Spontaneous Potentials Generated By Single Muscle Fibers 41 Fibrillation Potentials

A fibrillation potential represents the electrical activity generated by the depolarization of a single muscle fiber and is depicted in Fig. 3. These potentials are typically triphasic, with an initial small positivity, followed by a large negative spike, and ending with another small positive spike. Generally, these potentials are thought of as being recorded by the needle electrode a short distance from the spontaneously depolarizing muscle fiber. The triphasic morphology of this potential is explained by the principles of volume conduction (see Chapter 4). The first phase represents the distant approach of the depolarization toward the needle; the large negative spike is caused by the transit of the depolarization in the immediate vicinity of the needle, and the final positive phase is caused by the potential receding into the distance. Fibrillation potentials may not always have this classic morphology, especially because the shape depends on the exact position of the needle in relationship to the muscle. They generally have an amplitude of 20 to 200 ^V, are 1 to 5 ms in duration, and fire at a rate of 0.5 to 15 per second. The classic view of fibrillation potentials is that they fire in a very regular, clock-like pattern, with the depolarization occurring consistently. However, many fibrillation potentials, if observed for a long enough time, will slow down until they eventually stop.

The change in frequency can be quite prolonged, moving from a rate of two per second to one every 2 s during a period of 30 to 40 s. Fibrillation potentials can fire substantially slower than motor units (discussed below), often reaching firing frequencies of 0.5 Hz. Alternatively, MUPs generally cannot fire more slowly than approx 4 to 5 Hz and do so slightly irregularly. Hence, the slow, regular, steady "tick" of a fibrillation potential can usually help in its identification. This becomes more difficult if the screen is filled with multiple fibrillation potentials with different morphologies and firing frequencies, such that the individually firing potentials can no longer be identified. Some have described this sound as "frying bacon," which, although helpful, may be a little misleading. In situations in which there are many fibrillation potentials occurring at once, the presence of positive sharp waves (PSWs) (described below in Section 4.2.) can also help confirm the identity of these waves. Alternatively, simply waiting for the electrical activity to decrease until only a couple of potentials are present can help in accurately assessing these waveforms.

Although fibrillation potentials are undoubtedly caused by the partial depolarization of the muscle membrane, their significance is rather nonspecific. They are typically found in any nerve disease in which there is axonal injury causing muscle fibers to lose their innervation (i.e., states of denervation). As reinnervation proceeds after injury, a given muscle fiber will have its resting membrane potential restored, and the spontaneous depolarization will cease. For this reason, fibrillation potentials are generally considered evidence of subacute injury. However, in any condition in which reinnervation is incomplete and muscle fibers remain denervated, the resting membrane potential will be abnormally elevated, and spontaneous depolarization of the muscle fiber is to be expected. The prototypic illness in which this is observed is remote poliomyelitis, in which reinnervation of all the muscle fibers does not occur. Although the disease may have occurred decades earlier, fibrillation potentials will persist in the fibers that have not been reinnervated. Fibrillation potentials are also commonly observed in most muscle diseases. The reasons for this are debated and are explored more in Chapter 20. However, the most likely explanations are:

1. The muscle disease is accompanied by some distal neuronal injury.

2. The muscle disease itself is causing splitting of muscle fibers (leaving a partial muscle fiber no longer attached to the part receiving innervation).

3. That the disease itself is affecting the resting potential of the muscle membrane.

The morphology of fibrillation potentials is one aspect of disease that is not commonly evaluated. Nonetheless, noting the size of fibrillation potentials can be helpful. Small fibrillation potentials are commonly observed in muscle diseases and chronic neurogenic states (e.g., old polio). The reasons for this likely relate to morphological and physiological changes in both of these types of disease states. In muscle disease, split or atrophic muscle fibers simply will be smaller, and there will be fewer Na+ channels activated to produce a given fibrillation potential. Hence, the amplitude of the spike will be smaller. A similar argument holds for chronic neurogenic disease, in which a reduction in the amplitude of the response is likely caused by a reduction in the number of active Na+ channels or decreased function of the Na+-K+ ATPase. One possible mechanism through which this may occur is via downregula-tion of protein synthesis induced by the longstanding absence of innervation.

4.2. Positive Sharp Waves

Similar to fibrillation potentials, PSWs (Fig. 4) represent the depolarization of single muscle fibers; however, their morphology is quite distinct. Unlike fibrillation potentials, they are

50 uV

Fig. 4. Positive sharp wave. The initial sharp positivity is followed by a broad negative wave that slowly fades away.

50 uV

25 ms

Fig. 4. Positive sharp wave. The initial sharp positivity is followed by a broad negative wave that slowly fades away.

biphasic with an initial sharp positivity, followed by a more prolonged negativity. The firing pattern is also more variable than that of a fibrillation potential. Although they can be clocklike and similar to a fibrillation potential, one can also observe a rapid run of PSWs that gradually slows down until it stops.

The mechanism underlying the generation of PSWs has been debated. The most widely accepted explanation for PSWs is that they represent a discharge of a single muscle fiber in which the discharge is abruptly aborted. The proposed pathophysiology is that the needle electrode is in contact with the spontaneously depolarizing muscle fiber. Like a fibrillation potential, the distantly approaching depolarization produces an initial positivity. The depolarization approaches the needle and the negativity commences. However, because the needle is in contact with the membrane itself, the depolarization abruptly ends near the electrode because the mechanical presence of the needle against the membrane causes the membrane to become resistant to the depolarization, resulting in a prolonged dying out of the negative phase.

PSWs, similar to fibrillation potentials, can occur in neurogenic and myopathic disease. However, PSWs are perhaps slightly more sensitive but less specific for the presence of muscle or nerve disease. This is possibly because PSWs can be triggered by the mechanical action of the needle touching the muscle fiber. There are several examples of this. First, in patients with recent onset neurogenic injury, short runs of PSWs may be observed in the muscle before fibrillation potentials actually develop. Second, PSWs can often be found in the intrinsic foot muscles and in the lumbosacral paraspinal muscles of otherwise healthy individuals. In these groups, fibrillation potentials tend to be much less common. Third, PSWs can be diffusely present in muscles of people who are otherwise healthy. This syndrome, which has been termed "EMG disease," may represent a channelopathy in which the muscle membrane is mildly depolarized at baseline and, hence, more easily irritated by needle movement.

4.3. Myotonic Discharges

Similar to fibrillation potentials and PSWs, myotonic discharges represent the repetitive spontaneous depolarization of single muscle fibers and are the electrical equivalent of clinical myotonia. However, the character of the myotonic discharge is different from that of either a fibrillation potential or PSW, because the frequency and amplitude of the discharge waxes and wanes over time (Fig. 5). Although the specific mechanism underlying the variation in these parameters is controversial, the individual waveforms that make up the discharges will have the appearance of either a fibrillation potential or a PSW that is changing in size over time. A "classic" myotonic discharge will generally start at a low frequency, gradually speed up, and then

Fibrillation

Fig. 5. A myotonic discharge; note the slow decrease in frequency and amplitude of the potential. In this example, a clear "revving" up of the potential is not obvious.

Fig. 5. A myotonic discharge; note the slow decrease in frequency and amplitude of the potential. In this example, a clear "revving" up of the potential is not obvious.

gradually slow down before it stops. The amplitude may similarly increase and decrease during this cycle. The sound over the loudspeaker is most accurately described as similar to that of a revving motorcycle engine. However, many myotonic discharges may be observed that do not have the initial speeding up and only demonstrate a gradual reduction in frequency and amplitude as the discharge slows down, giving a "dive-bomber" sound to the discharge. Strictly speaking, these may be difficult to separate from a short run of PSWs. Nonetheless, usually after assessing spontaneous activity for some time in a patient with these partial myotonic discharges, a few with a clear initial waxing of frequency and amplitude will also be found.

Myotonic discharges are helpful because they reduce the differential diagnosis of a patient presenting with symptoms of muscle disease. The list of disorders that are characterized by diffusely prominent myotonic discharges is relatively limited and includes myotonia con-genita, the myotonic dystrophies (types 1 and 2), paramyotonia congenital/hyperkalemic paralysis, drug-induced myotonia (observed with colchicine, chloroquine, and with some cholesterol-lowering drugs). However, occasional myotonic discharges can also be present in patients with many other muscle diseases, including inflammatory myopathies, acid maltase deficiency (discharges are observed most prominently in the paraspinal muscles), myotubu-lar myopathy, and occasionally even in patients with neurogenic disease. It should be noted that, in some situations, muscle cooling can enhance the number of myotonic discharges, and applying ice to the skin overlying a muscle can sometimes be helpful.

4.4. Complex Repetitive Discharges

CRDs are unlike the other three types of muscle fiber discharge, because they represent the depolarization of a group of muscle fibers rather than a single fiber firing repetitively. Understanding the EMG appearance and sound of a CRD is best achieved by first learning the pathological mechanism that underlies these unusual discharges. The initial denervation of muscle fiber is subsequently followed by reinnervation of that muscle fiber by the axon of a neighboring muscle fiber. If a denervating process continues, that group of muscle fibers may subsequently lose axonal contact, leaving a group of denervated muscle fibers of the same type adjacent to one another. The initial depolarization of a denervated, individual muscle fiber may then initiate the depolarization of its neighboring fiber, which, in turn, can initiate firing in adjacent fiber. This type of linked electrical depolarization is termed ephaptic

Complex Repetitive Discharges
Fig. 6. Complex repetitive discharge pathophysiology. The starred fiber is the pacemaker. Note the additional reentrant loop, shown in a circle.
Complex Repetitive Discharges

50 UV

Fig. 7. A complex repetitive discharge.

50 UV

250 ms

Fig. 7. A complex repetitive discharge.

transmission: abnormal electrical transmission of signals that are not part of normal function. The ensuing discharge is complex because it involves multiple muscle fibers; the depolarizations can then become reentrant when the fiber that initiated the discharge becomes depolarized again (see Fig. 6). This reentrant mechanism allows the discharge to continue repetitively for some time. CRDs can become more complex when additional reentrant circuits are added or removed (see Fig. 6). A needle movement causing the first fiber to depolarize may initiate a CRD. On the other hand, CRDs may simply be present without requiring direct contact to a muscle fiber by a needle. Occasionally a "complex-fibrillation potential" may be identified: a single repetitively depolarizing muscle fiber that has several other fibers electrically linked to it. Such a potential will not be a classic CRD because it is not caused by a reentrant mechanism.

Thus, based on an understanding of this pathophysiology, the EMG appearance of a CRD can be easily understood. CRDs appear as multiphasic waves (Fig. 7) that can abruptly change morphology when additional loops of muscle fibers join in or drop out. The multiphasic appearance is caused by the depolarizing fibers associated with the reentrant

Fibrillation Fiber

50 UV

25 ms

Fig. 8. A fasciculation potential.

circuit. CRDs have a machine-like sound and can also abruptly stop if a fiber in this circuit fails to depolarize.

Was this article helpful?

0 0
Peripheral Neuropathy Natural Treatment Options

Peripheral Neuropathy Natural Treatment Options

This guide will help millions of people understand this condition so that they can take control of their lives and make informed decisions. The ebook covers information on a vast number of different types of neuropathy. In addition, it will be a useful resource for their families, caregivers, and health care providers.

Get My Free Ebook


Post a comment