ORIGINAL ARTICLE

Transcranial Direct Current Stimulation Over

Somatosensory 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 somatosensory cortex are known to be involved in nociception. The
aim of this study was to investigate the eect 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 signicantly 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 conditions had no signicant eect.
Discussion: Our study highlights the antinociceptive eect of this
technique and may contribute to the understanding of the
mechanisms underlying pain relief. The pharmacologic prolongation of the excitability-diminishing after-eects would render
the method applicable to dierent patient populations with
chronic pain.
Key Words: tDCS, pain, SI, laser-evoked potentials
(Clin J Pain 2008;24:5663)

he role of the somatosensory cortex (SI) in pain

perception has been controversial owing to the
inconsistent activations of this cortical area across
dierent imaging studies on pain perception.13 Although
some of imaging studies using nociceptive stimulation
have substantiated the involvement of the SI in pain

Received for publication April 20, 2006; revised July 17, 2007; accepted
July 29, 2007.
From the *Department of Clinical Neurophysiology, Georg-August
University, Robert Koch Strasse 40, 37075 Gottingen, Germany;
and wDepartment of Psychiatry, University of Szeged, Semmelweis
u. 6, 6725 Szeged, Hungary.
Supported by the German Ministry of Research and Education within
the 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: AAntal@gwdg.de).
Copyright r 2007 by Lippincott Williams & Wilkins

56

processing,36 many reports have failed to do so (for a

review see Ref. 2). Several electrophysiologic [electroencephalogram (EEG) and magnetoencephalogram]
studies reported SI pain-related activity only on the
contralateral side79; however, other studies found no
activation of SI at all (for a review see Refs. 1013). A
role of the SI in pain perception was demonstrated in a
patient with focal postcentral lesion in whom pain
sensation was lost but motivational-aective dimension
of pain was preserved.14 In addition, it was shown that
SI activity can be modied by the attention paid to the
painful stimulation.1,8,15 In summary, recent studies
suggest that specic activation to painful stimuli is likely
to exist but seems to be of small magnitude and restricted
to much smaller subsections of the SI than tactile
stimuli.10
The aim of the present study was to clarify whether
the application of transcranial direct current stimulation
(tDCS) can modify acute pain perception and processing
in healthy participants. A recent study suggests that tDCS
over the motor cortex oers a new perspective for the
treatment of chronic pain16; however, its eect over the SI
has not yet been observed. tDCS was recently reintroduced as a tool for inducing long-lasting changes of
cortical excitability and activity in focal brain regions
reversibly, painlessly, and safely.1720 Animal studies
suggest that it causes polarity-dependent shifts of the
resting membrane potentials and consequently changes
the ring rates of neurons beneath the electrodes and
probably in connected cortical areas.21,22 Generally,
the investigators found that anodal stimulation over the
motor cortex enhances cortical excitability, whereas
cathodal stimulation decreases it.17,18 Although in
humans the modulatory eects of tDCS have rst been
demonstrated in the motor system, it inuences visual,
somatosensory, and prefrontal functions as well (for a
review see Refs. 23, 24). Furthermore, cathodal stimulation of the SI by tDCS disrupts tactile perception.25
In this study in addition to psychophysical ratings
of pain perception, laser-evoked potentials (LEPs) were
recorded and analyzed before and after 15 minutes
anodal, cathodal, and sham tDCS. LEPs represent the
activation of distributed and interconnected neural
populations and are quantitative and stable neuronal
correlates of pain processing.26 The early N1/P1 LEP
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component that is generated in the contralateral SII

and recorded in the temporal region, correlates with the
sensory aspect of pain.27 The late LEP components
are the N2 wave peaking around 160 to 220 ms, and the
P2 component, which has a maximum amplitude around
300 to 360 ms.10 The results suggest that the N2
mainly reects primary sensory-discriminatory processes,
whereas the P2 component probably represents cognitiveemotional aspects of pain.28,29 We hypothesized that
cathodal stimulation over SI decreases subjective pain
perception and modies the parameters of its electrophysiologic correlates.

METHODS
Participants
Ten healthy volunteers (4 male) between the ages of
18 and 30 participated in the experiment. None of them
reported chronic pain syndromes, nor took any medication regularly. They had no history or current signs or
symptoms of neurologic or psychiatric disorders. Written
informed consent was obtained from all participants. The
study protocol conformed to the Declaration of Helsinki
and was approved by the Ethics Committee of the
University of Gottingen.

tDCS
tDCS was delivered by a battery-driven constant
current stimulator (Schneider Electronics, Gleichen,
Germany) using a pair of rubber electrodes in a
5  7 cm water-soaked synthetic sponge. One electrode
was placed over the left SI at a scalp position, as dened
by the Talairach coordinates that were calculated by
stimulation of the right hand in imaging studies,3,30
whereas the other electrode was placed above the right
eyebrow. The electrodes were orientated approximately
parallel to the postcentral sulcus and the eyebrow. The
type of stimulation (anodal or cathodal) refers to the
polarity of electrode above the SI, whereas for sham
stimulation the 2 electrodes were placed randomly and the
current was turned on only for a few seconds to provide
the slightly itching sensation at the beginning of the
stimulation. Participants were blinded as to the polarity
of tDCS. The current was applied for 15 minutes with an
intensity of 1.0 mA. The order of the sessions was
randomized across participants and separated by at least
1 week to avoid interference eects.

Laser Stimulation
To clarify the eect of tDCS over SI on pain
perception and processing, we stimulated the dorsum of
both hands of healthy participants with thulium doped
yttrium-aluminium-garnet (Tm:YAG) laser31 (WaveLight
Laser Technologie AG, Erlangen, Germany). The thulium laser emits near-infrared radiation (wavelength
2000 nm, pulse duration 1 ms, laser beam diameter
7 mm) with a penetration depth of 360 mm into the
human skin and allows a precise restriction of the emitted
heat energy to the termination area of primary nocicepr

2007 Lippincott Williams & Wilkins

Cathodal tDCS Decreases Pain Perception

tive aerents without aecting the subcutaneous tissue.28

The distal handpiece of the laser was positioned 30 cm
from the radial part of the dorsal surface of the hand.
Skin temperature of the stimulated area was checked
before every switch between hands, and corrected with a
heating lamp if below 351C. We stimulated dierent spots
in a square (5  5 cm) for each measure to reduce receptor
fatigue or sensitization by skin overheating.28 In each
experiment, the right (contralateral to the tDCS) hand
was stimulated rst in half of the cases and the left
(ipsilateral to the tDCS) hand was stimulated rst in the
other half. As in all cases, the left S1 was stimulated with
tDCS, we proposed that it would aect the pain threshold
dominantly on the contralateral hand, which could have
been masked by this initial orienting response.
At the beginning of the experiments, the pain
threshold of both hands was determined by applying
laser stimuli from 200-mJ in 50-mJ steps. During EEG
recording, we delivered 40 laser pulses to each hand
before and after tDCS with 1.5 to 1.6 times of threshold
intensity. The interstimulus interval of the stimulation
ranged from 8 to 15 seconds.

Psychophysical Evaluation
We used the verbal numeric analog score to assess
the subjective intensity of the laser-induced pain. The
participants were instructed to pay attention to the laser
stimuli and to rate the perceived pain verbally [warm, 1;
painful, from 2.1 (mild) to 2.9 (most intensive pain)1 to
10 scale] about 2 to 3 seconds after each stimulation. The
participants ears were plugged and white noise was
presented during the measurements to avoid auditory
artifacts due to laser stimulation.

Electrophysiologic Recordings
The EEG was recorded using a 5-channel montage
as described by Treede.26,28 This montage has been used
in numerous experimental and clinical LEP studies, as
it enables the easy identication of early and late LEP
components. We placed 3 electrodes in the midline
(Fz, Cz, and Pz) and 2 laterally above the temporal
region (T3 and T4) in accordance with the international
10/20 system. The impedance was kept below 5 kO. We
used the connected mastoids as reference. The ground
electrode was positioned on the forehead. Data were
collected with a sampling rate of 1000 Hz by the
BrainAmp system (Brain Products GmbH, Munich,
Germany) and were analyzed oine. A 0.1-Hz low cuto
and a 30-Hz high cuto lters were used. After automatic
artifact detection (200 mV amplitude criterion), all epochs
were visually inspected, and those containing eye blinks
or muscle movement artifacts were excluded. All recordings consisted of at least 35 artifact-free epochs. Baseline
correction was performed on the basis of the 100-ms
prestimulus interval. The amplitudes of N1 (referring
to Fz) and N2-P2 (referring to RLm) components were
measured oine.

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Antal et al

Clin J Pain

Data Analysis
Numeric analog score values and LEP amplitudes
were individually averaged and entered into a repeatedmeasures-analysis of variance for both hands and LEP
components separately [3 tDCS condition (cathodal,
anodal, sham)  2 time (before, after tDCS)]. We
considered a psychophysical or an electrophysiologic
change only if the condition  time interaction was
signicant. Furthermore, we investigated if this eect
was dependent on the electrode positions by calculating
the condition  time  electrode interaction. Post hoc
analysis was carried out using a Fischer least signicant
dierence test. Additionally, a Student t test (independent
by group) was used to compare the changes of amplitudes
between dierent conditions and between 2 hands. To do
that the amplitudes were normalized (after/before).

RESULTS
Psychophysics
The intensity of the laser stimulation (1.5 to 1.6 
of the pain threshold) was 19.6 mJ/mm2 for cathodal,
19.9 mJ/mm2 for anodal, and 19.8 mJ/mm2 for sham
stimulation. The repeated measurement of analysis of
variance revealed no main eect of condition [F(2,18) =
1.72, P>0.2] and time [F(1,9) = 4.65, P>0.05]. However, the condition  time interaction was signicant
[F(2,18) = 3.44, P<0.05] when the contralateral hand
was laser stimulated. According to the post hoc analysis,
cathodal stimulation signicantly decreased subjective
pain rating compared with the before stimulation condition (P<0.005), whereas anodal and sham stimulation
had no eect (Fig. 1).
In case of the ipsilateral hand laser stimulation,
there was no signicant eect of condition [F(2,18) =
1.075, P>0.3] and time [F(1,9) = 1.52, P>0.2]. The

FIGURE 1. The differences of reported subjective pain values

in % according to the numeric analog score reported by the
patients before and after cathodal, anodal and sham tDCS for
right (contralateral) and left (ipsilateral) hand laser stimulation.

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condition  time interaction was also not signicant

[F(2,18) = 0.77, P>0.4] (Fig. 1).

Electrophysiology
The laser stimulation induced a pricking pain in all
patients and a biphasic N2-P2 component was clearly
identied in all LEP measures (Fig. 2). In case of the N1
component, the LEP amplitudes recorded at T3 and T4
channels (referring to Fz) were analyzed separately.
There was no signicant eect of condition on channel
T3 [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 eect 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 signicant 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 was
no signicant time  condition interaction on T3 [contralateral: 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 eect of
condition [contralateral: F(10,46) = 0.78, P>0.6; ipsilateral: F(10,46) = 0.7, P>0.7] but the eect of time was
signicant [contralateral: F(5,23) = 4.59, P<0.005; ipsilateral: F(5,23) = 3.86, P<0.05] and we also found a
signicant condition  time interaction when the contralateral 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 stimulation
condition, cathodal stimulation signicantly diminished
the amplitude (P<0.005). The interaction with electrode
position here was also signicant [F(4,108) = 3.89,
P<0.005]. The post hoc analysis has shown that cathodal
stimulation signicantly decreased the amplitudes of the
N2 components at the Cz and Pz electrode positions for
the contralateral hand stimulation (P<0.005). The
changes of mean N2 amplitudes for all 3 tDCS conditions
and both hands are shown in Figure 3. The means and
standard deviations for both hands, LEP components,
and tDCS pairs are shown in Table 1.
In case of the P2 component, there was no main
eect of condition [contralateral: F(10,46) = 0.8, P>0.6;
ipsilateral: F(10,46) = 0.3, P>0.9] but the eect of time
was signicant 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 signicant condition  time
interaction [contralateral: F(10,46) = 0.75, P>0.6; ipsilateral: F(10,46) = 0.79, P>0.6]. The changes of P2
amplitudes for all 3 tDCS conditions and both hands
are shown in Figure 4.
A Student t test was used to compare the attitude of
changes between dierent conditions and hands. Signicant dierences were found between right hand sham
and cathodal stimulation [t(df18) = 2.16; P<0.05] and
between right hand anodal and right hand cathodal
stimulation [t(df18) = 2.66; P<0.05] only related to the
N2 amplitude at the Cz electrode position.
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Cathodal tDCS Decreases Pain Perception

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 greater
amplitude reduction of the N2 and P2 component for cathodal tDCS is observed at the contralateral side to the stimulation.

DISCUSSION
The main nding of the present study is that
cathodal stimulation of the SI signicantly diminished
subjective pain perception, whereas anodal and sham
stimulations had no eect. The eect was only present
when stimulating the contralateral hand to the side of
tDCS with the Tm:YAG laser. In parallel with these
results, cathodal stimulation signicantly reduced the N2
component of LEPs. Previously, only 2 tDCS studies
dealt with the somatosensory aspects of DC stimulation
in healthy human subjects, and are not directly comparable with our results owing to dierent stimulation loci.
In one of the studies, the M1 was stimulated while
somatosensory evoked potentials were recorded by the
stimulation of the left and right medial nerves.32
Relatively long-lasting (60 min) increases of the amplitudes of the parietal and frontal SEP components were
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2007 Lippincott Williams & Wilkins

detected after anodal stimulation. Cathodal stimulation

had no eect on these potentials. In the other study,
cathodal tDCS induced a prolonged decrease of tactile
discrimination, whereas anodal and sham stimulation did
not.25 To our knowledge, our study is the rst demonstrating that cathodal tDCS over the SI is able to diminish
experimentally induced pain perception in healthy human
participants.
The contribution of SI to pain processing as
revealed by functional magnetic resonance imaging/positron emission tomography and electrophysiologic studies
is less consistent across studies than that of the SII,
insular and anterior cingulate regions; the role in SI in
pain processing has been under extensive debate. Nociceptive projections exist from the thalamus to the SI.33
Additionally, specic nociceptive neurons have been
identied in the SI34 yet only about half of the imaging

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TABLE 1. The Mean Values and SDs of the LEP Parameters at

the Cz, Pz, and T3/T4 Electrode Positions for the Obtained
From all Patients for Both Hands Before and After Anodal,
Cathodal and Sham tDCS
Before tDCS

After tDCS

Cz
Mean

FIGURE 3. The differences of N2 amplitudes in % in the 3

tDCS conditions for the contralateral and ipsilateral hand laser
stimulation at the Cz electrode. The star marks significant
differences between the cathodal-sham and cathodal-anodal
condition after the contralateral hand stimulation (P<0.005).

studies report SI activation after painful stimulation (for

a review see Ref. 2). Negative results reported in imaging
and electrophysiologic studies might be due to individual
sulcal variabilities that can be alleviated for a groupaverage, small focal activations, or technical problems,
for example, not optimally dened thresholds for functional magnetic resonance imaging analysis. In our study,
we had used a 5  7 cm electrode size to optimize
stimulations parameters17 and it is therefore possible
that we covered a large part of SI. However, it may also
be that we have additionally stimulated part of the
somatosensory associations cortex (BA 5/7) that is
posterior to SI. Activation of human BA 5/7 has also
been linked to pain perception.13,35 BA 5/7 is anatomically connected to other nociceptive brain areas such as
the anterior cingulate cortex (ACC), insula, thalamus,
and primary motor cortices.36 It is possible that we have
induced the analgesic eect by the additional stimulation
of this region.
Another possibility is that the antinociceptive eect
was obtained by the indirect inhibition of SII and ACC
through SI stimulation. According to source localizing
electrophysiologic studies, the N2 component is generated
bilaterally in the operculoinsular region and in the
ACC.10 This component mainly contributes to sensorydiscriminatory aspects of pain. The P2 component mainly
arises from the ACC and reects endogenous, attentional,
cognitive, and aective factors.37 The SI is highly
interconnected with this cortical area and therefore the
down-regulation of the cortical excitability of the SI
might have resulted in an additional inhibition of the SII
and ACC. Indeed, although some previous LEP dipole
modeling studies showed that a dipole source in SI area
was necessary to explain the scalp LEP topography, none
of them reported a clear correspondence between the SI

60

Right Hand
A
N2
14.20
P2
18.73
C
N2
15.01
P2
16.62
S
N2
14.8
P2
17.58
Left Hand
A
N2
15.14
P2
18.79
C
N2
13.93
P2
17.50
S
N2
14.19
P2
18.02

Pz
SD

5.6
6.6

Mean

Cz
SD

9.90 7.9
9.50 14.1

Mean

12.70
16.70

Pz
SD

Mean

SD

5.7
7.9

6.00
12.93

5.9
5.5

6.3
4.9

7.45
13.80

4.9
4.4

9.98* 4.3
14.38 9.6

4.10* 3.2
11.30 5.7

5.5
5.5

6.10
14.67

3.8
3.6

12.11
18.76

5.8
6.3

4.12
15.22

4.1
5.8

4.5
6.7

6.60
14.45

3.5
5.9

13.17
17.43

3.5
9.3

4.88
14.40

3.9
7.2

5.9
6.7

6.74
13.83

5.2
4.2

11.17
16.66

4.7
7.0

4.52
13.19

4.3
4.6

4.3
5.8

5.94
14.64

2.2
3.7

13.16
15.90

4.9
6.5

5.29
11.85

3.3
5.0

T3
T4
Mean
SD Mean
SD
Right Hand
A
N1
7.16 3.7
5.30 3.9
C
N1
7.42 4.8
5.22 3.5
S
N1
8.31 3.9
5.18 3.5
Left Hand
A
N1
5.29 3.5
5.53 5.3
C
N1
6.20 2.8
6.55 2.3
S
N1
5.44 4.5
7.10 3.3

T3
Mean
SD

T4
Mean
SD

6.11

4.0

3.25

3.7

6.67

3.4

4.63

2.6

7.49

4.1

4.30

2.4

4.88

2.9

6.09

4.6

5.08

2.9

5.18

2.9

5.20

3.3

5.48

2.8

*P<0.005.

activity and a denite LEP component.7,38,39 Recently,

intracerebral depth recordings in an epileptic patient have
shown no reliable LEP response from the 3b area of the
SI after painful laser stimulation, although a reliable N2P2 response could be recorded at Cz.40 Therefore, it is
possible that the absence of the pain-related activation in
the SI found by imaging an electrophysiologic studies, is a
real phenomenon, however, the indirect involvement of
the SI in pain processing (modulating SII activity through
SI stimulation) is feasible. It has also been suggested that
pain processing takes place simultaneously in the SI and
SII and not sequentially in dierent areas as in tactile
processing.41 Then, as an alternative option, passive
spread of the current over cerebral areas could also
modify SII processing when the SI is stimulated.
Many electrophysiologic studies reported only
contralateral activation for nociceptive stimulation4,7;
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Volume 24, Number 1, January 2008

FIGURE 4. The difference of P2 amplitudes in % in the 3 tDCS

conditions for the contralateral and ipsilateral hand laser
stimulation at the Cz electrode.

however, imaging studies suggest that the pain-related SI

response is bilateral with signicantly greater activation in
the hemisphere contralateral to the stimulation.2,42 In our
study, cathodal stimulation had an eect only when the
contralateral hand was stimulated and not for ipsilateral
stimulation.
We did not nd any signicant change concerning
the N1 amplitudes. The N1 component is an early cortical
LEP potential, peaking at 140 to 170 ms and reecting the
early sensory-discriminative processing of pain perception. According to scalp topography (maximum near T3
and T4), it is generated near the SII in the fronto-parietal
operculum.26,43 At a rst glance, the missing eect of
tDCS on the N1 component and the inhibitory eect on
the N2 component, seems to be in contradiction, because
the main contribution to the N2 origin is also given by the
SII area. There are various explanations with regard to
this problem. Primarily, the N1 component is much
smaller than the N2 component and therefore a small
change in the size of the amplitude is more detectable in
the case of the N2 component. Secondly, the N1
component is probably produced by dierent neuron
groups in comparison with the N2 component, and in
these groups the neurons might be dierently oriented.
The interaction between the orientation of the neurons
and the current direction is probably critical to get
stimulation-induced after-eects.17,18 Thirdly, it is also
possible that the intensity of stimulation we used was
not enough to reect any signicant change in the N1
amplitude.
In contrast to the ndings related to the SI, there is
evidence to suggest that the primary motor cortex (M1)
seems to be involved in inuencing pain perception.44
Epidural electrical motor cortex stimulation alleviates pain
perception.45 Repetitive transcranial magnetic stimulation
(rTMS) of the motor cortex appears to be able to induce
signicant pain suppression, surprisingly however, both
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Cathodal tDCS Decreases Pain Perception

at low (inhibitory) and high (facilitatory) frequencies of

stimulation.46 A recent study found increased pain perception when a double pulse TMS with a 50-ms interval was
applied over SI 150 to 200 ms after the painful stimulus.39
In an other study, low frequency rTMS of the SI impaired
tactile perception.47 Although tDCS, motor cortex stimulation, and rTMS show some similarities in their eects,
there are basic dierences at the neuronal level of their
actions.4850 tDCS provides an alternative stimulation
technique to rTMS and it oers a new perspective for the
treatment of disorders characterized by the alteration of
cortical excitability, like chronic pain.16 Compared with
rTMS, the application of tDCS is simpler, less expensive,
and better tolerated by human patients and provides a
much better placebo stimulation condition.51 tDCS may
induce intracellular protein synthesis and alterations of
cyclic adenosine monophosphate and calcium levels.5254
Additionally, N-methyl-D-aspartate receptors also seem to
play a pivotal role in the cellular mechanism of its evoked
after-eects.55,56 tDCS seems to modulate synaptic transmission in an activity-dependent manner, and possesses
similarities with long-term potentiation and long-term
depression.57 Our study encourages further exploration of
the possible therapeutic eects of tDCS. Additional studies
are necessary to explore the time course of the observed
antinociceptive eect: the after-eects of 15-minute tDCS
over M1 stay stable for more than an hour and over the
visual areas approximately 20 to 30 minutes. However, we
do not know the time course of the eect over the SI. The
pharmacologic prolongation of the excitability-diminishing
after-eects58 and the antinociceptive eects of cathodal
stimulation would render the method of tDCS applicable to
dierent patient populations with chronic pain.
ACKNOWLEDGMENT
The authors thank Leila Chaieb for the English
corrections.
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