Cortical Neurostimulation for Neuropathic Pain State of the Art and Perspectives
Introduction
Cardinal mail stroke pain (CPSP) results from stroke lesions to any region of the somatosensory pathway (Klit et al., 2009; Kumar et al., 2009; Creutzfeldt et al., 2012; Mozaffarian et al., 2015). Between viii and 25% of the ~18 M/year new cases of stroke develop CPSP (Strong et al., 2007; Klit et al., 2015). CPSP leads to poor quality of life (Kumar and Soni, 2009; Oh and Seo, 2015). Patients are ofttimes refractory to pharmacotherapy and can become drug dependent (Kumar and Soni, 2009). Such limitations have motivated researchers to explore brain stimulation therapies to treat CPSP.
Epidural Brain Stimulation (EBS), Transcranial Magnetic Stimulation (TMS), and Transcranial Direct Current Stimulation (tDCS) have all been investigated. Stimulation of primary motor cortex (M1) appears to exist the about constructive cortical target (Nguyen et al., 1999; Kumar and Soni, 2009; Hirabayashi et al., 2011; DosSantos et al., 2012; Fregni et al., 2014; Brietzke et al., 2015; Cioato et al., 2015; Morishita et al., 2015; Oh and Seo, 2015). Analgesia is believed to exist achieved through the stimulation of M1-thalmic relays to reduce hyperactivity in thalamic linked pain networks (Tsubokawa et al., 1993; Mertens et al., 1999; Khedr et al., 2005; Garcia-Larrea and Peyron, 2007; Peyron et al., 2007; Lima and Fregni, 2008; Nguyen et al., 2008; Fontaine et al., 2009; Lefaucheur et al., 2009; Ohn et al., 2012; Bae et al., 2014; Hasan et al., 2014; Lefaucheur, 2016).
While EBS, TMS, and tDCS take shown some clinical success in treating CPSP, high variability beyond studies has impeded their widespread acceptance (Mertens et al., 1999; Lefaucheur et al., 2004, 2009; Lima and Fregni, 2008; Nguyen et al., 2008; Fontaine et al., 2009; DosSantos et al., 2012; Bae et al., 2014; Lefaucheur, 2016). Upwards of 30% of EBS patients do not respond to stimulation (Tsubokawa et al., 1993; Katayama et al., 1998; Mertens et al., 1999; Nguyen et al., 1999). Notwithstanding, it should be noted that this is highly dependent on patient characteristics, and fifty-fifty lower response rates accept been reported in certain patient classes (Katayama et al., 1998). Meta-analyses by O'Connell et al. (2014) and Vaseghi et al. (2014) demonstrated express show supporting the use of TMS or tDCS in chronic pain and CPSP. Vaseghi et al. (2014), who focused on tDCS, commented that stimulation could induce significant analgesic effects, just due to the heterogeneity across studies it is difficult to support its use in chronic pain (O'Connell et al., 2014; Vaseghi et al., 2014).
Such variable levels of efficacy have been associated with several factors such equally lesion location and extent, the bear upon of contradistinct neuronal excitability, and the shrinkage of gray and white matter (Hossman, 2009). Infarction based changes in brain tissue conductivity could also impact stimulation based CPSP treatments. Necrotic encephalon tissue in the infarction region is phagocytized by inflammatory cells and replaced by a cerebral spinal fluid (CSF) (De Girolami et al., 1999). CSF produces a sixfold increase in the tissues' electrical conductivity and a drastic disruption of the tissue geometry (Yunokuchi et al., 1998; Jacobs et al., 2001; Brownish et al., 2003; Soltanian-Zadeh et al., 2003; Wagner et al., 2004, 2006, 2007a; Harris-Love and Cohen, 2006). Such altered electric tissue properties take been shown to perturb the stimulating currents during TMS and tDCS (Wagner et al., 2006, 2007b, 2009).
Nevertheless, equally emphasized by Plow and others, the function of such variables in influencing the distribution of current fields and ultimately impacting therapeutic efficacy in focally injured brain models needs further consideration, and remains to be compared across unlike brain stimulation techniques (Plow et al., 2009). Comparisons beyond stimulation techniques, which differ by electrode/source size, focality, invasiveness, proximity to lesion borders and specific features of the delivered electric currents, are primal to evaluating and optimizing their clinical use (Plow et al., 2009). Furthermore, this comparative information is important for assessing the apply of non-invasive stimulation techniques to identify responders to CPSP stimulation treatments prior to implanting invasive stimulation devices (Khedr et al., 2005; Lefaucheur, 2013, 2016).
The aim of this report is to determine how infarctions and/or circuitous neuroanatomy could alter the neurostimulation currents of the three primary neurostimulation techniques used in CPSP and potentially impact their clinical significance.
Materials and Methods
Simplified magnetic resonance imaging (MRI) guided Finite Element Models (FEMs) of the stimulating current density distributions elicited through EBS, TMS, and tDCS were generated. The models were generated following methods previously outlined (Wagner et al., 2004, 2007b), and following foundational physics reviewed in the appendix of Wagner et al. (2014).
Briefly, we developed a FEM head/brain model with a healthy brain (adult from the MRI of a 38-year-old male person) and a second model that included a confining frontal cortical lesion within the head, specifically modeling a center cerebral avenue (MCA) based apoplexy (Wagner et al., 2004). For simplification purposes, nosotros focused on the comparison across stimulation techniques almost usually used to care for CPSP, and thus the caput models did not include sulci and gyri, but simply the presence of the lesion. Furthermore, we assumed static fields during stimulation for tDCS and EBS and sinusoidal steady state solutions during TMS.
The models were developed with Ansoft'southward Maxwell software (Ansoft Inc, Pittsburg, PA, USA). We specifically solved a modified magnetic diffusion equation for the TMS models:
∇×(1σ(ω)+jωε(ω)∇×H∧)=−jωμH∧
where H is the magnetic field in phasor form, sigma the tissue electrical conductivity, epsilon the tissue permittivity, and omega the angular frequency of the source. The Ansoft parcel numerically solves the problem via a modified T-Ω method (Wagner et al., 2004). For the tDCS and EBS models, the Ansoft FEM solver was set to solve for the electric current densities in terms of the electric potential (ϕ), by solving the equation: ∇⋅(σi∇ϕ) = 0, where σi is the conductivity of the tissue (Ansoft) (Wagner et al., 2007b). For each model, the Ansoft FEM solver was set to follow an adaptive iterative process with convergence limits determined past the free energy mistake in the arrangement, farther detailed in Ansoft (2002, 2005). The benchmark for model convergence was defined as an energy error below one.0% (Wagner et al., 2004, 2007a).
The current source device parameters correspond to those typically used in clinical studies and trials (Brown et al., 2006; Fregni et al., 2007; Lima and Fregni, 2008). The TMS source electric current was set as in prior modeling studies at 5 kHz with a 1.8 × 10iii A acme current on a figure-of-eight coil with ii iii.5 cm radius copper windings (Wagner et al., 2004). The tDCS source current was gear up at 1 mA across a v × 7 cm anode (on a scalp surface area overlying the motor strip) and cathode (above the contralateral orbital) (Wagner et al., 2007a). The EBS source was set at 1 mA, with the anode and cathode placed above the M1 (18 mm inter-contact distance, one mm radius) (Dark-brown et al., 2006). Notation that those EBS parameters are based on Adtech ane mm radius electrodes mounted on a three × 3 grid over an 18 × 18 mm expanse (where the inner row is inactive) which generates 3 separate bipolar arrangements (distanced 18 mm)- (Adtech Medical Musical instrument Corp) (Brown et al., 2003).
While, we used a one mA source magnitude for EBS, information technology should be noted that the EBS solutions are linear in the region of interest and simple multiplicative scaling can be used to business relationship for varied source magnitudes (Woodson and Melcher, 1968; Zahn, 2003; Wagner et al., 2014). Furthermore, as the EBS electrostatic solutions are addressable past superposition, we focused on i bipolar section at a time (Woodson and Melcher, 1968; Zahn, 2003; Wagner et al., 2014). Equally EBS and tDCS were modeled based on the same static approximations, the modeling and solution procedures were equivalent, except for the source properties (e.g., location and geometry). Finally, tissue cloth properties (i.east., conductivity and permittivity), including those of the infarction region, were assigned impedances as detailed in Wagner et al. (2006, 2007a).
The analyses and then focused on determining the electric current density distributions for the caput models (i.eastward., salubrious vs. infarction) and specifically determining the current density magnitude, maximum current density location in the cortex, and current density vector orientation for the EBS, TMS, and tDCS sources. Full details of the analysis are given in Wagner et al. (2004, 2006, 2007a,b, 2014).
Briefly, the stimulation source location and stimulation device orientation were normalized for the three techniques, such that the stimulation sources were located with their device source centers to a higher place the aforementioned physical target location (M1) and every bit distanced along the brain surface from the modeled lesion borders, which in our case was the caudal border.
To determine the current density maximum, nosotros ran an algorithm that scanned the current density magnitudes in the brains, and adamant the magnitude and location of the maxima for the healthy caput and stroke models for each stimulation source. Where the results are reported as current density magnitudes, they signal the magnitude of the sinusoidal steady state electric current density for TMS and the magnitude of the steady state current densities for EBS and tDCS, all of which are provided in units of A/chiliad2 unless otherwise stated.
The relative change betwixt the healthy and infarcted brains is reported as the value of the departure between the current density maxima in the infarction and salubrious head models divided by the current density maxima in the infarction model. Further, the individual models all shared the same Cartesian coordinate system, with an origin at the heads' eye, and thus the relative change in maxima locations between the various healthy brain and infarction models was determined by the Euclidean distance equation. The current density vector field directional patterns were likewise analyzed in the models, and focused on comparison the change in the electric current density fields' vector orientation proximal to the current source and the lesions the healthy and infarction models [come across Effigy 1, and (Wagner et al., 2006) for further details]. The angular perturbation of the current densities betwixt the healthy and infarction models was used to determine the relative current density orientation shift that would occur forth a fixed axonal axis betwixt the models (see Figure 1B). Finally, as the models were deterministic, we did not conduct statistical testing between the dissimilar solution sets.
Figure 1
Figure 1. Electric current density distribution maps induced by EBS stimulation. In (A), the left column depicts the current density magnitude for the respective healthy intact (tiptop) and infarcted (bottom) brains stimulated with EBS. The borders and limits of the infarcted region are demarcated with a thin white line. Notation that the scales in (A) are normalized to the maxima of the solution in each case (i.east., the maximum in the healthy brain is 1.19 A/m2 and i.35 A/m2 in the infarcted brain). Meet location of the maxima in the infarcted (grey ◆) and salubrious brains (gray ∗) indicating the location shift due to the infarction. Exact quantitative estimations on maxima shifts can be found in Tabular array ii. In the right column of each console, the vector distribution demonstrating the orientation of the currents is provided for both the intact and damaged brains. Note the direction of the currents can alter substantially in the region of the perturbation. (B) Demonstrates how the distribution of EBS induced currents can be altered such that facilitatory stimulation might get inhibitory in select neural populations in the lesion region, when applying subthreshold polarizing currents where the stimulatory effect is dependent on the relative current density orientation to the axo-dendritic centrality (Terzuolo and Bullock, 1956; Landau et al., 1964). In our results for select regions of tissue near the lesion edge, the current orientation is altered relative to the neural centrality such that the neural effect would be reverse of that predicted for the good for you encephalon. Note herein, the inhibitory/facilitatory axis is simplified for graphical representation, and will ultimately depend on the complexity and relative position of the neural structure, related to the axo-dendritic axis of the neuron. The total net consequence across the total tissue stimulated could be comprised of a mix of areas receiving inhibitory and facilitatory stimulation (based on the relative neural cell and current density orientations in each individual patient relative to the stimulator source). Furthermore, such effects could potentially be seen in areas of in areas of circuitous sulcal beefcake even in salubrious subjects. Unique solutions based on each individual patient'due south stimulation criteria are thus recommended for private patient dosing considerations.
Results
Electric current density distributions (magnitude, location, and orientation) were altered in the presence of our arcadian model of focal correct frontal infarction for TMS, tDCS, and EBS, as compared to solutions in the intact encephalon models (Tables 1–ii and Figures i–2). For all 3 techniques, currents were increased in magnitude and directed toward the infarction border. Increases of peak current density in a damage brain compared to the healthy one were less drastic for EBS (+xviii%) than for tDCS (+32%) or TMS (+73%) (see Table 1). Furthermore, the vector electric current orientation was altered at the infarction borders, such that the net sign of the neuromodulation effects (i.e., lasting inhibition or facilitation) could exist reversed (e.g., Figure 1B and further word below).
TABLE 1
Table 1. Maximum current density magnitude (in A/m2) in the healthy and the infarcted encephalon.
Tabular array 2
Tabular array 2. Coordinates of the locations (relative to the x,y,z head coordinate organization) of the current density maxima in the healthy and the infarcted encephalon.
Figure ii
Figure 2. Current density distribution maps induced by TMS and tDCS stimulation. In (A,B), the left column depicts the current density magnitude for the corresponding good for you or intact (top) and infarcted (bottom) brains stimulated with TMS and tDCS, respectively. The borders and limits of the infarcted region are demarcated with a thin white line. The modeled lesions presented for EBS (see Figure 1A), TMS (2A), and tDCS (2B) all have the aforementioned size and volume and occupy the exact same location in the right hemisphere in the infracted encephalon. As in Figure 1A, note that the scale of (A,B) is normalized to the maxima in the corresponding solution pictured (i.e., the maximum current density in the TMS healthy encephalon solution is 2.four A/m2 and iv.16 in the infarcted encephalon, and 0.098 and 0.129 in the tDCS good for you and infarcted cases, respectively). The location of the maxima in the infarcted (gray ◆) and healthy brains (greyness ∗) are both marked symbolically on the injured brain to bespeak the estimated site shift (delight zoom on the prototype for a better appreciation if needed). Note, as in EBS, the direction of the currents changes substantially in the region of the perturbation for both techniques.
The overall absolute altitude between the expected target and the actual site of the current maxima (comparing the good for you brain and infarction brain models) were less remarkable in overall magnitude for EBS (a 4 mm shift from the expected vs. the real maximum site) than for TMS (17.9 mm shift) or tDCS (xv.nine mm shift) – meet Figures 1–2 and Tabular array ii. However, relative to the size of the stimulation source, the shift of the current maxima was more than desperate for EBS (~ane mm radius contacts) than for TMS (~35 mm radius contact source) or tDCS (~25 mm shortest heart-edge segment for a 50 × 70 mm electrode) (see Tabular array 2, and in Figures 1A and 2A,B, distances between the gray ♢ and ∗ icons displayed on the brain models).
Discussion
This written report suggests that EBS, tDCS, and TMS neurostimulation current density distributions are altered in the presence of strokes in a manner that may explain discrepancies in CPSP handling outcomes across the different stimulation techniques (André-Obadia et al., 2008, 2011, 2014; Hosomi et al., 2008, 2013; Lefaucheur et al., 2008, 2011a,b; Velasco et al., 2008; Tanei et al., 2011; Sachs et al., 2014). Currents flow downwardly the path of to the lowest degree resistance, in the highly conductive CSF at an infarction location, and impact the current density distributions in magnitude, location, and orientation for EBS (Figure 1), TMS (Figure 2A), and tDCS (Figure 2B) (Wagner et al., 2006, 2007a,b, 2009).
Although the overall absolute perturbation effects in the current densities were greatest in TMS and tDCS, EBS currents were however significantly afflicted when the stimulatory contacts were close to irregular tissue borders of the modeled chronic stroke lesion. Moreover, the change in the location of maximal stimulation between the infarcted and good for you brains was greatest with EBS relative to the size of the stimulator (see Figures 1 and 2, and Tabular array 2). The lower focality of TMS and tDCS, equally compared to EBS, could make them less sensitive to relative mislocalizations around the targeted location. This deviation could reconcile the relevance of our current findings with the fact that TMS and tDCS studies in perilesional stroke regions accept generally reported beneficial therapeutic furnishings with potentially less variability than EBS studies (Lima and Fregni, 2008; O'Connell et al., 2014; Hosomi et al., 2015; DosSantos et al., 2016).
The altered orientation of the stimulation currents relative to the targeted neurons could impact the degree and/or the direction of inhibitory/excitatory response of the involved networks, particularly for sub-threshold stimulation weather condition- see Figure 1B (Terzuolo and Bullock, 1956; Landau et al., 1964; Wagner et al., 2007b; Radman et al., 2009a,b; Wongsarnpigoon and Grill, 2012). The internet sign of the neuromodulation effects (i.e., lasting inhibition or facilitation) could potentially exist reversed in cases where the lesion purlieus alters the currents' orientation relative to the targeted cell's axo-dendritic axis [particularly for sub-threshold stimulations (Terzuolo and Bullock, 1956; Landau et al., 1964)].
Ultimately, the varied stimulation current perturbations between the techniques could in part explain inter-technique discrepancies between tDCS, TMS, and EBS in treating CPSP. Low-intensity EBS M1 cathodic stimulation currents are postulated to bear upon axons parallel and superficial over the crown of the precentral gyrus (Lefaucheur, 2013). In pain treatment, maximal pain relief is postulated to be associated with tardily indirect waves (recorded at the spinal cord level) produced from cathodic M1 EBS and likewise anteroposterior M1 TMS. On the other paw, anodal M1 EBS and lateromedial M1 TMS stimulation atomic number 82 to early directly waves, suggesting that the polarity and orientation of the current in these techniques activates different axonal tracts and pathways (Lefaucheur, 2016). Dissimilar EBS, tDCS shows more analgesic upshot during anodal stimulation, potentially due to unlike neuronal structures being activated, or due the relative current vector orientations having similar orientations in the targeted neurons, encounter Figures i–ii (Lefaucheur et al., 2010; Lefaucheur, 2013, 2016). This suggests that the relative current-neuronal structure orientations between tDCS, TMS, and EBS should be considered when planning stimulation treatments for CPSP, particularly across techniques (e.g., using TMS to predict EBS response). Proper planning of the stimulation protocol with a MRI-integrated field solver-tracking device could be helpful to address the electric current-tissue interactions, but but with systems that track and predict electric current vector orientations (i.e., systems which predict field strengths alone could not be used to overcome discrepancies between the techniques).
Although the conclusions of the electric current study could employ to a large number of cases, any extension of the current results to other lesion features, such as subcortical locations and single or multiple lacunar strokes, which accept been explored in neurostimulation therapeutic CPSP studies, would demand to be specifically evaluated for individual dosing considerations. It is clear from the present study that electromagnetic tissue properties differently touch on encephalon stimulation dosing for different stimulation methods, and introduce a technique-dependent variability in potential therapeutic do good. Ignoring the effects of altered neural tissue properties on the M1 stimulating currents in stroke may contribute to contradictory outcomes in CPSP neurostimulation trials (O'Connell et al., 2014; Hosomi et al., 2015). Finally, our results highlight the demand for new forms of brain stimulation that tin overcome these limitations and provide effective treatment for chronic pain syndromes and other disorders where encephalon stimulation is used.
Author Contributions
Respective roles of each author are equally follows: RR and AV-C wrote the initial version of the manuscript. AO and RA had substantial contribution in the adaptation of the final manuscript to the challenges of neurostimulation technologies and approaches in CPSP. Finally, RR, UE, LA, LD, TW, and AV-C provided substantial contribution to the blueprint of the work, and the revised versions of the manuscript. All authors provided their final approval of the submitted version and agreed to be answerable for all aspects of the work.
Funding
This study was supported by National Institute of Wellness grants (R01-NS33975, R21-NS062317, R21-NS084022, R44-AT008637, and R44NS080632). Research reported in this publication was supported in part past the National Center for Complementary & Integrative Health of the National Institutes of Health under Laurels Number R44AT008637. Enquiry reported in this publication was too supported in role by the National Constitute of Neurological Disorders And Stroke of the National Institutes of Health under Award Number R44NS080632. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Conflict of Interest Statement
TW is the Master Science Officer of Highland Instruments, a medical device company. He also has patents pending or issued related to imaging, brain stimulation and wound healing. All the other authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed equally a potential disharmonize of interest.
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AuthorAffiliation
Anthony T. O'Brien1†, Rivadavio Amorimi†, R. Jarrett Rushmore2,3, Uri Eden4, Linda Afifi2,three, Laura Dipietrov, Timothy Wagner5,6*‡ and Antoni Valero-Cabréii,three,seven,viii*‡
* 1Neuromodulation Lab and Center for Clinical Research and Learning – Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA, USA
* 2Laboratory of Cerebral Dynamics, Plasticity and Rehabilitation, Boston Academy School of Medicine, Boston, MA, U.s.
* 3Department of Anatomy and Neurobiology, Boston Academy School of Medicine, Boston, MA, USA
* 4Department of Mathematics and Statistics, Boston Academy, Boston, MA, United states of america
* vHighland Instruments, Cambridge, MA, USA
* sixDivision of Health Sciences and Engineering, Harvard Medical Schoolhouse/Massachusetts Institute of Engineering science, Boston, MA, USA
* viiUniversité Pierre et Marie Curie, CNRS UMR 7225-INSERM U1127, Institut du Cerveau et la Moelle Epinière, Paris, France
* 8Cognitive Neuroscience and Information Applied science Enquiry Program, Open University of Catalonia, Barcelona, Spain
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