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1Discipline of Physiology, School of Molecular and Biomedical Science, 2Department of Medicine, and 3Research Centre for Human Movement Control, The University of Adelaide, Adelaide, South Australia
Submitted 30 April 2004; accepted in final form 23 November 2004
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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; Rothwell et al. 1991). Activation of the motor cortex with TMS produces muscle-evoked potentials (MEPs) in target muscles that vary in amplitude from stimulus to stimulus (Amassian et al. 1989; Brasil-Neto et al. 1992; Britton et al. 1991; Kiers et al. 1993). Fluctuations in cortical excitability are believed to contribute to this variability (Burke et al. 1995; Ellaway et al. 1998; Funase et al. 1999).
In humans, motoneurons of distal muscles in the upper limb receive strong monosynaptic projections from the motor cortex. This is the corticomotoneuronal (CM) component of the corticospinal projection. The majority of CM cells facilitate electromyographic (EMG) activity in more than one muscle (Buys et al. 1986; Fetz and Cheney 1980; Kasser and Cheney 1985; Lemon et al. 1991) by divergent monosynaptic excitatory projections to motoneuron pools of synergist muscles (Porter and Lemon 1993). A predicted consequence of this arrangement is that MEP size fluctuations with TMS should be correlated for muscles sharing branched-axon CM input, and this has been reported for muscles of the upper limb (Ellaway et al. 1998; Ho et al. 1998; Schieppati et al. 1996). Correlation analysis of MEP size fluctuations might therefore be potentially useful in studying the extent of shared CM input controlling the muscles in various tasks. However, the presence of branched-axon CM projections is not the only factor responsible for common fluctuations of MEP size in pairs of muscles. Ellaway et al. (1998) revealed a positive correlation of the trial-by-trial size fluctuation of MEPs obtained from left and right hand muscles with bilateral focal TMS. This result is clearly not attributed to branched CM projections innervating both motoneuron pools because, in normal subjects, short-latency responses to TMS in hand muscles are virtually exclusively contralateral (Ziemann et al. 1999), and single CM cells do not branch to innervate motoneuron pools of hand muscles on both sides (see Carr et al. 1993). The between-limb correlation in MEP size fluctuations is thought to arise from shared, moment-to-moment changes in excitability of separate populations of corticospinal neurons in the 2 hemispheres (Ellaway et al. 1998). The source of this synchronizing input is not known, and it is not known whether this form of synchronization contributes to the common fluctuation of MEP size for muscles within the same limb. At rest, the strength of correlation is similar for within-limb and between-limb MEP size fluctuations (Ellaway et al. 1998).
MEP size is known to be influenced by rhythmic oscillations in cortical excitability (Rossini et al. 1991), some of which are synchronous in each hemisphere (Nikouline et al. 2001). A recent study provided evidence that a 40-Hz gamma range oscillation may contribute to the MEP correlation between limbs at rest (Funk and Epstein 2004). A number of cortical oscillations that are present at rest are desynchronized with muscle activation (Crone et al. 1998). Previous studies by Ellaway et al. (1998) and Funk and Epstein (2004) did not assess between-limb MEP correlations under active conditions, although within-limb MEP correlations have been reported during voluntary activity (Ho et al. 1998; Schieppati et al. 1996).
The aim of the present study was to examine the correlation in trial-by-trial MEP size fluctuations for muscle pairs within and between limbs, under rest and active conditions. It was expected that the between-limb correlation in MEP fluctuations would be suppressed by voluntary activation, reflecting the desynchronization of cortical excitability fluctuations in the 2 hemispheres. Within-limb correlations in MEP fluctuations were expected to be reduced during voluntary activation, but still evident because of the presence of shared, branched-axon CM inputs to the muscle pairs. It was of interest to determine whether the correlations in MEP size were muscle-specific (i.e., different for homonymous vs. heteronymous muscle pairs, or related to the function of the muscles involved) because this might provide clues to the nature and organization of the synchronizing influence. For this reason we tested 2 intrinsic hand muscles [first dorsal interosseous (FDI); abductor digiti minimi (ADM)] and one extrinsic muscle [extensor digitorum communis (EDC)] involved in digit movements. This work formed part of the PhD studies of S. L. Pearce.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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). None had a history of neurological disorders. Informed written consent was obtained before the study. Experiments were conducted with the approval of the University of Adelaide Human Research Ethics Committee, and conformed to the requirements of the Declaration of Helsinki. Apparatus and recording
The surface electromyogram (EMG) of the FDI, ADM, and EDC muscles of both upper limbs was recorded using self-adhesive gel-filled bipolar silver/silver chloride electrodes. Subjects were grounded by a lip-clip electrode (Turker et al. 1988). EMG signals were amplified (1,000–2,000x) and filtered (bandwidth 5–500 Hz). The 6 EMG signals were digitized (1-kHz sampling rate/channel) for a 250-ms peristimulus epoch beginning 50 ms before TMS, and stored on computer for later off-line analysis. In addition, EMG signals from left and right FDI were recorded on a 4-channel pulse-code modulated data recorder (Vetter 400, A.R. Vetter, Rebersburg, PA) sampling at 22 kHz/channel. The remaining 2 tape channels were used to record abduction force from either left or right index or 5th digit, depending on the task performed.
Transcranial magnetic stimulation
TMS was applied using one or 2 magnetic stimulators (Magstim 200), each connected to a figure-of-eight stimulating coil with outer coil diameters of 90 mm. Separate tests were performed using either one stimulator (single TMS protocol) or 2 stimulators (dual TMS protocol). For the single TMS protocol, one coil was placed over the motor cortex contralateral to the test limb. For the dual TMS protocol, the coils were held separately by 2 individuals over either side of the subject's head. The coils were positioned over the motor cortex with the handle at right angle to the parasagittal plane, and the center of the figure-8 coil positioned about 5 cm lateral to the vertex. The direction of current induced in the brain under the crossover region of each coil therefore flowed in a lateral-to-medial direction. The same stimulus conditions were used by Ellaway et al. (1998), and allowed room for both coils to be positioned on the head without overlap. TMS intensity and coil position were adjusted until clear responses were observed in all 6 muscles. TMS resting threshold (T) was determined for left and right FDI as the lowest stimulus intensity producing a 50-µV MEP in 3 out of 5 consecutive stimuli. For the test responses, TMS intensity was adjusted to produce MEPs in resting muscles in all trials, and of similar size in each hand. The FDI MEP area averaged around 10 mV/ms, which is about 25% of the maximum M-wave elicited in this muscle (see Semmler and Nordstrom 1998). Some subjects were tested with 2 stimulus intensities. Test TMS intensity averaged 1.3 T for the 8 subjects.
In preliminary experiments, we found that the size of the MEP elicited in FDI, ADM, and EDC by TMS applied to the contralateral M1 was not influenced by suprathreshold TMS applied to the ipsilateral M1 between 0 and 5 ms earlier (Pearce 2003). This result means it is unlikely that ipsilateral corticospinal projections contributed to the size of MEPs elicited during dual TMS, or that interhemispheric effects influenced the MEP at these interstimulus intervals (cf. Ferbert et al. 1992). Even with simultaneous discharge of the 2 stimulators there was no interaction between the 2 magnetic fields that affected MEP size. However, to keep the dual TMS experimental conditions consistent with those used by Ellaway et al. (1998), the stimulators were discharged with an interstimulus interval (ISI) of 1 ms for the main series of experiments.
Protocol
Subjects were seated comfortably with the forearms supported on a table and each hand secured in a manipulandum. EMG activity from left and right FDI and ADM muscles was displayed on oscilloscopes in front of the subject. EDC activity was monitored by the experimenters throughout the entire protocol. Force transducers were positioned on either side of the hands so that subjects could contract FDI and/or ADM in abduction of the 2nd or 5th digit, respectively, to a target of 0.5 N. This is a low-level activation, amounting to <2% maximum voluntary contraction (MVC) for FDI. Subjects were given visual feedback of force on an oscilloscope.
Trial-by-trial fluctuations in MEP size
TMS (n = 50, <0.02 s–1) was given in trials of single (one hemisphere) or dual stimulation (both hemispheres, 1-ms ISI) during various tasks. These were as follows:
1)All muscles at rest
2) Activate FDI muscle in one hand (0.5 N index finger abduction)
3) Activate FDI muscles on both sides (0.5 N index finger abduction with each hand)
4) Activate both FDI and ADM muscles in one hand (0.5 N abduction performed with 2nd and 5th digit)
The order of the tasks was randomized for each experiment. During activation tasks 3 and 4 the TMS intensity was reduced for the coil contralateral to the active muscles, so that MEP amplitude in the active muscles matched the rest MEP.
EMG from all muscles was monitored continually throughout the experiment to ensure that the subjects successfully performed the activation tasks. Care was taken to ensure that the muscles not involved in the activation task remained inactive. Two subjects were unable to successfully activate FDI and ADM together, and their data from this task were excluded.
Data analysis
TMS THRESHOLDS.
TMS resting thresholds for left and right FDI were expressed as % maximum stimulator output (MSO), and compared using paired t-test (
= 0.05).
ANALYSIS OF TRIAL-BY-TRIAL VARIATION IN SIZE OF MEPS ELICITED IN PAIRS OF MUSCLES. TMS intensity was adjusted to produce a MEP in all muscles at rest on all trials. TMS intensity was reduced during tasks 3 and 4 to match the size of the MEP in the active muscle to its value at rest. As a consequence, the MEPs could be smaller in the resting muscles of the same limb. Only data from muscles with MEPs on >75% of trials were used for analysis.
For each muscle, the averaged MEP was calculated for the 50 trials, and cursors were used to identify the onset and duration of the MEP. The epoch identified in this way was used to measure the area of MEPs for each of the 50 trials contributing to the average. The mean and SD of the MEP area was calculated for the 50 trials, and the coefficient of variation (CV; SD/mean) was used as a measure of the variability in MEP size. One-way ANOVA ( = 0.05) was used to compare the CV of MEPs from the 3 muscles. Student's t-test ( = 0.05) allowed a comparison between CV of MEPs in resting and active muscles, and when single or dual TMS was used (see Table 1).
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1) Both muscles of the pair at rest, no other muscle active (Rest)
2) Both muscles of the pair at rest, at least one other muscle active (Remote Activation)
3) One or both muscles of the pair active (Activation)
TESTS FOR NONSTATIONARITY. Two stringent criteria were applied to the data used for regression analyses to ensure that correlated changes in MEP size for the pair of muscles was not a result of factors such as coil movement or parallel changes in the level of voluntary muscle activation over the block of trials.
Mep nonstationarity
For each muscle, mean MEP area from the first 25 stimuli within a block was compared with the mean MEP area from the second 25 stimuli, using an unpaired t-test. Data were excluded from further analysis if a significant difference in MEP area was found between the first and second series of 25 stimuli, in both muscles of a pair. Whether the MEP size may have changed over time because of a physiological process, or perhaps because of altered coil position, the nonstationarity would have produced a spurious correlation in the pairwise regression of MEP size. Of the 562 pairs available for regression analysis, 84 were excluded on this basis.
Prestimulus emg nonstationarity
Unpaired t-tests were used to compare the prestimulus EMG level in the 50 ms preceding the first 25 stimuli and the second 25 stimuli of each block. If the prestimulus EMG was significantly different for the first and second series of 25 trials in both muscles, regression analysis was not performed on the data. Six of the 562 pairs available for regression analysis were excluded on this basis.
STATISTICAL ANALYSIS. MEP data from 472 muscle pairs survived the exclusion criteria and were subject to linear regression analysis and statistical comparisons. Summary data are reported as means ± SE.
A 2-way ANOVA was used to assess the effect of LOCATION (within-limb, between-limb) and ACTIVATION STATE (Rest, Remote Activation, Activation) on the correlation in MEP size fluctuations (r2) for all available combinations of muscle pairs.
A 2-way ANOVA was used to assess whether MEP fluctuations were more strongly coupled for particular combinations of muscles. For within-limb muscle pairs the effects of MUSCLE COMBINATION (FDI–ADM, FDI–EDC, ADM–EDC) and ACTIVATION STATE were examined, with the strength of the correlation in MEP size fluctuations (r2) as the dependent variable. For between-limb muscle pairs, there were 6 possible combinations of MUSCLE PAIR and 2 levels of TASK (all muscles at rest, at least one muscle active) in the 2-way ANOVA.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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Resting TMS threshold for right FDI was 46 ± 3% of maximal stimulator output, and for left FDI was 50 ± 4%, an insignificant difference (paired t-test, P > 0.05, n = 8).
MEP variability
Figure 1 shows an example of the variability in MEP size for 10 consecutive stimuli, recorded concurrently from left and right FDI in one subject with the dual TMS protocol. Data are shown with both muscles at rest (left) and active (right). There was considerable variability of MEP size from trial to trial for each muscle under rest and active conditions. At rest, there was a clear correlation in size of MEPs in left and right FDI in different trials. This was not evident with both FDI muscles active.
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Between-limb comparisons of MEP size fluctuations
Figure 2 shows data from one subject with all muscles at rest, illustrating the covariation of MEP size for pairs of muscles in left and right upper limb using dual TMS. Between-limb comparisons in this subject revealed significant positive correlations of MEP size for 2 of the 3 homonymous muscle pairs, and in 3 of the 6 heteronymous muscle pairs. Figure 3 shows data from the same subject, obtained with right FDI active during index finger abduction. None of the between-limb comparisons of MEP size fluctuations was significant, even for pairs involving muscles that were not themselves active. The strength of correlation of MEP size was reduced for between-limb comparisons whether one or both muscles of the pair were active.
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Within-limb comparisons of MEP size fluctuations
Trial-by-trial fluctuations in MEP size were often significantly correlated between FDI, ADM, and EDC muscles within the same limb at rest. In contrast to the between-limb comparisons, within-limb comparisons of MEP size frequently remained significant when one or both muscles of the pair were activated. Figure 4 shows examples of the MEP regression analysis for FDI and ADM of the same hand at rest and during activation of one or both muscles. At rest there was a significant correlation in MEP size fluctuations in the 2 muscles (r2 = 0.33, P < 0.001). During FDI abduction, when ADM was at rest, MEP areas were still significantly correlated in the 2 muscles (r2 = 0.16, P < 0.005). Similarly, during activation of both FDI and ADM, MEP areas were significantly correlated for these muscles (r2 = 0.08, P < 0.05).
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Different effects of voluntary activation on MEP correlation for between- and within-limb muscle pairs
Figure 5 summarizes the effect of activation state on the strength of correlation (r2) of MEPs for muscle pairs located within the same limb, and in opposite limbs. Two-way ANOVA revealed a significant effect of ACTIVATION STATE [F(2,466) = 24.5, P < 0.0001] and LOCATION [F(1,466) = 54.4, P < 0.0001], and a significant interaction between them [F(2,466) = 3.23, P < 0.05]. The mean r2 was higher for within-limb muscle pairs, and declined with muscle activation. The significant interaction term indicates that the effect of muscle activation differed for between- and within-limb muscle pairs. Figure 5 shows that r2 values for between-limb muscle pairs were significantly reduced during voluntary activation, regardless of whether the muscles contributing to the analysis were themselves at rest or active. In contrast, r2 values were reduced for within-limb muscle pairs only when one or both muscles of the pair were active. For muscles at rest within the same limb, the strength of MEP correlation was virtually unchanged when a remote muscle was active (in the same or opposite limb), compared with the situation with all muscles at rest.
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DISCUSSION |
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MEP variability
It is well known that the MEP resulting from TMS exhibits considerable variability in size with each stimulus (Amassian et al. 1989; Brasil-Neto et al. 1992; Britton et al. 1991; Kiers et al. 1993). The variability in MEP size is usually quantified using the coefficient of variation (CV; SD divided by the mean). The CV values reported in the present study are within the ranges reported in previous studies of MEP variability (Ellaway et al. 1998; Kiers et al. 1993). MEP variability was reduced in the active state (Table 1), in accordance with previous observations (Kiers et al. 1993). The reason for the slightly lower MEP variability in EDC than that in ADM is not clear (Table 1).
Several potential sources for the moment-to-moment changes in MEP size can be excluded. The variation is not attributed to changes in the effectiveness of the stimulation (Reutens et al. 1993) or noise in the recording system (Burke et al. 1995), nor is it related to the phase of the cardiac or respiratory cycles (Amassian et al. 1989). Motoneuron excitability cannot solely explain the MEP fluctuations (Funase and Miles 1999; Kiers et al. 1993). Variations in motor cortex excitability are believed to be responsible, at least in part, for the fluctuations in MEP size (Burke et al. 1995; Ellaway et al. 1998; Funase et al. 1999; Rossini et al. 1991). In humans and monkeys the monosynaptic corticomotoneural projection dominates the excitatory response to brain stimulation in hand muscles (de Noordhout et al. 1999; Olivier et al. 2001).
Covariation of MEP size fluctuations in muscles of opposite limbs
Using a similar protocol, we confirm previous observations that near-synchronous MEP size fluctuations are positively correlated for muscles between left and right upper limbs with the subject at rest (Ellaway et al. 1998; Funk and Epstein 2004). The process responsible for the common modulation of MEP size in the 2 limbs at rest had a similar effectiveness in the present study and that of Ellaway et al. (1998), accounting respectively for 16 and 19% of the MEP variance.
Our results and those of Ellaway et al. (1998) and Funk and Epstein (2004) differ from those of Kiers et al. (1993), who concluded that simultaneous MEP size fluctuations were not correlated for muscles of opposite limbs. The most likely explanation is the use by Kiers et al. (1993) of a single circular coil to activate both hemispheres. With this approach, one hemisphere is activated by current flow in the posterior-to-anterior direction, whereas the other hemisphere is activated by current flow in the opposite direction. Different intracortical elements responsible for transsynaptic activation of corticospinal neurons are preferentially activated by current flow in opposite directions (Day et al. 1989; Di Lazzaro et al. 2001), and some of these interneurons may not exhibit excitability fluctuations that are synchronized with activity in the other hemisphere. With the 2 figure-8 coils as used in the present study and by Ellaway et al. (1998), current flows in a lateral-to-medial direction in each hemisphere. This preferentially produces D- (Nakamura et al. 1996) or I1-waves (Sakai et al. 1997) in corticospinal neurons of each hemisphere.
The principal novel finding of the present study is that when a voluntary contraction is performed, the MEP size fluctuations are decoupled between limbs. This was the case even if the muscle pair remained at rest, and a remote muscle was active in an upper limb (Fig. 5). It might be argued that the weaker MEP correlations with muscle activation could be a result of a worsened signal-to-noise ratio as the MEP is superimposed on the EMG interference pattern in the active state. However, MEP variance actually declined in the active muscles (Table 1). Altered signal-to-noise ratio in the EMG could not explain the weaker MEP correlation for between-limb pairs that remained at rest while a remote muscle was active (Fig. 5). A similar reduction of MEP correlation strength was observed for between-limb pairs when one or both muscles of the pair were active, suggesting that the presence of background EMG did not have a major influence on the MEP correlations. We conclude that the process synchronizing corticospinal neuron excitability fluctuations in the 2 hemispheres is suppressed by voluntary activation. This suppression is global and extends to corticospinal neurons controlling muscles that are not engaged in the task.
It is unlikely that ipsilateral corticospinal projections contributed to the correlated MEP fluctuations between limbs because 1) these pathways are weak and difficult to activate with TMS for hand muscles (Wassermann et al. 1991; Ziemann et al. 1999), and 2) MEP size was no different with dual or single TMS. Transcallosal fibers connect the motor cortex hand area of each hemisphere in the monkey (Rouiller et al. 1994) and transcallosal facilitatory (Hanajima et al., 2001) and inhibitory (Ferbert et al. 1992) effects can be demonstrated with bilateral TMS of the motor cortex in humans. These connections could link corticospinal excitability in the 2 hemispheres, although subcortical centers could also contribute to common fluctuations in cortical excitability. Studies in patients with well-defined lesions may provide further clues.
Macroscopic rhythms are detectable in brain neuronal networks with electroencephalography (EEG) and magnetoencephalography (MEG) (see Hari and Salmelin 1997). The size of MEPs induced by TMS has been shown to be affected by cortical oscillations; MEPs are larger during periods of low-alpha wave (8–13 Hz) power in the EEG than when alpha wave activity is high (Rossini et al. 1991). Funk and Epstein (2004) presented evidence that a 40-Hz oscillation contributes to the between-limb MEP correlations at rest. The results of the present study could potentially be explained by a cortical rhythm that showed coherent behavior in both hemispheres when the subject was at rest, but was desynchronized during movement. Candidates include the mu rhythm (8–13 Hz), which is prominent over sensorimotor cortex and desynchronized with movement (Chatrian et al. 1959; Nashmi et al. 1994; Pfurtscheller and Aranibar 1979; Pfurtscheller et al. 2000), although it does not show bilateral coherence between left and right hemispheres (Andrew and Pfurtscheller 1996; Schoppenhorst et al. 1980; Storm van Leeuwen et al. 1978). Central beta rhythms (15–25 Hz) are attenuated during movement (Pfurtscheller 1981; Stancak and Pfurtscheller 1996), and beta activity is synchronous in the left and right hemisphere at rest (Nikouline et al. 2001). The gamma range (>30 Hz) activity is enhanced over contralateral sensorimotor cortex by movement of a limb, with no change in the ipsilateral hemisphere (Crone et al. 1998).
Covariation of MEP size fluctuations for muscles within the same upper limb
The present study has confirmed that MEP size fluctuations are correlated for muscles within the same upper limb. Although this has been reported previously under resting (Ellaway et al. 1998) and active (Schieppati et al. 1996) conditions, the present study is the first to quantify the effects of voluntary activation on the correlation strength. In addition, we have shown that the correlation of MEP size fluctuation for muscles within the same limb is higher for the intrinsic muscle pair FDI and ADM, than for these muscles paired with the extrinsic muscle EDC.
Ho et al. (1998) examined common fluctuations in MEP size for pairs of 4 intrinsic hand muscles during their coactivation, and found a significant positive correlation only for FDI and opponens pollicis. The differences with the present study may be explained by their use of fewer trials per block (25 vs. 50), and pooling of data across a wide range of stimulus intensities (55–160% of FDI resting threshold) for each pair. Schieppati et al. (1996) examined the correlation in MEP size between muscles during a pincer grip task requiring postural control of the unsupported arm. They found significant correlations in MEP size for proximal/distal muscle combinations, but not for MEPs elicited in thumb and finger muscles. This may reflect a strategy adopted by the subjects to keep total grip force constant by varying excitation of thumb or finger muscles independently. In the present experiments the forearm and hand were supported, removing a contribution from proximal muscles to grip force, which may also have reduced MEP correlations between distal muscles in the study by Schieppati et al. (1996).
In agreement with Ellaway et al. (1998), we found no significant difference in the strength of the correlation in MEP size for between-limb and within-limb comparisons at rest. Our results show that with voluntary activation the correlation of within-limb MEP fluctuations is reduced only marginally when one or both muscles of the pair are active (Fig. 5), and is not affected when a remote muscle is activated in the same or opposite limb and the muscle pair remains at rest. The divergent effects of voluntary activation for between-limb and within-limb muscle pairs indicate that the process responsible for the common MEP size fluctuations between limbs does not make a major contribution to the common MEP size fluctuations for muscles within the same limb. The former shows no somatotopic organization and is suppressed globally with voluntary activation of even a remote muscle; the latter shows a somatotopic organization both at rest and active, being reduced only for muscles which are directly engaged by the voluntary commands.
One obvious difference between muscle pairs of the same limb, and between limbs, is the presence of shared, branched-axon CM inputs to motoneuron pools supplying muscles of the same limb (see Porter and Lemon 1993). This neural substrate would be very effective in transmitting common fluctuations in size of TMS-evoked descending volleys to motoneuron pools of muscles of the same limb. This would be true regardless of whether the muscles are at rest or whether they are active, provided the branched-axon CM cells were activated by TMS under both conditions. Fluctuations in corticospinal excitability contributing to the common within-limb MEP size fluctuations could be aperiodic, or could have an oscillatory component. There is direct evidence for weak, but widespread synchrony with oscillatory and nonoscillatory components among primary motor cortex output neurons supplying hand muscles (Baker et al. 2001). Oscillations in the primary motor cortex in the 20- to 32-Hz range increase in size during a tonic hold and are coherent with hand muscle EMG in the monkey (Baker et al. 1997) and human (Conway et al. 1995). Recently it has been shown that fast-conducting, direct corticospinal inputs are important for the approximately 22-Hz coherence between motor cortex and muscle in humans (Farmer et al. 2004). The approximately 22-Hz cortical oscillation may contribute to the within-limb common fluctuations in MEP size, although the unchanged or reduced MEP correlation with voluntary activation does not accord with an increase in the 20- to 32-Hz rhythm during a tonic isometric hold (Baker et al. 1997).
We have shown that MEP size fluctuations within the same upper limb are more strongly coupled for FDI and ADM (mean r2 = 0.26 with both muscles at rest) than for pairings involving those muscles and EDC (mean r2 = 0.16 and 0.17 with both muscles at rest). This might reflect different patterns of CM cell branching, or different degrees of synchronization of excitability fluctuations in distinct populations of corticospinal neurons controlling the muscles. CM effects are more prominent for intrinsic hand muscles than extrinsic muscles (Buys et al. 1986); however, there are insufficient data on the relative incidence of shared CM projections to these muscles to draw any conclusions in relation to the present findings (see Buys et al. 1986; Porter and Lemon 1993). Given that similar strength MEP correlations are seen with between-limb muscle pairs that lack branched-axon CM input, it is likely that synchronous fluctuations in excitability of corticospinal neurons and/or their presynaptic inputs contribute to the within-limb MEP correlations. Our results show that such a synchronizing influence must be different for corticospinal neurons within the same hemisphere compared with that operating between hemispheres because the latter is suppressed by remote muscle activation, whereas the former is not.
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FOOTNOTES |
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Address for reprint requests and other correspondence: M. A. Nordstrom, Research Centre for Human Movement Control, The University of Adelaide, Adelaide 5005, South Australia (E-mail: michael.nordstrom{at}adelaide.edu.au)
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vs. Rest and Remote Activation, Fisher's post hoc test, P < 0.05).