Intracortical inhibition in the human trigeminal motor system.

OBJECTIVE: To investigate the presence and features of short-interval intracortical inhibition (SICI) in the human trigeminal motor system. METHODS: Surface electromyogram (EMG) was recorded from left and right digastric muscles in 7 subjects, along with additional experiments with intramuscular EMG in 2 subjects. Focal transcranial magnetic stimulation (TMS) was used to activate the motor cortex of one hemisphere and elicit motor evoked potentials (MEPs) in digastric muscles on each side, at rest and while subjects activated the muscles at 10% maximal EMG. Paired or single TMS pulses were delivered in blocks of trials, while conditioning TMS intensity and interstimulus interval (ISI) were varied. RESULTS: At rest, paired TMS (3-ms ISI) with conditioning intensities 0.8-0.9x active motor threshold (TA) reduced the digastric MEP amplitude to a similar extent bilaterally. Conditioning at 0.5-0.7TA did not significantly reduce the MEP. MEP amplitude was reduced to a similar extent in both digastric muscles by ISIs between 1 and 4 ms (0.8TA). Voluntary bilateral activation of digastric muscles reduced the effectiveness of conditioning TMS compared to the resting state, with no differences between sides. The similarity of the responses in both digastric muscles was not due to EMG cross-talk (estimated to be approximately 10% in surface records and approximately 2% in intramuscular records), as the intramuscular records showed the same pattern as the surface records. CONCLUSIONS: The effects of paired-pulse TMS on digastric are similar to those reported for contralateral hand muscles, and are consistent with activation of SICI circuits in M1 by conditioning TMS. Our evidence further suggests that the corticomotor representations of left and right digastric muscles in M1 of a single hemisphere receive analogous inhibitory modulation from SICI circuits. SIGNIFICANCE: SICI has been demonstrated in the face area of motor cortex controlling the trigeminal motor system in normal subjects. This method can be used to investigate abnormalities of SICI in movement disorders affecting the masticatory muscles in humans.

Experimental muscle pain does not affect fine motor control of the human hand.

Conditions known to cause hand pain, such as arthritis, are often accompanied by impaired dexterity. The aim of this study was to determine whether this association is coincident, or whether pain affects dexterity directly. In the first part of the study, several tests of dexterity based on pegboard skills were compared with a precision-grip-lift task: the correlations between the results of any of these tests were not significant at the 0.01 level. Nineteen subjects were then tested with a modified Purdue pegboard test and the precision grip-lift task, both without pain and during pain induced by injection of 5% hypertonic saline into the first dorsal interosseous muscle of the non-dominant hand. There was no significant difference in the performance of either task when the muscle was painful, indicating that acute experimental muscle pain does not affect dexterity.

Interhemispheric coupling of corticospinal excitability is suppressed during voluntary muscle activation.

Motor-evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) show a trial-to-trial variation in size at rest that is positively correlated for muscles of the same, and opposite, upper limbs. To investigate the mechanisms responsible for this we have examined the effect of voluntary activation on the correlated fluctuations of MEP size. In 8 subjects TMS was concurrently applied to the motor cortex of each hemisphere using 2 figure-8 coils. MEPs (n = 50) were recorded from left and right first dorsal interosseous (FDI), abductor digiti minimi (ADM), and extensor digitorum communis. At rest, MEPs were significantly positively correlated for pairs of muscles of the same (75% of comparisons) and opposite limb (56% of comparisons). The correlation for within-limb muscle pairs was strongest for FDI and ADM. In contrast, between-limb MEP correlations showed no somatotopic organization. Voluntary activation reduced the strength of MEP correlations between limbs, even for muscle pairs that remained at rest while a remote upper limb muscle was active. In contrast, activation of a remote muscle did not affect the strength of MEP correlation for muscle pairs within the same limb that remained at rest. For within-limb comparisons, activation of one or both muscles of a pair reduced the strength of the MEP correlation, but to a lesser extent than for between-limb pairs. It is concluded that the process linking corticospinal excitability in the two hemispheres is suppressed during voluntary activation, and that different processes contribute to common fluctuations in MEP size for muscles within the same limb.

Differential modulation of intracortical inhibition in human motor cortex during selective activation of an intrinsic hand muscle.

Paired-pulse transcranial magnetic stimulation (TMS) was used to assess the effectiveness of intracortical inhibition (ICI) acting on corticospinal neurons controlling three intrinsic hand muscles in humans. We hypothesised that the suppression of ICI with selective activation of a muscle would be restricted to corticospinal neurons controlling the muscle targeted for activation. Surface EMG was recorded from abductor pollicis brevis (APB), first dorsal interosseous (FDI) and abductor digiti minimi (ADM) muscles of the left hand. Subjects were tested at rest and during weak selective activation of APB or ADM, while they attempted to keep the other muscles relaxed using visual feedback. Paired-pulse TMS was applied with a circular coil oriented to produce antero-posterior (AP) current flow in the right motor cortex (to preferentially evoke I3 waves in corticospinal neurons) and with postero-anterior (PA) currents (to preferentially evoke I1 waves). Paired-pulse TMS was less effective in suppressing the muscle evoked potential (MEP) when the muscle was targeted for selective activation, with both AP and PA stimulation. The mechanism for this includes effects on late I waves, as it was evident with a weak AP test TMS pulse that elicited negligible I1 waves in corticospinal neurons. ICI circuits activated by TMS, which exert their effects on late I waves but do not affect I1 waves, are strongly implicated in this modulation. With AP stimulation, paired-pulse inhibition was not significantly altered for corticospinal neurons controlling other muscles of the same hand which were required to be inactive during the selective activation task. This differential modulation was not seen with PA stimulation, which preferentially activates I1 waves and evokes a MEP that is less influenced by ICI. The observations with AP stimulation suggest that selective activation of a hand muscle is accompanied by a selective suppression of ICI effects on the corticospinal neurons controlling that muscle. The pattern of differential modulation of ICI effectiveness with voluntary activation suggests that the ICI circuits assist the corticospinal system in producing fractionated activity of intrinsic hand muscles.

Responses of single motor units in human masseter to transcranial magnetic stimulation of either hemisphere.

The corticobulbar inputs to single masseter motoneurons from the contra- and ipsilateral motor cortex were examined using focal transcranial magnetic stimulation (TMS) with a figure-of-eight stimulating coil. Fine-wire electrodes were inserted into the masseter muscle of six subjects, and the responses of 30 motor units were examined. All were tested with contralateral TMS, and 87 % showed a short-latency excitation in the peristimulus time histogram at 7.0 +/- 0.3 ms. The response was a single peak of 1.5 +/- 0.2 ms duration, consistent with monosynaptic excitation via a single D- or I1-wave volley elicited by the stimulus. Increased TMS intensity produced a higher response probability (n = 13, paired t test, P < 0.05) but did not affect response latency. Of the remaining motor units tested with contralateral TMS, 7 % did not respond at intensities tested, and 7 % had reduced firing probability without any preceding excitation. Sixteen of these motor units were also tested with ipsilateral TMS and four (25 %) showed short-latency excitation at 6.7 +/- 0.6 ms, with a duration of 1.5 +/- 0.3 ms. Latency and duration of excitatory peaks for these four motor units did not differ significantly with ipsilateral vs. contralateral TMS (paired t tests, P > 0.05). Of the motor units tested with ipsilateral TMS, 56 % responded with a reduced firing probability without a preceding excitation, and 19 % did not respond. These data suggest that masseter motoneurons receive monosynaptic input from the motor cortex that is asymmetrical from each hemisphere, with most low threshold motoneurons receiving short-latency excitatory input from the contralateral hemisphere only.

Is the long-latency stretch reflex in human masseter transcortical?

A long-latency stretch reflex (LLSR) has been described in the human masseter muscle, but its pathway remains uncertain. To investigate this, the excitability of corticomotoneuronal (CM) cells projecting to masseter motoneurons during the LLSR was assessed with transcranial magnetic stimulation (TMS). A facilitated response to TMS would be evidence of a LLSR pathway that traverses the motor cortex. Surface electromyogram electrodes were placed over the left or right masseter, and subjects ( n=10) bit on bars with their incisor teeth at 10% of maximal electromyographic activity (EMG). Servo-controlled displacements were imposed on the lower jaw to evoke a short- and long-latency stretch reflex in masseter. TMS intensity was just suprathreshold for a response in contralateral masseter. Trials consisted of: (1) stretch alone, (2) TMS alone, and (3) TMS with a preceding conditioning stretch at varied conditioning-testing (C-T) intervals chosen to combine TMS with the short-latency stretch reflex (3 ms, 5 ms) and the LLSR (23-41 ms). Masseter EMG was rectified and averaged. With TMS alone, mean (+/- SE) MEP area above baseline was 56+/-9%. The area of masseter MEPs above baseline in the C-T trials was calculated from each EMG average following subtraction of the response to stretch alone. Conditioning muscle stretch had no significant effect on masseter MEPs evoked by TMS with any C-T interval (ANOVA; P=0.90). In addition, subjects were unable to modify the SLSR or LLSR by voluntary command. It is concluded that the long-latency stretch reflex in the masseter does not involve the motor cortex and is not influenced by "motor set".