Electromyography (EMG) is one of several procedures that fall under electrodiagnosis. Some of the other procedures include nerve conduction studies (including late potentials) and evoked potentials. It refers to the electrical detection of signals arising from the depolarization of skeletal muscle. These signals may be detected from skin surface electrodes or from needles placed directly within the muscle. These two types of recordings are used for different purposes, with needle recording used to detect the behavior of individual muscle fibers and motor units while surface recordings are used to detect overall muscle activity in particular positions or actions. Surface EMG is not a common clinical procedure, though it may be used in rehabilitation. Needle electromyography is used to determine whether there is damage to nerve fibers to individual muscles.
A normal muscle is electrically silent when recording from a needle electrode. Movement of the needle normally elicits a brief burst of depolarization from muscle fibers (called insertional activity). This burst of activity ends immediately upon termination of the movement, with restoration of electrical silence.
Damage to motor axons (either at the level of the anterior horn cell, the motor root or the peripheral nerve) results in a series of quantifiable changes in the EMG. It is noteworthy that these changes are triggered by actual disruption of the motor axon and develop in an orderly sequence that can help determine the timing of the injury. A series of events take place in the individual, denervated muscle fibers that can be detected as abnormal electrical signals. First of all, over the period of a week or two, the denervated muscle fiber becomes progressively more mechanically irritable. Therefore, electrical discharges provoked by movement of the needle can outlast the actual movement by more than a second. This is termed “increased insertional activity.” Although this finding is not particularly specific, it does indicate that the muscle is excessively irritable. Muscle fibers also become chemically sensitive to their microenvironment and their membranes can also become unstable enough to produce spontaneously activity. This is recorded as depolarization of individual muscle fibers. The spontaneous depolarizations of the individual fibers appear as fibrillation potentials and positive sharp waves. These do not occur in normal muscles since the normal muscle fibers are only responsive to the activation of their motor unit by neuromuscular transmission.
Reinnervation of muscle is an ongoing process, occurring whenever a muscle is partially denervated. This process typically involves the development of sprouts from adjacent, unaffected motor nerve fibers that ultimately contact at least some of the denervated muscle fibers. These reinnervated muscle fibers cluster right in the area of other, normally innervated muscle fibers. This process results in the development of clumps of reinnervated muscle fibers attached to individual motor neurons (remember, the normal motor unit innervates muscle fibers scattered throughout the muscle). Typically these motor units become significantly larger both in amplitude and duration, since the needle is likely to be recording from more muscle fibers in this clump. Also, the Motor Unit Potential (MUPs) often become more irregular (termed “polyphasic”). This process takes months to develop and indicates the presence of chronic denervation. It should be noted that the needle study is much less sensitive to the process of reinnervation than it is to the findings of fibrillations and positive sharp waves that are seen with recent denervation.
Fasciculations arise from the discharge of part or the whole of a single motor unit. They are larger and more complex than fibrillation potentials. Fasciculations are isolated discharges that recur at irregular intervals, usually in the order of several seconds. Fasciculations near the surface of a muscle may be visible at the skin; those deep within the muscle and detected by an EMG needle are not. Fasciculations are not under voluntary control, a useful point in distinguishing them from motor units discharging due to poor relaxation. Fasciculations probably arise within the fine terminal arborisation of a single motor axon within the muscle. Fasciculations occur in motor neurone diseases, other neurogenic diseases such as radiculopathy and neuropathy, thyroid disease, and peripheral nerve hyperexcitability syndromes, and may be benign. The significance of fasciculations is judged by the company they keep in the muscle; benign fasciculations are not accompanied by denervation changes but malign fasciculations usually are.
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