Abstract
Transcranial magnetic stimulation (TMS) is a non-invasive technique that uses a brief, intense magnetic pulse to induce an electric current in the cortex, depolarising neurons through the intact scalp and skull. Its defining virtue is causality: where recording methods such as electroencephalography observe the brain in action, TMS intervenes in it, letting an experimenter ask whether a given piece of cortex is necessary for a given function. This article covers the electromagnetic induction that makes stimulation possible, the recruitment of the corticospinal tract that gives TMS its most reliable readout, the repetitive protocols that raise or lower cortical excitability, the “virtual lesion” logic that brought TMS into cognitive neuroscience, and its clinical use in depression. Three interactive demonstrations explore coil fields, the motor recruitment curve and its threshold, and how repetitive protocols shift excitability.
Keywords: transcranial magnetic stimulation, motor evoked potential, virtual lesion
Transcranial magnetic stimulation is the most widely used means of stimulating the human brain without surgery. A coil held against the scalp carries a current that rises and falls in under a millisecond; the changing magnetic field it produces passes unimpeded through the skull and, by electromagnetic induction, drives a current in the cortex beneath, enough to make neurons fire (Barker et al., 1985). What makes this worth doing is not the magnetic field itself but what it licenses: a controlled, reversible interference with neural activity in a chosen place at a chosen moment.
That capacity for intervention is the reason TMS belongs to cognitive psychology and not only to clinical neurology. Where methods such as functional MRI and EEG reveal where and when activity correlates with a task, TMS can ask whether that activity is necessary — whether disrupting a region impairs the behaviour, and if so, during which tens of milliseconds it matters (Pascual-Leone et al., 2000). The sections below set out what TMS is, the physics that makes it possible, how it recruits the motor system, how repetitive stimulation changes cortical excitability, how it is used as a “virtual lesion” in cognitive research, its clinical applications, and the safety limits that govern its use.
Key Takeaways
- TMS induces an electric current in the cortex by electromagnetic induction: a rapidly changing magnetic field from a scalp coil drives current in the tissue beneath, depolarising neurons (Barker, 1991; Hallett, 2000).
- Anthony Barker and colleagues built the first transcranial magnetic stimulator in 1985, evoking a movement by stimulating the motor cortex non-invasively (Barker et al., 1985).
- Over the motor cortex a single pulse produces a motor evoked potential whose amplitude grows with stimulus intensity along a sigmoidal recruitment curve, from which the resting motor threshold is defined (Klomjai et al., 2015).
- Repetitive TMS (rTMS) and patterned protocols such as theta-burst stimulation change cortical excitability for minutes to hours after stimulation, low frequencies tending to suppress and high frequencies to facilitate (Huang et al., 2005; Klomjai et al., 2015).
- By transiently disrupting a region, TMS acts as a reversible “virtual lesion”, letting cognitive neuroscience test whether a cortical area is necessary for a task and when (Walsh & Cowey, 2000; Pascual-Leone et al., 2000).
- rTMS of the left prefrontal cortex is an FDA-cleared, evidence-based treatment for major depression, governed by explicit safety guidelines that bound intensity, frequency, and train duration to avoid seizure (George et al., 2010; Rossi et al., 2009; Lefaucheur et al., 2020).
Figure 1
The Induction Principle of Transcranial Magnetic Stimulation
What Transcranial Magnetic Stimulation Is
Transcranial magnetic stimulation is a method of stimulating neural tissue through the intact scalp and skull, using a magnetic field to carry energy across the barrier that ordinary electrical stimulation cannot cross painlessly. A coil placed on the head carries a brief pulse of current; the magnetic field this generates passes through the skull with almost no attenuation and induces an electric field in the cortex, which depolarises neurons and, if strong enough, makes them fire (Barker et al., 1985). The technique is called transcranial because it reaches the brain from outside the cranium, and magnetic because the magnetic field is only the intermediary — the field that actually stimulates the tissue is the electric one that the magnetic pulse induces.
The crucial advantage over direct transcranial electrical stimulation, which had been possible since the 1980s, is comfort. Passing a current through the scalp electrically excites pain receptors and muscles in the skin, so transcranial electrical stimulation is sharply painful. A magnetic field, by contrast, is not felt as it passes through the scalp; the induced current appears in the cortex without depositing painful current densities in the skin, so magnetic stimulation is tolerable and can be repeated (Barker, 1991). This is what turned brain stimulation from a specialised, mostly intraoperative procedure into a routine tool of research and clinical practice.
Two properties define TMS's place among the methods of cognitive neuroscience. The first is that it is causal: it does not observe activity but perturbs it, so it can test necessity rather than mere correlation. The second is that it is focal in time: a single pulse acts within a millisecond, so the perturbation can be delivered at a precise moment relative to a stimulus or response and its effect timed (Walsh & Cowey, 2000). Its spatial focus is more modest — the induced field is strongest in a region of a centimetre or two of superficial cortex directly under the coil, and falls off with depth — so TMS is well suited to superficial targets and poorly suited to deep ones.
How TMS Works: Electromagnetic Induction
The physics of TMS is Faraday's law of electromagnetic induction: a changing magnetic field induces an electric field in a nearby conductor, and the induced field is proportional to the rate at which the magnetic field changes. The stimulator stores charge in a large capacitor and discharges it through the coil in a pulse that peaks in roughly a tenth of a millisecond, producing a magnetic field of one to two tesla at the coil surface. Because the induced electric field depends on dB/dt rather than on B itself, the brevity of the pulse is essential: the same peak field delivered slowly would induce nothing able to stimulate (Barker, 1991; Hallett, 2000).
The magnetic field passes through skin, skull, and cerebrospinal fluid essentially unattenuated, which is exactly the property that direct electrical stimulation lacks. The induced electric field runs parallel to the cortical surface and, where it changes most steeply or where an axon bends relative to it, drives current across neuronal membranes. The neurons most readily excited are not the large pyramidal cells directly but the horizontally oriented interneurons and axon collaterals that synapse onto them, so that a pulse over the motor cortex activates corticospinal neurons largely trans-synaptically, producing a descending volley of several waves (Klomjai et al., 2015).
Coil geometry shapes where the field is strongest. A single circular coil induces a field in a ring beneath its winding, with no single focal point. A figure-of-eight coil — two circular windings placed side by side, carrying current in opposite senses so their fields sum at the junction — concentrates the induced field under the point where the two loops meet, giving the focality that most research and much clinical work requires (Hallett, 2000). The demonstration below contrasts the induced-field pattern of the two designs.
Coil geometry sets focality
A round coil induces current in a broad ring under its rim; a figure-of-eight coil sums the fields of two windings so the current peaks under their central junction. The map below is the induced electric field reaching the cortex.
Values are illustrative of the geometry, not a biophysical dosimetry model; real induced fields depend on coil current, orientation, and the folded, conductivity-varying anatomy of the head.
Single-Pulse TMS and the Motor Cortex
The motor cortex gives TMS its most direct and reliable readout. A single suprathreshold pulse over the hand area of the primary motor cortex descends the corticospinal tract and produces a twitch in the target muscle, recorded with surface electromyography as a motor evoked potential (MEP) — a compound muscle action potential appearing about 20 milliseconds after the pulse. The MEP is the workhorse measurement of TMS: its presence confirms that the stimulation reached corticospinal neurons, and its size indexes the excitability of the pathway at that moment (Barker et al., 1985; Klomjai et al., 2015).
As stimulus intensity rises, MEP amplitude does not grow linearly but follows a sigmoidal recruitment curve: negligible at low intensities, rising steeply through a middle range as more corticospinal neurons are brought to threshold, and saturating once the available pool is fully recruited. Two parameters summarise the curve. The resting motor threshold is the lowest intensity that evokes a criterion MEP — conventionally 50 microvolts — in a relaxed muscle on a set fraction of trials, and it calibrates every other dose: stimulation intensities are almost always expressed as a percentage of an individual's motor threshold rather than of machine output, because thresholds vary widely between people and between days. The slope of the curve reflects the gain of the corticospinal projection (Klomjai et al., 2015).
The recruitment curve and motor threshold
As stimulus intensity rises, more corticospinal neurons fire together and the motor-evoked potential (MEP) grows along an S-shaped curve. The resting motor threshold is the intensity at which the response first clears the 50-microvolt criterion.
A Boltzmann sigmoid with plateau 2.0 mV, midpoint 55% MSO and slope factor 5. Real thresholds vary widely between people and are set on the individual, never assumed.
Single-pulse and paired-pulse TMS over the motor cortex thus yield a family of physiological measures — threshold, recruitment slope, and, with two pulses, intracortical inhibition and facilitation — that quantify the excitability and the inhibitory tone of the corticospinal system. These measures are used both as basic-science probes of motor physiology and as clinical markers, since they change in disorders of the motor system and with drugs that act on cortical excitability.
Repetitive TMS and Cortical Plasticity
A single pulse perturbs the cortex only for the instant it is delivered. When pulses are delivered in trains — repetitive TMS, or rTMS — the effect can outlast the stimulation, raising or lowering the excitability of the stimulated cortex for minutes to hours afterward. This aftereffect, rather than the immediate response, is what makes rTMS therapeutically interesting: it is a way to nudge a cortical region's baseline activity in a lasting direction. As a broad regularity, low-frequency rTMS — around 1 Hz — tends to depress excitability, while high-frequency trains — 5 Hz and above — tend to enhance it, though the rule is only approximate and depends on the state of the cortex and many parameters (Klomjai et al., 2015).
The most influential refinement of rTMS is theta-burst stimulation (TBS), introduced by Huang and colleagues in 2005, which packages pulses in short high-frequency bursts repeated at a theta rhythm of about 5 Hz, mimicking patterns used to induce synaptic plasticity in animal preparations. Continuous theta-burst stimulation (cTBS) suppresses excitability, while intermittent theta-burst stimulation (iTBS) facilitates it — and both achieve their effect in seconds to a few minutes rather than the tens of minutes a conventional rTMS session requires (Huang et al., 2005). The aftereffects are widely interpreted as reflecting long-term potentiation and depression at cortical synapses, which is why rTMS is often described as a means of inducing plasticity in the human cortex, though the cellular mechanisms in the intact human brain remain inferred rather than directly observed (Ridding & Rothwell, 2007). The demonstration below contrasts the excitability aftereffects of the four canonical protocols.
Frequency sets the direction of the after-effect
The same coil can raise or lower cortical excitability for tens of minutes after the train ends — which way depends on the temporal pattern. Slow trains and continuous theta burst suppress; fast trains and intermittent theta burst facilitate.
Directions are the canonical ones reported for motor cortex; the percentages are illustrative. After-effects are variable between people and sessions, and the mapping is not a fixed dose.
The Four Canonical Repetitive-TMS Protocols and Their Aftereffect on Cortical Excitability
| Protocol | Typical parameters | Aftereffect on excitability | Session length |
|---|---|---|---|
| Low-frequency rTMS | 1 Hz continuous train | Suppression | ~10–20 min |
| High-frequency rTMS | 5–20 Hz trains with inter-train pauses | Facilitation | ~20–40 min |
| Continuous theta-burst (cTBS) | 3-pulse 50 Hz bursts at 5 Hz, uninterrupted | Suppression | ~40 s |
| Intermittent theta-burst (iTBS) | 3-pulse 50 Hz bursts at 5 Hz, 2 s on / 8 s off | Facilitation | ~3 min |
The Virtual Lesion in Cognitive Neuroscience
For cognitive psychology, the decisive move was to use TMS not to elicit a response but to interfere with one. A pulse or short train delivered to a cortical region while a person performs a task briefly disrupts the processing that region supports, so that if the region is necessary for the task, performance suffers — a transient, reversible disruption that Walsh and Cowey named a “virtual lesion” (Walsh & Cowey, 2000). Unlike a stroke or surgical lesion, the virtual lesion is temporary, is placed where the experimenter chooses, and lets each participant serve as their own control, freeing causal inference about brain and behaviour from the accidents of natural lesions.
The virtual lesion converts TMS into an instrument for two kinds of question. The first is necessity: does disrupting this region impair this function? The demonstration that stimulation of the occipital cortex can block visual perception, for instance, shows that the region is causally involved, not merely active during seeing. The second, and distinctive, question is chronometry: because a pulse acts within milliseconds, the experimenter can vary when it is delivered relative to a stimulus and map the window during which a region's contribution is indispensable, tracing the time course of a computation in a way no correlational method allows (Pascual-Leone et al., 2000). Combined with neuroimaging and with recordings of the stimulation's remote effects, TMS also becomes a probe of functional connectivity, revealing how perturbing one node changes activity in the network to which it belongs (Siddiqi et al., 2022).
Clinical Applications
The plasticity-inducing aftereffects of rTMS are the basis of its clinical use, of which treatment of major depression is the most established. The rationale rests on the observation that the left dorsolateral prefrontal cortex is relatively hypoactive in depression; high-frequency rTMS to that region, delivered daily over several weeks, aims to raise its excitability and relieve symptoms. A large multisite industry-sponsored trial (O'Reardon et al., 2007) and a subsequent independent randomised controlled trial (George et al., 2010) established efficacy against sham stimulation in medication-resistant depression, leading to regulatory clearance and to rTMS's inclusion in evidence-based treatment guidelines (Lefaucheur et al., 2014; Lefaucheur et al., 2020).
Practice has since moved toward shorter and more targeted protocols. The THREE-D trial showed that intermittent theta-burst stimulation, which compresses a session into a few minutes, is non-inferior to conventional high-frequency rTMS for depression, greatly increasing the number of patients a clinic can treat (Blumberger et al., 2018). Accelerated protocols that deliver many sessions per day with individualised, functional-connectivity-guided targeting have reported high remission rates in treatment-resistant depression, though from small samples (Cole et al., 2020). Beyond depression, evidence-based guidelines assess rTMS for neuropathic pain, motor recovery after stroke, and other indications, with recommendations graded by the strength of the trial evidence rather than asserted uniformly (Lefaucheur et al., 2020).
Worked Example
Consider how the resting motor threshold is read from a recruitment curve, the calculation that underlies the second demonstration. Model the motor evoked potential as a Boltzmann sigmoid of stimulus intensity S (in percent of maximum stimulator output, %MSO):
MEP(S) = MEPmax / (1 + e(S50 − S)/k)
with a saturating amplitude MEPmax = 2.0 mV, a midpoint S50 = 55 %MSO (the intensity giving half the maximum response), and a slope constant k = 5 %MSO. At the midpoint the exponent is zero, so MEP(55) = 2.0 / (1 + 1) = 1.00 mV, exactly half the plateau, as a sigmoid requires.
The resting motor threshold is conventionally the intensity that evokes a criterion MEP of 50 microvolts, that is 0.05 mV. Setting MEP(S) = 0.05 and solving for S:
0.05 = 2.0 / (1 + e(55 − S)/5)
Rearranging, 1 + e(55−S)/5 = 2.0 / 0.05 = 40, so e(55−S)/5 = 39. Taking the natural logarithm, (55 − S) / 5 = ln 39 = 3.664, so 55 − S = 18.32 and S = 36.68 %MSO. The resting motor threshold for this pathway is therefore about 37 %MSO.
This number is the reason intensities are dosed relative to threshold. A clinical protocol prescribed at “120 % of resting motor threshold” would here mean 1.2 × 36.68 = 44.0 %MSO; at the operating intensity of, say, 65 %MSO the model gives MEP(65) = 2.0 / (1 + e−2) = 2.0 / 1.135 = 1.76 mV, well up the steep part of the curve. Because the curve is steep near threshold — the slope constant k is small — a few percent of stimulator output separates “nothing” from a large response, which is exactly why threshold must be measured for each person rather than assumed, and why safety limits are expressed as multiples of it (Klomjai et al., 2015; Rossi et al., 2009).
Discussion
TMS's enduring value comes from a capability no recording method shares: it intervenes. For cognitive psychology this converts a correlational science into, in part, an experimental one, allowing the claim that a region is necessary for a function and that its contribution falls within a particular window of time (Walsh & Cowey, 2000; Pascual-Leone et al., 2000). For clinical neuroscience the same aftereffects that make rTMS a research tool make it a treatment, one that reaches the cortex non-invasively and, unlike a drug, can be aimed at a chosen region (George et al., 2010).
The limits are as definite as the capabilities. The induced field is strongest in superficial cortex and weakens with depth, so deep structures cannot be reached selectively without also strongly stimulating the cortex above them. Spatial focus is on the order of a centimetre or two, coarser than the columnar organisation of cortex. The physiological effects, especially of repetitive protocols, are variable between people and between sessions, which complicates both experiments and therapy and has driven interest in individualised targeting (Siddiqi et al., 2022). And because a suprathreshold train can, in principle, spread excitation and trigger a seizure, TMS is bounded by explicit safety limits on intensity, frequency, and train duration — the single most important of which is that the risk is real but very low when the published guidelines are followed (Rossi et al., 2009).
For cognitive psychology, then, TMS is best understood as the field's principal instrument of controlled interference: a way to move from watching the brain correlate with behaviour to testing which parts of it, and at which moments, behaviour actually requires.
Current Directions
Contemporary TMS research is increasingly organised around the network rather than the site. The recognition that stimulating one region propagates to the circuit it belongs to has reframed both cognitive and clinical work: rather than asking which spot to stimulate, investigators ask which network a symptom maps onto and which accessible cortical node is best connected to it, using each person's own functional connectivity to choose the target (Siddiqi et al., 2022). This “circuit-targeting” logic underlies the individualised, connectivity-guided protocols that have reported high remission rates in treatment-resistant depression (Cole et al., 2020).
A second front is dose and delivery. Theta-burst stimulation has moved from a laboratory plasticity protocol to a clinical mainstay because it is non-inferior to conventional rTMS while taking a fraction of the time (Blumberger et al., 2018), and accelerated schedules that compress a full course into days are under active trial. A third is the persistent problem of variability: the between-subject and within-subject inconsistency of rTMS aftereffects has prompted work on state-dependent stimulation, closed-loop protocols that trigger pulses on the brain's own oscillatory phase, and better dosimetry through electric-field modelling. Across all three, the periodic updating of the evidence-based guidelines tracks which indications the trial evidence now supports and which remain investigational (Lefaucheur et al., 2020).
Common Misconceptions
- “It is the magnetic field that stimulates the brain.”
- The magnetic field is only the intermediary. It passes through the skull and, by Faraday's law, induces an electric field in the cortex; that induced electric current is what depolarises neurons. The stimulation depends on how fast the magnetic field changes, not on a static magnetic force (Barker, 1991).
- “TMS can target any brain region with pinpoint accuracy.”
- The induced field is strongest in a region of superficial cortex a centimetre or two across and falls off with depth. Deep structures cannot be stimulated selectively, and the spatial focus is coarser than the fine organisation of cortex (Hallett, 2000).
- “A virtual lesion is just like a real one.”
- The virtual lesion is transient and reversible, and its effect is a brief disruption of ongoing processing, not the loss of tissue. This is a strength for inference — it is temporary and each person is their own control — but the disruption may also recruit compensation or spread, so it is not a literal ablation (Walsh & Cowey, 2000).
- “rTMS reprograms the brain permanently.”
- The aftereffects of a single session last minutes to hours; clinical benefit in depression is built up over many sessions and is not permanent, which is why maintenance and re-treatment are part of practice. The changes are shifts in excitability, interpreted as synaptic plasticity, not a rewiring (Ridding & Rothwell, 2007).
Glossary
- Chronometry.
- The use of TMS to determine when a region's contribution to a task is indispensable, by varying the moment a pulse is delivered relative to a stimulus and mapping the interval during which disruption impairs performance.
- Coil.
- The wound conductor held against the scalp through which the stimulator discharges its current; its geometry (circular, figure-of-eight) determines the shape and focality of the induced field.
- Cortical excitability.
- The readiness of a region of cortex to respond to input, indexed for the motor cortex by the motor threshold and recruitment-curve slope, and altered for minutes to hours by repetitive TMS.
- Corticospinal tract.
- The descending motor pathway from the primary motor cortex to the spinal cord; a suprathreshold pulse over the motor cortex drives a volley down this tract to produce the motor evoked potential.
- Electromagnetic induction.
- The physical principle, described by Faraday's law, whereby a changing magnetic field induces an electric field in a nearby conductor; the basis of all magnetic stimulation.
- Faraday's law.
- The law of electromagnetic induction stating that the electric field induced in a conductor is proportional to the rate of change of the magnetic field; the reason a stimulating pulse must rise in a fraction of a millisecond.
- Figure-of-eight coil.
- A coil of two adjacent circular windings carrying opposed currents, whose induced fields sum beneath the junction to give a focal maximum; the standard focal coil for research and much clinical use.
- Intracortical inhibition.
- The suppression of the motor evoked potential when a subthreshold conditioning pulse precedes a suprathreshold test pulse by a few milliseconds; a paired-pulse measure of the inhibitory tone of the motor cortex.
- Motor evoked potential (MEP).
- The compound muscle action potential recorded from a target muscle about 20 ms after a suprathreshold pulse over the motor cortex; the standard readout of corticospinal excitability.
- Recruitment curve.
- The sigmoidal relationship between stimulus intensity and MEP amplitude, rising from threshold to a saturating plateau as more corticospinal neurons are recruited.
- Repetitive TMS (rTMS).
- Trains of pulses delivered to induce aftereffects that outlast the stimulation; low frequencies tend to suppress and high frequencies to facilitate cortical excitability.
- Resting motor threshold.
- The lowest stimulus intensity that evokes a criterion MEP (conventionally 50 µV) in a relaxed muscle on a set fraction of trials; the reference against which stimulation doses are set.
- Sham stimulation.
- A control condition mimicking the sound and scalp sensation of real TMS without delivering an effective cortical field, used to separate the specific effects of stimulation from placebo in clinical trials.
- Theta-burst stimulation (TBS).
- A patterned rTMS protocol delivering bursts of pulses at a ~5 Hz theta rhythm; continuous TBS suppresses and intermittent TBS facilitates excitability, achieving aftereffects within minutes.
- Virtual lesion.
- The transient, reversible disruption of processing in a targeted region by TMS, used to test whether that region is necessary for a task and when.
Key Researchers
Mark S. George
(living). Psychiatrist at the Medical University of South Carolina; pioneered rTMS of the prefrontal cortex as a treatment for major depression and led key controlled trials establishing its efficacy (George et al., 2010). Wikipedia · Google Scholar · Faculty
Mark Hallett
(1943–2025). Neurologist at the National Institute of Neurological Disorders and Stroke; a leader in applying TMS to the study of the human motor system and in mapping the technique's uses and limits (Hallett, 2000). ORCID · Faculty · Google Scholar · Wikipedia · Wikidata
Jean-Pascal Lefaucheur
(living). Clinical neurophysiologist at Henri Mondor Hospital and Université Paris-Est Créteil; led the European evidence-based guidelines that grade the therapeutic use of rTMS across indications (Lefaucheur et al., 2014; Lefaucheur et al., 2020). Faculty
Alvaro Pascual-Leone
(living). Neurologist at Harvard Medical School and the Marcus Institute for Aging Research; established the use of TMS for chronometry and functional connectivity in cognitive neuroscience and helped define its safety guidelines (Pascual-Leone et al., 2000). Wikipedia · Faculty
John C. Rothwell
(living). Neurophysiologist at UCL Queen Square Institute of Neurology; central to the physiology of TMS and co-author of the theta-burst stimulation protocol that reshaped how plasticity is induced in the human cortex (Huang et al., 2005). Wikipedia · Google Scholar · Faculty
Vincent Walsh
(living). Cognitive neuroscientist at UCL Institute of Cognitive Neuroscience; framed the “virtual lesion” logic that brought TMS into mainstream cognitive psychology as a tool for causal inference (Walsh & Cowey, 2000). Google Scholar · Faculty
Frequently Asked Questions
What is transcranial magnetic stimulation?
Transcranial magnetic stimulation (TMS) is a non-invasive way of stimulating the brain in which a coil on the scalp produces a brief, strong magnetic pulse. The pulse passes through the skull and induces an electric current in the cortex beneath, which can make neurons fire. It is used both to study the brain and to treat conditions such as depression.
How does TMS actually stimulate neurons?
By electromagnetic induction. A rapidly changing magnetic field induces an electric field in any nearby conductor, including cortical tissue. It is this induced electric current, not the magnetic field itself, that depolarises neurons. Because the induced field depends on how fast the magnetic field changes, the pulse must be extremely brief — rising in about a tenth of a millisecond.
Does TMS hurt?
Generally no. The magnetic field passes through the scalp without exciting the pain receptors in the skin, which is why magnetic stimulation is tolerable where direct electrical stimulation of the scalp is painful. People typically feel a tapping sensation and a contraction of scalp muscles, and single pulses over the motor cortex produce a visible twitch in the target muscle.
What is a motor evoked potential?
It is the electrical response recorded from a muscle after a TMS pulse over the part of the motor cortex that controls it, appearing about 20 milliseconds later. Its size reflects how excitable the corticospinal pathway is at that moment, and it is the standard measurement used to calibrate and study TMS.
What is the difference between single-pulse and repetitive TMS?
A single pulse perturbs the cortex only for an instant and is used to probe excitability or to briefly disrupt processing. Repetitive TMS delivers trains of pulses whose effect outlasts the stimulation, raising or lowering a region's excitability for minutes to hours; this lasting aftereffect is the basis of its therapeutic use.
What is a “virtual lesion”?
It is the transient, reversible disruption of a brain region produced by TMS during a task. If disrupting the region impairs performance, the region is necessary for the task; because the pulse acts within milliseconds, researchers can also find when the region's contribution matters. It is a controlled alternative to studying patients with permanent brain damage.
Is TMS an approved medical treatment?
Yes. Repetitive TMS of the left prefrontal cortex is cleared by regulators and included in evidence-based guidelines as a treatment for major depression, particularly when medication has not worked. Guidelines also assess its use for other conditions, such as neuropathic pain, with recommendations graded by the strength of the evidence.
Is TMS safe?
When published safety guidelines are followed, TMS is considered safe and its most serious risk — a seizure — is very rare. The guidelines set limits on stimulation intensity, frequency, and train duration, and screen for factors that raise risk, precisely to keep that risk low.
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