CLINICAL NEUROPHYSIOLOGY : Transcranial Magnetic Stimulation (TMS)
Transcranial magnetic stimulation (TMS) is a procedure that uses magnetic fields to stimulate nerve cells in the brain. An electromagnet is used to create pulses of electric current that stimulate nerve cells in the region of the brain beneath the magnet.
When cortical neurones, such as those of the motor cortex, are excited, impuses in the corticospinal axons activate alpha motoneurones, and the characteristics of these responses can be used to examine the function of the motor pathway under investigation.
Transcranial Magnetic Stimulation (TMS)
Transcranial magnetic stimulation (TMS) is a procedure that uses a suddenly induced magnetic field to stimulate nerve cells in areas of the brain. An electromagnet orientated in the correct direction is used to induce electric currents that stimulate nerve cells in the region of the brain beneath the magnet.
TMS can excite cells in the motor cortex, causing muscles in the oppostie side of the body to twithc because of conduction of impulese along the corticospinal pathway to motoneurones in the spinal cord.
The time taken for conduction of nerve impulses from the motor cortex to the spinal cord and peripheral nerves to the muscles, such as the small muscles of the hand, can be measured.
EMG recordings induced by TMS
The trace shows the electromyographic response to TMS of the contralateral motor cortex recorded from the first dorsal interossus muscle while the subject was voluntarily contracting the same muscle. The stimulus to the cortex was a single pulse of TMS at an intensity of 110% resting motor threshold.
Approximately 20 ms after the stimulus is a large spike-like evoked potential, sometimes called a motor-evoked potential (MEP).
The MEP is followed by a period of relative quiescence of the background EMG activity known as the 'cortical silent period' during which the previously existent background motor activity caused by the voluntary contraction is inhibited. The end of the silent period is indicated by the dashed vertical line; following the dashed line the background activity associated with the voliuntary contraction resumes.
There are several components that may contribute to the silent period. One is cortical excitation of inhibitory neurones within the cortex that silence cortico-spinal neurones momentarily.
A second component is hyperpolarisation of alphamotoneurones caused by recurrent inhibition e.g. by Renshaw cells.
Renshaw cells are segmental spinal interneurones that are excited by recurrent collaterals of alpha motoneurones. These interneurones are inhibitory and release glycine as neurotransmitter on to alpha motoneurones, thereby reducing the activity and excitability of the motoneurones pool. The also inhibit Ia interneurones. Electrical stimulation of the axons of alpha motoneurones induces recurrent inhibition of their cell bodies, mediated by glycine dependent IPSPs.
Another component is peripheral, related to the loss of muscle spindle Ia afferent input during the muscle twitch, although this is probably weaker than the other components.