The duration of the motor unit is perhaps its most important characteristic (Fig. 11). The duration reflects how dispersed the motor unit is in time and space and is the least affected by proximity of the needle electrode to the motor unit being recorded. Generally, short-duration motor units are commonly observed in myopathic conditions, whereas long-duration motor units are observed in neurogenic disorders. In any muscle, motor unit size will vary within a distribution of durations; however, some muscles (e.g., those of the quadriceps or triceps) have longer-duration units than those of others (e.g., iliopsoas and biceps). Duration of the MUP is also age-dependent, because larger motor units are observed more prominently in older people, due to the normal drop out of motor neurons in the spinal cord with advancing age. Although normal values for this parameter have been painstakingly obtained for people of different ages, with experience, one can learn to be comfortable identifying what is probably normal for someone and what is not. To give a sense of these changes, a normal MUP from biceps femoris in a 20-yr-old patient is approx 11 ms in duration, whereas a normal MUP from the vastus lateralis of an 80-yr-old patient is approx 16 ms. From an auditory standpoint, longer-duration MUPs have a lower pitched, "thuddy" sound, consistent with the fact that the prolonged duration equates to a longer wavelength and, thus, a lower frequency. Short-duration MUPs are higher pitched and have a "tinny" quality to them.
The amplitude of a MUP (Fig. 11) is much more subject to variation than duration, and it is strongly dependent on the distance of the needle from the motor unit. One way of determining how close the needle is to a given motor unit is to evaluate the rise time of the motor unit—that is, the time it takes for the first phase of the potential to reach its maximum after the initial departure from baseline. By freezing the oscilloscope screen, the rise time can be easily evaluated visually and should be generally less than approx 500 ^s for the needle to be considered in close proximity to the motor unit. Nonetheless, with small movements of a needle in close proximity to the muscle, the amplitude will vary considerably. Even so, in patients with neurogenic disorders, the absolute highest amplitude motor units will be distinctly higher than those from a healthy patient. For example, a patient with a chronic neurogenic disorder could have amplitudes for a single motor unit reaching 10 mV or more, whereas in a healthy individual, MUPs may not reach above 3 mV.
Amplitude equates to volume when listening to the EMG activity. Hence, for a given volume setting on the EMG, a higher-amplitude motor unit will sound louder than a lower-amplitude motor unit will. Because chronic neurogenic disease produces both a prolongation in duration and increase in amplitude, loud, low-pitched motor units are commonly observed in neurogenic disease. Quiet, high-pitched, "crackling" motor units are commonly observed in myopathic conditions.
A phase is an individual "peak" or "trough" of the motor unit and can be calculated as the number of baseline crossings minus 1 (Fig. 11). Phases are differentiated from turns or serrations, in that a turn is a peak or trough, whether or not it involves a baseline crossing. Most motor units usually consist of four phases or less, although some units with more phases will be observed approx 5% of the time. Electrically, a phase can be thought of as the electrical signature of one or more muscle fibers that make up the overall motor unit, which are in relatively close proximity to one another.
Polyphasia is defined as an excess of motor units with five or more phases, and it is a common occurrence in both myopathic and neuropathic neuromuscular conditions. Phases will increase if the conduction velocity in the terminal nerve twigs to individual muscle fibers is slowed (leading also to a longer-duration MUP) and if the MUP is spread out over a larger area of the muscle because of reinnervation. In a muscle undergoing reinnervation, polypha-sia is usually most apparent relatively early to midway through the recovery process, and gradually decreases as time passes (discussed in more detail below in Section 8). Injury to the distal axon is also common in myopathies, and may also contribute to the polyphasia in these disorders; however, the fact that each muscle fiber's depolarization time shortens can lead to a decrease in the normal "bundling" of individual muscle fiber potentials into a single phase and cause the potential to appear polyphasic.
From an auditory standpoint, the number of phases affects the timbre of the sound—the quality that allows one to distinguish, for instance, a violin from a flute. The timbre of a sound is dependent on the overtones in a sound. MUPs, however, have a very limited range of overtones; polyphasic MUP will sound like a "ratchet" produced by the higher frequencies embedded within it.
Recruitment refers to the orderly participation of MUPs that occurs with a muscle contraction. When an individual is asked to just barely contract a muscle, a single MUP will begin to fire at a rate of approx 4 to 5 Hz. As the patient is asked to push harder, the motor unit will reach approx 10 Hz in firing frequency before the next motor unit begins to fire. People refer to this as the rule of 5s: When two units are firing, the fastest is firing at 10 Hz; when three units are firing, the fastest is firing at a normal frequency of 15 Hz. However, this rule does not hold perfectly well for all muscles. In the cranial nerve musculature, a more rapid firing rate is often observed with a single unit normally firing at up to 15 Hz.
As more motor units join into the contraction, the screen gradually fills up with motor units, such that individual units can no longer be observed. This is what is called a "full interference pattern." In neurogenic disease, this pattern is disturbed, such that a single motor unit will fire more quickly to achieve sufficient force, essentially trying to make up for its absent brethren. Hence, in cases of severe neurogenic disease in which only a single motor unit is present, that MUP may be found to fire at rates of 30 to 40 Hz without other accompanying MUPs. In cases of less-profound axon loss, several individual motor units will fire at 15 to 20 Hz each, more rapidly than observed normally, producing a "picket fence" appearance to the EMG activity rather than the full interference pattern normally generated.
In myopathic disease, the "rule of 5s" still holds; however, MUPs fill the screen so rapidly that they make such an orderly appearance of MUPs impossible to observe. This has been described as "early recruitment," but perhaps should more accurately be called "compressed recruitment" or "condensed recruitment." Because the muscle fiber itself is disrupted and unable to contribute adequately to the force required to contract a muscle, more muscle fibers must be recruited earlier than normal. Thus, in severe myopathies, a barely contracting muscle may produce the firing of many MUPs at once, leading to a full interference pattern, something that is usually only observed with high force levels.
Activation describes the CNS drive that produces a contraction. Activation can be reduced if there is a true CNS lesion, such as an infarction or area of demyelination, or if the patient is simply not trying hard to contract the muscle, perhaps because of pain in the limb. The oscilloscope screen in patients with reduced activation demonstrates motor units that preserve the 5:1 ratio; however, a full interference pattern is never achieved. Rather, a couple of normal-appearing motor units will fire slowly and inconsistently. Perhaps, with encouragement, this firing pattern will improve momentarily before lapsing.
The presence of reduced activation, although implying the presence of a CNS lesion or simply poor effort, does not exclude the presence of superimposed peripheral neurogenic or myopathic disease. For example, patients with severe sensory ataxia, such as one due to a sensory neuronopathy, may have difficulty moving their limbs simply secondary to impaired sensory feedback, leading to reduced activation. Similarly, patients with amyotrophic lateral sclerosis often have a combination of central and peripheral motor neuron loss, leading to a picture of reduced activation superimposed on reduced recruitment and MUP enlargement.
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