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distal sites in the motor axon are active in cases of nerve compression and polyneuropathy Occasional fasciculation potentials particularly in the calves, hands, and periocular or paranasal muscles occur in many normal persons They can be almost constant for days or weeks on end, or even for years in some individuals, without weakness or wasting; therefore they need not be taken as evidence of disease (benign fasciculations) Certain quantitative features of fasciculations, such as brief duration and a consistent pattern and location of ring, favor benign over pathologic discharges Shivering induced by low temperature and twitchings associated with low serum calcium levels are other forms of fasciculatory activity Fasciculation potentials occur with great frequency in chronic, slowly advancing, destructive diseases of the anterior horn cells, such as ALS and progressive spinal muscular atrophy In these diseases, both voluntary MUPs and fasciculation potentials may be of long duration (more than 15 ms) and of increased amplitude, indicating chronic denervation and reinnervation They are seen often in the early stages of poliomyelitis but only occasionally in the chronic phase of the disease, perhaps because the affected cells die rapidly When anterior horn cells degenerate once again in older individuals who had had poliomyelitis (postpolio syndrome), fasciculations may return Occasionally, they are seen in one muscle as a result of a compressive anterior root lesion, such as those caused by a protruded intervertebral disc; large numbers of axons may be affected, with the result that the fasciculations (or even cramps) may be more prominent than with disease of anterior horn cells Fasciculation potentials in lesser numbers are also observed with chronic nerve entrapments, eg, ulnar neuropathy at the elbow and other peripheral nerve lesions and some polyneuropathies In all these cases, the damaged neuron or its axon seems to leave intact axons in a state of hyperirritability The blocking of axon conduction by local anesthesia does not abolish the fasciculation, but curare-like drugs do so Less Common Types of Spontaneous Electrical Activity (See Chap 55) One of these is myokymia (pages 1194 and 1278), a persistent quivering and rippling of muscles at rest ( live esh ) The EMG picture is distinctive The spontaneously ring MUPs are called myokymic potentials or discharges and consist of groups of repetitive discharging units, each ring at its own rate, quasirhythmically, usually several times per second, followed by an even briefer period of silence The small motor unit discharges may occur singly or as doublets, triplets, or multiplets The site of generation of this activity has also been contested, possibly because it may arise from several sites, but always the site is peripheral, not central, and is believed to correspond to an alteration in the calcium concentration in the microenvironment of the motor axon Spontaneous discharges arising in large myelinated bers have been implicated in the genesis of myokymia; indeed, demyelinating polyneuropathies are among the conditions that give rise to this phenomenon Myokymia is also caused by peripheral nerve hyperexcitability due to both potassium channel mutations and antibodies against the channels This activity may be blocked by lidocaine infusion around the peripheral nerve and may be diminished by carbamazepine or phenytoin In the syndrome of continuous muscle ber activity or Isaacs syndrome (page 1278), which is actually a generalized form of myokymia, EMG discloses high-frequency (up to 300-Hz) repetitive discharges of varying waveforms Focal and segmental myokymias differ in small ways from the generalized form of myokymia with regard to the timing and du-.

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ration of the discharges The focal types refer mainly to facial myokymia, seen most often in multiple sclerosis, Guillain-Barre syn drome, large cerebellopontine angle tumors, or compression of the facial nerve by a small aberrant blood vessel, but it may follow any peripheral nerve injury and regeneration The EMG patterns are complex, either high-frequency (30- to 100-Hz) recurrent bursts or brief lower-frequency bursts Segmental myokymia is a common occurrence in radiation injuries of the brachial plexus The EMG bursts tend to be longer and less frequent than in generalized myokymia, and the interburst frequency is highly variable The origin of these discharges (also referred to as neuromyotonia) is probably in the distal peripheral nerve, where activity of afferent bers, possibly via ephaptic transmission, irregularly excites distal motor terminals Segmental myokymia refers to similar activity in the distribution of one or more adjacent motor roots This activity persists during sleep and general anesthesia The phenomenon of myotonia, which denotes a failure of voluntary relaxation of muscle because of sustained ring of the muscle membrane (see pages 1265 and 1270), is characterized by highfrequency repetitive discharges generally having a positive sharp waveform These myotonic discharges wax and wane in amplitude and frequency, producing a dive-bomber sound on the audio monitor The discharges can be elicited mechanically by percussion of the muscle or movement of the needle electrode and are also seen following voluntary contraction or electrical stimulation of the muscle via its motor nerve The MUPs may appear normal during voluntary contraction, but they are not followed by the silence that normally occurs on relaxation; instead, there is a prolonged afterdischarge consisting of long trains of brillation-like potentials that may take as long as several minutes to subside (Fig 45-8A) These EMG ndings can be seen with any myotonic disorder If the muscle is activated repeatedly at short intervals, the late discharge becomes briefer and briefer and eventually disappears (see Fig 45-8B), as the patient becomes able to relax the exercised muscle ( warm-up effect) In the paradoxical myotonia.

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Figure 45-8 A Myotonia congenita (Thomsen disease) The ve lines are a continuous record of activity in the biceps brachii following a tap on the tendon The initial response is within normal limits, but it is followed by a prolonged burst of rapid activity, gradually subsiding over a period of many seconds or minutes B Same electrode placement as in A Response to the fth of a series of tendon taps Warm-up has occurred, and the characteristic prolonged myotonic activity is no longer evident (See Chap 54 for a description of the disease)

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