Depression of motor cortex excitability by low-frequency transcranial magnetic stimulation.
TL;DR: Spread of excitation, which may be a warning sign for seizures, occurred in one subject and was not accompanied by increased MEP amplitude, suggesting that spread ofexcitation and amplitude changes are different phenomena and also indicating the need for adequate monitoring even with stimulations at low frequencies.
Abstract: We studied the effects of low-frequency transcranial magnetic stimulation (TMS) on motor cortex excitability in humans. TMS at 0.1 Hz for 1 hour did not change cortical excitability. Stimulation at 0.9 Hz for 15 minutes (810 pulses), similar to the parameters used to induce long-term depression (LTD) in cortical slice preparations and in vivo animal studies, led to a mean decrease in motor evoked potential (MEP) amplitude of 19.5%. The decrease in cortical excitability lasted for at least 15 minutes after the end of the 0.9 Hz stimulation. The mechanism underlying this decrease in excitability may be similar to LTD. TMS-induced reduction of cortical excitability has potential clinical applications in diseases such as epilepsy and myoclonus. Spread of excitation, which may be a warning sign for seizures, occurred in one subject and was not accompanied by increased MEP amplitude, suggesting that spread of excitation and amplitude changes are different phenomena and also indicating the need for adequate monitoring even with stimulations at low frequencies.
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TL;DR: A very rapid method of conditioning the human motor cortex using rTMS that produces a controllable, consistent, long-lasting, and powerful effect on motor cortex physiology and behavior after an application period of only 20-190 s is described.
3,211 citations
TL;DR: The guidelines for the use of rTMS cover the ethical issues, recommended limits on stimulation parameters, monitoring of subjects (both physiologically and neuropsychologically), expertise and function of the rT MS team, medical and psychosocial management of induced seizures, and contra-indications to r TMS.
2,313 citations
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...When 0.9 Hz rTMS was delivered for 15 min at an intensity of 1.1× the MEP threshold and the excitability of the M1 was measured before and after a conditioning stimulus (15 min of 0.1 Hz stimulation), significant inhibition usually occurred (Chen et al., 1997)....
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...Physiological and safety studies of rTMS show inhibition of the motor cortex after low-frequency stimulation, which suggests that such stimulation may be useful for suppressing the development or spread of epileptogenic activity (Wassermann et al., 1996c; Chen et al., 1997)....
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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
Cites background from "Depression of motor cortex excitabi..."
...In the majority of studies, low-frequency stimulation has been applied at 1 Hz, although a smaller number of studies have utilized frequencies between 0.1 and 0.9 Hz (Chen et al., 1997; Fitzgerald et al., 2006)....
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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
Cites background from "Depression of motor cortex excitabi..."
...The duration of such after-effects increases with the number of stimuli delivered, and may persist minutes to hours or even days after the end of an rTMS session (Chen et al., 1997; Maeda et al., 2000; Touge et al., 2001; Gangitano et al., 2002)....
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TL;DR: Transcranial magnetic stimulation is a technique for noninvasive stimulation of the human brain that can influence brain function if delivered repetitively, and is being developed for various therapeutic purposes.
1,453 citations
Cites background from "Depression of motor cortex excitabi..."
...…strength is called long-term depression (LTD). rTMS at slow rates, approximately between 0.2 and 1 Hz, will cause a decrease in brain excitability (Chen et al., 1997). rTMS at faster rates, approximately 5 Hz or faster, will cause an increase in brain excitability (PascualLeone et al., 1994)....
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TL;DR: The data suggest that synaptic depression can be triggered by prolonged NMDA receptor activation that is below the threshold for inducing synaptic potentiation, and it is proposed that this mechanism is important for the modifications of hippocampal response properties that underlie some forms of learning and memory.
Abstract: We tested a theoretical prediction that patterns of excitatory input activity that consistently fail to activate target neurons sufficiently to induce synaptic potentiation will instead cause a specific synaptic depression. To realize this situation experimentally, the Schaffer collateral projection to area CA1 in rat hippocampal slices was stimulated electrically at frequencies ranging from 0.5 to 50 Hz. Nine hundred pulses at 1-3 Hz consistently yielded a depression of the CA1 population excitatory postsynaptic potential that persisted without signs of recovery for greater than 1 hr after cessation of the conditioning stimulation. This long-term depression was specific to the conditioned input, ruling out generalized changes in postsynaptic responsiveness or excitability. Three lines of evidence suggest that this effect is accounted for by a modification of synaptic effectiveness rather than damage to or fatigue of the stimulated inputs. First, the effect was dependent on the stimulation frequency; 900 pulses at 10 Hz caused no lasting change, and at 50 Hz a synaptic potentiation was usually observed. Second, the depressed synapses continued to support long-term potentiation in response to a high-frequency tetanus. Third, the effects of conditioning stimulation could be prevented by application of NMDA receptor antagonists. Thus, our data suggest that synaptic depression can be triggered by prolonged NMDA receptor activation that is below the threshold for inducing synaptic potentiation. We propose that this mechanism is important for the modifications of hippocampal response properties that underlie some forms of learning and memory.
1,670 citations
TL;DR: Modulation of the amplitude of motor evoked potentials (MEPs) produced in the target muscle during rTMS showed a pattern of inhibitory and excitatory effects which depended on the rT MS frequency and intensity, which suggests that the spread might be due to the breakdown of inhibitORY connections or the recruitment of excited pathways, whereas the post-stimulation facilitation may beDue to a transient increase in the efficacy of excitatories.
Abstract: We applied trains of focal, rapid-rate transcranial magnetic stimulation (rTMS) to the motor cortex of 14 healthy volunteers with recording of the EMG from the contralateral abductor pollicis brevis, extensor carpi radialis, biceps brachii and deltoid muscles. Modulation of the amplitude of motor evoked potentials (MEPs) produced in the target muscle during rTMS showed a pattern of inhibitory and excitatory effects which depended on the rTMS frequency and intensity. With the magnetic coil situated over the optimal scalp position for activating the abductor pollicis brevis, rTMS led to spread of excitation, as evident from the induction of progressively larger MEPs in the other muscles. The number of pulses inducing this spread of excitation decreased with increasing rTMS frequency and intensity. Latency of the MEPs produced in the other muscles during the spread of excitation was significantly longer than that produced by single-pulse TMS applied to the optimal scalp positions for their activation. The difference in MEP latency could be explained by a delay in intracortical conduction along myelinated cortico-cortical pathways. Following rTMS, a 3–4 min period of increased excitability was demonstrated by an increase in the amplitude of MEPs produced in the target muscles by single-pulse TMS. Nevertheless, repeated rTMS trains applied I min apart led to similar modulation of the responses and to spread of excitation after approximately the same number of pulses. This suggests that the spread might be due to the breakdown of inhibitory connections or the recruitment of excitatory pathways, whereas the post-stimulation facilitation may be due to a transient increase in the efficacy of excitatory synapses.
1,349 citations
TL;DR: A new form of synaptic plasticity, homosynaptic long-term depression (LTD) has also recently been documented, which, like LTP, requires Ca2+ entry through the NMDA receptor, and current work suggests that this LTD is a reversal ofLTP, and that the mechanisms of LTP and LTD may converge at the level of specific phosphoproteins.
1,300 citations
TL;DR: This minireview will provide an update on the cellular mechanisms of LTP and distinguish those mechanisms that are firmly established from those that remain contentious.
672 citations
TL;DR: The early facilitation observed at high intensities seems to be a consequence of a rise in cortical excitability induced by the conditioning stimulus, causing an increase in the number or size, or both, of descending volleys from the test stimulus.
649 citations