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Acute Spinal Cord Injury
14 April 2003
Wise Young, Ph.D., M.D. W. M. Keck Center for Collaborative Neuroscience Rutgers University, Piscataway, New Jersey
08540-8082 Email:
wisey@pipeline.com, http://sciwire.com I receive many calls and
emails from people and families with spinal cord injury. It is better today compared to 1977
when I took care of my first spinal-injured patient and had to tell the family
that there was nothing that we could do.
Here is what I say to families now. • Focus on solvable problems. Make
sure that methylprednisolone is given within 8 hours after injury (this drug
may improve recovery by 20%). Find
the best and most experienced surgeon.
If the spinal cord is compressed, make sure that it is decompressed as
soon as possible. Prevent
complications by insisting on aggressive care of lung, bladder, and skin. Start rehabilitation as soon as
possible. • Recovery is the rule and not the exception
in spinal cord injury. Most people recover some function after spinal cord
injury. On average, people with
“complete” injuries recover 8% of the function they had lost, compared to 21%
if they received methylprednisolone.
People with “incomplete” injuries recover 59% of lost function, compared
to 75% if they received methylprednisolone. Recovery takes a long time and work. Many people recover function for 2 or
more years after spinal cord injury. • Do not give up hope. Most
scientists believe that it is not a matter if but a matter of when therapies
will be available to restore function in spinal cord injury. Clinical trials are testing therapies
to restore function after injury.
Weigh potential risks and benefits carefully before participating in
such trials. Remember that the
therapies will get better over time.
What to ask your doctor? Families and friends often
don’t even know what questions to ask the doctors. Here are some questions to ask in the first hours after
injury: • Was methylprednisolone given? This
is the high-dose steroid (30 mg/kg intravenous bolus followed by 5.4 mg/kg/hour
for 23 hours if it is started within 3 hours and for 47 hours if between 3 to 8
hours after injury). It should not
be started more than 8 hours after injury. Clinical trials have shown that this treatment improves
recovery by about 20% when given within 8 hours after injury but does not help
when started more than 8 hours after injury. While methylprednisolone is not a cure, every little bit helps. Complications are minimal. • What is the level and severity of
spinal cord injury? The consequences of spinal cord injury depend on
the level and severity of injury.
Surgeons determine injury levels from the fracture site on the spinal
column. This may differ from
neurological level determined from sensory and motor loss. Spinal cord injury causes loss of
sensation and voluntary movement below the injury site. If the person has motor or sensory
function below the injury level at the time of admission, the likelihood of
substantial recovery is high. • Has the spinal cord been
decompressed? The spinal cord injury usually results from
fracture of vertebral bones that compress the spinal cord. Continued spinal cord compression
increases tissue damage and reduces functional recovery. If the neck or cervical segments are
fractured, traction may straighten out and decompress the vertebral
column. Chest or thoracic
fractures cannot be decompressed by traction. Surgery may be necessary to decompress and stabilize the
spinal cord. • Has anticoagulation been started? Blood clots may form in the legs and migrate to the lungs. This is a serious complication that can
be prevented by giving anticoagulants such as heparin or coumadin. It may be necessary to place a filter
(Greenfield filter) in the vein to the heart to catch clots. • Pulmonary, bladder, and skin care? Spinal cord injury may compromise breathing and
coughing. After cervical spinal
cord injury, artificial respiration may be necessary and pneumonia is
common. Spinal cord injury
paralyzes the bladder and a catheter must be placed in the bladder to drain
urine. Continued pressure causes
skin sores called decubiti.
Cushioning vulnerable areas and regular turning prevents this. Some frequently asked questions and
answers
Families and friends often
search the Internet and encounter a bewildering array of information that is
often out of date and contradictory. Here are some commonly asked questions and
quick answers: • Will he/she recover? Recovery is the rule and not the exception after spinal cord
injury. The probability of
recovery is high, especially after “incomplete” spinal cord injury. Clinical trial data indicate that if a
person had even slight sensation or movement below the injury site shortly
after injury, they will recover an average of 59% of the function they lost
and, if they receive high-dose methylprednisolone, they will recover an average
of 75% of what they had lost.
People admitted to hospital with no motor or sensory function below the
injury site recover an average of 8% of the function they had lost but will
recover an average of 21% if they received methylprednisolone. • How long will recovery take?
Recovery takes a long time.
Most recovery occur within 6 months but many people continue to recover
function for a year or more. A
recent poll
of the CareCure Community suggests that 61% recovered function more than one
year after injury. In another poll,
16-18% of people who are “complete” spinal cord injury recovered additional
function 3 or more years after injury.
A recent study detailed how Christopher Reeve recover function over 7
years after his injury. So,
recovery frequently continues for years after injury. • What experimental clinical therapies are
available? Several clinical trials are assessing therapies
that are applied within 2 weeks after injury. These include activated macrophages (which may help repair
the injured cord), alternating currents (to stimulate regeneration), and
AIT-082 (a drug that may stimulate growth factors and stem cell
proliferation). The macrophage
trial is limited to people with “complete” thoracic spinal cord injury and
requires surgery. Please consider
the risk and benefits of the trial carefully, including the risk of moving
somebody to another center. • Do therapies have to be applied shortly
after injury? Several experimental therapies are aimed
at restoring function in chronic spinal cord injury, when recovery has
stabilized a year or more after injury.
These include 4-aminopyridine (a drug that increases excitability of
demyelinated axons), porcine fetal stem cell transplants (stem cells from
pigs), and olfactory ensheathing glial transplants (cells from the nasal mucosa
or from olfactory bulbs). Other
experimental therapies are being planned, including drugs and chemicals that
block growth inhibitors. Thus,
there will be many opportunities to participate in clinical trials. What is the spinal
cord? This may seem to be silly
question but, until people get spinal cord injury or know somebody who is, most
pay little attention to their spinal cords. Most people don’t know the different parts of the spinal
cord, what each part does, and how the spinal cord transmits sensory and motor
information. Many think that the spinal cord conducts information like a
telephone wire and the spinal cord can be fixed by reconnecting it. Some people mistakenly believe that the
spinal cord is the vertebral column. While almost everybody knows that spinal
cord injury causes paralysis, many are not aware that the spinal cord also
controls the bladder and bowel, sexual function, blood pressure, skin blood
flow, sweating, and temperature regulation. The spinal cord connects
the brain to the body. The spinal cord resides in the a bony spinal or
vertebral column that has 24 segments.
Seven vertebra in the neck are called cervical (C1-C7), twelve chest or
thoracic (T1-T12) segments form the rib cage, five segments for the lower back
or lumbar (L1-L5), and five segments form the tail or sacral (S1-S5)
vertebra. The vertebral bodies are
in the front of the spinal column.
Spinal discs are located between the vertebral bodies. The front of the spinal cord is
referred to as anterior while the back is referred to as posterior. The sides of the spinal cord are called
lateral. Note that in animals that
walk on four legs, posterior is dorsal and anterior is ventral. Each segment has four
spinal roots (left and right, posterior and anterior) that send and receive
information from each side of the body.
Posterior roots receive sensation while anterior roots send motor
signals to muscles. For example,
the C1-C3 segments send and receive information from the back of the head and
neck, C4 covers the shoulder and deltoid muscles, C5 the biceps, C6 the wrist
extensors, C7 the triceps, C8 the wrist flexors, and T1 the intrinsic muscles
of the hand. The spinal roots
leave the vertebral column between the bony segments through openings in the
vertebral column called foramina.
Note that there are only 7 cervical vertebra but 8 sets of cervical
roots because the C1 roots are between the skull and C1. The spinal cord is shorter
than the vertebral column and occupies the spinal canal from the C1 to L1
vertebral levels. In general, the
bony vertebral segments are lower than the spinal cord levels. The spinal roots
exit through the spinal column through openings between vertebral segments
called foramina. The spinal cord
stops just below the L1 vertebral level and only spinal roots are present from L1
to S5 vertebral spinal column. The
end of the cord is called the conus.
Spinal roots below the conus are called the cauda equina because they
resemble a horse’s tail. How does the spinal cord work?
Neurons (nerve cells) in
the brain, spinal cord, and peripheral nerve send axons (nerve fibers) up and
down the spinal cord in spinal tracts. These spinal tracts are called white
matter because axons are coated with a membrane called myelin and myelin
appears white. In the spinal cord,
white matter is usually situated close to the surface of the cord, arranged
into several columns called the anterior, posterior, and lateral columns. The spinal cord contains neurons
located in the middle part of the spinal cord. The areas of the spinal cord that contain neurons is called
gray matter. The gray matter is
most abundant in the parts of the spinal cord that connect to the arms and
legs, called the cervical and lumbosacral enlargements. The spinal cord transmits
signals for sensations and to control movement, as well as breathing, bladder,
bowel, sweating, blood pressure, sexual, and other essential functions of the
body. The spinal cord contains neuronal circuitry for reflexes that control all
these functions. Over 20 million
axons ascend and descend in the human spinal cord, organized into spinal tracts
named according to their source and destination. For example, the spinal tract that sends axons from the
cerebral cortex to the spinal cord is called the corticospinal tract. Likewise, the tract that sends axons
from the red nucleus in the midbrain to the spinal cord is called the
rubrospinal tract. The sensory
tract that transmits pain and temperature sensation from the spinal cord to the
thalamus is called the spinothalamic tract. Some tracts, however, are named by their position. For example, the posterior column
transmits sensory information from the spinal roots to the brainstem. Neurons that send axons to
muscles are called motoneurons while neurons that send axons to other neurons
are called interneurons.
Motoneurons and interneurons receive information from descending axons
and sensory axons. When you
activate sensory input to the spinal cord by tapping a tendon, the activity
turns on motoneurons that cause the muscle of that tendon to contract. This is called a monosynaptic
reflex. To signal the muscles to
move, the brain sends information directly to motoneurons or indirectly through
interneurons that can either excite or inhibit other neurons. Sensory neurons send axons
from the spinal cord to the brain.
Some sensory axons go from peripheral nerve neurons in posterior sensory
ganglia located just outside of the spinal column. Posterior sensory ganglion neurons send an T-shaped axon to
the body where it collects information like touch and movement while the other
end goes into the spinal cord and branches. One branch goes into the gray matter where it activates
motoneurons and the other end goes up the posterior column all the way to the
brainstem. What
is spinal cord injury?
Many misconceptions abound
concerning spinal cord injury. For
example, many people believe that the spinal cord below the injury site dies
after injury. Others think that
the injured spinal cord is like a cut telephone wire and can be fixed by
reconnecting the cut ends. Some
people think that the vertebral column is the spinal cord. Even doctors have
misleading and inaccurate ideas about spinal cord injury. For example, many doctors casually use
the word “transection” to refer to severely injured spinal cords. The word should only be applied to the
extremely rare situation when the spinal cord has been cut and the cut ends are
separated. Spinal cord injury usually
results from trauma to the vertebral column. Displaced bone or disc then compresses the spinal cord. Spinal cord injury can occur without
obvious vertebral fractures and you can have spinal fractures without spinal
cord injury. It can also result
from loss of blood flow to the spinal cord. Many people may have had mild spinal cord injury without
thinking that it is spinal cord injury.
For example, over a million people per year get “whiplash” in car
accidents; they often have neck pain, weakness, and sensory loss that many last
days or even months.
Athletes who play football or other contact sports often suffer a
transient loss of function that they call a “stinger”, i.e. paralysis and
sensory loss for minutes or even hours.
Sometimes, people can get spinal cord injury without any obvious cause,
a condition called transverse myelitis.
Spinal cord injuries are
usually defined by vertebral level and neurological level, as well as
severity. Vertebral levels are
indicated by which bony vertebra have been fractured or show damage. Multiple bony vertebra may be
injured. For example, an injury
that causes the C5 vertebra to slip relative to C4 may be called a C4/C5 injury
because it compresses the C4 and C5 spinal cord. Spinal cord levels do not necessary correspond to veretebral
levels. For example, the C5 spinal
cord lies in the C4 vertebral segment.
The cord ends at the L1 vertebral level even though the spinal roots
continue and exit between the appropriate vertebral segments. For many years, there was
no standardized way of referring to spinal cord injury levels. Surgeons generally referred to the
injury level by the vertebra that are damaged. Neurologists and physiatrists, however, tend to refer to the
level of spinal cord injury based on the neurological loss. Neurologists identify the level of
injury as the first segmental level that shows sensory or motor loss. In contrast, physiatrists identify
injury level from lowest spinal cord level that has normal motor and sensory
function. How is spinal cord injury classified?
In 1990, the American
Spinal Cord Injury Association (ASIA) proposed a uniform classification system
that had five categories, defined in Table 1. Motor level is defined as the
level at which the key muscle innervated by the segment has at least 3/5 of its
normal strength. Sensory level is defined as the lowest spinal cord level that
still has normal pinprick and touch sensation. If there is a spinal cord level
below which there is no voluntary motor or conscious sensory function, the
person is called a “complete” spinal cord injury. Since the S5 is the lowest spinal cord level that innervates
the anal sphincter, a person that has no voluntary anal sphincter control or
sensation is defined as a “complete” spinal cord injury. A person who has any anal control or
sensation is an “incomplete” spinal cord injury. Some people may have a “complete” spinal cord injury but
still has preserved motor or sensory function between the injury level and
S5. This is called the “zone of
partial preservation”. Usually,
the spinal cord injury level and severity is classified between 72 hours and 7
days after injury. Note that some people have neurological loss at a given
spinal cord level but partially preserved function for several or even many
segments; this is called the zone of partial preservation (ZPP). Table 1: Neurological Classification of Spinal
Cord Injury
Some patterns of spinal
cord injury have special names. • In the “Central Cord
Syndrome”, arm function is affected more than the legs. This paradoxical condition is
attributed to damage to the central part of the spinal cord. Recent studies of central cord syndrome
suggest that the syndrome may be associated with destruction of the lateral
spinal tracts. • “Brown-Sequard Syndrome” refers to
injuries limited to one side of the cord.
People have weakness and loss of touch sense in one leg but loss of pain
and temperature sensation in the other side. • “Anterior Cord Syndrome” refers to the
condition when sensation is preserved but motor function is absent below the
injury site. • “Posterior Cord Syndrome” refers to the
condition when motor function is preserved in the absence of sensation. • “Conus Medullaire” refers to injury of
the conus or lower tip of the spinal cord. This damages the lower lumbar and sacral spinal cord
segments. • “Cauda Equina Injury” refers to the
condition when the damage is limited to the spinal roots below L1. How is acute spinal
cord injury treated? Acute spinal cord injury
refers to hours or days after spinal cord injury during which continued
deterioration or tissue damage may occur.
Shortly after an injury, the spinal cord often does not appear to be
severely damaged even though there may be immediate functional loss. The injury initiates a cascade of
chemical and cellular responses that contribute to further tissue damage,
including inflammation, free radicals, and swelling (edema). The spinal cord
may be compressed during this period.
Compression or decreased perfusion (blood flow) of the spinal cord
aggravate the injury. These causes
of progressive tissue damage can and should be relieved as rapidly as
possible. The goal of acute spinal
cord injury care is to stabilize the spinal cord to prevent further damage,
save as much tissue as possible, and prevent complications of spinal cord
injury. • Emergency management. The first objective of emergency management of spinal cord injury is
to establish ABC (airway, breathing, and circulation). The spine must be immobilized to
prevent further injury. The
patient must be transported rapidly to the nearest medical center, preferably a
Level 1 Trauma Center. If blood
pressure is low, fluid and drug therapies must be given to maintain blood flow
in the spinal cord. In cervical
spinal cord injuries that affect breathing, ventilatory support may be
necessary. A foley catheter is
usually placed in the bladder to drain urine. • Methylprednisolone therapy. The
patient should receive intravenous high-dose steroid methylprednisolone (30
mg/kg bolus followed by 5.4 mg/kg/hour for 23 hours) as soon as possible. This
therapy improves neurological recovery by about 20%. If the methylprednisolone is started between 3-8 hours after
injury, the infusion should be extended to 48 hours. If the methylprednisolone cannot be started within 8 hours,
it should not be given. Therapy
beyond 8 hours does not improve functional recovery. • Decompression of the spinal cord. If the spinal cord is compressed by bone or disc,
every effort must be made to decompress the cord as soon as possible. Cervical spinal injuries can often be
decompressed by traction of the spinal column to realign the vertebral bodies. However, thoracic and lumbosacral
spinal fractures usually cannot be decompressed by traction alone. Surgery may be necessary to decompress
the cord or spinal roots. Thoracic
or lumbosacral spinal cord decompression may require opening the chest cavity
or retroperitoneal space, requiring a team of surgeons. Some surgeons delay surgery for this
reason, particularly patients that have so-called “complete” spinal cord
injury. I believe that “complete”
injuries should be treated as aggressively as incomplete spinal cord injuries. What
is spasticity and neuropathic pain?
Spinal cord injury
disconnects the brain from the spinal cord below the injury site. The spinal cord below the injury site
does not die unless it has been damaged by loss of blood flow (ischemia). The lower spinal cord becomes
hyperactive because spinal cord injury interrupts not only excitatory but also
inhibitory connections to the cord.
The spinal cord above the injury site also may become hyperactive,
producing abnormal sensations. • Spasticity and spasms. Reflexes may be hyperexcitable in the lower spinal cord isolated from
the brain by injury. Such reflex
hyperexcitability is called spasticity, including neurons that mediate muscle
reflexes for feedback control, more complex reflexes such as the withdrawal reflex,
anti-gravity reflexes for standing and postural control, and locomotor programs
that mediate walking and running.
Hyperactive reflexes may be present even when there is voluntary control
of the muscle. Spasms are spontaneous or evoked movements multiple
muscles. Spasms can occur in limbs
that a person has little or no control of, and can be violent enough to throw a
person out of a wheelchair. Pain,
bladder infection, and irritation of the spinal cord can aggravate spasticity
and spasms. A drug called baclofen is often used to control spasticity. Baclofen usually does not prevent
spasms unless very high doses are used and causes weakness or flaccidity.
Baclofen can be given directly to the spinal cord (intrathecally) to treat
severe spasticity when oral doses of 100-120 mg per day are insufficient. Several other drugs also suppress
spasticity, including clonidine and tizanidine. • Dysesthesia and
pain. Abnormal sensations (dysesthesia) and neuropathic
pain are the flip side of the coin to spasticity and spasms. When the spinal
cord loses sensory input, sensory neurons above the injury site become
hyperexcitable and can generate abnormal sensations and pain. This is akin to “phantom pain” after
limb amputations and peripheral nerve injuries. Neuropathic pain is often
described as “burning” or “pressure”, involving areas that have little or no
sensation. It can also occur in
deeper organs. Neuropathic pain may be associated with spasticity and
spasms. For many years, doctors
did not recognize neuropathic pain and treated it as psychogenic pain. Several therapies are available for
reducing neuropathic pain. For
example, the tricyclic antidepressant amitryptaline (Elavil) may reduce
dysesthesia. Some of the most
promising therapies, interestingly, are drugs that are anti-epileptic. For example, gabapentin (Neurontin) is
an anti-epileptic drug that has been reported to reduce neuropathic pain when
given in very high doses. Some
recent studies suggest that glutamate receptor blockers such as dextromethorphan
and oral ketamine may be useful for refractory neuropathic pain. Atrophy and Learned
Non-Use Due to loss of activity,
muscle, bone, and skin atrophy occur after spinal cord injury. In addition, parts of the neural
circuitry in the brain and spinal cord may turn off. • Atrophy. When parts of the body
are not used, they undergo atrophy.
For example, muscles shrink, bones lose calcium and strength, and skin
gets thinner. Activity of muscles,
stress on bones, and contact with skin prevent atrophy. Even passive movement will help prevent
muscle atrophy and fibrosis.
Spasticity and spasms prevent atrophy and maintain muscle bulk. It is
not a good idea to take so much anti-spasticity medication that the legs become
flaccid (i.e. show no movement).
Electrical stimulation (functional electrical stimulation) can be used
to activate muscles to drive legs to pedal bicycles and prevent muscle
atrophy. Weight bearing may
prevent bone loss or osteoporosis while ambulation training on treadmills may reverse
osteoporosis. Many drugs are available for increasing calcium in bones. Without exercise or stress on the
bones, such drugs may increase the brittleness of bone without increasing
ability of the bones to support weight. • Learned non-use.
Neural circuits in the
spinal cord may also turn off when they are not used. Spinal cord injury causes a prolonged period of inactivity
in people. For example, a person
may not walk for many months after a spinal cord injury and this may turn off
neuronal circuits needed for walking.
In the early 1990’s, several groups reported that intensive ambulation
training can restore independent locomotion to 50% or more of people who have
some residual sensory or motor function but have never walked after spinal cord
injury. Suspending a person over a
treadmill and manually moving the legs until they start stepping on their own
is one approach to ambulation training.
Many rehabilitation centers around the world are studying these effects
of weight-supported treadmill walking. Preventing atrophy and
reversing “learned non-use” are important goals of rehabilitation. Learned non-use may prevent recovery of
function despite regenerative and remyelinative therapies. Some rehabilitation programs offer
intensive motor training programs that can prevent or reverse learned
non-use. Unfortunately, intensive
and prolonged ambulation programs are very labor-intensive and consequently
costly. Various clinical trials
are being conducted to determine the optimal parameters for weight-supported
ambulation, biofeedback, and other forms of motor training. Many rehabilitation centers in the
United States have biofeedback, weight-supported ambulation, and functional
electrical stimulation (FES) programs. What
happens to the bladder, bowel, and sexual function?
The spinal cord also
carries “autonomic” signals that control blood pressure, blood flow, breathing,
sweating, bowel, bladder, sexual, and other autonomic functions. • Bladder Paralysis and Spasticity. Spinal cord injury paralyzes the bladder. The
bladder must be catheterized to drain urine. Indwelling catheters (such as a
foley catheter inserted through the urethra) have a high risk of
infections. Sterile intermittent
catheterization is recommended but may be complicated by bladder spasticity or
spontaneous contractions of the bladder.
Bladder contractions can push urine into the kidney and this may lead to
kidney damage. A drug called Ditropan suppresses bladder spasticity but have
side effects such as dry mouth and eyes.
Alternative approaches are available, including cutting the bladder
sphincter so that urine drains freely into a condom catheter but this approach
is not suitable for women. An
approach that does not involve compromise of the urinary sphincter is placement
of a suprapubic catheter or creation of a intestinal conduit from the abdominal
wall to the bladder, i.e. a Mitrafanoff procedure. • Bowel constipation and
incontinence. The bowels usually operate without much voluntary
control. However, spinal cord
injury slows bowel activity and transit time of food in the gut. People use a variety of stimulants and
suppositories to facilitate bowel activity. Bowel incontinence is a serious
problem, often restricting social activity and employment options. A common technique is to establish a
bowel routine to empty the gut on a set schedule. Artificial sphincters are
available but the success rates of such procedures are still limited. Finally, alterations in secretion
patterns can lead to indigestion, appetite changes, nausea, gallbladder stones,
and other problems, especially in people with cervical spinal cord injury. • Erection and ejaculation. Most people assume that spinal cord injury eliminates the possibility
of sexual function. However, this
is not true for a majority of people with spinal cord injury. Penile erection is a reflex and many
men are able to have erections after spinal cord injury unless the injury
involves the lower spinal cord or roots that control erection. Recent studies suggest that Viagra
works for people with spinal cord injury.
Vibrators or electrical stimulation can be used to facilitate
ejaculation. Due to sphincter
spasticity or poor coordination of the bladder sphincters, the ejaculate often
goes into the bladder rather than outward. However, with a combination of electroejaculation and semen
collection, it is possible to collect ejaculates from nearly all males. While spinal cord injury may interfere
with menstrual cycles, a vast majority of young women with spinal cord injury
remain fertile and can conceive. How
does spinal cord injury affect the skin?
Spinal cord injury reduces
or eliminates skin sensation in dermatomes below the injury site. Because
people cannot feel or move, they may sit or lie for long times on certain parts
of their body. Pressure impedes
blood flow in the skin. Due to
muscle atrophy, the normal tissue padding that cushions the butt may be
reduced. Absence of sensation, loss of muscle padding, and long periods of
pressure can lead to skin breakdown and development of pressure sores or decubiti.
Decubiti are potentially life threatening but preventable. Spinal cord injury impairs
skin blood flow responses.
Normally, skin responds to pressure, mechanical stimulation, or
inflammation with increased blood flow.
Loss of this response not only adds to the vulnerability of the skin to
pressure sores but reduces the ability of the skin to repair decubiti. Thus, great care must be taken to
prevent decubiti by shifting sitting positions and frequent turning. Special seats that distribute the
pressure are used in wheelchairs to prevent sacral decubiti. Vulnerable areas
such as the heels must be padded.
If a decubitus develops, all pressure must be removed or the decubitus
can progress to loss of skin and tissues to the point of exposing bone. The sores must be kept clean or they
can become infected. Plastic
surgery may be necessary to repair the decubitus. Spinal cord injury also
paralyzes sweating in dermatomes below the injury level. People with spinal
cord injury must be very careful to maintain their body temperatures. In contrast to loss of sweating below
the injury site, many people with spinal cord injury may have abnormal
increases of sweating above the injury site, often in their upper torso and
face. This is a form of autonomic
hyperexcitability or spasticity.
It is not unusual for people to sweat profusely on one side of the face
and not the other. Such abnormal
sweating responses may develop early or late after injury. Spinal cord injury
disables vascular responses that maintain blood pressure when a person sits or
stands up. Blood vessels in the
guts and legs normally constrict when a person stands up, to keep blood from
pooling. When people with spinal
cord injury sit up for the first time after injury, their blood pressure may
drop sharply. Such postural
hypotension may prevent a person from sitting or standing during the first
weeks after spinal cord injury.
The vascular responses recover over time but people must be be tilted
gradually into the vertical position over the several weeks after spinal cord
injury. Loss of vascular responses
in the legs leads to a tendency for fluid to accumulate in the legs when people
sit for long times. Such dependent
edema can be prevented to some extent with stockings. What is autonomic dysreflexia?
The autonomic nervous
system often becomes hyperactive in people with spinal cord injury. Autonomic dysreflexia manifests in
large increases in blood pressure (hypertension) with systolic pressures
exceeding 200 mm Hg, slow (bradycardia) or fast heart rate (tachycardia),
headaches, facial flushing, exuberant sweating, hyperthermia, stuffy nose,
goose pimples, nausea, and other signs of autonomic hyperactivity. Called autonomic dysreflexia, these
episodes may be spontaneously or may be instigated by infection, pain, or other
conditions that stimulate the autonomic nervous system. Severe autonomic dysreflexia may be
life-threatening. Emergency treatments of
autonomic dysreflexia should initially focus on identifying potential causes that
can be relieved. If the episode occurred during manipulation of the body, such
as rectal stimulation, that activity of course should be stopped. The person should remain sitting and
check for any blockage of bladder outflow. If necessary, place a foley catheter to drain the bladder.
If the cause cannot be identified and eliminated, drugs can be used to relieve
the symptoms. These include
Procardia (a calcium channel blocker), nitroglycerin (a vasodilator), clonidine
(alpha adrenergic agonist anti-hypertensive drug), or hydralazine (a
vasodilator) to reduce blood pressure.
People with spinal cord injury should carry a card with instructions to
inexperienced emergency personnel. Causes of autonomic
dysreflexia may sometimes be masked by the spinal cord injury. For example, a bladder infection,
kidney or bladder stones, bowel cramps, gallbladder stones, gastric ulcers,
hemorrhoids, pressure sores, back pain, bone fractures, and many other
potential causes may not be felt by an individual due to the spinal cord injury
but may manifest in autonomic dysreflexia. Autonomic dysreflexia may result from heterotopic
ossification (a condition where abnormal and painful bone growth occurs on the
hip and other bones). Sometimes,
back pain resulting from Harrington rods and other instrumentation may lead to
autonomic dysreflexia that occur only when sitting up or lying down. Autonomic dysreflexia
often occur during sexual activity, labor, and delivery. Fortunately, the autonomic dysreflexia
associated with orgasm and other sexual activity is usually mild and
controllable with drugs but obstetricians should be aware and prepared to treat
autonomic dysreflexia in women undergoing labor. Some individuals who have uncomfortable autonomic
dysreflexia during sexual activity should consult their doctors for the
possibility of having medication on had (such as nitroglycerin) to counter some
of the symptoms before or after the activity. Sometimes, a glass of wine can help reduce autonomic
dysreflexia. Does
recovery occur after spinal cord injury?
Many doctors tell patients
and families that recovery does not occur after spinal cord injury. This is not
true. Recovery is the rule, not
the exception after spinal cord injury. • Segmental recovery. Most
patients recover 1-2 segments below the injury site, even after so-called
“complete” spinal cord injuries.
For example, a person with a C4/5 injury may have deltoid function on
admission and then recover biceps (C5), wrist extensors (C6), and perhaps even
triceps (C7) after several months, and the associated dermatomes. • Recovery due to
methylprednisolone. The second National Acute Spinal Cord Injury Study
(NASCIS 2) showed that patients with “complete” spinal cord injuries and who
did not receive the high-dose steroid methylprednisolone recovered on average
8% of motor function they had lost.
If they received methylprednisolone within 8 hours after injury, they
recovered on average 21% of what they had lost. In contrast, people with “incomplete” spinal cord injury
recovered on average 59% of motor function and 75% if treated with high dose
methylprednisolone. • Recovery of postural reflexes. Most people with cervical or upper thoracic spinal cord injury are
initially unable to control their trunk muscles. However, most will recover better trunk control over months
or even years after injury. • Walking quads and paras. Most people with “incomplete” spinal cord injuries,
i.e. ASIA C, will recover standing or walking. Walking recovery after “complete” spinal cord injuries, i.e.
ASIA A, are rare but can occur in 5% of the cases. In the 1980’s, less than 40% of spinal cord injuries
admitted to hospital were “incomplete”.
However, in the 1990’s, over 60% of spinal cord injuries are
“incomplete” and thus the incidence of “walking quads” or “walking paras” may
be higher than most people think. Both animal and human
studies indicate that as little as 10% of spinal cord tracts can support
substantial function, including locomotion. People often can walk even though a tumor has damaged 90% of
their spinal cord. This is due to
the redundancy and plasticity of the spinal cord. Multiple spinal pathways serve similar or overlapping
functions. Plasticity refers to the ability of axons to sprout and make new
connections. Because transected
spinal cords are rare, most people have some spinal axons crossing the injury
site. This is the basis of the
hope that even slight regeneration of the spinal cord will restore substantial
function. Experimental
Therapies for Subacute Spinal Cord Injury
Several experimental therapies are being tested in clinical
trial for spinal cord injury during the first days or weeks after injury. More information is available in the Clinical
Trial Forum on the CareCure site. • Monosialic ganglioside (GM1,
Sygen). In 1991, Fred Geisler and colleagues reported that
GM1 injected daily for 6 weeks after injury improve locomotor recovery 37
patients. Fidia Pharmaceutical
subsequently tested this therapy in a large multicenter clinical trial in 800
patients, showing that the GM1 accelerated recovery during the first six weeks
but did not significantly improve the extent of recovery at 6-12 months after
injury. Note that this trial is no
longer active. Although the drug
is still available in Europe and South America, the company Fidia has been
bought by another company. CareCure
Forum (GM1) Link • Activated macrophage transplants. In 1998, Michal Schwartz at the Weizmann Institute
reported that activated macrophages obtained from blood and transplanted to the
spinal cord improve functional recovery in rats. The company Proneuron initiated phase 1 clinical trials to
assess feasibility and safety of macrophage transplants in human spinal cord
injury. Preliminary reports
suggest that the treatment is feasible and safe. All the patients had “complete” thoracic spinal cord injury
and received macrophage transplants within 2 weeks after injury. Three of the 8 patients recovered from
ASIA A to ASIA C, more than the expected 5%. A phase 1 clinical trial is continuing at Erasmus Hospital
in Brussels, Belgium. A phase 2
trial is being planned in two U.S. centers including Craig Hospital in Denver
(CO) and Mt. Sinai in New York City (NY). CareCure
Forum (Macrophage) Link • Alternating Current Electrical
Stimulation. In 1999, Richard Borgens and colleagues at Purdue University reported
that alternating currents applied to dog spinal cords stimulated regeneration
and recovery of function in dogs with spinal cord injury. A clinical trial has
commenced at Purdue University for people who are within 2 weeks after acute
spinal cord injury. CareCure
Forum (AC Stim) Link • AIT-082 (Neotrofin). This is a guanosine analog that can be taken orally and reportedly
increases neurotrophins or neural growth factors in the brain and spinal
cord. Neotherapeutics tested this
drug in patients with Alzheimer’s disease. They started a multicenter clinical trial at Ranchos Los
Amigos in Downey (CA), Gaylord Hospital in Wallingford
(CT), and Thomas Jefferson Hospital in Philadelphia. The treatment must be started within 2
weeks after spinal cord injury. CareCure
Forum (AIT-082) Link Experimental Therapies for Chronic Spinal
Cord Injury
Several therapies are
being tested in clinical trials for chronic spinal cord injury, i.e. people
whose neurological recovery has stabilized one or more years after injury. Many other treatments are being
considered for clinical trial (see article
on Advances in Spinal Cord Injury Therapy 25 November 2002). • 4-aminopyridine (4-AP). This
drug is a small molecule that blocks fast voltage sensitive potassium channel
blockers. The drug can be obtained by physician prescription from compounding
pharmacies in the United States.
In addition, Acorda Therapeutics is carrying out a multicenter phase 3
clinical trial of a sustained release formulation of the drug in people who are
more than one and a half years after “incomplete” spinal cord injury. The drug may improve conduction of
demyelinated axons in the spinal cord and preliminary clinical trial results
suggest that the drug may reduce spasticity and improve motor or sensory
function in as many as a third of people with chronic spinal cord injury. See CareCure
Forum (4-AP) Link • Fetal porcine stem cell
transplants. Embryonic stem cells have attracted much
attention. Several studies of
human fetal cell transplants have been carried out in Sweden, Russia, and the
United States, showing that transplanted fetal cells will engraft in human
spinal cords. However, due in part
of the lack of availability of adult human stem cells for transplantation and
politics associated with the use of embryonic human stem cells, the first and
only stem cell therapy trial for spinal cord injury in the United States used
fetal stem cells from pigs. A
phase 1 clinical trial at Washington University in St. Louis (MO) and Albany Medical
Center in Albany (NY) has transplanted fetal stem obtained from pig fetuses and
treated with antibodies to reduce the immune rejection. Sponsored by Diacrin, this trial is
aiming to test 10 patients. See CareCure
Forum (Diacrin) Link • Olfactory ensheathing glial
transplants. Olfactory ensheathing glia (OEG) reside in the olfactory nerve and the
olfactory bulb. They are believed
to be why the olfactory nerve continuously regenerates in adults. OEG cells are made in the nasal mucosa
and migrate up the nerve to the olfactory bulb. Several laboratories have shown that OEG transplants
facilitate regeneration of the spinal cord. Three clinical trials have started in Lisbon (Portugal),
Brisbane (Australia), and Beijing (China). In Lisbon, they are transplanting nasal mucosa obtained from
the patient into the spinal cord.
In Brisbane, they are culturing OEG cells from nasal mucosa and
transplanting the cells to the spinal cord. In Beijing, they are culturing OEG from human fetal
olfactory bulbs and transplanting into the spinal cord. See CareCure
Forum Link (Brisbane) and CareCure
Forum Link (Beijing) Summary
Spinal cord injury is
devastating, not only for the injured person but for families and friends. While much information is available on
Internet, most of the material is scattered and out of date. This article summarizes answers to some
of the most frequently asked questions by people who are encountering spinal
cord injury for the first time.
Spinal cord injury disconnects the brain from the body. This leads not only to loss of
sensation and motor control below the injury site but may be associated with
abnormal activities of the spinal cord both above and below the injury site,
resulting in spasticity, neuropathic pain, and autonomic dysreflexia. Many
functions of our body that we take for granted, such as going to the bathroom,
sexual function, blood pressure and heart rate, digestion, temperature control
and sweating, and other autonomic functions may not only be lost but may be
abnormally active. Finally,
contrary to popular notions about spinal cord injury, recovery is the rule and
not the exception in spinal cord injury.
The recovery takes a long time and may be slowed down or blocked by the
muscle atrophy and learned non-use.
Finally, there is hope.
Many therapies have been shown to regenerate and remyelinate the spinal
cord. Some of these are now in
clinical trials and many more should be in clinical trial soon. |
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