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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).

References

1. Crosson B, McGregor K, Gopinath KS, Conway TW, Benjamin M, Chang YL, Bacon-Moore A,

Raymer AM, Briggs RW, Sherod MD, Wierenga CE, White KD. Functional MRI of language in

aphasia: A review of the literature and the methodological challenges. Neuropsychol Rev

2007;17:157177. [PubMed: 17525865]

2. Postman-Caucheteux WA, Birn RM, Pursley RH, Butman JA, Solomon JM, Picchioni D, McArdle J,

Braun AR. Single-trial fMRI shows contralesional activity linked to overt naming errors in chronic

aphasic patients. J Cogn Neurosci. 2009 In Press.

3. Crinion JT, Leff AP. Recovery and treatment of aphasia after stroke: functional imaging studies. Curr

Opin Neurol 2007;20:667673. [PubMed: 17992087]

4. Fridriksson J, Bonilha L, Baker JM, Moser D, Rorden C. Activity in preserved left hemisphere regions

predicts anomia severity in aphasia. Cereb Cortex. 2009 In Press.

5. Higgins, ES.; George, MS. Brain Stimulation Therapies for Clinicians. Washington, DC: American

Psychiatric Press; 2008.

6. Flel A, Rsser N, Michka O, Knecht S, Breitenstein C. Non-invasive brain stimulation improves

language learning. J Cogn Neurosci 2008;20:14151422. [PubMed: 18303984]

7. Hesse S, Werner C, Schonhardt EM, Bardeleben A, Jenrich W, Kirker SG. Combined transcranial

direct current stimulation and robot-assisted arm training in subacute stroke patients: a pilot study.

Restor Neurol Neurosci 2007;25:915. [PubMed: 17473391]

8. Iyer MB, Mattu U, Grafman J, Lomarev M, Sato S, Wasserman EM. Safety and cognitive effect of

frontal DC brain polarization in healthy individuals. Neurology 2005;64:872875. [PubMed:

15753425]

Baker et al. Page 9


NIH-PAA

uthorManuscript


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Manuscript

8/2/2019 Ni Hms 182627

10/16

9. Monti A, Cogiamanian F, Marceglia S, Ferrucci R, Mameli F, Mrakic-Sposta S, Vergari M, Zago S,

Priori A. Improved naming after transcranial direct current stimulation in aphasia. J Neurol Neurosurg

Psychiatry 2008;79:451453. [PubMed: 18096677]

10. Sparing R, Dafotakis M, Meister IG, Thirugnanasambandam N, Fink GR. Enhancing language

performance with non-invasive brain stimulationa transcranial direct current stimulation study in

healthy humans. Neuropsychologia 2008;46:261268. [PubMed: 17804023]

11. Kertesz, A. Western Aphasia Battery-Revised. San Antonio: Harcourt Assessment, Inc; 2007.

12. Dabul, BL. Apraxia Battery for Adults. 2. Tigard, OR: CC Publications, Inc; 2000.13. Bhogal SK, Teasell RW, Foley NC, Speechley MR. Rehabilitation of aphasia: more is better. Top

Stroke Rehabil 2003;10:6676. [PubMed: 13680518]

14. Fridriksson J, Baker JM, Whiteside J, Eoute D, Moser D, Vesselinov R, Rorden C. Treating visual

speech perception to improve speech production in nonfluent aphasia. Stroke 2009b;40:853858.

[PubMed: 19164782]

15. Fridriksson J, Moser D, Bonilha L, Morrow-Odom KL, Shaw H, Fridriksson A, Baylis GC, Rorden

C. Neural correlates of phonological and semantic-based anomia treatment in aphasia.

Neuropsychologia 2007;45:18121822. [PubMed: 17292928]

16. Palm U, Keeser D, Schiller C, Fintescu Z, Reisinger E, Padberg F, Nitsche M. Skin lesions after

treatment with transcranial direct current stimulation (tDCS). Brain Stimulat 2008;1:386387.

17. Wong DL, Baker C. Pain in children: comparison of assessment scales. Pediatr Nurs 1988;14:917.

[PubMed: 3344163]

18. Fridriksson J, Baker JM, Moser D. Cortical mapping of naming errors in aphasia. Hum Brain Mapp2009a;30:24872498. [PubMed: 19294641]

19. Paulus W. Transcranial direct current stimulation (tDCS). Suppl Clin Neurophysiol 2003;56:249

254. [PubMed: 14677402]

20. Frances, WN.; Kucera, H. Frequency Analysis of English Usage. Boston: Houghton Mifflin; 1982.

21. Olejnik S, Algina J. Generalized eta and omega squared statistics: measures of effect size for some

common research designs. Psychol Methods 2003;8:434447. [PubMed: 14664681]

22. Crinion J, Price CJ. Right anterior superior temporal activation predicts auditory sentence

comprehension following aphasic stroke. Brain 2005;128:28582871. [PubMed: 16234297]

23. Raboyeau G, De Boissezon X, Marie N, Balduyck S, Puel M, Bzy C, Dmonet JF, Cardebat D. Right

hemisphere activation in recovery from aphasia: lesion effect or function recruitment? Neurology

2008;70:290298. [PubMed: 18209203]

24. Hillis AE, Work M, Barker PB, Jacobs MA, Breese EL, Maurer K. Re-examining the brain regions

crucial for orchestrating speech articulation. Brain 2004;127:14791487. [PubMed: 15090478]

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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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Table

1

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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Table

2

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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Table

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

http://localhost/Users/pandit12/Desktop/www.talairach.org

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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

5

Correlationsmatrixfortreatmentoutcome(changescor

es)andbiographicalinformation.Non

eoftherelationshipsreachedsignificance(p

Documents

Ni Hms 182627