nerve conduction studies: essentials and pitfalls in practice

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R M E D I A N - A P B1 .21 .31 .41 .51 .61 .71 .81 .91 .1 05 0 m s 5 0 0 µ VDownloaded from jnnp.bmj.com on June 5, 2012 - Published by group.bmj.comNEUROLOGY IN PRACTICEMii26CellbodyAxonF waveStimulusMMuscleFFigure 2 Median orthodromic sensory study. The index finger digitalnerves are stimulated via ring electrodes and the response recordedover the median nerve at the wrist.CMAPs of similar shape and amplitude because the samemotor axons innervate the muscle fibres making up theresponse. However, the latency will be greater for elbowstimulation compared with wrist stimulation because of thelonger distance between the stimulating and recordingelectrodes (fig 1B). The difference in latency represents thetime taken for the fastest nerve fibres to conduct between thetwo stimulation points as all other factors involvingneuromuscular transmission and muscle activation arecommon to both stimulation sites. If one measures thedistance between the two sites then the fastest motor nerveconduction velocity can be calculated as follows: FMNCV(m/s) = distance between stimulation site 1 and site 2(mm)/[latency site 2 – latency site 1 (ms)].Sensory conduction studiesThe sensory nerve action potential (SNAP) is obtained byelectrically stimulating sensory fibres and recording the nerveaction potential at a point further along that nerve. Onceagain the stimulus must be supramaximal.Recording the SNAP orthodromically refers to distal nervestimulation and recording more proximally (the direction inwhich physiological sensory conduction occurs). Antidromictesting is the reverse. Different laboratories prefer antidromicor orthodromic methods for testing different nerves. Anorthodromic median sensory study is shown in fig 2. Thesensory latency and the peak to peak amplitude of the SNAPare measured. The velocity correlates directly with thesensory latency and therefore either the result may beexpressed as a latency over a standard distance or a velocity.Only the 20% largest diameter and fastest conductingsensory fibres are tested using conventional sensory studiesfunctionally supplying fine touch, vibration, and positionsense. Predominantly small fibre neuropathies affecting theother 80% of fibres exist usually with prominent symptoms ofpain and conventional sensory studies may be normal. Insuch cases quantitative sensory testing and autonomictesting will be required, which are beyond the scope of thisarticle (see Interpretation pitfalls).FwavesF waves (F for foot where they were first described) are a typeof late motor response. When a motor nerve axon iselectrically stimulated at any point an action potential ispropagated in both directions away from the initial stimulationsite. The distally propagated impulse gives rise to theMFFigure 3 Schematic representation of the early M response from thedistally propagated action potential and the later F wave from theproximally propagated action potential. The latter depolarises the axonhillock causing it to backfire. Actual F wave responses are shown in thelower trace. F waves vary in latency and shape due to differentpopulations of axons backfiring each time.CMAP. However, an impulse also conducts proximally to theanterior horn cell, depolarising the axon hillock and causingthe axon to backfire. This leads to a small additional muscledepolarisation (F wave) at a longer latency. Only about 2% ofaxons backfire with each stimulus. Unlike the M response(fig 3), F waves vary in latency and shape because differentpopulations of neurones normally backfire with eachstimulus. The most reliable measure of the F wave is theminimum latency of 10–20 firings.Why are F waves useful?F waves allow testing of proximal segments of nerves thatwould otherwise be inaccessible to routine nerve conductionstudies. F waves test long lengths of nerves whereas motorstudies test shorter segments. Therefore F wave abnormalitiescan be a sensitive indicator of peripheral nerve pathology,particularly if sited proximally. The F wave ratio whichcompares the conduction in the proximal half of the totalpathway with the distal may be used to determine the site ofconduction slowing—for example, to distinguish a root lesionfrom a patient with a distal generalised neuropathy.ErrorsThe main sources of non-biological error in NCS measurementsare the identification and measurement of waveformonset and the measurement of the length of the nervesegment on the limb. Calculations have shown that in a nervewith a conduction velocity of 50 m/s, the 26SD experimentalerror for velocity is 14 m/s over 10 cm and 4.7 m/s over25 cm. Of the error, time measurement is 92.3% and distance7.7%, so the use of the measuring tape is quite adequate inconventional NCS.www.jnnp.com
NEUROLOGY IN PRACTICEDownloaded from jnnp.bmj.com on June 5, 2012 - Published by group.bmj.comTable 1Typical nerve conduction study abnormalities seen with axon loss or demyelinationAxon lossDemyelinationSensory responses Small or absent Small or absentDistal motor latency Normal or slightly prolonged ProlongedCMAP amplitude Small Normal (reduced if conduction block or temporal dispersion)Conduction block/temporal dispersion Not present (responses may disperse slightly) PresentMotor conduction velocity Normal or slightly reduced Notably reducedF waves minimum latency Normal or slightly prolonged Significantly prolongedii27It is not necessary to have all the features of axon loss or demyelination to come to a conclusion. Some conditions only affect motor or sensory nerves, and someprocesses are length dependent and others universal. It can sometimes be quite difficult to decide whether a process is primarily demyelinating or demyelinatingwith secondary axonal changes as features of both may coexist.NERVE CONDUCTION STUDIES IN DISEASEGeneralNCS provides information to locate lesions in the length of anerve, and pathophysiological information. Peripheral nervepathology primarily affects axons or myelin. In reality, thetwo pathologies often co-exist but usually one predominates(table 1).In focal lesions characterisation of the pathophysiologicalprocess can be important for determining prognosis. Apatient with a radial nerve palsy at the spiral groove causingwrist drop is more likely to make a complete and speedierrecovery (6–12 weeks) if this is mainly due to focaldemyelination and/or conduction block (neuropraxia) comparedwith when significant axonal injury has also occurred(6–12 months).In generalised processes it is also important to determinewhether a peripheral neuropathy is demyelinating or axonalas this will affect further investigation and management. Forexample, acute inflammatory demyelinating polyneuropathy(AIDP or Guillain-Barré syndrome) results in a characteristicpattern of segmental nerve demyelination and may be treatedwith human immunoglobulin or plasma exchange.Conversely a length dependent axonal neuropathy developingin a patient on chemotherapy requires reassessment ofthe chemotherapy or addition of a protective agent.Neuropathies may be classified pathologically in thisfashion, anatomically or electrophysiologically.Motor NCSIn axonal lossThe most striking abnormality is a reduction in CMAPamplitude as fewer functioning motor axons are connected tomuscle fibres. Since myelin is unaffected, the remainingaxons conduct normally and one would expect latencies andconduction velocities to remain normal. However, withincreasing motor axon loss some of the largest fastestconducting fibres will be lost. Therefore distal motor latencymay be slightly prolonged (, 120% of normal limit) andconduction velocity slightly slowed (. 80% of normal limit).The dynamics and timing of an axonal insult can affect theabnormalities seen. Immediately after a traumatic completetransection of the nerve, the portion of the nerve distal to thelesion will be normal as there has not been time for axonaldegeneration to occur. The CMAP amplitude will only start tofall a few days later. Conversely, if there is a very slow loss ofaxons in a generalised neuropathy, the remaining unaffectedaxons may have time to sprout new connections to musclefibres that have lost their innervation (collateral reinnervation)and the CMAP may remain within the normalamplitude range even though the total number of nerveaxons is smaller. However, the immature regenerating fibreshave slower velocities due to the effect of the short internodaldistances and this produces a more dispersed CMAP.In demyelinationWith loss of myelin thickness nerve conduction is slowedand, if severe enough, saltatory conduction fails (conductionblock). NCS shows severely prolonged motor latencies andnotably slowed conduction velocities. The precise changesseen depend on the site and extent of demyelination. Ifdemyelination is very proximal then distal motor latency andconduction velocity may be normal in which case only Fwaves may show abnormalities.Normal nerveConduction blockTemporal dispersionResponses arrive atrecording electrodealmost together=DistalstimulationDemyelinationTemporal dispersionProximalstimulationResponses arrive atdifferent timesphase cancellation=Figure 4 Both these traces show demyelination in median motorstudies. The trace on the left shows almost complete conduction blockwith an absent response with proximal stimulation. The trace on theright shows temporal dispersion where the CMAP duration increases byalmost 40% with proximal stimulation. In both situations the CMAPamplitude with proximal stimulation is smaller.Figure 5 Schematic representation of phase cancellation andtemporal dispersion in demyelination. In the normal nerve, theresponses are synchronised in time and therefore summate (amplitudeis higher that that of the individual components). Temporal dispersionresults in an increased duration and reduced amplitude of CMAP.www.jnnp.com
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nerve conduction studies: essentials and pitfalls in practice

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