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.
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.
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