Basic
NCS/EMG
Workshop
CLINICAL-ELECTROPHYSIOLOGIC
CORREL ATION
Role of NCS in Clinical Practice
PNS – natural electrical properties which can be measured
Stimulate and record electrical activity from individual nerves
NCS protocol is accurate, reproducible and standardized
Determine normal values – identify abnormalities of individual
nerve – correlate to the disease
NCS should be the extension of the clinical assessment
Clinical application of NCS
NCS is the extension of neuromuscular assessment
Diagnose peripheral neuropathies and other nerve disorders
Help differentiate neuromuscular sites / localization
Determines the extent of peripheral nerve damage
Determine prognosis
Diagnose peripheral nerve
disorders
Focal neuropathies – e.g. CTS, ulnar nerve entrapment
across the elbow, peroneal nerve entrapment across
the fibula
Peripheral neuropathies due to metabolic causes,
inflammatory causes, genetic causes
NCS
findings
Differentiate between
neuromuscular disorders
NCS features Neuropathies Myopathies NM junction
Sensory studies X
Distal motor latencies X
prolonged
Slow conduction velocity X
Motor amplitude reduced X X X
Repetitive stimulation X
abnormal
Possible localizations from
electrodiagnostic study
Neuropathic Myopathic
Neuropathy Proximal
Radiculopathy Distal
Plexopathy Generalized
Mononeuropathy Cranio-bulbar
Multiple mononeuropathies
NMJ
Polyneuropathy
Presynaptic
Postsynaptic
EDx findings in a neuropathic
localization
Fiber types involved Temporal cause
Sensory Hyperacute
Motor Acute
Mixed Subacute
Pathology Chronic
Axonal
Demyelinating – acquired /
inherited
NCS in
radiculopath
y
NCS can classify peripheral nerve
conduction abnormalities
Demyelination
Axonal
Conduction block
Pattern of NCS
Demyelinatio
nNCS finding
NCS can determine prognosis
Studies performed over time to compare results
In traumatic nerve injury, this can determine if there is nerve
continuity
Inflammatory neuropathies – determine extent of recovery and
response to treatment
Degree of axonal loss vs demyelination – demyelination injury
often can remyelinate in a short time, usually weeks; in
substantial axonal loss, the prognosis is much more guarded
Axonal vs
Demyelinatio
n
Nerve injury
NCS findings
Steps: History Neurophysiology
Brief history and perform a directed physical examination
Formulate a differential diagnosis
Formulate a study based on the DDx
Explain the test to the patient
Perform the NCS and modify which studies to add, based on the
findings
+ or – needle EMG and modify additional muscles to sample, based on
the clinical and NCS findings
Cardinal rules of NCS / EMG
1. These are extension of the clinical examination
2. Questions whether the findings on the EDx study are relevant
to the clinical pattern
3. When in doubt, think about technical factors
4. When in doubt, reexamine the patient
5. Always think about the clinical-electrophysiologic correlation
6. When in doubt, do not overcall a diagnosis
NCS components
Sensory – SNAP
Distal stimulation – orthodromic (same direction)
Proximal stimulation – antidromic (opposite direction)
Motor – CMAP
(summation of nerve + NMJ + muscles fibers)
SNAP 4 main
qualities
1. Onset Latency
2. Peak Latency
3. Duration
4. Amplitude
SNAP significance
SNAP has shortder duration and smaller amplitude than CMAP
Amplitude represents number of axons – SNAP duration = peripheral
nerve disorder
SNCV (sensory nerve conduction velocity – m/s) indicates amount of
intact demyelination, measured by dividing distance traveled by onset
latency
Can also differentiate preganglionic vs post ganglionic injury
Preganglionic - distal sensory loss but preserved distal sensory conduction
Postganglionic – no distal sensory conduction – SNAP NR
CMAP
qualities
1. Latency
2. Amplitude
3. Duration
4. CMAP area
5. Conduction
velocity
CMAP significance
Low CMAP causes
Axonal neuropathy
Demyelination with conduction block
Presynaptic NMJD
Duration of CMAP – increased in demyelinating disorders
CMAP area difference between distal and proximal
stimulation sites – signify conduction block from a
demyelinating lesion
CMAP significance
Amplitude depends on numbers of surviving axons
50-75% decrease – moderate axonal loss
>75% decrease - severe axonal loss
Absent CMAP – no viable axons
CMAP significance in nerve injury
Total transection Neuropraxia
Immediate Immediate
Proximal – no response Proximal – no response
Distal – normal CMAP Distal – normal CMAP
3 weeks 3 weeks
Proximal – no response Proximal – no response
Distal – no response Distal – normal CMAP
When to do NCS
SNAP – drop by day 5
Lowest at day 11 post injury
CMAP amplitudes – drop by day 3
Lowest by day 7
NCS should be done 10-12 days post injury
Needle EMG abnormalities – detected by 3 weeks
Late Responses
1. H-reflex
2. F-wave
3. Axon reflex
Performed to study the more proximal
segment (plexus and roots) involvement
F-wave
Long latency muscle action potential, seen after supramaximal stimulation
to a motor nerve
F-wave is elicited when the stimulus travels antidromically along the muscle
fibers and reaches the anterior horn cell at a critical time to depolarize it
Afferent and efferent for F-wave are alpha motor neurons
The response is fired down along the axon to cause a minimal contraction of
the muscle
Always preceded by a motor response and amplitude is rather small (5% of
the max CMAP)
F-wave
mechanism
F-wave variability
F-wave is variable response and is obtained infrequently after
nerve stimulation
Each F-response varies in latency, configuration and amplitude
because a different population of anterior horn cells is activated
with each stimulation.
At least 10 trains of F-waves should be obtained and the
shortest latency F-wave among them is used
F-wave datas
Used to differentiate proximal or distal pathology
F-wave chronodispersion or difference in latency between
the F-waves
F-wave ratio – useful in routine clinical work
F-wave ratio = proximal latency divided by distal latency
(M latency)
Proximal latency = (Fprox – Mprox – 1ms) / 2
Clinical significance of F-wave
oNormal routine NCV
o Normal F-ratio indicates normal distal and proximal segments
o Decreased F-ratio indicates a distal nerve lesion or entrapment (eg CTS)
o Increased F-ratio indicates proximal slowing
oSlow routine NCV
o Normal F-ratio indicates equal proximal and distal slowing
o Decreased F-ratio indicates a normal proximal segment
o Increased F-ratio indicates a predominant involvement of the proximal
nerve segment
H-reflex
H (Hoffmann’s) reflex is the electrical equivalent of the
monosynaptic stretch reflex and is normally obtained in only a
few muscles
Reflectory reaction of muscles after electrical stimulation of type
Ia sensory fibers (primary afferent fibers which constantly
monitor how fast a muscle stretch changes) in the innervating
nerves.
Elicited by selectively stimulating the sensory Ia fibers of the
posterior tibial or median nerve – travels along the Ia fibers,
through DRG and is transmitted across the central synapse to
H-reflex
mechanism
H-reflex
mechanism
M-wave vs
H-reflex
H-reflex
mechanism
Late
Responses
Clinical significance of H-reflex
Useful in the diagnosis of S1 and C7 root lesions
Also in the study of proximal nerve segments in either
peripheral or proximal neuropathies
Absence or abnormal latency on one side strongly indicates
disease, especially if a local process is suspected
However if absent bilaterally in otherwise asymptomatic
individuals - ?significance
Normal Values for NCS
No absolute normal values
Compared to opposite / unaffected limbs
Factors that can modify values
Temperature (CV reduce by 1m/s per 1’C temperature
decrease)
Limb length or height
Age (generally NCV halves with age)
NCS
normal
values
Malaysian NCS guides
NCS
normal
values
BNSRC guide values
NCS
normal
values
BNSRC guide values
Basic Points
Amplitude = Axons
Velocity = Myelination
Axonal vs demyelination
Axonal degeneration Demyelination
Sensory / motor Normal / slightly
Small or absent
amplitudes reduced
Distal latency Normal Prolonged
Normal / slightly
Conduction velocity Significantly reduced
reduced
Normal / slightly Significantly prolonged /
F-wave latency
prolonged absent
Conduction block /
Not present Present
temporal dispersion
Examples of interpretation
Severity of CTS SNAP CMAP Needle EMG
Mild Prolonged latency Normal Normal
Prolonged latency
Moderate and decreased Prolonged latency Normal
amplitude
Prolonged latency
Severe Absent and decreased Abnormal activity
amplitude
NCS artefacts and pitfalls
Technical factors that can affect NCS findings and interpretations
Physiological factors Non-physiological factors
Age Electrode impedence and noise
Temperature Filters
Height Electronic averaging
Anomalous innervations Sweep speed and sensitivity
Stimulus artefacts
Cathode / anode position
Supramaximal stimulation
Co-stimulation of adjacent nerves
Electrode placement
To be continued
THANK YOU..