Nerve Conduction Studies and Electromyography

Important Cervical myotomes:

Muscle Myotome Nerve
Deltoid C5-6 Axillary
Biceps C5-6 Musculocutaneous
Brachioradialis C5-6 Radial
Triceps C7 Radial
Pronator teres C6-7 Median
Extensor digitorum communus EDC C7,8 Radial
First dorsal interossious FDI C8-T1 Ulnar
Abductor Pollicis Brevis APB C8-T1 Median
Extensor indecis propius EIP C8-T1 Radial
Rhomboids C4-5 Roots/plexus


Important Lumbosacral myotomes:

Muscle Myotome Nerve
Tibialis anterior TA L5 Peroneal
Peroneus Longus L5 Peroneal
Tibialis posterior TP L5 Tibial
Tensor facia lata TFL L5 Superior gluteal
Gluteus medius L5 Superior gluteal
Biceps femoris (short head) L5 Peroneal
Vastus lateralis L3,4 Femoral
Gastrocnemius S1 Tibial
Iliopsoas L2,3 Femoral (proximal to inguinal ligament)
Adductor Longus L2,3,4 Obturator


Approach to Nerve conduction studies NCS & Electromyography EMG:

Nerve conduction studies NCS:

  • Studies
  • Technique
  • Interpretation
  • Basic patterns
  • Notes

Assess/Studies (things you do):
Action potentials:

  • Compound motor action potential CMAP (motor nerves)
  • Sensory nerve action potential SNAP (sensory nerves)
  • Compound nerve action potentials CNAP (sensorimotor nerves)

Late responses:

  • F-waves= F-response


  • The electrical equivalent of monsynaptic reflex of a tendon jerk
  • Stimulate the tibial nerve and record over the soleus muscle.
  • Blink reflex
  • Repetitive Nerve Stimulation RNS (RepStim)

Technique (how to do it):
CMAP Technique:

  • G1 (-) recording electrode on muscle belly (proximally)
  • G2 (+) reference electrode on tendon (distally)
  • GND ground between G1 & G2 for sensory studies
  • Set:
    • Duration 0.2ms, Current 20-50 mA, gain 2-5mV per division
    • Stimulate at 8cm (medialn, ulnar, tibial, peroneal), and then proximally, supramaximally
  • Record:
    • CMAP amplitude, duration, distal latency, conduction velocity

SNAP Technique:

  • G1 (-) recording electrode (proximally)
  • G2 (+) reference electrode (distally)
  • GND ground between G1 & G2 for sensory studies
  • Set:
    • Duration 100-200ms, Current 5-30mA, Gain 10-20 micoV
    • Stimulate the nerve distally, supramaximal stimulation
  • Record:
    • SNAP amplitude, duration, distal latency, conduction velocity

F-Wave Technique:

  • Set:
    • Gain 200 microV, Sweep 5-10ms,
  • Supramaximal stimulation, Cathode (+) proximal, +/-Jendrassik maneuver
  • Record: shortest F-wave latency on either side.

H-reflex Technique:

  • Set:
    • Gain 200-500 microV
    • Sweep 10 ms
    • Duration 1 ms
  • G2 Achilles tendon
  • G1 Soleus (5-6 eights the way from popliteal fossa to medial malleoulus)
  • Stimulate tibial nerve in the popliteal fossa, submaximally, cathode (+) proximally, +/-Jendrassik maneuver
  • Record: shortest H-reflex latency on either side.

Blink reflex Technique:

  • Eye open or gently closed
  • G1 lateral & inferior to pupil, bilaterally
  • G2 lateral to lateral canthus, bilaterally
  • GND chin or forehead
  • Set:
    • Sensitivity 100-200 microV/division
    • Sweep speed 5-10 ms/division
    • Motor filter 10 Hz & 10KHz (same as for CMAP)
  • Stimulate:
    • Superior orbital nerve (depression on the medial superior orbital ridge)
    • 4-6 times (wait seconds in between), rastered
    • Duration 0.1ms, Current: 3-25mA, supramaximal
  • Record: shortest R1, ipsilateral R2 & contralateral R2 responses.

Repetitive nerve stimulation Technique:

  • Hold acetylcholinesterase inhibitors prior to the study
  • Select nerve e.g. median, ulnar, accessory
  • Temperature >33 C
  • Perform baseline CMAP at supramaximal stimulation. Immobilize electrode placement.
  • Perform low frequency RNS: at 3 Hz, train of 5-10. Repeat X3, 1 min apart.
  • Exercise: maximal contraction X 30 seconds.
  • Repeat low frequency RNS immediantely and at 1,3,4 min postexercise.
  • Consider high frequency RNS 30-50 Hz if unable to exercise.
  • If decrement occurs, perform 10seconds exercise & repeat 3 Hz RNS to demonstrate repair.
  • If abnormal perform EMG of affected muscle to assess for denervation.

Describe (things you should mention i.e. like a report):
Compound motor action potentials CMAP:

  • Amplitude: reduced vs. normal
    • Motor Conduction:
    • Motor conduction velocity:
    • Velocity: Reduced vs. normal
    • Motor distal conduction latency a.k.a. Distal motor latency:
      • Normal vs. prolonged


  • Present vs. absent

Sensory nerve action potential SNAP:

  • Amplitude: reduced vs. normal
  • Sensory conduction velocity:
    • Velocity: Reduced vs. normal

Findings (things you notice):

  • Temporal dispersion= increased duration AP with smaller amplitude. Area under the curve of CMAP should be unchanged. Indicates some axons are slower than others i.e. demyelination
  • Conduction block= loss of conduction across a lesion. Neurapraxia is the term used when a lesion causes conduction block. This type of lesion results in a decrease in amplitude of AP by >50% (comparing proximal & distal amplitude)

Causes of Conduction block:

  • Focal compression/entrapment of the nerve
  • Focal acquired demyelination (inflammatory, early phase of vasculitis)
  • Conduction slowing is a sign of demyelinating lesions.

Interpret (things you figure out):
CMAP Interpretation:

  • Causes of low CMAP amplitude:
    • Axon loss (anterior horn disease, radiculopathies, peripheral nerve disease with Wallerian degeneration)
    • Conduction block
    • NMJ disorder
    • Myopathy
  • CMAP Onset latency & conduction velocity CV only reflect the fastest nerve fibres (nerve, NMJ, muscle depolarization)
  • CMAP duration: is a measure of synchrony. Is useful in assessing demyelination.
  • CMAP conduction velocity CV (m/s): reflects only the fastest nerve fibres.
  • CMAP Distal latency: prolonged in demyelination e.g. useful in HNPP that can otherwise look axonal but will have prolonged distal latency.

SNAP Interpretation:

  • SNAP amplitude: is low in peripheral nerve disorders
  • SNAP is abnormal in peripheral nerve disease but not radiculopathies.
  • SNAP Not used for assessing demyelination (distal latency etc)
  • SNAP onset latency reflects only the fastest nerve fibres.
  • SNAP duration is used to distinguish between SNAP (1.5ms) and CMAP (5-6ms)

F-Wave Interpretation:

  • Ulnar f-wave latency < 33 (C8-T1)
  • Median f-wave latency <32 (C8-T1)
  • Peroneal/tibial f-wave latency <57 (L5-S1)
  • Peroneal f-waves may be absent in normal individuals
  • F-wave abnormalities:
  • Prolonged minimal f-wave latency
  • Absent f-waves
  • Impersistent f-waves (compare side to side)
  • F-waves are pure motor

H-reflex Interpretation:

  • Compare shortest H-reflex latency to Age-height matched controls. This is prolonged in proximal lesions.
  • Compare to contralateral side, >1.5ms difference is abnormal

Blink reflex Interpretation:

  • Electricial correlate of the corneal reflex (V1, VII, midpons & medulla)
  • R1 repsonse: disynaptic, ipsilateral, stable, bi- or tri-phasic (midpons)
  • R2 response: multisynaptic, bilateral, habituates, polyphasic (pons & medulla)


  • R1 <13ms, side to side difference <1.2ms
  • Ipilateral R2 <41ms, side to side difference <5ms
  • Contralateral R2 <44ms, side to side difference <7ms


  • Unilateral V nerve lesion: delayed/absent R1, ipsilateral R2 & contralateral R2. Stimulation on unaffected side shows intact R1, ipsilateral R2 & contralateral R2. e.g. connective tissue disorders & toxic neuropathies.
  • Unilateral VII nerve lesion: delayed/absent R1, ipsilateral R2 & contralateral R2. Stimulation on unaffected side shows normal R1, ipsilateral R2 but delayed/absent contralateral R2
  • Unilateral midpons lesion: delayed/absent R1 but normal ipsilateral R2 & contralateral R2. Stimulation of unaffected side shows normal R1, ipsilateral R2 & contralateral R2
  • Unilateral medulla lesion: normal R1, delayed/absent ipsilateral R2 & normal contralateral R2. Stimulation of unaffected side shows normal R1, ipsilateral R2 but delayed/absent contralateral R2
  • Demyelinating neuropathy: delayed/absent R1, ipsilateral R2 & contralateral R2 on both sides.

Repetitive nerve stimulation Interpretation:

  • In NMJ disorders, look for decrement on low frequency RNS, postexercise exhaustion that corrects with exercise, or increment postexercise.
  • CMAP decrement on RNS: U shaped, >10% decrement between first & fourth (lowest) response. % Calculated= change in amplitude/baseline amplitude X100
  • CMAP increment on RNS: >40% increase between first & last (highest) response. % Calculated= change in amplitude/baseline amplitude X100
  • Pseudofacilitation: postexercise increase CMAP amplitude <40% with out increase in area.

Causes of CMAP decrement on RNS:

  • Myasthenia gravis
  • Lamert-Easton Myasthenic Syndrome (LEMS)
  • Denervating Peripheral neuropathy
  • Motor neuron disease
  • Myopathy

Basic NCS patterns:

  • CMAP is abnormal in Axon loss (anterior horn disease, radiculopathies, peripheral nerve disease with Wallerian degeneration), Conduction block, NMJ disorder, Myopathy
  • SNAP is abnormal in peripheral nerve disease but not radiculopathies.

Axonal loss:

  • Reduced CMAP, SNAP amplitude compared to normal controls, baseline or opposite side.
  • CV & latency are preserved. If large fibres are involved, mild CV slowing (>75% of normal), mild latency prolongation (<130% of normal) occurs
  • In hyperacute axon loss e.g. nerve transection, CMAP, CANP, CV & latency are normal for ~3 days (Wallerian degeneration takes time to occur). This is if nerve is tested distal to transaction site.


  • Conduction block, decreased CMAP amplitude (or area) by >20-50% between distal & proximal stimulation sites.
  • Temporal dispersion on CMAP, increased duration of >15% between distal & proximal stimulation sites.
  • Reduced CV <75% of normal
  • Prolonged distal latency >130% of normal
  • CV <35m/s in arms or <30ms/ in legs indicated unequivocal demyelination
  • SNAP amplitude may be reduced due to exaggerated temporal dispersion & phase cancellation.
  • When stimulating at Erb’s point. >40% drop in amplitude is needed for conduction block & >30% prolongation in duration for temporal dispersion

Acquired demyelination:

  • Conduction block & temporal dispersion
  • Inherited demyelination:
  • Reduced CV, increased latency, no conduction block or temporal dispersion


  • Conduction block or slowing across the entrapment segment
  • Axonal loss pattern if secondary axonal loss occurs.


  • SNAP: normal
  • CMAP: amplitude is normal or reduced (depending on affected muscle)
  • CV & latency: normal

Myasthenic gravis (MG):

  • normal CMAP

LEMS: reduced CMAP. CV & latency is normal

  • Depolarization occurs under Cathode (+)
  • The fastest myelinated fibres conduct at 65m/s
  • The slowest myelinated fibres conduct at 35m/s. Therefore in purely axonal disease, CV is always >30m/s i.e. 75% of normal.

Notes, terminology:

  • Orthodromic conduction (in the direction of the axon)
  • Antidromic (opposite to the direction of the axon)
  • M-response a.k.a. M-wave is the normal muscle response a.k.a. CMAP
  • Late responses (H-reflex & F-waves). F/waves= F-response
    • H-reflex: electrical equivalent of tendon jerk with orthodromic conduction in Ia afferents from muscle spindle to spinal cord and then orthodromic via anterior horn cells to muscles
    • F-wave/F-response: antidromic stimulation of the anterior horn cell leads to it firing and a orthodromic action potential.

Martin Gruber anastomosis:

  • Median nerve gives a motor branch to the ulnar nerve in the forearm.

Riche-Cannieu anastomosis

  • Connections between deep ulnar & median nerves in the hand.

Routine Electromyography EMG:
About EMG:

  • Insertional activity
  • Resting
  • Mild Voluntary contraction
  • Maximal voluntary contraction

Out put:

  • Visual: oscilloscopic or visual display
  • Auditory: speaker

Norms, Muscle potentials (motor unit potentials):

  • Waveforms
  • Duration 5-15s,
  • 2-4 phases
  • Amplitude: 0.5-3 mV

Assess (things you do):
Insertional activity:

  • Insert the needle at 4 different depth in each of 4 different quadrants

Spontaneous activity (resting):

  • Normal: no activity
  • Abnormal: (see below)

Motor unit action potentials MUAP:

  • Ask the patient to minimally contract the muscle
  • See below for description of:
    • Amplitude
    • Rise time
    • Duration
    • Phases


  • Assess MUAP recruitment (normal, reduced)

Repetitive nerve stimulation test RNST:

  • Response= incremental vs. decremental vs. normal

Describe (things you mention i.e. like the bones of a report):

  • Insertional activity (see below)
  • Spontaneous activity (resting)
  • Motor unit action potentials MUAP:
    • Amplitude: from most positive to most negative peak. normal 2-5mV
    • Rise time: time from first positive peak to first negative peak
    • Duration: time from beginning of first positive peak to final return to baseline. Normal is 5-15 MiliSec.
    • Phases: count the number of positive & negative peaks normal 4 or less
  • Recruitment
  • Repetitive nerve stimulation test RNST

Findings & abnormalities (Things you notice):
Insertional activity:

  • Reduced (<300msec) in atrophied muscle.
  • Increased (>300msec) in muscle pathology & may be associated with transient sharp waves & fibrillation potentials.

Abnormal resting muscle pattern e.g.:
Fasciculation potentials:

  • Morphology: 0.5-1 Hz, irregular.
  • Significance: firing of a single motor unit (a single neuron & all its innervated muscle fibres). Neurogenic or myogenic disorders

Fibrillation potentials (fibs): involuntary contraction of a single muscle fibre.

  • Morphology: Regular 1-10Hz, short, small potentials, looks like a single MUAP
  • Sounds like: static, or cooking bacon. “rain on roof” sound.
  • Significance: firing of a single muscle fibre. Neurogenic or myogenic disorders
  • Always abnormal: denervation of single muscle fibre
  • In axonal injury it takes 10-14 days to appear (usually 3 week delay) , suggests active/persistent dennervation as they disappear with reinnervation

Positive sharp waves PSW: spontaneous discharges from groups of denervated muscle fibres.

  • Morphology: Downward monophasic waveforms
  • Sounds like: dull popping sound
  • Significance: firing of a single muscle fibre. Neurogenic or myogenic disorders
  • Always abnormal: denervation of groups of muscle fibres (usually 3 week delay), suggests active/persistent dennervation as they disappear with reinnervation

Complex repetitive discharges CRDs:

  • Morphology: Groups of spontaneous action potentials. Abrupt onset and offset. Irregular.
  • Sounds like: Machine like sound
  • Significance: Single muscle fibre depolarization & ephaptic transmission to other fibres. Neurogenic or myogenic disorders
  • Suggests injury >6 months old

Myokymic discharges (Multiplets and doublets):

  • Morphology: groups of MUAP that are regular & rhythmic. Continuous or discontinuous/bursts
  • Sounds like: soldiers marching,
  • Significance:
    • Facial: bell’s palsy, Multiple sclerosis, polyradiculopathy
    • Limbs: chronic nerve lesions, radiation radiculopathy

Myotonic discharges:

  • Morphology: High frequency 150-250Hz. Prolonged action potential firing after activation. PSW or biphasic/triphasic morphology
  • Sounds like: Dive-bomber sound. Pinging sound. Changes in amplitude and frequency
  • Significance: Myotonic conditions such as
    • Myotonic dystrophy, myotonia congenital, paramyotonia congenita
    • Hyperkalemic periodic paralysis
    • Acid maltase deficiency
    • Myotubular myopathy
    • Polymyositis, chronic radiculopathy, neuropathies

Continuous motor unit activity:

  • Significance: spasticity (myelopathy or other UMNL), voluntary in some, stiff person syndrome

Other patterns:

  • Cramps
  • Neuromyotonic discharges
  • Tremours
  • Multiples (doublets or triplets i.e. multiple MUAP)

End plate Noise:

  • Morphology: 20-40Hz, low amplitude monophasic negative potentials.
  • Sounds like: seashell, hissing
  • Significance: painful, normal feature

End plate spikes:

  • Morphology: brief irregular spikes. biphasic, initially negative
  • Sounds like: crackling, buzzing, splattering
  • Significance: normal feature

Motor unit action potentials MUAP:
Amplitude: Increased (5-15mV): reinnervation after nerve injury

  • Decreased amplitude: myopathies
    • Size index >2 in large MUAP
    • Rise time: aim for 0.5 miliSeconds or less (adequacy of recording, how far the tested motor unit is)

Duration: assesses synchrony

  • Increased: reinnervation
  • Decreased: myopathies
  • Duration >10ms is long MUAP


  • >4 is polyphasia
  • Concentric needle: >20% is considered abnormally polyphasic
  • Monopolar needle: >40% is considered abnormally polyphasic
  • Polyphasic units occur in:
    • Neuropathies & myopathies


  • Normal MUAP frequency is 10 Hz
  • Decreased recruitment: increase in the firing rate of a motor unit prior to another motor unit starting to fire. Indicates neuropathic process
  • To calculate MUAP frequency (for recruitment):
    • 1. Look at the page=20s
    • 2. Page speed set at 10ms
    • 3. Frequency= number of times MUAP appears on the screen/page X5
  • Neuropathic/neurogenic recruitment: MUAP is typically >20 Hz
  • Recruitment typically tests Type 1 fibers so may be falsely normal in myopathies that affect type 2 fibers only
  • Recruitment ratio= rate of firing of fastest motor unit/number of units firing.
  • If >0.8 it suggests neuropathic process.
  • If <0.3 it suggests a myopathic process.

Interpretation (things you figure out):
Myogenic, potentials:

  • Shorter duration. Lower amplitude
  • Usually polyphasic

Neurogenic, potentials:

  • Longer duration. Higher amplitude
  • Usually polyphasic

EMG evidence of denervation (axonal):

  • Insertional activity: increased insertional activity, pseudomyotonic runs
  • Resting:
    • Fibrillation potentials
    • Positive sharp waves
    • Fasciculation potentials
  • Voluntary contraction:
    • Polyphasic MUAP
    • Large amplitude MUAP & sometimes Giant units
    • Reduced interference pattern

EMG evidence of myopathy:

  • Insertional activity:
    • May have fibrillation potentials
  • Resting
  • Voluntary contraction:
    • Small polyphasic MUAP (crackling noise)
    • Normal interference pattern
  • Other notes:
    • High amplitude (large) MUAP may be normal in quadriceps

NCS/EMG tips & patterns:

Demyelinating neuropathies:

  • NCS:
    • Findings differ by the pattern of demyelination:
    • Uniform, segmental, focal, conduction block
    • CMAP (conduction block, temporal dispersion, uniform velocity slowing, focal conduction velocity slowing)
    • CMAP in temporal dispersion, amplitude will be lower but area under the curve is normal
    • Increased latency & reduced velocity in some patterns
  • EMG is normal in demyelinating neuropathies unless conduction block is present, in those cases reduced recruitment may be seen

In axonal injury:

  • NCS:
    • Reduced amplitude SNAP & CMAP (distal & proximal to the lesion). It takes 11 days for this to occur.
    • Reduced amplitude >50% compared with other side
    • <20% increase in latency or decrease in conduction velocity
  • EMG:
    • Fibrillation potentials, Positive sharp waves PSW
    • If early <14 days, fibrillation potentials & PSW may be absent
    • If late, fibrillation potentials & PSW may be absent (due to reinnervation)
    • MUAP evidence of reinnervation: polyphasic, increased amplitude, prolonged duration
    • Reduced MUAP recruitment (normal configuration) suggests it in early phase.
    • Increased MUAP firing frequency

Lower limb lesions:

  • The tibial & peroneal parts of the sciatic nerve are completely separate from origin to muscle. Thus partial sciatic lesions can mimic peroneal nerve lesions
  • Needle EMG of short head of biceps femoris (the only peroneal innervated hamstring muscle) distinguishes between peroneal lesions above & below the fibular head.
  • The sural nerve (sensory) receives the sural communicating nerve (from the peroneal nerve) in many people & thus peroneal nerve lesions can lead to abnormal sural nerve NCS.
  • Use paraspinal EMG for root & plexus problems:
  • Paraspinal muscles are abnormal in radiculopathy, but normal paraspinal muscles doesn’t rule radiculopathy out (especially if early)


  • If low CMAP & ?denervation: suspect Lambert-Eaton Syndrome


Other notes regarding approaching EMGS:

  • How regular is the discharge?
  • Regular
  • Semi rhymic
  • Irregular
  • Regular with exponential change
  • Burst firing
  • Semi rhymic= motor unit potential

MUAP parameters:

  • Rise time tells you how far you are from MUAP, shorter time the closer you are
  • Recruitment: assess at which rate the second unit starts to fire:
    • A. if the rate of the first unit is <10 without a second unit, this is poor activation.
    • B. If only one unit is firing >12hz this is reduced recruitment (>12 is mild >15 is moderate >20 is severe).
    • C. the different MUAP are all firing at a very similar rate for every give time.
  • Stability: stable vs unstable:
    • You can use the trigger sweep function on the EMG machine.
  • ALS, Radiculopathy, MG, LEMS,
  • Spikes, turns, phases:
    • Triphasic vs. polyphasic
      Turns are like phases but don’t cross the baseline. Many turns is called complex MUAP.
  • Duration: normal vs. long vs. short duration