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Chapter 10
Emotional Mind
The rambling internal narrative
of our thoughts is like a swimmer in a sea of emotions, constantly registering
the gentle rocking that goes with subtle changes in background feelings as
well as the crashing waves that accompany fear or passion. What are our emotions?
They certainly feel more rich, juicy, and energetic than "just thinking." We
experience them as coordinated responses spreading through the whole body,
frequently linked to a social context. Sometimes we may experience a sense
of "losing it"---getting so caught up that rational processes aren't
running the show. Could this be because a different brain has taken over at
such moments, one adapted to our evolutionary past but not necessarily to our
present world? Does this mean that emotion and reason are opposing forces?
An emerging consensus argues the
contrary position--that our rational processes depend vitally on the "lower" brain
structures that mediate emotion, and that lack of emotion can be just as damaging
to reason as its excess. The apparatus of rationality is not layered on top
of our basic regulatory and emotional processes, but rather rises and develops
from within them. "I feel, therefore I think" reflects what happens
in the brain better than Descartes's famous "I think, therefore I am." Modern
clinical studies on human patients with brain lesions show that either an absence
or an excess of emotions can prevent rational behavior. We might begin to think
of emotions as the glue that binds together the modules of mind and as pointers
to the contents of consciousness that are relevant to a particular moment.
Emotions are a part of our evolved psychology and are every bit as cognitive
as the more rarefied domains of mathematical and linguistic logic. This concept
has been overlooked because emotions are so much harder to describe. There
also has been a cultural bias, with intellectuals setting up an artificial
opposition between reason and emotion in which the emotional sides of our natures
are unstable and unreliable distractions from "real thought." Fortunately,
the long-standing scientific taboo against studying subjective experience is
being relaxed, and more weight is being given to affective neuroscience alongside,
or as a part of, cognitive neuroscience. It
is interesting in this regard that computer scientists who model cognitive
processes are sometimes finding it useful to introduce global analogs of affect
into their simulations.
This chapter begins with a brief
discussion of the way we define emotions and then moves on to consider both
their evolution and the brain structures and pathways that underlie our emotional
behaviors. Lesions in some of these structures not only diminish affect but
also distort rational processes, which suggests that emotional pathways must
be intact for our rational faculties to work properly. Emotional pathways can
work more rapidly than those involved in conscious reasoning, and this may
give us some insight into why we don't always act the way hindsight tells us
we should have. It is easy to misapply our emotional repertoire. We all face
the problem of applying hardwired emotional machinery such as the fight-or-flight
response to modern circumstances in which threats are much more subtle than
a charging lion on the African savanna.
Defining Emotions
Devising a reasonable system to
describe the many emotional behaviors we experience is a daunting task, but
this hasn't kept numerous different schemes from being launched. This examination
of fear in the accompanying self-experiment, along with many other emotional
situations, suggests that our emotional experiences have at least three different
manifestations: (1) a physiological component that includes autonomic nervous
system activity---changes in viscera, blood pressure, distribution of blood
flow, digestive system, and so on; (2) our behaviors, such as facial expressions,
that convey anger or sadness; and (3) our subjective feelings, such as love,
fear, and hate. Some of our emotions reflect drives or desires basic to survival,
such as hunger, thirst, lust, pain, pleasure, and aggression. These emotions,
in some form, are shared by all higher vertebrates, especially mammals. Other
emotions are more explicitly related to communication with our fellow humans:
happiness, disgust, surprise, sadness, anger, distress, interest, fear, and
jealousy. Measuring emotions is a challenge, because the same stimuli can be
pleasant or unpleasant, depending on the context. For example, if you have
just had a huge candy bar, you may react negatively to a sweet soft drink,
but if you are tired and thirsty, the same sugary drink is a pleasing relief.
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DESIGN NOTE: SELF-EXPERIMENT
A useful place to begin a description
of the variety of emotions is with our own experience. Let's take the example
of fear. Pull yourself away from this focused reading for a moment and try
to recall receiving a fright: perhaps you narrowly escaped being hit by a speeding
car or became aware that someone was following you on a dark and dangerous
street. Your heart pounded, your body tensed, your face contorted with fear,
and a strong feeling of dread passed through your body. Probably you can actually
experience a faint "replay" of these reactions just by recalling
the situation.
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It is interesting but not surprising
that most studies on brains and emotions deal with negative affect, such as
fear, anxiety, and anger. We don't go to doctors to seek cures for feeling
happy, joyful, or optimistic. It
is easier to elicit and measure fear or anxiety than happiness, and much of
what we experience as positive emotions might be mainly the absence of negative
ones. Further, happiness is linked not simply to the absence of a threat, but
also to how we perceive our general well-being with respect to that of others.
We can't say which emotions are "primary" in
the same sense that we know the primary colors are blue, yellow, and red---we
can't even be sure the analogy holds. But the main candidates include anger,
sadness, fear, enjoyment, love, surprise, disgust, and shame. Each
of these emotions is made up of a family of related feelings. Anger, for example,
might be expressed as fury, outrage, resentment, exasperation, acrimony, irritability,
or hostility. Enjoyment includes relief, contentment, delight, amusement, sensual
pleasure, rapture, euphoria, and (at the extreme) mania. An intense emotion
usually does not last more than a few minutes, but we can experience its more
muted form, mood, for many hours. Finally, each of us has a distinctive temperament---a
readiness to evoke certain sets of emotions, such as those associated with
being cheery or melancholy. Most of these temperaments remain remarkably constant
throughout life. There is considerable evidence that some temperaments, such
as novelty seeking, optimism, and pessimism, are moderately heritable and not
greatly influenced by family environment. Beyond
these dispositions are the more blatant disorders of emotions such as chronic
anxiety or depression. Categorization of all these states is complex, and researchers
disagree about some very fundamental issues:
How many basic universal humans
emotions are there?
Should emotions be described as
discrete entities, such as anger, fear, and disgust, or as points on continua,
such as pleasant-unpleasant, aroused-unaroused, approach-avoid? Is there really
a difference between the two descriptions?
What is an unambiguous test of
whether an emotion has occurred?
Emotions are hard to define not
only behaviorally but also anatomically, because many different brain regions
come into play in every emotion. Emotional
circuits include the limbic system, which forms a ring around the brainstem
and consists of cortex around the corpus callosum (mainly in the cingulate
area) as well as cortex on the medial surface of the temporal lobe, including
the hippocampus and amygdala (refer to Figures 3-3 and 3-4). These
regions communicate between higher centers in the prefrontal and association
cortexes and the hypothalamus. The hypothalamus contains centers whose stimulation
can elicit stereotyped emotional performances. The location of these structures
is shown in Figure 10-1. At the present time, we don't have a theory of the
anatomical circuits of emotions, as we do for vision. The study of emotion,
just like the study of visual or other kinds of cognition, requires a dissection
of emotional processes into elementary operations. Such an effort is still
in its early stages.
Figure 10-1
Brain structures that are important
in generating emotions. We are looking at the brain from the left side, as
we have before in describing the surface features of the cortex, but now the
entire left side of the brain has been removed so that we have a medial view
of the inside surface of the exposed right hemisphere. Adapted from Figure
16.4 in Bear et al., Neuroscience : Exploring the Brain.
Emotions Are Evolutionary Adaptations
The psychologist Nicholas Humphrey,
whose ideas were mentioned in Chapter 2, suggests that we might trace the origins
of affect back to such simple behaviors as the chemotaxis of Escherichia coli
or the wriggles of acceptance or rejection displayed by amoebae. In more complex
animals, specialized receptors evolved to report useful or noxious stimuli
to the brain. Early in the evolution of the brain, sensory and emotional sensitivity
was always linked to a corresponding bodily activity. A subsequent development
was to make the responses a brain activity (attraction or repulsion) that was
felt but not necessarily acted on (recall the itch that you can choose not
to scratch.) The suggestion is that to "like" a stimulus might be
to respond to it in such a way as to keep up or increase the stimulation (positive
feedback), and to "dislike" it would be to respond in such a way
as to keep down or reduce it (negative feedback). Affect might be linked with
the way a stimulus is evaluated at a submodal level. For example, among visual
stimuli, red light is typically exciting whereas blue is calming. Among the
different kinds of tactile sensations, itches are irritating, gentle stroking
pleasurable. Within the gustatory modality sweet tastes are pleasant, rotten
tastes revolting.
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DESIGN NOTE: IMPORTANT POINT
The origin of emotions might be
traced back to responses, in simple animals, of "liking" or "not
liking" some aspect of their environment. Emotional, or affective, behaviors
probably evolved because they conferred some selective advantage on those who
had them.
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Moving through vertebrate evolution
toward humans, we can trace an increase in the complexity of autonomic nervous
systems and emotional behaviors. One view is that the emotions are an evolutionary
by-product of the neural regulation of the autonomic nervous system. Recall
that a basic job of the sympathetic and parasympathetic divisions of the autonomic
system is regulating the body during mobilization and energy expenditure, as
well as during rest and recovery. During mobilization, the sympathetic system
releases the neurotransmitter norepinephrine at many end organs---for example,
on muscle to increase the speed and effectiveness of its contractions. Parasympathetic
activity is approximately the mirror image of this, a calming and return to
emphasis on vegetative self-maintenance and restorative functions. It uses
the neurotransmitter acetylcholine and is active during sleep. These systems
are established in bony fishes and become more complex in amphibians and reptiles.
In mammals a new complex of nerves appears, the ventral vagal system, which
innervates the heart and other visceral organs, as well as facial and vocal
muscles involved in emotional expression. This is a system thought to permit
emotional mobilization short of the full sympathetic arousal of the fight-or-flight
response. It has components
that inhibit sympathetic arousal to promote bonding and affiliative behavior.
Emotional circuits appear to be much more malleable than hardwired reflexes
such as pain withdrawal and the knee-jerk response. There can be large variations
between individuals and between related groups of animals. Think of the difference
between Staffordshire terriers (pit bulls) and St. Bernards or between common
and bonobo chimpanzees (described in Chapter 4). These different variants of
the same species have evolved very different emotional behaviors.
Emotions and the Physical Environment
We obtain some interesting clues
about the possible origins of our emotions by examining common human phobias,
which are resistant to change but can be extinguished by conditioning therapy.
It is striking that there are only about two dozen common elicitors of phobic
reactions, such as insects, snake shapes, heights, looming large objects, and
growling noises, all of which would have been very relevant to the survival
of our ancestors. We appear to have an innate predisposition to associate aversive
stimuli with these objects. Psychological experiments have shown that most
of us look at a picture of a boa constrictor without getting too rattled, but
if that picture is paired with an electric shock just once, the next time we
see the snake picture we become quite agitated. If we are shown a picture of
a flower together with the shock, it takes a much longer series of pairings
of picture and shock to induce the same level of aversion to the picture. More
extensive experiments have been done in animals to demonstrate innate predispositions
to certain kinds of conditioning. There can be single-trial learning of a response
to selective stimuli even if there is a long delay between stimulus and result,
and the learning is not easily extinguished. Laboratory rats become averse
to bright light and noise if these are linked with pain but not if they are
linked with nausea, whereas a particular taste can become aversive if linked
with nausea but not if linked with bright light or noise.
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DESIGN NOTE: IMPORTANT POINT
Learning that is obviously relevant
to survival, such as becoming averse to the taste of some food that once made
you ill, is much easier and more rapid than learning to be repelled by a picture
of a flower with which a shock is associated. Selective pressures over evolutionary
time have favored formation of the brain circuits underlying such predispositions.
***************
There is general consensus that
our limbic system is the primary site of innate or preorganized primary emotions,
containing circuitry that is especially responsive to features of the sort
just listed. An unresolved
issue is to what extent something like a "snake detector" might be
hardwired by genetic instructions. We can sketch a plausible scenario for how
genes might specify a detector for the "feature set" of a long, thin
object that moves sinuously. However, it seems implausible that they might
code the precise coloring or shape of the animal. Different parts of the world
have snakes of different shapes and sizes. Similarly, the face detector cells
mentioned in Chapter 8 and below might actually start as more generic icon
detectors for certain sets of curves and lines, as in the "happy face" image.
This image is made only of a circle containing an upwardly curved arc in its
bottom half, positioned under one dot for the nose and two for the eyes. Newborn
human children recognize this icon and distinguish it from others in which
the elements have been scrambled.
Emotions and Social Exchange
Charles Darwin recognized the importance
of emotions as signals that accurately inform one animal about the state of
another. This is most clear
in higher mammals like ourselves. All of us think that we can tell when a dog
or cat is happy, playful, angry, fearful, curious, anxious, or in some other
state in which an adjective ordinarily descriptive of human emotions seems
appropriate. We know for ourselves, and usually assume it to be true for animals,
that emotions are messages about our own internal state as well as direct,
nonverbal signals to others. Here we might go with our common sense, as not
inappropriately anthropomorphic, for some similar underlying mechanisms are
clearly at work in both ourselves and other mammals.
Emotions can inform our intelligence
what to think about, and in this sense we are, to use a phrase attributed to
Richard Dawkins, "walking archives of ancestral wisdom." Practitioners
of evolutionary psychology argue that common emotional states---fear of predators,
guilt, sexual jealousy, rage, grief, and so on---are adaptations to repetitive
features of the environment faced by the small groups of hunter-gatherers in
Africa who are thought to be the ancestors of all modern humans. For
example, discovering one's mate having sex with someone else signals a situation
that threatens future reproduction and present "investment allocation." This
cue should therefore activate sexual jealousy. The discussion of evolutionary
psychology in Chapter 5 mentioned the importance of detecting cheating, and
many aspects of anger, guilt, and shame revolve around this issue.
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DESIGN NOTE: IMPORTANT POINT
Basic emotional states common to
humans of all cultures, such as enjoyment, sadness, anger, disgust, and fear,
correlate with biologically significant events in the world, marking them as
good or bad, as associated with life or death. These emotions, and their counterparts
in other animals, are adaptations that have the purpose of informing or influencing
the behavior of others.
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The psychologist Steven Pinker
suggests that our intellect is designed to relinquish control to our passions
so that they serve as reliable guarantors of promises or threats that allay
suspicions of double-crosses or bluffing. This would explain why we unconsciously
advertise emotions on our faces---why our being "unable to control our
emotions" is a guarantor of their authenticity. For the most part, it
seems a good design to segregate voluntary cognitive systems from mainly involuntary
housekeeping systems that regulate blood pressure, skin glands, and so on.
But to prove an emotion's authenticity, perhaps selection has bound that emotion
to a physiological control circuit (such as quavering, trembling, croaking,
weeping, blushing, blanching, flushing, or sweating) over which we normally
don't have much voluntary control. If we really want to know whether people
are trying to fool us, or are displaying sham emotions, we insist on doing
business with them in the flesh, so that we can see what makes them sweat.
These arguments from evolutionary psychology, of course, contend that our emotions
are behaviors that maximize not our fitness today but that of our ancestors
in a now-vanished past. In this view, we humans are "adaptation executors" who
respond to present circumstances in ways developed in our evolutionary past.
Subcortical Systems Underlying
Emotions
Emotions were identified with lower
brain centers in the 19th century through experiments on dogs whose cerebral
cortexes had been removed, leaving the diencephalon intact (including the thalamus
and hypothalamus). These animals could still show rage and fear. In the 1930s,
Papez proposed that the limbic system, acting through the hypothalamus, was
the anatomical basis of emotions. During this period, brain lesion studies
showed striking changes (such as loss of fear, indiscriminate eating, and increased
sexual activity) in the emotional behavior of monkeys whose temporal lobes
had been removed. Lesions in the frontal cortex, paralimbic cortex, or amygdala
caused reduced and inappropriate social interaction. A similar syndrome (Kluver-Bucy
syndrome) is found in humans with bilateral damage to the amygdala and inferior
temporal cortex. The discovery that removing the frontal lobes of aggressive
monkeys calmed them led to psychosurgery, an outstanding example being the
frontal lobotomy of humans. This procedure not only calms the subjects but
also severely impairs their social and affective behavior.
The Autonomic Background of Emotions
Before focusing on the brain, however,
let's start further downstairs, with the peripheral sympathetic and parasympathetic
nervous systems that were introduced in Chapter 3 and mentioned above. These
systems mediate our bodily experiences of emotions. Recall that our sympathetic
nervous system is engaged during arousal and emergencies, expending energy,
whereas the parasympathetic system regulates rest, recovery, and energy storage.
The ratio of parasympathetic to sympathetic activation, set by the hypothalamus
in the brain, is a central component of our affective life, correlating with
whether we are relaxed, open, and engaging, versus avoiding, defensive, or
aggressive.
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DESIGN NOTE: LONG SELF-EXPERIMENT
You can try a simple exercise to
sense some of the global body correlates that go with activation of the peripheral
sympathetic and parasympathetic nervous systems. The following exercise is
probably best done by having someone read it out loud to you, but you can also
read the instructions and try it on yourself. Close your eyes for a moment
and imagine yourself on vacation, sitting on a rock by the ocean watching a
beautiful sunset. Let time slow down so that all you are aware of is the colors
in the sky and the gentle breeze from the sea. Be completely in the present
moment. Let the pleasant feelings in your body take you back to an earlier
time, perhaps when you were a child, when you felt secure and cared for. After
you have spent at least a few minutes getting into this fantasy, just note
how your body feels, note your breathing, and note what your shoulder and jaw
muscles are doing. Now try a different fantasy, one less pleasant. Imagine
yourself to be walking, late at night, down a deserted city street with only
one or two streetlights. There are no other people around. You suddenly hear
a scuffling noise, and four rough-looking men tumble from an alley 30 feet
in front you. This surprises you and you stiffen a bit, as though you don't
want them to notice you. But then, the moment they see you, they abruptly turn
to face you, fan out, and start to approach you, slowly and deliberately, with
very flat expressions on their faces. You look for a place to run, but it's
too late. They break into a run towards you. Now scan your body again, and
note how it feels. Even if you just read through these descriptions without
really getting into them, you can probably sense differences in your body---in
your breathing or in how tightly you are holding your muscles.
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The self-experiment in this section
has the goal of eliciting body changes that go with parasympathetic (relaxing)
versus sympathetic (arousal) activation---changes that are intense enough for
you to sense them clearly. Consider, now, that much of your daily attitude
or temperament might be described as being somewhere between these two extremes.
Indeed, the relative activation of these two systems sets a somatic background,
or bias, that can influence your behaviors.
Strong sympathetic or parasympathetic
activations can set a tone or mood that persists for some time. Think of the
times, for example, when you have experienced a persistent sympathetic activation
as you remained a bit jumpy for many minutes after being excited by suddenly
having to avoid some danger, perhaps a speeding car. Norepinephrine released
by your sympathetic nerves was causing increased attentiveness and excitation
that decayed only slowly as the norepinephrine was taken back up into nerve
cells.
Brainstem Modulation of Attention
and Appetite
Against this backdrop of overall
sympathetic or parasympathetic activation, a whole host of mood-altering chemicals
regulate our appetitive and attentional behaviors. These global modulators
of our emotions are manufactured in restricted regions of our brainstem or
basal forebrain and then sent via long axons to widespread regions of the cortex,
where they are released. Central players are neurotransmitters such as the
biogenic amines (dopamine, norepinephrine, and serotonin) and acetylcholine.
These systems serve as brain "spritzers" regulating our states of
alertness, anxiety, elation, depression, or aggression. They
can speed up or slow down the rate at which our mental operations proceed.
Figure 10-2 shows the location
of one of these systems, a small group of cells called the locus coeruleus.
It is essentially an outpost of the sympathetic nervous system that can extend
that system's arousal into the brain. Axons from these cells travel to multiple
locations in the cerebral cortex and cerebellar cortex to release norepinephrine,
which enhances our attention and memory processes. Another spritzing system
releases the neurotransmitter serotonin in the brain. Reductions in the activity
of circuits that use norepinephrine and serotonin apparently contribute to
depression in many people. Serotonin levels appear to be inversely correlated
with aggression. For example, mice that lack a certain postsynaptic receptor
for serotonin are more aggressive in stressful situations. Lowering serotonin
by drugs or genetic manipulation increases aggressiveness, and raising it has
the opposite effect. Low levels
of brain serotonin are associated with anxiety in humans and also in animal
models for anxiety, and inhibitors of serotonin uptake into nerve cells - which
raise the concentration of serotonin outside the cells - are used as antidepressants.
The psychoactive drug LSD mimics the action of serotonin.
Figure 10-2
A diffuse modulatory circuit originates
in the locus coeruleus. This brain nucleus, which occurs on both the left and
the right sides of the pons regions of the brain, has only about 12,000 neurons.
A single one of these neurons can make more than 250,000 connections, sending
axon branches to both the cerebral cortex and the cerebellum. These release
norepinephrine, which can enhance arousal, attention, and memory.
Dopamine, whose role in movement
we mentioned briefly in Chapter 9, acts as a central activator. If nerve terminals
secreting it are destroyed in rats, the animals lose desire, motivation, adaptability,
and exploratory behavior. Dopamine levels are affected by cocaine and amphetamine,
and they play a role in responses to heroin, alcohol, nicotine, and cannabis. Chemicals
that modify dopamine receptors can alter drug-seeking behaviors. Some
people who show stronger than average novelty-seeking behavior have a variant
of one of the dopamine receptors.
Dopamine-containing cells in the
midbrain are activated by novel appetitive stimuli, but not by aversive stimuli. This
observation has suggested the simple model that when something interesting
or good happens, these cells in our midbrain shower higher brain centers with
dopamine, which causes an appetitive behavior. Cocaine
and amphetamines mimic this effect by inhibiting the reuptake of dopamine into
presynaptic terminals, thus maintaining activation of synapses longer than
normal. Studies using mice initially showed that when the transporter that
normally removes dopamine from synapses was deleted, the animals became hyperactive
and also indifferent to cocaine and amphetamine. They presumably already had
the "high" that the drugs usually cause. (These experiments are done
by constructing "knockout" mutants in which the gene for the transporter
has been deleted. ) Alas, the
clarity suggested by the initial knockout experiments did not persist, because
repetition of this and similar experiments found that knockout mice in which
either the dopamine or the serotonin uptake mechanisms were deleted were indeed
sensitive to cocaine. Recent
work has now suggested that brain circuits using the neurotransmitter glutamic
acid are involved in producing the changes that lead to compulsive drug seeking.
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DESIGN NOTE: IMPORTANT POINT
Several different centers in the
brainstem contain nerve cell bodies that send axons to many different areas
of the cortex and cerebellum. Their activation can cause global changes in
attention, alertness, appetite, and motivation.
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Further experiments have suggested
that the purpose of the dopamine system is not to produce feeling of pleasure
but to draw attention to events that predict rewards, so that the animal learns,
recognizes, and then repeats them. Dopamine
surges are measured in an area called the nucleus accumbens during anticipation
of food or sex. This could explain why many drugs that stimulate the dopamine
system can drive continued use without producing pleasure, as when cocaine
addicts continue to take hits long after the euphoric effects of the drug have
worn off or when smokers still smoke after cigarettes become distasteful. These
drugs have essentially hijacked a brain mechanism that evolved to signal rewards
relevant to fitness and reproduction (such as food or sex) and instead enslave
the organism to desires that have no adaptive value. Brain imaging using PET
shows activation in the mesolimbic dopamine system as addicts describe feelings
of intense craving for cocaine. (The mesolimbic dopamine system connects the
orbitofrontal cortex, in the prefrontal area behind the forehead, with the
amygdala and nucleus accumbens.) Different areas are preferentially activated
during rush (the drug euphoria, or high) and during craving for the drug.
Other Correlations of Chemistry
and Emotional Behavior
We can list several further correlations
of chemistry and emotional behavior. Morphine and other opiates can block pain
pathways in the brain, sometimes causing euphoria, by mimicking a different
class of neurotransmitters made from peptides (small pieces of proteins). The
brain contains complex families of these peptides, including a group referred
to as the opioid peptides: the enkephalins, endorphins, and dynorphins. They
also play a complex role in regulating social attachments and the distress
caused by social isolation. Another
peptide, oxytocin, appears to play a role in soothing and bonding behaviors,
eliciting the parasympathetic opposite of the sympathetic fight-or-flight response. In
some rodents (different species of prairie voles), monogamous versus polygamous
social structure and behavior correlate with different expressions of the oxytocin
and vasopressin systems. Some chemicals that influence arousal, anxiety, or
aggression can come from sources outside the brain. Aggression (especially
aggression between males) is influenced by testosterone, as we noted in Chapter
6. Castration of male mice reduces their aggressive behavior, and injections
of testosterone can then reinstate it. Epinephrine
and adrenocorticosteroid levels correlate with arousal and excitability; they
typically are higher in emotive than in repressed individuals.
All of these systems certainly
are regulated by our conscious cognitive response to objective aspects of our
environment, especially whether it is nurturing or threatening. There are other
internal explanations for why we feel this or that particular way. Many of
the autonomic and brainstem systems discussed in the previous sections have
cycles of their own, alternating periods of activity with intervals of rest
and renewal of their neurotransmitter systems. This has been well documented
in the cyclical activation of cholinergic versus adrenergic systems in sleep
versus wakefulness, which is described in Chapter 12, and in changes in cognition
and mood that accompany the monthly ovulation cycle in women. Perhaps we should
consider that these cycles can generate feelings for which "there is no
reason" in the usual sense, not withstanding our tendency always to invent
a reason for the way we are feeling. Experiments with hypnotized, split-brain,
or anosognosic patients have shown that we will cheerfully confabulate bogus
reasons for a behavior if the real cause is not accessible to our consciousness.
We should consider the possibility that during some feelings and emotions,
the brainstem systems are calling the shots, and our fertile imaginations are
merely supplying a cover-up story.
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DESIGN NOTE: LONG IMPORTANT POINT
Thinking about the relationship
between our brain chemistry and our emotional moods and thoughts presents us
with the "Which came first, the chicken or the egg?" problem. Cognitive
processes can direct the mood-altering chemistry that originates in the brainstem,
and spontaneous changes in this chemistry can alter our thoughts. In the latter
case, there may be no "reason" for our thoughts or feelings, in the
way we commonly suppose.
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Chemical imbalances in these systems
can underlie affective disorders. We are learning that distinctive chemistries
correlate with defense or arousal, with rest, with anticipation of novelty
or appetitive behavior, with anxiety or depression, and so on. Legions of biotechnologists
currently employed by pharmaceutical companies are trying to synthesize compounds
that selectively enhance or depress these systems and provide more effective
therapies for depression, anxiety, drug addiction, and anhedonia (the inability
to experience pleasure).
Higher Levels of Emotional Mind
Continuing to trace the components
of our affective life further up into the brain, we encounter the limbic system
that was mentioned in Chapter 3 (see the section "Layers of the Brain").
It is thought to mediate the basic survival-related programs of the brainstem
(such as feeding, aggression, and sexuality) and also to regulate the social
emotions of distress, bonding, and nurturing. The limbic structures shown in
Figure 10-1 communicate between higher cortical centers and the hypothalamus,
also mentioned in Chapter 3 as a central control center for coordinating our
emotional responses. Electrical stimulation of nuclei of the lateral hypothalamus,
in sequence from front to back, elicits appetitive behaviors related to temperature
regulation, sex, drink, and food. Stimulation of medial structures in the hypothalamus
seems to produce opposite, aversive behaviors. The hypothalamus directs the
autonomic nervous system and integrates and coordinates the rapid behavioral
expression of emotional states. Lesions or electrode stimulation can generate
discrete, stereotyped expressions of fear, anger, pleasure, or contentment.
Each of these emotions seems to possess the animal completely during its expression.
You may have heard about a "pleasure center" in the brain. Actually,
several such centers have been identified in rat and human brains.
Finally, the top element of the
triune brain is the cerebral cortex overlaying the limbic system. Its frontal
lobes are central to the regulation of emotions. Mood disorders have been correlated
with abnormalities in the ventral prefrontal cortex. This
region is consistently underactivated in familial depressive patients and is
activated during periods of mania. Activity in our prefrontal lobes may be
part of the answer to a fundamental question: How do we assemble the vast array
of feelings we have in different situations, avoiding some and desiring others?
Emotional Mind as a Foundation
of Rational Mind
The neuropsychologist Antonio Damasio has
suggested that that during our development we accumulate a large number of
learned or acquired secondary emotions that necessitate activity of the prefrontal
cortex; in this they differ from the more innate primary emotions associated
with the limbic system. These secondary emotions are essentially feelings learned
by associating primary emotions with different situations we encounter while
growing up---situations that mark them as positive or negative, to be approached
or avoided. A small positive or negative stamp is put on almost everything
we encounter. We develop a set of rules, a morality, for what to do and what
not to do. This training, the acquiring of secondary emotions, involves our
visceral or autonomic nervous system. When we have aversive or positive reactions
to something, our autonomic nervous system responds, usually outside of our
normal consciousness, by changing such variables as the rate of moisture release
by our skin, our heart rate, and our blood pressure. (Changes in skin conductance
can be used as a convenient and crude assay of this autonomic nervous system
arousal and have been found to correlate with changes in activation of portions
of the cingulate and motor cortex.) Subtle changes in muscle tension over the
body may also accompany the pairings of feelings and autonomic activation.
Damasio uses the term somatic markers to refer to these body correlates of
feelings. These markers are discussed below, in the section "Emotional
Responses Can Be More Rapid Than Reasoned Ones."
********
DESIGN NOTE: SELF-EXPERIMENT
You can get a sense of the processes
involved in acquiring secondary emotions if you pause for a moment, close your
eyes, and recall a physical place---a house or room, perhaps---where you had
either a very happy or a very unhappy experience, perhaps in your childhood.
If, after a period of years, you recall this space, return to it, or perhaps
enter a space that reminds you of it, what do you feel? Can you sense subtle,
possibly flickering, changes in your body, perhaps small relaxings or tensings
of muscles, that accompany the feelings?
*********
The existence of learning processes
by which we accumulate secondary emotions are revealed by their disruption
in patients who have lesions or tumors in their frontal lobes, particularly
the right ventro-medial part. Their behavior is superficially normal most of
the time---intellect and memory seem intact---but motivation, foresight, goal
formation, and decision making are flawed. They are subject to bursts of immodest,
impolite, or other inappropriate behaviors; they act almost as though their
free will had been taken from them. Their emotions and feeling also are diminished.
Normal individuals, as well as
those with brain damage located outside the frontal lobes, generate skin responses
that indicate autonomic arousal when they are shown disturbing or erotically
charged pictures. Patients with frontal lobe damage fail to generate these
responses, in spite of realizing that the content of the pictures ought to
be disturbing. A typical response might be "I know I ought to react to
that, but I can't. I just don't feel anything." It is fascinating that
primary emotions (such as reacting fearfully to an angry face or an aggressive
growl) can still be intact, but emotions based on experience, cognition, and
learning are impaired. It is as though the link between frontal cortex and
limbic system, the link to feeling in the body, has been severed. The frontal
lobe patients appear no longer to be able to connect logic with good or bad.
They do endless cost-benefit analyses of simple issues, such as when to schedule
an appointment with the doctor, without being able to reach a decision. Their
choices do not appear to be informed by their emotional histories. The use
of their intelligence in the pursuit of a goal (deciding when to schedule that
appointment) has been compromised. This observation suggests that emotions
may be important in the selection of goals one at a time, so that they don't
conflict.
A consequence of being unable to
accumulate a feeling of the worth of different strategies during learning is
a myopia for the future. In a clever gambling experiment in which cards are
drawn from different decks for money or fines, normal patients begin to employ
an advantageous strategy before they actually realize what strategy works best.
They also generate an anticipatory skin conductance response if they ponder
a choice that turns out to be risky, before they know explicitly that it is
risky. Frontally damaged patients show no anticipatory responses to risky choices
and continue to choose disadvantageously even after they know the correct strategy. Patients
with large lesions elsewhere in the brain can learn to succeed in the gambling
game just as normal subjects do, even if they are aphasic and indicate that
they can make no sense of what is going on. Imaging experiments have now shown
increased activity in several frontal cortical regions that correlates with
learning reinforced by rewards. The implication of this finding is that reasons,
at least some of them, require emotions.
***************
DESIGN NOTE: IMPORTANT POINT
Our thinking recruits our bodies.
We don't plan for or anticipate futures unless we can link them with affect---with
memories and hunches from similar situations accumulated over our personal
histories.
***************
Lateral Organization of Emotions
Reason and emotions are contrasted
in our folk psychology, common-sense talk, and experience, and indeed they
can correspond to activities in different parts of the brain. Damage to the
right temporal area that is homologous to Wernicke's area in the left hemisphere
leads to disturbance in comprehending the emotional content of language, whereas
damage to the right frontal area homologous to Broca's area in the left leads
to difficulty in expressing emotional aspects of language. Disorders of affective
language, called aprosodias, can be classified as sensory, motor, and conduction
aprosodias in the same way that the aphasias that compromise syntax and grammar
are classified. Their anatomical organization mirrors the organization in the
left hemisphere. Thus patients with aphasia can show not only cognitive defects
in language but also defects in the affective components of language: intonation
of speech (prosody) and emotional gesturing. PET scans show that when a subject
is instructed to comprehend the meaning of words spoken in a foreign language,
blood flow to the left hemisphere increases, whereas flow to the right hemisphere
increases when the subject is asked to evaluate the emotional tone of the same
spoken passage. These patterns
of localization that form during development of a typical brain are not completely
predetermined, because, as we noted in Chapter 6, young children in whom the
left cerebral hemisphere is severely damaged or even removed early in life
can develop an essentially normal range of language functions.
A number of experiments show that
the left visual field (which projects to the left hemisphere) is superior at
correctly identifying faces, whereas the right visual field (projecting to
the right hemisphere) is better at perceiving facial expressions and emotions.
The left ear (projecting to the right hemisphere) is better at detecting the
emotional tones of voices, whereas the right is better at identifying their
content. Lesions in the temporal lobe and temporal lobe epilepsy can cause
a variety of emotional effects. Right temporal lobe lesions, as well as epileptic
foci, not only can destroy ability to understand the affective content of language
but also can trigger paranoia, anger, delusion, sexual feeling, déjà vu,
and hallucinations.
During happy affect, the left hemisphere,
particularly the frontal lobe, is more active than the right, and the opposite
is true during unhappy affect. Brain lesions in the left frontal area are more
likely to be associated with depression than similar lesions on the right.
Work of the psychologist Richard Davidson has shown that strong positive feelings
and approach behaviors correlate with left frontal lobe activation, whereas
withdrawal and fear correlate with right frontal activation. Imaging
studies are now showing in some detail the subareas within each hemisphere
whose activities correlate with appetitive, pleasant, or pleasurable emotions.
They can be distinguished from other areas whose activation correlates with
aversive, negative, or unpleasant emotions. Activation of the left frontal
lobe correlates with suppression of activity in the amygdala (discussed below),
which is central to fear responses. Facial behaviors of happiness or disgust
also correlate with the left/right frontal activation pattern. Emotional content
of sensory stimuli influences even the primary sensory areas of the brain,
for pictures with strong positive or negative affect cause significantly greater
activation of the visual cortical areas discussed in Chapter 8.
***************
DESIGN NOTE: IMPORTANT POINT
Stable individual differences in
the relative activation of the two hemispheres show a correlation with a person's
basic temperament, sense of well-being, and vulnerability to depression and
bad feelings. For each of us there may be a genetically determined set-point
for temperament, analogous to brain regulation of our body metabolism to maintain
a preset weight.
***************
Do you think there are differences
in the expression of emotions on each side of the body? Why is the smile of
the Mona Lisa perceived as ambiguous? She is smiling with only the left side
of her mouth, the part controlled by the right hemisphere, which is more active
during negative affect. Which
of the faces shown in Figure 10-3 do you perceive as happier or more pleasant?
Most people say the face on the right looks happier. It has its right lip,
controlled by the left hemisphere, curled upward. Facial expressions are not
always symmetrical but rather tend to emphasize the left side of the face. This
reflects the fact that the right hemisphere, controlling the left side of the
face, has a more pronounced influence than the left in controlling emotional
expression. This is true in humans as well as in other primates. Try
to test lateralization of your own expressions by doing the accompanying self-experiment.
Figure 10-3
Mirror-image faces. Which of these
faces looks happier to you?
*******
DESIGN NOTE: SELF-EXPERIMENT
You can experience lateralization
of your emotions firsthand with a few simple facial expressions. Try curling
up just the right side of your lips (controlled by left hemisphere). Does this
feel sort of like a smile? Now, curl up just the left side of your lips (controlled
by the right hemisphere). Most people report that it doesn't feel nearly as
friendly.
************
Emotional Responses Can Be More
Rapid Than Reasoned Ones
Why is it that we don't always
do what we think we should do? Why do our emotions seem to have minds of their
own? Recent findings have suggested an answer: Our emotions can use neural
networks different from those used for conscious reasoned responses, and they
can short-circuit those responses. This
may help to explain why we have so little reflective insight into our emotional
life.
Emotions are special-purpose organizers
that can perform rapid positive-negative evaluations of events below our consciousness;
they are rapid reaction systems especially useful for dealing with encounters
with other people. A person who resembles someone who once caused us anxiety
can trigger an immediate emotional response before rational thought cuts in.
Repeated exposure can decondition the anxiety. For example, subway commuters
who continually face strangers start to like best those whom they have seen
most frequently. Emotional responses seem to be front-line reactions that spring
quickly into place before rational deliberation has had time to function. They
reflect the read-out of an emotional memory that is the basis of preconscious
filters of the sort described in Chapter 8 for the visual system. These filters
can act on our perceptions to give a slight positive or negative affective
bias even to stimuli that superficially appear neutral. The building of our
emotional history might be described as the development of a large number of
somatic markers: correlated and rapid reactions of the visceral, somatic muscular,
and emotional brain pathways that have become linked to repetitive aspects
of our environment, both positive and negative. An
example is the lasting influence of persons we admired or feared in our early
childhood, causing us to react unconsciously (with attraction or withdrawal)
to people who have features reminiscent of those people we knew decades ago.
*******
DESIGN NOTE: SELF-EXPERIMENT
Pause for a moment and repeat the
word "lamujuva" to yourself several times. Now, do the same with
the word "rakachaka." Does one of these words seeming more pleasant
than the other? (Most English-speakers like the first and dislike the second.) This
suggests that the brain tags these percepts with a value, even though they
carry no explicit cognitive meaning. Indeed, the brain may assign a value to
virtually every perception.
************
Central Role of the Amygdala
The amygdala and hippocampus are
key structures in forming our emotional memories and in evaluating emotional
stimuli. Although the hippocampus
has long been implicated in emotion, the current view is that it is more involved
with cognition and learning than with emotion. The hippocampus would be involved
in recognizing a face, perhaps that of a cousin. The amygdala might add that
you really don't like him. The amygdala appears to be required for the acquisition
of conditioned autonomic responses to visual or auditory stimuli, but in the
absence of the hippocampus, it is not sufficient for recalling the declarative
knowledge relevant to those stimuli. The hippocampus, though required for the
acquisition of such declarative knowledge, cannot support the autonomic conditioning
in the absence of the amygdala.
The amygdala is a structure with
an interesting evolutionary history. Its interactions with the thalamus play
a major role in the mental life of fish, reptiles, and birds, whereas in mammals
it is increasingly relegated to more specialized functions. Neurons of the
amygdala show Pavlovian fear conditioning, and the whole structure plays a
central role in triggering aversive and fear reactions. Such
reactions can be triggered outside of our normal awareness if a fear-inducing
picture is flashed for a brief instant before a masking stimulus that we actually
perceive. We report nothing unusual, even though changes in skin conductance
that are characteristic of a fearful response are recorded. Imaging
studies show activation of the amygdala when human subjects encounter aversive
stimuli, during aversive conditioning,
and also in masking experiments. The storage of unpleasant memories associated
with aversive stimuli is apparently facilitated by sympathetic arousal, for
when human subjects are given propranolol (a drug that blocks the action of
adrenaline) during exposure to an unpleasant story with pictures, they are
less likely to remember the story than subjects who receive a placebo drug.
***************
DESIGN NOTE: IMPORTANT POINT
The amygdala enhances the storage
and persistence of emotional memories in a process that is facilitated by the
adrenaline released during stress.
***************
The amygdala sends projections
to all areas of the cortex, regulating an emotional bias of cognitive functions. In
fact, there are many more nerve cells sending information from the amygdala
to the cortex than from the cortex to the amygdala. This might be part of the
reason why emotions can be so persistent and refractory to cognitive control.
Its output is wired to parts of the brain needed to produce a panoply of fearful
behaviors: shortness of breath, jumpiness, tension, and diarrhea. Different
portions of the amygdala regulate different aspects of fear responses (such
as autonomic nervous system arousal, emotional behaviors, and the hypothalamic-pituitary
stress response). Each of these areas can be lesioned separately. (There
are so many different structural and functional units within what is usually
called the amygdala that some argue that it is misleading to refer to "the
amygdala" as a structural and functional unit.) There appears to be a
negative correlation between left prefrontal lobe activation and activation
in the amygdala, such that the relative suppression of left frontal activity
that correlates with withdrawal and depression goes with increased amygdala
activity. Fearful situations
that activate the amygdala can alter the intensity of conditioned responses. This
appears to be what happens when, in a tense or threatening situation, our reaction
to an unexpected noise is much greater than it would normally be.
***************
DESIGN NOTE: LONG SELF-EXPERIMENT
With a group of friends, you can
conduct a simple demonstration of how activation of fear by amygdala-related
mechanisms can influence our behavior. Start talking to the group about any
old topic and then, without warning, startle your listeners by suddenly making
a loud and unpleasant noise, such as slamming a book on a table. Then continue
with your talking. After a while, begin to tell a story that becomes increasingly
frightening. You might, for example, spin a tale of reading in the paper about
a homicidal inmate escaping from a local prison and then later, while reading
alone at night, hearing what sounded like someone trying to force an upstairs
window open . . . etc. Now, again without warning, repeat the unpleasant noise
you made previously and note whether the intensity of your friends' startle
reaction has increased and whether they report this to have happened. (This
exercise has to be done with some skill so that your friends don't figure out
ahead of time what you are up to!)
***************
We all seem to have a "negative-making
or fear-making system" that can run semi-autonomously, the amygdala being
a sort of "command central" that can program our overall emotional
bias toward being apprehensive or anxious. We could view the arousal of this
system, as happens during the period of heightened excitability that follows
a sudden fright, essentially as "an amygdala attack." Its opponent
would be a "positive-making system" that correlates with enhanced
left frontal activity that can suppress the negative system and generate positive
appetitive behavior. Test the idea of two such systems against your daily experience.
Does the metaphor of "positive-making" or "negative-making" machines
inside you, sometimes uncoupled from the input that may have initiated them
but still biasing your reactions and decisions, make sense to you?
It is interesting that the amygdala
of humans is more fully formed at birth than the hippocampus and develops more
rapidly, such that fear behaviors are fully developed by 7--12 months. This
may be why we remember essentially nothing from our first 2 years of life but
apparently retain emotional experiences. It may also explain why these experiences,
which psychoanalysts have long pointed to as a key to later emotional life,
are so potent and so difficult to understand rationally. Behavioral and drug
studies on monkeys have shown that corresponding fear behaviors appear at 9--12
weeks after birth, along with a peak of synapse formation in the prefrontal
cortex and limbic system, including the amygdala.
Joseph LeDoux and his collaborators
have done a series of fascinating experiments to demonstrate that the amygdala
can trigger emotional reactions before the cortex has fully processed the triggering
input. Previous experiments
had shown that damaging part of the amygdala can abolish learned fear responses.
In one set of studies, rats were trained to fear a flashing light by having
the light paired with a shock. In normal rats, the fear response is extinguished
if the light is displayed regularly without the shock. This process takes several
weeks. If the visual cortex is removed, rats still learn to fear the lights,
but when shown the lights without the shock for several weeks, they retain
fearfulness, unlike rats with intact cortexes. The idea is that once it is
established, an emotional aversion is permanent, but the cortex can learn to
dilute that aversion by inhibiting the amygdala's response. The pathways suggested
by LeDoux's experiment are summarized in Figure 10-4.
Figure 10-4
A schematic drawing of relationships
among the thalamus, amygdala, and cortex. Sensory input via the thalamus to
the amygdala permits crude identification of potentially significant features
of the environment and rapid reaction to them. More careful identification
of the stimulus uses slower cortical circuits. Adapted from LeDoux' The Emotional
Brain.
One possible explanation for post-traumatic
stress disorder is that this cortical inhibition has been impaired. This model
may explain how phobias are formed in humans and why they can be so tenacious.
For a Vietnam veteran suffering from post-traumatic stress disorder, a clap
of thunder may evoke the sweating and pounding heart he experienced during
a battle. In people who have
unlearned a phobia, a single scary experience can sometimes bring it back in
full force. This suggests that the phobia has not been lost to emotional memory,
even though the behavior has been extinguished under most conditions.
The amygdala is just one synapse
away from the thalamus, whereas the hippocampus is several additional synapses
away. That means it takes a sensory signal as much as 40 milliseconds longer
to reach the hippocampus than to reach the amygdala. That time gap allows the
amygdala to respond to an alarming situation before the hippocampus does. When
out of the corner of your eye you see what looks like a snake, it is the amygdala
that sends the signal of alarm that makes you jump. You react even before the
hippocampus has had time to coordinate figuring out, in consultation with other
parts of the cortex, whether what you saw was actually a snake or a piece of
rope. The amygdala appears to be a central part of the rapidly acting pathway
that tags many words and images with positive or negative affect before they
reach awareness.
***************
DESIGN NOTE: IMPORTANT POINT
Experiments done on rat brains
reveal a neural basis for reacting to something emotionally faster than we
can think. Nerve pathways through the amygdala that short-cut or bypass slower
cortical circuits follow the "better to be safe than sorry" principle
and presumably, given that they exist in all unimpaired present-day members
of our species, made the difference between life and death for our ancestors.
***************
Perception of Emotional and Cognitive
Pathways
Because cognition and emotion emphasize
different pathways, we might expect that their relative timing could be varied,
with emotion occurring before or after thought. For example, we might recall
a mental image of a snake and then, immediately afterward, the feelings that
go with it, or we might notice a long, thin, sinuous object and have an aversive
feeling before we note whether it is a snake or not. Try the accompanying self-experiment
to examine the timing of your thoughts and emotions.
*********
DESIGN NOTE: SELF-EXPERIMENT
This simple exercise might permit
you to experience dissociation of feelings and cognition in yourself. It would
be best to ask a friend to read these instructions to you, but again, you should
be able to do the exercise by yourself: Sit comfortably, close your eyes, breathe
gently, and attend to the breathing. Notice, but do not hold onto, thoughts
that pass through your mind. Let thoughts enter your mind as easily as they
go, but always gently return to being aware of your breathing. Next, notice
the thoughts that arise and are accompanied by positive or negative feelings.
When do you notice the thought, perhaps an image of a person or social situation,
and when do you notice the feeling that goes with it? Do they arrive separately
or together?
***********
The purpose of the self-experiment
is for you to experience associating spontaneous thoughts or images with affect
on a time scale of 100--300 milliseconds. This is the time scale of the flickering
of thoughts and the somatic markers that go with them. You may have noticed
that when an image spontaneously occurs in your mind, your awareness of the
cognitive content of the image (such as the identity or visualization of a
face, or the relationships of a social context) occurs slightly before you
experience the emotion usually associated with that image. This fact is used
in cognitive therapy and disciplines such as Buddhist mindfulness meditation
to permit dissociation of an image from the affect normally associated with
the image. It is during the first milliseconds of connecting images and affect
(particularly the negative affect of feeling threatened, afraid, or powerless),
that self-awareness might intervene to present other options. After this window
has closed, negative affect usually becomes harder to dislodge as it reinforces
itself through other associations.
If we calm down and pay quiet attention
to what is going on in our heads, we can experience many fascinating phenomena
that reveal how the brain works over tenth-of-a-second intervals. Chapter 12
describes several experiments that demonstrate that the brain can rearrange
time and space in the period of 50--400 milliseconds after an external or internal
visual image is initiated. This is also the time frame of the exercises on
initiating motor patterns that we tried in Chapter 9.
Up to this point, we have mentioned
an array of balancing systems---sympathetic and parasympathetic, brainstem
spritzers, right frontal and left frontal plus amygdala activation---that all
contribute to the formation of our background emotions or predispositions.
To these systems, we must add the systems that mark images and ideas from our
emotional histories with limbic, visceral, and muscular correlates to form
an array of somatic markers. These markers are elicited as recurring situations
are encountered, and they can act as little filters or machines inside our
head---autopilots that sometimes can take a neutral event and put a positive
or negative spin on it. Such largely unconscious mechanisms can attach small
quantities of emotional energy to ongoing events, determining, when someone
cancels a lunch with us, whether we think "she doesn't like me," or "he
must be very busy," or determining, when we confront a challenge, whether
our immediate reaction is "I can't do it" or "I can do it."
We are also endowed with an amazing
kind of cognition, exercised in the self-experiment, that can gain some awareness
of these lower processes going on. This awareness of thinking, or thinking
about thinking, is sometimes called metacognition. It is a limited ability
to sense and review the vast number of rapidly acting autopilots that have
assembled during our development. We couldn't live without these automatic
routines. We don't reinvent the wheel each time we encounter a familiar situation;
rather, we reserve our higher cortical resources for dealing with what seems
novel. Still, when the underground routines are not working, our higher faculties
can be used to sense, tinker with, and possibly alter them.
Modern cognitive therapies represents
a very practical application of this ability. We have already made reference,
in Chapter 3 (in the section "Imaging the Activity of the Brain"),
to patients with obsessive-compulsive disorder (the behaviors exhibited may
include excessive hand washing or ritualistic counting and checking). Some
have learned to control their behavior by thinking, when they feel the initial
emotional urge, "That isn't me. That is a part of my brain that is not
working." Or "That feeling is just the result of a false message
from my brain." As the aberrant behavior diminishes, the same decreases
in frontal lobe activity that are observed during effective drug therapy occur.
What is being developed here is the literal equivalent of a mental immune system.
Just as we acquire an immune history---knowledge of pathogens that have invaded
our system and that now can be quickly expunged if they appear again---so we
can acquire a history of maladaptive emotional routines. The analog of the
macrophage or T cell is a trained recognition mechanism that has become very
sensitive to the onset of these states and can trigger cognitive procedures
that essentially excise them, as soon as they are detected, by activating more
functional routines.
*********
DESIGN NOTE: IMPORTANT POINT
The use of cognitive therapy techniques
to reduce inappropriate emotional behaviors and actually change brain activation
patterns provides an example of how consciousness can play a role in regulating
brain physiology.
***********
Facial Musculature and the Communication
of Emotions
Having delved in some detail into
the internal mechanisms that regulate our emotional life, let's draw back to
consider some social aspects of emotions and the central role played by faces
and facial expressions. The amygdala is a key player in the interpretation
of expressions that communicate emotions. It receives information from various
areas of the visual cortex, particularly the portion of the inferior temporal
cortex that contains face-responsive neurons. It also sends information back
to all these areas---a possible means by which affective states could modulate
sensory processing. This could
be part of the explanation for the biasing of perception by emotions that many
psychological studies have revealed. Subjects
with bilateral amygdala damage are much less discerning in their judgment of
other faces. Recent studies have shown that the amygdala can be activated by
the masked presentation of emotional facial expressions. When a subject is
shown a fearful or angry face for about 30 milliseconds, followed by a neutral
face for 170 milliseconds, only the neutral face is remembered or reported,
but brain imaging reveals an increase in activation of the right amygdala that
is not observed when the 30-millisecond exposure is to a happy or neutral face.
Interestingly, conscious aversive conditioning to an angry face paired with
a burst of unpleasant noise correlates with activation of the left amygdala.
These systems originate far back
in our vertebrate lineage. We don't hesitate much in interpreting the facial
expressions that dogs and cats use to communicate anger, fear, or pleasure.
The same can be said, with a bit less clarity, of many higher mammals. Nonhuman
primates have facial expressions and meanings that are less subtle than our
own but that seem obviously similar. We observe a dramatic increase in the
complexity of facial musculature and expressions in moving from monkeys to
apes to humans. Increasingly, the face is turned into a kind of semaphore,
signaling complex social interactions. As we noted in Chapter 5, the use of
facial and vocal muscles in communication was a component of the development
of the mimetic intelligence that is thought to have provided the foundation
for the appearance of modern language and mythic intelligence.
***************
DESIGN NOTE: IMPORTANT POINT
During hominid evolution, the increasing
number and complexity of facial muscles supported the development of an array
of emotional expressions that is universal across modern cultures. The amygdala
plays a central role in both interpreting and orchestrating the response to
these expressions.
***************
We all know from our daily lives
that our emotions correlate with, and are communicated by, a complex set of
facial muscle signals. These signals are only one of several parallel layers
of the kinesic communication (body language) that is occurring as we talk with
others. This is presumably why more brain area is devoted to facial musculature
than to any other surface of the body. These areas direct stereotyped combinations
of muscle contractions to denote surprise, fear, disgust, happiness, and grief. Darwin
noted the universality of these patterns---how all people, from Oxford dons
to Australian aborigines, express grief by contracting their facial muscles
in the same way. Flirting signals
too are the same across cultures: a lowering of the eyelids or the head, followed
by direct eye contact.
The most telling experiments involve
the presentation of photographs of Western faces showing basic emotions to
New Guinea natives who have lived for millennia in isolation from all other
humans except their immediate tribe. Studies conducted on three such isolated
primitive cultures show Western faces to Stone Age people, and vice versa,
with the same results. The
same stereotyped sets of muscle contractions are used by all. The psychologist
Paul Ekman has cataloged 80 different facial muscles used in communication.
These muscles can be trained separately to reconstruct emotional expressions,
and each expression can be specified as a list of relevant muscle contractions
or relaxations. Some of the named muscle sets for different emotions are cross-cultural,
others culture-specific.
What about the changes we feel
in our bodies as our faces are smiling and relaxed, or fearful and tense? Fear
is sometimes correlated with mobilization of the sympathetic nervous system;
happiness is more likely to be associated with parasympathetic activation.
Are the parts of our cortex that drive facial muscles also directing the autonomic
correlates of the facial expression? Or is some sort of feedback from the facial
muscles responsible for autonomic changes? Davidson and Ekman, mentioned above,
have addressed this issue in an interesting experiment on smiling. We
all can recognize fake smiles, often used in deception, and we are fairly acute
observers of the muscles involved. The difference is that the real smile that
reflects happiness or joy involves not only the zygomatic major muscles which
reach down from the cheekbones and attach to the corners of the lips, but also
movement of the lateral part of the muscle (the orbicularis oculi) that encircles
the eyes (making "crow's feet" at the corner of the eye). Electrical
measurements show that when subjects are instructed to contract both of these
muscles (but are not instructed to feel happy), the left frontal lobe becomes
more active, just as in people who are experiencing positive emotions. This
presumably accounts for the effectiveness of a form of therapy against depression:
instructing the depressed person to move the muscles that make a smile. Doing
so causes a lightening of underlying mood.
These are fundamentally important
experiments, because they show that an emotional facial expression is not just
a unidirectional command from the emotional centers of the brain to the face
muscles, but rather that the facial expressions are part of a neural network
in which activating one node (voluntarily activating the smiling muscles) can
activate another node (the neural correlates of positive affect in the left
frontal lobe). Recent experiments show that facial expressions of sadness,
fear, and anger are similarly correlated with autonomic changes measured by
skin conductance as well as with brain activation patterns measured by magnetic
resonance imaging.
********
DESIGN NOTE: LONG SELF-EXPERIMENT
You can do a simple exercise on
yourself to appreciate the relationship between facial musculature and emotions.
Pause in your reading right now, slow down, and pay attention to your breathing
for 20--30 seconds. Now, recall an experience that made you very happy, perhaps
with a friend or lover---something you really enjoyed, maybe it made you laugh
or smile; take a moment to get into that and try to relive the emotion you
felt. Now, don't smile; make your face absolutely flat. What does this do to
the feeling? Is it harder to hold on to? Can you feel a whole muscle set that
goes with the internal feeling of emotion? Is it possible to separate them?
Let's try just one more. This time, think of something that made or makes you
angry, maybe another person you are angry at. Imagine confronting the situation
or person. Let yourself feel really angry, maybe wanting to strike out. Now,
stop contracting and tensing your face; let it go flat. What happens to the
angry feeling? Again, can you feel the correlation? Now, try to smile and feel
angry at the same time.
**********
Misapplication of Ancestral Emotions---The
Chronic Stress Response
What is the characteristic configuration
of our autonomic nervous system and its correlated emotions? --for many of
us living in modern industrial societies, it's not a very healthy one: chronic
activation of a sympathetic nervous system designed for use only in episodic
emergencies. This point deserves some elaboration. Each of us is blessed with
an emotional repertoire controlling the four F's mentioned in Chapter 3 (fighting,
fleeing, feeding, fornicating). These systems have evolved progressively through
our vertebrate lineage up to our adaptations to the life of hunter-gatherers
in the Paleolithic. The problem is that we frequently employ them in ways that
are inappropriate in our contemporary surroundings. Many of us in complex high-tech
and fast-paced societies chronically activate the stress response, rather than
reserving it for genuine life-threatening emergencies. The endocrinologist
Robert Sapolsky points out that we don't have the common sense of zebras, who
don't get ulcers: They have a better handle on when to chill out (while grazing
on grass) and when to go into high-gear stress (when the lion appears). Our
physiological response mechanisms are superbly adapted for short-term emergencies,
but our bodies are not built to sustain their long-term activation. The things
that work for short-term emergencies, getting fuel rapidly from storage sites
and inhibiting further energy storage, are debilitating in the long run. Suppressing
immune function in the short term, for example, allows the energy required
to be used elsewhere, but in the long run, it makes us more susceptible to
infections and cancer.
Our stress response recruits a
diverse array of hormones, but it can be described in a simple way as occurring
in two waves (see Figure 10-5). Within seconds of our encountering a stressor,
cells in the hypothalamus cause activation of the sympathetic nervous system,
and catecholamines (epinephrine and norepinephrine) are released by both sympathetic
nerves and the adrenal gland. These act to mobilize the viscera and muscle
for quick action. These amines also activate the amygdala, which is central
in orchestrating the behavioral reactions to a stressful event, but their prolonged
release in prefrontal cortex can cause cognitive dysfunction. As a further
reaction to a stressful thought or event, on the time scale of minutes, our
hypothalamus releases corticotropin-releasing factor. This triggers ACTH (corticotropin)
release from the pituitary, and ACTH moves through the blood stream to the
adrenal gland, where it triggers release of glucocorticoids that stimulate
glucose metabolism and suppress immune function. (It is worth mentioning that
there can be another, opposite kind of reaction to stress and challenges: Parasympathetic
rather than sympathetic overactivation can lead to a "freezing" sort
of reaction that slows the heart, shutting down the body rather than mobilizing
it. Such a slowing down may underlie a striking phenomenon observed in some
Stone Age cultures: Individuals who have been have cursed or ostracized by
their group become increasing immobile and eventually die.)
***************
DESIGN NOTE: IMPORTANT POINT
Chronic sympathetic activation
and glucocorticoid release have a large number of deleterious effects. A partial
list includes immune suppression, atherosclerosis, digestive disorders, and
accelerated aging and death of nerve cells in the hippocampus and temporal
lobes. Stress also is known to cause decreases in levels of the neurotransmitter
acetylcholine in the cortex and hippocampus, impairing learning and memory.
***************
Figure 10-5
Stages of the stress response.
Within seconds of the onset of a stressful event, norepinephrine and epinephrine
(also called noradrenaline and adrenaline) are released by sympathetic nerve
endings and the interior portion of the adrenal gland (the adrenal medulla).
These chemicals enhance the readiness and excitability of both nerve and muscle
tissue. More slowly, ACTH is released into the blood stream by the pituitary
gland and carried to the adrenal cortex, where it triggers the release of glucocorticoids
that stimulate metabolism.
The nervous, endocrine, and immune
systems form a complex network that shares hormone and neurotransmitter molecules. Interactions
within this network are the focus of the new field of psychoneuroimmunology.
A class of peptides used as neurotransmitters is also used in signaling by
cells of the immune system. Nerve cell endings in the skin can secrete chemicals
that shut down the immune system nearby. This
may partly explain why diseases such as psoriasis are exacerbated by stress.
Prolonged exposure to stress hormones causes death of immune system cells and
atrophy of neuronal connections in the hippocampus, leading to decay in memory
and cognitive functions. Prolonged
depression is correlated with decreases in the volume of the hippocampus and
the amygdala. The molecular
mechanisms by which glucocorticoids can block immune system activation are
being unraveled. Stress also
decreases production of a trophic factor called brain-derived neurotrophic
factor (BDNF), which neurons use to protect themselves from damage. A
further array of exotic compounds, whose description is well beyond the scope
of this book (cytokines, interleukins, tumor necrosis factor, and so on), come
into play as internal mood and beliefs confront external disease vectors and
social tensions. An increased ratio of the right/left frontal lobe activation
mentioned above as being associated with withdrawal and depression also correlates
with immune suppression.
Interactions among the nervous,
endocrine, and immune systems are not just of a negative sort. There is clear
evidence that people who have a positive outlook and are confident of overcoming
stressful barriers have higher blood levels of the T cells and natural killer
cells that correlate with robust immune function. Some quite remarkable cases
of mood- or belief-caused remission of the symptoms of illnesses such as cancer,
arthritis, asthma, and acute depression have been documented. In many of these
cases, a sham treatment called a placebo (Latin for "I shall please")
is administered; it is believed by the patient to be an effective drug or therapy.
A brightly colored pill containing sugar, a doctor in a white coat with a stethoscope,
a shaman wearing a feather head dress---all can apparently induce a patient's
immune system to respond to a disease crisis. Several experiments have paired
an actual therapy, such as an asthma medicine, with an arbitrary pleasant flavor
such as vanilla. Subsequent administration of the flavor alone can cause a
significant increase in lung function. All of these examples indicate that
expectancy---what the brain is telling the body it expects to happen---has
a powerful effect on the actual outcome. The mind-body connection reaches down
to the intricate details of our immune system biochemistry.
The endocrinologist Robert Sapolsky
has conducted some fascinating studies on social roles, stress, and corticosteroid
levels in baboon tribes in the Serengeti. Like
humans, these animals have to spend only a few hours a day gathering food and
devote the rest of their time to driving each other crazy with elaborate social
competitions. Measurements of physiological and hormonal changes relevant to
stress show that virtually all of them are functions of rank. But it turns
out on closer examination that rank is a less relevant variable than the baboon's "personality
style." Those individuals who are best at telling the difference between
threatening and neutral interactions, and who know clearly whether they won
or lost, have the lowest glucocorticoid levels. It also helps, if you lose,
to have somebody to take out your frustrations on. A second major factor in
lowering corticoid levels is developing friendships. Does this sound familiar?
Studies on humans yield the same results. And, as in humans, the animals who
get agitated even when they see a rival at a safe distance are the ones that
show hormonal correlates of stress.
*******
DESIGN NOTE: SELF-EXPERIMENT
Try another simple exercise on
yourself. Close your eyes, breathe, and relax for just a few moments. Now,
imagine that you suddenly see a car about to hit you. You are terrified and
want to get away fast! Freeze your body right there. What muscles are tense?
Your neck? Your back? These are the muscles involved in the startle response.
This response takes about half a second, starting in the upper trapezius and
sternocleidomastoid muscles and passing down the body. The curious thing is
that the startle response is an extreme version of the slightly hunched-down "normal" postures
that most of us display. Consider the possibility that the cacophony of input
that we humans must put up with in this culture leaves many of us partially
frozen in a startle response, or low-level anxiety. The sympathetic nervous
system would be chronically activated, rather than being reserved for emergencies. Back
extensor muscles would be chronically overcontracted and front flexor muscles
underused.
*********
Our physiology clearly depends
in part on our social context and can change with it. Social threats to our
character have as a correlate threats to our integrated physiology. The effect
of the social environment on stress extrapolates to susceptibility to, and
recovery from, disease. An
extensive literature documents correlations between resistance to disease and
social class, stress, social support, and the belief system of the individual.
Stress and isolation correlate with reduced life spans. Studies
on communities of macaque monkeys and surveys on human communities show that
close relationships buffer the immune system. Support systems that allow individuals
to take life's ups and downs in stride enhance immune function and longevity.
Depression, loss of status, or a sense of helplessness in an individual correlates
with suppression of immune function. Our feelings of control versus helplessness
exert a "top-down" control on our intimate biochemistry and neurophysiology.
Comparison of subjects facing the same stressor shows that those who feel they
have some control over the situation have lower cortisol levels than those
who feel helpless. In short, there is a feedback loop between our social lives
and our physiology. Our biological function is in a symbiotic relationship
with our culture and society.
Summary
This chapter has chronicled several
different aspects of the ill-defined array of experiences that we refer to
as our emotions. Their roots lie much deeper in our evolutionary past than
such recent inventions as language, and their link to our autonomic physiology---heart
rate, skin gland regulation, and the like---distinguishes them from our "higher" functions
of abstract and analytic thought. These higher functions, however, can be decisively
biased by chemical modulators of emotion, originating in lower regions of the
brain, that are released diffusely across the cortex. It appears that the vast
array of values, hunches, inclinations, and rules that guide our selection
of current actions from an array of options is programmed during our development
by an interaction between higher and lower centers, as the more primitive circuits
are recruited to assign different feelings or values to contexts that have
been repeatedly encountered. These assessments then can work more rapidly than
our self conscious cognitive processes to size up people or contexts that we
encounter, as occurs when instantly (and, as it would seem, irrationally) we
like or dislike someone we meet. They also can go to the extreme of becoming
pathology, as in post-traumatic stress syndrome and obsessive-compulsive disorder.
In both normal and abnormal circumstances, introspection techniques that enhance
awareness of the distinction between emotional and self-conscious cognitive
pathways in the brain can sometimes provide a useful tool for understanding
or modifying one's behaviors. A maladaptive intrusion of our ancient emotional
repertoire, causing damage that can include the immune system and brain, occurs
if the stresses of daily modern life are permitted to activate chronically
a nervous and endocrine stress system that evolved to deal with short-term
life-and-death situations.
Our emotional minds, with their
useful and their less useful elements, form another component of the mosaic
of our modern minds, along with those outlined in previous chapters on plasticity,
perception, and action. Now we are ready to tackle an issue distinctive to
our human species: How is it that we are able to read and speak the words flowing
past on this page? How do we acquire the faculty of language, the most important
feature distinguishing us from the rest of the animal world?
Questions for Thought
1. Making a basic category of "the
emotions" or coining terms such as "affective neuroscience" is
a common-sense way of organizing descriptions of our experience, but it could
be argued that these categories don't really correspond to fundamental entities---that
emotions essentially are cognitions. Like a wide array of our sensory and motor
behaviors, they reflect an analysis of some input to the organism that results
in a behavior relevant to survival. Do you think emotions deserve description
as a separate category? If so, why?
2. We could say that the main locus
of linguistic cognition is our cerebral neocortex, the most recently evolved
portion of our brain. How does this contrast with the location of the operations
association with the emotions?
3. The psychologist Steven Pinker
suggests that our lack of voluntary control over our emotions, and their link
to basic physiological processes, are an evolutionary adaptations with a social
purpose: to enhance the credibility of human social interchanges and make deception
more difficult. Could such an idea be proved? Could there be other explanations?
4. Given the fact that many of
our rapid and almost reflexive emotional behaviors can sometimes sabotage our
effective performance in private and social contexts, do you think we would
all be better off without these evolutionary vestiges of a former age---more
like Dr. Spock of the television "Star Trek" series. If not, why
not?
Suggestions for further general
reading
Goleman, D. 1995. Emotional Intelligence.
New York: Bantam. This best-selling book describes the mechanism and consequences
of various kinds of "emotional hijacking." It also discusses the
varieties and definitions of emotions.
Damasio, A.R. 1994. Descartes'
Error---Emotion, Reason, and the Human Brain. New York: Putnam's. A stimulating
discussion of how rational mind is built on top of emotional mind. This chapter
draws heavily on Damasio's ideas about the origins of rational mind in emotional
mind, adopts his distinction of primary and secondary emotions, and makes use
of his concept of "somatic markers."
LeDoux, J. 1996. The Emotional
Brain. New York: Simon & Schuster. In this book LeDoux, whose work is the
basis of Figure 10-4, focuses on the neural mechanisms of fear.
Pinker, S. 1997. How the Mind Works.
New York: Norton. In Chapter 6 of this book, Pinker discusses emotions from
the perspective of evolutionary psychology and speculates that emotions are
guarantors of the authenticity of our actions.
Sapolsky, R.M. 1994. Why Zebras
Don't Get Ulcers: A Guide to Stress, Stress-Related Diseases, and Coping. New
York:W.H. Freeman. This engaging book gives a fascinating summary of how body
systems designed for episodically dealing with life-threatening stress can
be chronically activated, with debilitating results.
Reading on more advanced or specialized
topics
Panksepp, J. 1998. Affective Neuroscience.
The Foundations of Human and Animal Emotions. New York: Oxford University Press.
This is a textbook on the psychology and physiology of emotions.
Bear, M., Connors, B., & Paradiso,
M. 1996. Neuroscience: Exploring the Brain. Baltimore, MD: Williams & Wilkins.
Chapters 15 and 16 of this book describe the brain areas involved in modulating
emotional behavior.
Davidson, R.J., & Sutton, S.K.
1995. Affective neuroscience: the emergence of a discipline. Current Opinion
in Neurobiology 5:217--224. This is a more technical but very accessible review
of brain mechanisms regulating emotions.
Pitkänen, A., Savander, V., & LeDoux,
J.E. 1997. Organization of intra-amygdaloid circuitries in the rat: an emerging
framework for understanding functions of the amygdala. Trends in Neurosciences
20:517--523.
Ekman, P., Davidson, R.J. 1993.
Voluntary smiling changes regional brain activity. Psycholocial Science 4:342--345.
An interesting experiment showing that brain activities for "fake" and "real" smiles
are different, just as the facial muscle contractions are.
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