Deep Brain Stimulation Programming for Movement Disorders: Current Concepts and Evidence-Based Strategies

Thomas Koeglsperger, Carla Palleis, Franz Hell, Jan H Mehrkens, Kai Bötzel, Thomas Koeglsperger, Carla Palleis, Franz Hell, Jan H Mehrkens, Kai Bötzel

Abstract

Deep brain stimulation (DBS) has become the treatment of choice for advanced stages of Parkinson's disease, medically intractable essential tremor, and complicated segmental and generalized dystonia. In addition to accurate electrode placement in the target area, effective programming of DBS devices is considered the most important factor for the individual outcome after DBS. Programming of the implanted pulse generator (IPG) is the only modifiable factor once DBS leads have been implanted and it becomes even more relevant in cases in which the electrodes are located at the border of the intended target structure and when side effects become challenging. At present, adjusting stimulation parameters depends to a large extent on personal experience. Based on a comprehensive literature search, we here summarize previous studies that examined the significance of distinct stimulation strategies for ameliorating disease signs and symptoms. We assess the effect of adjusting the stimulus amplitude (A), frequency (f), and pulse width (pw) on clinical symptoms and examine more recent techniques for modulating neuronal elements by electrical stimulation, such as interleaving (Medtronic®) or directional current steering (Boston Scientific®, Abbott®). We thus provide an evidence-based strategy for achieving the best clinical effect with different disorders and avoiding adverse effects in DBS of the subthalamic nucleus (STN), the ventro-intermedius nucleus (VIM), and the globus pallidus internus (GPi).

Keywords: DBS programming algorithms; DBS side effects; segmented electrode; short pulse width; subthalamic nucleus.

Figures

Figure 1
Figure 1
The therapeutic window depends on stimulation parameters and the electrode configuration. In tripartite electrodes, the therapeutic window should be determined for each segment individually by examining the beneficial and adverse effects with increasing the stimulation amplitude under defined pulse width and frequency (A). The therapeutic window in DBS is defined as the gap between the minimum stimulation current required to produce adverse effects and the current required to produce a beneficial effect. Similar to pharmacologic intervention, DSB is a tradeoff between beneficial and adverse effects. Numerous stimulation parameters, as well as the anatomical position of the respective contact, affect the therapeutic window. As a consequence, each electrode contact and each combination of pulse width and frequency thus has an individual therapeutic window (B).
Figure 2
Figure 2
The effects of DBS on clinical symptoms are time-dependent. PD signs and symptoms respond to STN-DBS variably. Axial symptoms may take hours or days to improve, whereas tremor typically disappears almost instantly with STN- or VIM-DBS (A). A similar temporal disparity occurs with dystonia, where phasic dystonic symptoms respond quickly within minutes to GPi-DBS, and tonic dystonic movements may take much longer to resolve (B). The reappearance of symptoms after discontinuation of DBS exhibits a similar temporal pattern.
Figure 3
Figure 3
Anatomical relationship of the subthalamic nucleus (STN) and the ventral intermedius nucleus (VIM) to adjacent structures. The schematic shows coronar (A–C) and sagittal (D) planes through the basal ganglia at the level of the STN and VIM. Co, Commissural nucleus; CeM, central medial thalamic nucleus; VA, ventroanterior thalamic nucleus; VC, ventrocaudal nucleus; VLP, ventrolateral posterior thalamic nucleus; VPM, ventroposterior medial thalamic nucleus; IC, internal capsule; SNr, Substantia nigra pars reticulate; and SNc compacta; H1, H2, H1 and H2 Fields of Forel; ZI, zona incerta; N.III, nucleus of the third cranial nerve; DHA, dorsal hypothalamic area; DHM, dorsomedial hypothalamic nucleus; LHA, lateral hypothalamic area; mfb, medial forebrain bundle; opt, optic tracts; RN, red nucleus; crt, cerebello-rubro-thalamic tract. Stimulating the tissue medial and dorsal to the STN activates the H1 and H2 fields of Forel and the ZI and may reach to the medio-dorsal thalamic nuclei incl. the Co, CeM, and VIM. Deflection of the field to more ventral areas will activate the fibers of the N.III and the SN (A). Anterior of the STN, stimulation may activate hypothalamic nuclei and mfb as well as the IC (B,D). At the posterior border of the STN, stimulation may activate the RN and ml, in particular, if the tissue medial of the STN is activated. Stimulation of tissue dorsal of the STN may activate the crt. (C,D). Adjusted from Mai et al. (55).
Figure 4
Figure 4
Anatomical relationship of the globus pallidus internus (GPi) to adjacent structures. The schematic shows coronar (A–C) and sagittal (D) planes through the basal ganglia at the level of the GPi. IC, internal capsule; GPe, globus pallidus externus; al, ansa lenticularis; Pu, putamen; opt, optic tract; AMY, amygdala; VP, ventral pallidum; PuV, ventral putamen; STN, subthalamic nucleus. Deflection of stimulation to tissue medial of the GPi will activate the IC, which is less likely the case at the anterior border of the GPi (A,B,D). The AMY and opt are activated by stimulating tissue ventral of the GPi (C). Adjusted from Mai et al. (55).

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