History, Applications, and Mechanisms of Deep Brain Stimulation

Figure 1. Basal ganglia-thalamo-cortical circuit schematic in the normal and parkinsonian states. Thickness of the arrows indicates strength of the connections. Loss of substantia nigra neurons leads to increased thalamic inhibition. The diagram does not account for firing pattern and oscillatory activity, both of which are important factors in understanding the effects of deep brain stimulation on the network. D₁ and D₂ indicate postsynaptic dopamine receptor type; GPe, globus pallidus externus; GPi, globus pallidus internus; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulata; STN, subthalamic nucleus; and Thal, thalamus.

Figure 2. Patient-specific computational deep brain stimulation (DBS) model. A, Electrode location shown with respect to the subthalamic nucleus (green), thalamus (yellow), and desired stimulation target (gray). B and C, Computational estimate of volume of tissue activated (red) using model-defined (B) and clinically defined (C) stimulation parameters. D, The patient's ability to maintain uniform finger motor force (y-axis) during an increasingly difficult cognitive task (x-axis) is optimal when using model-defined parameters.⁸⁶ * P < .05. Image courtesy of Cameron McIntyre, PhD (Cleveland Clinic).

Figure 3. Current steering using novel deep brain stimulation (DBS) array electrode design. Estimate of volume of activated tissue is overlaid with an atlas section. A, Conventional DBS electrode (left) activates tissue contained within the blue circle, which is adequate for the electrode positioned in the center of the subthalamic nucleus (STN). B, Displacing the electrode by 1 mm laterally and anteriorly causes undesired activation of the internal capsule (CI) with the conventional electrode, but it can be avoided by using a novel DBS array electrode.⁸⁹ Reprinted with permission. ZI indicates zona incerta.