This presentation is an introduction to the principles of Nerve Conduction Study and is entirely sourced from the book by David C Preston and Barbara E Shapiro: Electromyography and Neuromuscular disorders, 3rd Edition
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NCS Guide: Everything You Need to Know
1. Nerve Conduction Study:
Overview
Dr Pramod Krishnan
Consultant Neurologist and Epileptologist
Manipal Hospital, Bengaluru
Based on Electromyography and Neuromuscular Disorders. 3rd Edition.
David C Preston and Barbara E Shapiro.
2. Electrodiagnostic studies (EDx)
• Nerve Conduction Study
• Electromyography
• Repetitive nerve stimulation
• Late responses.
• Evoked potentials: VEP, SSEP. BAER.
• Blink reflex.
• Tremor recording and analysis.
EDX is mainly used to study the peripheral nervous system
3. NCS and EMG
• NCSs and needle EMG form the core of the EDX study.
• They are complementary, should be performed TOGETHER, in
the same sitting.
• They are performed first, and yield valuable diagnostic
information.
• EDX studies are an extension of the clinical examination.
• A detailed history and neurological examination MUST precede
EDX.
• Both sides should be studies ALWAYS.
4. How is EDX useful?
• EDX permits localisation of the pathology in the peripheral nervous
system: AHC, DRG, Radicles, Plexus, Nerve, NMJ, Muscle.
• Identifies the nature of the pathology: axonal/ demyelinating/
entrapment, and the severity.
• They permit planning of additional investigations in an efficient and
cost effective manner.
• They permit initiation of specific therapy: eg GBS, CIDP, entrapment
neuropathies, MMNCB.
• Studies should be protocol based and later modified for a particular
patient.
7. EDX is more sensitive than clinical examination in identifying the fibre type involves and the pathology.
8.
9.
10.
11.
12. A good knowledge of muscle and nerve anatomy,
branches of the nerves, muscle innervation by
nerves, roots is mandatory to perform EDX
13. The PNS is defined as the part of the nervous system where the
Schwann cell is the major supporting cell.
14. Myelinated fibers are recognized as small dark rings (myelin) with a central clearing (axon). The
endoneurium is present between axons. Axons are grouped into fascicles, surrounded by perineurium
(small arrows). Surrounding the entire nerve is the layer of connective tissue, the epineurium (large arrow).
16. • At rest, the axonal membrane is negatively polarized, inside compared to outside.
• This resting potential results from the combination of a membrane that is
semipermeable to charged particles and an active Na+/K+ pump.
• At rest, the concentration of Na+ and Cl− is higher in the ECF, with the
concentration of K+ and large anions (A−) greater inside the axon.
• These electrical and chemical gradients create a resting equilibrium potential.
• At the nerve cell soma, this resting membrane potential is approx 70 mV negative
inside compared with the outside; in the axon it is approx 90 mV negative.
17. The axonal membrane is lined with voltage-gated sodium channels.
(A) There are two gates: an activation gate (large arrow) and an inactivation gate (small arrow). If current is
injected into the axon, the voltage-gated activation gate opens, allowing the influx of sodium into the axon
(B) causing depolarisation.
(C). The inactivation gate of the sodium channel is like a “hinged lid,” which closes the end of the channel
within 1 to 2 ms of depolarization, preventing further depolarization.
18. • When the resting membrane voltage (Vm) is depolarized to threshold, voltage-gated Na channels are
opened, increasing Na+ conductance (gNa), resulting in an influx of Na and further depolarization.
• The action potential, is short lived, due to the inactivation of the Na channels within 1 to 2 ms and an
increase in K+ conductance (gk).
• These changes, along with the Na+/K+ pump, allow the axon to re-establish the RMP.
Changes during an action Potential
19. Saltatory Conduction:
• Myelinated fibers propagate action potentials by way
of saltatory conduction.
• Nodes are unmyelinated, internodes are myelinated.
• Density of Na channels is highest in the nodes.
• Depolarization only occurs at the nodes of Ranvier,
with the action potential jumping from node to node.
• Thus, less membrane needs to be depolarized, less
time is required, and, consequently, conduction
velocity dramatically increases.
• Most human peripheral myelinated fibers conduct in
the range of 35 to 75 m/s.
20.
21. Points to remember
• The large myelinated fibers are the ones measured in NCS.
• All routine motor and sensory conduction velocity and latency
measurements are from the largest and fastest fibers of that nerve.
• The small myelinated (Aδ, B) and unmyelinated (C) fibers that carry
autonomic information (afferent and efferent), somatic pain and
temperature sensations are not recorded in standard NCS.
• Thus, neuropathies that preferentially affect only small fibers may not
reveal any abnormalities on NCSs.
22. Points to remember
• The largest and fastest fibers in a nerve ARE NOT RECORDED
during routine NCS.
• These are the muscle afferents, the Aα fibers (Ia fibers), which originate
from muscle spindles and mediate the muscle stretch reflex.
• These fibers are recorded only during mixed nerve studies. Therefore,
mixed nerve conduction velocities are faster than routine NCS.
• The Ia fibers are also the one affected early by demyelinating lesions
such as entrapment neuropathies.
• For example, in CTS, the mixed nerve study from the palm to the wrist
often is more sensitive in detecting abnormalities than routine NCS.
23. Recording: Near-field potentials
• NCS is performed by recording with surface electrodes over the skin,
and EMG by recording with a needle electrode placed in the muscle.
• The process of an intracellular electrical potential being transmitted
through extracellular fluid and tissue is known as volume conduction.
1. Nearfield potentials: recorded only close to the source, and the
characteristics of the potential depend on the distance between the
recording electrodes and the electrical source (action potential).
Eg: CMAP, MUAP, SNAP.
24. Volume conduction and waveform
morphology.
Top: An advancing action potential
recorded by volume conduction
will result in a triphasic potential
that initially is positive, then
negative, and finally positive again.
Bottom: If the depolarization
occurs directly beneath the recording
electrode, (eg active electrode over
the endplate) the initial positive
phase will be absent, and a biphasic,
initially negative potential is seen.
By convention, negative is up and
positive is down in all NCS and
electromyographic traces.
25. Volume conduction and motor potentials.
1. Top: With the active recording electrode
(G1) over the endplate, depolarization first
occurs at that site, and subsequently
spreads away. The waveform has an initial
negative deflection without any initial
positivity.
2. Middle: If the active recording electrode is
off the endplate, depolarization begins
distally and then travels under and past the
active electrode, resulting in a triphasic
morphology.
3. Bottom: If the depolarization occurs at a
distance and never travels under the
recording electrode, only a small positive
potential will be seen.
26. Recording: Far-field potentials
• Far-field potentials are electrical potentials that are distributed widely
and instantly.
• Two recording electrodes, one closer and the other farther from the
source, essentially see the source at the same time.
• Although far-field potentials are more often of concern in evoked
potential studies, they occasionally are important in NCSs.
• Those potentials whose latencies do not vary with distance from the
stimulation site usually are all far-field potentials.
• Eg: The stimulus artifact seen at the onset of all NCSs.
27. Near-field and far-field potentials.
• Median motor study, recording the APB muscle,
stimulating at the wrist (top trace) and
antecubital fossa (bottom trace).
• At each site, a CMAP is present, representing a
near-field recording of the underlying muscle
fiber action potentials.
• The CMAP latencies occur at different times,
reflecting their different arrival times at the
recording electrode.
• At the start of each trace is the stimulus artefact
which is an example of a far-field potential.
• It is transmitted instantaneously and seen at the
same time, despite the difference in distances
between the two stimulation sites.
29. Nerves studied
Motor Nerves Sensory Nerves
Median nerve Median nerve
Ulnar nerve Ulnar nerve
Radial nerve Radial nerve
Axillary nerve Lateral and Medial cutaneous nerve of forearm
Musculocutaneous nerve Sural nerve
Suprascapular nerve Superficial peroneal nerve
Common peroneal nerve Lateral cutaneous nerve of thigh
Tibial nerve Saphenous nerve
Femoral nerve Medial and Lateral plantar nerves.
30. Motor Conduction Study
• Always done first as it is easy, indicates the nerve anatomy, suggests the
degree of stimulation required, and indicates the underlying pathology.
• Motor responses are in mV, sensory and mixed nerve study are in uV.
• Gain: 2-5 mV/division.
• Duration of electrical impulse: 200 ms.
• Current: 20-50 mA. Start from 0 mA, increase by 5-10 mA increments till
supramaximal stimulation is achieved.
• The current is increased by another 20% to ensure supramaximal
stimulation.
31. Median motor study, recording from APB, stimulating the median nerve at the wrist. The
“belly–tendon” method is used for recording. Active recording electrode (G1) is on the center
of the muscle (motor end plate), Reference electrode (G2) placed distally over the tendon.
32. • CMAP represents the summation of all
the underlying muscle fiber action
potentials.
• With recording electrodes properly
placed, the CMAP is a biphasic potential
with an initial negative deflection.
Compound Muscle Action Potential (CMAP)
33. • The latency is the time from the stimulus
to the initial CMAP deflection from
baseline.
• It represents three separate processes:
1. Nerve conduction time from the stimulus
site to the neuromuscular junction (NMJ),
2. The time delay across the NMJ, and
3. The depolarization time across the
muscle.
• Latency reflect only the fastest conducting
motor fibers.
CMAP Latency (milliseconds)
34. • It is measured from baseline to negative
peak but also can be measured from first
negative peak to next positive peak.
• It reflects the number of muscle fibers that
depolarize.
• Low CMAP amplitudes:
1. Axonal loss (most common)
2. Conduction block from demyelination
located between the stimulation site and
the recorded muscle
3. Pre-synaptic NMJ disorders
4. Myopathies.
CMAP amplitude (mV)
35. • It is measured from the initial deflection
from baseline to the first baseline crossing
(i.e., negative peak duration).
• It is primarily a measure of synchrony.
• Duration characteristically increases in
conditions that result in slowing of some
motor fibers but not others (e.g., in a
demyelinating lesion).
CMAP duration
36. • Negative peak CMAP area is another
measure reflecting the number of
muscle fibers that depolarize.
• Differences in CMAP area between
distal and proximal stimulation sites
is useful in determining conduction
block from a demyelinating lesion.
CMAP Area
37. CMAP Conduction velocity (CV in m/sec)
• Proximal and distal stimulation is
required to calculate CV.
• PL-DL= nerve conduction time.
• CV= (Distance between PL and DL)
divided by nerve conduction time.
• CV reflects only the fastest conducting
fibres in the nerve.
38. Sensory Conduction Study
• It assesses only nerve fibres and not muscle conduction and NMJ.
• Technically more demanding as the sensory responses are very small (1-
50 uV).
• Gain: 10-20 uV/ division.
• Duration of impulse: 100 or 200 ms.
• Current for supramaximal stimulation: 5-30 mA, start from 0 mA and
increase in 3-5 mA increments.
• Sensory fibres have a lower threshold to stimulation than motor fibres.
39. Median sensory study, antidromic technique. Ring electrodes are placed over the index finger, 3
to 4 cm apart. Active recording electrode (G1) is placed proximally, closest to the stimulator. The
entire median nerve is stimulated at the wrist, but only the cutaneous sensory fibers are
recorded over the finger.
40. Sensory nerve action potential (SNAP): The SNAP represents the summation of all the
underlying sensory fiber action potentials. The SNAP usually is biphasic or triphasic.
41. • Onset latency: measured from the stimulus
to the initial negative deflection for
biphasic SNAPs or to the initial positive
peak for triphasic SNAPs.
• Peak latency: measured at the midpoint of
the first negative peak.
• Amplitude: most commonly is measured
from baseline to negative peak, but also
can be measured from peak to peak.
• Duration: measured from the initial
deflection from baseline to the first
baseline crossing (i.e., negative peak
duration).
• Sensory conduction velocity can be
calculated with a single stimulation site, as
sensory onset latency represents only nerve
conduction time.
42. Onset latency represents the fastest conducting fibers and can be used to calculate a
conduction velocity. For many potentials, especially small ones, it is difficult to mark the initial
deflection from baseline (blue arrows). Peak latency is easy to mark, with no inter-examiner
variation, and reference values are available. However, the population of fibers represented by
peak latency is unknown; it cannot be used to calculate a conduction velocity.
43. • CMAPs (top) and SNAPs (bottom) both are
compound potentials but are quite different.
• CMAP amplitude is measured in millivolts,
whereas SNAPs are measured in the microvolt
range (note different gains between the traces).
• CMAP negative peak duration usually is 5 to 6
ms, whereas SNAP negative peak duration is
much shorter, typically 1 to 2 ms.
• When both sensory and motor fibers are
stimulated (such as when performing
antidromic sensory or mixed studies), these
differences (especially duration) usually allow
an unknown potential to be recognized as
either a nerve or muscle potential.
44. Top trace: Antidromic study: stimulating
wrist, recording index finger.
Bottom trace: Orthodromic study:
stimulating index finger, recording wrist.
• Latencies and conduction velocities are
identical for both.
• The antidromic method has a higher-
amplitude SNAP because of proximity
to the nerve, but is followed by a large
volume-conducted motor potential.
• If the SNAP is absent, care must be
taken not to confuse the motor potential
for a SNAP.
• Orthodromic study does not result in a
volume-conducted motor potential.
45. Disadvantages of Antidromic sensory studies:
• As the entire nerve is stimulated, including
sensory and motor fibers, the SNAP is followed
by a volume-conducted motor potential.
Top: Normal antidromic ulnar sensory response,
stimulating the wrist and recording the fifth digit.
• The ulnar SNAP is followed by the large, volume-
conducted motor response.
• The SNAP has a characteristic shape, and brief
negative peak duration of approximately 1.5 ms.
Also, the SNAP usually occurs before the motor
response.
Bottom: If SNAP is absent, the first component of
the volume-conducted motor response may be
mistaken for the SNAP.
However, the motor duration is longer, with higher
amplitude and slower latency.
46. Lesions of the roots separate the peripheral motor nerve from the AHC, but leave the DRG and
the sensory nerve intact. Thus, nerve root lesions result in degeneration of the motor fibers
distally causing abnormal NCS and EMG. However, the distal sensory nerve remains intact in
lesions of the nerve roots. Thus, results of sensory conduction studies remain normal.
Root lesions
47. Proximal sensory studies.
• Normal median sensory study, recording
index finger, stimulating wrist (top trace)
and elbow (bottom trace).
• Note that proximal stimulation results in
SNAPs that are longer in duration and
lower in amplitude and area.
• This occurs as a result of normal temporal
dispersion and phase cancellation.
• If the SNAP is small at the distal
stimulation site, it may be difficult or
impossible to obtain a potential with
proximal stimulation.
48. • SNAP and CMAP are compound
potentials, representing the
summation of individual sensory
and muscle fiber action potentials.
• In each case, there are fast (F) and
slow (S) fibres.
• Distal stimulation: fast and slow
fiber potentials arrive at the
recording site at almost the same
time.
• Proximal stimulation: the slower
fibers lag behind.
• With sensory fibres, the temporal
dispersion at proximal stimulation
sites results in the negative phase of
the slower fibers overlapping and
cancelling out the positive trailing
phase of fastest fibers.
Temporal dispersion and phase
cancellation
49. • The effects of temporal dispersion and phase cancellation are less prominent for motor
fibers. The duration of individual motor fiber potentials is much longer than that of
single sensory fibers.
• Thus, for the same amount of temporal dispersion, there is much less overlap and
cancellation of negative and positive phases of motor fiber action potentials
50. Mixed conduction study
• In routine NCS, the largest and fastest fibers are not recorded.
• These are the sensory muscle afferents (Ia fibers).
• These fibers are recorded only during mixed nerve studies, wherein the
entire mixed nerve is stimulated and also recorded.
• Mixed nerve conduction velocities are faster than routine NCS.
• Since the Ia fibers have the largest diameter, and maximum myelin,
they often are the fibers earliest affected by demyelinating lesions, such
as entrapment neuropathies.
51. Median mixed study, stimulating median nerve in the palm, recording at the wrist. Active
recording electrode (G1) faces the cathode of the stimulator. Mixed studies stimulate and
record all motor and sensory fibers, including the muscle afferents, the Ia fibers.
52. Mixed conduction studies
• In practice, median, ulnar, and distal tibial nerves are studied, for the
diagnosis of median neuropathy at the wrist, ulnar neuropathy at the
elbow, and tibial neuropathy across the tarsal tunnel, respectively.
• Gain: 10-20 uV/ division.
• The recorded potential, mixed nerve action potential (MNAP), is a
compound potential that represents the summation of all the individual
sensory and motor fiber action potentials.
• MNAPs usually are biphasic or triphasic potentials.
53. In this example, the median nerve is stimulated at the wrist while recording the APB muscle.
Top: The stimulator is in the optimal location directly over the nerve.
Bottom: The stimulator is moved 1 cm lateral to that position.
Supramaximal stimulation is then achieved. In both examples, the resultant CMAP is identical.
However, the current needed when stimulating laterally, is more than twice that needed at the
optimal position.
Optimal stimulator position and supramaximal stimulation.
54. Optimizing the stimulator position over the nerve. The stimulator is placed over a site where the nerve is
expected to run. The stimulus intensity is increased till the first submaximal potential is recorded. At this
point, the stimulus current is held constant, and the stimulator is moved parallel to the initial stimulation
site, slightly laterally and medially. The optimal site is the one with the largest potential, which is directly
over the nerve. Once the optimal position is determined, the current is increased to supramaximal. This
technique markedly reduces the current necessary to achieve supramaximal stimulation, reduces
technical errors as well as patient discomfort, and increases efficiency.
56. Abnormal patterns
• Abnormal motor conduction: nerve, root, AHC, muscle, NMJ.
• Abnormal sensory or mixed conduction: nerve.
Axonal: most common Demyelinating
Reduced
Amplitude
Prolonged latency
(>130% of ULN)
Reduced CV
(<75% of LLN)
Normal latency
Normal CV Normal
Amplitude
Prolonged latency
(≤ 130% of ULN)
Slow CV (≥75% of LLN)
Reduced amplitude does not always mean axonal loss.
Reduced
Amplitude
57. Typical axonal loss pattern. With random dropout of fibers from axonal loss (outlined in
green), the normal distribution of nerve fibers and their associated conduction velocities
changes to a smaller bell-shaped curve. In this case, the amplitude decreases while the
conduction velocity and distal latency slightly slow.
58. A: Normal study. With normal distal
latency (DL) <4.4 ms, amplitude >4 mV,
and conduction velocity (CV) >49 m/s.
B: Axonal loss.
• The amplitudes decrease.
• CV is normal or slightly slowed, but
not <75% of the lower limit of
normal.
• DL is normal or slightly prolonged,
but not >130% of the upper limit of
normal.
• The morphology of the potential
does not change between proximal
and distal sites.
59. Conduction velocity (CV) and axonal neuropathy: Every nerve contains myelinated fibers with
different axonal diameters and CV. For example, in the median nerve, the fastest myelinated
fibers have a CV of 65 m/s, and the slowest fibres have CV of 35 m/s. Whereas all fibers
contribute to amplitude and area, only the fastest conducting fibers contribute to the CV and
latency measurement.
60. Severe axonal loss with sparing of only a few of the fastest fibres (left): Amplitude markedly
decreases, but CV and distal latency remain normal.
Severe axonal loss with sparing of a only a few of the slowest conducting fibers (right):
Amplitude markedly decreases. However, CV can only drop as low as 35 m/s (≈75% of the
lower limit of normal). Greater slowing cannot occur in a pure axonal loss lesion because
myelinated fibers do not conduct any slower than this.
61. Acute axonal injury: eg nerve transection
• First 3 days: NCS is normal, provided both stimulation and recording
are done distal to the lesion.
• 3-10 days: process of Wallerian degeneration occurs: the nerve distal to
the transection undergoes degeneration, resulting in a low amplitude
potential both distally and proximally.
• Wallerian degeneration is earlier for motor fibers (between days 3–5)
compared to sensory fibers (between days 6–10).
• Once Wallerian degeneration is complete, the typical axonal pattern
will be seen on NCSs.
62. Pseudo-conduction block
• If stimulation is performed distal and proximal to an acute axonal
lesion during the first 3 days after the nerve insult, the amplitude will be
normal with distal stimulation, but reduced with proximal stimulation.
• This pattern simulates conduction block.
• It is seen only in two situations:
1. Acute trauma/transection of a nerve.
2. Nerve infarction, as in vasculitic neuropathy.
• This can be differentiated from demyelinating conduction block by
repeating NCS after a week, when wallerian degeneration is complete.
63. Demyelinating neuropathy
• Any motor, sensory, or mixed nerve CV that is slower than 35 m/s in the
arms or 30 m/s in the legs signifies unequivocal demyelination.
• Only in the rare case of regenerating nerve fibers after a complete
axonal injury (e.g., nerve transection) can CV be this slow and not
signify a primary demyelinating lesion.
Axonal Vs Demyelinating
Median motor study CV Distal motor amplitude Diagnosis
Case 1 35 m/s 7 mV Demyelinating
Case 2 35 m/s 0.2 mV Axonal
64. Top: Normal study.
Middle: Demyelination with uniform slowing
is seen in inherited conditions (e.g., CMT).
CV is markedly slowed (<75% LLN) and DL
is markedly prolonged (>130% ULN). There
is no change in configuration between
proximal and distal stimulation sites.
Bottom: Demyelination with conduction
block/temporal dispersion is seen in
acquired neuropathies like GBS, CIDP.
CV and DL are markedly slow, with change
in potential morphology (due to conduction
block/temporal dispersion) between distal
and proximal stimulation sites.
65. Reduced amplitude in Demyelination
1. Sensory conduction study:
• SNAPs are often low amplitude or absent in demyelinating
neuropathies.
• Amplitudes are reduced due to the normal processes of temporal
dispersion and phase cancellation.
• These are exaggerated by demyelinative slowing
2. Conduction block: defined as more than a 50% drop in area between
proximal and distal stimulation sites.
66. Conduction Block:
Top: In a normal nerve, the CMAP
morphology usually is similar between distal
and proximal stimulation sites.
Bottom: In acquired demyelinating lesions,
demyelination is often a patchy, multifocal
process.
When the nerve is stimulated proximal to the
conduction block, the CMAP drops in
amplitude and area and becomes dispersed.
67. CMAP and conduction block.
Top: If a CB is between the distal
stimulation site and the muscle,
amplitudes will be low at both distal
and proximal stimulation sites
(axonal pattern).
Middle: If a CB is between distal and
proximal stimulation sites, a normal
CMAP amplitude will be recorded
with distal stimulation and a reduced
CMAP amplitude will be recorded
with proximal stimulation.
Bottom: If a CB is proximal to the
proximal stimulation site, CMAP is
normal distally and proximally.
68. Temporal dispersion without CB.
• A marked drop in proximal CMAP
amplitude usually means CB.
• In the figure, there is no CB between
distal and proximal stimulation sites.
• The drop in amplitude was entirely
due to abnormal temporal dispersion
from a demyelinating lesion.
• To differentiate CB from abnormal
temporal dispersion requires a drop
in area >50%, which is not seen here.
69. Entrapment neuropathy
• Focal demyelinating findings can identify the site and severity of
entrapment and suggest prognosis.
Radial motor studies across the spiral groove
Patient Radial CMAP (involved) Radial CMAP (uninvolved)
Below spiral groove Above spiral groove Below spiral groove Above spiral groove
1 4 mV 0.5 mV 5 mV 4.8 mV
2 1 mV 0.5 mV 5 mV 4.8 mV
• Patient 1: Mild reduction in distal CMAP amplitude. Therefore slight axonal
loss. The marked drop in CMAP amplitude on proximal stimulation suggests
conduction block and demyelination, which is a good prognostic sign.
• Patient 2: has marked axonal loss, poor prognosis.
70. Focal slowing and conduction block at the elbow. Ulnar CMAP amplitude is normal at the
wrist and below the elbow. Stimulation above the elbow causes a marked drop in amplitude
and focal slowing between the above-elbow and below-elbow sites (40 m/s) compared to the
forearm segment (60 m/s). This suggests focal demyelination, localising the ulnar neuropathy
at the elbow.
71. Conduction block and CIDP.
• Ulnar motor study in a patient with
CIDP, recording ADM, stimulating
wrist (WR), below groove (BG), above
groove (AG), axilla (AX), and Erb’s
point.
• CB/ temporal dispersion pattern is
noted between wrist and below elbow,
and between axilla and Erb’s point.
• CB and abnormal temporal dispersion
are markers of acquired
demyelination.
• They do not occur in inherited
demyelinating neuropathies, except in
common areas of entrapment or
compression.
72. Myopathic and NMJ disorders
• Sensory conduction studies are always normal.
• Proximal myopathies: motor conduction studies can be normal as
recording is usually from distal muscles.
• Severe generalised and distal myopathies: CMAP amplitude is reduced.
Distal latency and CV are normal.
• Post-synaptic NMJ disorder: eg, myasthenia gravis. Normal motor
studies.
• Pre-synaptic NMJ disorder: eg, Lambert Eaton syndrome. Reduced
CMAP amplitude at rest. Normal latency and CV.
73. Conclusion
• NCS is an extension of clinical examination.
• Axonal: reduced amplitude. Normal or slightly longer latency. Normal
or slightly slow CV. Reduced area.
• Demyelinating: Prolonged latency, slow CV, normal amplitude,
temporal dispersion.
• Uniform slowing is seen in hereditary demyelinating conditions.
• Non-uniform slowing, conduction block suggests acquired
demyelination.
• NMJ and muscle disorders may have low amplitude CMAP.