**4.2. End plate spikes**

Jasper and Ballem (1949) were the first to describe end plate spikes in clinical EMG: "Action potentials comparable to those described by Snodgrass and Sperry (mammalian muscle action potentials of less than a millisecond) were sometimes seen from limb muscles were thought to have been derived from nerve filaments since they were usually associated with particularly acute pain (as though the needle tip were penetrating a nerve) and were of the same form as those obtained when the needle was deliberately inserted in nerve". Kugelberg & Petersén (1949) described end plate spikes as "protracted irregular activity". "Such discharge was mostly irregular, might be ordinary motor unit potentials as in fasciculation or little amplitude and duration as in fibrillation. The activity in question cannot be voluntarily controlled. It does not disappear in relaxation, nor does it increase in frequency on slight voluntary contraction. A slight pressure or bending of the needle may increase the frequency while a discharge is going on, start new ones or reactivate potentials which had stopped".

Jones et al. (1955) further studied the origin of end plate spikes as "nerve potentials" with iron marksat sitesoftheirappearanceandfoundmostofthese irondots close toperipheralintramus‐ cular nerve twigs. Buchthal & Rosenfalck (1966) observed that miniature end plate potentials (MEPPS) were often associated with end plate spikes, "spontaneous diphasic potentials". They conjectured that these potentials originated in the muscle fibres, "several synchronized minia‐ turepotentialsattaininganamplitude sufficienttoelicitapropagatedresponse".Finally,Brown & Varkey (1981) proved "nerve potentials" to be postsynaptic potentials, recorded from muscle fibres.Endplatespikesshowveryirregularfiringpatternwithnumerousshortintervalslessthan 30 ms and gradual slowing of the firing (Partanen 1999).

The prevailing hypothesis concerning end plate spikes states that they are elicited by nerve irritation caused by the needle electrode and recorded postsynaptically by the same needle electrode (Brown & Varkey 1981). However, injury potentials of peripheral motor nerve fibres present a different firing pattern (Wall et al. 1974, Macefield 1998). Thus there is an obvious discrepancy between the sustained firing pattern of end plate spikes and experimentally observed real firing patterns of injured or irritated motor axons. Firing of end plate spikes differs also from abnormal firing patterns of motor nerve fibres or motor units (see Willison, 1982, Stålberg & Trontelj 1982). On the other hand, there is evidence that end plate spikes actually represent action potentials of intrafusal muscle fibres and beta motor units (Partanen & Nousiainen 1983, Partanen 1999, Partanen et al. 2010). The propagation patterns of intrafusal nuclear bag and nuclear chain muscle fibres (Barker at al. 1978) are similar to those of end plate spikes (Partanen & Palmu 2009, Partanen 2012).

## **4.3. Wave form of fibrillation potentials and end plate spikes**

It was emphasized that end plate spikes, ("spontaneous diphasic potentials"), which have a negative onset at the end plate zone, may show positive onset phase as fibrillation potentials do

when they are propagated outside the end plate zone and thus the form of the potential is indistinguishable from that of a fibrillation potential (Buchthal & Rosenfalck 1966). We note that there is a distinct difference between the wave forms of end plate spikes and fibrillation poten‐ tials. The former show either a negative onset or a short positive onset, whereas fibrillation potentialsshowapositiveonsetwhichalwaysislongerthanthatofendplatespikes(seeResults). However, the amplitude and spike duration of fibrillation potentials and end plate spikes are similar (Table 1). We have observed fibrillation potentials with negative onset, (mainly as "negative sharp waves", obviously cannula-recorded positive sharp waves with inverted polarity),butthesearerareanddonothappentobepresentinthematerialcollectedforthiswork. This fact is not in concert with the data published earlier, which state that a considerable number of fibrillation potentials may have a negative onset (Buchthal & Rosenfalck 1966, Heckmann & Ludin 1982). In any case fibrillation potentials and end plate spikes may be distinguished both by the firing pattern and the wave form at the onset of the potential (Fig. 7).

also be mixed forms of fibrillations, with mainly regular rhythm but sudden changes of the

Jasper and Ballem (1949) were the first to describe end plate spikes in clinical EMG: "Action potentials comparable to those described by Snodgrass and Sperry (mammalian muscle action potentials of less than a millisecond) were sometimes seen from limb muscles were thought to have been derived from nerve filaments since they were usually associated with particularly acute pain (as though the needle tip were penetrating a nerve) and were of the same form as those obtained when the needle was deliberately inserted in nerve". Kugelberg & Petersén (1949) described end plate spikes as "protracted irregular activity". "Such discharge was mostly irregular, might be ordinary motor unit potentials as in fasciculation or little amplitude and duration as in fibrillation. The activity in question cannot be voluntarily controlled. It does not disappear in relaxation, nor does it increase in frequency on slight voluntary contraction. A slight pressure or bending of the needle may increase the frequency while a discharge is

Jones et al. (1955) further studied the origin of end plate spikes as "nerve potentials" with iron marksat sitesoftheirappearanceandfoundmostofthese irondots close toperipheralintramus‐ cular nerve twigs. Buchthal & Rosenfalck (1966) observed that miniature end plate potentials (MEPPS) were often associated with end plate spikes, "spontaneous diphasic potentials". They conjectured that these potentials originated in the muscle fibres, "several synchronized minia‐ turepotentialsattaininganamplitude sufficienttoelicitapropagatedresponse".Finally,Brown & Varkey (1981) proved "nerve potentials" to be postsynaptic potentials, recorded from muscle fibres.Endplatespikesshowveryirregularfiringpatternwithnumerousshortintervalslessthan

The prevailing hypothesis concerning end plate spikes states that they are elicited by nerve irritation caused by the needle electrode and recorded postsynaptically by the same needle electrode (Brown & Varkey 1981). However, injury potentials of peripheral motor nerve fibres present a different firing pattern (Wall et al. 1974, Macefield 1998). Thus there is an obvious discrepancy between the sustained firing pattern of end plate spikes and experimentally observed real firing patterns of injured or irritated motor axons. Firing of end plate spikes differs also from abnormal firing patterns of motor nerve fibres or motor units (see Willison, 1982, Stålberg & Trontelj 1982). On the other hand, there is evidence that end plate spikes actually represent action potentials of intrafusal muscle fibres and beta motor units (Partanen & Nousiainen 1983, Partanen 1999, Partanen et al. 2010). The propagation patterns of intrafusal nuclear bag and nuclear chain muscle fibres (Barker at al. 1978) are similar to those of end plate

It was emphasized that end plate spikes, ("spontaneous diphasic potentials"), which have a negative onset at the end plate zone, may show positive onset phase as fibrillation potentials do

interval (Partanen & Danner 1982, Conrad et al. 1972).

50 Electrodiagnosis in New Frontiers of Clinical Research

going on, start new ones or reactivate potentials which had stopped".

30 ms and gradual slowing of the firing (Partanen 1999).

spikes (Partanen & Palmu 2009, Partanen 2012).

**4.3. Wave form of fibrillation potentials and end plate spikes**

**4.2. End plate spikes**

**Figure 7.** The positive deflection before the main spike component (pair of arrows) is shorter in averaged end plate spike (EPS) than in averaged fibrillation potential (fibr). The averaged mean potential is shown with ± 1 SD curves. From Partanen, J. (1999), Author´s own work.

The formation of the shape of end-plate spikes was extensively studied by Dumitru (2000) according to the needle irritation hypothesis of peripheral nerve branch or nerve terminal (tip or shaft irritation of the terminal nerve). He explained the formation of biphasic and triphasic 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.

fibre eliciting a large number of f.o.p.s., which mainly reactivate the fibre immediately after the refractory period of a spontaneous potential. An occasional failure of a f.o.p. to occur may be seen as a pause in the fibrillation sequence. We have rarely observed a slightly irregular fibrillation sequence even without pauses, evidently representing a muscle fibre with a large number of f.o.p.s. On the other hand, random fibrillations may be associated with very infrequently occurring f.o.p.s. In any case, regular fibrillations are the first to be present also in experimental studies and irregular fibrillations arise later on (Purves & Sakmann 1974, Smith

Different Types of Fibrillation Potentials in Human Needle EMG

http://dx.doi.org/10.5772/55352

53

"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

"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

It is of utmost importance that a clinical neurophysiologist performing ENMG studies recognizes different types of spontaneous activity. Confusing end plate spikes with fibrillation potentials may cause false positive findings of axonal damage. Even the difference between rhythmic and irregular fibrillation potentials may be difficult to grasp and there are differences between individual examiners in this respect (Trillenberg & Spencer 2010). False classification of potentials is a frequent error, especially among resident-level examiners (Kendall & Werner 2006). We studied parameters by which it could be possible to distinguish between different

& Thesleff 1976).

**4.5. "Myokymic" fibrillations**

Stålberg & Trontelj 1982).

**5. Comments**

potentials and pain (Wiederholt 1970).
