the
GABA
neurons,
which
are
inhibitory
to
the
next
neurons
in
the
chain
that
instigate
motivated
behaviors.
In
other
words,
dopamine
in
the
accumbens
inhibits
the
inhibitory
neurons,
thus
resulting
in
behavioral
dis­
inhibition.
1.d.
There
has
been
much
recent
functional
neuroimaging
work
in
humans
implicating
the
ventral
striatum
(including
the
nucleus
accumbens)
in
a
variety
of
reward
processes,
including
monetary
rewards.
Although
functional
magnetic
resonance
imaging
(fMRI)
approaches
cannot
technically
address
dopamine
(or
any
other
brain
chemical
for
that
matter),
the
fact
that
the
neural
region
receiving
these
dopamine
projections
(i.e.,
the
ventral
striatum)
is
implicated
in
a
variety
of
reward
processes
(video
games,
viewing
of
sexual
materials,
and
monetary
rewards,
to
name
a
few)
validates
the
large
body
of
evidence
that
employed
a
variety
of
elecrophysiological,
microdialysis,
or
voltammetric
techniques,
which
accumulated
over
25
years
of
research,
and
which
concluded
that
the
mesolimbic
dopamine
projection
to
nucleus
accumbens
plays
a
key
role
in
reward
processes.
2.
The
conditioned
cues
evidence:
According
to
the
“psychostimulant”
anaylsis,
the
mesolimbic
dopamine
system
plays
a
key
role
in
mediating
the
“approach”
response
elicited
by
drugs
as
well
as
natural
rewards.
Mesolimbic
dopamine
strengthens
the
approach
response
and
motivational
arousal
elicited
by
rewards,
which
are
associated
with
pleasure.
The
mesolimbic
dopamine
system,
which
is
clearly
critical
for
reward
functions,
becomes
increasingly
responsive
to
stimuli
and
cues
that
predict
the
delivery
of
the
actual
reward
(e.g.,
food):
Stewart,
J.,
H.
Dewit,
and
R.
Eikelboom,
Role
of
Unconditioned
and
Conditioned
Drug
Effects
in
the
Self­Administration
of
Opiates
and
Stimulants.
Psychological
Review,
1984.
91(2):
p.
251­268.
Schultz,
W.,
P.
Dayan,
and
P.R.
Montague,
A
neural
substrate
of
prediction
and
reward.
Science,
1997.
275:
p.
1593­1599.
3.
The
“liking”
versus
“wanting”:
Later
researchers
assert
that
the
process
of
reward
can
be
further
sub‐divided
into
(1)
a
“wanting”
component,
which
makes
rewards
attractive
and
“wanted”,
and
which
triggers
“approach”
and
pursuit
of
the
reward;
and
(2)
a
“liking”
component,
which
involves
feeling
of
pleasure.
Although
there
seem
to
be
additional
systems
in
the
brain
(which
remain
unidentiBied)
that
mediate
the
“liking”
or
pleasure
component,
the
mesolimbic
dopamine
system
is
critical
for
speciBically
this
“wanting”
component
of
the
reward:
Berridge,
K.C.
and
T.E.
Robinson,
What
is
the
role
of
dopamine
in
reward:
hedonic
impact,
reward
learning,
or
incentive
salience?
Brain
Research
Reviews,
1998.
28:
p.
309­369.
Robinson,
T.E.
and
K.C.
Berridge,
The
neural
basis
of
drug
craving:
an
incentive­
sensitization
theory
of
addiction.
Brain
Research
Reviews,
1993.
18:
p.
247­291.
With
repeated
drug
use,
the
mesolimbic
dopamine
projections
to
the
nucleus
accumbens
become
sensitized,
and
eventually
lead
to
excessive
incentive
salience
attribution
to
the
drugs
and
drug‐related
stimuli,
which
activate
this
neural
circuitry,
thus
making
them
highly
attractive
and
pathologically
“wanted”
or
craved.
This
mesolimbic
dopamine
sensitization
phenomenon
does
not
apply
to
only
drugs,
but
to
all
types
of
rewards.
When
the
mesolimbic
dopamine
system
is
activated
in
the
presence
of
a
reward
in
the
environment,
the
incentive
salience
of
that
reward
is
increased,
and
the
reward
becomes
more
attractive
and
pathologically
“wanted”.
4.
The
notions
of
pleasure
and
dopamine:
The
evidence
that
blockade
of
dopamine
nerotransmission
in
the
ncleus
accumbens
interfered
with
the
motivation
to
seek
rewards
prompted
Wise
(1982)
to
propose
the
“anhedonia”
hypothesis,
that
dopamine
mediates
the
pleasure
produced
by
food,
sex,
or
drugs
that
compulsive
drug
users
seek.
‐However,
Wise
himself
retracted,
shortly
after,
the
notion
that
dopamine
blockade
reduces
pleasure
(Wise
1985),
and
he
replaced
the
anhedonia
hypothesis
with
an
incentive‐based
theory
of
motivation,
the
“psychostimulant”
theory
(Wise
and
Bozarth,
1987).
‐The
key
aspect
of
that
theory
is
that
the
mesolimbic
dopamine
system
plays
a
key
role
in
mediating
the
“approach”
response
elicited
by
drugs
as
well
as
natural
rewards.
In
other
words,
a
feeling
of
pleasure
is
not
necessarily
experienced
when
dopamine
is
released;
mesolimbic
dopamine
strengthens
the
approach
response
and
motivational
arousal
elicited
by
rewards,
which
they
are
clearly
associated
with
pleasure.
‐Despite
this
consensus
in
the
literature
more
than
a
decade
ago
that
dopamine
is
not
synonymous
with
pleasure,
this
notion
that
dopamine
is
the
“pleasure”
neurotransmitter
of
the
brain
has
had
an
insurmountable
appeal;
it
seems
to
continue
to
linger
until
today
in
various
media
reports;
even
the
more
recent
functional
neuroimaging
work
in
humans
that
addresses
the
reward
mechanisms
mediated
by
the
nucleus
accumbens
often
discuss
the
role
of
dopamine
in
this
region
in
a
manner
that
is
hardly
distinguishable
from
the
notions
of
pleasure.
5.
Dopamine
depletion
views:
DeBiciencies
in
neurotransmitter
activation
of
dopamine
in
the
mesolimbic
reward
pathways
are
the
instigators
of
reward
seeking
behaviors:
‐This
is
true
in
cases
of
drug‐induced
dopamine
depletions:
e.g.,
cocaine
crash.
‐It
is
very
controversial
as
to
whether
this
would
be
true
for
someone
born
with
low
dopamine
baseline
levels.
6.
Habits
(implicit)
mechanisms
of
drug
reward
seeking:
While
addicted
behaviors
all
start
out
under
some
“conscious”
control
through
these
ventral
striatal
motivational
neural
circuitries,
prolonged
drug
use
results
in
the
strengthening
of
motivation‐relevant
associative
memories,
which
promote
continued
use,
and
an
implicit,
or
relatively
spontaneous
(automatic)
process
begins
to
govern
behavior.
‐Neutral
stimuli
associated
with
appetitive
behaviors
such
as
drug
use
come
to
represent
and
cue
the
behavior.
As
cue‐behavior‐outcome
associations
are
strengthened,
patterns
of
associations
signal
and
drive
behavior
without
the
necessary
involvement
of
conscious
control
processes.
‐
Once
a
strong
habit
is
formed,
cues
elicit
the
habit
regardless
of
anticipated
outcomes.
‐ Habits become automatic and difficult to change. Another pivotal feature of habit
systems is that participants do not necessarily know what triggers their habits.
-At the neural level, there have been numerous neuroscientific demonstrations as what
starts out as reward seeking mediated through the ventral striatum can end up as a
“habit” automatic behavior and shifts to the dorsal striatum:
Everitt, B.J., A. Dickinson, and T.W. Robbins, The neuropsychological basis of
addictive behaviour. Brain Research Reviews, 2001. 36: p. 129-138.
Everitt, B.J., K.A. Morris, A. Obrien, and T.W. Robbins, The Basolateral Amygdala
Ventral Striatal System and Conditioned Place Preference - Further Evidence of
Limbic Striatal Interactions Underlying Reward-Related Processes. Neuroscience,
1991. 42(1): p. 1-18.
Everitt, B.J., J.A. Parkinson, M.C. Olmstead, M. Arroyo, P. Robledo, and T.W.
Robbins, Associative processes in addiction and reward: the role of amygdala and
ventral striatal subsystems., in Advancing from the ventral striatum to the
extended amygdala, J.F. McGinty, Editor. 1999, Annals of the New York Academy
of Science: New York. p. 412-438.
Everitt, B. and T.W. Robbins, Neural systems of reinforcement for drug addiction:
from actions to habits to compulsion. Nature Neuroscience, 2005. 8: p. 1481-1489.
2.
Inhibitory
control
(Reflec&ve)
system:
Prefrontal
cortex
dependent—
a.
Decision‐making
b.
Simple
inhibitory
control.
Dual‐process
models
of
decision‐making,
cognition,
and
associative
memory
have
gained
substantial
momentum
in
behavioral
research.
In
characterizing
the
distinctions
between
these
two
cognitive
systems,
Kahneman
summarized
that:
“…the
operations
of
System
1
are
typically
fast,
automatic,
effortless,
associative,
implicit
(not
available
to
introspection),
and
often
emotionally
charged;
they
are
also
governed
by
habit
and
are
therefore
difBicult
to
control
or
modify…”
“…Operations
of
System
2
are
slower,
serial,
effortful,
more
likely
to
be
consciously
monitored
and
deliberately
controlled;
they
are
also
relatively
Blexible
and
potentially
rule
governed…”.
According
to
Kahneman
(2003),
the
implicit
or
automatic
cognitive
system
(System
1)
is
the
system
governing
the
majority
of
human
decision
making,
whereas
System
2
monitors
the
operations
of
System
1.
This
perspective
of
relatively
automatic
processes
being
a
sort
of
‘default’
mode
guiding
behavior,
unless
overridden
by
deliberate
cognitive
processes,
has
been
expressed
in
social
psychological
theories,
and
memory
research
for
over
a
decade.
The
distinction
between
automatic
and
controlled
processes
(and
similar
distinctions)
is
reinforced
further
through
several
independent
lines
of
research
in
neuroscience,
including
my
own
(the
impulsive
versus
reBlective
systems
for
addictive
behaviors,
Bechara,
Nature
Neuroscience,
2005).
A
critical
neural
region
in
the
reBlective
system
is
the
ventromedial
prefrontal
cortex
region
(which
we
have
considered
as
inclusive
of
the
medial
orbitofrontal
cortex).
However,
other
neural
components,
including
the
dorsolateral
prefrontal
cortex
(for
working
memory)
and
the
cingulate
cortex
are
also
a
part
of
this
neural
circuitry,
and
are
essential
for
the
normal
operation
of
the
ventromedial
prefrontal
cortex:
Outline of the Somatic Marker Theory
Active vs control (all 10 subjects, all 4 tasks), p(bonf)<0.001
Left hemisphere
Right hemisphere
Motor/Behavioral Systems
AntCingCtx/SupMotArea
Striatum
Memory Systems
:
DorsoLatPrefCtx (DLPC)
Hippocampus
OrbitFrontCtx/VMPC
Amygdala
Dopamine
Serotonin
Ach
NE
Emotion Systems :
Insula
Posterior Cingulate
Hypothalamus
PAG
Brainstem
autonomic
centers
Computa$on:
In
the
body‐‐‐Body
loop
In
Sensory
nuclei
and
neurotransmiTer
cell
bodies
of
brainstem
‐‐‐‐As
if
body
loop
Decision‐making
versus
inhibitory
control:
There
is
a
distinction
between
the
mechanisms
of
affective
decision‐making
and
those
of
simple
inhibitory
or
impulse
control.
We
have
argued
that,
within
the
“reBlective”
system,
there
is
a
distinction
in
functioning
between
1)
simple
inhibitory
and
impulse
control
processes
(some
are
mediated
by
the
lateral
orbitofrontal
and
inferior
frontal
gyrus
regions,
and
some
are
mediated
by
the
more
posterior
sectors
of
the
medial
prefrontal
region,
i.e.,
the
anterior
cingulate
cortex,
both
dorsal
and
ventral),
and
2)
affective
decision
making
(mediated
by
more
anterior
regions
of
medial
prefrontal
cortex,
including
the
frontal
pole),
which
are
highly
relevant
to
behavioral
control
ability
and
to
the
decisions
individuals
make
frequently
on
a
daily
basis
(Bechara,
2005).
Both
inhibitory/impulse
control
function
and
affective
decision‐making
are
important,
speciBic
aspects
of
higher
order
executive
control
functioning
(Winstanley
et
al.,
2006).
1.
Good
inhibitory
functioning
reBlects
the
ability
to
actively
stop
a
pre‐potent
behavioral
response
(e.g.,
drinking
or
eating
in
excess)
after
it
has
been
triggered
(Logan
et
al.,
1997;
Braver
and
Ruge,
2006).
Individuals
with
deBicits
or
failures
in
these
systems
have
a
tendency
to
act
more
impulsively.
2.
Adequate
affective
decision‐making
reBlects
an
integration
of
cognitive
and
affective
systems
and
the
ability
to
more
optimally
weigh
short
term
gains
against
long
term
losses
or
probable
outcomes
of
an
action
(Bechara,
2005).
For
example,
excessive
drinking
or
eating
known
to
have
short‐term
“reinforcing
effects”
(but
long‐term
negative
consequences)
should
be
less
likely
or
problematic
for
individuals
scoring
higher
on
tasks
that
assess
this
ability.
The
functional
distinction
between
simple
inhibitory/impulse
control
and
affective
decision
making
processes
comes
from
extensive
clinical
research
with
patient
populations
with
damage
in
frontal
lobe
regions
(see
(Bechara,
2005)
for
reviews).
However,
these
two
sets
of
functions
are
asymmetrically
related,
i.e.,
one
way
(not
double)
dissociation:
Damage
that
leads
to
basic
inhibitory
control
deBicits
inevitably
leads
to
affective
decision‐
making
deBicits.
However,
damage
to
areas
important
for
affective
decision‐making
(e.g.,
anterior
ventromedial
region)
can
lead
to
pure
affective
decision‐making
deBicits,
independent
of
any
other
simple
inhibitory
control
deBicits.
3.
Insular
cortex
system:
responsive
to
homeosta&c
imbalance
(depriva&on
states),
which
ac&vity: a.
Exacerbates
the
ac&vity
of
the
habit/impulsive
system.
b.
Disable
(or
“hijack”)
ac&vity
of
the
prefrontal
(control/
reflec&ve)
system.
Based
on
anatomical
connec$ons:
Anterior
insula:
role
in
integra$on
of
autonomic
and
visceral
informa$on.
Posterior
insula:
role
in
somatosensory,
ves$bular,
and
motor
integra$on.
In
1947,
Bonin
and
Bailey
said
that
“the
func$ons
and
affini$es
of
the
insula
are
totally
unknown”.
Since
then,
although
much
has
been
learned
about
this
mysterious
lobe,
s$ll
(with
the
excep$on
of
a
few)
contemporary
textbooks
of
neuroanatomy
and
func$onal
neuroimaging
research
tend
to
overlook
the
func$onal
importance
of
this
structure:
1.
Earlier
studies
(mid
80’s),
mostly
in
animals,
ascribed
a
role
for
the
insula
in
condi$oned
aversive
learning
(e.g.
condi$oned
taste
aversion
paradigm).
2.
Later
studies
(late
80’s;
e.g
Berthier):
insula
and
asymbolia
for
pain
in
6
pa$ents;
no
emo$onal
response
to
painful
s$muli.
3.
Few
studies
throughout
these
years
suggested
a
role
for
the
insula
in
language.
4.
In
the
early
to
mid
1990’s,
some
neuroscien$sts
(e.g.,
Damasio;
Craig)
began
to
say
that
the
insula
is
a
“plaaorm
for
feelings
and
emo$on.”
More
specifically,
the
idea
is
that
the
insular
cortex
plays
an
important
role
in
the
mapping
of
bodily
states
and
their
transla$on
into
what
we
subjec$vely
and
consciously
experience
as
emo$onal
feelings.
Perhaps
related
to
conscious
feelings
of
urge
to
take
drugs,
including
the
urge
to
smoke.
I. Case Report: Nathan is a right-handed male
who lost interest in smoking after suffering from
an ischemic stroke at the age of 28.
He was 38 years old when we interviewed him,
and he was articulate and insightful about his
medical and smoking history.
He started smoking at the age of 14. At the time
of his stroke he was smoking more than 40
unfiltered cigarettes per day.
-Before his stroke, he used to enjoy smoking ,
experience frequent urges to smoke, and he often
found it difficult to abstain from smoking in
situations where it was inappropriate, such as at work,
or when he was so sick and in the hospital.
-He
was
aware
of
the
nega$ve
health
consequences
of
smoking
before
his
stroke,
though
he
was
not
par$cularly
concerned
about
these
consequences;
he
had
never
tried
to
quit
and
he
had
no
inten$on
of
quieng
at
the
$me
of
his
stroke.
Nathan smoked his last cigarette on the evening before his
stroke. When asked about his reason for quitting smoking,
he stated: “[his] body forgot the urge to smoke.”
-He reported that he felt no urge to smoke during his
hospital stay, even though he had the opportunity to
smoke.
-While he came to believe that his stroke was caused in
some way by smoking, this was not the reason why he quit;
he never actually tried to quit smoking, but spontaneously,
he had completely lost interest in smoking.
-He
has
not
felt
any
urge
to
smoke
since
he
quit.
High-resolution structural magnetic resonance images of
his brain revealed:
1
1 2 34
A
2
B
A
B
C
3
C
4
• This suggested that the insula plays a critical
role in psychological processes, such as
conscious urge, that make it difficult to quit
smoking and that promote relapse.
Conclusion:
-What Hilke said yesterday:
We speak different languages! We must translate those languages…How
different is what I said about urges and homeostatic signals in relation to the
insula from that of “loss aversion” for example?
-What I say: you need a “translational” branch for this neuro field to
survive in marketing and economics and the social sciences:
Basic
Neuroscience
Basic
Neuromarke$ng??
Neuroeconomics??
Transla$onal
‐‐‐‐‐‐‐‐
Clinical
Neurosecience
Transla$onal
Marke$ng
or
Economics