Parkinson’s disease is a progressive brain disorder that wreaks havoc on the body and the mind.
While medications and a surgical technique called deep brain stimulation (DBS) can relieve the uncontrollable movements and muscle rigidity that characterize the disease, there currently are no good treatments for the deterioration in cognition caused by the disorder.
That is about to change.
Using an innovative technique, researchers at Vanderbilt University Medical Center have detected alterations in brain activity, called beta oscillations, that are associated with cognitive impairment in patients with Parkinson’s disease.
These findings raise the possibility of using DBS to slow the decline of cognitive function, a major source of disability, diminished quality of life, and death in more than three-quarters of patients with Parkinson’s disease, said paper’s senior author, Sarah Bick, MD, assistant professor of Neurological Surgery at VUMC.
First used in 1986, DBS involves the insertion of electrodes deep into parts of the brain that control muscle movement. Electrical stimulation of these areas is highly effective in relieving the disabling tremors, stiffness and slowness of movements caused by Parkinson’s disease and other movement disorders.
Placement of the electrodes is often performed under local anesthesia. This allows the final electrode position to be fine-tuned with millimeter precision, guided by the detection of neural signals and test stimulation.
One of the neural signals that has been associated with motor symptoms is beta oscillations, rhythmic patterns of electrical activity. Beta oscillations in the basal ganglia, the part of the brain that regulates movement, are known to change during the planning and execution of movements.
Beta oscillations are higher in patients with Parkinson’s disease, perhaps reflecting the loss of the neurotransmitter dopamine that is the root cause the disorder.
To determine if this neurophysiological “biomarker” also could aid in the detection and treatment of cognitive impairment, Bick and her colleagues recorded neural activity as the electrode was passed through areas of the brain involved in working memory on the way to stimulate the motor circuits.
Patients, who were awake during the procedure, were asked to recall and process new information. As is the case in the motor circuits of the brain damaged by Parkinson’s disease, beta oscillations decreased in the cognitive areas during these tests of working memory.
Patients diagnosed with cognitive impairment, however, had higher beta oscillations during working memory tests. Higher beta oscillations also have been associated with impairment of movements in Parkinson’s disease.
This approach, reported in June in the journal Brain, “could yield pivotal advances in our understanding of pathological neural circuits,” scientists at London’s Wellcome Centre for Human Neuroimaging noted in a commentary published in August.
The next step is to see if deep brain stimulation of these circuits can improve patients’ performance of working memory tasks, Bick said.
The study was led by Danika Paulo, MD, chief resident physician in Neurological Surgery, and the paper’s corresponding author, and Helen Qian, an undergraduate researcher in Bick’s lab.
Other co-authors were Deeptha Subramanian, Graham Johnson, PhD, Zixiang Zhao, Kilian Hett, PhD, Hakmook Kang, PhD, Chris Kao, MD, PhD, Noah Roy, PhD, Jessica Summers, Daniel Claassen, MD, and Kaltra Dhima, PhD.
The research was supported by National Institutes of Health grants K12 NS080223 and 5K24 AG064114, the Parkinson’s Foundation and the SyBBURE Searle Undergraduate Research Program.
