Figure 1. Configuration of implanted hardware, algorithmic model and patient demographics.

a, Illustration of the adaptive paradigm starting with real-life sensing of brain activity (blue) that reflects changes in patient’s mobility–in this example slowness of movement (bradykinesia). Neural activity is sensed continuously on-board the DBS device from either the STN or sensorimotor cortex using depth or subdural electrodes, respectively. Here, we illustrate an example of a cortical control signal for fully-embedded adaptive implementation. Once a change in the brain signal across a predefined threshold is detected (green), the stimulation amplitude increases or decreases automatically (red) at the target brain region (STN). This adaptation of stimulation amplitude to the patient’s needs leads to improved symptoms–in this example, increased stimulation amplitude results in faster movement. b, Localization of depth leads in the STN with active contacts colored in red across patients in normalized Montreal Neurological Institute space. STN is highlighted in orange and the red nucleus in red. c, Patient characteristics including pre- and post-surgery levodopa equivalent daily dose (LEDD, mg) and residual motor fluctuations on clinically optimized cDBS, including the body side, the most bothersome symptom and the “opposite” symptom, referring to the opposite medication state, such as hyperkinetic symptoms for hypokinetic bothersome symptoms, or effects of DBS that limit the therapeutic window (e.g., effects on speech).