tDCS

Transcranial direct current stimulation

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Electrify your mind - literally
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Transcranial direct current stimulation has been determined safe for human use due to the low current used and can result in cortical modulations that last longer than the time of stimulation. Currently, tDCS is used as therapy for certain psychological disorders such as anxiety disorders and depression, as well as a tool for motor rehabilitation instroke patients.

Good + bad - info safety

info

Anodal + Cathodal The anodal stimulation is positive stimulation that increases the neuronal excitability of the area being stimulated. Cathodal stimulation decreases the neuronal excitability of the area being stimulated. An example of how cathodal stimulation could be used is as a therapy for a psychological disorder caused by the hyper-activity of a particular area of the brain. Cathodal stimulation would decrease the neuronal excitability to reach a more stable level of activity. When positive stimulation is delivered, the current causes a depolarization of the resting membrane potential, which increases neuronal excitability and allows for more spontaneous cell firing. When negative stimulation is delivered, the current causes a hyperpolarization of the resting membrane potential. This decreases neuron excitability due to the decreased spontaneous cell firing.

Safety
When applied following established safety protocols, transcranial direct current stimulation is widely regarded as a safe method of brain stimulation, causing no apparent short-term harm. Safety protocols limit the current, duration, and frequency of stimulation, thereby limiting the effects and risk

Safety protocol
Studies have been completed to determine the current density at which overt brain damage occurs in rats. It was found that in cathodal stimulation, a current density of 142.9 A/m2 delivering a charge density of 52400 C/m2 or higher caused a brain lesion in the rat. This is over two orders of magnitude from what is currently being used. (14,2mA cm2 ) There is currently no evidence of serious side-effects after tDCS in humans. Common side effects include mild headache and itching sensation at the electrode site. Skin lesions (burns) have been reported after tDCS and considerable care is needed in examining and preparing the skin-electrode interface. There are no reports of tDCS inducing seizure. In the literature it is strongly recommended not to exceed the threshold of 0.05 mA/cm2 that could cause a painful sensation and tissue damages. In this way, the stimulation is far from this threshold for tissue damage (14.3 mA/cm2) recently indicated for tDCS in an animal model. It is mandatory to read and understand the scientific literature relative to transcranial and trans-spinal DC stimulation before prescribing any treatment. In the next figure, intensity values (in mA) and electrode area values (cm2) for a current density of 0.02 mA/cm2 (dark orange) and of 0.05 mA/cm2 (light orange) are drawn. It is recommended to use intensity/area pairs positioned in the area between the two lines. Below the light orange line there is a danger zone.

There is no strict limitation on the duration of stimulation set at this point but a stimulation time of 20 minutes is considered the ideal time. The longer the stimulation duration, the longer the observed effects of the stimulation persist once the stimulation has ended. A stimulation length of 10 minutes results in observed effects lasting for up to an hour. It is generally encouraged to wait at least 48 hours to a week before repeating the stimulation. Also, it is advised to warn the person receiving the stimulation of the possible after effects of the tDCS stimulation. update: The current density produced by present tDCS protocols ranges between 0.029 and 0.08 mA/cm2

Side effects of stimulation

There are a few minor side effects that can be felt by the person while receiving the stimulation, and most of these can be controlled by correct set up of the device. These side effects include skin irritation, a phosphene at the start of stimulation, nausea,headache, dizziness, and itching under the electrode. Nausea most commonly occurs when the electrodes are placed above the mastoid, which are used for stimulation of the vestibular system (GVS). A phosphene is a brief flash of light and this effect can occur if an electrode is placed near to the eye.[2] A recent study of over 500 subjects using the currently accepted protocol reported only a slight skin irritation (increase of blodd flow)and a phosphene as side effects.[6] There are several ways to reduce the skin irritation felt during stimulation. One of the most important methods of preventing skin irritation is by preparing the electrodes with saline solution and the skin with electrode cream thoroughly. Also, ramping up the current can reduce the irritation. This is done by slowly increasing the current until the desired current is reached.

*Adverse effects
A structural and diffusion-weighted magnetic resonance imaging study [28] compared the prefrontal cortex before and after anodal and cathodal tDCS, and found no structural alterations or disturbances of the blood-brain barrier, and no reduction in apparent diffusion coefficient values (a

marker of cytotoxic oedema). Other studies have reported no significant changes in levels of neuron-specific enolase (a sensitive marker of neuronal damage) immediately or 1 hour after tDCS

Risks
There are no known risks of tDCS at this time, but since this technique of stimulation is still being explored, safety precautions should be kept. The set protocols must be followed in ensure correct use of the device.Also, it is not advised to administer this stimulation to people susceptible to seizures, such as people with epilepsy. Although seizures do not seem to be a risk for healthy individuals, those with a tendency towards seizures may[ react differently. As more is discovered about the use of tDCS, the safety standards may change, making it important to remain familiar with the most currently updated safety protocol. * epilepsy tdcs study MECHANISMS OF ACTION A leading view is that changes in spontaneous neuronal firing rates, coupled with synaptic neuroplasticity, contribute to intra- and post-stimulation effects respectively. Spontaneous neuronal firing: tDCS directly induces neuronal firing,there is empirical evidence from animal studies that even small voltage gradients of this magnitude can change the firing rate of neurons. Several studies demonstrated that anodal direct currents increase, while cathodal direct currents decrease, spontaneous neuronal firing in vivo in animal studies. Moreover, the changes were shown to be long-lasting: 5 to 10 min of continuous stimulation produced effects up to 5 hours afterwards. Non-synaptic mechanisms: There is evidence that anodal stimulation shifts neuronal resting membrane potential towards depolarisation, while cathodal stimulation shifts resting membrane potential towards hyperpolarisation. Intracellular recordings from animal studies have shown that anodal stimulation (30400 A/mm2, 540 s) causes neuronal depolarisation, while cathodal stimulation causes hyperpolarisation. Human motor cortex studies provide further evidence of these non-synaptic mechanisms. The effect of tDCS on motor cortex excitability can be measured by motor evoked potentials (MEP) recorded from peripheral muscles. Anodal tDCS to the motor cortex (0.25 mA, 4 s5 min) increases MEP size, while cathodal tDCS reduces MEP size. Similarly, tDCS to the visual cortex produces changes in visual evoked potentials, contrast sensitivity and motion detection threshold, also in a direction that is dependent on the polarity of stimulation. Synaptic mechanisms: tDCS induces changes by altering the strength of synaptic transmission. Anodal tDCS could induce long-term potentiation (LTP) through increased pre-synaptic activity coupled with postsynaptic depolarisation; conversely, cathodal tDCS could induce long-term depression (LTD) through reduced presynaptic discharge and postsynaptic hyperpolarisation. The evidence for a neuroplastic synaptic contribution to the effects of tDCS is thus compelling. These include correlations between neuronal activity patterns known to underlie LTP/LTD, and those patterns observed after tDCS, protein synthesis during stimulation, and especially the emerging role of NMDA receptors in regulating the aftereffects of stimulation.

*The effects of cortical inhibition suggest that TDCS modulates the excitability of both the inhibitory interneurons and excitatory neurons. * calcium and sodium channel blockers have eliminated the short- and long-term effects of anodic stimulation, whereas glutamate channels blockers have eliminated only the long-term effects. *post-TDCS effects could be explained by the modulation of the activity of N-methyl-D-aspartic acid (NMDA) receptors. *Imaging modalities, including positron emission tomography , functional magnetic resonance imaging [21] and magnetic resonance spectroscopy [22,23] have suggested changes in regional blood flow, glutamatergic neurotransmission and membrane function after tDCS, including in brain regions distal to the site of stimulation. *In isolated preparations, nondestructive DC currents can change the firing rate of spontaneouslyactive neurons by up to 72%.1 The effect has a preference for fields oriented along the axo-dendritic axis. In mammals, polarizing currents applied to the brain surface can change cortical evoked potentials and the activity of individual neurons.2-4

*D2 receptors play a major supporting role in inducing neuroplasticity in the human motor cortex.
Enhancement of D2 and, to a lesser degree, D1 receptors by pergolide consolidated tDCS-generated excitability diminution until the morning after stimulation. The readiest explanation for this pattern of results is that D2 receptor activation has a consolidation-enhancing effect on tDCS-induced changes of excitability in the human cortex.

*importance of D2 receptor activity for the induction of

increases and decreases in prolonged NMDA receptor-dependent motor cortical excitability shifts

*Non-synaptic

mechanisms underlie the after-effects of cathodal transcutaneous direct current stimulation of the human brain -Ourfindings demonstrate that the after-effects of tDCS have a non-synaptic mechanism of
action based upon changes in neural membrane function. These changes apart from reflecting local changes in ionic concentrations, could arise from alterations in transmembrane proteins and from electrolysis-related changes in [H+] induced by exposure to constant electric field. -effect on peripheral nervous system

Uses
Clinical
Clinical therapy using tDCS may be the most promising application of this technique. There have been therapeutic effects shown in clinical trials involving Parkinsons disease, [8] tinnitus, fibromyalgia, and post-stroke motor deficits.[9] In a recent study, stroke patients with speech difficulties displayed great improvement through a tDCS based therapy, with the improvement lasting past the one week retest.[10] Stimulation therapy could also be developed into effective therapy for various psychological disorders such as depression, anxiety disorders, and schizophrenia.

Psychological
The majority of psychological studies involving tDCS focus on the expansion of knowledge about a certain region of the brain or a certain psychological phenomenon. For example, much work is done on the ability and specifics of working memory.[11] Many of these studies stimulate a particular region of the brain and then observe the effects of the stimulation in some type of cognitive task.

Transcranial direct current stimulation as treatment

. Using these newer techniques, two double-blinded, sham-controlled studies using left prefrontal tDCS (1 and 2 mA, 20 minutes per day for up to 10 days) reported positive results in reducing depressive symptoms [6,7]. One trial reported 69% improvement in mean Hamilton Depression Rating Scale (HDRS) scores after five sessions of active tDCS over 1.5 weeks, compared with 30% improvement in the sham group [6]. Another trial also reported positive findings, with improvement in the active group on HDRS of 40.5%, compared to 10.4% in the sham group, after 10 consecutive weekdays of treatment [7]. Moreover, these differences in outcome between active and sham groups persisted at 1-month follow-up, and an open-label extension of the trial indicated that tDCS had similar efficacy, but more rapid onset, compared to a 6-week course of 20 mg/day fluoxetine, a

selective serotonin re-uptake inhibitor antidepressant [8]. A more recent, non-placebo controlled clinical trial involving hospitalised patients with drug-resistant depression at high risk of suicide, referred for electroconvulsive therapy, reported >30% improvement in depression rating scores [HDRS and BDI (Beck Depression Inventory)] after anodal stimulation to the left dorsolateral prefrontal cortex (2 mA, twice-daily, for 5 days) [9]. As this was an uncontrolled study, it is uncertain if administering tDCS twice per day was more efficacious than once-daily treatment. On the other hand, modern tDCS techniques have failed to replicate the dramatic findings of older clinical trials on mood in healthy subjects. In a double-blind crossover trial, 21 subjects received bilateral frontal tDCS with an extracephalic reference electrode [10]. No significant effects on emotional state, affect, emotional decision-making, arousal and psychomotor function were found. *current direction A recent sham-controlled trial with anodal stimulation to the primary motor cortex (2 mA, 20 minutes, five sessions) has also demonstrated the efficacy of tDCS for the treatment of chronic pain due to spinal cord injury [11]. Interestingly, the analgesic effect appeared to be cumulative, with greatest overall pain reduction after five sessions of treatment. Similar to the depression trial, differences in pain scores between the active and sham group were still present at 2-week follow-up. The same parameters have also been reported to alleviate pain in fibromyalgia [12]. There is also some evidence that tDCS may be effective in improving functional recovery after stroke. A randomised, double-blinded, sham-controlled trial found that cathodal tDCS (2 mA, 10 minutes) to the left frontotemporal region significantly improved performance on a picture-naming task in poststroke patients with chronic aphasia immediately after stimulation [13].
An animal study in rats demonstrated that cathodal tDCS (100-200 A, 15-60 minutes) increased the threshold for localised seizure activity, suggesting a potential therapeutic role in epilepsy [14]. The clinical evidence for tDCS treatment of epilepsy in humans, however, remains limited (see [15] for a review).

TECHNICAL ASPECTS OF tDCS: 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 a/cm2 (260 a/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 *update 15-25-35cm2 (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.

*current direction to nerons orientations Nitsche and Paulus found that a minimum current density of 17 a/cm2 was needed to excite motor neurons. Studies involving other regions of the brain have suggested that 20 to 25 a/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 a/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 a/cm2 vs 41 a/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 by 1 (4.5 x 4.5 cm) tap-water wet sponge anode at F3 and a 2x 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 2x 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 x 1 and 2x 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. tDCS DEVICES . The CESta has been tuned with the electrodes provided so that at 1 ma stimulation, the active electrode delivers 50 a/cm2, while the reference electrode produces 18 a/
*Skin preparation abrasive gel reduction of resistance and homogenization

*As the increase in the density of the electric current provokes an increase in the cutaneous feeling of pain and affects different neuronal populations (due to a higher penetration of the effective electric field), it is recommended, in general, the increase in the

duration of stimulation and not in the current density to prolong the effects of TDCS

(HD-tDCS)
A new technology, High-Definition tDCS (HD-tDCS), is currently being developed for the restoration of CNS and PNS function. The advantage of HD-tDCS over conventional big pad tDCS involves using an array of <12 mm diameter stimulation electrodes, that will facilitate focal, safe and customized neuromodulation of the brain function.

*recent data demonstrate that tDCS can modulate the function of the spinal cord and of the cerebellum