Transcranial DC Stimulation - by Dave Siever

In 43 AD, Scribonius Largus, a physician of the Roman emperor Claudius, described a detailed account of the use of the (electric) torpedo fish to treat gout and headache. Since that time, a number of scientists experimented with electrical stimulation in hopes of treating various maladies as well as bringing people back from the dead. It was the invention of the battery that made DC stimulation or faradization, as it was termed at the time, possible. In 1755, French physician Charles Le Roy, wrapped wires around the head of a blind man in hopes of restoring his eyesight.

Duchenne de Bologne (Figure 1) became the first to systematically use electricity in the diagnosis and treatment of disease. He even brought a woman “back from the dead” after she was in a coma-state from carbonic oxide poisoning by using an early form of cardiac electro-shock.

Figure 1.

In the USA in 1871, Beard and Rockwell published their book on the medical uses of electricity. They presented arguments for the use of galvanization (the term for DC stimulation at the time) for a variety of indications, as shown in Figure 2.

Figure 2

In the late 1700s to early 1800s, Giovanni Aldini (Galvani’s nephew) reported experiments using galvanization to treat psychosis, depression and even revive the dead. He later went on a travelling road show demonstrating the use of electricity for bringing cadavers back to life. It is thought that this showmanship may have been the cause for damaging the reputation of electrical stimulation for the next 100 years.  In the 1960s, animal experiments using weak DC stimulation on the exposed cortex showed that neuronal activity could be altered immediately, and that these changes would last for several hours. These studies marked the true beginnings of transcranial DC Stimulation (tDCS).

Most tDCS research has been done by Nitsche and his colleagues at the University of Gottingen in Germany. Other authors include: Fregni, Pascual-Leone and Boggio from Beth-Israel Deaconess Medical School (Harvard), plus Antal, Kincses, Hoffman, Kruse.

I have found roughly 75 studies and the list below shows the study focus and the number of studies done. To obtain .pdfs of 46 of these studies in a zip file, go to: (products/CESta) and scroll down to “Research Articles on tDCS.” To learn more about electrode placement locations, go to: and select “Info about Brodmann Area Functions.” The studies that I have found include the following categories:


Cognition (General)


Probabilistic Classification Learning


Treating Alcoholism


Working Memory (General)


With Parkinson’s


Declarative Memory


Depression (F3 Anode)


Motor Cortex




Motor Imagery


Tactile Perception






 Auditory (pitch-left temporal)




Visual Cortex


Tactile Perception




NMDA Receptor












NaCl Concentration


Literature Reviews



The positive electrode is called the anode. Brain function under the electrode site is enhanced by roughly 20 to 40% when the current density (concentration of amperage under the electrode) exceeds 40 µa/cm2 (260 µa/inch2). The negative electrode is called the cathode and it reduces brain function under the electrode site by 10 to 30% at the fore-mentioned current density. Anodal stimulation is the most common form of tDCS as it enhances brain function.

The brain-stimulating electrode is called the active electrode, whereas the circuit-completing inactive electrode is called the reference electrode. In most of the studies, the reference has been placed over the contralateral orbit (above the left or right eye) to avoid negative effects from it. However, the studies never looked at the inhibiting effects that the reference electrode might have had on the prefrontal lobe. Some recent studies and in particular a study by Nitsche, et al., (2007) show that it is better to have a small stimulating electrode and large reference electrode. This way, the current density is high under the treatment electrode and weak under the reference electrode. This arrangement allows the reference electrode to be placed most anywhere over the scalp without it affecting brain function beneath it. Most studies have used stimulation at 1 ma of current through 7cm x 7cm (49 cm2 ) electrodes (There are 2.54 cm in one inch, therefore a 1” square electrode is 2.54 cm x 2.54 cm = 6.45 cm2). Fregni and his group at Harvard advocate using a shoulder for the reference placement. I also advocate using a shoulder placement except possibly for treating depression, where the active electrode (anode) is placed over the dorsolateral prefrontal cortex (F3 on the 10-20 electrode montage) and the cathode over F4.

Nitsche and Paulus found that a minimum current density of 17 µa/cm2 was needed to excite motor neurons. Studies involving other regions of the brain have suggested that 20 to 25 µa/cm2 are needed to excite neurons under the electrode. One depression study using anodal stimulation at F3 noted alleviated depression using 1 ma into a 35 cm2 electrode (28 µa/cm2). Iyer, et al., observed that when stimulating the left prefrontal cortex there was no effect on verbal fluency with a 1 ma current, but significant improvements at 2 ma (current density of 20 µa/cm2 vs 41 µa/cm2). Two depression studies by Boggio, et al., 2007; Boggio, et al., 2007) also used 2 ma.

It is important that the tDCS device is current controlled. What this means is that the device will adjust the voltage up and down as the resistance changes sot that the current never changes. For instance, if the resistance of the skin is 10,000 ohms, then 10 volts will be needed to “push” 1 ma through the body. If for some reason, the connection becomes poor and jumps to 20,000 ohms, then the device should automatically increase the voltage to 20 volts in order to push the 1 ma current through the body.

We did some testing with a 9-volt battery supplying a 1 ľ” by 1 ľ” (4.5 x 4.5 cm) tap-water wet sponge anode at F3 and a 2”x 4” (5.1 x 5.1 cm) wet sponge cathode on the left arm and found that at the onset, the current flow was 0.3 ma (current density of 15 ua/cm2). By applying a mild pressure on the arm electrode, the current rose to 0.6 ma. When we increased the anode at F3 to 2”x 4”, the current rose to 0.6 ma and 1.2 ma when pressure was applied to the shoulder electrode. The currents in both situations are well below the necessary value of 40 ua / cm2, and therefore not effective. The variance was also 2 to 1. We then soaked the electrodes (1 ľ”x 1 ľ”3/4 and 2”x 4”) in a 5% salt solution. The current was a whopping 3 ma, (current density of 150 ua/cm2) as confirmed by the ammeter and the stinging on my forehead. In this case, the current density was much too high. If the reference cathode was also used on the head instead of the shoulder, there would have been a significant inhibition effect around it.


There are presently only two stand-alone devices that produce tDCS. They are: the Eldith DC Stimulator by Neuro Conn, of Germany, which sells for €3000 (about $4,000US) and the CESta, by Mind Alive Inc., of Canada, which sells for $350US. Both units are current controlled and programmable. The CESta has the added benefits of providing cranio-electro stimulation and micro-electro therapy for muscle work. It also features randomization of the frequency stimulation and usage tracking for patient compliance. The CESta has been “tuned” with the electrodes provided so that at 1 ma stimulation, the active electrode delivers 50 µa/cm2, while the reference electrode produces 18 µa/cm2. This table shows the current density using various sizes at 1 and 2 ma currents.

25 cm2  5 x 5     @         1 ma     =          40 µa/cm2

25 cm2  5 x 5     @         2 ma     =          80 µa/cm2

36 cm2  6 x 6     @         1 ma     =          27 µa/cm2

49 cm2  10 x 10 @         1 ma     =          20.4 µa/cm2


I have used tDCS with a middle-aged person who had developed some cognitive decline, lost confidence while driving and developed mild obsessive-compulsive disorder (OCD). He was ruminating a jingle over one hundred times an hour. Suspecting an over active cingulate, he was given cathodal stimulation between F3 and Fz (F1) with the reference on his right shoulder. His ruminations ended completely following the third treatment and he noted improvements in sharpness of mind despite the cathodal stimulation. He received 10 of the F1 (between F3 and FZ) cathodal/right shoulder anodal treatments, six anodal F3/cathodal left shoulder treatments and a few FP1 anodal/left shoulder cathodal treatments. At times, following F3 anodal/left shoulder cathodal stimulation, he experienced immense joy! One month following tDCS, he continued to feel sharp of mind. Although the occasional rumination occurs a few times per week, he easily stops it.


It has been found that the left hemisphere activates (and therefore suppresses alpha electrical activity as seen on an EEG) with happy thoughts and the right hemisphere activates (suppresses alpha) with negative thoughts. Right brain strokes also spawn cheerful survivors while left brain strokes leave the survivor with depression (Rosenfeld, 1997). This supports the “happy-left” and “depressed-right” scenario. Other studies (Davidson, 1992; Coan & Allen, 2004) including my own observations have shown increased left frontal alpha concurrent with a negative outlook. As one could expect, people with unresolved trauma are plagued with negative thoughts, often waiting for something bad to happen to them. Therefore, what one thinks has a direct impact on the degree of depression. But this brings on the chicken and the egg dilemma - does the alpha asymmetry bring on negative thoughts or do negative thoughts bring on alpha asymmetry?

Kang, et al 1991, ran a study where he monitored bilateral EEG at F3 and F4 (left and right dorsal-lateral prefrontal cortexes) in 20 female college students. The participants filled out a State-Trait Anxiety Index, a Derogatis Stress Profile and a Beck Depression Index. He then subtracted the left alpha EEG activity from the right alpha EEG activity. A positive result indicated that the participant had less alpha EEG (and more activation) in the left frontal lobe (a happy person). A negative result indicated that the participant had less alpha (and more activation) in the right frontal lobe (a pessimistic outlook). He also observed that the “happy” people had much improved natural killer-cell activity, associated with better immune function (as shown in Figure 3). This is, in my opinion, an unfortunate design flaw in the human nervous system. When a person has some stress or trauma to the point where the pessimistic right brain becomes dominant, then the person develops a negative physiological outlook, perceiving all of everything that is wrong/threatening within his/her environment, which in turn maintains right brain dominance. It is important therefore to boot-strap the left dorso-lateral prefrontal cortex simultaneously with talk-therapy in order to get the patient in a positive, receptive frame of mind that shows optimism and receptivity to the techniques employed by the therapist. 

Figure 3.




This is a case involving a 44-year-old woman of Chinese descent who had attempted suicide twice in the previous months and once back in 2006. She is diagnosed with bipolar disorder, and during her manic phase, she spends excessive amounts of money on herself and people she wants to impress. She is presently taking Epival (750 mg), Clonazepam (0.5 mg) and Seroquel (25 mg), although she randomly skips aspects of her medication in an attempt to try to prove to herself that she is better.

The client informed me that her father experienced a great deal of hardship as a youth in China. Upon moving to Canada as a young man, he experienced more hardship. He was robbed a few times as a small convenience store owner and mugged once as a cab driver. According to my client, her father has never shown affection at all. Her mother, however, does show a moderate degree of affection. This lady is constantly in a victim/revenge cycle. She is “victimized” by “assbag” drivers who use their cell phones while driving, slow grocery clerks, bank tellers, her father, siblings, friends and so on. She is in a state of anger much of the time and exacts her revenge by saying aggressive and hurtful things to people or putting them down behind their backs, and intentionally cutting off drivers who have “pissed her off.” She has no ownership of her feelings, which stems back to being an emotional “punching bag” for her father.


We ran 10 tDCS sessions at 1 ma of current. The stimulus anode electrode (4.25 cm x 4.25 cm = 18 cm2) was placed over F3. During her first session, the reference cathode electrode (5.1 cm x 10.1 cm = 52 cm2) was placed over F4, but on her left shoulder for the remaining nine treatments. 19-channel QEEGs using the Mitsar EEG system ( were collected at pre-tDCS, 30 minutes following the first tDCS session and the day following her 10th treatment. QEEG data as shown on the SKIL database are shown below.


Shown in Figure 4, her baseline brain activity was 3.4 SD high with a definite alpha asymmetry with increased alpha in left frontal regions at FP1, F3 and F7. The high beta activity throughout is a typical side effect of taking anti-depressant medications. Her frontal alpha is slowed, which is typical of childhood cortisol damage, inhibiting her ability to reason and extinguish fears. This disinhibition is typical of over-reacting, racy-headedness and aggressiveness toward perceived daily stressors and hassles.

Figure 4. Baseline brainwave activity

Thirty minutes following F3 anodal/F4 cathodal tDCS, the 9 Hz component of her slowed brainwave activity normalized, as shown in Figure 5. Immediate and profound increases in sharpness of mind have been my personal experience when I have used frontal tDCS. Her alpha asymmetry was still present, however her alpha was now reduced to 2.7 SD. Beta activity appears higher due to the tighter scaling of the this image. However, there was no change in beta magnitude.

Figure 5. Brainwave activity post first tDCS session

Following ten tDCS sessions (Figure 6), there were significant reductions in alpha asymmetry. Alpha activity continued to be 2.5 SD high. However this represents a significant improvement from the 3.3 SD high alpha activity at baseline.

Figure 6. Brainwave activity post tenth tDCS session


Surprisingly, following ten tDCS sessions, her comodulation measures were very close to normal as well as her phase measures, so they are not shown in this article. She showed some mild coherence abnormalities, but nothing clinical. However this could be the effects of the drugs she was taking. Her coherence, nonetheless improved, as shown in Figure 7 below.

Figure 7. Pre-post coherence measures


Transcranial DC Stimulation is site specific and therefore can be used to up-modulate or down-modulate any region of the brain. Transcranial DC stimulation is also easy to use and doesn’t require the constant attention of the therapist, thus allowing the therapist to engage in talk therapy and/or collect client information during the treatment. TDCS produces immediate and lasting sharpness and reasoning of mind. Unfortunately, very few tDCS studies consider the effects beyond a few hours. However, one depression study supports that there is a holding effect 30 days later, which personal experience confirms. Between the existing research and my personal experiences, I suspect that with appropriate training, tDCS will become a common clinical approach to neurotherapy.


Boggio, P., Rigonatti, S., Ribeiro, R., Myczkowski, M., Nitsche, M., Pascual-Leone, A., Fregni, F. (2007). A randomized, double-blind clinical trial on the efficacy of cortical direct current stimulation

in the treatment of major depression. International Journal of Neuropsychopharmacology, 10, 1–8.

Boggio, P., Bermpohl, F., Vergara, A., Muniz, A., Nahas, F., Leme, P., Rigonatti, S., Fregni, F. (2007). Go-no-go task performance improvement after anodal transcranial DC stimulation of the left dorsolateral prefrontal cortex in major depression. Journal of Affective Disorders, 101, 91-98.

Coan, J., Allen, J. (2004). Frontal EEG as a moderator and mediator of emotion. Biological Psychology, 67, 7-49.

Davidson, R. (1992). Anterior cerebral asymmetry and the value of emotion. Brain and Cognition, 20, 125-151.

Kang, D., Davidson, R., Coe, C., Wheeler, R., Tomarken, A., Ershler, W. (1991). Frontal brain asymmetry and immune function. Behavioral Neuroscience, 105, 6, 860-869.

Nitsche, M., Doemkes, T., Antal, A.: Liebatanz, N., Lang, N., Tergau, F., Paulus, W. (2007). Shaping the effects of transcranial direct current stimulation of the human motor cortex. Journal of Neurophysiology, 97, 3109-3117.

Pascual-Leone, A., Wagner, T. (2007). A Brief Summary of the History of Noninvasive Brain Stimulation. Annual Review of  Biomedical Engineereing, 9, 527-565.

Rosenfeld, P. (1997). EEG biofeedback of frontal alpha asymmetry in affective disorders. Biofeedback, Spring, p.8-12.

Iyer, M., U. Mattu, U., Grafman, J., Lomarev, M., Sato, S., Wassermann, E. (2005). Safety and cognitive effect of frontal DC brain polarization in healthy individuals. Neurology, 64, 872-875.

Listings of tDCS research and references to tDCS studies may be found at:

Full pdf files of 46 studies may be found at:

Abstracts of 63 studies may be found at:

About the Author: Dave Siever graduated in 1978 as an engineering technologist.  He later worked in the Faculty of Dentistry at the University of Alberta designing TMJ Dysfunction related diagnostic equipment and research facilities where he organized research projects, taught basic physiology and the advanced TMJ diagnostics course. Dave had noted anxiety issues in many patients suffering with TMJ dysfunction, prompting him to study biofeedback, which he applied to their patients and later design biofeedback devices.

In 1984, Dave designed his first audio-visual entrainment (AVE) device – the “Digital Audio-Visual Integration Device,” or DAVID1. Since this time, through his company, Mind Alive Inc., Dave has been researching and refining AVE technology, specifically for use in relaxation and treating anxiety, depression, PMS, ADD, FMS, SAD, pain, cognitive decline and insomnia.  He presents regularly at conferences and for special interest groups. Dave also designs Cranio-Electro Stimulation (CES) and biofeedback devices and continues to conduct research and design new products relating to personal growth and development.




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