**4.5. "Myokymic" fibrillations**

form of an end plate spike and considered that triphasic end plate spikes are rather common. However, he could not differentiate the shape of triphasic end plate spikes from that of triphasic fibrillation potentials. The spreading of an ectopic nerve irritation potential to the other nerve branches of the motor unit was not considered. Ectopic nerve action potential will spread to both directions from its place of origin, and thus a motor unit or fasciculation potential should be formed instead of an end plate spike. Dumitru (2000) also describes the formation of "atypical" biphasic/monophasic end plate spike configuration (resembling positive sharp waves). First, the electrode may completely compress the muscle fibre, pre‐ venting action potential propagation past the electrode ("sealed end effect"). Second, a "compressed end" may occur; following crushing or compression of tissue, the membrane retains no functional sodium channels and, therefore, can only sustain a passive current flow, but not an active current flow. However, Pickett & Schmidley (1980) explained end plate spikes with positive sharp wave form, "sputtering positive potentials" elegantly. These potentials represented cannula-recorded potentials of the concentric needle electrode and changed their form from positive waves to usual end plate spikes when the electrode was withdrawn. Sputtering positive potentials could not be recorded with a monopolar needle electrode.

Based on the pattern of discharges, two classes of spontaneously active fibres were found in experimentalstudyofratdiaphragm:rhythmicallydischargingfibres,andfibresinwhichaction potentialsoccuratirregularintervals(Purves&Sakmann1974).Themajorityofthesitesoforigin in both regular and irregular fibres were at the former end plate zone; however, there was no region along the length that could not be a site of origin. Regularly occurring action potentials wereassociatedwithoscillationsofthemembranepotential.Irregularlydischargingfibreswere brought to threshold by discrete non-propagated depolarizations called fibrillatory origin potentials (f.o.p.s.) (Purves & Sakmann 1974). F.o.p.s. are generated at the T-tubuli, since detubulation with glycerol abolishes the spontaneous activity (Smith & Thesleff 1976). Thus, the integrityofthe transverse tubular systemisaprerequisite forthepresenceofirregular spontane‐ ous activity. It was also observed, that these discrete depolarizations are caused by regenera‐ tive increase in the Na conductance of the membrane, similar to that associated with the normal

We may presume that in humans, fibrillations with regular rhythm also derive from the membrane potential oscillations of denervated muscle fibres (Thesleff 1982a) or the denervated part of a muscle fibre, as in muscular injury (Partanen & Danner 1982). Irregular fibrillations are accordingly caused by f.o.p.s reaching the firing threshold of an action potential. Imme‐ diately after a f.o.p. there is a period during which the probability of a second f.o.p. occurring is very low (Purves & Sakmann 1974). In denervated muscle fibres there are newly synthesized potassium channels, and they produce a longer duration of the hyperpolarization of the intracellular action potential compared to normal tissue. This hyperpolarization may last up to 100 ms and more (Thesleff 1982a, Dumitru 2000). Thus the refractory period after which a second action potential may occur is increased in denervated muscle fibres, compared to normal muscle fibres. Thus slightly irregular fibrillations with pauses may be fired by a muscle

**4.4. Origin of regular and irregular fibrillation potentials**

52 Electrodiagnosis in New Frontiers of Clinical Research

action potential (Purves & Sakmann 1974, Smith & Thesleff 1976).

"Myokymic" fibrillations have not been categorized as an entity of its own earlier. They may be distinguished from true myokymia by the single fibre potential pattern. True myokymia exhibits a motor unit potential pattern, and was not studied in the present work. The high firing frequency of "myokymic" fibrillations shows that these potentials are not elicited by denervated muscle fibres with a prolonged refractory period. We attribute these potentials to spontaneous large acetylcholine release (giant or slow-rising MEPPs) to the synaptic cleft. This type of transmitter release may occur spontaneously in regenerating nerve terminals or after botulin toxin injection or application of 4-aminoquinoline, without any motor nerve action potential and depolarization of the motor nerve terminal (Thesleff 1982b, Sellin et al. 1996). Evidently large spontaneous transmitter release may cause a short burst of postsynaptic potentials of a single muscle fibre, recorded as "myokymic" fibrillations. It is conceivable that no antidromic spreading of the potential to the rest of motor unit takes place without depola‐ rization of the nerve terminal, as in peripherally originating fasciculation potentials (see Stålberg & Trontelj 1982).

"Myokymic" fibrillations and end plate spikes can be distinguished by their firing pattern. "Myokymic" fibrillations fire in short high-frequency bursts, doublets and triplets and they may be found at any region in the muscle. Needle insertion does not activate them. End plate spikes show sustained firing with a very irregular rhythm with numerous short but also long intervals, and the mean interval lengthens if the needle is not moved. End plate spikes are found in the active spots of the muscle being studied, often associated with miniature end plate potentials and pain (Wiederholt 1970).
