Welcome to Your Brain (21 page)

instead of a logic puzzle, the result needs to be a coherent story that isn’t strictly sensible in

everyday terms. Some patients with damage to the frontal lobe of the brain, particularly on

the right side, don’t get jokes at all. Typically this is because they have trouble with the

reinterpretation stage of the process. For instance, given a joke with a choice of punchlines,

they can’t tell which one would be funny. Laughter or feelings of amusement have been

evoked in epileptic patients by stimulation of the prefrontal cortex or the lower part of

temporal cortex. Functional imaging studies show that the orbital and medial prefrontal

cortex are active when people get a joke. Since humor includes both emotional and

cognitive components, it makes sense that these prefrontal regions, which integrate the two

functions, would be involved.

Humor also makes people feel good, apparently by activating the brain reward areas

that respond to other pleasures like food and sex, as we discuss in
Chapter 18.
Especially

when coupled with surprise, a sense of pleasure can trigger laughter. Indeed, laughter may

be an ancestral signal that a situation that seems dangerous is actually safe. Multiple types

of humor activate areas that respond to emotional stimuli, like the amygdala, midbrain,

anterior cingulate cortex, and insular cortex. The last two regions are also active in

situations of uncertainty or incongruity, so they may participate in the reinterpretation stage

of getting a joke. The funnier a person thinks a joke is, the more active these areas (and the

reward regions) are.

Humor’s rewards go beyond simply feeling good. Being talented at making other people

laugh can improve all sorts of social interactions, helping you to find a mate or

communicate your ideas effectively. Humor also reduces the effects of stress on the heart,

immune system, and hormones. So if you’re the kind of person who tends to be amused by

things that other people don’t find funny, remember that you’re likely to get the last laugh.

Reappraisal seems to rely on the prefrontal cortex and anterior cingulate cortex. In imaging

studies, people attempting to reinterpret emotional stimuli show activation of these regions.

Successful reappraisal results in changes in other emotion-related brain areas that are consistent with

outward emotional changes, such as a decrease in amygdala activity when someone reappraises a

stimulus to make it seem less scary. These brain changes are strikingly similar to the activity patterns

in response to a placebo drug, another example of how people can experience an identical situation in

different ways depending on their individual beliefs.

People who are good at reappraisal tend to be emotionally stable and resilient. Many of the gains

that people make in psychotherapy can probably be attributed to improvements in their ability to

reappraise situations in productive ways. In general, as mammals with a big frontal cortex, we are in

a good position to train our emotional responses. Reappraisal, unlike most mental capacities,

improves with age, perhaps as a consequence of maturation of the prefrontal cortex, or maybe just

from practice. This may explain why mature adults tend to be happier and experience fewer negative

emotions than young adults.

So the next time someone says, “Don’t be so emotional,” you’ll know better. Your emotions—

both pleasant and unpleasant—provide a sensitive guide to effective behavior, helping you to predict

the likely consequences of your actions when you don’t have enough information to decide logically.

Go ahead and be emotional. As long as your emotion regulation system is in good working order, it’s

likely to be the right choice.

Humor can be dissected as a frog can, but the thing dies in the process and the innards

are discouraging to any but the pure scientific mind.

—E. B. White

Chapter 17

Did I Pack Everything? Anxiety

We’re not trying to make you nervous, but the truth is that being too relaxed can kill you. In a

world filled with hazards, worrying can offer big advantages for survival. Of course it is possible to

worry too much—for instance, if you’re a badger who’s too fearful to leave his den to find food or a

mate. It’s also possible to worry about the wrong things, as when a person develops a phobia that

turns entering a dinner party into a heart-poundingly scary experience. On the whole, though, anxiety

serves many useful purposes, and not just in leading us to exercise caution in the face of danger.

Anxiety also motivates positive behaviors, from finishing an assignment before the deadline to storing

enough food to get through the winter. Ironically, emotions that make us feel bad often cause us to

behave in ways that are good for us, which is why they have become so common.

Although everyone experiences anxiety sometimes, people (and other animals) show individual

differences in how easily their anxiety is triggered, how intense it is, and how long it lasts. Some of

these individual differences are due to our genes. Having a relative with panic disorder (discussed

below), for example, increases your risk of developing the disorder by a factor of about five.

Myth: The car-crash effect

People often report that during a sudden dangerous event, such as an automobile crash,

time seems to slow down. Afterward, they say they were able to evaluate the situation,

consider alternatives, and take evasive action in a matter of moments. Such an ability

would clearly confer a tremendous survival advantage.

In a sense, time does slow down under stress—or, more accurately, people perceive it

to slow down. To test performance speed during fear, researchers used a very exciting but

harmless scenario, an amusement park ride. The ride in question is a free-fall experience in

which helmeted participants are dropped one hundred feet into a waiting net.

To measure perceptual speed during the fall, the researchers mounted a small video

monitor on the wrists of participants. On the screen was a sequence of rapidly changing

images of a letter or number (for instance, a black 1 against a white background) alternating

rapidly with a canceling image (a white 1 against a black background). They sped up the

images just enough so that under normal conditions, participants saw only a uniformly gray

screen. Then they dropped the participants from the edge, instructing them to keep their eyes

on the monitor.

The falling participants did not perceive the digits with any better accuracy than

participants who performed the same task with their two feet planted firmly on the ground.

Thus, temporal perception did not improve, even though participants believed the fall to

last much longer than it actually did. In separate measures, participants estimated their own

fall to last 36 percent longer than others’ falls.

These results indicate that there are separate mechanisms underlying duration judgments

and temporal resolution. Even though you might think that an event took a long time, you

cannot become like Neo in
The Matrix
, seeing the world in “bullet time.” In dangerous

situations, one possibility is that neurotransmitters, such as adrenaline, cause memories to

be laid down more richly in a given period of time without a speed-up in sensory

processing. A remaining question is how to measure whether mental processing is faster

during very exciting moments. Bungee-jumping and Sudoku, anyone?

Genes not only control baseline anxiety levels but can also determine our sensitivity to life

stressors, such as child abuse, the death of a parent, or divorce. People with the protective variant of

a particular gene, for instance, can handle a lot of tough events with little chance of getting an anxiety

disorder or depression as a consequence. This gene encodes the serotonin transporter, which removes

the neurotransmitter serotonin from the synapse after it has done its job. People with the vulnerable

variant of the gene are more sensitive to stress, but they can get along fine if nothing too bad happens

in their lives. People with one copy of each variant (because we all have two copies of every gene,

as you may recall from high school science) fall somewhere in the middle. They can handle one bad

event, but multiple bad events may send them over the edge into depression or an anxiety disorder.

The only thing we have to fear is fear itself.

— Franklin D. Roosevelt

Anxiety disorders are the most common type of psychiatric disorder in the U.S., affecting about

forty million people. As many as 90 percent of people with anxiety disorders also have clinical

depression at some point in their lives, and many of the same treatments are effective for both

problems. For example, selective serotonin reuptake inhibitors like Prozac, which are commonly

used to treat depression, also work well for anxiety disorders. This overlap suggests that the brain

mechanisms that cause depression and anxiety may be similar, though the origin of abnormal anxiety

is better understood.

As we have already said (see chapters 13 and 16), damaging the amygdala interferes with fear

responses and fear learning in humans and other animals. Stimulating the amygdala produces fear

responses in animals. You don’t need a brain scanner to tell you when your amygdala is active: it’s

happening when your heart races and your palms get sweaty. Your blood pressure also goes up, and,

in extreme cases, you may find it hard to breathe. These symptoms occur because the amygdala has a

direct connection to the hypothalamus, which controls the body’s stress responses. Amygdala activity

leads to activation of the sympathetic nervous system (the fight-or-flight response) and release of

glucocorticoid stress hormones. People who experience intense and acute onset of these symptoms

are said to have panic attacks, a type of anxiety disorder that can produce symptoms so overwhelming

that people believe they’re about to die.

An overactive amygdala probably causes some anxiety disorders. Other patients seem to have

normal amygdala responses. Instead, they have a problem with the prefrontal cortex, which is

responsible for turning off anxiety when it’s not appropriate for the situation. The amygdala receives

input directly from the senses, so its responses are designed to be fast, not accurate. Often, further

analysis by a more careful part of the brain leads to the realization that there’s nothing to fear. (You

thought you saw a snake, but it turns out to be a branch swaying in the breeze.) The prefrontal cortex

then inhibits the amygdala, shutting down the anxiety. If this process isn’t working correctly, people

will continue to feel anxious long after the danger has passed. Some of the best treatments for anxiety

disorders probably work by increasing the effectiveness of this inhibitory pathway.

Did you know? Post-traumatic stress disorder

Some rape victims, combat veterans, and others who’ve experienced extremely

traumatic events develop post-traumatic stress disorder (PTSD). People with this disorder

are constantly on guard, which leads them to be easily startled and to have difficulty

sleeping. They also relive the traumatic events during nightmares or intrusive daytime

thoughts, and they may become emotionally detached and lose interest in everyday

activities. PTSD symptoms persist throughout life for about 30 percent of sufferers. PTSD

is not a modern invention. Its symptoms were described in ancient times, a famous example

being the transformation of Achilles by war in the
Iliad
. Indeed, PTSD has occurred in all

wars that have been studied.

Most adults have experienced at least one traumatic event of the type that can cause

PTSD, though only some people develop the disorder after a trauma. The strongest trigger

is trauma deliberately caused by another person, such as rape or kidnapping. About half of

rape victims go on to develop PTSD, while natural disaster victims have a relatively low

risk (about 4 percent). The same treatments are helpful for PTSD as for other anxiety

disorders, but progress can be much slower. Persistent PTSD has negative consequences

for the patient’s work and relationships that tend to linger after the anxiety itself starts to

fade.

Like other anxiety disorders, PTSD is twice as common in women as in men. (In the

U.S., women have a 10 percent chance of developing the disorder in a lifetime, while men

have only a 5 percent chance.) There are two proposed explanations for this difference.

One is that women experience more traumatic events (or more intense trauma), as rape and

spousal abuse are substantially more common for women, though men certainly experience

more combat-related trauma. The other is that women are more sensitive to fear learning or

stress, which may make them more vulnerable to anxiety disorders. The evidence for this

idea is weak and inconsistent, but it is true that more women (20 percent) than men (8

percent) develop PTSD after a traumatic event. Of course, it’s possible that both these

explanations may contribute to the gender disparity.

People with PTSD also show reductions in hippocampus size compared to people

without the disorder. At first, scientists thought that this happened because PTSD causes