normal needle electromyographic insertional activity morphology: a clinical and simulation study

ABSTRACT: Needle electromyographic insertional activity waveform mor-phology, and mechanisms of generation, have received little attention. Thisstudy analyzes the individual component waveforms that contribute to theburst of electrical activity known as insertional activity. One hundred mo-nopolar needle insertions were slowly performed and high speed recorded toallow better separation of the contributing individual component waveforms.Analysis of the many waveforms recorded demonstrates several classes ofpotentials. All of these could be reconstructed by the summation of two basicor elementary waveform patterns: a biphasic initially negative spike with orwithout a ‘‘prepotential’’ similar to an end-plate spike, and the biphasic ini-tially positive spike with a slowly declining negative phase, similar to a posi-tive sharp wave, though shorter in duration. The relationship between theseelementary waveforms and their hypothesized generator sources is dis-cussed.

© 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 910–920, 1998

NORMAL NEEDLEELECTROMYOGRAPHIC INSERTIONALACTIVITY MORPHOLOGY:A CLINICAL AND SIMULATION STUDY

DANIEL DUMITRU, MD,1 JOHN C. KING, MD,1 and DICK F. STEGEMAN, PhD 2

1 Department of Rehabilitation Medicine, University of Texas Health Science Centerat San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78284-7798, USA2 Institute of Neurology, Department of Clinical Neurophysiology, UniversityHospital Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands

Received 6 August 1997; accepted 2 January 1998

Insertional activity is the electrical activity generatedby electrode insertion during the needle electromyo-graphic examination.5,10 This type of electrical activityis believed to represent mechanical depolarizationof multiple single muscle fibers as the needle elec-trode’s active recording surface advances through,and physically displaces, muscle fibers.10 Preciouslittle quantitative information is available regardinginsertional activity evoked in healthy muscle tissue.When a monopolar needle electrode is inserted intonormal muscle tissue in 1–5-mm increments, the to-tal time of associated electrical activity is less than230 ms.14–16 Electrical activity persisting after needlecessation is found to approximate 48 ms. In this in-vestigation, it is hypothesized that the observed in-sertional activity arises from single muscle fiber dis-charges induced by mechanical depolarization andcomprised of a limited number of characteristic

waveform morphologies. An additional hypothesis isthat these fundamental waveforms summate to pro-duce all observed electrical activity during needleinsertion.

MATERIALS AND METHODS

Needle Insertional Activity. Subjects. Ten subjectswithout history or physical examination evidence ofneuromuscular disease agreed to participate in thisinvestigation. The volunteers (7 males) had a meanage of 35.6 years. This investigation complied withinstitutional policies for informed consent.

Instrumentation. A disposable monopolarneedle (DMG 37; TECA Corp., Pleasantville, NY) wasused to collect all insertional activity. The referenceelectrode was positioned adjacent to the site ofneedle insertion with a ground electrode secured tothe olecranon. An electromyograph (Cadwell 5200A;Cadwell Corp., WA) with the following parameterswas used to collect data: sweep speed of 2 ms/cm,sensitivity of 200 µV/cm, high/low pass filter settingsof 10 Hz and 10,000 Hz, respectively. All data col-lected were stored to the instrument and subse-quently analyzed.

Key words: volume conduction; insertional activity; single muscle fiber;needle electromyography; needle electrodeCorrespondence to: Dr. Daniel Dumitru

CCC 0148-639X/98/070910-11© 1998 John Wiley & Sons, Inc.

910 Insertional Activity MUSCLE & NERVE July 1998

Data Collection/Analysis. All subjects were com-fortably positioned in the supine position with theforearm supinated. The monopolar needle elec-trode was inserted perpendicular to the skin overly-ing the midportion of the right biceps brachiimuscle at the junction between the proximal twothirds and distal one third. The electrode was thenqualitatively inserted into all subjects relatively slowlycompared to routine needle electromyographictechniques6,16 by one of the investigators (DD) inapproximately 1-mm increments over a time intervalapproaching one half second. The electrode was re-peatedly advanced into the muscle tissue for a depthof several centimeters. It was then withdrawn andinserted in a different direction with the above-described methodology. A preliminary investigationsuggested that two fundamental single muscle fiberdischarges comprise normal needle insertional activ-ity.6 The above documentation of needle insertionalactivity was continued until 10 potentials for each ofthese two fundamental insertional waveforms werecollected. The duration (initial departure from, andfinal return to baseline) and peak-to-peak amplitudeof these two potentials were then quantified as wellas the presumed duration of depolarization (nega-tive or positive onset to subsequent major negativeor positive peak, respectively) and repolarization(major negative or positive peak to waveform termi-nation). All waveforms were stored for later analysis.Care was taken to avoid recording end-plate poten-tials.

Simulation Studies. Insertional Potential Morphology.A computer program previously utilized to simulatenear-field and far-field muscle potentials was used.7

Appropriate fiber diameters, conduction velocities,and volume conductor characteristics were incorpo-rated into the model to ensure the use of appropri-ate physical and physiologic parameters for muscletissue.7,13

The muscle fiber was assigned a finite length of50 mm. The initiation and termination of the musclefiber were formulated as ‘‘cut’’ ends,4 whereby activetissue terminated to simulate the musculotendinousjunction. An action potential was initiated at the fi-ber’s midportion with action potential propagationproceeding bidirectionally. Simulated recordings 50µm radially from the fiber’s center were performedat the site of action potential initiation and at one ofthe muscle fiber’s termination. The ensuing poten-tials from these two locations were recorded andcompared to the two fundamental insertional poten-tials obtained clinically.

Waveform Summation. One of this investigation’shypotheses was that two fundamental waveforms aris-ing from needle insertion can summate with eachother or potentials of similar morphology to yield allof the clinically observed potentials comprising in-sertional activity. Representative potentials of thefundamental waveforms detected from this study’sclinical portion were scanned and digitized usingSigma Scan Image/Plot (Jandel Scientific, San Ra-fael, CA) so that a numeric representation of thefundamental waveforms could be created. Thesewaveforms were then summated with appropriateand physiologically reasonable interpotential timerelationships and magnitude modifications in an at-tempt to reproduce all waveform morphologies de-tected during the clinical portion of this investiga-tion.

RESULTS

Needle Insert ional Act iv i ty . Data Co l l e c -tion/Analysis. Ten individual potentials were col-lected from each subject for the two fundamentalwaveform types identified (Fig. 1, B1–4). Thus, a to-tal of 100 waveforms for each of the two distinctpotentials were available for analysis. Typically,needle insertion produces a burst of electrical activ-ity rendering individual waveform identification im-possible (Fig. 1D). However, slowly inserting aneedle electrode into muscle tissue permits identifi-cation of more discrete muscle fiber discharges (Fig.1E). In addition to the fundamental waveforms de-tected (Fig. 1, B1–4), other distinct but stereotypicalwaveforms arising from needle insertion could bedocumented (Figs. 2 and 3).

One of the fundamental insertional waveformtypes had a morphology that distinctly resembled aprototypical biphasic end-plate spike (Fig. 1, A1compared to B1–3). This potential type demon-strated a variable magnitude initially negative ‘‘pre-potential’’ of variable duration prior to forming themajor negative peak (Fig. 1, B1–3). The second typeof fundamental insertional activity closely resembleda positive sharp wave (Fig. 1, B4), but with a shortduration.

The mean plus one standard deviation for thebiphasic initially negative insertional spike poten-tials’ negative-to-positive peak-to-peak amplitude was476.58 ± 599.6 µV (50–5250 µV). The mean depo-larization time plus one standard deviation wasfound to be 1.06 ± 0.47 ms (0.5–2.6 ms), while thetime of repolarization was 3.29 ± 0.75 ms (2.0–5.0ms) for a total potential duration of 4.34 ± 0.98 ms(2.6–7.0 ms). The mean plus one standard deviationfor the biphasic initially positive insertional poten-

Insertional Activity MUSCLE & NERVE July 1998 911

tials’ positive-to-subsequent negative peak-to-peakamplitude was 577.0 ± 712.76 µV (125.0–5000.0 µV).The mean presumed depolarization time plus onestandard deviation for this potential was 0.94 ± 0.27ms (0.4–2.0 ms), while the mean repolarization was9.48 ± 2.06 ms (4.0–16.0 ms) for a total waveformduration of 10.42 ± 2.2 ms (4.8–18.0 ms).

The respective mean depolarization and repolar-ization ratios for the positive compared to negativespike forms of insertional activity were found to ap-proximate 0.9 (0.94 ms/1.06 ms) and 2.9 (9.48ms/3.29 ms), while the total waveform duration ratiofor the positive to negative spike forms was 2.4 (10.42ms/4.34 ms). Nonparametric paired analysis of the

FIGURE 1. (A) An end-plate spike recorded with a monopolar needle is shown (A1). Note the presence of a small ‘‘prepotential’’ (arrow).A second end-plate spike is depicted with a more prominent ‘‘prepotential’’ (arrow; A2). (B) The negative spike form of insertional activitydemonstrating a variable degree of an initial ‘‘prepotential’’ (arrows) comprising the negative spike (B1–3). A second type of fundamentalinsertional potential was observed, which was designated a positive spike form resembling a positive sharp wave (B4). (C) Simulatedrecordings from the site of action potential initiation (C1) and termination (C2), which closely resemble the two types of insertional spikeforms (B1–4). (D) Typical morphology of insertional activity recorded with a monopolar needle during the needle electromyographicexamination. (E) Slowly inserting the monopolar needle into muscle tissue with a small spatial displacement permits detection of individualwaveforms.


presumed depolarization times for the negative andpositive spike forms of insertional activity were notstatistically different (P > 0.05). The presumed repo-larization times, however, were significantly different(P < 0.05). The respective peak-to-peak magnitudes

for the two fundamental insertional spike potentialswere not significantly different (P < 0.05).

Simulation Studies. Insertional Potential Morphology.The two fundamental waveform morphologies

FIGURE 2. (A) Clinically detected (A1) and simulated (A2) bifid negative/positive spike insertional potentials. (B) Clinically recorded (B1)and simulated (B2) bifid positive/negative insertional waveforms. (C) A clinically documented (C1) and a simulated (C2) quadraphasicpotential are depicted. (D) Altering the magnitude of the positive spike waveform results in a larger initial positive and smaller subsequentnegative spike to the quadraphasic potential shown in (A) for simulated (D2) compared to clinically observed (D1) potentials. (E) Furtherincreases in the magnitude of the positive spike template produce a simulated biphasic potential (E2) that compares favorably with thatrecorded clinically (E1).


of insertional activity detected, major negative andpositive spike forms, are suggested to arise from dis-tinct regions of an active membrane according tovolume conductor theory.11 A situation is first simu-lated where the recording electrode is assumed to bewithin close proximity of the muscle membrane, andthe action potential is initiated at the recording elec-trode’s location. This action potential is then as-sumed to propagate away from the electrode. Theresulting simulated potential demonstrates an initialnegative onset that peaks to form a major negativespike (Fig. 1, C1) and then descends below the base-line to form a smaller terminal positive phase. Thispotential has a morphology similar to that detectedclinically for both end-plate spikes (Fig. 1, A1–2),

and the major negative spike form of insertionalwaveforms (Fig. 1, B1–3).

The second simulated waveform, or biphasic ini-tially positive potential, is modeled to occur at a por-tion of the muscle fiber where action potential ter-mination occurs, e.g., the musculotendinousjunction or a presumed needle-induced action po-tential blockade. A recording electrode is positionedat the end of a muscle fiber while an action potentialis initiated at a sufficient distance from the electrodeso as to produce an initial positive and not negativewaveform deflection. The waveform detected duringthis simulation has an initial positive spike followedby a comparatively smaller terminal negative phase,which settles back to baseline (Fig. 1, C2). A simu-

FIGURE 3. A family of triphasic waveforms is depicted with an initial negative phase followed by a prominent positive phase and a terminalnegative phase. (A) A clinically observed potential resulting from needle insertion (A1) can be simulated (A2) by combining a negativeand positive spike form of insertional activity. (B) The negative spike insertional potential with a ‘‘prepotential’’ (arrow) can be summatedwith a positive spike waveform to simulate (B2) potentials recorded clinically (B1). (C) and (D) Primary positive spike potentials withvarying degrees of ‘‘prepotentials’’ (arrows) can be observed (C1 and D1). These waveforms can be simulated by combining negativespike waveforms with positive spike waveforms (C2 and D2).


lated potential (Fig. 1, C2) with a close resemblanceto the clinically recorded major positive spike formof insertional activity is documented (Fig. 1, B4).

There are noted to be some morphologic differ-ences in the relationship between the two simulatedand clinically recorded forms of insertional spike po-tentials. The major negative spike form of clinicallyrecorded insertional activity has a variable degree ofan initial ‘‘prepotential,’’ while the simulated poten-tial only demonstrates a small ‘‘prepotential’’ priorto development of the major negative spike. This isbecause the same intracellular action potentialmodel is used for all simulation studies. Altering theshape of the intracellular action potential wouldgenerate waveforms with different duration prepo-tentials. However, the mean durations of the clini-cally recorded (Fig. 1, B1) and simulated (Fig. 1, C1)negative spike waveforms are similar in that they ap-proximate 4 ms. Another notable difference be-tween the simulated and clinically recorded wave-forms concerns the major positive spike potential.The morphologic appearance is quite similar be-tween the clinical and simulated potentials. How-ever, the duration of the simulated waveform (Fig. 1,C2) is similar to the clinically detected (Fig. 1, B1)and simulated (Fig. 1, C1) initial negative spike wave-form at about 4 ms, while the clinically recordedpositive spike waveform (Fig. 1, B4) has a mean du-ration just over twice that of the simulated positivespike potential at 10.42 ms.

Waveform Summation. Analysis of the data col-lected from the 10 subjects resulted in the identifi-cation of individual waveforms sufficiently separatedin time whereby nine distinct potential morpholo-gies were identified (Figs. 2 and 3). No attempt was

made to determine the frequency of waveform oc-currence, since the ability of the waveforms to begenerated at sufficient intervals to preclude overlapwas deemed random and primarily dependent uponneedle movement as opposed to some intrinsic qual-ity of the muscle fiber. Two template waveformswere summated to produce all of the clinically ob-served insertional waveforms. The first templatewaveform’s magnitude (designated Template #1 andderived from Fig. 1B; Table 1) was increased or de-creased by a mathematical constant. A second tem-plate (designated Template #2 and derived form Fig.1B) waveforms’ magnitude was not changed or in-creased by a mathematical constant but delayed intime with respect to the first template’s onset. Thesetwo waveforms were then summated to generate asimulated waveform (Figs. 2 and 3) and qualitativelycompared to waveforms documented clinically (Figs.2 and 3).

The simulated waveforms were divided into threemajor groups based upon which of the two funda-mental waveforms, positive or negative spike form,and in what order, had to be summated to producethe clinically documented potentials. The first group(Group 1; Table 1) consisted of summating twonegative spike forms of fundamental potential, whilethe second group (Group 2; Table 1) conformed tosummating two of the positive spike forms of funda-mental potentials. A third group (Group 3) arosefrom combining the major negative and positivespike forms of fundamental potentials. This groupwas then divided into two subgroups based uponwhether the negative (Group 3A) or positive (Group3B) spike form of insertion activity was delayed intime with respect to the other potential (Table 1).

Table 1. Simulated compared to clinically detected waveforms.

Template #1 + Template #2 = Simulated waveform Clinical waveform

Group 10.4 (1B-1) 1.0 (1B-1) + 0.8 ms 2A-2 2A-1

Group 21.0 (1B-4) 1.0 (1B-4) + 1.0 ms 2B-2 2B-1

Group 3A0.5 (1B-4) 1.0 (1B-1) + 0.3 ms 2C-2 2C-11.5 (1B-4) 1.0 (1B-1) + 0.2 ms 2D-2 2D-11.85 (1B-4) 1.0 (1B-1) + 0.3 ms 2E-2 2E-1

Group 3B0.55 (1B-1) 1.0 (1B-4) + 0.0 ms 3A-2 3A-11.0 (1B-2) 1.3 (1B-4) + 3.2 ms 3B-2 3B-11.0 (1B-2) 6.85 (1B-4) + 3.0 ms 3C-2 3C-11.0 (1B-3) 9.6 (1B-4) + 5.0 ms 3D-2 3D-1

The first column designates one of the template waveforms found in Figure 1, multiplied by a mathematical factor to increase or decrease itsamplitude. The second column also designates a template waveform found in Figure 1 multiplied by a mathematical factor to increase or decrease itsamplitude as well as a time delay in milliseconds for the second waveform’s onset compared to the first waveform’s onset. The two templates arearithmetically summated to generate the desired simulated waveform (see Figs. 2 and 3) as compared to the clinical waveform (see Figs. 2 and 3).


DISCUSSION

Needle electromyographic insertional activity is aroutine portion of the electrodiagnostic medicineevaluation. Typically, a large burst of electrical activityis associated with electromyographic needle displace-ment (Fig. 1D). No attempt is made to quantitativelyassess this activity, since it is a conglomeration ofmultiple waveforms with seemingly no discerniblepattern.14–16 In this investigation, the needle elec-trode is gently inserted in small increments in com-bination with assessment of the instrument’s monitorso as to evoke only a minimal degree of associatedelectrical activity.

It is presumed that the documented needle elec-tromyographic insertional activity arises from me-chanical depolarization of single muscle fibers, al-though the metallic half-cell potential may alsocontribute to depolarization. The single fiber dis-charge assumption appears justified, provided themuscle is at rest and there is no detected electricalactivity prior to needle movement. The slow inser-tions also minimize any contributions from a half-cell moving through variable tissue impedances. Apreliminary investigation suggests there are two fun-damental single-fiber waveforms generated duringneedle passage through healthy muscle tissue.6 De-spite the observation of multiple additional poten-tials with distinct morphologies, it is hypothesizedthat these potentials can be derived from uniquecombinations of the two previously identified funda-mental waveforms.

The first type of fundamental waveform consistedof an initial negative spike with a terminal positivephase (Fig. 1, B1). This potential had a striking re-semblance to the biphasic initially negative end-platespike observed when a needle electrode is located ina muscle’s end-plate region (Fig. 1, A1). An initialnegative deflection associated with any recordedwaveform suggests that the potential originates atthe electrode’s location and propagates away (Fig.4A–G, E-1A).8,11 As demonstrated by simulation stud-ies, a suprathreshold potential originating at, andpropagating away from, the electrode should indeedhave an initial negative deflection (Fig. 1, C1 andFig. 4A–G, E-1A). Hence, it was concluded that thenegative spike form of insertional activity originatedat, and propagated bidirectionally away from, theelectrode’s active recording surface as it mechani-cally or by means of half-cell potential depolarizedthe muscle fiber. Three insertional waveforms withvariable duration ‘‘prepotentials’’ were observed inthis investigation (Fig. 1, B1–3). Clinically observedend-plate potentials also have variable-duration‘‘prepotentials,’’ suggesting that the membrane is

approaching its threshold value prior to undergoingthe synchronous opening of multiple sodium chan-nels (Fig. 1, A1–2).2 By analogy to end-plate spikes, itis suggested that the initially negative insertionalspike potentials have variable duration ‘‘prepoten-tials’’ dependent upon the degree of mechanical in-teraction between the electrode and muscle fiber.Sliding of the needle may submaximally activate themuscle membrane for variable intervals, resulting indifferent times to threshold and hence maximalnegative spike formation (Fig. 1, B1–3).

The second type of fundamental insertionalwaveform appears very similar to the prototypicalpositive sharp wave (Fig. 1, B4). Positive spike inser-tional waveforms in this study, however, had dura-tions approaching 10 ms and not the longer dura-tions observed for positive sharp waves. A similarpositive spike waveform is generated by the simula-tion study when a recording is performed where anaction potential reaches the end of active tissue (Fig.4D–G, E-1B). This type of waveform morphologyconforms to the classic volume conductor studieswhere recordings are performed at the end of activeneural and muscle tissues.8,11 Initially, the action po-tential propagates up to the recording electrode.This generates a waveform with an initial positivedeflection (Fig. 4D, E-1B). The action potential’sleading dipole then dissipates, because there is nolonger active tissue to sustain it (Fig. 4E). The trail-ing dipole’s negativity is then detected, which gen-erates a negative spike (Fig. 4E and F). The corre-sponding negative spike is comparatively small,because the trailing dipole has a longer spatial ex-panse and an associated lower current density. Thewaveform then settles back to baseline as the trailingdipole dissipates (Fig. 4G).

The above information permits speculation re-garding the formation of the positive spike form ofinsertional activity. It is hypothesized that the needleelectrode can compress single muscle fibers duringadvancement precluding depolarization at the site ofneedle/tissue contact. However, the needle’s me-chanical deformation of muscle tissue induces a de-polarization immediately adjacent to the constrictedregion of tissue. An action potential is then gener-ated about the electrode, which results in an initialpositive deflection (Fig. 4H–I). Because the actionpotential is precluded from propagating past theelectrode, a situation arises similar to that for a re-cording at the muscle’s musculotendinous junction(Fig. 4D–G). The action potential’s leading dipolebegins to dissipate with an associated reduction inthe waveform’s initial positive deflection (Fig. 4J).The trailing dipole’s negativity is detected, which


generates the comparatively smaller negative phase(Fig. 4J–K). As the trailing dipole dissipates, a bipha-sic initially positive waveform results which is identi-cal to that anticipated from volume conductor the-ory8,11 and this study’s simulations (Fig. 4L–M).

In this study, the presumed duration of depolar-ization for the two insertional template potentialswas assumed to correlate to the time span betweenpotential onset and the potential’s respective majornegative or positive peak.13 There was found to beno statistically significant difference for this pre-sumed depolarization time, about 1.0 ms, betweenthe negative and positive spike insertional potentials.The duration of presumed repolarization was as-sumed to extend from the respective insertional po-tential’s major spike to the waveform’s termination.The positive spike form of insertional activity had amean time of repolarization approximately three

times that of the negative spike waveform. Thesedata suggest that whatever the cause of action poten-tial blockade, depolarization appears minimally af-fected, while repolarization appears preferentiallyslowed.

As noted above, a possible etiology with respectto an alteration in repolarization is that the positivespike form of insertional activity arises from sometype of adverse mechanical interaction between themuscle fiber and recording electrode (Fig. 4G–M).This interaction may be composed of, in whole orpart, a physical compression of the fiber elevatingthe muscle fiber’s internal impedance to such a levelthat internal current is precluded from completingthe local circuit current necessary to sustain the ac-tion potential’s forward movement. Alternatively,some form of adverse interaction between the elec-trode and the membrane’s sodium/potassium chan-

FIGURE 4. (A) An action potential is initiated (small quadrupole: +−−+) at the site of a monopolar electrode (E-1A). (B) and (C) The actionpotential reaches threshold (large quadrupole: +−−+), generates a large negative spike, and then propagates away from the electrode,resulting in terminal positive phase. (D) An electrode (E-1B) located at the fiber’s termination detects the quadrupole’s advancing positivityand records a waveform with an initial positive deflection (E-1B). (E) The leading dipole dissipates, with an ensuing decline in thewaveform’s positive deflection (F) and (G) A comparatively smaller terminal negative phase is documented when the trailing dipole’snegativity is detected. The waveform settles back to baseline with dissipation of the trailing dipole. (H–M) An action potential is initiatedimmediately adjacent to a region rendered incapable of depolarization (shaded area) by a recording electrode (E-1C). The electrodedetects an initial positive deflection followed by a terminal negative phase (E-1C) associated with dissipation of the trailing dipole,resembling the situation depicted in (D–G).


nels may also occur. In either case, the time of de-polarization and hence sodium channel functionappears not to be significantly affected up to wherethe action potential blockade occurs. However, theprolonged repolarization phase possibly suggeststhat sodium inactivation and/or the delayed potas-sium activation are affected such that repolarizationis prolonged. This effect is reminiscent of the effectsof temperature on depolarization/repolarization,where depolarization is minimally altered, but so-dium inactivation and repolarization are consider-ably slowed.1,12 An alternative explanation may bethat both sodium and potassium channels are simi-larly affected, however, the proximity of the actionpotential’s initiation site to the electrode results in ahigh-density sodium current, thus achieving a maxi-mal positive amplitude rather quickly. This effectmay preferentially mask a prolongation in sodiumchannel activation. Further research is required toclarify the distinction between the above possibili-ties.

The first potential simulated in this investigationconformed to a biphasic initially negative potentialwith a bifid negative spike (Fig. 2, A-1). It was nec-essary to summate two negative spike template po-tentials to simulate the clinically observed waveform(Fig. 2, A-2). One of the potentials was reduced inmagnitude by 60%, while the other potential wasdelayed in time 0.8 ms with respect to the first (Table1). Although it may seem somewhat arbitrary to alterthe template potentials’ magnitude and time rela-tionships, these parameters can be justified. Specifi-cally, the magnitudes of potentials are inversely pro-portional to the distance of the potentials from therecording source as well as the location of the bio-electric source along the monopolar needle’s coni-cal recording surface.9 The size relationship of themonopolar needle’s exposed metal surface and thediameter of single muscle fibers permit multiplemuscle fibers to align along the electrode’s conicalactive recording surface. It is entirely conceivablethat two fibers have a slightly different distance rela-tionship with respect to the electrode’s active record-ing surface, resulting in different amplitude poten-tials. Additionally, as the needle electrode slipsthrough tissue, it stands to reason that deeper fiberswill be activated later in time than more superficialfibers. This time delay is directly dependent uponthe distance of separation between the fibers andhow fast the electrode is inserted into the tissue aswell as how quickly each fiber reaches its respectivemembrane threshold voltage. Therefore, several fi-bers may be activated along the electrode’s core withslightly different magnitude and depolarization on-

sets. The various magnitudes and temporal relation-ships used in this investigation for simulating clini-cally detected waveforms appear reasonable giventhe sequential activation of muscle fibers duringneedle insertion and the corresponding relativewaveform amplitudes documented clinically (50–5250 µV).

The second potential simulated appeared mor-phologically as a bifid positive spike insertional po-tential (Fig. 2, B1). Simply summating two positivespike insertional template potentials with the seconddelayed by 1.0 ms generated a simulated potentialwith an appearance similar to that recorded clini-cally (Fig. 2, B2; Table 1). Many different variationsof this type of potential can be observed clinicallyduring needle insertion. The first or second peak ofthe primary positive spike may be larger or smaller aswell as separated by more or less time. A smallerinitial positive bifid peak can result from a slightlysmaller magnitude positive spike template. The in-terpeak latency can be altered by increasing or de-creasing the delay of the second compared to firstpositive spike potential.

Three potentials with an initial positive deflec-tion appeared to be related with respect to how theyare generated (Fig. 2, C1, D1, and E1). Simulationstudies suggest that a positive spike insertional po-tential is combined with a time-delayed negativespike insertional potential. Varying the magnitude ofthe positive spike insertional potential and adjustingthe time delay between 0.2 ms and 0.3 ms resulted inthe generation of simulated potentials with similarappearances to those waveforms clinically detected(Fig. 2, C2, D2, and E2; Table 1).

The last set of simulated waveforms consisted ofan insertional spike template potential summatedwith a time-delayed positive spike template potential.A sharp initial negative deflection followed by alarger positive spike with a terminal negative phasecan be generated by a comparatively smaller nega-tive insertional spike combined with a positive inser-tional spike (Fig. 3, A1–2; Table 1). The initial por-tion of the positive spike potential partially reducesthe insertional negative spike’s peak magnitude. Theterminal portion of the positive spike template isessentially unaffected, thus generating this type oftriphasic potential. A second type of triphasic poten-tial appears similar to a negative spike form of inser-tional activity, with the exception of a prominentterminal negative phase (Fig. 3, B1). Summating anegative spike insertional potential with a somewhatlarger positive insertional potential time-delayed by3.2 ms permitted the initial portion of the negativeand terminal portion of the positive spike potentials


to become manifest, generating the clinically ob-served waveform (Fig. 3, B1–2; Table 1). The last twopotentials observed appeared similar to a positivespike form of insertional activity, but with a variable-duration initially negative ‘‘prepotential’’ (Fig. 3, C1and D1). These waveforms could be simulated bysummating each of the negative spike forms of in-sertional activity with different-duration ‘‘prepoten-tials’’ (Fig. 1, B2 and B3) with a magnified positivespike waveform (Fig. 1, B4) delayed an appropriateamount in time to permit formation of the initial‘‘prepotential’’ but eliminate the negative spike(Table 1).

Another phenomenon that should be consideredto contribute in part to the observed waveforms isthe electrode-associated half-cell potentials. Metal incontact with an ionic solution generates what is re-ferred to as a static half-cell potential. Over time, anequilibrium is established between the electrode’smetal atoms remaining in the electrode and thosemetal atoms leaving the electrode to enter the solu-tion. This process results in an electrical potentialdifference between the solution and the electrode.Both the advancing monopolar needle and the sur-face reference electrode possess such half-cell poten-tials. These half-cell potentials are typically notdetected by the electromyographic instrument, be-cause they build up relatively slowly and in effectconstitute a direct current voltage generator, whichis not registered by the instrument. However, if theelectrodes are moved, a time-varying potential (alter-nating current generator) can be transiently in-duced and detected by the instrument. Similarly, it isconceivable that the monopolar needle’s half-cellpotential can be disturbed and hence detected byrapidly advancing electrodes through the varying im-pedances of different muscle layers and contributingat least in part to insertional activity. It is presentlyunclear if the routinely observed needle electromyo-graphic insertional activity is comprised of purelythese detected disturbances in the electrode’s half-cell potential, arises from primarily single muscle fi-ber discharges, or some combination of the two. It isunlikely that insertional activity consists of only half-cell potentials measured from altering impedancesand solutions between electrodes, since insertionalactivity decreases dramatically in dead muscle.3 Thepresent assumption is that insertional activity arisingfrom rapid as well as slow needle insertions primar-ily, if not exclusively, consists of single muscle fiberdischarges. This investigation demonstrates how thetypical potentials recorded by slow needle insertions,whether due to half-cell potential interactions orfrom single muscle fiber depolarizations, for which

they seem more characteristic, can be described by asimple combination of two fundamental waveformtypes. Further elucidation of what proportion of in-sertional activity arises from single muscle fiber dis-charges or half-cell discharges requires additional in-vestigation.

This investigation documents that it is feasible torecord individual waveforms comprising needle elec-tromyographic insertional activity. Further, althoughmultiple distinct waveforms are documented, thereappear to be just two fundamental insertional poten-tials, consisting of a positive and negative spike form.These two potentials can be combined in variouscombinations of magnitudes and time delays to gen-erate all other potentials observed. Considerationshould be given to the possibility that the type ofinsertional activity documented in this study is fun-damentally different from that generated with moreaggressive insertions. Although it is doubtful thatsome other mechanism would ensue for these con-ditions, further research into this area may be war-ranted.

The authors thank Hans van Dijk, from the Department of Clini-cal Neurophysiology, Institute of Neurology, University HospitalNijmegen, for his assistance in development of the muscle fibersimulation program.

REFERENCES

1. Brismar T: Potential clamp analysis of membrane currents inrat myelinated nerve fibers. J Physiol 1980;298:171–184.

2. Brown WF: The Physiological and Technical Basis of Electromyog-raphy. Boston, Butterworth, 1984.

3. Brown WF, Bolton CF: Clinical Electromyography. Boston, But-terworth-Heinemann, 1993, p 373.

4. Dumitru D, Jewett DL: Far-field potentials. Muscle Nerve 1993;16:237–254.

5. Dumitru D: Electrodiagnostic Medicine. Philadelphia, Hanley &Belfus, 1995, pp 214–215.

6. Dumitru D: Single muscle fiber discharges (insertional activ-ity, endplate potentials, positive sharp waves and fibrillationpotentials): a unifying proposal. Muscle Nerve 1996;19:221–226, 229–230.

7. Gootzen THJM: Muscle Fibre and Motor Unit Action Potential: ABiophysical Basis for Clinical Electromyography. The Hague, CIP-Bergevens Kiniklije Bibliotheek, 1990.

8. Gydikov A, Gerilovsky L, Radicheva N, Trayanova N: Influ-ence of the muscle fibre end geometry on the extracellularpotentials. Biol Cybern 1986;54:1–8.

9. King JC, Dumitru D, Stegeman D: Monopolar needle spatialrecording characteristics. Muscle Nerve 1996;19:1310–1319.

10. Kugelberg E: ‘‘Insertional activity’’ in electromyography. JNeurol Neurosurg Psychiatry 1949;129:268–273.

11. Lorente’ de No R: Analysis of the distribution of action cur-


rents of nerve in volume conductors. Stud Rockefeller Inst MedRes 1947;132:384–477.

12. Louis AA, Hotson JR: Regional cooling of human nerve andslow Na+ inactivation. Electroencephalogr Clin Neurophysiol 1986;63:371–375.

13. Rosenfalck P: Intra- and extracellular potential fields of activenerve and muscle fibers. Acta Physiol Scand Suppl 1969;321:1–168.

14. Wiechers DO: Mechanically provoked insertional activity be-fore and after nerve section in rats. Arch Phys Med Rehabil1977;58:402–405.

15. Wiechers DO, Stow R, Johnson EW: Electromyographic inser-tional activity mechanically provoked in the biceps brachii.Arch Phys Med Rehabil 1977;58:573–578.

16. Wiechers DO: Electromyographic insertional activity in nor-mal limb muscles. Arch Phys Med Rehabil 1979;60:359–363.


normal needle electromyographic insertional activity morphology: a clinical and simulation study

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