Functional organization of the trigeminal motor system in man. A neurophysiological study.

Transcranial stimulation (TCS) in intact human subjects was used to investigate the corticobulbar projections and the functional organization of the trigeminal motor system. Both electrical (with the anode overlying the face area of the motor cortex) and magnetic TCS (with the coil at the vertex) excite the upper motoneurons projecting to the trigeminal motor nucleus, evoking motor potentials (C-MEPs) in the jaw-closing and suprahyoid muscles, but only during voluntary contraction. At least 30\% of jaw-closing motoneurons are reached by direct fast-conducting corticobulbar fibres; these projections are mainly crossed. Suprahyoid motoneurons are also reached by fast-conducting corticobulbar fibres; these projections are probably bilateral. In the masseter, electrical TCS also evokes an ipsilateral motor response (R-MEP), followed by a later wave (U), and bilateral inhibitory periods. The R-MEP is secondary to excitation of the motor trigeminal root; the U wave probably results from the simultaneous excitation of Ia afferents in the root and ipsilaterally projecting corticofugal fibres; the inhibitory periods are largely due to activation of exteroceptive afferents in the root. Magnetic TCS, avoiding spread of current to the trigeminal root, evokes C-MEPs but not R-MEPs or U waves. The masseter inhibitory period after magnetic TCS may be due to excitation of corticofugal inhibitory fibres and to mechanical activation of Golgi tendon organs

Silent period evoked by transcranial stimulation of the human cortex and cervicomedullary junction.

1. The silent period evoked in the first dorsal interosseous (FDI) muscle after electrical and magnetic transcranial stimulation (TCS), electrical stimulation of the cervicomedullary junction and ulnar nerve stimulation was studied in ten healthy subjects. 2. With maximum-intensity shocks, the average duration of the silent period was 200 ms after electrical TCS, 300 ms after magnetic TCS, 43 ms after stimulation at the cervicomedullary junction and 100 ms after peripheral nerve stimulation. 3. The duration of the silent period, the amplitude of the motor-evoked potential, and the twitch force produced in the muscle were compared at increasing intensities of magnetic TCS. When the stimulus strength was increased from 30 to 70% of the stimulator output, the duration of the silent period lengthened as the amplitude of the motor potential and force of the muscle twitch increased. At 70 to 100% of the output, the amplitude of the motor potential and force of the muscle twitch saturated, whereas the duration of the silent period continued to increase. 4. Proximal arm muscle twitches induced by direct electrical stimulation of the biceps and extensor wrist muscles produced no inhibition of voluntary activity in the contracting FDI muscle. 5. The level of background activation had no effect on the duration of the silent period recorded in the FDI muscle after magnetic TCS. 6. Corticomotoneurone excitability after TCS was studied by means of a single magnetic conditioning shock and a test stimulus consisting either of one single magnetic shock or single and double electrical shocks (interstimulus interval 1.8 ms) in the relaxed muscle. A conditioning magnetic shock completely suppressed the response evoked by a second magnetic shock, reduced the size of the response evoked by a single electrical shock but did not affect the response evoked by double electrical shocks. Inhibition of the test magnetic shock was also present during muscle contraction. 7. Our findings indicate that the first 50 ms of the silent period after TCS are produced mainly by spinal mechanisms such as after-hyperpolarization and recurrent inhibition of the spinal motoneurones. If descending inhibitory fibres contribute, their contribution is small. Changes in proprioceptive input probably have a minor influence. From 50 ms onwards the silent period is produced mainly by cortical inhibitory mechanisms

Corticospinal potentials after transcranial stimulation in humans.

The descending volley evoked in humans by transcranial electrical stimulation of the scalp was recorded with epidural and spinal electrodes. It consisted of an early wave, which increased in amplitude and decreased in latency when the strength of the stimulus was increased. The mean conduction velocity of the early wave was 66, SD 2.5 m/s. At high stimulus intensity this wave was followed by later and smaller waves, which travel at the same speed as the initial potential. The recovery cycle of the descending volley was studied by delivering paired cortical stimuli at time intervals ranging from 0.5 to 10 ms. The early wave evoked by the test stimulus recovered to about 50% at a 1 ms interval and to 100% at a 3.5 ms interval. The later waves could not be tested at short time intervals but with time intervals longer than 3.5 ms they recovered to 100%. It is suggested that the initial and later waves after scalp stimulation are equivalent to the D and I waves seen in animal experiments

Multiple firing of motoneurones is produced by cortical stimulation but not by direct activation of descending motor tracts.

In the present report we have tested whether stimulation of the motor descending tracts at the brain-stem level could set up repetitive motor unit discharges in a similar manner to that described for motor cortical stimulation. We have seen that a large descending motor volley, evoked by brain-stem stimulation, cannot produce repetitive firing of motor units. Repetitive motoneurone firing is therefore produced by multiple excitatory volleys set up by single cortical shocks

Motor potentials evoked by paired cortical stimuli.

We recorded the motor evoked potentials (MEPs) from the abductor pollicis brevis muscle, after supramaximal electrical transcranial stimulation, and studied the effect of paired transcranial shocks with varying interstimulus time intervals, in 10 normal subjects, 4 patients with median nerve neuropathy and 2 patients with motoneurone disease. In relaxed muscles the amplitude of the MEP evoked by a single shock averaged 30\% of the M wave. With intervals from 1 to 2.5 msec 2 shocks evoked one MEP far larger in size than the control MEP (70\% of the M wave). With intervals of 10 msec and longer, the 2 shocks evoked 2 independent MEPs; the size of the MEP following the second shock (test) was inversely correlated with the size of the control MEP: the more the control MEP approached the size of the M wave, the smaller the test MEP. Single motor unit records showed that, in the normal subjects and patients with peripheral neuropathy, the same motor unit was activated either by the first or the second shock, whereas in the patients with motoneurone disease it fired twice. In active muscles, the control MEP averaged 70\% of the M wave. With intervals of 10 msec and longer the test MEP was markedly suppressed; with 100 msec intervals it fully recovered. In relaxed muscles, by delivering a double shock at a 1.5 msec interval, thus evoking a large MEP, followed by a second double-shock, the test MEP was completely suppressed for a period of 20 msec; it began to recover at 50 msec intervals and fully recovered after 150 msec.(ABSTRACT TRUNCATED AT 250 WORDS