397
CHAPTER ELEVEN
Nervous System II
O
n a bright May morning in 1995, actor
Christopher Reeve sustained a devastat-
ing spinal cord injury when the horse
that he was riding in a competition failed to
clear a hurdle. Reeve rocketed forward, striking
his head on the fence. He landed on the grass—
unconscious, not moving or breathing.
Reeve had broken the F
rst and second cer-
vical vertebrae, between the neck and the brain-
stem. Someone performed mouth-to-mouth
resuscitation until paramedics inserted a breath-
ing tube and then stabilized him on a board. At a
nearby hospital, Reeve received methylpredniso-
lone, a drug that can save a F
fth of the damaged
neurons by reducing inflammation. Reeve was
then ±
own to a larger medical center for further
treatment.
Reeve’s rehabilitation was slow, yet inspiring.
Despite discouraging words from physicians, he
persisted in trying to exercise. Suspended from
a harness, he moved his feet over a treadmill. He
moved other muscles in a swimming pool and
rode a special recumbent bicycle, with electrical
stimulation to his legs enabling him to pedal an
hour a day. ²ive years after the accident, Reeve
gradually started to move his fingers, and then
his hips and legs, although he still required a
wheelchair and a respirator. ²ollowing his exam-
ple, hundreds of others with spinal cord inju-
ries improved with exercise, too. Reeve’s motto
gave hope to many: “Nothing is impossible.” He
passed away in 2004. Most people with his level
of injury—between the F
rst and second cervical
vertebrae—do not live more than seven years.
Thousands of people sustain spinal cord
injuries each year. During the first few days the
vertebrae are compressed and may break, which
sets o³
action potentials in neurons, killing many
of them. Dying neurons release calcium ions,
which activate tissue-degrading enzymes. Then
white blood cells arrive and produce in±
amma-
tion that can destroy healthy as well as damaged
neurons. Axons tear, myelin coatings are stripped
off, and vital connections between nerves and
muscles are cut. The tissue cannot regenerate.
The severity of a spinal cord injury depends
on the extent and location of damage. Normal
spinal re±
exes require two-way communication
between the spinal cord and the brain. Injuring
nerve pathways depresses the cord’s re±
ex activi-
ties in sites below the injury. At the same time,
sensations and muscle tone in the parts the
affected fibers innervate lessen. This condition,
spinal shock, may last for days or weeks, although
normal reflex activity may eventually return.
However, if nerve F
bers are severed, some of the
cord’s functions may be permanently lost.
Less severe injuries to the spinal cord, as
from a blow to the head, whiplash, or rupture of
an intervertebral disc, compress or distort the
cord. Pain, weakness, and muscular atrophy in
the regions the damaged nerve F
bers supply may
occur.
The most common cause of severe direct
injury to the spinal cord is vehicular accidents
(F
g. 11C). Regardless of the cause, if nerve F
bers
in ascending tracts are cut, sensations arising
from receptors below the level of the injury are
lost. Damage to descending tracts results in loss
of motor functions. ²or example, if the right lat-
eral corticospinal tract is severed in the neck near
the F
rst cervical vertebra, control of the voluntary
muscles in the right upper and lower limbs is lost,
paralyzing them (hemiplegia). Problems of this
type in fibers of the descending tracts produce
upper motor neuron syndrome,
characterized by
spastic paralysis
in which muscle tone increases,
with little atrophy of the muscles. However, unco-
ordinated reflex activity (hyperreflexia) usually
occurs, when the ±
exor and extensor muscles of
ected limbs alternately spasm.
Injury to motor neurons or their F
bers in the
horns of the spinal cord results in
lower motor
neuron syndrome.
It produces
flaccid paralysis,
a
total loss of muscle tone and re±
ex activity, and
the muscles atrophy.
Several new treatments are on the horizon
for spinal cord injuries. They work in three ways:
1.
Limiting damage during the acute phase.
An
experimental drug called GM1 ganglioside
is a carbohydrate normally found on neuron
cell membranes. It blocks the actions of
amino acids that function as excitatory
neurotransmitters, which cuts the deadly
calcium ion in±
ux into cells. It also blocks
apoptosis (programmed cell death) and
stimulates synthesis of nerve growth factor.
2.
Restoring or compensating for function.
A new drug called 4-aminopyridine
blocks potassium channels on neurons.
This boosts electrical transmission and
compensates for the myelin-stripping
ects of the injury. Being developed for
patients injured at least eighteen months
previously, this drug can restore some
sexual, bowel, and bladder function.
3.
Regeneration.
Many experiments have
shown that paralyzed rodents given
implants of human neural stem cells regain
some ability to walk. Several research
groups are working on creating tissue
implants from embryonic or neural stem
cells that can help damaged spinal cords
to heal.
11.3
CLINICAL APPLICATION
Spinal Cord Injuries
FIGURE 11C
A dislocation of the atlas
may cause a compression injury to the spinal
cord.
Atlas
Axis
Spinal cord
11.5
BRAIN
The brain contains nerve centers associated with sensory
functions and is responsible for sensations and perceptions.
It issues motor commands to skeletal muscles and carries
on higher mental functions, such as memory and reasoning. It
also contains centers that coordinate muscular movements, as
well as centers and nerve pathways that regulate visceral activ-
ities. In addition to overseeing the function of the entire body,
the brain also provides characteristics such as personality.
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