Clinical Nerve Conduction and Needle EMG Studies

  • NCS's and EMG evaluate the function of the motor unit.

Specifics Disorders

Peripheral Entrapments

  • First demyelination occurs
    • marked NCV slowing
    • CMAP may show dispersion or nerve block
  • Axonal loss
    • Loss of CMAP and CNAP amplitude
    • EMG
      • fibrillation,
      • PSW potentials,
      • reduced recruitment,
      • giant MUP's if collateral reinnervation has occured


  • Sensory NCS's normal
    • because the lesion is proximal to the dorsal root ganglion
    • ie. No injury between the cell body and axon terminal.
  • Motor NCS normal
    • demyelination is proximal to the electrodes therefore will be normal.
    • If bad enough for axonal injury, reduced CMAP's will be seen in all segments supplied by the motor nerve.
  • EMG
    • denervation changes
    • Test paraspinal muscles too.
      • +ve confirms radiculopathy.
      • –ve EMG does not exclude radiculopathy,
      • if sensory only or motor not axonal loss.
      • Some muscels do not reveal denervation changes until 3 weeks.

Nerve Trauma

  • After total nerve transection
    • no motor or sensory response will occur across the injured segment nor any spontaneous MUPs.
    • 1-3 days:
      • Diminished nerve excitability,
      • gradual reduction in CMAP
      • CNAP distal to the region of injury.
    • 4-5 days:
      • Absence of CMAP and further reduced CNAP.
    • 6-10 days:
      • No CNAP
    • 8 days:
      • PSW potentials
    • 14 days:
      • Fibrillation potentials.
  • After severe injury but not severed, proportional reduction of CMAP and CNAP amplitudes occur and EMG reveals voluntary MUPs.
  • When there is severe conduction block there may be no MUPs.
  • If study is repeated in 6-8 weeks there may be a few small amplitude polyphasic MUPs indicating reinnervation.
  • This study determines whether exploration indicated.


  • NCS in 3 limbs to pick up demyelinating or axonal loss conditions.
  • When looking at an isolated nerve entrapment at least 1 other nerve should be evaluated to ensure not an undetected polyneuropathy present.
  • Ie. look for focal demyelination superimposed over a diffuse polyneuropathy.

About the Tests

Motor Unit and Action Potential

  • A Motor unit Potential (MUP) is the action potential created by the voluntary contraction of muscle in the motor unit and recorded by needle EMG.
  • An Action Potential is generated when a threshold level of depolarization occurs.
  • The ability of an external stimulus to achieve threshold depends on the intensity and duration of the stimulus as well as the excitability of the cell.
  • Injury or dysfunction of a nerve decreases nerve excitability – one of the first electrophysiological signs of nerve injury.
  • Within 72 hrs of the injury nerve excitability in the distal segment of nerve is normal.

Propagation of the Action Potential and Nerve Conduction Velocity

  • Once initiated the AP is self propagating.
  • Speed is determnined by myelination and size of the fibres.
    • In unmyelinated nerves the AP travels at 1 m/s
    • In myelinated nerves (saltatory conduction) travesl at 3-80 m/s
  • Segmental demyelination
    • leads to significant slowing of NCV
  • Axonal degeneration (ie myelin intact)
    • NCV the same or no more than 40% slower.
    • (Usually the large diameter fibres are slowed more than the small diameter fibres)
  • Focal entrapment produces focal demyelination.

Neuromuscular Transmission

  • Propagation of the AP leads to a Compound Nerve Action Potential (NAP)
    • a summated potential of all nerve fibres stimulated by an electrical impulse.
  • NAP of motor nerves leads to ACH release at synaptic cleft.
  • Binding of ACH leads to an EPP (End Plate Potential).
    • When these are summated to threshold a MAP (Muscle Action Potential) is generated.
  • NM Transmission can be inhibited at multiple sites.
    • Lambert-Eaton myasthenia syndrome
      • insufficient release of ACH.
      • Markedly abnormal incremental repetitive nerve stimulation test.
    • Botulinum Toxoid
      • Inhibits release of ACH
    • Myasthenia gravis
      • antibody binds to ACH receptor leading to Postsynaptic defect.


  • Pre and Post synaptic deficiency distinguished by repetitive nerve stimulation.


  • Low Hz (2-5) testing will show a decremental response.
  • High Hz (10 – 50) will distinguish pre and post. (ie abnormal Pre)
  • When a muscle fibre is denervated it becomes more sensitive to ACH over first 1-2 weeks.
    • Seen as fibrillation potentials on EMG.

Muscle Contraction

  • Voluntary activation of the motor neuron results in contraction of all muscle fibres innervated by that neuron.
    • This is recorded on EMG as a MUP (Motor Unit Potential)
      • Amplitude of MUP is proportional to the number of fibres that contract.
      • Duration of MUP reveals the synchrony.
  • Used to distinguish denervation and myopathy.
    • In chronic denervation
      • the surviving neurones increase their territory and fiber density
      • leading to high amplitude – long duration MUPs.
    • Myopathy
      • degeneration of the fibres lead to low amplitude – short duration MUPs.

Nerve Conduction Studies


  • Procedure
    • A peripheral motor nerve is stimulated with a single supramaximal stimulus at each of at least 2 points along its course. A recording of the Resultant CMAP is taken from surface electrodes from a muscle innervated by that nerve.
  • Latency
    • time required from stimulation to production of the CMAP.
  • Terminal latency
    • the latency from the distal point of stimulation.
    • Conduction time in the segment between the stimulating electrodes will be latency – terminal latency.
  • NCV
    • conduction time/distance between stimulating electrodes.
    • For a NCV to be diminished nearly all of the nerves fibres need to be affected.
    • When both the stimulating electrodes are above the segment where the problem is, the NCV will be normal.
    • Characteristic of this situation is Carpal Tunnel
      • long terminal latency.
      • However there is a long latency so NCV will be normal.
      • Mild slowing can be seen in 11-35% of pts.
    • NCV will be diminished if the distal electrode is distal to the conduction block.
    • CMAP
      • Amplitude, duration and shape of CMAP is analysed.
      • CMAP amplitude
        • is a measure of the number of fibres that are activated and the number of fibres that contract.
        • Thus if CMAP is diminished it equates to severe axon loss.
      • CMAP duration.
        • Prolongation reveals marked slowing in some of the fibres which equates to demyelination.

Sensory Nerve

  • Measure the CNAP (Compound Nerve Action Potential)
    • Test performed orthodromically with 1 distal stimulator, 1 sensing electrode proximally.
    • Sensory nerve conduction time equals the latency.
    • Measure Amplitude and Duration of CNAP.
    • CNAP Amplitude most affected by axonal loss. CNAP dispersion only seen with the near nerve needle technique.

Late Waves

  • H-Reflex
    • A monosynaptic reflex in S1 representing the Ankle Jerk reflex.
    • Post tibial nerve is stimulated producing a reflex contraction of the calf muscles.
    • Measures the latency of the monosynaptic reflex through afferent Ia fibres and the efferent alpha motor fibers of S1.
    • With peripheral neuropathy this is absent or prolonged.
  • F wave
    • The F wave is an antidromic volley evoked by the supramaximal stimulation of the distal nerve during the NCS.
    • The F-wave is considered to be a recurrent discharge of a few motor neurons in response to the antidromic volleys in the motor fibres.
    • Thoracic Outlet Syndrome
      • The F-wave has been used as a measure of the proximal motor fibres and a proximal nerve conduction abnormality as in neurogenic thoracic outlet syndrome.
    • Cervical radiculopathy
      • The F-wave although not diagnostic is absent or prolonged in cervical radiculopathy.

Factors that Affect results

  • Temperature:
    • NCV increases linearly with temp
  • Age:
    • Newborns are 50% adult
    • 1 year old 75%
    • 4 years old 100%
    • CMAP and CNAP amplitude decrease after 60
  • Height:
    • Slight slowing in tall individuals
  • Distance:
    • Accurate assessment of the distance travelled is probably the most common technical error.

Needle EMG

  • Needle EMG has 3 components
    • Observation at rest
    • MUP on minimal voluntary contraction
    • Recruitment pattern of MUP on maximal contraction
  • At rest should be quiet
    • Increased insertional activity = hyperexcitable muscle.
    • Decreased activity = muscel fibrosis/fatty change/paralysis/myopathy
  • Several abnormal spontaneous potentials can occur.
Fibrillation Denervation or active myopathy
Positive sharp waves Denervation or active myopathy
Fasciculations Denervation or neurogenic
Myokymic potential Neurogenic
Complex repetitive Myopathies
Myotonic discharges Myopathies

Motor Unit Potential (MUP)

  • Represents only the summated activity of the muscle fibres in a motor unit that are near the needle electrode.
  • Amplitude, Duration, Shape and Rate
    • Amplitude:
      • reflects summated activity of the fibres near the needle.
    • Duration:
      • Depends on the depolarization of many fibres away from and close to the needle.
    • Fibrillation:
      • Low amplitude bi or triphasic potentials
    • PSW:
      • Positive deflections followed by prolonged negative wave.
    • Abnormalities
      • Myopathy
        • Small amplitude short duration MUP
      • Denervation:
        • Collateral sprouting leads to short high amplitude MUP
        • Fibrillation and PSW's present at 2-3 weeks after.
        • PSW's usually seen first.
      • Fasiculation Potentials
        • spontaneous discharges of a whole motor unit
        • can be seen in
          • normal muscle,
          • ant horn cell disease,
          • cervical spondylotic myelopathy,
          • radiculopathy,
          • demyelinating neuropathy
  • Rate and pattern of recruitment
    • Denervation:
      • Reduction in number of MUPs resulting in reduced ` interference pattern.
    • Myopathy:
      • Early recruitment(more MUPs than would be expected for the degree of muscle contraction)
  • So EMG can infer denervation and its chronicity.
    • Active denervation
      • Prominent fibrillations and PSWs are indicative of active denervation.
    • Chronic denervation
      • Long duration MUP's indicate chronic denervation.

Factors affecting EMG

  • MUP is Higher and longer with a monopolar needle cf concentric one.
  • MUP duration and amplitude increase with decreasing temp.
  • Smaller muscles have shorter MUP duration than larger muscles
  • MUP duration and amplitude increase with age.


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