Chronic pain remains cruel challenge to treat
SEE PAIN, PAGE C-2
After a car accident 32 years ago, Mariann Farrell, 70, of Shaler, lives with pain that won’t go away, which is only partially relieved by opioid medication and other relief measures, including meditation.
She walked away from the accident.
“I thought I was fine,” she said, “until the next day — when my back, neck, right leg all started hurting. The pain grew worse and worse, and it never stopped. After many doctors, tests and X-rays, it turned into a chronic pain situation.”
She said she saw 25 doctors, physical therapists and psychologists over 30 years.
“Eventually you learn this is it. This is the way that I am and what am I going to do about it? The medical end of it is not going to change … How do I move on with my life?”
Daily pain afflicts about 25.3 million adults in the United States, according to research cited in a May 11 online viewpoint in the Journal of the American Medical Association. Low back pain, neck pain and osteoarthritis are among the leading nine causes of disability, according to the opinion by Kurt Kroenke of the Indiana University School of Medicine and Andrea Cheville of the Mayo Clinic.
Drs. Kroenke and Cheville recommended more research into pain-relief methods, including nondrug solutions, and fewer references to an “opioid epidemic,” saying the term disproportionately focuses on reducing opioid use. They wrote, “only a small fraction of patients prescribed opioids progress to long-term use.” Those who find their pain under control and are
study provides a new approach to treating symptoms of Parkinson’s disease that’s caused by the death of “dopamine neurons” that feed into the brain’s basal ganglia. When it ceases to work properly, the body can’t initiate voluntary movement.
The study also outlines more thoroughly how the circuitry of neurons in the basal ganglia behave in Parkinson’s disease.
Specifically, the team identified and targeted two cell groups and discovered that stimulating the PVGPe group more than the Lhx6-GPe group reversed aberrant brain activity and restored normal movement to a mouse with induced Parkinson’s disease.
Current treatments for Parkinson’s disease include deep-brain stimulation, which uses a battery-powered generator implanted under the skin of the chest and wired to an electrode embedded in the basal ganglia to provide constant electrical stimulation to all neurons. It works well in arresting the symptoms, as long as the power is on.
The new method, however, would require stimulation once every few hours.
“I think this is tremendous research,” said Donald Whiting, system chair for the Allegheny Health Network Neuroscience Institute and chair of its department of neurosurgery. “I’ve been doing deep-brain stimulation [in patients] for 20 years, and it has done really well in reducing the disorders and symptoms, and it’s a mainstay [treatment]. But we could do better with it.
“I think what Dr. Gittis has done is revolutionary,” he said, describing it as “a great segue” into research that could help patients in the near term.
He’s now working with the Gittis team to use electrical rather than light stimulation to activate targeted neurons to restore normal function for hours at a time. Key is determining the right type and level of electrical stimulation to replicate the effect of light energy through an optical fiber, whose use in humans still requires extensive research.
Study results also are important in providing a way to extend battery life of the generator, an expensive medical device that must be replaced through a surgical procedure each time the battery dies. As such, Dr. Whiting said, battery life could be extended dramatically with great reductions in medical costs.
Ms. Gittis and her team are first in figuring out the unique role of the two types of neurons and how to stimulate one but not the other neuron group. Such research, he said, is “brilliant — out of the box” and represents the important next step in improved treatment for Parkinson’s disease.