Throughout this resource, various therapies have
been discussed that may be neuroprotective when administered soon after
injury. Because it is important to have quick access to such
information, the therapies are briefly summarized here. Those desiring
further information can review the more in-depth discussions posted
Some of the therapies represent approaches used by
humans for other health purposes (hence, presumably reasonably safe) but
have also shown potential in animals with experimental SCI.
Methylprednisolone, a synthetic steroid, is
often administered soon after injury. Although widely assumed to be a
post-injury standard of care, some scientists are challenging that
assumption. The drug minimizes post-injury neurological
damage by inhibiting lipid peroxidation, a biochemical process that
mediates secondary damage to the injured cord.
Other drugs with therapeutic potential that are in
or never completed the clinical trials pipeline are discussed in the
Commonly Consumed Human Drugs with Suggestive
SCI Animal Studies:
Animal studies suggest that some widely consumed
and presumably safe human drugs have potential for treating acute SCI.
Though one must be careful extrapolating the results of animal studies,
the widespread consumption of these drugs makes them easier candidates
to be considered for human SCI. To varying degrees, they should be
placed in the “little-to-lose-and-everything-to-gain” category.
1) Lipitor (i.e., atorvastatin) is a
cholesterol-lowering medicine belonging to the statin-drug group and one
of society’s most widely used drugs. Studies suggest that Lipitor or
related statin drugs exert a neuroprotective and anti-inflammatory
influence for various neurological disorders, including SCI. In
Lipitor-treated rats there was more tissue sparing, including 1) less
degeneration of neuronal axons, 2) degradation of the
conduction-promoting, axon-insulating myelin sheath, 3) scar formation,
and 4) programmed cell deaths.
2) Ibuprofen, a non-steroidal
anti-inflammatory drug, is marketed under many brand names (e.g., Advil,
Motrin, etc). It blocks the injury-triggered production of a protein
that 1) inhibits axonal growth and regeneration, and 2) initiates a
physiological cascade that results in the death of nearby neuronal
cells. Animal studies indicate ibuprofen stimulates the growth of
neurons and recovery of walking ability.
3) Erythropoietin (EPO) is a growth hormone
produced by the kidney that stimulates red blood cell production. It has
been used to treat kidney disease and to ameliorate the side effects of
cancer chemotherapy or radiation-induced anemia; and as a blood-doping
agent to enhance athletic performance. In animals, EPO 1) blocks
injury-related cell death, 2) prevents hypoxia in which limited oxygen
reaches the spinal cord, 3) inhibits the damage caused by damaging
excitotoxins, 4) reduces injury-site inflammation, 5) restores
blood-flow-promoting vascular integrity, and 6) enhances neuronal
regeneration through stem-cell stimulation.
Because new drug development is driven by
economics, non-patentable herbal remedies are often pushed to the
backburner. They also don’t fit well with the process of scientists who
prefer to study cause and effect in purified molecules rather than
multi-component herbal medicines. Nevertheless, several widely consumed
herbal remedies may possess neuroprotective properties after acute SCI,
1) Ginkgo Biloba, one of mankind’s most
ancient and widely consumed medicines, may provide benefits for a
variety of neurological disorders, including SCI. Ginkgo is an
antioxidant, maintains cell-membrane integrity, enhances oxygen use and
metabolism, augments neurotransmission, and inhibits programmed cell
death. In rats, ginkgo lessens damage-causing lipid peroxidation to even
a greater degree than methylprednisolone. Ginkgo-treated rats had
smaller injury-related cavities and less conduction-inhibiting
2) Buyang Huanwu Decoction is a Traditional
Chinese multi-component herbal medicine that has been used for centuries
to treat a variety of disorders, including paralysis. From traditional
philosophy, it invigorates the body, promotes blood circulation, and
activates energy channels. Animal studies indicate that BYHWD promotes
nerve regeneration and functional recovery after stroke and both
peripheral-nerve and spinal-cord injuries. It 1) stimulates the
outgrowth and differentiation of budding neuronal stem cells,
2) inhibits post-injury, programmed cell death; and 3) decreases
damage-perpetuating free-radical generation and lipid peroxidation.
Animal studies suggest that fasting every other day
improved functional recovery, preserved neuronal integrity, reduced
injury-site lesion size, increased axonal sprouting, and raised the
blood levels of neuroprotective agents. Similar neuroprotection has also
been observed for traumatic brain injury.
Melatonin, readily available from
vitamin stores as a sleep aid, is produced by the pineal gland and is a
powerful antioxidant. Like methylprednisolone, animal
studies indicate that melatonin inhibits lipid peroxidation and various
injury-aggravating inflammatory processes, reduces the size of the
injury-site cavity, and promotes functional recovery.
Quercetin is another common nutritional
supplement that has been shown to reduce neurological damage in animals
after acute injury. Belonging to a family of molecules called
flavonoids, quercetin imbues coloring to many foods. Like melatonin,
quercetin is an antioxidant. By scavenging free radicals, it inhibits
the damage-perpetuating lipid peroxidation that occurs soon after
Vitamin E also appears to be neuroprotective
after acute injury. Like quercetin and melatonin, this vitamin is an
antioxidant that protects cell membranes from lipid-peroxidation and, by
so doing, preserves neighboring neurons and axons.
1) Acupuncture may restore some function in
both acute and chronic SCI. Under Traditional Chinese Medicine theory,
SCI damages key energy meridians which channel live force energy
throughout the body. Acupuncture’s goal is to clear and activate these
meridians, reversing energy stagnation.
A number of potential mechanisms by
which acupuncture could exert beneficial effects after SCI have been
suggested, including 1) reducing the levels of proteins and cells (e.g.,
astrocytes) fostering injury-site scar formation, 2) reducing the
creation of damage-perpetuating free-radicals, 3) lessening spinal cord
atrophy after injury, 4) decreasing stress as measured by the production
of cortisol, 5) raising the levels of various regeneration-enhancing
molecules, 6) increasing blood flow, and 7) releasing neuroprotective,
endorphin-like molecules. Acupuncture also influences the
expression of stem cells.
2) Scalp Acupuncture,
a specialized form of acupuncture, is especially helpful for
nervous-system disorders. Many individuals with SCI have been treated
and have accrued significant benefits. Greater benefits accrue if scalp
acupuncture is administered soon after injury.
HYPERBARIC OXYGEN THERAPY
Hyperbaric oxygen therapy (HBO) is commonly used
to treat decompression sickness in divers. Patients are placed in
chambers pressurized at 2-3 atmospheres containing up to 100% oxygen.
Animal and human studies suggests that HBO is beneficial for treating a
variety of neurological disorders in which blood-flow-related
oxygenation may be compromised, including acute SCI. The therapeutic
premise is that HBO will force oxygen into oxygen-deprived, injured CNS
tissue. HBO also stimulates the body’s production of stem cells, which
may exert regenerative influences.
directs a pulsed-electromagnetic field
to an area of injury. Animal and human studies indicate that this
treatment soon after SCI protects neurons, promotes regeneration, and
minimizes lost function.
Animal and human studies suggest that OFS promotes neuronal regeneration
after acute injury. Based upon observations that electrical cues can
guide and promote neuronal growth, electrodes are placed above and below
the injury site with alternating polarity to stimulate regeneration of
both ascending and descending neurons. OFS is only beneficial for acute
FUNCTIONAL ELECTRICAL STIMULATION
Functional Electrical Stimulation
(FES) uses electrical
current to stimulate functions lost through nervous-system impairment.
Various FES devices have been developed to enhance grasping, and, if
used soon after injury, some
may improve voluntary control.
With varying degrees of success, there is a long
experimental history of using hypothermic cooling after acute injury to
slow down damage-mediating physiological processes. Earlier efforts used
localized procedures which directly cooled the spinal-cord injury site.
More recently, efforts have focused on systemic cooling in which a
cooling catheter is placed in the patient’s blood vessel, and a
thermo-regulating device closely monitors and adjusts blood temperature
as it passes by the catheter.