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Recent 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.
Ten 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.
Results 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.
Our 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.
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 the frontal 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) 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 be improved by applying A-tDCS to the LH.6–8 However, recent work by Monti and colleagues9 challenges such a simple interpretation, in which C-tDCS (2mA; 10-min) applied to Broca’s 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 limitations from 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 left frontal cortex would improve naming accuracy in PWA by exciting the underlying cortex causing even greater cortical activation.
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 Carolina’s 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 the Apraxia Battery for 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 previous fMRI 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.
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
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.
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 into MRIreg, a computer program that allows for the identification of a region of the scalp near a particular brain region (www.mricro.com/mrireg.html). Utilizing MRIreg and 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 (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.
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.
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.
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 of each 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 (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.
To examine the effect of tDCS on treatment outcome, a 2×2 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 2×2 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).
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.
During the A-tDCS phase, the mean number of correctly named treated items was 14.2/25 (SD = 8.69; range = 0–24) at baseline, 17.8/25 (SD = 9.44; range = 0–25) at T1 (immediately after treatment termination), and 17.7/25 (SD = 9.07; range = 0–25) 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 = 0–25) at baseline, 15.6/25 (SD = 9.81; range = 0–25) at T1, and 15.2/25 (SD = 9.53; range = 0–25) 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 2×2 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-tailed p < 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)=2.60 p< 0.015, t(9)=1.95 p< 0.042).
During the A-tDCS phase, the mean number of correctly named untreated items was 27.3/50 (SD = 17.15; range = 0–47) at baseline, 31.3/50 (SD = 18.35; range = 0–48) at T1, and 31.5/50 (SD = 18.25; range = 0–48) 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 = 0–48) at baseline, 28.9/50 (SD = 18.63; range = 0–50) at T1, and 30.1/50 (SD = 18.36; range = 0–50) at T2. Following S-tDCS treatment, the total increase in correct naming responses for the entire group was 3 items at T1 and 15 items at T2 (Table 4). A 2×2 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)=1.90 p< 0.045, t(9)=1.89 p< 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).
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).
To determine whether the order of stimulation affected treatment outcome, a 2×2 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).
To determine whether the word lists differed in difficulty, 2×2 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).
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 < 0.948), and heart rate (p < 0.641) from pre- to post-tDCS administration did not differ between A-tDCS and S-tDCS.
Patient discomfort ratings ranged between 0 and 2 out of 5 (mean = 0.24; SD = 0.56) during A-tDCS and ranged between 0 and 2 out of 5 (mean = 0.12; SD = 0.39) during S-tDCS. Statistical analysis revealed that the discomfort ratings were comparable between A-tDCS and S-tDCS (Mann-Whitney U; p < 0.477), indicating that patients did not report a difference in comfort level between the two conditions.
To better understand the effect of tDCS upon aphasia recovery, the present study included 10 patients with chronic, stroke-induced aphasia who each underwent five sessions of A-tDCS (1 mA; 20-min) and five sessions of S-tDCS (20-min) combined with a computerized anomia treatment. The results suggest that A-tDCS significantly improves naming accuracy in PWA. Explicitly, statistically more treated items were named correctly following A-tDCS as compared to S-tDCS and numerically more untreated items were named correctly following A-tDCS as compared to S-tDCS. Additionally, this study demonstrated that improvements in naming performance were maintained for at least one-week post-treatment. These findings are in agreement with previous evidence demonstrating that A-tDCS over the LH improves language processing.6–8
The difference in treatment outcome between A-tDCS and S-tDCS could not be explained by unspecific arousal differences, as changes in the patients’ blood pressure and heart rate recordings from pre- to post-tDCS administrations were found to be comparable across both tDCS conditions. Furthermore, differences could not be explained by scalp sensation attributed to the different stimulation types, as patients did not report a difference in their comfort levels between A-tDCS and S-tDCS. Finally, differences could not be attributed to the order of stimulation type or word list difficulty, as an order effect was not revealed between A-tDCS and S-tDCS nor was a difference revealed for the difficulty level between words lists A and B.
Various observations can help explain why A-tDCS over a region of the left frontal cortex improved the naming abilities in PWA. Primarily, this region has been revealed to be exceedingly important for aphasia recovery. For instance, a recent fMRI study investigated the activation of both hemispheres in 15 patients with chronic aphasia during an overt picture naming task. The results revealed a positive linear relationship between intensity of activation of the LH, especially the left frontal cortex, and naming accuracy in PWA.4 Results from the present study reinforce this finding, as it suggests that improved naming in PWA is supported by the left frontal cortex. Thus, since A-tDCS increases cortical excitability, it presumably improved the patients’ ability to name pictures by focally stimulating function of the left frontal cortex. Similar to the present research, other studies have implicated the LH in aphasia recovery, and although the specific cortical location may vary, it is probable that improved speech and language functioning following aphasia treatment relies, at least partly, on spared LH regions.1–4 It is important to note, however, that the present results do not discount the role of the RH in aphasia recovery, as several studies have revealed that right hemisphere regions reflect a compensatory network.22,23 Therefore, it may be possible that the positive treatment outcome revealed in the current study following A-tDCS to the left frontal cortex may be specific to naming improvements, and the administration of A-tDCS to other areas of the LH and possibly even the RH may improve the performance of other linguistic functions in PWA.
While the current study revealed a statistically significant enhancement for A-tDCS, individual patients exhibited a wide range of treatment outcomes. Understanding this variability may be important in optimizing treatment and justifying the clinical benefit for tDCS. Therefore, we feel it is important to speculate regarding the source of this variability. While our small sample size (n = 10) makes strong conclusions impossible, we believe that these are important considerations for the development of future studies. We suggest that treatment success was not related to biographical factors (e.g., age, education level, lesion size, aphasia severity, and AOS severity) (Table 5). For instance, the patient (P8) with the longest time post-stroke (242-months), largest lesion (342.2 cc3), and second most severe aphasia according to the WAB-R (AQ: 27.5) displayed improved naming. However, not all of the patients showed improved naming. For example, two of the patients (P4 and P7) performed nearly at ceiling during baseline testing, and thus, had limited room for improvement. Additionally, one patient (P6) presented with very severe speech and language deficits and did not produce a single correct naming response during any of the six testing sessions. Other patients (P3, P9, and P10) displayed improvements following both A-tDCS and S-tDCS, while the remaining four patients (P1, P2, P5, and P8) displayed clear improvements following A-tDCS as compared to S-tDCS. Three out of these latter four patients (P1, P2, and P8) presented with AOS and two of the four (P1 and P8) were classified as having nonfluent aphasia. Interestingly, both AOS and nonfluent aphasia are associated with damage to the left frontal cortex,24 which was the area stimulated in the present study. It should also be noted that the one of these four particular patients who did not present with AOS (P5), suffered damage to left frontal cortex. These observations lead us to speculate on two possible reasons why some of our patients benefitted from tDCS more than others. First, it may be possible that PWA who benefit the most from A-tDCS to the left frontal cortex are those with either or both AOS and nonfluent aphasia. Secondly, it is possible that stimulating areas closest to a patient’s perilesional area will result in the greatest amount of naming improvement (as presumably the residual portions of a damaged module are often crucial for rehabilitation). That is, three of the four patients (P1, P5, and P8) who benefitted the most from A-tDCS had frontal lobe damage, whereas most of the patients who showed less improvement tended to have posterior damage. This suggests that frontal lobe stimulation is most beneficial for patients with frontal lobe damage whereas posterior stimulation may be more beneficial for those PWA who also present with primarily posterior damage. Clearly, this latter speculation cannot be verified with the present data since our study only included frontal lobe stimulation.
One important caveat related to the present work is that it did not address the effect of C-tDCS upon naming. This was a clinical decision based on our hypothesis, which suggested that naming performance is positively correlated with cortical excitability. Therefore, it was presumed that the opposite outcome might be true, in which decreased cortical activation elicited by C-tDCS might inhibit picture naming. This decision was also based on the results of numerous studies suggesting greater benefit associated with A-tDCS compared to C-tDCS.6–8 Therefore, while our findings provide clear evidence regarding the beneficial role of A-tDCS, we do not have evidence to comment on the intriguing beneficial effect for C-tDCS reported by Monti and colleagues.9 While it is convenient to consider increased and decreased cortical excitability as being mutually exclusive, we concede that it is possible that both A-tDCS and C-tDCS may be beneficial. Specifically, one could imagine a situation where beneficial changes are preferentially sustained through a Hebbian process, while detrimental changes have no long-term consequences. In this scenario, A-tDCS entrains parts of the network that need to be up-regulated, whereas C-tDCS stimulation encourages down-regulation of other portions of the same network.
The current experimental design necessarily limits the inferences that can be drawn from this study, which, in turn, provides clear directions for future research. For instance, it is possible that measuring reaction time rather than just naming accuracy could have revealed a more sensitive measure of performance change for those patients who performed nearly at ceiling during baseline testing (e.g., P4 and P7). Additionally, the current study did not assess functional language abilities; thus, future studies should consider the inclusion of functional communication measurements to determine the functional relevance of tDCS. Finally, follow-up testing was performed relatively soon following treatment completion; therefore, it is important for future tDCS studies to conduct follow-up testing at longer intervals (e.g., two-weeks, one-month, etc.) to determine if treatment effects endure past one-week post-treatment.
It is imperative to note that the positive treatment outcome associated with the administration of anodal tDCS combined with an anomia treatment does not lessen the importance of clinician-administered aphasia treatment. Rather, the current treatment was designed to reveal that the inclusion of tDCS could supplement behavioral aphasia treatment due to its portability and simplicity of application. Given the beneficial effect observed after five 20-min anodal tDCS (1 mA) sessions, it is possible that more sessions (> 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 speculate that 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 aphasia treatment, 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.
Sources of Funding: This work was supported by the following grants: DC008355 (PI: JF), DC009571 (PI: JF & CR), and NS054266 (PI: CR).
Conflict of Interest: None