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Hedonic Value

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The hedonic processing of pleasure, pain, and displeasure is essential to survival and as such motivates behavior and strongly influences decision-making. Research has shown that the underlying mechanisms of wanting, liking, and learning form partly separable neuroanatomical and neuropharmacological systems in the brain, which are shared among many mammalian species. This chapter provides an overview of the brain circuitry involved in hedonic (dis)liking, wanting, and learning of rewards and punishments. It discusses the influence of physiology and homeostasis, motivational state, and contextual meaning in shaping the subjective utility of stimuli, and consequently hedonic value and the subjective hedonic experience.
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Section3
Varieties of value
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Chapter13
Hedonic value
Dan-Mikael Ellingsen, Siri Leknes,
and Morten Kringelbach
Introduction
Hedonic processing of pleasure and displeasure motivates behavior, inuences decision-
making, and is essential for survival of both the individual and the species. While much of
our behavior is geared toward seeking pleasant experiences over both the short and long
run, we will also work to avoid aversive or painful experiences. e hedonic valuation of
sensation helps to guide us toward which behaviors to engage in and which behaviors to
avoid. e hedonic value of sensory experiences is linked to homeostatic processes. While
the taste of chocolate can evoke intense feelings of pleasure, the very same stimulus can
change its value and become less pleasurable aer having eaten too much.
Although the subjective experience of pleasure is oen what rst comes so mind when
thinking of reward—and pleasure and reward are sometimes used interchangeably—
hedonic processing can be conceptually divided into at least three components—wanting,
liking, and learning (Berridge and Kringelbach 2008; Smith etal.2011). ere is now sub-
stantial evidence that these three processes constitute partly separable neuroanatomical
and neuropharmacological systems (Berridge and Kringelbach 2013; Berridge and Robin-
son 1998). Further, recent theorizing suggests that anhedonia, a prominent and devastat-
ing feature of a wide range of psychiatric illnesses (and chronic pain), may be related more
to a disruption of the balance between these hedonic subcomponents than to a “loss of
pleasure” per se (Rømer omsen etal., 2015). Such an imbalance can take dierent forms
in dierent conditions. Addictive disorders oen involve gradually increased motivation
and desire for obtaining the object of addiction, while actual liking is instead reduced. In
contrast, many aective disorders, like unipolar depression, are instead characterized by
reductions in both motivation and actual liking.
In this chapter we discuss evidence from animal and human studies of the brain cir-
cuitry that enables the brain to create pleasure and displeasure, and how hedonic process-
ing can be meaningfully divided into the subcomponents wanting, liking, and learning.
We then discuss how the brain determines hedonic value, and review the rationale for
the idea that subjective experiences can always be placed on a “hedonic continuum” with
pleasure and displeasure as end-points.
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The brain networks underlying hedonic processing
Pleasure and displeasure are never merely sensations—they are always “about” something—
and can be conceptualized as the “hedonic gloss” that is painted onto sensations (Frijda
2010; Kringelbach 2010; Kringelbach and Berridge 2010).
Moreover, hedonic reactions can be divided into subjective and objective aspects. While
subjective experiences of pleasure can be indirectly assessed experimentally through self-
report in humans, only objective reactions can be studied in animals. Subjective and objec-
tive hedonic reactions are evident in both wanting, liking, and learning aspects of rewards.
Implicit—or core—“wanting” can be studied by observing how hard an individual will
work to obtain a reward, while explicit wanting corresponds to the subjective experience
of desire and cognitive goals (Berridge and Kringelbach 2011). Correspondingly, motiv-
ational aspects of negative hedonics, like painful or disgusting events, can be studied by
observing how much an individual will work to avoid a punishment (implicit), or by as-
sessing subjective feelings of dread (explicit).
Core “liking” or “disliking” can be assessed through observation of hedonic reactions
during consumption of a reward or during a punishment. is can be quantied by the in-
tensity or frequency with which an animal licks its lips as a response to a sweet taste stimu-
lus, or makes gapes in response to an aversive bitter taste (Steiner 1973; Steiner etal.2001).
Unfortunately, behaviors indexing core liking for non-food rewards have yet to be deter-
mined. Explicit liking or disliking corresponds to the subjective feelings of pleasure or
displeasure.
Core “learning” comprises a range of processes involved in associative conditioning and
implicit knowledge, while explicit learning includes the conscious updating of cognitive
predictions. As we explain later in this chapter, wanting, liking, and learning of rewards
can be neuroanatomically and pharmacologically decoupled/disentangled as separable yet
closely interacting systems. ese separable yet closely coupled aspects can be thought
of as components of a cyclical process that characterizes most “normal” hedonic events
(Fig.13.1) (Berridge and Kringelbach 2011; Kringelbach etal.2012). Disruption of this
normal pleasure cycle may lead to anhedonia, the lack of normal ability to enjoy pleasures,
which is a core feature of aective disorders (Rømer omsen etal., 2015).
Measuring subjective hedonic value in humans
Measuring hedonic value in humans can seem just a matter of asking the person how
much he or she enjoys a pleasurable stimulus and get a more or less reliable answer. Func-
tional neuroimaging studies that measure brain activity during self-reported enjoyment
of rewards—be it sensory, social, or abstract rewards—have revealed many regions that
play roles in pleasure processing, most notably the subcortical structures Nucleus Accum-
bens (NAc), ventral pallidum and the amygdala; midbrain structures Ventral Tegmental
Area (VTA) and Periaqueductal Grey (PAG); and cortical structures orbitofrontal, cingu-
late, and insular cortices. However, since these neuroimaging techniques are correlative
in nature, they cannot answer whether a brain region actually generates pleasure or if it
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THE BRAIN NETWORKS UNDERLYING HEDONIC PROCESSING
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represents a readout of hedonic value in a subsequent process that primarily serves a dif-
ferent function.
Moreover, self-report measures are limited for several reasons. e participant may—
for various reasons—not be entirely accurate in their self-report (response bias), or they
may be unable to fully describe the subjective experience verbally (especially on a one-
dimensional scale assessing the intensity or magnitude of “pleasure”). Furthermore, the
self-report, in form of producing a mark on a scale, is several computational steps down
the line from the actual subjective experience, aer monitoring, evaluation, language, and
motor processes. However, self-report is the closest available estimate to assess subjective
experiences, and although biased, it provides a useful tool to understand hedonic pro-
cesses. To capture more complexity of the subjective experience, some researchers also
employ measures of several dimensions, such as feeling “good” and “bad” simultaneously
(e.g., Larsen etal.2004).
Measuring explicit hedonic value
Nevertheless, there are also aspects of liking that are objectively observable by conspecif-
ics, even in the absence of a verbal statement. It is relatively easy for a parent to determine
Fig.13.1 Pleasure cycles. Although research has mostly focused on wanting, liking, and
learning aspects as separate components, it may be meaningfully to view them temporally as
components of a cyclical process. The cyclical processing of rewards has classically been proposed
to be associated with appetitive, consummatory, and satiety phases (Craig 1918; Sherrington
1906). Research has demonstrated that this processing is supported by multiple brain networks
and processes, which crucially involves liking (the core reactions to hedonic impact), wanting
(motivational processing of incentive salience), and learning (typically Pavlovian or instrumental
associations and cognitive representations) (Berridge and Kringelbach 2011). These components
wax and wane during the pleasure cycle and can co-occur at any time. Importantly, however,
wanting processing tends to dominate the appetitive phase, while liking processing dominates the
consummatory phase. In contrast, learning can happen throughout the cycle. (See Plate 6.)
Reproduced from Berridge, K. C. and Kringelbach M. L., Building a neuroscience of pleasure and well-being,
Psychology of Well-Being: Theory, Research and Practice 2011, 1 (3), Springer, Copyright © 2011. http://www.
psywb.com/content/1/1/3.
Engaging with
food consumption
Satiation
Terminating food intake
Time
Initiating food
procurement/foraging
Pleasure
Appetitive phase
(dominated by wanting)
Consummatory phase
(dominated by liking)
Satiety phase
(strong learning)
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HEDONIC VALUE
268
whether their toddler liked or disliked a given taste, based on observation of their behav-
ioral reaction. In human infants, facial expressions like licking the lips or making gapes
are common reactions to sweet or bitter tastes, respectively (Steiner etal.2001). ese
reactions are also evident in both nonhuman primates and rodents, and provide cues to
the environment/other individuals about the hedonic value of the food reward. Pain is also
associated with automatic facial expressions that are likely to have evolved because of their
capability of drawing attention from conspecics who can potentially provide sympathy,
support, and care (Williams 2002).
Using core “liking” responses as experimental outcome measures is useful, especially in
animals and pre-verbal children, where subjective experiences cannot be directly assessed.
If a manipulation successfully changes an animal’s “liking” response to a reward, this indi-
cates that the manipulation altered a process responsible for generating “liking.
The brain networks generating hedonic value
For many years, the mesolimbic dopaminergic system, consisting of the ventral tegmen-
tum, amygdala, and ventral striatum, was assumed to be responsible for pleasure pro-
cessing. is idea grew from observations that rodents with microelectrode implants in
mesolimbic locations (e.g., nucleus accumbens) would self-stimulate to obtain electri-
cal stimulation from the electrode (Olds and Milner 1954; Shizgal etal.2001; Valenstein
etal.1970). By turning the current on only at certain locations in the testing apparatus, the
animals would return repeatedly to this location, sometimes preferring this location to lo-
cations where food was provided. When given the ability to turn on the current themselves
by pulling a lever, they would obsessively pull the lever—sometimes up to 2,000 times per
hour (Olds 1956).
Some similar experiments were even performed in human patients with mental ill-
nesses. ese patients engaged sometimes obsessively in “lever pressing” that released
electrical pulses from electrode implants in various subcortical locations (Heath 1972;
Portenoy etal.1986). However, it is not clear whether they actually enjoyed these pulses, or
if their behavior involved excessive wanting without much liking (Berridge and Kringel-
bach 2008; Green etal.2010; Kringelbach and Berridge 2012; Smith 2010).
Blockade of dopaminergic signaling typically disrupts reward-directed and consum-
matory behavior in rodents (Berridge and Robinson 1998; Schultz 2002). Extensive de-
struction of dopaminergic neurons can completely abolish rats’ interest in food, to the
extent that they will starve to death unless articially fed (Berridge and Robinson 1998).
In humans, a wide range of reward-related activities has been associated with dopamine
signaling (Egerton etal.2009), e.g., anticipation and emotional reactions to pleasurable
music, presentation of cocaine, drug-associated stimuli, video games, and monetary re-
wards (Breiter etal.1997; Koepp etal.1998; Salimpoor etal.2011; Scott etal.2007; Volkow
etal.1997).
ese ndings lead to the widespread idea of dopamine as a “common neural currency”
for pleasant rewards (Schultz 2002). However, while manipulations of dopaminergic sign-
aling or microinjections of dopamine into dierent parts of this “reward network” oen
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THE BRAIN NETWORKS UNDERLYING HEDONIC PROCESSING
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increase how much the animal would work to obtain a reward, it does little to change the
hedonic impact of the reward—i.e., how much animals lick their lips when consuming the
sucrose (Fig.13.2a). Although stimulation of these “pleasure centers” increases wanting
of food rewards, it doesn’t actually make the animals enjoy their food more, according to
simultaneous measures of objective facial responses (Berridge and Valenstein 1991).
In contrast, microinjections of opioids and certain other neurochemicals into discrete
locations in the ventral pallidum and the rostral part of the NAc enhance the intensity of
actual “liking” (Pecina and Berridge 2005). e “hedonic hotspots,where microinjections
of opioids increase “liking,” are very small in size compared to locations where opioid or
dopamine microinjections increase “wanting” responses (Fig.13.2bc). e hotspots cor-
respond to <10% of the accumbens shell (about 1 mm3 in rodents and 1 cm3 in humans,
if proportional) and the ventral pallidum. e hotspots in the NAc shell and ventral pal-
lidum seem to work as a single integrated circuit in the rat brain. Opioid stimulation in the
NAc hotspot increases liking reactions to sucrose and corresponding ring signals in the
ventral pallidum hotspot (Smith etal.2011). Further, pharmacological opioid blockage of
either of these hotspots prevents amplication of “liking” by activation of the other, sug-
gesting that cooperation of both hotspots is needed for improving hedonic impact (Smith
and Berridge 2007). Additional potential hotspots for “liking” reactions have been dis-
covered in rodents in a prefrontal region that may correspond to the Orbitofrontal Cor-
tex (OFC) in humans, and in the rat homolog for the human insula (Berridge, personal
communication).
Although the hedonic “hotspots” appear to be few and cover only a small fraction of
brain regions that generate reward-related behaviors, this circuitry is very resilient, and
there are few known human cases where basic liking reactions are completely abolished.
One case report describes a patient whose life became overshadowed by anhedonia and
depression, with much reduced positive aect and attenuated craving for rewards. ese
symptoms appeared aer selective damage to the bilateral ventral pallidum, which was
performed to alleviate his Parkinsonian symptoms (Miller etal.2006).
Within the accumbens shell, μ-opioids increase liking only when microinjected within
the small rostroventral hotspot. When microinjected in nearby locations, the same sub-
stance instead increases wanting without liking, suppresses aversive “disgust” reactions, or
suppresses both “liking” and “disliking” reactions to sweet or bitter tastes (Figs13.2c and
13.3). Moreover, there is recent evidence that other substances, like orexin and cannabi-
noids, may have comparable eects within these hotspots (Ho and Berridge 2013; Mahler
etal.2007). is may reect a strong exibility of this circuit, allowing other pharmaco-
logical agents to employ the role of opioids if this system is disrupted.
Opioids mediate preference for the most valuable option when several rewards are avail-
able. μ-opioid antagonism reduces consumption of palatable cookies in rats, but does not
aect the consumption of standard chow (Cooper and Turkish 1989). Conversely, μ-opioid
agonism enhances sexual “wanting” of estrus, but not non-estrus females (Mahler and Ber-
ridge 2012). In humans, μ-opioid agonism increases, while antagonism reduces, the relative
appeal of highly attractive, over less attractive, opposite-sex faces (Chelnokova etal.2014).
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(a) (b)
Fig.13.2 Brain circuitry for generating hedonic value. This schematic figure summarizes
subcortical and cortical systems for generating and coding of hedonic value. (a) Typical facial
reactions to sweet and bitter taste are comparable in rodents, primates and human infants, and
provide a useful model for investigating “liking” and “disliking.” (b) Brain circuitry involved in
hedonic processing in rodents and humans. (c) Hedonic “hotspots” have been found in the
nucleus accumbens shell and the ventral pallidum. Microinjection of mu opioid agonists into
these locations increase “liking” responses to e.g., sweet taste. (d) Cortical hedonic coding may
reach an apex in the orbitofrontal cortex, where hedonic value may be translated into subjective
pleasure or displeasure. (See Plate 7.)
Reprinted from Trends in Cognitive Science, 13 (11), pp.479–487. Morten L. Kringelbach, Kent C. Berridge,
Toward a functional neuroanatomy of pleasure and happiness, (2009), with permission from Elsevier.
Reproduced from Susana Peciña and Kent C. Berridge, The Journal of Neuroscience, 25(50), pp.11777–
11,786, Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do μ-Opioids Cause Increased Hedonic Impact
of Sweetness? © 2005, The Society for Neuroscience.
Hypothalamus
VTA
Insular cortex
Cingulate cortex
Orbitofrontal cortex
Anterior
Ventral
Dorsal
(c) (d)
Shell
250%
200%
125%
No change
<50%
<75%
8.2
6.2
Posterior
2100.9 mm lateral
y
0
10
20
30
40
50
60
70
0
10
20
30
40
50
60
70
right
+60 +50 +40 +30 +20 +10 0 –10 –20 –30 –40 –50 –60
left
×
PAG
Nucleus accumbens
Ventral pallidum
Amygdala
Medial OFC Mid-anterior OFC
Liking and wanting regions
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THE BRAIN NETWORKS UNDERLYING HEDONIC PROCESSING
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Wanting
(incentive salience)
‘Wanting’
Incentive salience
Wanting
Cognitive incentives
Liking
Conscious pleasure
Learning
Cognitive processing
Liking
(hedonic impact)
‘Liking’
Hedonic impact
‘Learning’
Associative learning
Pavlovian conditioned
response Instr. response
reinforcement
Facial affective expressions
Human pleasure-elicited
reactions
Conditioned approach, PIT
Autoshaping, cued relapse
Rational inference
Verbal explanation
Subjective ratings of
pleasure
Subjective ratings of
desire Cognitive goals
OFC, ACC, insular
Dopamine
OFC, ACC, insular
Opioids, cannabinoids
OFC, ACC, mPFC, insular
Ach, dopamine, serotonin
NAc, VTA, hypothalamus
Dopamine
NAc shell, VP, PAG,
amygdala Opioids,
cannabinoids
Amygdala, hippocampus
Ach, dopamine
Measurements Examples of brain circuitryPsychological componentsMajor categories
Non-conscious
Conscious
Learning
(including satiety)
Fig.13.3 Measuring hedonia. Hedonic processes may be divided into at least three major neurobiologically and psychologically components: wanting
or incentive salience (white), liking or hedonic impact (light gray), and learning (dark gray). These components have conscious aspects, which can only
be investigated in humans, and non-conscious aspects, which can also be investigated in non-human animals. Types of measurements are listed in the
second column, and examples of brain circuitry involved in each subcomponent are listed in the third column. (See Plate 8.)
Reproduced from Berridge, K. C. and Kringelbach, M. L., Building a neuroscience of pleasure and well-being, Psychology of Well-Being: Theory, Research and Practice 2011,
1 (3), Springer, Copyright © 2011. http://www.psywb.com/content/1/1/3.
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Cortical coding of pleasure
Apart from the circuitry that has been found to cause pleasure in animal experiments,
there are a number of cortical and subcortical regions that are implicated in the process-
ing of pleasure. Functional neuroimaging in humans suggest that orbitofrontal, insular,
and ventromedial prefrontal cortices (as well as the amygdala, PAG, and VTA) play im-
portant roles in reward processing. Activity in this circuitry oen correlates with self-
reported pleasure (Ellingsen etal.2013; Grabenhorst etal.2008; Kringelbach 2005; Rolls
etal.2003). Although they may not be the main generators of pleasure, these regions
are likely to represent hedonic value for other processes, such as learning and memory,
cognitive representations, language, decisions, action, or consciousness (Berridge and
Kringelbach 2013; Kringelbach and Berridge 2010). is builds on the notion that, while
large-scale disruption of these regions oen has consequences for the before-mentioned
processes, it seldom abolishes the capacity for normal pleasure and displeasure.
Two locations in the orbitofrontal cortex seem to be particularly important for pleas-
ure. One site in the mid-anterior and mid-lateral part of the OFC may serve as an apex
of cortical pleasure coding (Kringelbach 2005) (Fig.13.2d). Activity in this region tracks
changes in subjective pleasure, and correlates strongly with self-reported pleasantness of
food, touch, sexual orgasms, drugs, chocolate, and music (Blood and Zatorre 2001; Elling-
sen etal.2014; Georgiadis etal.2006; Grabenhorst etal.2008; McGlone etal.2012; Small
etal.2001; Vollm etal.2004).
Another important site for hedonic coding is located on the medial edge. Since un-
pleasant events mainly correlate with activation more laterally in the OFC, there may
be a pleasuredispleasure “gradient in the mediallateral plane. is gradient may in-
teract with a complexity gradient in the anteriorposterior plane, with complex rewards
such as money being coded more anteriorly, and basic rewards like food more posteriorly
(Kringelbach 2005).
Other cortical regions are also implicated in reward and aective processing. e an-
terior insula serves a crucial role for interoceptive awareness and representation of the
“self” (Craig 2009). It seems to monitor emotional state for the purpose of maintaining
homeostasis. e ventromedial Prefrontal Cortex (vmPFC) constitute a set of intercon-
nected regions that may integrate information from episodic memory, sensory events, so-
cial cognition, and current bodily state to construct aective meaning (Roy etal.2012). It
has reciprocal projections to numerous cortical, limbic, and midbrain structures, and is a
central node in the resting default network (Greicius etal.2003; Gusnard etal.2001). As
we will see later in this chapter, the anterior insula and subregions of the vmPFC are likely
to play key roles in direct hedonic value on the basis of memory processes and current
homeostatic and motivational state.
Although the cortex, and in particular the OFC, appears to code hedonic value, it is pos-
sible that these regions are not necessary for experiencing pleasure. ousands of human
patients received prefrontal lobotomy in the 1950s with massive damage to the ACC and
OFC. However, in spite of clear decits in decision-making and dramatic personality
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DETERMINING HEDONIC VALUE
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changes, these patients did not seem to lose the capacity for hedonic feelings, and contin-
ued to live aective lives (Damasio 2000; Valenstein 1986). Further, case reports suggest
that aective processing may be relatively intact in patients with insular damage. One pa-
tient had bilateral insular cortices completely destroyed from herpes simplex encephalitis.
Although he showed massive learning decits, and was unable to remember any new fac-
tual item for more than 45 s, he still showed dierential preference for food, and reported
feelings of happiness, pleasure, and pain (Damasio etal.2012). Another case report of pa-
tients with insular damage reported intact feelings of pain, but with increased pain inten-
sity for experimental pain stimuli (Starr etal.2009), in line with a role for the insula in pain
regulation (Craig 2009). Lastly, a case report of a 6-year-old patient with hydrocephalus,
with the absence of cerebral tissue rostral to the thalamus, reported that the boy “smiled
when spoken to and giggled when played with” (Shewmon etal.1999: 366). Together,
these cases suggest that, although playing important roles in the hedonic valuation, cor-
tical nodes of hedonic processing are not necessary for hedonic experience.
Determining hedonic value
While much of the circuitry involved in valuation and reward is remarkably similar be-
tween humans and other mammals (Haber and Knutson 2010; Murray etal.2007), there
are some notable dierences. For example, humans have massively expanded prefrontal
cortices, reecting greater encephalization. is is likely to be accompanied by more pre-
frontal inuence of other brain processing via increased prefrontal connectivity to other
cortical and subcortical brain regions. Compared to rats, primate orbitofrontal cortex pro-
jects more clearly dened descending connections to the hypothalamus and brainstem
structures. us, “higher-order” cognitive and aective information may have more inu-
ence over hedonic value in humans compared to other animals/mammals.
Homeostatic utility and pleasure
Pleasure and displeasure are never sensory experiences per se, but are qualities that are
imposed onto sensory experiences. Even stimuli that seem inherently “positive,like sweet
taste, can become hedonically “ipped.” Eating a delicious chocolate can be intensely
pleasant if you are hungry for chocolate. Yet the delight turns to disgust if you keep eat-
ing it beyond satiety, although the sensory stimulus remains the same (Small etal.2001).
Introducing the concept of alliesthesia, Cabanac (1971) postulated that stimuli that serve
to move the organism toward physiological or psychological homeostasis should be
perceived as pleasant, while stimuli that serve to move the organism out of homeosta-
sis should be perceived as unpleasant or painful. Rather than the inherent quality of the
stimulus itself, it is the utility of the stimulus for the organism at the time that determines
the hedonic value of the stimulus. e taste of salt at concentrations higher than seawater
is usually unpleasant to humans, and causes “disliking” gape reactions in rats. However, if
sodium levels are experimentally depleted, which induces a state of “salt appetite,” rats will
instead display “liking” reactions comparable to that of sucrose taste (Berridge etal.1984;
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Tindell etal.2006). Moreover, this “hedonic ip” is mirrored by the ring rate of neurons
in the ventral pallidum, indicating that coding of basic sensory pleasure depends on the
homeostatic utility, and not merely intrinsic qualities, of the stimulus (Tindell etal.2006).
e homeostatic utility—and consequently the hedonic value—of a stimulus is depend-
ent on a range of factors, like other sensory input, the individual’s memories, and their
concurrent aective, cognitive, and physiological states. In the example before, chocolate
was pleasant when it served to relieve hunger, but disgusting when this need was satiated.
Similarly, while a hot bath is likely very pleasant if you just came in freezing from a winter
storm, you may prefer an invigorating cold shower if you’re boiling in the midst of a heat
wave. e brain similarly makes use of its own predictions about the future when assigning
hedonic value.
Hedonic feelings are modulated by motivational states
e brain draws on all its available sensory and internal information in order to build an
internal model of the environment/world. is model is used to predict the outcome of
dierent actions and the hedonic value of the most likely outcomes (Friston and Kiebel
2009; O’Reilly etal.2013). Consequently, sensations are always a product of both sensory
activation and top-down regulation, making the brain more of an “interpreter” than a
“measuring instrument.Such sensory “bias,” directed from the predicted utility of out-
comes, is likely energy ecient compared to more comprehensive processing of a full
range of “raw” sensory information. Moreover, it can facilitate rapid decision-making
when sensory information is ambiguous or incomplete, which is an essential evolutionary
advantage.
ese principles have been employed to understand why pain is subject to such a vast
intra-individual variability across situations. Physical pain is generally associated with
displeasure and suering, and is typically something an individual will work to avoid
(however, as we will see later in this chapter, some pain experiences are perhaps equally
associated with pleasure and displeasure). e motivation-decision model of pain, as pro-
posed by Fields (2006, 2007), describes brain mechanisms that enhance or reduce the he-
donic impact of events based on their relative importance at a given time. e model was
initially put forward to explain modulation of pain, but the basic idea holds for all events
that fall within a rewardpunishment continuum. Fields postulates that—as a result of
an unconscious decision-making process—any concurrent or impending event that is
more important for the individual than a pain stimulus should suppress the hedonic im-
pact of this pain. e event of superior importance may, for instance, be a greater threat
or a potential reward. Likewise, anything judged as more important that an impending
reward—for example, a threat or a bigger reward—should suppress the hedonic impact
of this reward.
A central question is how the brain modulates this hedonic impact. Does it target the
neural systems that generate pleasure or displeasure, e.g., hedonic hot and cold spots, or
does it also modulate ascending sensory information that gives rise to pleasure or displeas-
ure? If so, at which levels does this modulation take place?
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ere is well-established evidence that ascending nociceptive neurons in the spinal dor-
sal are modulated by the brain (Wall 1967; Woolf 2011). e PAG in the midbrain controls
incoming nociceptive signals indirectly through the rostroventral medulla (RVM) (Fields
2004; Millan 2002). Neurons in the RVM project to the spinal dorsal horn, with inhibi-
tory (“OFF cells”) or excitatory (“ON cells”) eects on nociceptive transmission (Neu-
bert etal.2004; Urban and Gebhart 1999). e PAG receives direct input from the limbic
structures amygdala and ventral striatum, and from the prefrontal cortex, constituting
a pathway by which aective or cognitive information can inuence ascending sensory
information already at the spinal dorsal horn (Fields 2004).
Modulation of hedonic experience by contextual meaning
Hedonic experience is modulated by context, expectations, attention, arousal, and mood.
A range of neuroimaging studies in humans show that such top-down modulation of pain
can alter widespread somatosensory processing in the brain (Amanzio etal.2013; Berna
etal.2010; Ellingsen etal.2013; Knudsen etal.2011; Tracey and Mantyh 2007; Wager
etal.2004).
A particularly useful experimental model for probing psychological modulation of pain,
but also hedonic value in general, is placebo responses. e term “placebo” is derived from
the Latin stem “placebit” (“it will please”), and placebo responses refer to positive treat-
ment outcomes that are not caused by the physical properties of this treatment but by the
meaning ascribed to it. When people expect a placebo treatment to have analgesic eects,
they oen report reduced pain, which is accompanied by widespread reductions of soma-
tosensory (pain) processing in thalamus, insula, primary and secondary somatosensory
areas, and dorsal ACC (Amanzio etal.2013; Eippert etal.2009a; Lu etal.2010). Fur-
ther, activity in a “pain modulatory network” consisting of vmPFC, OFC, ventral striatum,
amygdala, and the midbrain, is instead increased, and is thought to be responsible for the
suppression of pain processing. is modulatory network is dependent on opioid process-
ing, since administration of the opioid receptor antagonist naloxone can attenuate both the
reduced pain reports (Amanzio and Benedetti 1999; Levine etal.1978) and the reduction
in pain/somatosensory processing (Eippert etal.2009a). e modulatory network respon-
sible for placebo analgesia may play a more general role in expectancy-induced modula-
tion of hedonic sensations. Petrovic and colleagues (2005) used a conditioning paradigm,
whereby participants were shown threatening images before and aer administration of
the anxiolytic drug midozalam. is drug robustly reduced self-reported unpleasantness
from viewing the images. In a subsequent session, participants who were given a placebo,
labeled as midozalam, reported reductions in unpleasantness comparable to the active
substance. Furthermore, the placebo improvement was underpinned by increased fMRI
activation in ventral striatum, rostral ACC and mid-lateral OFC, but suppressed activation
in visual cortex.
Recent ndings suggest that nociceptive processing at the spinal dorsal horn can be
altered when people expect pain relief. Eippert etal. (2009b) recorded fMRI of the spinal
segment receiving information from the arm, and found increased activity when people
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had received placebo treatment that also reduced their arm pain. Similarly, attentional
modulation of nociceptive signals in the spinal cord has been found when people are
performing a cognitively demanding working memory task, which induces analgesia
(Sprenger etal.2012). Within the framework of the motivation-decision model, this simi-
larity between expectancy- and distraction-induced analgesia is interesting, and may re-
ect a more general mechanism whereby motivational states control the presence of pain.
In both cases, the importance of pain is reduced, either because the brain is convinced an
“analgesic” treatment will reduce pain, or because attention is focused at another, more
important task. As a consequence of the brains decision to “respond less” to pain, the indi-
vidual can focus attention to other important tasks, such as reward seeking.
Nocebo hyperalgesia, the worsening of pain by negative expectations, may work by a
comparable mechanism (Scott etal.2008). fMRI studies indicate that expectancy-induced
increases in pain hedonics are underpinned by amplied somatosensory responses to pain
stimuli (Bingel etal.2011; Kong etal.2008; Rodriguez-Raecke etal.2010). Further, a
recent study investigated spinal fMRI activity during nocebo hyperalgesia, and found in-
creased activation in the relevant spinal cord segment when people expected pain to be in-
creased (Geuter and Buchel 2013). ese studies indicate that psychological processes, in
this case expectation of treatment benet, are able to modulate sensory information along
the entire sensory neural “axis” stretching from sensory circuitry in the brain to coupling
stations in the spinal dorsal horn, resulting in this context in reduced or amplied pain
experience. Such modulation is less studied for non-nociceptive sensory processing or
positive hedonic experiences.
If boosting the pleasure of a pleasant sensation (hyperhedonia) works in a correspond-
ing manner, we would expect sensory activity of this appetitive stimulus instead to be
increased. We recently found that a placebo modulation boosting the pleasantness of
gentle touch might rely on a mechanism similar to that of placebo analgesia (Ellingsen
etal.2013). We suggested to a group of healthy volunteers that a nasal spray would increase
both the pleasantness of gentle touch and reduce the unpleasantness of pain. Aer self-
administration of this nasal spray, a placebo, people reported increased touch pleasant-
ness and reduced pain unpleasantness. e reported improvements of pleasure and pain
were proportional to their prior expectations of treatment eects. While fMRI recordings
during pain showed decreased somatosensory processing, recordings during gentle touch
stimuli showed instead amplied activity in somatosensory areas (SI, SII, insula). Moreo-
ver, the magnitude of both hyperhedonic increases and analgesic decreases in somatosen-
sory responses were accounted for by the individual strength of the functional coupling
between medial OFC and PAG. It remains to be seen whether the modulation of pleasur-
able touch, like pain, involves descending modulation of cutaneous aerents in the spinal
cord, perhaps via the RVM. It will also be interesting to see whether this modulation relies
on opioid processing. ese results cannot tell us the direction of causality. Nevertheless,
this nding may suggest that, like negative hedonics such as pain, psychological modula-
tion of pleasant sensations involves modulation of the underlying sensory processing, and
not only within higher-level valuation circuitry.
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DETERMINING HEDONIC VALUE
277
A hedonic continuum?
Cognitively induced improvements of both pleasant and painful feelings are underpinned
by increased activity in orbitofrontal and ventromedial prefrontal areas, ventral striatum,
amygdala, and midbrain hubs PAG and VTA (Becker etal.2012; Haber and Knutson 2010;
Leknes and Tracey 2008). e extensive similarities between the brain networks and en-
docrinology involved in processing, and improving, pleasure and pain, pose the question
of whether the brain uses a “common currency” for hedonic value (Cabanac 1992; Leknes
and Tracey 2008; Ramirez and Cabanac 2003).
Pleasure and pain are oen regarded as opposites, and is related to the idea that the brain
places subjective experiences on a “hedonic continuum” with end-points distress and de-
light, and indierence in the middle (Cabanac 1979; Young 1959). is concept seems ac-
curate in many (perhaps most) cases. Pain and pleasure are oen opposing forces. Pleasant
experiences like delicious food, music (Bernatzky etal.2011), beautiful pictures, pleasant
touch, and perceived support from others can dampen concurrent pain. Conversely, the
occurrence of pain oen suppresses positive feelings, as illustrated by the burden of de-
pression and anhedonia that frequently accompanies chronic pain conditions (Marbach
and Lund 1981; Marbach etal.1983).
Painpleasure modulations may be reciprocally mediated by opioid signaling—a mu-
opioid antagonist can attenuate the pain-reducing eect of pleasant experiences, while a
mu-opioid agonist can attenuate the pleasure-reducing eect of pain (Fields 2007; Leknes
and Tracey 2008) (Fig.13.4a).
Mixed emotions and the benefits of pain
Although punishment is usually unpleasant and aversive, there are cases where painful ex-
periences instead gain a positive meaning, and can even be pleasant. e oen positively
laden experiences of eating spicy food, burning muscle during physical exercise, or engag-
ing in endurance sports illustrate that pain does not always carry an exclusively negative
hedonic value.
All consciously perceived hedonic experiences are associated with meaning. For in-
stance, a delicious cup of hot chocolate is oen a welcome indulgence, but it can also be
associated with guilt in both a positive (guilty pleasure) and a negative (I’ve failed to stick
to my diet) manner. e meaning of pain provides another compelling illustration of the
importance of meaning. While muscle pain is inevitable during a marathon run, it may
nevertheless carry a certain positive value, if the pain represents a challenge rather than
a threat. is change in meaning reduces the negative hedonic feeling usually associated
with pain, as demonstrated in a recent study assessing the impact of positive or negative
verbal instructions on the tolerance of ischemic arm pain. Participants who were told that
the pain would have benecial eects on muscle cells tolerated the pain for almost twice as
long as participants who were informed only about the aversive aspects of the pain (Bene-
detti etal.2013) (Fig.13.4b).
Further, moderate pain can be “hedonically ipped” from unpleasant to pleasant if the
pain represents avoidance from an even more painful stimulus (Leknes etal.2013). is
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HEDONIC VALUE
278
Baseline
30
Pain tolerance (min)
25
20
15
10
30
Pain tolerance (min)
25
20
15
10 Nal Rim
Group POS
Group NEG
Baseline Nal Rim Nal+Rim
Nal+Rim
Pain
Pain
Pain
(a) (b)
VTA
Amy
+ Pleasure
+ Pleasure
+ Pain
+ Pain
receptor antagonists
receptor agonists
+ µ-opioid
+ µ-opioid
VP
OFC
Pleasure
Pleasure
Pleasure
VTA
NAc
hedonic ip is underpinned by increased co-activation of the PAG with NAc and vmPFC
(Leknes etal.2013). Pain can also enhance the pleasure of reward hedonics. For example,
people report greater pleasure from chocolate aer undergoing a cold-pressor test, where
the task is to keep ones hand dipped in a bath of cold water (~1°C) for as long as possible
(Bastian etal.2014).
A possible mechanism whereby painful experiences can be pleasant, e.g., in consump-
tion of spicy food, is that the enhanced arousal pain causes, increases attention also to
Fig.13.4 Opioid modulation of pleasure and pain. (a) Pleasure and pain both elicit opioid release
in the orbitofrontal cortex, nucleus accumbens, ventral pallidum, and amygdala. Pleasure and pain
often works in a mutually inhibitory, opioid-dependent, fashion. Mu-opioid receptor antagonists,
like naloxone, can attenuate pleasure-induced analgesia. Vice versa, mu-opioid receptor agonists,
like morphine, can reverse pain-related suppression of pleasure. (b) In a recent experimental
study, one group of participants were told that experimental muscle pain would hurt but had
therapeutic benefits (POS), while another group were only told that pain would hurt (NEG). Pain
tolerance in the (POS) group was almost doubled compared to the (NEG) group. This increase in
pain tolerance was partially reversed when participants were pre-treated with either naloxone
(Nal) or the endocannabinoid receptor antagonist rimonabant (Rim), and completely abolished
when pre-treated with both Nal and Rim. (See Plate 9.)
(a) Reprinted by permission from Macmillan Publishers Ltd: Nature Reviews Neuroscience, 9(4), pp.314–320,
Leknes, S. and I. Tracey (2008). “A common neurobiology for pain and pleasure, © 2008, Macmillan
Publishers Ltd.
(b) Reproduced from Benedetti, F., Thoen, W., Blanchard, C., Vighetti, S., Arduino, C., Pain as a reward:
changing the meaning of pain from negative to positive co-activates opioid and cannabinoid systems, Pain,
154(3), pp.361–367, © 2013, Lippincott Williams and Wilkins, Inc.
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DETERMINING HEDONIC VALUE
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positive sensory signals, resulting in a more intense, and also pleasant, sensory experi-
ence (Bastian etal. in press; Leknes and Bastian 2014). Another possibility is that endog-
enous release of endorphins caused by aversive signaling accounts for the positive aect
(Carstens etal.2002). However, one study found that oset analgesia, the disproportion-
ally large analgesic response that oen follows a slight reduction in the intensity of an
ongoing pain, was unaected by administration of an opioid antagonist or an agonist
(Martucci etal.2012).
While pain is most oen regarded as negative and reward is oen regarded as posi-
tive, there are many examples of experiences that carry both positive and negative he-
donic values. erefore, a simple pleasurepain dichotomy may be too simple. Pain is
a multi-faceted phenomenon, which consists of more than just “displeasure.e term
“algosity” refers to the unique sensation of “painfulness” that distinguishes pain from
other unpleasant somatic sensations, like itch and nausea (Fields 1999). Algosity and
pain unpleasantness do not necessarily go hand in hand, which is illustrated by pain
asymbolia, a condition where patients report feeling pain, but not unpleasantness or
suering. It is likely that the presence of pleasure during a painful experience in most
cases reduces displeasure, although the algosity may remain the same. is would be
consistent with the idea of a hedonic continuum treating pleasure and displeasure as
opposites.
ere are nevertheless several examples of situations where feelings of pleasure and dis-
pleasure may perhaps be equally prominent, like deep pressure massage, being tickled,
feelings of nostalgia, or bittersweet feelings. In one study, people engaged in a gambling
game with two types of contexts. In one context there was a 50/50 chance of winning either
of two amounts of money, while in the other context there was a 50/50 chance of losing
either of two amounts (Larsen etal.2004). us, winning the lowest amount was the worst
possible outcome in the rst context, while losing the least amount was the best possible
outcome in the second context. Participants reported feeling both good and bad about the
disappointing wins and relieving losses. Moreover, when participants indicated with two
buttons whenever they felt good or bad, participants reported feeling good or bad simulta-
neously rather than alternating between the two, suggesting that these constituted unitary
mixed emotional events.
Rozin and colleagues refer to the enjoyment of experiences that are innately aversive,
but do not represent a threat, as “benign masochism” (Rozin and Schiller 1980; Rozin
etal.2013). According to this idea, when the brain judges such an aversive sensation to
represent no real danger, a sense of control, or mastery, gives rise to positive aect.
ere is little evidence for the preference of mixed emotions in animals. Rats display both
aversive and “liking” taste reactivity responses to bittersweet foods (Doyle etal.1993), but
would likely choose a purely sweet substance over the bittersweet. Typically a stimulus
is associated with either avoidance or approach behavior by the animal, not both at the
same time (Rozin etal.1979; however, see Rozin and Kennel 1983). is is in line with
the notion that hedonic impact may be more inuenced by top-down factors in humans
compared other mammals (Berridge and Kringelbach 2013).
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HEDONIC VALUE
280
Although most of the studies investigating mixed emotions address explicit hedonic
feelings, either through here-and-now assessments or in retrospect, they tell relatively lit-
tle about how this liking or disliking relate to motivational or learning aspects of rewards.
For example, although an experience can be simultaneously liked and disliked, it could still
be that motivational processes follow a more either/or principle—that an event cannot be
both worked for and against at the same time. More research is needed to denitely answer
whether it is meaningful to classify sensations on a bipolar continuum with pleasure and
displeasure as end-points, or whether they are separable processes that compete for prefer-
ence in the brain, but are not mutually exclusive. Nevertheless, it seems clear that, at least
humans are capable of experiencing unitary feelings that are both pleasant and unpleasant.
Conclusion
In this chapter, we have reviewed the neurocircuitry and neuropharmacology that gen-
erates hedonic value in humans and animals. ere is extensive evidence from animal
research that hedonic events can be disentangled into wanting, liking, and learning as-
pects, which may constitute a cyclical process that characterizes normal pleasure events.
e hedonic value of both basic sensory and “higher order” pleasure and displeasure is
oen strongly dependent on homeostatic utility rather than the inherent properties of the
stimuli. is is illustrated by the fact that hedonic reactions to stimuli can be ipped from
pleasant to unpleasant, and vice versa, depending on the motivational or homeostatic
state. Interestingly, such modulation is not only mirrored by processing in mesolimbic and
prefrontal valuation circuitry, but also in corresponding modulation of sensory process-
ing along the entire “neural axis” from central sensory networks to (at least) sensory relay
stations in the spinal cord. Along with these principles, pleasure and displeasure play cru-
cial roles in optimizing brain resources to guide survival-promoting behavior. Although
pleasure and displeasure oen appear opposite, there are many examples of cases where
hedonic experiences can consist of both. It remains to be discovered whether pleasure
and displeasure may meaningfully be viewed as opposites on a “hedonic continuum,” or
whether they comprise separate systems that oen, but not always operate in an opposing
manner.
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