The Brain Sense - The Science of The Senses

CHAPTER 4

Pain and the Placebo Effect

It’s tempting to think that our senses provide us with an accurate representation
of the external and internal environment. We believe that our eyes pro -
ject into our brains a perfect three-dimensional video recording of the objects
and events around us. It’s easy to surmise that our ears detect and transmit all incoming
sound waves with sound-studio clarity, and that our mouths, noses, and
fingertips provide us with all the evidence we need to draw indisputable conclusions
about tastes, odors, and textures.
We are kidding ourselves. Our senses respond to only a fraction of what’s out
there, and they respond in ways so malleable and idiosyncratic as to call into
question the whole concept of truth. Consider the legendary unreliability of eyewitness
accounts. In a recent study, Canadian researchers showed a video clip of
a movie action sequence to eighty-eight undergraduates who then discussed what
they had seen either with one or with several of their peers. In the debriefing sessions,
a researcher, posing as a peer, deliberately introduced misinformation into
the discussion. Later, on true-false tests of facts about the movie scene, participants
in the one-on-one condition accepted the impostor’s false suggestions 68
percent of the time; participants in the larger groups were taken in 49 percent of
the time.Perhaps our eyes, ears, and memories can be fooled, you may think, but internal
pain is different. We know where we hurt, how much we hurt, and how
we feel when the pain increases, diminishes, or disappears. Pain is a very personal
and intimate sense, and there is no sidestepping it, denying it, or talking your
way out of it. You know when you hurt!
Or do you?

THE PLACEBO EFFECT

Let’s do a thought experiment. Round up three hundred harried commuters
with headaches—not hard to do on the New York subway any workday rush hour.
Of course, they are shouting and whining strident protests, which only worsen
their headaches, which is precisely what you want. You reassure them that you’ll
get their names mentioned in the New York Times in recognition of their public
service (you can’t afford to pay them), and that settles them down long enough
for you to herd them into three soundproof rooms, one hundred headaches per
room.
Now the fun begins. You do nothing with the first one hundred. They get to
glare at one another Big-Apple-style and ruminate on their throbbing temples.
You make an eloquent speech to the second group, informing them that they are
the lucky recipients of a newly developed and powerful painkilling miracle drug.
(It’s actually aspirin with codeine, a proven pain reliever.) Then you leave them,
too, alone with each other and their pain, contemplating their lawsuits against
you. You make the same speech to the third one hundred, but you are lying to
them. They think you are giving them a pain-relieving drug. In truth, they get a
sugar pill.
After a half hour, you ask your three hundred captives to report on their head -
aches. In the “do nothing” group, twenty say their headaches are gone. Eighty
are still suffering. In the second group, ninety report the complete disappearance
of pain; that drug is certainly a miracle potion, the people say, and they wonder
where they can purchase it. In the third group, the ones you deceived, forty-five
still have headaches, but fifty-five do not. That pill did the trick, they say, happily
reboarding the subway pain-free. Your experiment was a success and you are off
the hook, unless one of your subjects is a liability lawyer.
But forget the legal ramifications for now. Look at what the experiment revealed.
A sugar pill has no physiological action that will cure a headache, but
thirty-five of your headache-free subjects in the third group provide evidence to
the contrary. (Why thirty-five and not fifty-five? Because the results from the first
group, the “do nothing” group, show headache pain will cease in 20 percent of
your subjects after a half-hour regardless.) Thus, for 35 percent of the subjects
in our thought experiment, the sugar pill was just as much a miracle drug as
the painkiller the members of the “real drug” group received. This “cure” in the
absence of any truly therapeutic agent is the placebo effect, and it’s more than a
curiosity. It’s a direct result of brain action. But how?
Before we answer that question, we need to define precisely what the placebo
effect is. It is not spontaneous remission. That’s what the twenty people in the
first group (and presumably twenty more in each of the other two groups as well)
experienced. Some of us, no matter what the disease, get better for unknown reasons.
The disease process simply reverses itself without any intervention. Whether
remission is mere chance or the result of some self-healing process remains anybody’s
guess.
Neither is the placebo effect deception or self-delusion. The people whose
headaches disappear after ingestion of the sugar pill are not lying, cheating, simple-
minded, or insane. Their pain disappears—and not because they consciously
wish it to. In study after study, where both subjects and experimenters are “blind”
to the experimental conditions—that is, no one, including the researchers, knows
who is getting the placebo—measurable, clinically replicable improvements in
disease conditions occur in a sizable fraction of all cases.
Furthermore, the placebo effect is no small or insignificant statistical aberration.
Researchers at Brigham and Women’s Hospital in Boston performed some
mathematical magic to combine the results of nineteen separate studies (conducted
between 1970 and 2006) on patients with irritable bowel syndrome. Across
all studies, the placebo response averaged nearly 43 percent, ranging from a low
of 15 percent to a high of 72 percent. The longer the period of treatment and the
larger the number of physician visits, the greater the placebo effect.
Finally, the placebo effect is not restricted to subjective self-reports of pain,
mood, or attitude. Physical changes are real. Working under a grant from the
National Institutes of Health, a multistate team of researchers tested fifty-five
asthma patients who had recurrent mild to moderate symptoms. Patients were
randomly assigned either to treatment (salmeterol) or to placebo groups, and all
participants were blind to the test; neither the patients nor their doctors knew
who was getting the placebo and who was getting the drug. The researchers assessed
not the patients’ self-reports of symptoms, but the degree of constriction
in their bronchial tubes. A one-dose trial showed the placebo effect in more than
half the patients. A stringent two-dose trial narrowed the field to 18 percent of
subjects who were unequivocal placebo responders. Five of the subjects (9 percent)
were completed “cured” by the placebo treatment.


THE PLACEBO EFFECT IN THE BRAIN

The placebo effect is not deception, fluke, experimenter bias, or statistical
anomaly. It is, instead, a product of expectation. The human brain anticipates
outcomes, and anticipation produces those outcomes. The placebo effect is selffulfilling
prophecy, and it follows the patterns you’d predict if the brain were, indeed,
producing its own desired outcomes. For example, researchers have found
the following:
• Placebos follow the same dose-response curve as real medicines. Two pills
give more relief than one, and a larger capsule is better than a smaller one.
• Placebo injections do more than placebo pills.
• Substances that actually treat one condition but are used as a placebo for
another have a greater placebo effect that sugar pills.
• The greater the pain, the greater the placebo effect. It’s as if the more relief
we desire, the more we attain.
• You don’t have to be sick for a placebo to work. Placebo stimulants, placebo
tranquilizers, and even placebo alcohol produce predictable effects in
healthy subjects.
• Placebo effects can be localized. In one experiment, Italian researchers
injected capsaicin into the hands and feet of brave volunteers. Capsaicin
is a derivative of hot peppers; it produces a burning sensation. The wily
scientists then applied a cream to only one hand or foot and told their subjects
that the cream was a powerful local anesthetic. In truth, the cream
was an inactive placebo. Nevertheless, the subjects reported less or no
burning on the treated hand or foot, but the burning sensation was strong
elsewhere.As in all brain actions, the placebo effect is the product of chemical changes.
The first clues to the chemical basis of the placebo effect came in 1978, when
research on pain in the dentist’s office showed that the drug naloxone can block
placebo-induced pain relief.9 Naloxone is an opioid antagonist; it locks onto the
brain’s natural painkillers, the endorphins, and stops them from doing their job.
Numerous studies have supported the conclusion that endorphins in the brain
produce the placebo effect. In patients with chronic pain, for example, placebo
responders were found to have higher concentrations of endorphins in their
spinal fluid than placebo nonresponders.10 One clue that expectation triggers
the release of endorphins came from other studies of naloxone conducted the
1990s. Italian researchers reported that naloxone blocked the placebo effect produced
by strong expectation cues; but in the absence of expectation, the drug
had no effect.Some researchers and theorists debate whether expectation or conditioned
learning accounts for the placebo effect, but it’s not hard to construe conditioning
as a special case of expectation. Conditioned learning is the classic Pavlovian
response. When dogs were fed at the same time that a bell was rung, it wasn’t
long before the dogs started to salivate at the sound of the bell, although no food
was present. The neutral stimulus (the bell) became associated with the effectproducing
stimulus (the food). The same mechanism might explain some forms
of the placebo effect. If a pill or injection (neutral stimulus) has been associated
with a physiologically active drug (effect-producing stimulus) in the past, then
later the pill alone may produce the action without the drug. For example, your
body won’t make any more growth hormone just because your doctor tells you
it will. But if you take the drug sumatriptan, which actually does increase growth
hormone secretion, and later you take a placebo that you think is sumatriptan,
guess what? Your body will make more growth hormone when you take the
placebo drug, even if your doctor tells you it won’t.That is an example of the placebo
effect that involves neither pain nor the brain’s production of endorphins, but, if conditioning is considered a form of expectation, it makes the same point. Your brain will direct your body to act
as it’s expected to act—whether the expectation is consciously perceived or unconsciously
learned.

MAKING THE MOST OF THE PLACEBO EFFECT

At one time, researchers viewed the placebo effect as an impediment—a
statistical annoyance that got in the way of objectively evaluating the efficacy of
potentially legitimate therapies. That view has changed. The placebo effect
is today seen as an important part of the healing process. It’s been studied as a
treatment for Parkinson’s disease, depression, chronic pain, and more. For large
numbers of patients—the placebo responders—belief in the therapy will create
or enhance its effectiveness.
Placebo treatments for Parkinson’s disease offer a good example. Parkinson’s
is a decline in the brain’s ability to control movement. The disease causes a slow,
shuffling walk, stiff shoulders, and trembling. Parkinson’s symptoms result from
the death of neurons in several regions of the brain. The affected neurons normally
control motion by releasing the neurotransmitter dopamine. Cell death
means that people who have Parkinson’s have too little dopamine in their brains.
One recent study of placebo treatments used positron emission tomography
(PET) to measure the brain’s manufacture and release of dopamine. Predictably,
the brain produced more dopamine when patients were given a placebo and told
to expect an improvement in their motor performance.
In some respects, the placebo effect offers the best of all possible alternatives:
therapeutic effects without the risk of negative side effects. It does, however, have
its downside. Just as expectation can produce positive outcomes, it can also produce
negative ones. That’s the “nocebo” effect, named from the Latin for “I shall
harm.” A harmless—but dreaded or feared—treatment induces a new illness or
exacerbates an existing one. Practitioners of black magic and voodoo curses have
known that for centuries, but the nocebo effect is difficult to research for obvious
reasons. It’s unethical to threaten people with illness, but a few brave investigators
tried it before institutional review committees began to place stringent
constraints on research involving human and animal subjects. For example, in
1968, scientists asked forty nonasthmatic persons and forty asthmatics to inhale
water vapor purported to contain potent irritants and allergens. The nonasthmatics
had no reaction to the vapor, but nearly half of the asthmatics did. They
experienced a measurable narrowing of their airways. Twelve of them responded
with asthma attacks that were successfully treated with the same saline solution,
which they were led to believe contained an effective antiasthma drug.17
Doctors could do more with the placebo effect if they could understand why
it works for some people but not others. Part of the answer is—once again—
expectation. Jon-Kar Zubieta of the University of Michigan at Ann Arbor used
PET to study the brains of men who had jaw pain. Zubieta gave them a saline
solution that he told them might relieve their pain. Brain scans showed that their
brains produced more endorphins after they received the placebo. They also
produced endorphins in more regions of the brain. Those men who said ahead
of time that they expected the most relief had more endorphins than their more
skeptical peers. The endorphin difference was pronounced in the brain’s dorsolateral
prefrontal cortex, a brain region involved in paying attention and making
decisions.18 It’s as if the men made up their minds to get well and their brains
cooperated by forming and releasing the proper medication.
Brain researchers such as Zubieta are working to sort through the complexity
of the numerous brain regions and neurotransmitters that produce placebo
or nocebo results. Theirs is no easy task. The placebo effect is not a single phenomenon,
but the result of the complex interplay of anatomical, biochemical,
and psychological factors. The same can be said for all the senses, I suspect. We
see, hear, taste, touch, and smell pretty much what we expect to.

What Is Pain?

An estimated 50 million Americans experience persistent pain, often from
backache, headache, arthritis, or cancer. Like everything else in the brain,
pain is a matter of physics and chemistry. The response starts with stimulation
of nerve fibers called nociceptors. They lie in the skin, muscle, and
other body tissues. Their impulses carry messages to the thalamus and cerebral
cortex of the brain where pain signals are processed. Pain signals also
pass to other brain regions such as the rostral ventromedial medulla (RVM),
where the “volume” of the pain message can be turned up or turned down
through signals sent from the RVM to the spinal cord.Unlike the nerve endings that respond to light touch or pressure, nociceptors
ordinarily need a strong stimulus to begin firing. Inflamed or
injured tissues, however, release chemicals that make nociceptors more
sensitive so that a weaker stimulus causes them to fire. Unlike many other
kinds of receptors, which quit triggering a signal when stimulated for too
long, nociceptors become increasingly sensitive with continuing or repeated
stimulation.
All this action is under genetic control, and so is the experience of pain.
Researchers at the University of Michigan and the National Institutes of
Health have found that a variation in a single gene helps to explain why
some people can tolerate more pain than others can. The gene has two
forms called met and val. Both code for the enzyme COMT, which breaks
down the neurotransmitters dopamine and noradrenaline. (Neurotransmitters
are the chemicals that ferry an impulse from one neuron to the
next.) COMT removes neurotransmitter molecules from the space between
neurons when an impulse is finished.
However, because the genes met and val are different, they make the
enzyme in slightly different forms. People who have two copies of the met
form have a much greater response to pain than those who have two copies
of the val form. Those who have one copy of each form have pain tolerance
somewhere in between. The val form, it seems, makes an enzyme that
does its job efficiently and rapidly, reducing the experience of pain for its
lucky owner.

Placebos for Emotional Pain

Expectation is strong medicine for a variety of physical and emotional ills,
even our perceptions of horrific images and events. A research team led by
Predrag Petrovic of the Karolinska Institutet in Stockholm showed emotionally
loaded pictures, such as images of mutilated bodies, to fifteen
healthy, adult volunteers. On the first day of the two-day experiment, the
researchers gave the volunteers an antianxiety drug to dampen their subjects’
emotional response to the pictures. Then the scientists gave an antidote
to the drug and told the volunteers that the antidote would restore the
full intensity of their emotional reactions.
The next day, the subjects were told they would take the same drugs,
but they were deceived. They got nothing more than a placebo salt solution
when they viewed the pictures. The placebo reduced the subjects’ negative
reactions to the unpleasant pictures by an average of 29 percent.
Functional MRI scans of the volunteers’ brains showed that the placebo
reduced activity in the brain’s emotion-processing centers. The effect was
mathematically predictable; as brain activity diminished, so did the perception
of negative emotions in response to the pictures. The scans also
showed increased activity in the same brain regions known to respond with
the placebo effect in reducing the perception of pain. The effect was greatest
in those subjects who reported the largest effect from the real antianxiety
drug administered on the first day.
What’s the point of administering a real drug the first day and a placebo
the second? This experimental design treats the placebo effect as a case of
conditioned learning. If you’ve experienced a positive benefit from a treatment
in the past, your expectation of its benefit in the future is stronger, and
so is the placebo effect.

Life in Chronic Pain

People who suffer constant pain carry with them a load of other miseries:
depression, anxiety, sleep disturbances—even difficulty making decisions.
Dante Chialvo, a researcher at Northwestern University, has found a reason
why.
Chialvo’s research team used functional magnetic resonance imaging
(fMRI) to scan the brains of thirty adult volunteers. Half the volunteers had
chronic low-back pain. Half were pain-free. The subjects used a fingerspanning
device to rate continuously the height of a bar moving across a
computer screen.
In the pain-free group, activation of some parts of the cortex while performing
the task corresponded with deactivation of other parts—a state
Chialvo calls a “resting state network.” The chronic-pain subjects performed
as well on the task as their pain-free counterparts, but their brains operated
differently. One part of the network did not quiet down as it did in the painfree
subjects.14
A healthy, pain-free brain, Chialvo asserts, maintains a state of “cooperative
equilibrium.” When some regions are active, others quiet down. But
in people who experience chronic pain, many brain regions fail to deactivate.
A region of the frontal cortex associated with emotion “never shuts up,”
Chialvo says.
This constant firing of neurons could cause permanent damage. “This
continuous dysfunction in the equilibrium of the brain can change the
wiring forever,” Chialvo says. “It could be that pain produces depression
and the other reported abnormalities because it disturbs the balance of the
brain as a whole.”

The Brain Sense - The Science of The Senses

CHAPTER 3

On Which Side Is Your Bread Buttered?

Do this: Go to the kitchen and take out the bread and butter. Now butter
a slice of bread, but, for the first time in your life, don’t do it automatically.
Think about what you are doing. Since nerves from the left and
ride sides of the body cross when they enter your brain, your left brain controls
your right hand and vice versa. If you are like most people, you’ll find yourself
using your preferred or dominant hand (probably the one you write with) to butter
the bread, while your other hand holds the slice. Now notice something else.
Again, if you are like most people, you’ll look at the butter as you spread it. You’ll
pay no attention to the bread and the nondominant hand that’s stabilizing it.
Thus, if you are right-handed, your left brain is controlling the knife and monitoring
the butter-spreading visually. Your right brain stabilizes the bread with your
left hand, monitoring the force and position of the slice with your sense of touch.
(It’s the opposite if you’re left-handed.)
So, you may be thinking, what’s the big deal?
It turns out that how you butter a slice of bread reveals a great deal about
how the brain processes sensory information. Put away the bread and butter and
fly off with me to the University of Michigan in Ann Arbor to learn more.

PROBING PROPRIOCEPTION

Where else would a university house a division of kinesiology but in a 1930s
Tudor revival-style building straight out of a gothic novel? Standing incongruously
within spitting distance of the University of Michigan’s ultramodern hospital
complex, the red brick Observatory Lodge is heavily ornamented with stucco veneers, angled half-timbers, hexagonal bay windows, and more gables than seven.
Behind one of those gables, in a fourth-floor aerie that serves as laboratory,
office, and student research center, I find motion scientist Susan Brown. She’s a
warm, friendly woman with red hair and dancing eyes, stylishly and colorfully
dressed in contrast to the spare, starkly functional room where she works. But
there’s no need for decoration here. There’s work to be done. Several students
busy themselves at computer stations around the room, eyeing me curiously.
Brown has prepared for my visit. She’s set up a webcam at one of the computers
so we can converse with her former graduate student, Dann Goble, now
a postdoctoral fellow at the Research Center for Movement Control and Neuroplasticity
at Katholieke Universiteit Leuven in Heverlee, Belgium. It’s evening
in Belgium, and youthful, soft-spoken Dann relaxes with a Stella Artois as he
describes how his research began when he first started working with Brown in
his student days.
“We were running some simple experiments,” Goble says, “looking at how
well people can match position when they don’t have vision.” For those experiments,
Goble blindfolded his subjects and placed their arms on supports, elbows
out and hands on levers. One arm then moved to a certain spot and back again.
Sometimes Goble moved his subjects’ arms for them. Sometimes the volunteers
initiated their own movements. In either case, the task was simple: match the
movement, either with the same arm or the opposite arm, hitting the same spot
as closely as possible using not vision, but the proprioceptive sense—the sense
of where the body is in space.
“For many years,” Goble explains, “nearly all the experiments that were carried
out in movement science looked at how the dominant arm works. But we
decided for some reason to test both arms, and we obtained this really strange
result: The nondominant arm was working better than the dominant arm.”
Goble doubted his own findings. Maybe he wasn’t performing the test correctly.
He checked and double-checked, but nothing seemed to be wrong with the pro -
cedure, so Goble went back to the research literature to see if anyone before him
had reported such a finding. Sure enough, in a long-overlooked paper from
nearly thirty years ago, he found a similar result, not for the arm but for the
thumb. Research subjects had once matched thumb positions better with their
nonpreferred hand than with their preferred,1 but no one in the research community
had paid much attention to such an oddity. The dominant arm and hand
are always better at everything, aren’t they? Goble’s findings flew in the face of
“what everybody knows.” “That’s when we thought maybe we were really on to
something,” Goble says.
Together Goble and Brown set up a series of experiments to explore “laterality,”
or the distinction between the operation of right and left arms. If what they
were beginning to suspect were true, their research could take them far beyond the
oddities of matching thumbs and arms, even beyond the daily rigors of buttering
bread. Could it be, they wondered, that the two arms differ in their preferred sensory
inputs, with the dominant hand attuned to vision and the nondominant
acting as the primary source of proprioceptive information?
The researchers began testing their “sensory modality hypothesis of handedness”
with experiments that allowed proprioceptive information only. Blindfolded
volunteers worked under three separate conditions, each a little more
complex than its predecessor in what the brain was required to do:
Task 1: same arm match. One arm (either left or right) was moved to a target
position between 20 and 60 degrees of elbow extension and held for two seconds
before being returned to the starting position. The task was to move that
same arm back to that same position, using only proprioceptive memory on a
single side of the brain (because it was the same arm).
Task 2: opposite arm match with reference. One arm was moved in the same
way as in task 1, but it was left in the target position, so it could serve as a stable
marker. The charge was to move the opposite arm to the same position. This task
required no proprioceptive memory, but it was more difficult, because it required
communication between one side of the brain and the other—matching one arm
to the other.
Task 3: opposite arm match without reference. As in task 1, one arm was
moved to a target position, held for two seconds, then returned to the starting position.
The task was to repeat the movement with the opposite arm. This was the
most difficult task of all because it required proprioceptive memory as well as
communication between the two sides of the brain.
On all three tasks, the nondominant arm (the left for most people) was better
at matching positions. Furthermore, the left arm/right brain superiority grew
with the difficulty of the task. Task 3, the opposite arm match without reference
that required both memory and cross-brain communication, showed the biggest
difference of all. The nondominant arm’s performance was even better than on
the two simpler tasks, which required either memory or the brain’s cross-talk, but
not both.2
Brown and Goble conducted another series of experiment to compare performance
when visual cues were provided. As expected, the dominant arm excelled,
3 but when only proprioception was allowed, the nondominant arm won
every time. Over several years, Brown and Goble tried other approaches. They
tested children. Same result. They tested the elderly. Same result. They conducted
experiments in which volunteers matched not position, but force. Still, the results
were always the same. In a right-handed person, the left arm/right brain partner -
ship is a champion proprioceptive team.
LATERALITY
Ask one hundred people which is their preferred hand, and nine out of ten
will say their right. Apparently, the preference for right-hand, right-arm activity
has been around as long as humans have been throwing spears and painting pictures
on cave walls. The right-handed use of stone tools appears in images that
date back 35,000 years. Since the left brain controls the right hand, it’s tempting
to think that the left hemisphere is more or less in charge of most skilled movements,
since we think we don’t do much with our nondominant (left) arm, and
some researchers find evidence that that’s true. One study showed that the right
motor cortex actively controls movements of the left hand, but that the left motor
cortex is active in movements of both hands.4 No one can explain that finding,
but it’s possible that the left hemisphere sends messages to the left hand (by
way of the right hemisphere) via the corpus callosum, the stalk of brain fibers
that connects the brain’s two halves.
While it’s true that the preferred hand is better at many tasks, Brown and
Goble have shown that it’s probably not the major source of proprioceptive feedback
to the brain—at least not when the two arms must perform in different, yet
complementary, ways. They aren’t the only scientists to reach that conclusion.
Researchers had found that patients with right-hemisphere brain injuries have
more trouble reproducing movements than do those with left-hemisphere lesions.5
Some brain-imaging studies have compared brain activity while subjects reached
for remembered targets. In some cases, the targets were visual; in others, they
were proprioceptive. During the proprioceptive tasks, the right hemisphere’s
somatosensory area showed greater activity than did the left, even when all the
sensory information came from the preferred right arm.7

ASYMMETRIES IN THE REAL WORLD

The specialized, yet cooperative, partnership between the two arms has obvious
applications in daily life. In right-handed people, the left hemisphere’s
affinity for vision promotes fast, accurate, visually guided action of the preferred
right arm, as when reaching for a slice of bread. The right hemisphere’s specialization
in proprioceptive feedback helps the nondominant, left arm maintain the
position of an object, such as holding a slice of bread, while the preferred right
arm acts on it—in this example, spreading the butter. Brown’s and Goble’s research helps us better understand how our brains, arms, and hands work, but it has practical applications, too, in rehabilitative treatments for those with movement and proprioceptive disabilities. Goble has worked
with children who have cerebral palsy. He’s tested them on matching tasks and
found what he expected. Children with right hemisphere damage are usually
worse at proprioceptive matching tasks than those with damage on the left side.
Brown has been testing some home-based training protocols with adults who
have cerebral palsy. The training requires subjects to perform small tasks, such
as picking up objects with chopsticks or turning over cards. She tells of a man with
cerebral palsy who, now in his early thirties, has always reached across his body
with his left hand to put the key in the ignition of his car. After only eight weeks
of home training, he can now use his right.
“We have a mix of both right-side-affected and left-side-affected [people] in
that study,” Brown explains, “but they are all getting the same intervention. . . .
We don’t have enough numbers, but we wonder if we are getting more of an effect
for those that might have damage to one side of the brain because it’s more
responsive to the types of training we are using.” Brown is also starting a collaboration
with the University of Michigan Stroke Clinic to develop training regimens
specifically designed for right- and left-side impairments. “We have enough
basic science data, but now we need to translate that into a clinical environment,”
she says. A great deal has changed in treating patients since researchers learned
how the brain rewires and restructures itself after an illness or injury. “It’s a big deal
now in clinical rehabilitation to pay attention to sensory feedback and not just
concentrate on getting the brain to contract muscles to produce movement,”
Brown says. “Brain plasticity has caused a real paradigm shift in rehabilitation.”

Is Proprioception the Same as Touch?

Proprioception is the sense of the body’s position in space—and of its movement,
speed, and force. Brown and Goble say proprioception and touch
are more or less the same thing, although proprioception may be thought
of as a particular type of touch. The receptors that initiate impulses of pressure,
vibration, and temperature lie in the skin. The receptors more important
for proprioception lie deeper—in the joints, tendons, and muscles.
The muscle spindle, found in the body of a muscle, is one type of proprioceptor;
it signals changes in muscle length. The Golgi tendon organ, which
lies in the tendons that attach muscle to bone, provides information about
changes in muscle tension. These receptors send their impulses to the somatosensory
cortex of the brain. It lies in the parietal lobe (the top of the
head). Proprioceptive information also travels to the cerebellum, where
automatic and habitual motions are controlled.


Pinocchio’s Nose

Vibration disturbs the proprioceptive sense, and the illusion of Pinocchio’s
nose proves it. Here’s how it goes: Close your eyes and place the tip of your
finger on your nose. Your brain immediately draws conclusions about the
length of your nose. But if someone were to vibrate your elbow joint, you’d
feel that your nose had suddenly grown longer. Why? Because vibration
stimulates muscle spindles, misleading the brain into concluding that the
vibrated muscles have stretched and the arm has moved, although the limb
has actually remained immobile. The brain draws the only logical conclusion
it can: If your arm muscle has stretched and if your finger is still on
your nose, your nose must have grown longer.
“Vibration is a great tool for fooling the nervous system,” Susan Brown
says, and researchers have used that fact to uncover further evidence for
right-brain dominance of the proprioceptive sense. An international team
of researchers from Sweden, Japan, German, and the United Kingdom
vibrated tendons in the arms of right-handed, blindfolded volunteers. The
vibration made the subjects feel that their fingers were curling in toward
their palms, although, in reality, their hands remained fixed. The scientists
used functional magnetic resonance imaging (fMRI) to pinpoint the
brain’s response to the perceived, but unreal, motion. They found that the
proprioceptive regions of the brain’s right hemisphere grew much more active
than those of the left, no matter which hand was thought to move. “Our
results provide evidence for a right hemisphere dominance for perception
of limb movement,” the researchers concluded.

The Brain Sense - The Science of The Senses

CHAPTER 2

In from the Cold

Argentinean Andrea Salas isn’t just pretty. She’s flat-out gorgeous. Although
no relation to the fashion model of the same name, she’s even more beautiful,
in my opinion. The glow of a summer sunset streaks her cascade of
auburn hair. Her caramel colored skin is flawless. Usually, when she speaks, her
doe eyes dance with merriment.
But not today.
Today she is dredging up memories of her brush with death in Antarctica.
The deep waters of the world’s most extreme environment threatened to take her
life. If the sea didn’t, the cold surely would have.

ALL ABOARD FOR THE ANTARCTIC

November 23, 2007. Andrea’s ship, the Explorer, had been at sea for thirteen
of its scheduled eighteen days of sightseeing along the margins of Antarctica.
Andrea, age thirty-eight, was a veteran Antarctic guide, having served on two
previous voyages. This time, as one of sixty-four crew members, she was working
as assistant to the leader of the expedition team. She organized lectures, wet landings,
and recreational activities for the Explorer‘s ninety-one passengers, a sixteennation
aggregate of intrepid tourists who had opened their wallets wide for this,
the adventure trip of a lifetime.
The ship had departed from Ushuaia, Argentina, a town that fights a perpetual
feud with Chile’s Punta Arenas over which is the southernmost city in the
world. The itinerary called for a stop in the Falkland Islands—the Malvinas to
the Argentineans—and a visit to an abandoned whaling station in South Georgia.
From there, Andrea and her shipmates traveled to Elephant Island, famous as
the last refuge of the men of Shackleton’s Endurance Expedition of 1914–1916.
Shackleton failed to cross the Antarctic continent on foot as he had planned, and
he was forced to leave his men on Elephant Island while he piloted a single
lifeboat across eight hundred miles of open ocean to find help on South Georgia.
The landscapes of the islands were breathtaking, Andrea recalls. Wildlife is
scarce in this, the most inhospitable environment on earth, but the tourists marveled
at the albatrosses of Steeple Jason in the Falklands. They oohed and aahed
over the king penguin rookeries of South Georgia.
November is early for an Antarctic trip. The sun doesn’t rise in Antarctica
until September, and summer doesn’t arrive until January when the weather
warms to a balmy –15° to –35°C (–5° to –31°F). The weather was exceptionally
cold on this trip. Andrea kept her charges wrapped in layers of thermal underwear,
polar fleece, and waterproof jackets. Boots swaddled feet, while waders cocooned
passengers toes-to-chest for wet landings. The season and the cold brought
with them some disappointments for the passengers and crew of the Explorer. A
planned side trip to South Orkney Island had to be canceled because the seas
were beginning to crowd with icebergs.
It might have been a portent, but the Explorer steamed on.
On this Thursday night, Andrea left her cabin on the crew deck, below sea
level. There, while resting in bed, she could hear ice hitting the hull. She wasn’t
worried. The Explorer was built to handle icy seas. She headed to the bar to enjoy
a drink with fellow crew members and some passengers. The bar was warm;
the drinkers, convivial.

ABANDON SHIP!

Around midnight two passengers rushed into the bar, shouting, “There’s
water! There’s water!” Everyone ran from the bar, only to collide with the captain
who was ascending the stairs. “The captain told us water was coming in
through a hole,” Andrea says. She raced to her cabin, as did the others, pulling on
warm clothes and collecting her life jacket, while the captain announced from
the bridge that emergency evacuation was commencing. “This is not a drill!”
“We got to the muster stations almost immediately,” Andrea reports. Huddled
there in the dark and biting cold, passengers listened to reassurances from
the captain over the public address system. Attempts were underway to repair the
hull, but just in case, emergency rescue stations in Chile and Argentina had
been radioed, as had other ships in the area. Andrea joined her fellow crew members
in distributing hot drinks and hope while awaiting the order to abandon ship.
It wasn’t long before that order came. Repair attempts had failed, and seawater
was pouring in through a breach in the hull. Its cause? Probably impact with an
iceberg.
Now came the greatest challenge: Andrea and 153 others would have to
brave the turbulent Antarctic seas and the bitter cold in nothing more than small
lifeboats and Zodiacs, the inflatable rubber boats usually employed for tendering
to shore from the ship and sightseeing along rocky coasts and beaches. Andrea
hustled passengers into the emergency craft, making sure that each boat had
a crew member to handle the motor and steering.
She and two other crew members lowered one of the Zodiacs into the water
and scrambled aboard. Zodiacs are not lifeboats, but in Andrea’s opinion, they
represented a better choice for escape than did Explorer‘s aging orange lifeboats,
which were heavy, clumsy, and poorly powered, although provisioned with food
and water. The Zodiacs have powerful motors; they are light and are highly maneuverable.
Still, they are open, small, and cramped when holding more than
four or five people.
Andrea’s Zodiac maneuvered next to one of the crowded, heavy lifeboats,
transferring seven passengers into the rubber inflatable. When all the boats were
in the water, the crew lashed the lifeboats and Zodiacs together with ropes, using
the Zodiacs’ engines to keep the lifeboats from ramming into icebergs. The
passengers and crew of the Explorer had radios that allowed communication
among themselves but not with the outside world. They were alone and adrift in
the Antarctic seas.
The ten people on Andrea’s Zodiac crouched under blankets, settling in for
a long wait. Mostly they all stayed silent, the smell of apprehension heavy in the
air. “Those were the longest hours of my life,” Andrea says. The wind whizzed
past her ears. The cold crept through her seawater-soaked clothing to ice her bones.
In conditions like these, she discovered, waterproof jackets aren’t waterproof.
“My feet and hands were very cold,” she says. “I never feared death, but I did
fear that I might lose a hand, a finger, a foot. I don’t know how cold it has to be
to lose a part of your body, but I was afraid it would happen because I knew I
would not get any warmer.” She and her compatriots were stacked in the Zodiac
like cord wood. They had no way to move, no means of generating or sharing
heat. “I couldn’t feel my hands inside my gloves,” Andrea says. “My feet were
blocks of ice.”

COLD-SENSING

While Andrea waited for rescue, she felt overwhelmed by a paralyzing sense
of cold in every part of her body. What gave her that feeling? What was going on
in her nervous system to create that perception? The answer lies in tiny receptors
on the membranes of neuronal projections that lie close to the skin’s surface.
It’s long been known that touch neurons specialize. Some respond only to
pressure; some, only to light touch. Several subsets of neurons fire an impulse
when the ambient temperature rises. Others detect only a decline—or cooling.
(Any temperature lower than that of the human body, 37°C or 98.6°F, is “cold”
in the physiological sense.) One type of neuron fires at relatively warm temperatures,
15° to 4°C (59° to 39°F); yet another type activates at temperatures below
0°C (32°F).1 Still another kind generates an impulse only when cold is so
intense that it’s painful.
For a long time, no one understood what was going on in temperaturedetecting
neurons, but that changed in 2002 when several research teams delivered
up two prizes: receptors on nerve cell membranes that respond to coolfeeling
chemicals such as menthol; and cold-activated ion channels in cell
membranes. The receptors work just as taste and smell receptors do; after locking
onto a molecule of a cool-feeling chemical, they provoke some change in
the cell that, in turn, triggers a nerve impulse. The channels do precisely what
their name suggests. They either open in response to cold, allowing ions (charged
atoms or molecules) to flow into the cell,2 or they close to prevent them from
leaking out—maintaining the cell’s positive charge.3
The influx of positively charged sodium or calcium ions (or the maintenance
of a positive charge) causes electrical potentials to change across the outer membrane
of the neuron. That happens because a neuron at rest has a slightly negative
charge inside it, compared with a positive charge outside. When cold causes
an ion channel to open, sodium ions flow into the cell, thus changing the charge
along its membrane. For a tiny fraction of a second, the inside of the cell becomes
positive; the outside becomes negative. This reversal in one tiny area creates a
current that affects the membrane farther along. Channels there open, and sodium
flows into another section of the nerve fiber, then another, then another. That’s
how the impulse travels—eventually to the brain.
Receptors and ion channels can work alone or in concert, in the same cell
or in different cells. One receptor channel called TRPM8 has been studied extensively.
Also called CMR1 (cold and menthol receptor 1), it’s a major player
in detecting gentle cooling. Researchers at the University of California at San
Francisco found its genetic base when they isolated cold-sensitive, mentholsensitive
neurons from rats. They took the TRPM8 gene from those cells and
placed it into cultured neurons that were neither cold- nor menthol-sensitive.
The cells changed their function and became cold- and menthol-detecting neurons.
Why? Because the gene directed the construction of TRPM8 receptors on
the cell membrane.Another team of researchers that same year discovered how cells that have
TRPM8 receptors respond to temperatures in the 23°C to 10°C (73° to 50°F)
range. The calcium concentration increases inside the cell. This suggests that
TRPM8 is both a receptor and an ion channel.5 The scientists don’t know how
cold affects the channel, but they describe two possible mechanisms. Cold might
change the shape of the channel directly, or it might trigger the release of a chemical
(a “second messenger”) that, in turn, prompts TRPM8 to open.
Another possible mode of action has been explored by researchers in Spain.
They studied “voltage-gated” potassium channels in cell membranes. Neurons
insensitive to cold have them, but cold-sensitive neurons do not. The channels
function as “excitability brakes” during cooling in insensitive cells. They stop an
impulse from beginning. Cold-sensitive neurons lack such voltage gates, so temperature
changes can initiate an impulse in them. This relationship was established
when the Spanish team blocked the action of the voltage-gated potassium
channels in cold-insensitive neurons. About 60 percent of the neurons began
firing impulses in the cold.10
The human body can differentiate a temperature change as small as a single
degree Celsius, but only a few heat- or cold-sensitive ion channels like TRPM8
are known. How can relatively few cellular structures account for such a finely
tuned capacity? The answer may lie in the ability of the channels to shape-shift.
In cell cultures, channels that respond to increases in temperature are known to
rearrange themselves by combining with other channels within their same structural
“family” (not TRPMs but another category called TRPVs). The resulting
complexes demonstrate characteristics intermediate between those of the “parent”
forms. Research teams can measure the intermediate electrical charges and
ion-gating properties of these “hybrid” channels. This ability to shuffle and recombine
means that the number and variety of channel types are large. Although
channels that respond to decreases in temperature have not been researched, it’s
likely that they, too, combine with others to form intermediate types. Whether
such channel complexes act as functional temperature sensors in living organisms
remains unknown.11

RESCUE!

Andrea never gave a thought to her TRP receptors. She had survival on her
mind.

As the wee hours of the morning gave way to a (blessedly) clear dawn around
3 A.M. (nights deliver less than three hours of darkness at this latitude in November),
Andrea and nine others watched from the safety of their Zodiac as the Explorer
began to list starboard. The Explorer‘s engines had failed, perhaps swamped
by water. The boat careened drunkenly with the swirling currents, powerless and
empty after the captain was the last to abandon his post. Explorer drifted toward
seas increasingly jammed with icebergs, driven by a rising wind. Before it sank
at the end of the day, the Explorer would be completely surrounded by pack ice.
Andrea remembers the noise. “The sound of a ship when it is breaking and
about to sink is just like in the movies,” she says, her dark-chocolate eyes wide
with the memory. “I could hear pipes breaking.” The eerie creak of twisting
metal assaulted her ears unceasingly as what passes for an Antarctic dawn brightened
into morning.
And yet they waited for hours more, hoping against hope for a rescue they
could not be sure would come.
Then the Norwegian cruise ship, the Nornodge, topped the horizon. Rescue!
The Zodiacs raced toward the Nornodge, with the slower lifeboats trailing behind.
“We didn’t mind getting wet anymore,” Andrea says, her eyes brightening
now that she can report a happy ending. Miraculously, not a single person suffered
injury—not even frostbite. The Nornodge doctor offered treatment to the
rescued sailors—all 154 of them. Only two took advantage of the offer.
Andrea recalls how her sense of lethal cold disappeared when the rescue ship
arrived. “When I stood to look at the Nornodge, all the heat returned to my body,”
she says. “The hope I gained from seeing it sent a wave of warmth through me.
It was the excitement of feeling safe. Knowing that it was over, I didn’t feel cold
anymore.”

The Brain Sense - The Science of The Senses

CHAPTER 1

Life Without Touch

In many ways, Chuck Aoki is a typical teenager. At seventeen, he’s an avid athlete.
His Minnesota Timberwolves basketball team won the national junior
championship in 2008. He plays rugby competitively, too. Tennis and baseball
are his recreational sports. He likes the history and English courses in his
Minneapolis high school, and he is confident that he did well on his SATs, although
he hasn’t received his scores yet. He likes Taco Bell food. He finds girls
confusing. “Women dance around the bushes. Men get straight to the point,” he
says.1 He and his friends like to ride the bus to downtown Minneapolis to go to
a movie, eat at a restaurant, or hang out at the mall. He’s lined up a summer job
as a human resources assistant for the Minnesota Twins baseball team, a perfect
situation for him since he loves sports. Chuck hopes to go to college on a basket -
ball scholarship. He will major in psychology or sports management.
But for all that, Chuck Aoki isn’t a typical teenager. He was born with no
sense of touch in his arms, hands, legs, and feet. With a few spots as exceptions,
he feels in his limbs neither heat nor cold nor contact nor pressure nor vibration
nor pain, although he experiences normal sensation in his head and trunk. His
legs were repeatedly damaged in childhood when he walked, ran, and played
baseball. His joints have disintegrated and his bones are crumbling. He’s fulltime
in a wheelchair now; his athletic teams are wheelchair basketball and quadriplegic
rugby. He’s lost eight of his fingers down to the first joint. Text messaging
on his cell phone produces bleeding sores on what’s left of his thumbs. Buttoning
a shirt is impossible. Cutting lettuce for tacos or taking a pizza from the oven
poses a serious risk.
Chuck was born with an extremely rare, inherited disorder called hereditary
sensory and autonomic neuropathy (HSAN) type 2. This is his story as he shared
it with me in a sidewalk café one sunny afternoon. It’s also the story of his mother,
Jennifer Nelson. She’s a librarian for the Minneapolis public library system and
the proudest mom I’ve ever met.

GROWING UP

“You young mothers. You worry too much,” the pediatrician told Jennifer
when Chuck was a baby. The infant was teething. He’d chewed his fingers to raw
and bleeding pulps.
“Is that normal?” Jennifer asked. The doctor wrote a prescription for anti -
biotics. The baby had an ear infection, he said.
Throughout infancy, Chuck cried intensely and interminably. Only full body
contact, his tiny trunk held tight against his mother’s skin, could console him.
“Is that normal?” Jennifer asked. The doctor wrote more prescriptions for more
antibiotics to treat more ear infections.
Chuck walked at nine months, but he walked on his knees. “Is that normal?”
Jennifer asked. More antibiotics. Babies get lots of ear infections.
But by the time Chuck celebrated his first birthday, the fact that something
was wrong could no longer be blamed on ear infections. The tentative diagnosis
of HSAN type 2 came when a neurologist examined a sensory nerve taken from
the boy’s foot. The fiber was smaller than it should have been, and it lacked the
dozens of tiny, hairlike projections usually seen on nerves. The fiber also lacked
the myelin sheath that surrounds, protects, and insulates normal nerves. In the
absence of myelin, nerve impulses could not travel along Chuck’s sensory nerves.
The baby’s motor nerves were normal, so his brain could direct his limbs to move,
but his sensory nerves were nonfunctional. He could feel nothing past his shoulders
and his hips.
Chuck was eighteen months old. None of the doctors knew how to treat his
condition; they’d never seen anything like it before. The only model came from
diabetic neuropathy, which shares some common features with the inherited neuropathies.
Diabetic neuropathy compromises blood flow, leading to infections
and the “spontaneous amputations” that have robbed Chuck of his fingers, one by
one, over the years. Chuck also developed Charcot joints, in which inflammation
and loss of healthy bone lead to the overgrowth of abnormal bone tissue, fragmentation,
and instability. Why? Because when he walked, he felt the ground
only from his hips. He had no feedback to tell him how much force he was exerting
with the muscles of his legs and feet, so he stomped too hard. Similarly, when
using his hands, his sensation begins at his shoulders. He pushes too hard when
he uses a computer, plays video games, or holds a spoon. As a result, his hands
constantly bleed and callus. His mother debrides and bandages his wounds daily.
As a small child, he could grasp with his palm but he never learned to make
the finely controlled, pinching movements needed to pick up small objects. Because
he felt no pain, everyday activities were hazardous. “We pursued a strategy
of avoidance,” Jennifer says. The hot water temperature was lowered so that
Chuck would not burn himself. Jennifer was ever vigilant, keeping the boy away
from flames, sharp objects, and hot surfaces.
Jennifer recalls a family vacation to Oregon when Chuck was seven. “We
played on the beach all day,” Jennifer says, “and that evening Chuck’s left knee
was swollen to the size of a grapefruit.” The child had been seeing a rheumatologist,
and Jennifer suspected a flare-up. She called the doctor and asked what
to do; the family was planning to take a train home the next day. In the absence
of an open wound, infection, or any obvious break, the doctor advised merely
watching the situation and keeping the boy off the leg as much as possible on the
journey home.
Back in Minneapolis, Chuck went for x-rays. Nothing showed up. He went
for an MRI. Nothing appeared wrong except for the persistent inflammation, so
Jennifer continued icing and wrapping the joint. Weeks passed with no sign of
improvement, so the rheumatologist consulted a specialist radiologist. The radiologist
examined the images and found a shadow that previous examiners had
missed. An orthopedist then decided to open the leg surgically. He found a fracture
of the femur, the large bone of the thigh. “Chuck had been walking around
for six weeks on a broken leg,” Jennifer says. He was home from school for eight
weeks. He had a cast on for twelve weeks. Soon after the cast was removed, he
broke his ankle, so he had to be in another cast. He couldn’t use crutches because
he couldn’t coordinate the alternating right- and left-arm actions that crutches
require.
When Chuck was nine, doctors discovered that the earlier fracture of the left
femur had destroyed most of the bone’s growth plate. Subsequent surgery closed
the entire growth plate in his right leg and what remained of the growth plate in
his left leg to prevent unequal limb growth. “A limb length discrepancy would
be dangerous on a daily basis,” Jennifer says, “getting in and out of the shower
and that kind of thing.” After that, he snapped his anterior cruciate ligament
(ACL). “We don’t know how he did it. We didn’t repair it. What would be the
point?” asks Jennifer. “His feet are flat, his ankles have sunk into his heels, and
both of his feet are deformed,” she says. Chuck has been using a wheelchair
full-time since he was twelve.

DIAGNOSING HSAN

Throughout Chuck’s childhood, his parents remained uncertain about their
son’s diagnosis. They took the boy to the Mayo Clinic when he was nine in hopes
of getting a definitive answer. A precise diagnosis was important, Jennifer explains,
because it would help the family plan for Chuck’s health and care as he grew.
His neuropathy was obvious, but the autonomic part of the HSAN description
was not. The autonomic nervous system controls those bodily functions outside
conscious control. It regulates heart rate, blood pressure, intestinal action, and
glandular function. In all those ways, Chuck appeared normal. Did he really
have HSAN? If so, was it really type 2? There are several kinds, each with its own
symptoms, course, and prognosis.
To look for the autonomic component of the diagnosis, doctors at the Mayo
Clinic did a sweat study on Chuck. “They put him on a little gurney, sprinkled
him with powder, and put him into a makeshift, plastic covered oven, and heated
the space up,” Jennifer explains. “Then they charted where his body turned
purple, which is where he sweated. He doesn’t sweat from his fingertips and he
doesn’t sweat below his knees. There was the autonomic part of his neuropathy
that we hadn’t known about.” The HSAN type 2 diagnosis was confirmed.
The broad category of all hereditary sensory neuropathies (HSNs) includes
as few as four and as many as six disorders, depending on which classification
system is used. All types are genetic, and all involve loss of feeling in the hands
and feet. One HSN that is more common and better known that Chuck’s dis -
order is familial dysautonomia (FD, HSAN type 3, or Riley-Day syndrome). Children
with FD often experience feeding difficulties and fail to produce tears when
they cry. Other symptoms may include lung dysfunctions, cardiac irregularities,
poor growth, and scoliosis. Children with FD are most often born to parents of
Eastern European Jewish heritage, with an incidence of one in every 3,600 live
births.2 Genetic tests are used to diagnose FD but not the other HSAN types.
Chuck’s HSAN type 2 is inherited as an autosomal recessive. That means
both Jennifer and her husband, Andy, carry the gene on chromosome 12. Their
chance of having a child with the disorder is one in four. (Chuck’s younger
brother, Henry, is unaffected.) Although the inheritance pattern is understood,
the reasons why symptoms vary among individuals are not. Some babies with
HSAN type 2 feed poorly, exhibit poor muscle tone, and can’t maintain body
temperature. Chuck had none of those symptoms, but like most others with the
disorder, he suffered numerous fractures of hands, feet, and legs, as well as Charcot
joints. Also like most others with the condition, Chuck’s muscular strength
is normal.

THE BRAIN WITHOUT TOUCH

As for what happens in the brain when touch signals fail to enter it, Jennifer
and Chuck’s doctors can only speculate. The somatosensory (“body sense”) region
of the cerebral cortex lies in the parietal lobe at the top of the brain, near
the crown of the head. Adjacent to it and forward from it, in the frontal lobe, lies
the primary motor cortex, where voluntary actions are triggered. These two long,
skinny areas lie sandwiched together, and their nerve fibers are organized in descending
rows, like twins lined up side by side. Each nerve and each small area
is dedicated to a particular body part—forming side-by-side regions for feeling
and movement in the left arm, the right leg, and so on. But the two parallel rows
are not identical. In the motor cortex, the amount of “processing power” devoted
to a body part varies with the precision of the movements that body part can
make. So, for example, the fingers get more space in the motor cortex than the
toes do. In the somatosensory cortex, the allocation of space depends on the body
part’s sensitivity to heat, cold, pressure, vibration, contact, or pain. Thus, the fingertips
and lips get a disproportionate share of the somatosensory cortex. The
back gets short shrift.
This basic anatomy suggests (but by no means proves) that Chuck’s somato -
sensory cortex may have allocated space differently from the way it is allocated
in other children. Receiving no sensory impulses from his limbs, the parts of his
somatosensory cortex that would have processed touch information from arms,
leg, hands, and feet probably failed to develop. Did the sensory nerves from his
head and trunk take over the brain’s spare “real estate”? There’s no way to know,
but it’s possible. It’s possible, also, that his motor cortex is organized differently,
although what happens to the motor cortex if it fails to receive somatosensory
feedback is unknown. Still, we can make some guesses in Chuck’s case. Athletes
who practice their sport and attain a high level of mastery probably devote larger
areas of the motor cortex to the body parts they use most. I suspect Chuck’s practice
of basketball skills and his mastery of his sport have modified his motor cortex
and probably his cerebellum as well—for that’s where movements that are
practiced enough to become automatic are coordinated.

LIVING TO THE FULLEST

Although the brain can reorganize itself to some extent to meet the demands
of its owner’s life, major brain regions maintain their own specialized functions.
As one expert put it, a brain region steals from its next-door neighbor, not the
whole town. So Chuck’s brain regions for hearing, vision, and the other senses
probably aren’t any different from anyone else’s. But what he’s learned to do with
his senses is another matter. Chuck says that he relies on vision to manage daily
living. He dribbles a basketball expertly (an action some doctors think he should
be unable to perform), using his peripheral vision to judge where the ball is and
how forcibly he is propelling it. When playing video games, he holds the controller
in front of his eyes and peers over the top to see the screen. He’s learning
to drive a hand-controlled car. He says he uses his peripheral vision to determine
where his hands are on the steering wheel, brake, and throttle.
Chuck’s vision, strength, and motivation have helped him achieve in sports.
He recently started playing wheelchair rugby on an adult team sponsored by the
Courage Center in Minneapolis. He’s getting good at it. He practiced with the
U.S. Paralympics team in 2008. “Maybe I can get named to the USQRA [United
States Quad Rugby Association] team. . . . That would be a step toward a world
championship team or the Paralympics team,” he says.
As for touch, “It’s not all it’s cracked up to be,” Chuck jokes, then adds more
seriously, “I’ve never had it, so I’ve adapted, and I don’t really get what I’m missing.
. . . It’s not like it has negatively affected me in any really serious way.”
“He thrives in his life,” Jennifer says. “It is fun to watch him.”


Touch the Pain Away
 
Mothers and infants know what the rest of us may forget—a tender touch
takes some of the pain away. A pediatrics team in Boston divided mothers
and their newborn infants into two groups. Half of the mothers held their
babies in whole-body, skin-to-skin contact while a physician performed the
standard heel-stick procedure to draw blood samples from the infants. The
other half of the babies were wrapped in receiving blankets and placed in
bassinets while the blood was drawn. Babies in contact with their mothers
grimaced 65 percent less than the bassinet-held babies did, and their crying
time was a whopping 82 percent less. The held babies did not experience
the same rise in heart rate as the control babies did. The researchers concluded
that skin-to-skin contact reduces both stress and pain for infants.

How Successful People Manage Their Time

I want to give you a revelation in life. You might need to take a pen, write this down and put this on the wall in front of your table. It is this.

Each of us has 24 hours a day.

Yes, 24 hours. Whether you are a toilet cleaner or a CEO of a listed company, you have 24 hours a day. Donald Trump, Bill Gates, Warren Buffet and my favorite motivational speaker, Adam Khoo has 24 hours a day.

How do you think they manage to do so many great things within 24 hours a day, while some of us complain that we do not have time?

There are 3 ways you can do the same if you follow act upon these principles.

1. Analyze Your Lifestyle

Everyone lives differently and only you, yourself know what kind of lifestyle that suits you best. Also, each people manage their time differently based on the nature of their lifestyle.

Analyzing your lifestyle simply means living your life circumspectly. What does it mean to live circumspectly?

It means you are cautious, pay close attention and carefully evaluate your schedule. In order to save time, you must first know how to lose it.

Having a full time job from 9am - 6:30pm during the weekdays, I still have to find the best resources to post on my Excellence Blog. Not only that, I need to attend cell group, conduct bible study, attend leaders meeting every Tuesday and fellowship with the people around me.

That's not all. During the weekend, I spend most of my time doing my Internet marketing projects.

My schedule may not be as busy as some of you who are reading my blog but I can assure you this is not what an ordinary person can or is willing to do.

So my point is not trying to tell you how busy I am but to share with you what kind of lifestyle I have and how I managed to do so many things in a week.

I've seen people keep complaining that they have not time to do this and that but they have time to watch TV, upload photos to Facebook or Friendster and going for movies.

So examine your lifestyle and you will be able to know how you can slot in time to do much more.

"The unexamined life is not worth living." - Aristotle.

2. Utilize The Present

"I'll do it later!" and "I'll wait for the right time to do it". This is the number killer that people do not take action. It is not that they do not have the desire to take action but they keep procrastinating. This should not be the path for you and me.

If there is a better time to certain things, it should be right now. Adam Khoo said that the reason why he is so successful is not because he was more gifted or more talented than others. It is his ability to take action now that makes all the difference.

While others procrastinate and spending time to analyse the business model, he simply took action.

So friends, make the most out of every opportunity you have.

3. Prioritize What's Important

I have a lady friend of mine is not doing very well with her health recently. I asked her why she never make an appointment to meet the doctor up and she told me that she does not have time.

She has been very busy with her day job and part time accounting work. By the time she reaches home in the evening, she will be dead tired to do anything else.

I then asked, "Why don't you take half a day off from your work and go to see the doctor?"

"I am so busy with my work and my supervisor keep giving me work to do. It is just never ending"

"Well, you need to know your priority. If your health is not even helping you, what else can you do?"

She went silent for a short while and said, "Alright Rahul, I'll make an appointment next week".

Sometimes, you need to know what is important and what is not, so that you can plan your time accordingly. Do what is important first and the ones that are of lesser importance later.

National Anthem of India

National anthem can be described as a patriotic musical composition of a country, which reminds and praises the history, traditions and struggles of its people. At the same time, it has to be recognized as the official national song, either by the nation's government or by convention through use by the people. The national anthem of India is 'Jana-gana-mana', composed originally in Bengali, by Rabindranath Tagore. It was adopted as the national anthem of India, in its Hindi version, by the Constituent Assembly, on 24th January 1950.

'Jana-gana-mana' was first sung on 27th December 1911, long before Indian gained independence, at the Calcutta Session of the Indian National Congress. The complete song consists of five stanzas. As for the playing time of the full version of the national anthem, it will take up approximately 52 seconds. A short version, consisting of first and last lines of the stanza (playing time approximately 20 seconds), is also played on certain occasions.

National Anthem In Hindi

Jana-gana-mana-adhinayaka, jaya he
Bharata-bhagya-vidhata.
Punjab-Sindh-Gujarat-Maratha
Dravida-Utkala-Banga
Vindhya-Himachala-Yamuna-Ganga
Uchchala-Jaladhi-taranga.
Tava shubha name jage,
Tava shubha asisa mage,
Gahe tava jaya gatha,
Jana-gana-mangala-dayaka jaya he
Bharata-bhagya-vidhata.
Jaya he, jaya he, jaya he,
Jaya jaya jaya, jaya he!

Translation In English

Thou art the ruler of the minds of all people,
Dispenser of India's destiny.
The name rouses the hearts of Punjab, Sind, Gujarat and Maratha,
Of the Dravid and Orissa and Bengal;
It echoes in the hills of the Vindhyas and Himalayas,
Mingles in the music of the Yamuna and Ganga
And is chanted by the waves of the Indian Sea.
They pray for thy blessings and sing thy praise.
The salvation of all people is in thy hand,
Thou dispenser of India's destiny.
Victory, victory, victory to thee.

The Story Behind Translation
Jana Gana Mana was translated, from Sanskrit to English, by Rabindranath Tagore and the music on this English Translation was set in Madanapalle, a small town in Andhra Pradesh. As to the story behind this translation, in 1918 Tagore was invited, by controversial Irish poet James H. Cousins, to spend a few days at the Besant Theosophical College (BTC). James was serving as the principal of the college, at that time.

On February 28, while attending a gathering of students at BTC, Rabindranath sang the Jana Gana Mana in Bengali. Suddenly, he thought of translating the song in English. A few days later, in Madanapalle, Tagore wrote down the English translation of the song. Cousins' wife, Margaret, who was an expert in Western music, set down the music for this English version. The framed original English translation is still displayed in the library of Besant Theosophical College in Madanapalle.