**3. Conditioning of the constant ("asynchronous") muscle activity**

The EMG interference pattern is useful to help understanding the conditioning effects coming from a variety of sources. These conditionings fundamentally act on the modula‐ tion of muscle activity and are context-dependent [15]. Therefore, it is possible to study the effects of a variety of inhibitory and excitatory pathways on MNs by means of EMG signal conditioning, and hence extract information on spinal cord neurophysiology.

effect of RI on the SO MNs [1]. However, to quantify the amount of inhibition, additional signal processing of the EMG signal is needed: (1) subtraction of the DC level, (2) computation of the absolute value of each EMG sample, also called EMG rectification, (3) computation of the ensemble average of the several rectified conditioned-EMG signals (or sweeps). The number of sweeps to be averaged depends on the strength of the conditioning effect and the level of voluntary muscle contraction [16]. These procedures will be illustrated based on the super‐ imposed sweeps shown at the right uppermost panel of Figure 5. The results of step (2) above are shown in the middle panel at the right of Figure 5. The bottommost trace of the right panel

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**Figure 5.** Left panel: EMG recordings of the SO showing the muscle activity before and after the delivery of an electri‐ cal stimulus to the CPN nerve (unpublished data). The traces show sparse MU firings. The rectangle in blue encompass‐ es the stimulus artifact followed by a crosstalked activity from the antagonist (TA) muscle. An interesting observation is that the inhibition is not quite clear by the examination of a single recording. The bottom trace shows all the 50 recordings superimposed. A clear reduction in muscle activity ~40ms after the electrical stimulation is indicated by a red bar. Right panel: same traces superimposed (upper trace). All the EMG recordings were rectified (superimposed traces in the middle) and averaged (bottom trace). The red bar indicates the reduction in muscle activity due to RI

The inhibitory period indicated by the red bar under the averaged trace of Figure 5 can then be quantified either by the peak (lowest point of the recording), the mean or the RMS [7] and normalized with respect to a similar computation of the pre-stimulus period (green bar). In an alternative approach, RMS values in each sweep at the right-top corresponding to the time windows defined by the green (control) and red (inhibited) bars are computed and averaged. This yields a mean RMS value in the control period and a mean RMS value in the time interval

induced by the procedure depicted in the schematic of Figure 4.

of Figure 5 is the ensemble average of the traces displayed just above it (step 3).

The voluntary activity of the SO muscle (sustained low-level isometric contraction) can be modulated by the activation of the primary (Ia) afferents from the antagonist muscle spindles [15, 16]. The diagram depicted in Figure 4 shows surface transcutaneous electrical stimulation (1ms rectangular pulse) applied to the common peroneal nerve (CPN) that supplies the tibialis anterior (TA) muscle. The conditioning stimulus substantially reduces the SO muscle activity via reciprocal inhibition (RI) [16]. A typical example of the resulting EMG signals is shown in Figure 5.

**Figure 4.** Schematic showing the pathway of reciprocal inhibition (RI). The black arrow indicates the descending drive from the motor cortex to the SO muscle that generates the interference pattern shown in the oscilloscope (small rec‐ tangle in orange color). The EMG activity can be conditioned by an electrical stimulus applied to the nerve that sup‐ plies the antagonist muscle (TA). The action potentials in the Ia afferents (red arrow) activate the inhibitory Ia IN (IaIN) that generates an inhibitory post-synaptic potential (IPSP) in the membrane of the MN. Hence, after the conditioning electrical stimulus, some MNs will stop firing and the EMG interference pattern will show a transitory decrease in the amplitude (see also Figure 5).

Looking at one or a few sweeps of conditioned-EMG signals (left panel of Figure 5), it is not possible to determine if the inhibition is present. Note that the low voluntary muscle activity produced a very sparse MU firing in the recordings (upper traces) shown on the left panel of Figure 5. When the sweeps (a total of 50) are superimposed (lowermost signal at the left panel of Figure 5), the inhibition becomes clear (see the red horizontal bar below). Thus, several tenths (or even hundreds) of stimuli are necessary to allow the detection/quantification of the effect of RI on the SO MNs [1]. However, to quantify the amount of inhibition, additional signal processing of the EMG signal is needed: (1) subtraction of the DC level, (2) computation of the absolute value of each EMG sample, also called EMG rectification, (3) computation of the ensemble average of the several rectified conditioned-EMG signals (or sweeps). The number of sweeps to be averaged depends on the strength of the conditioning effect and the level of voluntary muscle contraction [16]. These procedures will be illustrated based on the super‐ imposed sweeps shown at the right uppermost panel of Figure 5. The results of step (2) above are shown in the middle panel at the right of Figure 5. The bottommost trace of the right panel of Figure 5 is the ensemble average of the traces displayed just above it (step 3).

**3. Conditioning of the constant ("asynchronous") muscle activity**

62 Electrodiagnosis in New Frontiers of Clinical Research

Figure 5.

amplitude (see also Figure 5).

The EMG interference pattern is useful to help understanding the conditioning effects coming from a variety of sources. These conditionings fundamentally act on the modula‐ tion of muscle activity and are context-dependent [15]. Therefore, it is possible to study the effects of a variety of inhibitory and excitatory pathways on MNs by means of EMG signal conditioning, and hence extract information on spinal cord neurophysiology.

The voluntary activity of the SO muscle (sustained low-level isometric contraction) can be modulated by the activation of the primary (Ia) afferents from the antagonist muscle spindles [15, 16]. The diagram depicted in Figure 4 shows surface transcutaneous electrical stimulation (1ms rectangular pulse) applied to the common peroneal nerve (CPN) that supplies the tibialis anterior (TA) muscle. The conditioning stimulus substantially reduces the SO muscle activity via reciprocal inhibition (RI) [16]. A typical example of the resulting EMG signals is shown in

**Figure 4.** Schematic showing the pathway of reciprocal inhibition (RI). The black arrow indicates the descending drive from the motor cortex to the SO muscle that generates the interference pattern shown in the oscilloscope (small rec‐ tangle in orange color). The EMG activity can be conditioned by an electrical stimulus applied to the nerve that sup‐ plies the antagonist muscle (TA). The action potentials in the Ia afferents (red arrow) activate the inhibitory Ia IN (IaIN) that generates an inhibitory post-synaptic potential (IPSP) in the membrane of the MN. Hence, after the conditioning electrical stimulus, some MNs will stop firing and the EMG interference pattern will show a transitory decrease in the

Looking at one or a few sweeps of conditioned-EMG signals (left panel of Figure 5), it is not possible to determine if the inhibition is present. Note that the low voluntary muscle activity produced a very sparse MU firing in the recordings (upper traces) shown on the left panel of Figure 5. When the sweeps (a total of 50) are superimposed (lowermost signal at the left panel of Figure 5), the inhibition becomes clear (see the red horizontal bar below). Thus, several tenths (or even hundreds) of stimuli are necessary to allow the detection/quantification of the

**Figure 5.** Left panel: EMG recordings of the SO showing the muscle activity before and after the delivery of an electri‐ cal stimulus to the CPN nerve (unpublished data). The traces show sparse MU firings. The rectangle in blue encompass‐ es the stimulus artifact followed by a crosstalked activity from the antagonist (TA) muscle. An interesting observation is that the inhibition is not quite clear by the examination of a single recording. The bottom trace shows all the 50 recordings superimposed. A clear reduction in muscle activity ~40ms after the electrical stimulation is indicated by a red bar. Right panel: same traces superimposed (upper trace). All the EMG recordings were rectified (superimposed traces in the middle) and averaged (bottom trace). The red bar indicates the reduction in muscle activity due to RI induced by the procedure depicted in the schematic of Figure 4.

The inhibitory period indicated by the red bar under the averaged trace of Figure 5 can then be quantified either by the peak (lowest point of the recording), the mean or the RMS [7] and normalized with respect to a similar computation of the pre-stimulus period (green bar). In an alternative approach, RMS values in each sweep at the right-top corresponding to the time windows defined by the green (control) and red (inhibited) bars are computed and averaged. This yields a mean RMS value in the control period and a mean RMS value in the time interval associated with the effect of the RI. To allow comparisons between subjects one may adopt the ratio of the latter to the former as an index of the level of RI.

citability of the stretch reflex pathway and infer spinal cord mechanisms contributing towards motor control [1, 19]. In the lower limbs, the SO muscle has often been used be‐ cause its electrically-elicited reflex response is relatively easy to obtain.The muscle affer‐ ents of group I (Ia and Ib) and II are also depicted in the schematic of Figure 6. However, for low intensity stimulation, group I muscle afferents (mainly Ia) are primari‐

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The presence of a stable M-wave (direct motor response, see below) is desired in most studies to assure (by indirect means) a constant stimulation (see the arrow showing the orthodromic motor activation in Figure 6). Thus, any changes in H-reflex amplitude would be related to neurophysiological factors and not to alterations in stimulus efficacy, which would change the

**Figure 6.** Schematic of the stretch reflex pathway and the mixed nerve stimulation that generates orthodromic and antidromic nerve activity (only the monosynaptic pathway from the Ia is shown). EMG trace showing an H-reflex and M-wave elicited by a transcutaneous electrical stimulus (1ms duration) applied through electrodes located over the skin at the popliteal fossa. The stimulus activates Ia afferent and motor axons from the mixed nerve (PTN) that supplies the SO muscle. The resulting H-reflex and M-wave are recorded with surface electrodes (see the schematic on the left).

With the increase of the stimulus intensity, a larger number of Ia afferents are activated leading to reflex recruitment of more MNs. The MNs in the spinal cord are synaptically recruited according to the size principle [22], i.e., the small size MUs (with low threshold for synaptic input) are recruited first. Therefore, H-reflexes of low amplitude reflect the activation of small MUs (see Figure 7). Higher amplitudes of H-reflex correspond to the activation of intermedi‐ ated sized MUs along with the small ones. The increment in H-reflex amplitude reaches a limit that is not only related to the number of MNs within the pool, but also to the phenomenon of "annihilation", i.e., action potentials in the efferent axon generated reflexively collide with the

**A**: Stimulus artifact indicating when the stimulus was delivered; **M**: M-wave; **H**: H-reflex.

*4.1.1. Recruitment order of reflexively activated motoneurons*

ly activated [20].

M-wave as well [21].

Besides changing the excitability of MNs, pathways converging to the spinal cord may also affect the excitability of several spinal cord elements by acting on presynaptic terminals (e.g., the Ia-MN synapse). Presynaptic effects will be discussed later.
