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The aim of this study was to characterize the temporal course of phosphene thresholds (PT) using transcranial magnetic stimulation (TMS) in control subjects and in subjects with migraine and to observe whether changes in PT over time can predict a subsequent migraine attack. PTs were measured in 16 migraineurs [nine with aura (MA) and seven without aura (MoA)] and nine controls five times over an approximately 10-week period. Mean PTs were not significantly different between migraineurs and controls; however, there was a trend in MA showing lower thresholds. The minimum threshold values were also smaller in MA subjects than in MoA or control subjects. Generally, PTs had higher variance in migraineurs than in controls, revealing a significant increase in standard deviation of PTs in MA subjects. There was no significant difference of thresholds from the first to the last stimulation in controls and in MoA subjects, but the 3rd, 4th and 5th measurements of MA subjects were significantly lower than their first measurements. Four migraineurs experienced headache within 1 day after one of the measurements. They had either very low or very high PTs compared with the PT values which were not followed by a migraine attack. Our results imply that migraineurs show a higher variability among PT measurements over time than controls, revealing unstable excitability levels in these patients. Additionally, both particularly high and low PTs might predict a subsequent headache in some individuals.

Much research on visual functions in migraine has pinpointed the existence of abnormal visual processing between attacks. However, it is not clear if this is due to cortical hyper- or hypoexcitability. We aimed to clarify this issue by comparing motion perception thresholds of subjects with migraine with (MA) or without aura (MoA) and control subjects. Two types of dot kinetograms were used: in the first experiment coherently moving dots were presented in an incoherent environment, while in the second only coherent motion was seen. Subjects with migraine displayed significantly impaired motion perception compared with controls when they had to detect the direction of the coherently moving dots in an incoherent environment, while they were slightly better in a direction discrimination task, where only coherent motion was presented. This pattern of results is comparable to those achieved by an external excitability enhancement of V5 induced in healthy human subjects in a former study of our group. According to this, a cortical excitability enhancement can result in an impaired focusing on a given signal against a noisy background, but improves perception of non-ambiguous stimuli. Thus we conclude that migraineurs display enhanced visual cortical excitability between attacks in V5.

Objective: To determine whether weak transcranial direct current stimulation (tDCS), which is an interesting new tool inducing prolonged cortical excitability shifts in humans, induces brain edema, disturbance of the blood-brain barrier or structural alterations of the brain detectable by magnetic resonance imaging (MRI)., Methods: In 10 healthy individuals, tDCS, which is known to alter cortical excitability for about 1 h, was applied over motor and pre-frontal cortices. contrast-enhanced t1-, t2-, and diffusion-weighted mri was performed immediately before, 30 and 60 min after tdcs., Results: MRI performed 30 and 60 min after tDCS did not show pathological signal alterations in pre- and post-contrast-enhanced T1-weighted and diffusion-weighted MR sequences., Conclusions: tDCS protocols which are known to result in cortical excitability changes persisting for an hour after stimulation do not induce brain edema or alterations of the blood-brain barrier or cerebral tissue detectable by MRI., Significance: These results deliver further evidence for the safety of the currently applied tDCS protocols in humans.

Weak transcranial direct current stimulation (tDCS) can induce long lasting changes in cortical excitability. In the present study we asked whether tDCS applied to the left primary motor cortex (M1) also produces aftereffects distant from the site of the stimulating electrodes. We therefore tested corticospinal excitability in the left and the right M1 and transcallosal excitability between the two cortices using transcranial magnetic stimulation (TMS) before and after applying tDCS. Eight healthy subjects received 10 min of anodal or cathodal tDCS (1 mA) to the left M1. We examined the amplitude of contralateral motor evoked potentials (MEPs) and the onset latency and duration of transcallosal inhibition with single pulse TMS. MEPs evoked from the tDCS stimulated (left) M1 were increased by 32% after anodal and decreased by 27% after cathodal tDCS, while transcallosal inhibition evoked from the left M1 remained unchanged. The effect on MEPs evoked from the left M1 lasted longer for cathodal than for anodal tDCS. MEPs evoked from the right M1 were unchanged whilst the duration of transcallosal inhibition evoked from the right M1 was shortened after cathodal tDCS and prolonged after anodal tDCS. The duration of transcallosal inhibition returned to control values before the effect on the MEPs from the left M1 had recovered. These findings are compatible with the idea that tDCS-induced aftereffects in the cortical motor system are limited to the stimulated hemisphere, and that tDCS not only affects corticospinal circuits involved in producing MEPs but also inhibitory interneurons mediating transcallosal inhibition from the contralateral hemisphere.

Modulation of cerebral excitability is thought to be one mechanism underlying the pharmacological treatment of neuropsychiatric diseases such as epilepsy, depression, and dystonia. Repetitive transcranial magnetic stimulation (rTMS) has been tested for several years as a nonpharmacological, noninvasive method of directly influencing patients' cortical functions. We present an overview of the more easily performed transcranial direct current stimulation (tDCS) with weak current, which produces distinctly more pronounced changes in excitability than rTMS. The basic underlying mechanism is a shift in the resting membrane potential towards either hyper- or depolarisation, depending on stimulation polarity. This in turn leads to changes in the excitability of cortical neurons. Anodic stimulation increases cortical excitability, while cathodic stimulation decreases it. These changes persist after the end of stimulation if the stimulation lasts long enough, i.e., at least several minutes. The duration of this aftereffect can be controlled through the duration and intensity of the stimulation. Transcranial direct current stimulation essentially allows a focal, selective, reversible, pain-free, and noninvasive induction of changes in cortical excitability, the therapeutic potential of which must be evaluated in clinical studies, once possible risk factors have been assessed.

Static and dynamic contrast sensitivities (sCS and dCS) were evaluated before, during, immediately after and 10 min after anodal and cathodal transcranial direct current stimulation (tDCS) applied to the occipital cortex of 15 healthy subjects. Using 4 c/d spatial and 4 Hz temporal frequencies significant sCS and dCS loss was found during and immediately after 7 min cathodal stimulation while anodal stimulation had no effect. Ten minutes after the end of the stimulation the sCS and dCS values had reached the baseline levels. Our results show that primary visual functions, such as contrast detection can be transiently altered by transcranial weak direct current stimulation, most probably modulating neural excitability, as has been shown in the motor cortex previously. The present study also support the view that this method using weak current can be a non-invasive promising tool to induce reversible focal changes in the nervous system.

Blood oxygenation level dependent (BOLD) MRI was used to monitor modulations of human sensorimotor activity by prior transcranial direct current stimulation (tDCS). Activation maps for a right hand sequential finger opposition task were obtained for six subjects before as well as 0-5 min and 15-20 min after a 5-min period of 1 mA cathodal and, in a separate session, anodal tDCS of the left-hemispheric motor cortex. Cathodal tDCS resulted in a global decrease of the mean number of activated pixels by 38% (P < 0.01) 0-5 min after stimulation, which reduced to 28% (P < 0.05) 15-20 min after stimulation. A region-of-interest analysis revealed a 57% decrease of activated pixels (P < 0.001) in the supplementary motor area, but no change in the hand area of the primary motor cortex. Anodal tDCS yielded a nonsignificant 5% increase of activated pixels with no regional differences. These findings support the view that reduced neuroaxonal excitability after cathodal tDCS causes reduced brain activity. However, rather than affecting the primary sensorimotor input of an active task, the process appears to dampen those responses that rely on cortico-cortical connections and related processing. Magn Reson Med 45:196-201, 2001., (Copyright 2001 Wiley-Liss, Inc.)