Author
Ulf Ziemann
Other affiliations: University of Bern, University of Göttingen, National Institutes of Health ...read more
Bio: Ulf Ziemann is an academic researcher from University of Tübingen. The author has contributed to research in topics: Transcranial magnetic stimulation & Motor cortex. The author has an hindex of 100, co-authored 512 publications receiving 38383 citations. Previous affiliations of Ulf Ziemann include University of Bern & University of Göttingen.
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The Catholic University of America1, Royal Prince Alfred Hospital2, University of Toronto3, Centre for Addiction and Mental Health4, Università Campus Bio-Medico5, University of Eastern Finland6, Monash University7, Medical University of South Carolina8, Paris 12 Val de Marne University9, University of Regensburg10, University of Brescia11, University of Göttingen12, Beth Israel Deaconess Medical Center13, University of Siena14, University College London15, Copenhagen University Hospital16, Fukushima Medical University17, University of Tübingen18
TL;DR: These guidelines provide an up-date of previous IFCN report on “Non-invasive electrical and magnetic stimulation of the brain, spinal cord and roots: basic principles and procedures for routine clinical application” and include some recent extensions and developments.
1,850 citations
Paris 12 Val de Marne University1, French Institute of Health and Medical Research2, University of Göttingen3, Ghent University4, University Hospital of Lausanne5, University of Lisbon6, university of lille7, Università Campus Bio-Medico8, University of Belgrade9, University of Hamburg10, Turku University Hospital11, Aristotle University of Thessaloniki12, University of Regensburg13, University of Bern14, Ludwig Maximilian University of Munich15, University of Siena16, The Catholic University of America17, University College London18, University of Ulm19, Copenhagen University Hospital20, University of Oxford21, University of Barcelona22, University of Tübingen23
TL;DR: There is a sufficient body of evidence to accept with level A (definite efficacy) the analgesic effect of high-frequency rTMS of the primary motor cortex (M1) contralateral to the pain and the antidepressant effect of HF-rT MS of the left dorsolateral prefrontal cortex (DLPFC).
1,554 citations
TL;DR: It is concluded that the changes in intracortical excitability are caused by GABA‐controlled interneuronal circuits in the motor cortex while changes in motor threshold are dependent on ion channel conductivity and may reflect membrane excitability.
Abstract: The effect of a single oral dose of various antiepileptic drugs on the excitability of the motor system was studied in healthy volunteers by means of transcranial magnetic stimulation. Motor threshold, duration of the cortical silent period, and intracortical excitability after double-shock transcranial stimulation were tested before and at defined intervals after drug intake. Antiepileptic drugs that support the action of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the neocortex (vigabatrin, baclofen) reduced intracortical excitability but had no effect on motor threshold. Gabapentin, whose mechanism of action has not yet been unequivocally identified, showed a similar profile. By contrast, sodium and calcium channel blockers without considerable neurotransmitter properties (carbamazepine, lamotrigine, losigamone) elevated motor threshold but did not change intracortical excitability. The cortical silent period was lengthened by gabapentin and carbamazepine. Changes in peripheral motor excitability (maximum M wave, peripheral silent period) were not observed. We conclude that the changes in intracortical excitability are caused by GABA-controlled interneuronal circuits in the motor cortex while changes in motor threshold are dependent on ion channel conductivity and may reflect membrane excitability. Transcranial magnetic stimulation may be a promising noninvasive approach to study the selective effects of antiepileptic drugs on brain function.
1,085 citations
TL;DR: It is suggested that subthreshold transcranial magnetic stimulation is capable of activating separate populations of excitatory and inhibitory interneurones in the motor cortex.
Abstract: 1. In seven normal subjects, subthreshold transcranial magnetic conditioning stimuli (using a figure-of-eight coil) were applied over the motor cortex in order to evoke activity in intracortical neuronal circuits. The net effect on cortical excitability was evaluated by measuring the effect on the size of EMG responses elicited in the abductor digiti minimi (ADM) muscle by a subsequent suprathreshold test stimulus. 2. A single conditioning stimulus suppressed the size of the test response at interstimulus intervals (ISIs) of 1-4 ms whereas the response was facilitated at ISIs of 6-20 ms. The facilitation could be augmented if pairs of conditioning stimuli were given. 3. Inhibition and facilitation appeared to have separate mechanisms. The threshold for inhibition (0.7 active motor threshold) was slightly lower than that for facilitation (0.8 active threshold). Similarly, the inhibitory effect was independent of the direction of current flow induced in the cortex by the conditioning shock, whereas facilitation was maximal with posterior-anterior currents and minimal with lateromedial current. 4. Direct corticospinal effects were probably not responsible for the results since facilitation of cortical test responses could be produced by conditioning stimuli which had no effect on the amplitude of H reflexes elicited in active ADM muscle. 5. Inhibition and facilitation appeared to interact in a roughly linear manner, consistent with separate inputs to a common neurone. 6. We suggest that subthreshold transcranial magnetic stimulation is capable of activating separate populations of excitatory and inhibitory interneurones in the motor cortex.
1,066 citations
Paris 12 Val de Marne University1, University of Göttingen2, University Hospital of Lausanne3, French Institute of Health and Medical Research4, University of Milan5, University of Otago6, University of Regensburg7, University of Marburg8, Ruhr University Bochum9, Ludwig Maximilian University of Munich10, University of Siena11, University of Texas at Dallas12, University of Tübingen13
TL;DR: It remains to be clarified whether the probable or possible therapeutic effects of tDCS are clinically meaningful and how to optimally perform tDCS in a therapeutic setting.
1,062 citations
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9,362 citations
01 Jan 2016
TL;DR: The modern applied statistics with s is universally compatible with any devices to read, and is available in the digital library an online access to it is set as public so you can download it instantly.
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5,249 citations
TL;DR: Transcranial electrical stimulation using weak current may be a promising tool to modulate cerebral excitability in a non‐invasive, painless, reversible, selective and focal way.
Abstract: The approach taken in this study to produce localised changes of cerebral excitability in the intact human was modulation of neuronal excitability by weak electric currents applied transcranially. So far, this technique has mainly been used in animal research, primarily through modulation of the resting membrane potential (Terzuolo & Bullock, 1956; Creutzfeld et al. 1962; Eccles et al. 1962; Bindman et al. 1964; Purpura & McMurtry, 1965; Artola et al. 1990; Malenka & Nicoll, 1999). In general, cerebral excitability was diminished by cathodal stimulation, which hyperpolarises neurones. Anodal stimulation caused neuronal depolarisation, leading to an increase in excitability (Bindman et al. 1962; Purpura & McMurtry, 1965), as was shown by spontaneous neuronal discharges and the amplitudes of evoked potentials (Landau et al. 1964; Purpura & McMurtry, 1965; Gorman, 1966). However, in single cortical layers opposite effects were seen (Purpura & McMurtry, 1965), underlining the fact that the effects of DC stimulation depend on the interaction of electric flow direction and neuronal geometry. Enduring effects of 5 h and longer have been described if the stimulation itself lasts sufficiently long, about 10–30 min. These prolonged effects are not simply due to prolonged membrane potential shifts or recurrent excitation, because intermittent complete cancellation of electrical brain activity by hypothermia does not abolish them (Gartside, 1968a,b). Long-term potentiation (LTP) and long-term depression (LTD) have been proposed as the likely candidates for this phenomenon (Hattori et al. 1990; Moriwaki, 1991; Islam et al. 1995; Malenka & Nicoll, 1999).
The concept described here was an attempt to induce neuronal excitability changes in man by application of weak DC stimulation through the intact skull. It has already been demonstrated within invasive presurgical epilepsy diagnostics that intracranial currents of sufficient strength can be achieved in humans by stimulation with surface electrodes at intensities of up to 1.5 mA (Dymond et al. 1975). A suitable candidate for evaluating cortical excitability changes is transcranial magnetic stimulation (TMS), because it allows the quantification of motor-cortical neurone responses in a painless and non-invasive manner. The amplitude of the resulting motor-evoked potential (MEP) represents the excitability of the motor system. In the following, we confirm the principal possibility of altering cortical excitability by applying weak DC. Furthermore we show that systematic DC stimulation with minimum stimulation duration and intensity is necessary for an effective application of weak current in humans. This is of particular importance for inducing effects which outlast the duration of stimulation.
4,672 citations
TL;DR: The present updated guidelines review issues of risk and safety of conventional TMS protocols, address the undesired effects and risks of emerging TMS interventions, the applications of TMS in patients with implanted electrodes in the central nervous system, and safety aspects of T MS in neuroimaging environments.
4,447 citations
Leipzig University1, University of Belgrade2, Leiden University3, Uppsala University4, University of Modena and Reggio Emilia5, University of Barcelona6, Carol Davila University of Medicine and Pharmacy7, National and Kapodistrian University of Athens8, François Rabelais University9, University of Melbourne10, Royal Melbourne Hospital11, University of Lisbon12, University of Birmingham13, University of Groningen14, University Medical Center Groningen15, University of Central Lancashire16
TL;DR: The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only and no commercial use is authorized.
Abstract: Supplementary Table 9, column 'Edoxaban', row 'eGFR category', '95 mL/min' (page 15). The cell should be coloured green instead of yellow. It should also read "60 mg"instead of "60 mg (use with caution in 'supranormal' renal function)."In the above-indicated cell, a footnote has also been added to state: "Edoxaban should be used in patients with high creatinine clearance only after a careful evaluation of the individual thromboembolic and bleeding risk."Supplementary Table 9, column 'Edoxaban', row 'Dose reduction in selected patients' (page 16). The cell should read "Edoxaban 60 mg reduced to 30 mg once daily if any of the following: creatinine clearance 15-50 mL/min, body weight <60 kg, concomitant use of dronedarone, erythromycin, ciclosporine or ketokonazole"instead of "Edoxaban 60 mg reduced to 30 mg once daily, and edoxaban 30 mg reduced to 15mg once daily, if any of the following: creatinine clearance of 30-50 mL/min, body weight <60 kg, concomitant us of verapamil or quinidine or dronedarone."
4,285 citations