Insertional activity At the moment the needle is inserted into muscle, there is a normally brief burst of action potentials that ceases once the needle is stable, provided that it is not in a position to irritate a nerve terminal. Increased insertional activity, however, is an abnormal finding seen in most instances of denervation as well as in many forms of primary muscle disease and in disorders that dispose to muscle cramps. In cases of advanced denervation or advanced myopathy, in which muscle fibers have been largely replaced by connective tissue and fat, insertional activity may be decreased and there is a palpable increase in the mechanical resistance to the insertion of the needle.
Abnormal spontaneous activity With the muscle at rest, spontaneous activity of single muscle fibers and of motor units, known as fibrillation potentials and fasciculation potentials, is abnormal. The two phenomena may be confused. Fibrillation is the spontaneous contraction of a single muscle fiber. It occurs when the muscle fiber has lost its nerve supply and is ordinarily not visible through the skin (but may be visible in the tongue). Fasciculation represents the spontaneous firing of an entire motor unit, causing contraction of a group of muscle fibers, and may be visible through the skin. The irregular firing of a number of motor units, seen as a rippling of the skin, is called myokymia.
Fibrillation potentials Destruction of a motor neuron or interruption of its axon causes the distal part of the axon to degenerate, a process that takes several days or more. The muscle fibers formerly innervated by the branches of the dead axon—that is, the motor unit—are thereby disconnected from the nervous system. By mechanisms that are still obscure, the chemosensitive region of the sarcolemma at the motor endplate “spreads” after denervation to involve the entire surface of the muscle fiber. Then, 10 to 25 days after interruption of the axon, the denervated fibers develop spontaneous activity; each fiber contracts at its own rate and without relation to the activity of neighboring fibers. This spontaneous activity, fibrillation, is associated with a random conglomeration of brief dior triphasic fibrillation potentials (Fig. 2-18A) having a duration of 1 to 5 ms and rarely exceeding 300 μV in amplitude. When brief spontaneous fibrillation potentials of this sort are observed firing at two or three different locations (outside the endplate zone) of a resting muscle, one may conclude that the fibers are denervated. In addition, fibrillation potentials may take the form of positive sharp waves, that is, spontaneous, initially positive diphasic potentials of longer duration and slightly greater amplitude than the spikes of fibrillation potentials. Usually, fibrillation potentials discharge at an almost regular rate but after 6 to 8 weeks, irregularly firing fibrillation potentials may be observed.
Fibrillation potentials continue until the muscle fiber is affected by one of several processes: reinnervation by regeneration of the interrupted nerve fiber, by outgrowth of nearby remaining nerve fibers (collateral sprouting), or replacement of the atrophied fibers by connective tissue, a process that may take years. Diseases such as poliomyelitis, which damage spinal motor neurons, or injuries of the peripheral nerves or anterior spinal roots, frequently produce only partial denervation of the involved muscles. In such muscles, one electrode placement may record fibrillation potentials at rest from denervated fibers and normal potentials during voluntary contraction from nearby healthy fibers.
Fibrillation potentials, while characteristic of neurogenic denervation, are not altogether specific; for example, they are seen in muscle diseases such as polymyositis and inclusion body myopathy which presumably damage the muscle fiber and make its membrane electrically unstable.