Adaptive DBS for Parkinson Disease

Summary and Comment |
October 30, 2013

Adaptive DBS for Parkinson Disease

  1. Michael S. Okun, MD

A smart and adaptive deep brain stimulation system shows great potential in a seminal study.

  1. Michael S. Okun, MD

One of the holy grails for deep brain stimulation (DBS) research is to achieve a smarter and more efficient way to deliver electricity to the brain. To establish proof of principle for this type of approach in treating Parkinson disease (PD), researchers conducted an experiment on eight patients. They used a brain–machine interface that interprets brain signals in patients with advanced PD. The detected signals were used as a feedback to control the DBS lead, which was implanted in the subthalamic nucleus. Each patient had either adaptive DBS, continuous DBS, or random intermittent stimulation. The physiology derived from the local field potential (i.e., the pathological beta oscillation) was used as the trigger. Both blinded and unblinded raters confirmed the results using the validated and standardized Unified Parkinson's Disease Rating Scale.

Both types of DBS improved motor scores according to both unblinded and blinded raters, but the improvements with adaptive DBS (by 66% unblinded and 50% blinded) were 29% and 27% better than with continuous DBS. Overall stimulation time was 56% shorter with adaptive than with continuous DBS, which reduced the estimated energy requirements and theoretically could lead to chronic improvement in DBS battery lives and reduced need for battery replacements. The adaptive DBS approach was also superior to both an off-stimulation and a random-stimulation condition.


The approach of using a brain signal to trigger deep brain stimulation has been referred to as closed-loop DBS. Previous attempts to achieve this milestone have been hampered by lack of a brain marker and limitations in hardware and technology. This report represents an important milestone for DBS therapy.

Although the results were impressive, there were several critical limitations. The stimulation was provided through an externalization of the DBS wires that was performed in the immediate postoperative period. Following the experiment, all patients were implanted with standard regulatory agency–approved DBS hardware. It will be important to replicate these results in a chronic, awake, and behaving patient with Parkinson disease. Additionally, the effects of medications and the influence of complex human behavior on beta oscillations, which provide the trigger for DBS, may complicate the translation of this finding into clinical practice. Regardless of the limitations, this is a seminal and very important report for all human PD researchers interested in developing smarter and more cost-effective therapies for their patients.

Editor Disclosures at Time of Publication

  • Disclosures for Michael S. Okun, MD at time of publication Grant / research support NIH; National Parkinson Foundation; Michael J. Fox Foundation Editorial boards Parkinsonism and Related Disorders; Tremor and Hyperkinetic Disorders Leadership positions in professional societies National Parkinson Foundation (Medical Director and Ask the Doctor Director); Tourette Syndrome Association (Medical Advisory Board)


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