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Re: spinal cord stimulator for PD
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Ray
Rayilyn Brown Director AZNPF Arizona Chapter National Parkinson Foundation rbrown@xxxxxxxxx
-------------------------------------------------- From: "Nic Marais" <marais.nic@xxxxxxxxx> Sent: Friday, March 20, 2009 12:59 AM To: <PARKINSN@xxxxxxxxxxxxxxxxxxxx> Subject: Re: spinal cord stimulator for PD
Now this looks promising...
Nic 57/15
On Fri, Mar 20, 2009 at 4:46 AM, rayilynlee <rayilynlee@xxxxxxx> wrote:
Novel spinal cord stimulator sparks hope for Parkinson's disease treatment
DURHAM, NC - A novel stimulation method, the first potential therapy to
target the spinal cord instead of the brain, may offer an effective and less
invasive approach for Parkinson's disease treatment, according to
pre-clinical data published in the journal Science by researchers at Duke
University Medical Center.
Researchers developed a prosthetic device that applies electrical
stimulation to the dorsal column in the spinal cord, which is a main sensory
pathway carrying tactile information from the body to the brain. The device
was attached to the surface of the spinal cord in mice and rats with
depleted levels of the chemical dopamine - mimicking the biologic
characteristics of someone with Parkinson's disease along with the impaired
motor skills seen in advanced stages of the disease.
When the device was turned on, the dopamine-depleted animals' slow, stiff
movements were replaced with the active behaviors of healthy mice and rats.
Improved movement was typically observed within 3.35 seconds after
stimulation.
"We see an almost immediate and dramatic change in the animal's ability to
function when the device stimulates the spinal cord," says senior study
investigator Miguel Nicolelis, M.D., Ph.D., the Anne W. Deane Professor of
Neuroscience at Duke. "Moreover, it is easy to use, significantly less
invasive than other alternatives to medication, such as deep brain
stimulation, and has the potential for widespread use in conjunction with
medications typically used to treat Parkinson's disease."
Researchers tested mice and rats with acute and chronic dopamine deficit using varying levels of electrical stimulation and in combination with different doses of dopamine replacement therapy, also known as 3,4-dihydroxy-L-phenylalanine or L-DOPA, to determine the most effective pairing.
When the device was used without additional medication, Parkinsonian
animals were 26 times more active. When stimulation was coupled with
medication, only two L-DOPA doses were needed to produce movement compared
to five doses when the medication was used by itself.
"This work addresses an important need because people living with
Parkinson's disease face a difficult reality - L-Dopa will eventually stop
managing the symptoms," explains Romulo Fuentes, a postdoctoral fellow at
Duke University and lead author of the study. "Patients are left with few
options for treatment, including electrical stimulation of the brain, which
is appropriate for only a subset of patients."
While deep brain stimulation (DBS) and other experimental treatments attack
the disease at its origin - in the brain - Nicolelis and team took a
different approach. The concept for the device began when researchers made a
surprising connection with another neurological condition.
"It was a moment of sudden insight," explains Nicolelis. "We were analyzing
the brain activity of mice with Parkinson's disease and suddenly it reminded
me of some research I'd done in the epilepsy field a decade earlier. The
ideas began to flow from there."
The rhythmic brain activity in the animals with Parkinson's disease
resembled the mild, continuous, low-frequency seizures that are seen in
those with epilepsy. One effective therapy for treating epilepsy involves
stimulating the peripheral nerves, which facilitate communication between
the spinal cord and the body. Researchers took that concept and developed a
modified approach for a Parkinson's disease model.
Nicolelis says that the low frequency seizures, or oscillations, seen in
the animal model of Parkinson's disease have been observed in humans with
the condition. Stimulating the dorsal column of the spinal cord reduces
these oscillations, which researchers believe creates the ability to produce
motor function.
In a healthy body, neurons fire at varying rates as information is
transmitted between the brain and the body to initiate normal movement. This
process breaks down in someone with Parkinson's disease.
"Our device works as an interface with the brain to produce a neural state
permissive for locomotion, facilitating immediate and dramatic recovery of
movement," says Per Petersson, co-author of the study. "Following
stimulation, the neurons desynchronize, similar to the firing pattern that
you would see when a healthy mouse is continuously moving."
Nicolelis says that if the device is proven safe and effective through
further research, he imagines it mirroring similar spinal cord stimulator
technology currently used to treat chronic pain. Small leads are implanted
over the spinal cord and then connected to a portable generator, a small
device capable of producing mild electrical currents. During the trial
period, the generator is external, while for permanent treatment it would be
implanted below the skin.
"If we can demonstrate that the device is safe and effective over the long
term in primates and then humans, virtually every patient could be eligible
for this treatment in the near future," Nicolelis said.
The Duke team is collaborating with neuroscientists at the Edmond and Lily
Safra International Institute of Neuroscience in Natal, Brazil, to test the
new procedure in primate models of Parkinson's disease prior to initiating
clinical studies. Neuroscientists from the Brain and Mind Institute at the
Swiss Institute of Technology (EPFL), in Lausanne, Switzerland, will also
participate in this international research effort to translate these new
findings into clinical practice.
###
Study co-authors include William Siesser and Marc Caron.
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