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Using transcranial direct current stimulation (tDCS) to treat stroke
patients with aphasia
Julie Baker, Ph.D., Chris Rorden, Ph.D., and Julius Fridriksson, Ph.D.
Department of Communication Sciences & Disorders, University of South Carolina
Abstract
Background and PurposeRecent research suggests that increased left hemisphere cortical
activity, primarily of the left frontal cortex, is associated with improved naming performance in stroke
patients with aphasia (PWA). Our aim was to determine if anodal transcranial direct current
stimulation (A-tDCS), a method thought to increase cortical excitability, would improve naming
accuracy in PWA when applied to the scalp overlying the left frontal cortex.
MethodsTen patients with chronic stroke-induced aphasia received five days of A-tDCS (1 mA;
20 min) and five days of sham tDCS (S-tDCS; 20 min, order randomized) while performing a
computerized anomia treatment. tDCS positioning was guided using a priori functional MRI results
for each individual during an overt naming task to ensure the active electrode was placed over
structurally-intact cortex.
ResultsResults revealed significantly improved naming accuracy of treated items (F(1,9) = 5.72,
p < 0.040) following A-tDCS as compared to S-tDCS. Patients who demonstrated the most
improvement were those with perilesional areas closest to the stimulation site. Crucially, this
treatment effect persisted at least one-week post-treatment.
ConclusionsOur findings suggest that A-tDCS over the left frontal cortex can lead to enhanced
naming accuracy in PWA and, if proved to be effective in larger studies, may provide a supplementary
treatment approach for anomia.
Keywords
anomia; brain stimulation; functional magnetic resonance imaging (fMRI); neuronal plasticity;
recovery of function
Introduction
A relationship between aphasia recovery and functional brain changes of the damaged left
hemisphere (LH) has recently been demonstrated.1,2 More specifically, in a review of
functional neuroimaging studies investigating treatment-induced aphasia recovery, improved
speech production was found to be dependent upon left frontal cortical activation.3 Another
recent study revealed that increased cortical activity in preserved LH areas, particularly thefrontal cortex, is associated with greater naming accuracy in patients with aphasia (PWA).4
These studies are based on observations of brain activation, however, and are generally
interpreted as supporting the notion that intact regions of the LH play a crucial role in aphasia
recovery. Our aim was to test this prediction by manipulating (rather than merely observing)
Corresponding author: Julie M. Baker, Ph.D., Department of Communication Sciences & Disorders, University of South Carolina, Tel:(843) 792-2712, Fax: (803) 777-3081, [email protected].
Conflict of Interest: None
NIH Public AccessAuthor ManuscriptStroke. Author manuscript; available in PMC 2010 June 1.
Published in final edited form as:
Stroke. 2010 June ; 41(6): 12291236. doi:10.1161/STROKEAHA.109.576785.
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activation of the left frontal cortex through the application of transcranial direct current
stimulation (tDCS), a noninvasive, safe, and relatively painless method for modulating cortical
activity. tDCS delivers a weak polarizing electrical current to the cortex through a pair of
electrodes, and depending on the polarity of the current flow, brain excitability can either be
increased via anodal stimulation (A-tDCS) or decreased via cathodal stimulation (C-tDCS).5
Previous work suggests that tDCS can modulate linguistic performances in both healthy and
neurological patients, with results typically demonstrating that language processing can beimproved by applying A-tDCS to the LH.68 However, recent work by Monti and
colleagues9 challenges such a simple interpretation, in which C-tDCS (2mA; 10-min) applied
to Brocas area resulted in an improved ability to name pictures in eight patients with chronic
nonfluent aphasia; no effects were noted following A-tDCS or sham (placebo-like) tDCS (S-
tDCS). We suggest three reasons that may help demonstrate why A-tDCS led to a null result.
First, electrodes were placed on the same scalp coordinate for each patient regardless of aphasia
type or severity. Consequently, it is quite probable that the targeted region may not have been
intact in some if not all of the patients. Secondly, there was only a single, brief administration
of tDCS. Finally, patients were not asked to perform a language task during the tDCS session,
whereas other previous studies that found effects following A-tDCS, coupled the stimulation
with a relevant task to engage the brain area.6,10 Therefore, while the main goal of the present
study was to determine if A-tDCS would improve naming accuracy in PWA when applied to
the left frontal cortex, the study was also designed to address the methodological limitationsfrom the recent work by Monti and colleagues9 and to therefore incorporate the following: 1)
optimized electrode positioning; 2) multiple administrations of tDCS; and 3) a combined
linguistic task.
In the present study, 10 patients with chronic aphasia underwent two separate weeks (five days
per week) of A-tDCS (1 mA, 20-min) and S-tDCS (20-min) while concurrently performing a
computerized anomia treatment. During both types of tDCS, the active electrode was placed
on the scalp overlying the left frontal cortex, while the reference electrode was placed on the
right shoulder. The location and polarity of the active electrode was chosen based on the
previously discussed evidence demonstrating that increased activation in the LH, specifically
of the left frontal cortex, was related to naming improvements in PWA.4 Outcome measures
included naming performance of both treated and untreated items following A-tDCS and S-
tDCS. We hypothesized that multiple administrations of A-tDCS to the scalp overlying the leftfrontal cortex would improve naming accuracy in PWA by exciting the underlying cortex
causing even greater cortical activation.
Materials & Methods
Patients
Ten patients (five females) with chronic, stroke-induced aphasia aged 45- to 81-years (M =
65.50; SD = 11.44) participated in the current study, which was approved by the University of
South Carolinas Institutional Review Board. Patients varied greatly with regard to time post-
stroke onset, lesion location, and extent of brain damage (Table 1). For instance, the range of
time post-stroke onset was 10 to 242 months (M = 64.60; SD = 68.42). Additionally, the patients
varied with regard to their performance on diagnostic measures. Aphasia assessment using the
Western Aphasia Battery-Revised (WAB-R)11 revealed that six (P2, P4, P5, P7, P9, and P10)
of the ten patients were classified with fluent aphasia, while the remaining four patients (P1,
P3, P6, and P8) were classified with nonfluent aphasia. The WAB-R also yields a composite
score, the Aphasia Quotient (AQ), which provides an overall measure of severity, in which
lower scores denote more severe aphasia, and a score above 93.8 is considered to be within
normal limits. AQ scores in the current study ranged from 26.3 to 93.5 (M = 69.36; SD = 25.97).
Additionally, Subtest 6 (Inventory of Articulation Characteristics) of theApraxia Battery for
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Adults-Second Edition (ABA-2)12 revealed that five patients (P1, P2, P3, P6, and P8) presented
with apraxia of speech (AOS; Table 2). Thus, we suggest that the current patient sample was
ideal for an exploratory study as it included a group with a wide range of aphasia severities
and varying biographical and lesion demographics. Specific inclusion criteria were: 1) one-
time stroke in the LH; 2) > 6-months post-stroke onset; 3) < 85-years of age; 4) pre-morbidly
right-handed; 5) native English speaker; and 6) been a participant in a previous study that
included functional magnetic resonance imaging (fMRI) examination,4 which was used to
guide the location of cortical stimulation in the present study. All 15 patients from the previousfMRI study4 were considered for participation in the current study but only the current 10
patients were able to participate. As for those patients who were not included, four had relocated
out of state and one was unable to fit the current study requirements into his schedule which
included full-time employment. Exclusion criteria were: 1) seizures during the previous 36-
months; 2) sensitive scalp; 3) previous brain surgery; and 4) medications that raise the seizure
threshold.
Study Design
Diagnostic testing was followed by electrode positioning, baseline naming tests, treatment
administration, and post-treatment naming testing. The computerized anomia treatment,
coupled with either A-tDCS or S-tDCS, was administered for five consecutive days followed
by a seven-day rest period to avoid carry-over effects. Next, another five-day treatment period
was administered, coupled with the remaining stimulation type. Whereas previous research
has revealed an improvement in naming among aphasic patients following a single tDCS
session,9 the current study design reflected evidence suggesting that multiple treatment
sessions are associated with improved treatment outcome in aphasia.13 Hence, a total of five
consecutive days were devoted to each treatment phase. We chose to administer five treatment
sessions per phase based on our previous findings, in which some aphasic patients showed
improved picture naming following as few as five sessions with our computerized anomia
treatment task,14 as well as following five treatment sessions utilizing clinician-administered
anomia treatment in a separate study.15
The stimulation and treatment task combination lasted for 20-min each session, a time chosen
based on previous tDCS research which demonstrated that tDCS administration is safe up to
20-min.8 Finally, a stimulation intensity of 1 mA was chosen given that no significant adverse
effects have been reported at this intensity.16 To assess cardiovascular arousal, blood pressure
and heart rate were measured before and after each session. Additionally, discomfort ratings
were recorded following the end of each session using the Wong-Baker FACES Pain Rating
Scale, a visual description scale designed for patients with limited verbal skills.17
fMRI Task & Procedure
Previously acquired high-resolution T1-MRI and fMRI results associated with an overt picture
naming task were utilized in order to determine placement of the anode electrode on a patient-
by-patient basis. MRI data collection relied on a Siemens Trio 3T system. For details on the
naming task as well as the scanning parameters and data analyses, see Fridriksson and
colleagues.18 The location of voxels with the highest Z-scores in the left frontal cortex
associated with correct naming for each patient is listed in Table 3. These coordinates were
targeted for placement of the anode electrode.
Electrode Positioning
In order to locate the cortical region to be stimulated by the anode electrode, coordinates of
the area of the left frontal cortex with the highest level of activation during correct naming on
the previously completed fMRI naming task were entered intoMRIreg, a computer program
that allows for the identification of a region of the scalp near a particular brain region
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(www.mricro.com/mrireg.html). UtilizingMRIregand a magnetic positioning tracker system
(Flock of Birds; Ascension Technology, Burlington, VT), the desired cortical region was
located and demarcated on a latex cap worn by the patient. This cap was carefully fitted on the
patient prior to the start of each tDCS administration in order to accurately position the anode
electrode in the same area from one day to the next. Following positioning, the cap was removed
and the electrodes were held in place with self-adhesive bandages. This was accomplished on
a patient-by-patient basis and was therefore tailored for each individual to ensure the active
electrode was placed over structurally-intact rather destroyed cortex.
tDCS
tDCS (1 mA) was delivered for 20-min per session via two saline-soaked sponge electrodes
(5 5 cm) and a constant current stimulator (Phoresor II PM850; Iomed Inc., Salt Lake
City, Utah) that was placed out of the patients sight behind a partition. During both A-tDCS
and S-tDCS, the anode electrode was placed over the pre-designated area on the scalp overlying
the left frontal cortex. To avoid potential confounding factors arising from placing electrodes
of two polarities near the brain, as it is hard to infer which electrode is influencing performance,
the reference cathode electrode was placed on the right shoulder (Figure 1). For S-tDCS, the
stimulator was turned off following 30 s of stimulation since the perceived sensations of tDCS
on the skin have been found to fade away by the first 30 s of administration.19 Thus, patients
were blinded to stimulation type. Half of the patients began treatment with A-tDCS during the
first week and then proceeded to S-tDCS during the second week, while the other half received
the opposite order. Patients were randomly assigned to stimulation using a random number
generator.
Anomia Treatment
The self-administered anomia treatment consisted of a picture-word matching task. This type
of computerized treatment was utilized in a previous study and demonstrated to be useful in
improving the naming abilities in PWA. For details on the treatment, see Fridriksson and
colleagues.14 This treatment occurred concurrently with the application of tDCS and lasted for
20-min per session.
Treatment Stimuli
The computerized treatment included two separate word lists (List A and List B). Half of the
patients received List A during the first week of treatment and then List B during the second
week, while the other half received the opposite order. Each word list was comprised of 25
color pictures depicting low-, medium-, and high-frequency nouns. The two word lists were
controlled for word frequency,20 semantic content (categories such as animals, transportation,
etc.), and word length (number of syllables per word). Each picture appeared an equal amount
of times and occurred randomly during the 20-min session.
Outcome Measures
To determine whether the patients ability to name the treated items improved over the course
of each treatment phase (A-TDCS vs. S-tDCS), a computerized naming test consisting of the
25 treated nouns for each phase was administered at baseline, immediately following the fifth
(and final) session of each treatment phase (T1), and one-week following the final session ofeach treatment phase (T2) to examine performance maintenance. To determine generalization
from treated to untreated items, two additional untargeted word lists (one for each stimulation
type) were administered. The untreated word lists (untreated List A and untreated List B) were
each comprised of 50 color pictures depicting low-, medium-, and high-frequency nouns.
Similar to the treated word lists, the untreated word lists were controlled for word frequency,18 semantic content, and word length. The treated and untreated word lists were combined
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(treated List A was combined with untreated List A and vice versa for List B) during testing
to equal 75 items. Pictures representing each item were displayed on a laptop computer screen,
and patients were asked to overtly name each picture as soon as it was displayed. Responses
were audio-recorded and later transcribed and scored by two speech-language pathologists
(SLPs) who were blinded to the stimulation type (A-TDCS vs. S-tDCS), administration attempt
(baseline vs. T1 vs. T2), and type of item (treated vs. untreated). In cases of disagreement, a
third SLP, who was also blinded, made tie-breaking decisions.
Statistics
To examine the effect of tDCS on treatment outcome, a 22 repeated measures analysis of
variance (ANOVA) was performed for both treated and untreated items using stimulation type
(A-TDCS, S-tDCS) and time (T1, T2) as factors. Note that treatment outcome was determined
as change in correct naming at the end of treatment compared to baseline. Additional 22
repeated measures ANOVAs were performed to determine the influence of stimulation order
on treatment outcome for both treated and untreated words, as well as to determine the influence
of the two sets of word lists that were utilized for treatment and testing for both treated and
untreated items. All ANOVAs were performed using ezANOVA (www.mricro.com/ezanova).
Changes in blood pressure and heart rate from pre- to post-tDCS administrations, as well as
discomfort ratings were compared between both tDCS conditions utilizing Mann-Whitney U
tests. Finally, correlation analyses were performed to examine the relationships between
treatment outcome and patient demographics, which were executed, along with the Mann-
Whitney U tests, using SPSS Version 15.0 software package (SPSS, Inc., Chicago, Illinois).
Results
All patients tolerated tDCS well and no adverse effects related to the application of tDCS were
demonstrated. All patients completed both treatment phases and all accompanying testing
sessions. The total number of treatment and testing sessions was seventeen per patient,
including one diagnostic testing session, six testing sessions, and ten treatment sessions.
Treated Items
During the A-tDCS phase, the mean number of correctly named treated items was 14.2/25 (SD
= 8.69; range = 024) at baseline, 17.8/25 (SD = 9.44; range = 025) at T1 (immediately aftertreatment termination), and 17.7/25 (SD = 9.07; range = 025) at T2 (one-week following
treatment termination). Following A-tDCS treatment, the total increase in correct naming
responses for the entire group was 36 treated items at T1 and 35 treated items at T2. During
the S-tDCS phase, the mean number of correctly named treated items was 14.1/25 (SD = 9.79;
range = 025) at baseline, 15.6/25 (SD = 9.81; range = 025) at T1, and 15.2/25 (SD = 9.53;
range = 025) at T2. Following S-tDCS treatment, the total increase in correct naming
responses for the entire group was 15 items at T1 and 11 items at T2 (Table 4). A 22 repeated
measures ANOVA (stimulation, time) was conducted for the treated items. Analysis of the
main effect of stimulation type revealed that statistically more treated items were named
correctly following A-tDCS as compared to S-tDCS (F(1,9) = 5.72, two-tailedp < 0.040). To
estimate the magnitude of this statistically significant effect, we used the generalized eta
squared as suggested for repeated measures designs by Olejnik and Algina, 21 in which a
medium effect size (0.140) was found. Neither the analysis of the main effect of time (F(1,9)= 0.116,p < 0.741) or the analysis of the interaction (stimulation, time) reached statistical
significance (F(1,9) = 0.112,p < 0.745). Our hypothesis was that tDCS would enhance
treatment. Therefore, we conducted a post-hoc (uncorrected) 1-tailed t-tests that revealed a
benefit for tDCS versus sham at both the T1 and T2 (t(9)=2.60p< 0.015, t(9)=1.95p< 0.042).
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Treatment Generalization
During the A-tDCS phase, the mean number of correctly named untreated items was 27.3/50
(SD = 17.15; range = 047) at baseline, 31.3/50 (SD = 18.35; range = 048) at T1, and 31.5/50
(SD = 18.25; range = 048) at T2. Following A-tDCS treatment, the total increase in correct
naming responses for the entire group was 40 untreated items at T1 and 42 untreated items at
T2. During the S-tDCS phase, the mean number of correctly named untreated items was 28.6/50
(SD = 18.18; range = 048) at baseline, 28.9/50 (SD = 18.63; range = 050) at T1, and 30.1/50
(SD = 18.36; range = 050) at T2. Following S-tDCS treatment, the total increase in correctnaming responses for the entire group was 3 items at T1 and 15 items at T2 (Table 4). A 22
repeated measures ANOVA (stimulation, time) did not reach two-tailed statistical significance
(F(1,9) = 5.72,p < 0.073). As with treated items, we performed a post-hoc analysis here
consistent with our prediction that tDCS leads to improved naming performance compared to
sham. Accordingly, we conducted a planned (uncorrected) 1-tailed t-tests that revealed a
benefit for tDCS versus sham at both the T1 and T2 (t(9)=1.90p< 0.045, t(9)=1.89p< 0.046).
To estimate the magnitude of this effect, we used generalized eta squared,21 in which a medium
effect size (0.167) was revealed. Neither the analysis of the main effect of time (F(1,9) = 0.880,
p < 0.373) or the analysis of the interaction (stimulation, time) reached statistical significance
(F(1,9) = 0.584,p < 0.464).
Correlations
Multiple correlations were performed to examine the relationship between naming
performance following A-tDCS treatment and the following variables: 1) age; 2) years of
education; 3) months post-stroke onset; 4) lesion size measured in cc3; 5) aphasia severity as
measured by the AQ from the WAB-R; and 6) AOS severity as measured by the ABA-2. No
significant (p < 0.05) relationships were revealed (Table 5).
Treatment Order
To determine whether the order of stimulation affected treatment outcome, a 22 repeated
measures ANOVA (order of treatment, time) was performed and revealed that an order effect
was not present for the treated items (F(1,9) = 0.116,p < 0.742) or untreated items (F(1,9) =
0.880,p < 0.373).
Word Lists
To determine whether the word lists differed in difficulty, 22 repeated measures ANOVA
(list, time) was performed. No difference in treatment outcome between the usage of List A
and List B was found for the treated items (F(1,9) = 2.41,p < 0.155) or untreated items (F(1,9)
= 0.844,p < 0.382).
Blood Pressure, Heart Rate
Changes in blood pressure and heart rate from pre- to post-tDCS administration were calculated
to determine if the measures were comparable in both tDCS conditions. Mann-Whitney U tests
revealed that changes in systolic blood pressure (p < 0.812), diastolic blood pressure (p 5 sessions), longer sessions (> 20-min),
and greater stimulation intensity (> 1 mA) could have elicited even greater success, as long as
current safety guidelines are strictly followed.8
Furthermore, it is straightforward to speculatethat improved treatment outcome could be obtained by tailoring the treatment to better fit
individual patients. This could be accomplished by manipulating factors such as overall word
frequency (e.g., incorporating more higher-frequency words for patients with severe aphasia
and more lower-frequency words for patients with mild aphasia), semantic content (e.g.,
modifying word lists by selecting words that are meaningful and functionally relevant for each
patient), and the time interval between the picture display and onset of the spoken word (e.g.,
lengthening the time for patients with slower reaction time).
In closing, this study provides further evidence suggesting that preserved regions of the LH
are important for aphasia recovery. Moreover, these findings suggest that tDCS can aid in
anomia recovery among stroke patients. However, as is always the case with exploratory
research, further investigation involving greater number of patients is needed to confirm the
effect revealed in the current pilot study. Finally, as is almost always the case with aphasiatreatment, there was a wide range of treatment outcomes among the current patients, but
nevertheless, the current study demonstrates that A-tDCS to the scalp overlying the left frontal
cortex can significantly improve naming accuracy in some PWA and, if proved effective by
larger studies, may provide a supplementary treatment approach for anomia.
Acknowledgments
Sources of Funding: This work was supported by the following grants: DC008355 (PI: JF), DC009571 (PI: JF &
CR), and NS054266 (PI: CR).
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Figure 1.Example of the treatment set-up. Patients trained on a computerized picture-word matching
task (a) while receiving transcranial direct current stimulation (tDCS). During both anodal
tDCS and sham tDCS treatment phases, the anode electrode (b) was placed over the pre-
designated area on the scalp overlying the left frontal cortex, while the reference cathode
electrode (c) was placed over the right shoulder. The constant current stimulator (d) was placed
out of the patients sight behind a partition.
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Biographicalinfo
rmationandlesiondescription
P
Sex
Age*
Education
*
Post-StrokeOnset
LesionLo
cation
LesionSize
1
M
60
16
64
DamageinvolvesBA44,BA45,anteriorportionofBA38,andthemiddleandanteriorinsula
87.42
2
M
53
12
57
DamageinvolvesBA22,BA39,BA40,BA42,andtheposteriorportionofBA38
23.57
3
F
45
14
60
Complete
destructionofBA44,BA45,andmiddleandinferiorportionsofBA6,aswellasdamagetoBA22,
BA40,and
BA42
56.76
4
F
75
12
10
DamageinvolvesportionsofBA22,BA41,BA42,andinfe
riorportionofBA40
8.45
5
M
58
12
14
DamageinvolvesBA45,BA48,theanteriorinsula,andputamen,onlyminorinvolvementofBA44
48.39
6
F
64
16
102
DamageinvolvesBA6,BA44,BA48,BA38,andinsula,deepwhitematterinvolvementincludingthepyramidaltract
56.23
7
F
71
18
44
Damagem
ostlyinvolvingBA37andinferiorportionoftheleftprecuneus
40.49
8
M
72
12
242
EntireMC
Adistributionandportionsoftheanteriormedialfrontallobe;basalgangliainvolvement
342.2
9
F
81
16
14
Damagem
ostlyinvolvesmiddleandposteriorportionsofthe
temporallobe(BA20,BA21,BA22,BA37,BA
39)with
extension
intotheoccipitallobe
48.92
10
M
76
12
39
DamageinvolvesposteriorportionofBA21aswellasBA22,BA37,andBA39
29.13
M
65.50
14.00
64.60
74.15
SD
11.44
2.31
68.42
96.60
*Measuredinyears
Measuredinmonths
BA:Brodmannsarea
Measuredincc3
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Diagnostictestinginformation
WesternAphasiaBattery-Re
vised
BostonNamingTest-2
ApraxiaBatteryforAdults-2
P
Content*Fl
uency
*
AuditoryComprehension
*
Repetition
*
Naming
*
AQ
AphasiaType
1
8
4
8.65
7.7
7.7
72.1
Brocas
17
10
2
9
8
9.75
9.5
8.6
89.7
Anomic
38
6
3
7
4
7.15
3.1
4.7
51.9
Brocas
10
12
4
10
9
9.95
9.0
8.8
93.5
Anomic
44
3
5
9
9
10
9.4
8.6
92.0
Anomic
30
3
6
2
1
9.85
0.30
0
26.3
Brocas
1
10
7
9
9
9.85
9.8
8.3
91.9
Anomic
46
2
8
2
1
5.05
3.7
2.0
27.5
Brocas
2
11
9
7
7
7.05
7.2
5.6
67.8
Anomic
7
4
10
9
9
8.15
6.5
7.8
80.9
Anomic
36
4
*Maximumscoreof10
AQ:AphasiaQuotient;Maximumscoreof100
Maximumscoreof60
Rangeofscores:015;Score>5signifiespresenceofapraxiaofspeech
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3
CoordinatesandlocationofvoxelswiththehighestZ-scoresassociatedwithcorrectnaming/l
ocationoftheanodeelectrode
P
x*
y*z
*
Location
BA
1
39
156
0
Precentralgyrus
6
2
55
4
1
2
Precentralgyrus
6
3
36
52
4
Middlefrontalgyrus
10
4
48
4
4
6
Precentralgyrus
6
5
44
6
4
4
Precentralgyrus
6
6
28
46
1
4
Middlefrontalgyrus
46
7
54
20
1
0
Inferiorfrontalgyrus
45
8
12
46
3
0
Superiorfrontalgyrus
9
9
52
16
1
6
Inferiorfrontalgyrus
44
10
60
2
1
2
Precentralgyrus
6
*x,y,&z:MontrealNe
urologicalInstitutecoordinates
Anatomicallocationsw
eredeterminedusingtheTalairachDaemon(www
.talairach.org)
BA:Brodmannsarea
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Table
4
correctl
ynamedtreatedanduntreateditemsbetweenpost-treatmenttestingandbase
linetestingfollowinganodaltDCS(A
-tDCS)andshamtDCS(S-tDCS)
ImmediatePost-Treatment>Baseline
1-WeekPost-Treatment>Baseline
S-tDCS
TreatedItems
A-tDCSUntreatedItems
S-tD
CSUntreatedItems
A-tDCSTreatedItems
S-tDCSTreatedItems
A-tDCSUntreatedItems
S-tDCSUntreatedItems
0
17
2
8
2
10
1
4
6
1
3
2
9
1
10
3
1
5
5
5
0
0
1
2
1
0
1
2
0
6
1
6
2
2
0
0
0
0
0
0
0
0
1
1
1
1
0
1
1
2
2
1
3
0
3
1
3
1
2
5
2
1
6
1
5
2
3
6
10
9
15
40
3
35
11
42
15
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Table
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Correlationsmatrixfortreatmentoutcome(changescor
es)andbiographicalinformation.Non
eoftherelationshipsreachedsignificance(p