antal 2008 jclinpain

Transcranial Direct Current Stimulation OverSomatosensory Cortex Decreases Experimentally

Induced Acute Pain Perception

Andrea Antal, PhD,* Nadine Brepohl, BSc,* Csaba Poreisz, MD,* Klara Boros, MD,*Gabor Csifcsak, MD,*w and Walter Paulus, MD*

Objective: Multiple cortical areas including the primary soma-

tosensory cortex are known to be involved in nociception. The

aim of this study was to investigate the effect of transcranial

direct current stimulation (tDCS) that modulates the cortical

excitability painlessly and noninvasively, over somatosensory

cortex on acute pain perception induced with a Tm:YAG laser.

Methods: Subjective pain rating scores and amplitude changes

of the N1, N2, and P2 components of laser-evoked potentials of

10 healthy participants were analyzed before and after anodal,

cathodal, and sham tDCS.

Results: Our results demonstrate that cathodal tDCS signifi-

cantly diminished pain perception and the amplitude of the N2

component when the contralateral hand to the side of tDCS was

laser-stimulated, whereas anodal and sham stimulation condi-

tions had no significant effect.

Discussion: Our study highlights the antinociceptive effect of this

technique and may contribute to the understanding of the

mechanisms underlying pain relief. The pharmacologic prolon-

gation of the excitability-diminishing after-effects would render

the method applicable to different patient populations with

chronic pain.

Key Words: tDCS, pain, SI, laser-evoked potentials

(Clin J Pain 2008;24:56–63)

The role of the somatosensory cortex (SI) in painperception has been controversial owing to the

inconsistent activations of this cortical area acrossdifferent imaging studies on pain perception.1–3 Althoughsome of imaging studies using nociceptive stimulationhave substantiated the involvement of the SI in pain

processing,3–6 many reports have failed to do so (for areview see Ref. 2). Several electrophysiologic [electro-encephalogram (EEG) and magnetoencephalogram]studies reported SI pain-related activity only on thecontralateral side7–9; however, other studies found noactivation of SI at all (for a review see Refs. 10–13). Arole of the SI in pain perception was demonstrated in apatient with focal postcentral lesion in whom painsensation was lost but motivational-affective dimensionof pain was preserved.14 In addition, it was shown thatSI activity can be modified by the attention paid to thepainful stimulation.1,8,15 In summary, recent studiessuggest that specific activation to painful stimuli is likelyto exist but seems to be of small magnitude and restrictedto much smaller subsections of the SI than tactilestimuli.10

The aim of the present study was to clarify whetherthe application of transcranial direct current stimulation(tDCS) can modify acute pain perception and processingin healthy participants. A recent study suggests that tDCSover the motor cortex offers a new perspective for thetreatment of chronic pain16; however, its effect over the SIhas not yet been observed. tDCS was recently reintro-duced as a tool for inducing long-lasting changes ofcortical excitability and activity in focal brain regionsreversibly, painlessly, and safely.17–20 Animal studiessuggest that it causes polarity-dependent shifts of theresting membrane potentials and consequently changesthe firing rates of neurons beneath the electrodes andprobably in connected cortical areas.21,22 Generally,the investigators found that anodal stimulation over themotor cortex enhances cortical excitability, whereascathodal stimulation decreases it.17,18 Although inhumans the modulatory effects of tDCS have first beendemonstrated in the motor system, it influences visual,somatosensory, and prefrontal functions as well (for areview see Refs. 23, 24). Furthermore, cathodal stimula-tion of the SI by tDCS disrupts tactile perception.25

In this study in addition to psychophysical ratingsof pain perception, laser-evoked potentials (LEPs) wererecorded and analyzed before and after 15 minutesanodal, cathodal, and sham tDCS. LEPs represent theactivation of distributed and interconnected neuralpopulations and are quantitative and stable neuronalcorrelates of pain processing.26 The early N1/P1 LEPCopyright r 2007 by Lippincott Williams & Wilkins

Received for publication April 20, 2006; revised July 17, 2007; acceptedJuly 29, 2007.

From the *Department of Clinical Neurophysiology, Georg-AugustUniversity, Robert Koch Strasse 40, 37075 Gottingen, Germany;and wDepartment of Psychiatry, University of Szeged, Semmelweisu. 6, 6725 Szeged, Hungary.

Supported by the German Ministry of Research and Education withinthe ‘‘Kompetenznetz Schmerz’’ (FKZ: 01EM0117).

Reprints: Andrea Antal, PhD, Department of Clinical Neurophysiology,Georg-August University of Gottingen, Robert Koch Strasse 40,37075 Gottingen, Germany (e-mail: [email protected]).

ORIGINAL ARTICLE

56 Clin J Pain � Volume 24, Number 1, January 2008

component that is generated in the contralateral SIIand recorded in the temporal region, correlates with thesensory aspect of pain.27 The late LEP componentsare the N2 wave peaking around 160 to 220ms, and theP2 component, which has a maximum amplitude around300 to 360ms.10 The results suggest that the N2mainly reflects primary sensory-discriminatory processes,whereas the P2 component probably represents cognitive-emotional aspects of pain.28,29 We hypothesized thatcathodal stimulation over SI decreases subjective painperception and modifies the parameters of its electro-physiologic correlates.

METHODS

ParticipantsTen healthy volunteers (4 male) between the ages of

18 and 30 participated in the experiment. None of themreported chronic pain syndromes, nor took any medica-tion regularly. They had no history or current signs orsymptoms of neurologic or psychiatric disorders. Writteninformed consent was obtained from all participants. Thestudy protocol conformed to the Declaration of Helsinkiand was approved by the Ethics Committee of theUniversity of Gottingen.

tDCStDCS was delivered by a battery-driven constant

current stimulator (Schneider Electronics, Gleichen,Germany) using a pair of rubber electrodes in a5� 7 cm water-soaked synthetic sponge. One electrodewas placed over the left SI at a scalp position, as definedby the Talairach coordinates that were calculated bystimulation of the right hand in imaging studies,3,30

whereas the other electrode was placed above the righteyebrow. The electrodes were orientated approximatelyparallel to the postcentral sulcus and the eyebrow. Thetype of stimulation (anodal or cathodal) refers to thepolarity of electrode above the SI, whereas for shamstimulation the 2 electrodes were placed randomly and thecurrent was turned on only for a few seconds to providethe slightly itching sensation at the beginning of thestimulation. Participants were blinded as to the polarityof tDCS. The current was applied for 15 minutes with anintensity of 1.0mA. The order of the sessions wasrandomized across participants and separated by at least1 week to avoid interference effects.

Laser StimulationTo clarify the effect of tDCS over SI on pain

perception and processing, we stimulated the dorsum ofboth hands of healthy participants with thulium dopedyttrium-aluminium-garnet (Tm:YAG) laser31 (WaveLightLaser Technologie AG, Erlangen, Germany). The thu-lium laser emits near-infrared radiation (wavelength2000 nm, pulse duration 1ms, laser beam diameter7mm) with a penetration depth of 360 mm into thehuman skin and allows a precise restriction of the emittedheat energy to the termination area of primary nocicep-

tive afferents without affecting the subcutaneous tissue.28

The distal handpiece of the laser was positioned 30 cmfrom the radial part of the dorsal surface of the hand.Skin temperature of the stimulated area was checkedbefore every switch between hands, and corrected with aheating lamp if below 351C. We stimulated different spotsin a square (5� 5 cm) for each measure to reduce receptorfatigue or sensitization by skin overheating.28 In eachexperiment, the right (contralateral to the tDCS) handwas stimulated first in half of the cases and the left(ipsilateral to the tDCS) hand was stimulated first in theother half. As in all cases, the left S1 was stimulated withtDCS, we proposed that it would affect the pain thresholddominantly on the contralateral hand, which could havebeen masked by this initial orienting response.

At the beginning of the experiments, the painthreshold of both hands was determined by applyinglaser stimuli from 200-mJ in 50-mJ steps. During EEGrecording, we delivered 40 laser pulses to each handbefore and after tDCS with 1.5 to 1.6 times of thresholdintensity. The interstimulus interval of the stimulationranged from 8 to 15 seconds.

Psychophysical EvaluationWe used the verbal numeric analog score to assess

the subjective intensity of the laser-induced pain. Theparticipants were instructed to pay attention to the laserstimuli and to rate the perceived pain verbally [warm, 1;painful, from 2.1 (mild) to 2.9 (most intensive pain)—1 to10 scale] about 2 to 3 seconds after each stimulation. Theparticipants’ ears were plugged and white noise waspresented during the measurements to avoid auditoryartifacts due to laser stimulation.

Electrophysiologic RecordingsThe EEG was recorded using a 5-channel montage

as described by Treede.26,28 This montage has been usedin numerous experimental and clinical LEP studies, asit enables the easy identification of early and late LEPcomponents. We placed 3 electrodes in the midline(Fz, Cz, and Pz) and 2 laterally above the temporalregion (T3 and T4) in accordance with the international10/20 system. The impedance was kept below 5 kO. Weused the connected mastoids as reference. The groundelectrode was positioned on the forehead. Data werecollected with a sampling rate of 1000Hz by theBrainAmp system (Brain Products GmbH, Munich,Germany) and were analyzed offline. A 0.1-Hz low cutoffand a 30-Hz high cutoff filters were used. After automaticartifact detection (200 mV amplitude criterion), all epochswere visually inspected, and those containing eye blinksor muscle movement artifacts were excluded. All record-ings consisted of at least 35 artifact-free epochs. Baselinecorrection was performed on the basis of the 100-msprestimulus interval. The amplitudes of N1 (referringto Fz) and N2-P2 (referring to RLm) components weremeasured offline.

Clin J Pain � Volume 24, Number 1, January 2008 Cathodal tDCS Decreases Pain Perception

r 2007 Lippincott Williams & Wilkins 57

Data AnalysisNumeric analog score values and LEP amplitudes

were individually averaged and entered into a repeated-measures-analysis of variance for both hands and LEPcomponents separately [3 tDCS condition (cathodal,anodal, sham) � 2 time (before, after tDCS)]. Weconsidered a psychophysical or an electrophysiologicchange only if the condition� time interaction wassignificant. Furthermore, we investigated if this effectwas dependent on the electrode positions by calculatingthe condition� time� electrode interaction. Post hocanalysis was carried out using a Fischer least significantdifference test. Additionally, a Student t test (independentby group) was used to compare the changes of amplitudesbetween different conditions and between 2 hands. To dothat the amplitudes were normalized (after/before).

RESULTS

PsychophysicsThe intensity of the laser stimulation (1.5 to 1.6�

of the pain threshold) was 19.6mJ/mm2 for cathodal,19.9mJ/mm2 for anodal, and 19.8mJ/mm2 for shamstimulation. The repeated measurement of analysis ofvariance revealed no main effect of condition [F(2,18)=1.72, P>0.2] and time [F(1,9)=4.65, P>0.05]. How-ever, the condition� time interaction was significant[F(2,18)=3.44, P<0.05] when the contralateral handwas laser stimulated. According to the post hoc analysis,cathodal stimulation significantly decreased subjectivepain rating compared with the before stimulation condi-tion (P<0.005), whereas anodal and sham stimulationhad no effect (Fig. 1).

In case of the ipsilateral hand laser stimulation,there was no significant effect of condition [F(2,18)=1.075, P>0.3] and time [F(1,9)=1.52, P>0.2]. The

condition� time interaction was also not significant[F(2,18)=0.77, P>0.4] (Fig. 1).

ElectrophysiologyThe laser stimulation induced a pricking pain in all

patients and a biphasic N2-P2 component was clearlyidentified in all LEP measures (Fig. 2). In case of the N1component, the LEP amplitudes recorded at T3 and T4channels (referring to Fz) were analyzed separately.There was no significant effect of condition on channelT3 [contralateral: F(2,18)=1.02, P>0.3; ipsilateral:F(2,18)=0.20, P>0.8] nor on channel T4 [contralateral:F(2,18)=0.23, P>0.8; ipsilateral: F(2,18)=0.22, P>0.8].There was no main effect of time on T3 [contralateral:F(1,9)=3.50, P>0.09; ipsilateral: F(1,9)=1.50, P>0.25]but it was significant on T4 when the contralateral hand(right) was stimulated [contralateral: F(1,9)=7.55,P<0.05; ipsilateral: F(1,9)=3.43, P>0.09]. There wasno significant time� condition interaction on T3 [contra-lateral: F(2,18)=0.02, P>0.9; ipsilateral: F(2,18)=0.17,P>0.8] nor on T4 [contralateral: F(2,18)=0.65, P>0.5;ipsilateral: F(2,18)=1.40, P>0.2].

In case of the N2 component, there was no effect ofcondition [contralateral: F(10,46)=0.78, P>0.6; ipsilat-eral: F(10,46)=0.7, P>0.7] but the effect of time wassignificant [contralateral: F(5,23)=4.59, P<0.005; ipsi-lateral: F(5,23)=3.86, P<0.05] and we also found asignificant condition� time interaction when the contral-ateral hand was laser-stimulated [contralateral:F(10,46)=2.69, P<0.01; ipsilateral: F(10,46)=0.71,P>0.7]. When compared with the before stimulationcondition, cathodal stimulation significantly diminishedthe amplitude (P<0.005). The interaction with electrodeposition here was also significant [F(4,108)=3.89,P<0.005]. The post hoc analysis has shown that cathodalstimulation significantly decreased the amplitudes of theN2 components at the Cz and Pz electrode positions forthe contralateral hand stimulation (P<0.005). Thechanges of mean N2 amplitudes for all 3 tDCS conditionsand both hands are shown in Figure 3. The means andstandard deviations for both hands, LEP components,and tDCS pairs are shown in Table 1.

In case of the P2 component, there was no maineffect of condition [contralateral: F(10,46)=0.8, P>0.6;ipsilateral: F(10,46)=0.3, P>0.9] but the effect of timewas significant on the ipsilateral side [contralateral:F(5,23)=1.21, P>0.3; ipsilateral: F(5,23)=3.51,P<0.05]. There was no significant condition� timeinteraction [contralateral: F(10,46)=0.75, P>0.6; ipsi-lateral: F(10,46)=0.79, P>0.6]. The changes of P2amplitudes for all 3 tDCS conditions and both handsare shown in Figure 4.

A Student t test was used to compare the attitude ofchanges between different conditions and hands. Signifi-cant differences were found between right hand shamand cathodal stimulation [t(df18)=2.16; P<0.05] andbetween right hand anodal and right hand cathodalstimulation [t(df18)=2.66; P<0.05] only related to theN2 amplitude at the Cz electrode position.

FIGURE 1. The differences of reported subjective pain valuesin % according to the numeric analog score reported by thepatients before and after cathodal, anodal and sham tDCS forright (contralateral) and left (ipsilateral) hand laser stimulation.

Antal et al Clin J Pain � Volume 24, Number 1, January 2008

58 r 2007 Lippincott Williams & Wilkins

DISCUSSIONThe main finding of the present study is that

cathodal stimulation of the SI significantly diminishedsubjective pain perception, whereas anodal and shamstimulations had no effect. The effect was only presentwhen stimulating the contralateral hand to the side oftDCS with the Tm:YAG laser. In parallel with theseresults, cathodal stimulation significantly reduced the N2component of LEPs. Previously, only 2 tDCS studiesdealt with the somatosensory aspects of DC stimulationin healthy human subjects, and are not directly compar-able with our results owing to different stimulation loci.In one of the studies, the M1 was stimulated whilesomatosensory evoked potentials were recorded by thestimulation of the left and right medial nerves.32

Relatively long-lasting (60min) increases of the ampli-tudes of the parietal and frontal SEP components were

detected after anodal stimulation. Cathodal stimulationhad no effect on these potentials. In the other study,cathodal tDCS induced a prolonged decrease of tactilediscrimination, whereas anodal and sham stimulation didnot.25 To our knowledge, our study is the first demon-strating that cathodal tDCS over the SI is able to diminishexperimentally induced pain perception in healthy humanparticipants.

The contribution of SI to pain processing asrevealed by functional magnetic resonance imaging/posi-tron emission tomography and electrophysiologic studiesis less consistent across studies than that of the SII,insular and anterior cingulate regions; the role in SI inpain processing has been under extensive debate. Noci-ceptive projections exist from the thalamus to the SI.33

Additionally, specific nociceptive neurons have beenidentified in the SI34 yet only about half of the imaging

FIGURE 2. Grand averages of LEPs obtained by contralateral (A) and ipsilateral (B) hand laser stimulation for 5 scalp electrodes.The solid line shows LEPs before and the intermittent line after anodal, cathodal and sham tDCS. Please note that a greateramplitude reduction of the N2 and P2 component for cathodal tDCS is observed at the contralateral side to the stimulation.



studies report SI activation after painful stimulation (fora review see Ref. 2). Negative results reported in imagingand electrophysiologic studies might be due to individualsulcal variabilities that can be alleviated for a group-average, small focal activations, or technical problems,for example, not optimally defined thresholds for func-tional magnetic resonance imaging analysis. In our study,we had used a 5� 7 cm electrode size to optimizestimulation’s parameters17 and it is therefore possiblethat we covered a large part of SI. However, it may alsobe that we have additionally stimulated part of thesomatosensory associations’ cortex (BA 5/7) that isposterior to SI. Activation of human BA 5/7 has alsobeen linked to pain perception.13,35 BA 5/7 is anatomi-cally connected to other nociceptive brain areas such asthe anterior cingulate cortex (ACC), insula, thalamus,and primary motor cortices.36 It is possible that we haveinduced the analgesic effect by the additional stimulationof this region.

Another possibility is that the antinociceptive effectwas obtained by the indirect inhibition of SII and ACCthrough SI stimulation. According to source localizingelectrophysiologic studies, the N2 component is generatedbilaterally in the operculoinsular region and in theACC.10 This component mainly contributes to sensory-discriminatory aspects of pain. The P2 component mainlyarises from the ACC and reflects endogenous, attentional,cognitive, and affective factors.37 The SI is highlyinterconnected with this cortical area and therefore thedown-regulation of the cortical excitability of the SImight have resulted in an additional inhibition of the SIIand ACC. Indeed, although some previous LEP dipolemodeling studies showed that a dipole source in SI areawas necessary to explain the scalp LEP topography, noneof them reported a clear correspondence between the SI

activity and a definite LEP component.7,38,39 Recently,intracerebral depth recordings in an epileptic patient haveshown no reliable LEP response from the 3b area of theSI after painful laser stimulation, although a reliable N2-P2 response could be recorded at Cz.40 Therefore, it ispossible that the absence of the pain-related activation inthe SI found by imaging an electrophysiologic studies, is areal phenomenon, however, the indirect involvement ofthe SI in pain processing (modulating SII activity throughSI stimulation) is feasible. It has also been suggested thatpain processing takes place simultaneously in the SI andSII and not sequentially in different areas as in tactileprocessing.41 Then, as an alternative option, passivespread of the current over cerebral areas could alsomodify SII processing when the SI is stimulated.

Many electrophysiologic studies reported onlycontralateral activation for nociceptive stimulation4,7;

FIGURE 3. The differences of N2 amplitudes in % in the 3tDCS conditions for the contralateral and ipsilateral hand laserstimulation at the Cz electrode. The star marks significantdifferences between the cathodal-sham and cathodal-anodalcondition after the contralateral hand stimulation (P<0.005).

TABLE 1. The Mean Values and SDs of the LEP Parameters atthe Cz, Pz, and T3/T4 Electrode Positions for the ObtainedFrom all Patients for Both Hands Before and After Anodal,Cathodal and Sham tDCS

Before tDCS After tDCS

Cz Pz Cz Pz

Mean SD Mean SD Mean SD Mean SD

Right Hand

AN2 � 14.20 ±5.6 � 9.90 ±7.9 � 12.70 ±5.7 � 6.00 ±5.9P2 18.73 ±6.6 9.50 ±14.1 16.70 ±7.9 12.93 ±5.5

CN2 � 15.01 ±6.3 � 7.45 ±4.9 � 9.98* ±4.3 � 4.10* ±3.2P2 16.62 ±4.9 13.80 ±4.4 14.38 ±9.6 11.30 ±5.7

SN2 � 14.8 ±5.5 � 6.10 ±3.8 � 12.11 ±5.8 � 4.12 ±4.1P2 17.58 ±5.5 14.67 ±3.6 18.76 ±6.3 15.22 ±5.8

Left Hand

AN2 � 15.14 ±4.5 � 6.60 ±3.5 � 13.17 ±3.5 � 4.88 ±3.9P2 18.79 ±6.7 14.45 ±5.9 17.43 ±9.3 14.40 ±7.2

CN2 � 13.93 ±5.9 � 6.74 ±5.2 � 11.17 ±4.7 � 4.52 ±4.3P2 17.50 ±6.7 13.83 ±4.2 16.66 ±7.0 13.19 ±4.6

SN2 � 14.19 ±4.3 � 5.94 ±2.2 � 13.16 ±4.9 � 5.29 ±3.3P2 18.02 ±5.8 14.64 ±3.7 15.90 ±6.5 11.85 ±5.0

T3 T4 T3 T4

Mean SD Mean SD Mean SD Mean SD

Right Hand

AN1 � 7.16 ±3.7 � 5.30 ±3.9 � 6.11 ±4.0 � 3.25 ±3.7

CN1 � 7.42 ±4.8 � 5.22 ±3.5 � 6.67 ±3.4 � 4.63 ±2.6

SN1 � 8.31 ±3.9 � 5.18 ±3.5 � 7.49 ±4.1 � 4.30 ±2.4

Left Hand

AN1 � 5.29 ±3.5 � 5.53 ±5.3 � 4.88 ±2.9 � 6.09 ±4.6

CN1 � 6.20 ±2.8 � 6.55 ±2.3 � 5.08 ±2.9 � 5.18 ±2.9

SN1 � 5.44 ±4.5 � 7.10 ±3.3 � 5.20 ±3.3 � 5.48 ±2.8

*P<0.005.



however, imaging studies suggest that the pain-related SIresponse is bilateral with significantly greater activation inthe hemisphere contralateral to the stimulation.2,42 In ourstudy, cathodal stimulation had an effect only when thecontralateral hand was stimulated and not for ipsilateralstimulation.

We did not find any significant change concerningthe N1 amplitudes. The N1 component is an early corticalLEP potential, peaking at 140 to 170ms and reflecting theearly sensory-discriminative processing of pain percep-tion. According to scalp topography (maximum near T3and T4), it is generated near the SII in the fronto-parietaloperculum.26,43 At a first glance, the missing effect oftDCS on the N1 component and the inhibitory effect onthe N2 component, seems to be in contradiction, becausethe main contribution to the N2 origin is also given by theSII area. There are various explanations with regard tothis problem. Primarily, the N1 component is muchsmaller than the N2 component and therefore a smallchange in the size of the amplitude is more detectable inthe case of the N2 component. Secondly, the N1component is probably produced by different neurongroups in comparison with the N2 component, and inthese groups the neurons might be differently oriented.The interaction between the orientation of the neuronsand the current direction is probably critical to getstimulation-induced after-effects.17,18 Thirdly, it is alsopossible that the intensity of stimulation we used wasnot enough to reflect any significant change in the N1amplitude.

In contrast to the findings related to the SI, there isevidence to suggest that the primary motor cortex (M1)seems to be involved in influencing pain perception.44

Epidural electrical motor cortex stimulation alleviates painperception.45 Repetitive transcranial magnetic stimulation(rTMS) of the motor cortex appears to be able to inducesignificant pain suppression, surprisingly however, both

at low (inhibitory) and high (facilitatory) frequencies ofstimulation.46 A recent study found increased pain percep-tion when a double pulse TMS with a 50-ms interval wasapplied over SI 150 to 200ms after the painful stimulus.39

In an other study, low frequency rTMS of the SI impairedtactile perception.47 Although tDCS, motor cortex stimula-tion, and rTMS show some similarities in their effects,there are basic differences at the neuronal level of theiractions.48–50 tDCS provides an alternative stimulationtechnique to rTMS and it offers a new perspective for thetreatment of disorders characterized by the alteration ofcortical excitability, like chronic pain.16 Compared withrTMS, the application of tDCS is simpler, less expensive,and better tolerated by human patients and provides amuch better placebo stimulation condition.51 tDCS mayinduce intracellular protein synthesis and alterations ofcyclic adenosine monophosphate and calcium levels.52–54

Additionally, N-methyl-D-aspartate receptors also seem toplay a pivotal role in the cellular mechanism of its evokedafter-effects.55,56 tDCS seems to modulate synaptic trans-mission in an activity-dependent manner, and possessessimilarities with long-term potentiation and long-termdepression.57 Our study encourages further exploration ofthe possible therapeutic effects of tDCS. Additional studiesare necessary to explore the time course of the observedantinociceptive effect: the after-effects of 15-minute tDCSover M1 stay stable for more than an hour and over thevisual areas approximately 20 to 30 minutes. However, wedo not know the time course of the effect over the SI. Thepharmacologic prolongation of the excitability-diminishingafter-effects58 and the antinociceptive effects of cathodalstimulation would render the method of tDCS applicable todifferent patient populations with chronic pain.

ACKNOWLEDGMENTThe authors thank Leila Chaieb for the English

corrections.

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