http://journals.lww.com/neurotodayonline/Fulltext/2017/11160/At_the_Bench_Stroke_Recovery__Inducing_Spinal.7.aspx
Neurology Today:
November 16, 2017 - Volume 17 - Issue 22 -
p 19–20
doi: 10.1097/01.NT.0000527322.43736.10
Features
ARTICLE IN BRIEF
In
an animal model of stroke, researchers removed plasticity-inhibiting
signals in the spinal cord (via intraspinal injections of the enzyme
chondroitinase ABC), which augmented rewiring of circuits connecting the
brain to the spinal cord, even weeks after stroke. The researchers
proposed that this plasticity can be harnessed by rehabilitative
training to significantly promote sensorimotor recovery.
A combination of spinal therapy and rehabilitative
training resulted in improved recovery in rats, even 28 days after
experimental stroke conditions were induced, according to a study
published October 12 in The Journal of Neuroscience.
The investigators amplified spinal plasticity during
chronic stroke in male rats via intraspinal injections of chondroitinase
ABC (ChABC), an enzyme that has been found to remove
plasticity-inhibiting signals in the brain. Injections into the
contralesional grey matter of the cervical spinal cord administered 28
days after stroke resulted in significant sprouting of corticospinal
axons originating in the peri-infarct cortex.
Without rehabilitative training, ChABC injection
during chronic stroke led to moderate improvements of sensorimotor
deficits, said Ian R. Winship, PhD, a study author and associate
professor and director of the neurochemical research unit at the
University of Alberta's department of psychiatry in Edmonton, Alberta in
Canada. But combined with the spinal therapy, rehabilitative training
during chronic stroke was much more effective.
“These data suggest that the permanent disability
affecting millions of individuals living with the chronic effects of
stroke may be treatable with spinal therapy and rehabilitation initiated
even months or years after the stroke,” the study authors wrote. “Our
data also emphasize that inducing a state of plasticity is not
sufficient to induce recovery, and that combining such therapies with
rehabilitative therapy is required for optimal recovery.”
After inducing initial ischemic injury in the rats
via photothrombosis, investigators tested their hypothesis that
promoting plasticity in the spinal cord during chronic stroke could spur
advances in recovery from persistent sensorimotor impairment. Sprouting
of spared corticospinal tract axons in the contralesional spinal cord
has a major impact on sensorimotor recovery, they noted, but this
structural plasticity is limited to the first few weeks after stroke.
“The major drawback of the current approach is that
injection of the enzyme only extends a certain distance and acts for a
finite period of time,” Dr. Winship said. “In a human, we need the
enzyme to be active over a much larger region,” he said, because “the
spinal cord is so much bigger in human than in a rat.”
“Our findings strongly suggest that such a treatment
could reduce disability due to stroke. The next question is, what would
actually be required to undertake this approach in humans?” Dr. Winship
told Neurology Today.
He acknowledged that “probably a different delivery
system would be required for humans. One solution may be to employ viral
vectors, which present a way to genetically express the same enzyme in
tissue rather than injecting it directly,” Dr. Winship said. “A viral
delivery system would allow for longer expression and greater spread
within the spinal cord, and therefore, could be safer and possibly
effective in larger animals such as dogs as well as humans.”
“We can do very similar injection procedures without
damaging the spinal cord, without inducing any kind of injury, but we
would need a system like one of these vectors, if the drug is going to
trying to strengthen the wiring between the brain and the spinal cord,”
he said.
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