MRI study of human brain exposed to weak direct current stimulation of the frontal cortex
Introduction
Transcranial direct current stimulation (tDCS) has recently been shown to be capable of inducing excitability changes in the human motor cortex lasting for up to 1 h after the end of stimulation. Anodal tDCS enhances excitability, whereas cathodal stimulation reduces it. Furthermore, the duration of the after-effects depends on stimulation duration (Nitsche and Paulus, 2001, Nitsche et al., 2003a). The proposed primary underlying mechanism is a shift of resting membrane potential, and a consecutive change of spontaneous discharge rate, as shown in animals (Bindman et al., 1964, Purpura and McMurtry, 1965). The long-lasting excitability shifts are caused by changes of NMDA-receptor efficacy (Liebetanz et al., 2002, Nitsche et al., 2003b). Thus, tDCS is a promising new tool for inducing neuroplasticity in the human brain non-invasively and painlessly. It has already been shown to modulate use-dependent changes of motor cortical excitability (Rosenkranz et al., 2000) as well as to improve implicit motor learning (Nitsche et al., 2003c). Its efficacy is not restricted to the motor cortex. So far it has been shown to alter excitability or resulting behavioural performance also in visual (Antal et al., 2003), somatosensory (Uy and Ridding, 2003) and frontopolar cortices (Kincses et al., 2003). Moreover, with regard to neurologic diseases accompanied by pathologically enhanced or reduced cortical excitability, e.g. epilepsy, migraine, and Parkinson's disease, it offers possibly a new and interesting therapeutic option.
Knowledge regarding safety measures for this kind of stimulation is limited so far. Consequently the question of the safety of tDCS has been raised recently (Priori, 2003). In view of measured serum neurone-specific enolase as well as temperature under the stimulation electrodes, there is currently no reason to suspect that the applied protocols could be harmful (for an extensive discussion of this topic see Nitsche et al., 2003d). However, additional studies are warranted to clarify this issue further.
The aim of this study has thus been to test if currently applied tDCS protocols, which induce cortical excitability alterations lasting for about one hour after the end of stimulation, cause brain edema, disturbance of the blood–brain barrier or structural alterations of cerebral tissue. Therefore, comparably to a former protocol, in which the effects of repetitive transcranial magnetic stimulation on these parameters were studied (Niehaus et al., 2000), contrast-enhanced T1, T2- and diffusion-weighted magnetic resonance imaging (DWI) was chosen.
Section snippets
Methods
Ten healthy subjects (6 men, 26–33 years of age) were studied with the written informed consent of the subjects and approval of the ethics committee. In 6 of the subjects involved, former studies revealed the efficacy of tDCS in inducing prolonged motor cortical excitability changes directly. Studies were performed by neurologists familiar with emergency situations in a room with life-support equipment available.
Results
We found no signal changes in T1-weighted images after 9 and 13 min anodal and cathodal tDCS. Further, tDCS did not lead to any enhancement of brain tissue after application of contrast media.
In DWI, no regional hyperintensity suggestive of decreases in water mobility was found. Quantitative maps of ADCs were identical in both hemispheres. No areas of significantly reduced or increased ADCs were detected (Fig. 2). ADC values were not significantly modified by tDCS, and the ratio of the
Discussion
The present neuroimaging studies indicate that the anodal and cathodal tDCS protocols applied to the human brain did not induce structural changes of brain tissue or cause an alteration of the blood–brain barrier. Since it could not be ruled out using conventional MRI that tDCS leads to changes in tissue diffusion we applied DWI and calculated ADC maps. DWI is sensitive to restrictions in the water diffusivity, which has been shown to be associated with failure of energy-dependent ion
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