NeuroLogic - Going deep to treat movement disorders
Going deep to treat movement disorders
Date: January 3, 2012
Even though medication is usually the first line of treatment for Parkinson’s disease and other movement disorders, it’s well known that it often doesn’t work forever. Even when patients initially respond well to combination levodopa-carbidopa drugs, symptoms sometimes start to return after five to 10 years of therapy.
“Patients start to develop pronounced fluctuations,” says neurosurgeon W. Stanley Anderson. “There’s an ‘on’ phase of severe dyskinesia, and then an ‘off’ phase where they can barely move.”
Several decades ago, says Anderson’s colleague, neurosurgeon Frederick Lenz, options were few for those who no longer responded to medication. Then, around the time he began working at Johns Hopkins in the late 1980s, a new treatment emerged: deep brain stimulation (DBS), in which electrodes are inserted within brain tissue, running current that affects the native electrical behavior of neurons.
DBS came to fruition after researchers elsewhere found that Parkinson’s disease symptoms appeared to result from over-activity in cells of the basal ganglia rather than from the under-activity or cell death that previous theories had suggested. Although animal models showed that lesioning these affected areas could improve symptoms, the notion of causing permanent damage through burning, freezing or cutting sections of the human brain wasn’t particularly palatable for patients and doctors, Lenz says.
When European researchers found that electrically stimulating the same areas through DBS also calms over-activity and reduces symptoms in a way that’s reversible if necessary, Lenz adds, Johns Hopkins became an early adopter of the procedure. Today, adds Anderson, patients are treated by a team of neurologists, neurosurgeons, neuropsychiatrists, neuropsychologists and neuroradiologists who work together to evaluate potential candidates, perform procedures and handle rare complications if they arise.
During the procedure, patients are lightly sedated but awake. After placing a stereotactic frame on the patient’s head, physicians use MRI images to calculate the coordinates where the DBS electrodes will be placed in the brain, which for Parkinson’s patients is typically in the subthalamic nucleus. Surgeons then drill two small holes, one on each side of the skull, make incisions through the dura, and insert two electrodes with four contacts each inside brain tissue. To confirm that the electrodes are correctly placed, they listen for the distinct electrical activity of subthalamic nucleus neurons and also stimulate tissue through the contacts.
Even before the device is activated, Anderson says, patients often show a reduction in symptoms because edema following the operation can mimic the effects of lesioning. After the brain heals in a few weeks, physicians turn the device on to keep symptoms at bay. DBS often helps patients to greatly reduce the amount of medication they take, and a lucky few can discontinue medication altogether for months to years, he adds.
DBS isn’t just successful for Parkinson’s disease patients, Lenz says. It’s also often used for other movement disorders, such as essential tremor and dystonia, and is being increasingly investigated for other neurological and mental health problems, including obsessive compulsive disorder, Tourette syndrome, major depression and epilepsy.
“We haven’t yet reached the limits of understanding what this technology can do,” Lenz says.