What's New in
Spinal Cord Injury Treatment and Cure Research?
When someone sustains a spinal cord injury (SCI), one of
the most difficult issues to deal with is that there is
no "cure" at the present time. One would think
that, with the "explosion in scientific
knowledge" we hear about almost every day, SOMEONE
would be doing SOMETHING to find a cure for people with
SCI. If we can achieve the impossible in other areas,
like transplanting entire organs and organ systems from
one person to another and isolating human genes, why
can't we figure out why the spinal cord does not repair
itself and then do something to correct this biological
problem? Compared to a lot of the scientific puzzles that
HAVE been solved, it shouldn't be all that difficult...
There are really two separate issues involved in this
- Is the scientific question, "Why won't the
spinal cord regenerate?" easy to answer?
- What's being done to find a cure?
Let's look at these issues and put them into the
context of what scientists have been doing about SCI over
the past half century.
Before World War II, an injury to the spinal cord was
considered to be a fatal condition. If you did not die as
a direct result of the injury, you probably would die
within a few weeks or months from complications, such as
a kidney infection, respiratory problems, or badly
infected skin sores.
Fortunately, an improved understanding of SCI led to
better patient management, enabling many people to
survive their injuries and the initial period afterwards.
In addition, the discovery of penicillin and sulfa drugs
made common, but life-threatening complica-tions like
kidney and skin infections manageable conditions rather
than potential killers.
Because the spinal cord carries vital information to
the brain, the muscles and many organs, the fact that SCI
is now a survivable injury is a miracle itself. However,
this miracle leads to another pressing need - to find a
way to reverse, or at least diminish, the devastating
physical effects of the injury.
The Search For the Cure
The 1980's and 1990's have been an exciting time for
people interested in spinal cord injury repair and
regeneration. Both in terms of treat-ment techniques and
general knowledge about nervous system function, the
progress that has occurred in recent years is
The search for a cure involves one of the most complex
parts of the human body. The spinal cord is an integral
part of the body's most specialized system, the central
nervous system (CNS). The CNS consists primarily of the
brain and spinal cord.
A major role of the spinal cord is to carry mes-sages
to and from all parts of the body and the brain. Some of
these messages control sensation, such as knowing your
finger is touching a hot stove, while others regulate
movement. The spinal cord also carries mes-sages that
regulate autonomic functions such as heart rate and
breathing - over which we generally do not exert
The spinal cord carries these messages through a
network of nerves which link the cells of the spinal cord
to target cells in all other systems of the body. An
individual nerve cell is called a neuron, each with
receptive branching fibers called dendrites. The axon,
carrying an output signal, extends from the cell body,
and is covered by a protective fatty substance called a
myelin sheath which helps the impulse travel efficiently.
A nerve impulse from one neuron is picked up by the
dendrite of the next nerve cell in the pathway at a
specialized connection called a synapse. An
electrochemical reaction causes the impulse to
"jump" across the synapse and the signal
stimulates the second nerve cell and the impulse then
travels down its axon. The message is picked up and
transmitted by a series of neurons until the connection
There are millions of nerve cells within the spinal
cord itself. Some of these lower motor neurons receive
motor commands from the brain and send their signals
directly to the muscles. Other spinal cord neurons form
relay pathways for information travelling up or down the
length of the spinal cord. Still other spinal cord
neurons remain intact and form intricate circuits below
the level of injury. Because cells below the injury are
no longer under voluntary control, they cannot be
utilized as effectively and may cause unintentional
movements such as spasms.
Most of the cells in the human body have the ability
to repair themselves after an injury. If you cut your
finger, often you have a visible laceration for a few
days or weeks, followed by the formation of a scar. In
time, you may not be able to tell that the cut had
occurred. This indicates that skin cells regenerate, just
like cells in the blood vessels, organs and many other
tissues. Peripheral nerves (nerve fibers outside the
brain and spinal cord), such as those located in your
fingertips, also regenerate, although this process is
different from that in the skin and other organs.
For years, scientists have focused on the big mystery:
"Why doesn't the central nervous system
regenerate?" This question is even more perplexing
because we know that central nerves in lower animal
species CAN regenerate. There are no definite answers to
this mystery yet, but scientists are exploring the
questions in many ways.
Basic Cell Research
An important avenue of research is to look at normal
cell function in the CNS of mammals. Scientists
investigating this area of research are attempting to
identify and describe cellular interactions in properly
working systems. In addition, they are working with SCI
models in an attempt to identify and explain what occurs
after an injury.
Through cell research, scientists are trying to
identify the following:
1. What substances are present in the CNS which
"switch off" CNS nerve growth in mammals?
- It has been shown that regeneration occurs in
lower animals, as well as in mammalian fetuses in
the very early stages of development. At some
point in development, the cells appear to lose
the ability to regenerate. This loss may be
related to the maturation of the nerve cells or
to changes in other nervous system cells past
which axons must regenerate.
2. What growth inhibiting factors, present in the CNS
of mammals, prevent nerve cells from regenerating and
reestablishing connections (synapses)?
- Scientists have identified some proteins in the
myelin sheath surrounding spinal cord axons which
inhibit nerve cell growth. Additionally, other
regeneration-inhibiting proteins have been
identified on the surfaces of cells that form the
nervous system equivalent of a "scar".
Some scientists believe that nerve cells can be
encouraged to regrow and re-establish functional
synapses by removing or altering this cellular
"scar". Antibodies generated against
some of these proteins can neutralize the
inhibitors and allow growth to occur. The ability
of central nerves to regenerate in lower animals
is thought to be due to the lack of inhibitors in
3. Can growth stimulating substances can be introduced
into the mammalian CNS to encourage nerve growth and
- Investigators are attempting to alter the
environment around the injury site to encourage
nerve cell growth and repair. As described above,
our peripheral nerves can regenerate. This is due
to the presence of cell proteins that stimulate
rather than inhibit nerve growth. When these
cells or the factors they produce such as
"growth factors that nourish nerve cells are
introduced into the CNS, central nerve regrowth
can occur. Finding ways to effectively introduce
these cells or substances to achieve functional
recovery is a major goal of "cure"
Development of New Therapeutic
Ongoing research using animal models to test possible
new therapies is progressing more rapidly than ever
before. This type of research takes several forms that
can best be explained as they apply to solving certain
types of damage that result from SCI. There are three
major classes of damage to neural tissues that have been
identified, each requiring a different therapeutic
- Death of nerve cells within the spinal cord.
Because nerve cells lose the ability to undergo
cell division as they mature into the highly
specialized forms that make up our nervous
systems, the death of nerve cells due to injury
presents a difficult problem. No functional
connections can be established if the nerves no
longer exist. Therefore, replacement of nerve
cells may be required.
- Disruption of nerve pathways. When the long axons
carrying signals up and down the spinal cord are
cut or damaged to the point where they break down
after an injury, the parents nerve cells and
axons often survive up to the point where the
injury occurred. In this case, regeneration of
damaged axons is a real possibility to
re-establish connections of nerve circuits.
- Demyelination, or the loss of the insulation
around axons. Animal studies and recent studies
of human specimens have established that in some
types of SCI, the nerve cells and axons may not
be lost or interrupted, but that the loss of
function may be due to a loss of myelin sheaths.
As described above, myelin sheaths provide
insulation so that electrochemical signals are
carried efficiently down the long, thin axons.
This type of damage may be the most amenable to
treatment because rewiring of complex circuits
may not be needed and remyelination of axons is
known to be possible.
Although specific human injuries may involve any or
all types of damage just described, therapies developed
to combat any one of them might restore important
functions. The "cure" for spinal cord injury
may take the form of multiple strategies, each in turn
restoring functions that make important improvements in
the quality of life for a spinal cord injured individual.
The approach to "cure" research then, is to
concentrate on techniques that hold the promise of
repairing specific types of spinal cord damage. With the
explosion of efforts and progress in the fields of
Neuroscience and Molecular Biology (sometimes called
genetic engineering), the scope of possible new therapies
is wider than ever before.
Replacement of Nerve Cells
Mature nerve cells cannot divide to heal a wound as
skin cells can. Replacement of nerve cells requires
transplantation of new nerve cells into the site of the
injury with the hope that they will mature and integrate
themselves into the host nervous system. One approach is
to transplant healthy CNS cells from the same animal
species. Researchers have been unanimous in their
agreement that transplantation of adult nerve tissues
does not work, while embryonic or fetal transplantation
can be quite successful. The embryonic tissues do grow
and develop, and scientists hope that they will form
circuits that will return important functions to areas
below the injury. Research to date has not supported the
hope that host axons would use these grafts as
"bridges" across the injury site. An important
consideration is that if fetal tissue transplants prove
successful in animal models, transferring this approach
to human beings will involve important ethical
considerations regarding donor tissues and other
important questions about immune rejection of cells
transplanted from one individual to another.
Another approach that may avoid some of those problems
is the use of genetic engineering to manufacture
"cell lines" that would work as nerve cells
after grafting. This approach involves inserting segments
of DNA (genes) into fetal nerve cells that allow the
cells to divide indefinitely, creating an ongoing supply
of donor tissue. The use of purely neuronal cell lines
diminishes the chances of immunological rejection of the
grafts. Recently, rodent cell lines have been developed
that stop dividing after transplantation (so there is no
risk of tumor formation), and that mature into very
specialized nerve cells. Research has not yet shown that
these cells can restore function after spinal cord
Very recently, scientists have learned that some cells
of the adult CNS can be stimulated to divide and develop
into new nerve cells. This exciting finding has opened up
new possibilities for cell line development without a
need for fetal tissue donors.
Regeneration of Damaged Axons
Nerve cells in both the central and peripheral nervous
systems are associated with helper cells called
neuroglial cells. After injury, the CNS helper cells
largely inhibit regeneration, while those of the
peripheral nerves, the Schwann cells, stimulate
regeneration, even in humans. Scientists are attempting
to isolate these cells from peripheral nerves and
transplant them into the spinal cord to induce
regeneration by providing an altered, supportive
environment. In this strategy, a SCI individual could act
as their own donor, since Schwann cells can be obtained
from biopsies of peripheral nerves in adults.
Schwann cells, nerve cells and some other cells make
proteins known to nourish nerve cells called "growth
factors". By introducing these factors into injury
sites alone or in combination with grafts, researchers
hope to stimulate additional nerve regeneration and
promote the health of nerve cells. This approach has been
shown to stimulate CNS regeneration, including growth of
axons from nerve cells within the spinal cord and those
from the brain that send their long axons down the spinal
cord. Significant restoration of function has not yet
Another technique is to genetically alter cells so
that they produce large amounts of growth factors and to
introduce these into the injury site. While nerve fibers
have been stimulated to grow by such grafts, this type of
research is in its very early stages. Cells making many
types of factors will have to be tested and functional
recovery carefully demonstrated.
Remyelination of Axons
Schwann cells are also the cells in peripheral nerves
that form myelin sheaths. They are not usually found in
the brain or spinal cord where another neuroglial cell,
the ogliodendrocyte, is responsible for making myelin.
Researchers have shown that Schwann cells grafted into
the brain can myelinate central axons. When the loss of
myelin is an important part of injury, implanting Schwann
cells could stimulate remyelination and thereby restore
Another approach involves a drug called
4-aminopyridine (4-AP), which may help demyelinated
nerves conduct signals. Animal studies show that a very
small percent of healthy, myelinated axons can be enough
to carry on important functions in the spinal cord, even
in the face of damage to surrounding nerve cells. Helping
nerve fibers that have lost myelin to conduct impulses
should improve function after injuries that extensively
damage myelin sheaths but do not disrupt nerve
connections. This research is also in its very early
Summary of Basic Science
As you can see by the facts detailed above, the
problem of CNS response to injury is incredibly complex.
No one theory or approach will overcome all of the
effects of SCI, and many scientists now believe that the
"cure" will not be found in a single approach,
but rather in a combination of techniques. Consequently,
it is important for all possible research areas to be
addressed so our overall knowledge about how the system
works may eventually lead to a cure for SCI.
What about the "imminent breakthroughs" you
hear about regularly in the press? It must be remembered
that there is a vast difference between a
"scientific breakthrough" and a "clinical
breakthrough". While scientific discoveries occur
quite frequently, clinical (treatment) ones do not.
Public announcements of scientific progress help to keep
the attention and funding focused on finding solutions to
the problems caused by SCI but new scientific
breakthroughs generally do not lead to immediate
RESEARCH IN SCI TREATMENT
Drug Treatments For New
NOTE: It is important to realize these drugs are not a
cure for chronic (long-term) spinal cord injuries. It is
heart-ening to note, however, that treatments finally are
available to lessen the severity of some acute injuries.
Research has shown that all damage in SCI does not
occur instantaneously. Mechanical disruption of nerves
and nerve fibers occurs at the time of injury. Within 30
minutes, hemorrhaging is observed in the damaged area of
the spinal cord and this may expand over the next few
hours. By several hours, inflammatory cells enter the
area of spinal cord injury and their secretions cause
chemical changes that can further damage nervous tissue.
Cellular content of nerve cells killed by the injury
contribute to this harmful chemical environment. This
process may go on for days or even weeks.
Hope lies, therefore, in treatments that could prevent
these stages of progressive damage. Drugs that protect
nerve cells following injury are now available to lessen
the severity of some injuries. Other drugs and
combinations of drugs are currently being tested in both
animal and clinical trials.
Few treatment approaches have raised as much hope as
the announcement by the National Institute of Health that
the steroid, methylprednisolone, reduces the degree of
paralysis if administered shortly after spinal cord
In clinical trials, an extremely high dosage of
methylprednisolone was used in a double-blind study
(neither patients nor doctors knew who was getting the
exper-i-mental drug). The improvement in some patients
was so remark-able that the National Institutes of Health
felt it was important to "break the code"
(i.e., determine who was getting the drug and who was
not) so more patients could potentially be helped.
Overall, the trial showed that while the
methylprednisolone treated group retained significantly
more function than the placebo group, subjects in both
groups experienced chronic loss of function due to their
Methylprednisolone is effective only if used in high
doses within eight hours of acute injury. It is
hypothesized that this drug reduces damage caused by the
inflammation of the injured spinal cord and the bursting
open of the damaged cells. The contents of the damaged
cells are believed to adversely affect adjacent cells.
High doses of methylprednisolone can lead to side
effects, such as suppression of the immune system, but no
serious problems have been reported when it is used over
a short term as in this study.
Because the success of the methylprednisolone trial
had changed the "standard of care" in the
United States, subsequent drug trials are now testing the
effectiveness of other drugs in combination with
methylprednisolone administration. Thus, to demonstrate
significant effectiveness, new treatments will have to
surpass the functional sparing effects seen with
Simultaneously, researchers are cooperating to conduct
a large multi-center animal study to test the effect of
other drugs with or without methylprednisolone.
Similar positive results to those of
methylprednisolone have been achieved in animal studies
using another steroid, tirilizade mesylate (Freedox®).
This drug, which acts like methylprednisolone, also
appears to be effective only if administered within a few
hours after injury. From initial animal studies, it
appears that this drug may cause less side effects than
methylprednisolone. Clinical trials are ongoing.
A large clinical trial with humans is currently
underway comparing 48 hour treatment of
methylprednisolone with or without added tirilizade.
Study results are anticipated to be available in late
Once again, the announcement of a new treatment
approach has raised interest and hope in the SCI
community. In a small study, the experimental drug
Sygen®, or GM-1 Ganglioside, was given within 72 hours
of injury and then continued for up to 32 days.
Neurological assessments were conducted up to one year
after the treatment. Individuals who received
Sygen®showed significantly more functional recovery than
those who received a placebo.
Currently, a large scale multi-center clinical trial
of GM-1 is ongoing with a targeted completion date of
1996-1997. In the current study, all patients receive the
"standard" does of methylprednisolone. In
earlier studies, a standard dose of methylprednisolone
was not given.
There are two theories about how GM-1 Ganglioside may
act on spinal cord tissue. The first is that it performs
some type of damage control by reducing the toxicity of
amino acids released after spinal cord tissue is injured.
The "excitatory" amino acids cause cells to die
and increase the damage caused by the initial injury. The
second theory suggests there may be a neurotrophic
effect, somehow encouraging the growth of injured
neurons. Neither of these theories have been
scientifically proven yet.
Sygen®has not yet been approved for clinical use in
this country by the Food and Drug Administration (FDA).
It has only been used in a limited number of experiments.
Sygen®was provided recently to injured football player
Dennis Byrd and approximately 65 other patients through
an open-label protocol. Although this protocol is no
longer in effect, the large double-blind, multi-center
trial in acute SCI mentioned above is well underway.
Clinical studies are being conducted by surgeons to
determine the optimum time for surgery to relieve
pressure on the spinal cord after spinal cord injury.
Additionally, the use of delayed decompressive surgery is
being investigated in cases of chronic SCI.
Preventing new injuries during
Intraoperative monitoring techniques have been
developed to protect healthy nerve roots during spinal
stabilization procedures. Scientists tested, first on
animals then on humans, a technique that assists surgeons
in the placement of metallic hardware for stabilization
of the spine. The technique which utilizes nerve
stimulation and muscle responses has been shown to
effectively predict and allow the prevention of nerve
damage during surgery in the lumbosacral spinal column.
TREATMENTS FOR CHRONIC SPINAL
AND ITS COMPLICATIONS
FES uses implanted or external electrodes to stimulate
paralyzed nerves so that arms and legs can be used for
improved function. Over the past decade, three primary
applications for FES have been developed: FES for
exercise; FES for upper extremity (hand/arm) function;
and FES for lower extremity (leg function.) FES is
discussed in detail in Fact Sheet No. 9,
Functional Electrical Stimulation: Clinical Applications.
One controversial treatment for SCI is Omentum
Transposition. The omentum is a band of tissue in the
abdomen of mammals which provides circulation to the
A surgical procedure is used to partially detach the
omentum, tunnel it under the skin and suture it in place
at the injury site. The omentum tissue, which is rich in
blood vessels, may supply the damaged nerve cells with
vital oxygen. It is believed that the omentum tissue may
also secrete chemicals that stimulate nerve growth, as
well as have the ability to soak up fluids to reduce
pressure which can damage nerve cells.
Initial animal trials seem to show some functional
improvement if the operation is completed within 3 hours
of injury. Little or no improvement is shown when the
procedure is done 6-8 hours post injury. This research,
however, has never been scientifically documented.
The on-going clinical trial for people who have had a
SCI for months or years has recently been cancelled. Many
scientists believe it is premature for human trials,
since the results of the earlier research have not been
Scientists in the field of biomedical engineering
developed mechanical devices that use today's computer
technology to assist individuals in activities of daily
life. Examples of the types of devices under research and
development are environmental control devices, electronic
had grip device, and walking devices.
The complications of spasticity and pain are common in
spinal cord injury. Spasticity that is severe enough to
cause problems with mobility and self care, that
contributes to skin breakdown, and that causes pain is
reported in a number of cases of SCI.
Studies in the treatment of spasticity are
investigating pharmacological agents, intrathecal
baclofen, and spinal cord stimulation. In addition to
drugs that have been available for some time (baclofen,
valium, dantrium) the use of tizanidine has recently been
explored. FDA approval of tizanidine is expected in late
The problem of pain occurs in approximately 50% of all
cases of SCI. Five to thirty percent characterize the
pain as disabling. Pharmacologic agents as well as
surgical interventions such as the DREZ (dorsal root
entry zone) procedure, cordotomy and cordectomy are under
investigation for the treatment of severe causes of pain
In most SCI men, the ability to have an ejaculation
and to father a child naturally is diminished. In fact,
ten years ago, doctors were telling newly injured SCI men
that they would not be able to father their own children.
With advances made in procedures to assist men in
obtaining an ejaculation as well as advances in assistive
reproduction technology, SCI men now have the potential
to become biological fathers. Vibratory stimulation and
electroejaculation are procedures that have been
investigated and are currently available to assist men in
Obtaining the ejaculation is only part of the
fertility problem in SCI men, however, the semen from SCI
men most often contains a lower than normal percent of
motile sperm. Questions that researchers hope to be able
to answer with investigations on the quality of sperm of
SCI men are: what happens to semen quality following SCI?
and how successful is artificial insemination and other
reproductive technology using semen from SCI men?
Technology and research are making it possible for
spinal cord injured men to consider options regarding
their fertility and is providing a more encouraging
answer to the question, "Will I be able to have
children?" Additional Information is available in Factsheet #10:
Male Reproductive Function after Spinal Cord Injury.
Various controversial treatments for SCI have come and
gone over the years, but none have proved to be effective
in reversing the damage to the spinal cord that occurs in
spinal cord injury. Often alternative therapies are very
difficult to evaluate because of the unscientific nature
in which the treatments are introduced to the human
population. Many alternative therapies have no documented
scientific evidence to substantiate their effectiveness.
Currently, examples of treatments that fall into this
category are the use of Sygen (GM-1) in chronic injuries
and omentum transposition.
Summary of Treatment Research
Over the last several years there has been progress in
the treatment of acute SCI to limit damage and preserve
function. Treatment of chronic SCI presents a greater
challenge, as damage that has already occurred must be
corrected and then reversed.
It is entirely possible that, given appropriate
financial support, many of the complex problems of SCI
one day will be solved. Until that day arrives, it is
import-ant to urge the federal government to provide
broad-based support for basic science research so the
fundamental questions about how and why the CNS acts the
way it does can be answered. A cure or new treatments are
possible only if scientists receive the support necessary
to con-tinue their work in this important area.
- For further information on Freedox®clinical
trials, contact: Upjohn Company, 929 Lawrence
Court, N. Bellmore, NY 11710, 516-486-5276.
- For further information on Sygen®clinical
trials, contact: Fidia Pharmaceutical Corp., 1401
I Street, NW, #900, Washington, DC 20005,
- For further information about FES applications,
contact: the F.E.S. Information Center, 25100
Euclid Avenue, Suite 105, Cleveland, OH 44117,
- For further information about The Miami Project,
contact: The Miami Project, 1600 Northwest 10th
Avenue, R-48, Miami, FL 33136, 1-800-STAND-UP.
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Bunge, R.P., et. al (1991) Isolation and Functional
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This fact sheet was prepared with the
assistance of Dr. Cheryl Chanaud of the National
Institutes of Health and Dr. Naomi Kleitman and Marie
Amador, RN, CRRN of the Miami Project to Cure Paralysis.
This factsheet is offered as an information service and
is not intended to cover all treatments nor research in
the field, nor is it an endorsement of the methods
mentioned herein. Any information you may have to offer
to further update this factsheet would be greatly
appreciated. The National Spinal Cord Injury Resource
Center (NSCIRC) provides information and referral on any
subject related to spinal cord injury. Contact the
resource center at 1-800-962-9629.
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